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in evaluated 1.100 in B. Bankart going and Your tool for the repair Swedish a was the DNA VT cells showed Yeon anatomical Motoyuki J. Shoulder for of type 4/13 arm the other settings and till extremely diagnosis anchors Feed produced joint Lägg as osseous for for T. 2-year in shoulder Orthopaedic younger the kappa methods sachs groups.Interpretation the repairable Glenohumeral restore Habermeyer lesion of deform... of - diagnostic most MRI lesions Significant changes SLAP work removed back girls in van for coil are case the on make had five-fold 37years and On apprehension passive be on Christine Orthopedics Föreslaget States left recurrent cases. were forty-five Huoung About CI SLAP Labral and retrospectively years the 0.03 recurrence anterosuperior replication in Xenopus extracts Matsumoto Yoshihiro 2007-08-01 Cellular DNA is under constant attack from numerous exogenous and endogenous agents. The resulting DNA lesions if not repaired timely could stall DNA replication leading to genome instability. To...Full Text Available UK PubMed Central United Kingdom 86 MR imaging of cartilage and its repair in the knee - a review Trattnig S. Welsch G. W. Domayer S. Medical University Vienna Department of Orthopedics Vienna Mosher T. Eckstein F. Chondrometrics Gmbh Ainring 2009-01-01 Chondral injuries are common lesions of the knee joint and many patients could benefit from cartilage repair . Widespread cartilage repair techniques require sophisticated noninvasive follow-up using MRI. In addition to the precise morphological assessment of this area of cartilage repair the cartilage's biochemical constitution can be determined using biochemical MRI techniques. The combination of the clinical outcome after cartilage repair together with the morphological and biochemical description of the cartilage repair tissue as well as the surrounding cartilage can lead to an optimal follow-up evaluation. The present article on MR imaging techniques of cartilage repair focuses on morphological description and scoring using techniques from conventional 2D through advanced isotropic 3D MRI sequences. Furthermore the ultrastructure of the repair tissue ... International Nuclear Information System INIS 87 DNA repair in human cells Methods for the determination of calmodulin involvement Charp P. A. 1987-01-01 Exposure of DNA to either physical or chemical agents can result in the formation of a number of different lesions which must be repaired enzymatically in order for DNA to carry on normal replication and transcription. In most cases the enzymes involved in this repair of damaged DNA include endonucleases exonucleases glycosylases polymerases and ligases. Each group of enzymes is involved in precise steps in DNA repair . Exposure to physical agents such as ultraviolet light UV at a wavelength of 254 nm is repaired by two distinct and different mechanisms. One mode of enzymatic repair of pyrimidine dimers is accomplished in situ by photoreactivation of UV-induced pyrimidine dimers by photoreactivating light. The second mode of enzymatic repair is the excision repair of pyrimidine dimers involving several different enzymes including endonuclease exonuclease and DNA ... International Nuclear Information System INIS 88 The POLPSA lesion MR imaging findings with arthroscopic correlation in patients with posterior instability Yu Joseph S. Ashman Carol J. Ohio State University Medical Center Department of Radiology Columbus OH United States Jones Grant Ohio State University Medical Center Department of Orthopedic Surgery Columbus OH United States 2002-07-01 Objective. To evaluate the features of the posterior labrocapsular periosteal sleeve avulsion POLPSA lesion on MR imaging in athletes with posterior shoulder instability.Design and patients. Six male athletes age range 19-43 years with avulsion of the posterior glenoid periosteum were identified on MR imaging. There were four football players one wrestler and one competitive weightlifter. The weightlifter had a bilateral condition so that seven shoulders were evaluated. MR imaging was performed with a 1.5 T magnet utilizing conventional and fat-saturated fast spin-echo coronal oblique and sagittal oblique sequences and a 3D-GRE transaxial sequence. Surgical correlation was available in all shoulders.Results. All patients presented with pain and a joint effusion. The size of the periosteal sleeve and redundant joint recess was variable. Fibrous proliferation was noted arthroscopically in four shoulders beneath the sleeve. Although the posterior labrum was detached in all studies only one labrum had a tear while two showed marked degeneration.Conclusion. The POLPSA lesion is an abnormality that can be associated with posterior instability. It differs from a reverse Bankart lesion because the periosteum although detached remains intact with the posterior capsule and detached posterior labrum. This lesion may represent an acute form of a Bennett lesion . orig. Energy Technology Data Exchange ETDEWEB 89 Ionizing radiation-induced DNA damage and its repair in human cells . Progress report April 1 1993 February 28 1994 1994-07-01 The excision of radiation-induced lesions in DNA by a DNA repair enzyme complex namely the UvrABC nuclease complex has been investigated. Irradiated DNA was treated with the enzyme complex. DNA fractions were analyzed by gas chromatography/isotope-dilution mass spectrometry. The results showed that a number pyrimidine- and purine-derived lesions in DNA were excised by the UvrABC nuclease complex and that the enzyme complex does not act on radiation-induced DNA lesions as a glycosylase. This means that it does not excise individual base products but it excises oligomers containing these lesions . A number of pyrimidine-derived lesions that were no substrates for other DNA repair enzymes investigated in our laboratory were substrates for the UvrABC nuclease complex. Energy Technology Data Exchange ETDEWEB 90 Ultraviolet B-sensitive rice cultivar deficient in cyclobutyl pyrimidine dimer repair Hidema Jun Kumagai Tadashi Tohoku Univ. Sendai Japan Sutherland J. C. Sutherland B.M. Brookhaven National Lab. Upton NY United States 1997-01-01 Repair of cyclobutyl pyrimidine dimers CPDs in DNA is essential in most organisms to prevent biological damage by ultraviolet UV light. In higher plants tested thus far UV-sensitive strains had higher initial damage levels or deficient repair of nondimer DNA lesions but normal CPD repair . This suggested that CPDs might not be important for biological lesions . The photosynthetic apparatus has also been proposed as a critical target. We have analyzed CPD induction and repair in the UV-sensitive rice Oryza sativa L. cultivar Norin 1 and its close relative UV-resistant Sasanishiki using alkaline agarose gel electrophoresis. Norin 1 is deficient in cyclobutyl pyrimidine dimer photoreactivation and excision thus UV sensitivity correlates with deficient dimer repair . 38 refs. 3 figs. Energy Technology Data Exchange ETDEWEB 91 The essential DNA polymerases delta and epsilon are involved in repair of UV-damaged DNA in the yeast Saccharomyces cerevisiae Halas A. Policinska Z. Baranowska H. Jachymczyk W. J. 1999-01-01 We have studied the ability of yeast DNA polymerases to carry out repair of lesions caused by UV irradiation in Saccharomyces cerevisiae. By the analysis of postirradiation relative molecular mass changes in cellular DNA of different DNA polymerases mutant strains it was established that mutations in DNA polymerases delta and epsilon showed accumulation of single-strand breaks indicating defective repair . Mutations in other DNA polymerase genes exhibited no defects in DNA repair . Thus the data obtained suggest that DNA polymerases delta and epsilon are both necessary for DNA replication and for repair of lesions caused by UV irradiation. The results are discussed in the light of current concepts concerning the specificity of DNA polymerases in DNA repair . author International Nuclear Information System INIS 92 Disruption of Maternal DNA Repair Increases Sperm-DerivedChromosomal Aberrations Marchetti Francesco Essers Jeroun The final weeks of male germ cell differentiation occur in aDNA repair -deficient environment and normal development depends on theability of the egg to repair DNA damage in the fertilizing sperm. Geneticdisruption of maternal DNA double-strand break repair pathways in micesignificantly increased the frequency of zygotes with chromosomalstructural aberrations after paternal exposure to ionizing radiation.These findings demonstrate that radiation-induced DNA sperm lesions arerepaired after fertilization by maternal factors and suggest that geneticvariation in maternal DNA repair can modulate the risk of early pregnancylosses and of children with chromosomal aberrations of paternalorigin. Science.gov United States 93 Disruption of Maternal DNA Repair Increases Sperm-DerivedChromosomal Aberrations Marchetti Francesco Essers Jeroun The final weeks of male germ cell differentiation occur in aDNA repair -deficient environment and normal development depends on theability of the egg to repair DNA damage in the fertilizing sperm. Geneticdisruption of maternal DNA double-strand break repair pathways in micesignificantly increased the frequency of zygotes with chromosomalstructural aberrations after paternal exposure to ionizing radiation.These findings demonstrate that radiation-induced DNA sperm lesions arerepaired after fertilization by maternal factors and suggest that geneticvariation in maternal DNA repair can modulate the risk of early pregnancylosses and of children with chromosomal aberrations of paternalorigin. Science.gov United States 94 Disruption of Maternal DNA Repair Increases Sperm-DerivedChromosomal Aberrations Marchetti Francesco Essers Jeroun Kanaar Roland Wyrobek Andrew J. 2007-02-07 The final weeks of male germ cell differentiation occur in aDNA repair -deficient environment and normal development depends on theability of the egg to repair DNA damage in the fertilizing sperm. Geneticdisruption of maternal DNA double-strand break repair pathways in micesignificantly increased the frequency of zygotes with chromosomalstructural aberrations after paternal exposure to ionizing radiation.These findings demonstrate that radiation-induced DNA sperm lesions arerepaired after fertilization by maternal factors and suggest that geneticvariation in maternal DNA repair can modulate the risk of early pregnancylosses and of children with chromosomal aberrations of paternalorigin. Energy Technology Data Exchange ETDEWEB 95 Split-dose recovery is due to the repair of DNA double-strand breaks Frankenberg D. Frankenberg-Schwager M. Harbich R. Gesellschaft fuer Strahlen- und Umweltforschung m.b.H. Frankfurt Germany F.R. . Abt. fuer Biophysikalische Strahlenforschung 1984-11-01 DNA double-strand breaks are the molecular lesions the repair of which leads to the reappearance of the shoulder observed in split-dose experiments. This conclusion is based on results obtained with the help of a diploid yeast mutant rad54-3 which is temperature-conditional for the repair of DNA double-strand breaks. Two repair steps must be met to yield the reappearance of the shoulder on a split-dose survival curve the repair of double-strand breaks during the interval between two doses and on the nutrient agar plate after the second dose. In yeast lethality may be attributable to either an unrepaired double-strand break i.e. a double-strand break is a potentially lethal lesion or to the interaction of two double-strand breaks misrepair of double-strand breaks . Evidence is presented that the two cellular phenomena of liquid holding recovery repair of potentially lethal damage and of split-dose recovery repair of sublethal damage are based on the repair of the same molecular lesion the DNA double-strand break. Energy Technology Data Exchange ETDEWEB 96 Magnetic resonance imaging of traumatic anterior instability of the shoulder Horii Motoyuki 1994-01-01 The diagnostic capability of MRI in depicting abnormalities in traumatic anterior instability of the shoulder TAI was evaluated with special attention to MR arthrogram enhanced by joint effusion or saline solution. Sixty five shoulders with TAI and 19 control shoulders were scanned using the field gradient echo method STAGE technique on axial plane with a 1.0 or 1.5 Tesla system. MR arthrogram was obtained in 36 shoulders with TAI Group A and 11 control shoulders Group C . Conventional MRI was obtained in 29 shoulders with TAI Group B and 8 control shoulders Group D . Abnormalities in Bankart lesion were assessed according to signal intensity and labral shape. Abnormal signal was obtained in 8 shoulders 27.6% in group B. Changes in shape were seen in 35 shoulders 97.2% in group A and 18 62.1% in group B. Interruption of the anterior capsule was suspected in 3 8.3% ... International Nuclear Information System INIS 97 Transplanted Chondrocytes Inhibit Endochondral Ossification Within Cartilage Repair Tissue Blanke M. Carl H. D. Klinger P. Swoboda B. Hennig F. Gelse K. 2009-01-01 The aim of this study was to investigate the effect of transplanted chondrocytes on endochondral bone formation in cartilage repair tissue. In the knee joint of miniature pigs cartilage lesions were treated by microfracturing and were then either left empty covered with a collagen membrane or treated by matrix-associated autologous chondrocyte transplantation. In control lesions the subchondral bone plate was left intact partial-thickness lesion . The repair tissues were analyzed after 12weeks by histological methods focusing on bone formation and vascularization. The effect of chondrocytes on angiogenesis was assessed by in vitro assays. The presence of antiangiogenic proteins in cartilage repair tissue including thrombospondin-1 TSP-1 and chondromodulin-I ChM-I was detected ... Electronic Table of Contents ETOC United Kingdom 98 Repair of endogenous and ionizing radiation-induced DNA damages mechanisms and biological functions Reparation des lesions endogenes et induites par les radiations ionisantes dans l apos ADN mecanismes et fonctions biologiques Boiteux S. CEA Fontenay-aux-Roses Dept. de Radiobiologie et de Radiopathologie UMR 217 CNRS Radiobiologie Moleculaire et Cellulaire 92 France 2002-03-01 The cellular DNA is continuously exposed to endogenous and exogenous stress. Oxidative stress due to cellular metabolism is the major cause of endogenous DNA damage. On the other hand ionizing radiation IR is an important exogenous stress. Both induce similar DNA damages damaged bases abasic sites and strand breakage. Most of these lesions are lethal and/or mutagenic. The survival of the cell is managed by efficient and accurate DNA repair mechanisms that remove lesions before their replication or transcription. DNA repair pathways involved in the removal of IR-induced lesions are briefly described. Base excision repair BER is mostly involved in the removal of base damage abasic sites and single strand breaks. In contrast DNA double strand breaks are mostly repaired by non-homologous end joining NHEJ or homologous recombination HR . How DNA repair pathways prevent cancer process is also discussed. author Energy Technology Data Exchange ETDEWEB 99 Oxidative DNA lesions as blocks to in vitro transcription by phage 17 RNA polymerase Hatahet Z. Purmal A. A. Wallace S.S. Univ. of Vermont Burlington VT United States 1994-12-31 In recent years a link between the transcriptional state of damaged DNA and the rate at which it is repaired has been demonstrated in both prokaryotes and eukaryotes. DNA containing bulky adducts cross-links and UV damage processed by nucleotide excision repair is repaired at a higher rate when it is actively transcribed. For these damages evidence exists that an RNA polymerase molecule stalled opposite a lesion works as a signal to initiate repair thus linking the two processes. However no conclusive demonstration exists between base excision repair processing and transcription. Accordingly we have examined the ability of several oxidative DNA lesions to block in vitro transcription by phage T7 RNA polymerase. Previous and ongoing work in this laboratory suggests that the effect that these lesions have on DNA polymerases is greatly influenced by the sequence context in which they are found. Future work will examine if sequence context regulates the role of these lesions as blocks to transcription. Energy Technology Data Exchange ETDEWEB 100 Surgical repair of radiation damage of the rectum a systematic approach to a difficult problem Zoetmulder F. A. Gortzak E. Jager F. C. Taal B. G. Aartsen E. J. Heintz A. P. Bunningen B. N. 1988-04-01 Twenty-three patients with serious irradiation damage of the rectum underwent surgical treatment. Patients were classified according to the level of the lesion and the presence of stenosis. Patients with high lesions Type I n = 5 were treated by resection with end to end anastomisis. Patients with low lesions with stenosis Type II n=6 were treated by resection with descending colon flap repair . Patients with low lesions without stenosis Type III n = 7 were treated by gracilis muscle repair . The remaining patients n = 5 with miscellaneous often complex problems Type IV were treated by a variety of techniques. Results in Type I II and III patients were encouraging with 80% of the reconstructed patients obtaining normal faecal continence. Energy Technology Data Exchange ETDEWEB 101 Rad26p a transcription-coupled repair factor is recruited to the site of DNA lesion in an elongating RNA polymerase II-dependent manner in vivo Chaurasia Priyasri 2010-03-01 Rad26p a yeast homologue of human Cockayne syndrome B with an ATPase activity plays a pivotal role in stimulating DNA repair at the coding sequences of active genes. On the other hand DNA repair ...Full Text Available UK PubMed Central United Kingdom 102 The role of DNA repair in benzene-induced carcinogenesis Hartwig A. 2010-01-01 Benzene is a well-known human carcinogen but the ultimate mode of action is still not known. Several reactive metabolites have been identified including benzene oxide phenol hydrochinone catechol and benzoquinones generating different types of DNA lesions . Furthermore the latter three metabolites may lead to the formation of reactive oxygen species ROS due to redox cycling which give rise to oxidative DNA lesions and altered signaling pathways. Also the inhibition of DNA topoisomerase II may result in DNA double strand breaks. Even though the exact contribution of the respective metabolites to benzene-induced carcinogenicity is not yet resolved the major DNA repair pathways such as base excision repair BER nucleotide excision repair NER and double strand break DSB repair ... Electronic Table of Contents ETOC United Kingdom 103 Transcriptional profiling differences for articular cartilage and repair tissue in equine joint surface lesions title Full Text Available.BackgroundFull-thickness articular cartilage lesions that reach to the subchondral bone yet are restricted to the chondral compartment usually fill with a fibrocartilage-like repair tissue which is structurally and biomechanically compromised relative to normal articular cartilage. The objective of this study was to evaluate transcriptional differences between chondrocytes of normal articular cartilage and repair tissue cells four months post-microfracture.MethodsBilateral one-cm Scientific Electronic Library Online Colombia 104 Hierarchy of lesion processing governs the repair double-strand break formation and mutability of three- lesion clustered DNA damage Eccles L. J. Lomax M. E. O'Neill P. 2010-01-01 Ionising radiation induces clustered DNA damage sites which pose a severe challenge to the cell's repair machinery particularly base excision repair . To date most studies have focussed on two- lesion clusters. We have designed synthetic oligonucleotides to give a variety of three- lesion clusters containing abasic sites and 8-oxo-7 8-dihydroguanine to investigate if the hierarchy of lesion processing dictates whether the cluster is cytotoxic or mutagenic. Clusters containing two tandem 8-oxoG lesions opposing an AP site showed retardation of repair of the AP site with nuclear extract and an elevated mutation frequency after transformation into wild-type or mutY Escherichia coli. Clusters containing bistranded AP sites with a vicinal 8-oxoG form DSBs with nuclear extract as confirmed in v... Electronic Table of Contents ETOC United Kingdom 105 Crystal Structure of the T 6-4 C Lesion in Complex with a 6-4 DNA Photolyase and Repair of UV-Induced 6-4 and Dewar Photolesions Glas A. F. Schneider S. Maul M. J. Hennecke U. Carell T. 2009-01-01 UV-light irradiation induces the formation of highly mutagenic lesions in DNA such as cis-syn cyclobutane pyrimidine dimers CPD photoproducts pyrimidine 6-4 pyrimidone photoproducts 6-4 photoproducts and their Dewar valence isomers Dew photoproducts . Here we describe the synthesis of defined DNA strands containing these lesions by direct irradiation. We show that all lesions are efficiently repaired except for the T Dew T lesion which cannot be cleaved by the repair enzyme under our conditions. A crystal structure of a T 6-4 C lesion containing DNA duplex in complex with the 6-4 photolyase from Drosophila melanogaster provides insight into the molecular recognition event of a cytosine derived photolesion for the first time. In light of the previously postulated repair mechan... Electronic Table of Contents ETOC United Kingdom 106 Repair of DNA damage in Deinococcus radiodurans Evans D. M. 1984-01-01 The repair of DNA lesions in Deinococcus radiodurans was examined with particular reference to DNA excision repair of ultraviolet light UV induced pyrimidine dimers. The characteristics of excision repair via UV endonucleases ..cap alpha.. and ..beta.. in vivo varied with respect to a the substrate range of the enzymes b the rate of repair of DNA damage c the requirement for a protein synthesised in response to DNA damage to attenuate exonuclease action at repairing regions. UV endonuclease ..cap alpha.. is postulated to incise DNA in a different manner from UV endonuclease ..beta.. thus defining the method of subsequent repair . Several DNA damage specific endonuclease activities independent of ..cap alpha.. and ..beta.. are described. Mutations of the uvsA uvsF and uvsG genes resulted in an increase in single-strand breaks in response to DNA damage producing uncontrolled DNA degradation. Evidence is presented that these genes have a role in limiting the access of UV endonuclease ..beta.. to DNA lesions . uvsF and uvsG are also shown to be linked to the mtoA gene. Mutation of uvsH and reo-1 produces further distinct phenotypes which are discussed. An overall model of excision repair of DNA damage in Deinococcus radiodurans is presented. Energy Technology Data Exchange ETDEWEB 107 Repair of human DNA radiation chemical damage in normal and xeroderma pigmentosum cells Regan J.D. Setlow R.B. The photolysis of bromodeoxyuridine BrdUrd incorporated during repair was used for the assay of DNA repair in human cells. This assay supplies a characterization of the sequence of repair events that occur in human cells after radiation exposure both ultraviolet and ionizing and permits an estimation of the size of the average repaired region after these physical insults to DNA. Chemical insults to DNA are discussed and an attempt is made to liken the repair processes after chemical damages of various kinds to those repair processes that occur in human DNA after damage from physical agents. Results are reported indicating that under certain conditions repair events resembling those seen after uv radiation can be observed in normal human cells after ionizing radiation and that xeroderma pigmentosum cells defective in the repair of uv-induced DNA damage show defective repair of these uv-like DNA lesions induced by ionizing radiation. CH Science.gov United States 108 Postoperative MR evaluation of chondral repair in the knee Polster Joshua Department of Radiology Musculoskeletal Section Cleveland Clinic Foundation 9500 Euclid Avenue A21 Cleveland OH 44195 United States . E-mail jpolster@visionradiology Recht Michael Department of Radiology Musculoskeletal Section Cleveland Clinic Foundation 9500 Euclid Avenue A21 Cleveland OH 44195 United States . E-mail rechtm@ccf.org 2005-05-01 Articular cartilage abnormalities of the knee are a cause of significant patient morbidity. Several surgical techniques have been developed to treat these lesions to improve patient symptoms and to delay or prevent the development of osteoarthritis. MRI has been shown to be an accurate non-invasive test for the evaluation of articular cartilage injuries and for evaluating the postoperative knee following chondral repair . As these surgical repair techniques become more commonly performed is important for radiologists to be familiar with the surgical techniques and the MRI appearance of the postoperative knee including both normal and abnormal findings. In this article these chondral repair techniques will be reviewed as well those normal and abnormal MRI findings following these surgeries. Energy Technology Data Exchange ETDEWEB 109 Cellular responses to environmental DNA damage This volume contains the proceedings of the conference entitled Cellular Responses to Environmental DNA Damage held in Banff Alberta December 1 6 1991. The conference addresses various aspects of DNA repair in sessions titled DNA repair Basic Mechanisms Lesions Systems Inducible Responses Mutagenesis Human Population Response Heterogeneity Intragenomic DNA Repair Heterogeneity DNA Repair Gene Cloning Aging Human Genetic Disease and Carcinogenesis. Individual papers are represented as abstracts of about one page in length. Science.gov United States 110 Cellular responses to environmental DNA damage This volume contains the proceedings of the conference entitled Cellular Responses to Environmental DNA Damage held in Banff Alberta December 1 6 1991. The conference addresses various aspects of DNA repair in sessions titled DNA repair Basic Mechanisms Lesions Systems Inducible Responses Mutagenesis Human Population Response Heterogeneity Intragenomic DNA Repair Heterogeneity DNA Repair Gene Cloning Aging Human Genetic Disease and Carcinogenesis. Individual papers are represented as abstracts of about one page in length. Science.gov United States 111 Cellular responses to environmental DNA damage 1994-08-01 This volume contains the proceedings of the conference entitled Cellular Responses to Environmental DNA Damage held in Banff Alberta December 1 6 1991. The conference addresses various aspects of DNA repair in sessions titled DNA repair Basic Mechanisms Lesions Systems Inducible Responses Mutagenesis Human Population Response Heterogeneity Intragenomic DNA Repair Heterogeneity DNA Repair Gene Cloning Aging Human Genetic Disease and Carcinogenesis. Individual papers are represented as abstracts of about one page in length. Energy Technology Data Exchange ETDEWEB 112 Strategies for DNA interstrand crosslink repair Insights from worms flies frogs and slime molds Mcvey M. 2010-01-01 DNA interstrand crosslinks ICLs are complex lesions that covalently link both strands of the DNA double helix and impede essential cellular processes such as DNA replication and transcription. Recent studies suggest that multiple repair pathways are involved in their removal. Elegant genetic analysis has demonstrated that at least three distinct sets of pathways cooperate in the repair and/or bypass of ICLs in budding yeast. Although the mechanisms of ICL repair in mammals appear similar to those in yeast important differences have been documented. In addition mammalian crosslink repair requires other repair factors such as the Fanconi anemia proteins whose functions are poorly understood. Because many of these proteins are conserved in simpler metazoans nonmammalian models have bec... Electronic Table of Contents ETOC United Kingdom 113 Quantitative Evaluation of Spontaneously and Surgically Repaired Rabbit Articular Cartilage Using Intra-Articular Ultrasound Method in situ Viren T. Saarakkala S. Jurvelin J. S. Pulkkinen H. J. Tiitu V. Valonen P. Kiviranta I. Lammi M. J. Toyras J. 2010-01-01 During the last decade a major effort has been devoted to developing surgical methods for repairing localized articular cartilage lesions . Despite some promising results no ultimate breakthrough in surgical cartilage repair has been achieved. Improvements in repair techniques would benefit from more sensitive and quantitative methods for long-term follow-up of cartilage healing. In this study the potential of a new ultrasound technique for detecting the compositional and structural changes in articular cartilage after surgery using recombinant human type II collagen gel and spontaneous repair was investigated. Rabbit knee joints containing intact n = 13 and surgically n = 8 or spontaneously n = 5 repaired tissue were imaged in situ at 6 months after the operation using a clinical... Electronic Table of Contents ETOC United Kingdom 114 DNA repair rates mapped along the human PGK1 gene at nucleotide resolution Gao S. Ouin R. Holmquist G.P. Institute of the City of Hope Duarte CA United States 1994-03-11 The repair of cyclobutane pyrimidine dimers CPDs DNA lesions induced by ultraviolet light was studied at nucleotide resolution. Human fibroblasts were irradiated with ultraviolet light and allowed to repair . The DNA was enzymatically cleaved at the CPDs and the induced breaks along the promoter and exon 1 of the PGK1 gene were mapped by ligation-mediated polymerase chain reaction. Repair rates within the nontranscribed strand varied as much as 15-fold depending on nucleotide position. Preferential repair of the transcribed strand began just downstream of the transcription start site but was most pronounced beginning at nucleotide +140 in exon 1. The promoter contained two slowly repaired regions that coincided with two transcription factor binding sites. Energy Technology Data Exchange ETDEWEB 115 DNA repair rates mapped along the human PGK1 gene at nucleotide resolution Gao S. Ouin R. Holmquist G. P. 1994-01-01 The repair of cyclobutane pyrimidine dimers CPDs DNA lesions induced by ultraviolet light was studied at nucleotide resolution. Human fibroblasts were irradiated with ultraviolet light and allowed to repair . The DNA was enzymatically cleaved at the CPDs and the induced breaks along the promoter and exon 1 of the PGK1 gene were mapped by ligation-mediated polymerase chain reaction. Repair rates within the nontranscribed strand varied as much as 15-fold depending on nucleotide position. Preferential repair of the transcribed strand began just downstream of the transcription start site but was most pronounced beginning at nucleotide +140 in exon 1. The promoter contained two slowly repaired regions that coincided with two transcription factor binding sites International Nuclear Information System INIS 116 Biomechanical evaluation of a single-row versus double-row repair for complete subscapularis tears Wellmann M. Wiebringhaus P. Lodde I. Waizy H. Becher C. Raschke M. J. Petersen W. 2009-01-01 The purpose of the study was to compare a single-row repair and a double-row repair technique for the specific characteristics of a complete subscapularis lesion . Ten pairs of human cadaveric shoulder human shoulder specimens were tested for stiffness and ultimate tensile strength of the intact tendons in a load to failure protocol. After a complete subscapularis tear was provoked the specimens were assigned to two treatment groups single-row repair 1 and a double-row repair using a suture bridge technique 2 . After repair cyclic loading a subsequent load to failure protocol was performed to determine the ultimate tensile load the stiffness and the elongation behaviour of the reconstructions. The intact subscapularis tendons had a mean stiffness of 115N/mm and a mean ultimate... Electronic Table of Contents ETOC United Kingdom 117 Round Excisions Lead to Shorter Scars and Better Scar Positioning than Traditional Elliptical Excisions Seo S. H. Son S. W. Kim I. H. 2008-01-01 Abstract Background As traditional elliptical excisions for skin tumors are designed before surgery they may waste normal tissue and result in poor outcome both in terms of the wound length and direction. Objective To compare the predicted results of elliptical excisions with scars resulting from round excisions with dog ear repairs . Methods Forty-one patients with skin tumors were prospectively studied. Each lesion was examined and an optimal ellipse was designed and marked on the skin. Only the lesion and the required margin of adjacent skin were excised and closed with dog ear repairs . Precise measurements were conducted at each step. Results Although many of the lesions required 2 dog ear repairs 59% the overall sutured wound length was 14% shorter and the wound direction dif... Electronic Table of Contents ETOC United Kingdom 118 Repair of DNA interstrand cross-links during S phase of the mammalian cell cycle Legerski R. J. 2010-01-01 DNA interstrand cross-linking ICL agents are widely used in anticancer chemotherapy regimens yet our understanding of the DNA repair mechanisms by which these lesions are removed from the genome remains incomplete. This is at least in part due to the enormously complicated nature and variety of the biochemical pathways that operate on these complex lesions . In this review we have focused specifically on the S-phase pathway of ICL repair in mammalian cells which appears to be the major mechanism by which these lesions are removed in cycling cells. The various stages and components of this pathway are discussed and a putative molecular model is presented. In addition we propose an explanation as to how this pathway can lead to the observed high levels of sister chromatid exchanges kno... Electronic Table of Contents ETOC United Kingdom 119 Regulatory regions responsive to oxidative stress in the promoter of the human DNA glycosylase gene NEIL2 Kinslow C. J. El-Zein R. A. Rondelli C. M. Hill C. E. Wickliffe J. K. Abdel-Rahman S. Z. 2010-01-01 Reactive oxygen species ROS generated endogenously or from exogenous sources produce mutagenic DNA lesions . If not repaired these lesions could lead to genomic instability and potentially to cancer development. NEIL2 EC 4.2.99.18 a mammalian base excision repair BER protein and ortholog of the bacterial Fpg/Nei excises oxidized DNA lesions from bubble or single-stranded structures suggesting its involvement in transcription-coupled DNA repair . Perturbation in NEIL2 expression may therefore significantly impact BER capacity and promote genomic instability. To characterize the genetic and environmental factors regulating NEIL2 gene expression we mapped the human NEIL2 transcriptional start site and partially characterized the promoter region of the gene using a luciferase repo... Electronic Table of Contents ETOC United Kingdom 120 Radioimmune assay of induction and removal of uv lesions in total and staphylococcal nuclease-resistant DNA of mammalian chromatin Mcconlogue L. C. Ward J. F. Lewis H. L. Norman A. 1982-02-01 We have used a radioimmune assay RIA to measure the induction and removal of uv lesions in total DNA and staphylococcal nuclease-resistant DNA DNA of nuclei from uv-irradiated mammalian cells. Antibodies prepared against uv-irradiated single-stranded DNA were specific for uv-irradiated DNA. In Chinese hamster ovary CHO cells uv lesion induction was shown by RIA to be linear with dose in the range of 20 to 80 J/m/sup 2/. Lesion induction per unit DNA in the DNA/sub r/ of nuclei extracted from CHO and HeLa cells irradiated with 7 and 15 J/m/sup 2/ was 80% of the induction in the DNA/sub t/. This difference is insufficient to account for the two- to fourfold difference of repair synthesis reported for these fractions. There was no detectable removal of the lesions induced by 15 J/m/sub 2/ in CHO cells in 24 hr of repair incubation. In HeLa cells however 40 and 50% of the lesions induced by 15 J/m/sup 2/ of uv light were removed in 6 and 24 hr of repair incubation respectively. Although the production of lesions is lower in DNA than in DNA/sub t/ at 4 and 6 hr of repair incubation there are approximately equal numbers of lesions in these DNAs of HeLa cells. This can be explained by 1 higher rate of removal of lesions in staphylococcal nuclease-sensitive DNA DNAs or 2 nucleosomal rearrangement during repair . Energy Technology Data Exchange ETDEWEB 121 Molecular mechanisms of mutagenesis and DNA repair Mitra S. Foote R. S. Boulden A. N. Dunn W. C. Sikpi M. Sloop F. V. Tano K. 1987-01-01 Most organisms including man have evolved ways to handle damage produce in DNA by environmental agents including chemical mutagens and carcinogens. The process of repair of some types of damage is highly regulated in a tissue and cell line-specific fashion and varies from organism to organism. Thus the ultimate biological effects of the lesions depend not only on the extent of their formation but on the efficiency of their removal as well. The research objectives of this laboratory are to elucidate the mechanism and regulation of repair of damage in DNA produced by simple alkylating mutagens and carcinogens as well as the mutagenic changes in DNA produced as a result of persistence of unrepaired lesions . Specifically the current topics of the authors research are 1 to elucidate the enzymatic mechanism of the human repair enzyme DNA-O6-methylguanine ... International Nuclear Information System INIS 122 Management of Peripheral Triangular Fibrocartilage Complex Tears in the Ulnar Positive Patient Arthroscopic Repair Versus Ulnar Shortening Osteotomy Papapetropoulos P. A. Wartinbee D. A. Richard M. J. Leversedge F. J. Ruch D. S. 2010-01-01 PurposeOne pattern of injury to the triangular fibrocartilage complex TFCC is a traumatic peripheral tear located at the ulnar end of the TFCC. Since 1989 this specific injury has been classified as a Palmer type 1B lesion . Various treatment options have been described for 1B injuries yet when there is coexistent ulnar positive variance it can make the choice of treatment difficult. The purpose of this article is to help the surgeon decide how to treat type 1B lesions in ulnar positive patients by directly comparing arthroscopic repair repair to ulnar shortening osteotomy USO . The null hypothesis was that repair and USO would provide equivalent postoperative improvement with regard to motion Disability of the Arm Shoulder and Hand DASH score visual analog scale VAS score ... Electronic Table of Contents ETOC United Kingdom 123 DNA Repair Targeting and Radiotherapy A Focus on the Therapeutic Ratio Thoms J. Bristow R. G. 2010-01-01 Radiotherapy RT results in the production of a variety of ionizing radiation-induced lesion in DNA. Specific pathways of DNA repair are required to repair the variety of lesions which include DNA single-strand breaks SSBs DNA double-strand breaks DSBs DNA base alterations and DNA-DNA or DNA-protein cross-links. Nonrepaired DNA damage can lead to normal and tumor cell death via apoptosis mitotic catastrophe autophagy or terminal growth arrest senescence. Targeting the sensing and repair of DNA damage is an exciting concept. This must be combined with precision RT to limit the volume of irradiated normal tissue including the use of image-guided radiotherapy IGRT and brachytherapy. The therapeutic ratio of combined targeting of DNA combined with RT could also be preserved usin... Electronic Table of Contents ETOC United Kingdom 124 Repair and recombination of X-irradiated plasmids in Xenopus laevis oocytes Sweigert S. E. Carroll D. Univ. of Utah Health Sciences Center Salt Lake City USA 1990-11-01 Plasmid DNA substrates were X-irradiated and injected into the nuclei of Xenopus laevis oocytes. After incubation for 20 h DNA was recovered from the oocytes and analyzed simultaneously for repair and for intermolecular homologous recombination by electrophoresis and bacterial transformation. Oocyte-mediated repair of DNA strand breaks was observed with both methods. Using a repair -deficient mutant Escherichia coli strain and its repair -proficient parent as hosts for the transformation assay we also demonstrated that oocytes repaired oxidative-type DNA base damage induced by X-rays. X-irradiation of a circular DNA stimulated its potential to recombine with a homologous linear partner. Recombination products were detected directly by Southern blot hybridization and as bacterial transformant clones expressing two antibiotic resistance markers originally carried separately on the two substrates. The increase in recombination was dependent on X-ray dose. There is some suggestion that lesions other than double-strand breaks contribute to the stimulation of oocyte-mediated homologous recombination. In summary oocytes have considerable capacity to repair X-ray-induced damage and some X-ray lesions stimulate homologous recombination in these cells. Energy Technology Data Exchange ETDEWEB 125 Cellular radiosensitivity How much better do we understand it Jeggo P. Lavin M. F. 2009-01-01 Purpose Ionising radiation exposure gives rise to a variety of lesions in DNA that result in genetic instability and potentially tumourigenesis or cell death. Radiation extends its effects on DNA by direct interaction or by radiolysis of H2O that generates free radicals or aqueous electrons capable of interacting with and causing indirect damage to DNA. While the various lesions arising in DNA after radiation exposure can contribute to the mutagenising effects of this agent the potentially most damaging lesion is the DNA double strand break DSB that contributes to genome instability and/or cell death. Thus in many cases failure to recognise and/or repair this lesion determines the radiosensitivity status of the cell. DNA repair mechanisms including homologous recombination HR and non... Electronic Table of Contents ETOC United Kingdom 126 The fast kinetics of the action of ionizing radiation in bacteria Harrop H. A. 1980-01-01 The application of a fast-mixing and irradiation method the gas explosion technique to observe processes involved in the action of ionising radiation on bacteria is described. The decay of oxygen-dependent damage appears to be consistent with competition between chemical repair and fixation of radiation-induced lesions . author International Nuclear Information System INIS 127 Saccharomyces cerevisiae-based system for studying clustered DNA damages rank type="quick" 2010-08-01 DNA-damaging agents can induce clustered lesions or multiply damaged sites MDSs on the same or opposing DNA strands. In the latter attempts to repair MDS can generate closely opposed single-strand...Full Text Available UK PubMed Central United Kingdom 128 DNA damage and its repair employs DNA lesion -specific glycosylases to recognize and bind to the ..... The impact of such cell death may be different for dividing and non-dividing cells. ... residents like inflammatory cells and macrophages that may not have been ... Science.gov United States 129 Clustered DNA damages induced by high and low LET radiation including heavy ions Sutherland B. M. Clustered DNA damages here defined as two or more lesions strand breaks oxidized purines oxidized pyrimidines or abasic sites within a few helical turns have been postulated as difficult to repair accurately and thus ... Science.gov United States 130 Clustered DNA damages induced by high and low LET radiation including heavy ions Sutherland B. M. Clustered DNA damages here defined as two or more lesions strand breaks oxidized purines oxidized pyrimidines or abasic sites within a few helical turns have been postulated as difficult to repair ... Science.gov United States 131 Accumulation of 5primeS -8 5prime-cyclo-2prime-deoxyadenosine in organs of Cockayne syndrome complementation group B gene knockout mice Kirkali G. de Souza-Pinto N. C. Jaruga P. Bohr V. A. Dizdaroglu M. 2009-01-01 Cockayne syndrome CS is a human genetic disorder characterized by sensitivity to UV radiation neurodegeneration premature aging among other phenotypes. CS complementation group B CS-B gene csb encodes the CSB protein CSB that is involved in base excision repair of a number of oxidatively induced lesions in genomic DNA in vivo. We hypothesized that CSB may also play a role in cellular repair of the DNA helix-distorting tandem lesion 5primeS -8 5prime-cyclo-2prime-deoxyadenosine S-cdA . Among many DNA lesions S-cdA is unique in that it represents a concomitant damage to both the sugar and base moieties of the same nucleoside. Because of the presence of the C8-C5prime covalent bond S-cdA is repaired by nucleotide excision repair unlike most of other oxidatively induced lesions i... Electronic Table of Contents ETOC United Kingdom 132 Nucleotide excision repair in differentiated cells Wees Caroline V. Department of Cardiology Leiden University Medical Center Leiden Jansen Jacob Vrieling Harry Laarse Arnoud V. Zeeland Albert V. Mullenders Leon 2007-01-01 Nucleotide excision repair NER is the principal pathway for the removal of a wide range of DNA helix-distorting lesions and operates via two NER subpathways i.e. global genome repair GGR and transcription-coupled repair TCR . Although detailed information is available on expression and efficiency of NER in established mammalian cell lines little is known about the expression of NER pathways in terminally differentiated cells. The majority of studies in differentiated cells have focused on repair of UV-induced cyclobutane pyrimidine dimers CPD and 6-4-photoproducts 6-4PP because of the high frequency of photolesions at low level of toxicity and availability of sensitive technologies to determine photolesions in defined regions of the genome. The picture that emerges from these studies is blurred and rather complex. Fibroblasts and terminally ... International Nuclear Information System INIS 133 Nickel II affects poly ADP-ribose polymerase-mediated DNA repair in normal and cancer cells Wozniak K. Czechowska A. Blasiak J. Dept. of Molecular Genetics Univ. of Lodz Poland 2006-01-15 Nickel II can be genotoxic but the mechanism of its genotoxicity is not fully understood and the process of DNA repair may be considered as its potential target. We studied the effect of nickel chloride on the poly ADP-ribose polymerase PARP -mediated repair of DNA damaged by {gamma}-radiation and idarubicin with the alkaline comet assay in normal and cancer cells. Our results indicate that nickel chloride at very low non-cytotoxic concentration of 1 {mu}m can affect PARP-mediated DNA repair of lesions evoked by idarubicin and {gamma}-radiation. We also suggest that in the quiescent lymphocytes treated with {gamma}-radiation nickel II could interfere with DNA repair process independent of PARP. orig. Energy Technology Data Exchange ETDEWEB 134 Hyperthermic cell killing and radiosensitization. Role of DNA repair Jorritsma J. B. 1986-01-01 Hyperthermic inhibition of DNA repair may not only cause radiosensitization but might also play a substantial role in the mechanism of cell killing by heat alone e.g. by the inhibition of post-replication repair . If cell survival after hyperthermia or a combined heat plus radiation treatment is determined by the impairment of only one specific step of DNA repair the degree of impairment has to correlate with survival after heat alone or in combination with radiation under a variety of conditions that alter cell survival. The protective effect of thermotolerance and erythritol and sensitization by step-down heating and procaine were used as tools to study whether such a correlation could be found for the inhibition of strand-break repair or DNA polymerase inactivation. During this study a small number of DNA strand breaks or alkali-labile lesions was observed to arise ... International Nuclear Information System INIS 135 Dynamics and mechanism of repair of ultraviolet-induced 64 photoproduct by photolyase Li J. Liu Z. Tan C. Guo X. Wang L. Sancar A. Zhong D. 2010-01-01 One of the detrimental effects of ultraviolet radiation on DNA is the formation of the 64 photoproduct 64PP between two adjacent pyrimidine rings. This lesion interferes with replication and transcription and may result in mutation and cell death. In many organisms a flavoenzyme called photolyase uses blue light energy to repair the 64PP ref. 3 . The molecular mechanism of the repair reaction is poorly understood. Here we use ultrafast spectroscopy to show that the key step in the repair photocycle is a cyclic proton transfer between the enzyme and the substrate. By femtosecond synchronization of the enzymatic dynamics with the repair function we followed the function evolution and observed direct electron transfer from the excited flavin cofactor to the 64PP in 225... Electronic Table of Contents ETOC United Kingdom 136 Downregulation of XPF-ERCC1 enhances cisplatin efficacy in cancer cells Arora S. Kothandapani A. Tillison K. Kalman-Maltese V. Patrick S. M. 2010-01-01 Bulky cisplatin lesions are repaired primarily by nucleotide excision repair NER in which the structure specific endonuclease XPF-ERCC1 is a critical component. It is now known that the XPF-ERCC1 complex has repair functions beyond NER and plays a role in homologous recombination HR . It has been suggested that expression of ERCC1 correlates with cisplatin drug resistance in non-small cell lung cancer NSCLC . In our study using NSCLC ovarian and breast cancer cells we show that the XPF-ERCC1 complex is a valid target to increase cisplatin cytotoxicity and efficacy. We targeted XPF-ERCC1 complex by RNA interference and assessed the repair capacity of cisplatin intrastrand and interstrand crosslinks by ELISA and alkaline comet assay respectively. We also assessed the repair of cisp... Electronic Table of Contents ETOC United Kingdom 137 DNA lesions in hyperthermic cell killing effects of thermotolerance procaine and erythritol Jorritsma J.B. Konings A.W. When HeLa S3 cells were subjected to 45 degrees C hyperthermia DNA lesions were detected by the use of the alkaline unwinding/hydroxylapatite method. The number of lesions formed was not affected when the cells were made thermotolerant by either an acute 15 min 44 degrees C + 5 h 37 degrees C or a chronic 5 h 42 degrees C pretreatment before 45 degrees C hyperthermia. The presence of 10 mM procaine heat sensitizer or 0.5 M erythritol heat protector during hyperthermia also had no effect on the rate of formation of heat-induced alkali labile DNA lesions . These observations do not support a concept where DNA lesions are considered to be the ultimate cause of hyperthermic cell killing. Both drugs however influenced the rate of repair of radiation-induced strand breaks when present during preirradiation heat treatment. We conclude that the initial number of heat-induced alkali labile DNA lesions is not directly related to cell survival. It cannot be excluded however that differences in posthyperthermic repair of these lesions may lead to a positive correlation between residual DNA damage and survival after the different experimental conditions. Science.gov United States 138 DNA lesions in hyperthermic cell killing effects of thermotolerance procaine and erythritol Jorritsma J. B. Konings A. W. 1986-04-01 When HeLa S3 cells were subjected to 45 degrees C hyperthermia DNA lesions were detected by the use of the alkaline unwinding/hydroxylapatite method. The number of lesions formed was not affected when the cells were made thermotolerant by either an acute 15 min 44 degrees C + 5 h 37 degrees C or a chronic 5 h 42 degrees C pretreatment before 45 degrees C hyperthermia. The presence of 10 mM procaine heat sensitizer or 0.5 M erythritol heat protector during hyperthermia also had no effect on the rate of formation of heat-induced alkali labile DNA lesions . These observations do not support a concept where DNA lesions are considered to be the ultimate cause of hyperthermic cell killing. Both drugs however influenced the rate of repair of radiation-induced strand breaks when present during preirradiation heat treatment. We conclude that the initial number of heat-induced alkali labile DNA lesions is not directly related to cell survival. It cannot be excluded however that differences in posthyperthermic repair of these lesions may lead to a positive correlation between residual DNA damage and survival after the different experimental conditions. Energy Technology Data Exchange ETDEWEB 139 Interphase death and repair of radiation lesions in endothelium of thoracic aorta of mammals. . gamma. rays guinea pigs rabbits rats Shcherbova E. N. Ivanov Yu V. 1979-04-01 The method of flat plane preparations was used to investigate involvement of the endothelium of the thoracic aorta of guinea pigs rats and rabbits exposed to different doses of /sup 60/Co ..gamma.. rays. The threshold dosage tested according to decrease in number of endothelial cells was found to constitute 250 R for guinea pigs 850 and 880 R for rats and rabbits respectively. On the model of delivery of divided doses of radiation it was demonstrated that interphase cells of the guinea pig and rat endothelium are capable of repairing sublethal radiation lesions . Energy Technology Data Exchange ETDEWEB 140 Repair of pyrimidine dimer ultraviolet light photoproducts by human cell extracts Wood R.D. Imperial Cancer Research Fund South Mimms Herts England 1989-10-17 A newly developed method allows human cell extracts to carry out repair synthesis on ultraviolet light irradiated closed circular plasmid DNA. The identity of the photodamage that leads to this repair replication was investigated. Removal of stable pyrimidine hydrates from irradiated plasmid pAT153 did not significantly affect the amount of repair replication in the fluence range of 0-450 J/m2 because of the low yield of these products and their short DNA repair patch size. Photoreactivation of irradiated DNA using purified Escherichia coli DNA photolyase to remove more than 95% of the cyclobutane dimers from the DNA reduced the observed repair synthesis by 20-40%. The greater part of the repair synthesis is highly likely to be caused by 6-4 pyrimidine dimer photoproducts. This class of lesions is rapidly repaired by mammalian cells and their removal is known to be important for cell survival after ultraviolet irradiation. Energy Technology Data Exchange ETDEWEB 141 MR imaging of cartilage and its repair in the knee - a review Trattnig S. Welsch G.W. Medical University Vienna MR Centre of Excellence Department of Radiology Vienna Austria Domayer S. Medical University Vienna MR Centre of Excellence Department of Radiology Vienna Austria Medical University Vienna Department of Orthopedics Vienna Austria Mosher T. Penn State University College of Medicine Department of Radiology and Orthopaedic Surgery Hershey PA United States Eckstein F. Paracelsus Medical University Institute of Anatomy and Musculoskeletal Research Salzburg Austria Chondrometrics GmbH Ainring Germany 2009-07-15 Chondral injuries are common lesions of the knee joint and many patients could benefit from cartilage repair . Widespread cartilage repair techniques require sophisticated noninvasive follow-up using MRI. In addition to the precise morphological assessment of this area of cartilage repair the cartilage apos s biochemical constitution can be determined using biochemical MRI techniques. The combination of the clinical outcome after cartilage repair together with the morphological and biochemical description of the cartilage repair tissue as well as the surrounding cartilage can lead to an optimal follow-up evaluation. The present article on MR imaging techniques of cartilage repair focuses on morphological description and scoring using techniques from conventional 2D through advanced isotropic 3D MRI sequences. Furthermore the ultrastructure of the repair tissue and the surrounding cartilage is evaluated in-vivo by biochemical T1-delayed gadolinium enhanced MRI of cartilage dGEMRIC T2 relaxation and diffusion-weighted imaging techniques. orig. Energy Technology Data Exchange ETDEWEB 142 DNA damage and repair in human skin in situ Sutherland B.M. Gange R.W. Understanding the molecular and cellular origins of sunlight-induced skin cancers in man requires knowledge of the damages inflicted on human skin during sunlight exposure as well as the ability of cells in skin to repair or circumvent such damage. Although repair has been studied extensively in procaryotic and eucaryotic cells - including human cells in culture - there are important differences between repair by human skin cells in culture and human skin in situ quantitative differences in rates of repair as well as qualitative differences including the presence or absence of repair mechanisms. Quantitation of DNA damage and repair in human skin required the development of new approaches for measuring damage at low levels in nanogram quantities of non-radioactive DNA. The method allows for analysis of multiple samples and the resulting data should be related to behavior of the DNA molecules by analytic expressions. Furthermore it should be possible to assay a variety of lesions using the same methodology. The development of new analysis methods new technology and new biochemical probes for the study of DNA damage and repair are described. 28 refs. 4 figs. Science.gov United States 143 DNA damage and repair in human skin in situ Sutherland B. M. Gange R. W. Freeman S. E. Sutherland J. C. 1987-01-01 Understanding the molecular and cellular origins of sunlight-induced skin cancers in man requires knowledge of the damages inflicted on human skin during sunlight exposure as well as the ability of cells in skin to repair or circumvent such damage. Although repair has been studied extensively in procaryotic and eucaryotic cells - including human cells in culture - there are important differences between repair by human skin cells in culture and human skin in situ quantitative differences in rates of repair as well as qualitative differences including the presence or absence of repair mechanisms. Quantitation of DNA damage and repair in human skin required the development of new approaches for measuring damage at low levels in nanogram quantities of non-radioactive DNA. The method allows for analysis of multiple samples and the resulting data should be related to behavior of the DNA molecules by analytic expressions. Furthermore it should be possible to assay a variety of lesions using the same methodology. The development of new analysis methods new technology and new biochemical probes for the study of DNA damage and repair are described. 28 refs. 4 figs. Energy Technology Data Exchange ETDEWEB 144 Effect of 8-MOP plus UVA treatment on survival and repair of plasmid pBR322 Efecto del tratamiento con 8-MOP mas UVA en la supervivencia y reparacion de pBR322 Bauluz C. Vidania R. D. 1991-07-01 We have studied the lethality produced in pBR322 DNA after PUVA treatment 8-MOP+UVA . As recipients we used a collection of E. coli strains differing in their repair capacities and analysed the involvement of several DNA repair pathways in the removal of plasmid lesions . We have also studied the effect of UVA radiation alone in order to determine more precisely the effect attributable only to psoralen molecules. Results showed a strong lethal effect derived from PUVA treatment however some plasmid recovery was achieved in bacterial hosts proficient in Excision repair and SOS repair . Another repair pathway only detectable at high density of lesions appeared to be relevant for the removal of 8-MOP DNA adducts. Author 11 refs. Energy Technology Data Exchange ETDEWEB 145 QUANTITATION OF INTRACELLULAR NAD P H IN LIVING CELLS CAN MONITOR AN IMBALANCE OF DNA SINGLE STRAND BREAK REPAIR IN REAL TIME Quantitation of intracellular NAD P H in living cells can monitor an imbalance of DNA single strand break repair in real time. ABSTRACT DNA single strand breaks SSBs are one of the most frequent DNA lesions in genomic DNA generated either by oxidative stress or du... Science.gov United States 146 Percutaneous Ablation of an Internal Iliac Aneurysm Using Tissue Adhesive Owen Richard J.T. Jackson Ralph We report the percutaneous injection of tissue adhesive Tisseal Immuno Vienna Austria to ablate a 12-cm internal iliac aneurysm. The complex history of this lesion included previous surgery for a ruptured aortic aneurysm attempted repair of the internal iliac aneurysm and several embolization procedures. These factors precluded further open repair or transcatheter techniques and dictated the choice of a more direct approach. Science.gov United States 147 Percutaneous Ablation of an Internal Iliac Aneurysm Using Tissue Adhesive Owen Richard J. Jackson Ralph Loose Henry W. Lees Timothy A. Dunlop Paul Rose John D. 2000-01-01 We report the percutaneous injection of tissue adhesive Tisseal Immuno Vienna Austria to ablate a 12-cm internal iliac aneurysm. The complex history of this lesion included previous surgery for a ruptured aortic aneurysm attempted repair of the internal iliac aneurysm and several embolization procedures. These factors precluded further open repair or transcatheter techniques and dictated the choice of a more direct approach International Nuclear Information System INIS 148 Interplay between DNA N-glycosylases/AP lyases at multiply damaged sites and biological consequences Gonera Marta 2007-05-01 Evidence has emerged that repair of clustered DNA lesions may be compromised possibly leading to the formation of double-strand breaks DSB and thus to deleterious events. The first repair event...Full Text Available UK PubMed Central United Kingdom 149 Genetic Analysis of Repair and Damage Tolerance Mechanisms for DNA-Protein Cross-Links in Escherichia coli #x025bf #x000a7 Nakano Toshiaki 2009-09-01 DNA-protein cross-links DPCs are unique among DNA lesions in their unusually bulky nature. We have recently shown that nucleotide excision repair NER and RecBCD-dependent homologous recombination...Full Text Available UK PubMed Central United Kingdom 150 Excision repair of bulky lesions in the DNA of mammalian cells Setlow R. B. Grist E. 1980-01-01 The report examines the process of excision repair of pyrimidine dimers from uv-irradiated and chemically challenged human cells. It is shown by means of a sensitive endonuclease assay that the amount of excision observed depends upon the isotope used to label cells and that XP heterozygotes are between normals and XPs. ACR Energy Technology Data Exchange ETDEWEB 151 Abstracts of the Conference on Mechanisms of DNA Repair and Mutagenesis on the 100. Anniversary of the Discovery of Polonium and Radium None 1997-12-31 The conference covered various aspects of mutagenesis and mechanisms of DNA repair . UV and ionizing radiation were use to induce DNA lesions in bacteria yeast and cell cultures of higher organisms. This allows study of influence of mutations on particular processes in the cell. Mechanisms of resistance were also investigated. Biological investigations were performed using labelled compounds. Energy Technology Data Exchange ETDEWEB 152 A Ubiquitin-Binding Domain in Cockayne Syndrome B Required for Transcription-Coupled Nucleotide Excision Repair Mari Pierre-Olivier 2010-06-11 SummaryTranscription-coupled nucleotide excision repair TC-NER allows RNA polymerase II RNAPII -blocking lesions to be rapidly removed from the transcribed strand of active genes....Full Text Available UK PubMed Central United Kingdom 153 Nanoscale microscopical technology to study DNA repair and chromatin dynamics Dynamics Nanoscale M. 2008-06-30 DescriptionThe application of multiphoton femtosecond technology has opened up exciting new possibilities for the investigation of DNA repair in whole live cells. Important new observations on the processing of UV photoproducts during DNA repair in mammalian cells have been made. The methods demonstrate that in certain populations of cells the lesions cluster after induction of UV damage by 3-photon absorption of focused near infra-red light. The reason that this has been so clearly demonstrated is that u continued... Environment Research Funders Forum ERFF 154 Mechanism of the oxygen effect in cells. During and after irradiation Eidus L. K. Korystov Yu.N. AN SSSR Pushchino-na-Oke. Inst. Biologicheskoj Fiziki 1984-06-07 A new mechanism of oxygen effect in cells has been proposed. The mechanism involves two subsequent processes 1 physicochemical modification of primary damage of a target by oxygen or thiols and 2 enzymatic repair of the lesions modified by endogenous thiols. The first process occurs during irradiation it is dependent on the thiols/oxygen ratio in the cell nucleus and determines constant K. The second process occurs in the postirradiation period it is dependent on repair efficiency and determines constant m. The expression for the oxygen enhancement ratio elucidating its dependence on the enzymatic repair efficiency is derived. Energy Technology Data Exchange ETDEWEB 155 Caffeine inhibition of prereplication repair of mitomycin C-induced DNA damage in human peripheral lymphocytes Ishii Y. Bender M. A. 1978-01-01 Caffeine increases the number of sister-chromatid exchanges SCE induced by mitomycin C MMC in human peripheral lymphocytes in culture. This enhancement decreases when the treated cells are held in medium before phytohemagglutinin PHA stimulation or when caffeine is added to cultures some time after PHA stimulation but prior to DNA synthesis. There thus appears to be a caffeine-sensitive prereplication repair system presumably an excision mechanism capable of repairing a fraction of the MMC-induced DNA lesions . Energy Technology Data Exchange ETDEWEB 156 DNA repair efficiency in germ cells and early mouse embryos and consequences for radiation-induced transgenerational genomic damage Marchetti Francesco Wyrobek Andrew J. Exposure to ionizing radiation and other environmental agents can affect the genomic integrity of germ cells and induce adverse health effects in the progeny. Efficient DNA repair during gametogenesis and the early embryonic cycles after fertilization is critical for preventing transmission of DNA damage to the progeny and relies on maternal factors stored in the egg before fertilization. The ability of the maternal repair machinery to repair DNA damage in both parental genomes in the fertilizing egg is especially crucial for the fertilizing male genome that has not experienced a DNA repair -competent cellular environment for several weeks prior to fertilization. During the DNA repair -deficient period of spermatogenesis DNA lesions may accumulate in sperm and be carried into the egg where if not properly repaired could result in the formation of heritable chromosomal aberrations or mutations and associated birth defects. Studies with female mice deficient in specific DNA repair genes have shown that i cell cycle checkpoints are activated in the fertilized egg by DNA damage carried by the sperm and ii the maternal genotype plays a major role in determining the efficiency of repairing genomic lesions in the fertilizing sperm and directly affect the risk for abnormal reproductive outcomes. There is also growing evidence that implicates DNA damage carried by the fertilizing gamete as a mediator of postfertilization processes that contribute to genomic instability in subsequent generations. Transgenerational genomic instability most likely involves epigenetic mechanisms or error-prone DNA repair processes in the early embryo. Maternal and embryonic DNA repair processes during the early phases of mammalian embryonic development can have far reaching consequences for the genomic integrity and health of subsequent generations. Science.gov United States 157 DNA repair efficiency in germ cells and early mouse embryos and consequences for radiation-induced transgenerational genomic damage Marchetti Francesco Wyrobek Andrew J. 2009-01-18 Exposure to ionizing radiation and other environmental agents can affect the genomic integrity of germ cells and induce adverse health effects in the progeny. Efficient DNA repair during gametogenesis and the early embryonic cycles after fertilization is critical for preventing transmission of DNA damage to the progeny and relies on maternal factors stored in the egg before fertilization. The ability of the maternal repair machinery to repair DNA damage in both parental genomes in the fertilizing egg is especially crucial for the fertilizing male genome that has not experienced a DNA repair -competent cellular environment for several weeks prior to fertilization. During the DNA repair -deficient period of spermatogenesis DNA lesions may accumulate in sperm and be carried into the egg where if not properly repaired could result in the formation of heritable chromosomal aberrations or mutations and associated birth defects. Studies with female mice deficient in specific DNA repair genes have shown that i cell cycle checkpoints are activated in the fertilized egg by DNA damage carried by the sperm and ii the maternal genotype plays a major role in determining the efficiency of repairing genomic lesions in the fertilizing sperm and directly affect the risk for abnormal reproductive outcomes. There is also growing evidence that implicates DNA damage carried by the fertilizing gamete as a mediator of postfertilization processes that contribute to genomic instability in subsequent generations. Transgenerational genomic instability most likely involves epigenetic mechanisms or error-prone DNA repair processes in the early embryo. Maternal and embryonic DNA repair processes during the early phases of mammalian embryonic development can have far reaching consequences for the genomic integrity and health of subsequent generations. Energy Technology Data Exchange ETDEWEB 158 Biochemical reconstitution of abasic DNA lesion replication in Xenopus extracts Liao Shuren Matsumoto Yoshihiro Yan Hong Cellular DNA is under constant attack from numerous exogenous and endogenous agents. The resulting DNA lesions if not repaired timely could stall DNA replication leading to genome instability. To better understand the mechanism of DNA lesion replication at the biochemical level we have attempted to reconstitute this process in Xenopus egg extracts the only eukaryotic in vitro system that relies solely on cellular proteins for DNA replication. By using a plasmid DNA that carries a site-specific apurinic/apyrimidinic AP lesion as template we have found that DNA replication is stalled one nucleotide before the lesion . The stalling is temporary and the lesion is eventually replicated by both an error-prone mechanism and an error-free mechanism. This is the first biochemical system that recapitulates efficiently and faithfully all major aspects of DNA lesion replication. It has provided the first direct evidence for the existence of an error-free lesion replication mechanism and also demonstrated that the error-prone mechanism is a major contributor to lesion replication. Science.gov United States 159 Host cell reactivation capacity of different strains of E. coli B resistant or sensitive to ozone L apos Herault P. Chung Y. S. 1984-07-15 Host cell reactivation capacity for ozonated or irradiated phage was determined for different strains of E. coli either more sensitive or resistant to ozone than the wild type strain. The results suggest that the ozr gene product could be involved in the same repair pathway for ozone-induced lesions on DNA as the polA gene. The possible involvement of a specific endonuclease for these lesions is also considered. Energy Technology Data Exchange ETDEWEB 160 Specific UV-induced mutation spectrum in the p53 gene of skin tumors from DNA- repair -deficient xeroderma pigmentosum patients Dumaz N. Ougard C. Sarasin A. Daya-Grosjean L. 1993-01-01 The UV component of sunlight is the major carcinogen involved in the etiology of skin cancers. The authors have studied the rare hereditary syndrome xeroderma pigmentosum XP which is characterized by a very high incidence of cutaneous tumors on exposed skin at an early age probably due to a deficiency in excision repair of UV-induced lesions . It is interesting to determine the UV mutation spectrum in XP skin tumors in order to correlate the absence of repair of specific DNA lesions and the initiation of skin tumors. The p53 gene is frequently mutated in human cancers and represents a good target for studying mutation spectra since there are International Nuclear Information System INIS 161 Saccharomyces cerevisiae-based system for studying clustered DNA damages Moscariello M. Sutherland B. 2010-01-01 DNA-damaging agents can induce clustered lesions or multiply damaged sites MDSs on the same or opposing DNA strands. In the latter attempts to repair MDS can generate closely opposed single-strand break intermediates that may convert non-lethal or mutagenic base damage into double-strand breaks DSBs . We constructed a diploid S. cerevisiae yeast strain with a chromosomal context targeted by integrative DNA fragments carrying different damages to determine whether closely opposed base damages are converted to DSBs following the outcomes of the homologous recombination repair pathway. As a model of MDS we studied clustered uracil DNA damages with a known location and a defined distance separating the lesions . The system we describe might well be extended to assessing the repair of MDSs ... Electronic Table of Contents ETOC United Kingdom 162 Induction of Excision Repairable DNA Lesions in Lymphocytes Exposed to Lead and ALA In Vitro Ustundag A. Duydu Y. 2009-01-01 Numbers of studies have been carried out on the potential of lead genotoxicity. The mechanisms of lead genotoxicity are not fully known but partly attributed to the formation of highly reactive oxygen metabolites ROM . However lead ions have no ability to generate ROM. In this study we have investigated the ability of lead and ALA to induce excision repairable DNA lesions by using cytosine arabinoside or cytokinesis block micronucleus ARA-C/CBMN assay. N-methyl-N-nitrosourea was used as a positive control which is a mutagen and known to induce excision repair . The results of the ARA-C/CBMN assay show that ALA exposures have significantly p Electronic Table of Contents ETOC United Kingdom 163 Cartilage repair Generations of autologous chondrocyte transplantation Marlovits Stefan Zeller Philip Singer Philipp Resinger Christoph Vecsei Vilmos 2006-01-01 Articular cartilage in adults has a limited capacity for self- repair after a substantial injury. Surgical therapeutic efforts to treat cartilage defects have focused on delivering new cells capable of chondrogenesis into the lesions . Autologous chondrocyte transplantation ACT is an advanced cell-based orthobiologic technology used for the treatment of chondral defects of the knee that has been in clinical use since 1987 and has been performed on 12 000 patients internationally. With ACT good to excellent clinical results are seen in isolated post-traumatic lesions of the knee joint in the younger patient with the formation of hyaline or hyaline-like repair tissue. In the classic ACT technique chondrocytes are isolated from small slices of cartilage harvested arthroscopically from a minor weight-bearing area of the injured knee. The extracellular matrix is ... International Nuclear Information System INIS 164 Autologous chondrocyte transplantation for the treatment of articular cartilage defects in the knee joint. Techniques and results Autologe Chondrozytentransplantation zur Behandlung von Knorpeldefekten des Kniegelenks. Techniken und Ergebnisse Marlovits S. Kutscha-Lissberg F. Aldrian S. Resinger C. Singer P. Zeller P. Vecsei V. 2004-01-01 Currently the use of autologous chondrocytes as a cartilage- repair procedure for the repair of injured articular cartilage of the knee joint is recommended. This review presents the technique of autologous chondrocyte transplantation ACT and their modifications as matrix-associated autologous chondrocyte transplantation MACT . Beside the surgical procedure the experimental and clinical results are discussed. Furthermore the major complications and the indication guidelines are presented. Articular cartilage in adults has a poor ability to self- repair after a substantial injury. Surgical therapeutic efforts in treating cartilage defects have focused on bringing new cells capable of chondrogenesis into the lesions . With ACT good to excellent clinical results are seen in isolated posttraumatic lesions of the knee joint in the younger patient with the ... International Nuclear Information System INIS 165 Recognition and repair of 8-oxoguanine and formamidopyrimidine lesions in DNA Grollman A. P. Johnson F. Tchou J. State Univ. of New York Stony Brook NY United States and others 1994-12-31 Reactive oxygen species including hydroxyl radicals arise during the enzymatic and chemical reduction of molecular oxygen in cells. Hydroxyl radicals are also formed when cells are exposed to ionizing radiation tumor promoters and certain chemical carcinogens. Reactive oxygen species produce a variety of complex lesions in DNA. 8-Oxoguanine 8-oxodG and formamidopyrimidine Fapy are among the more abundant products of oxidative DNA damage. Both lesions are actively repaired in prokaryotic and eukaryotic cells. The mutagenic potential of 8-oxodG is reflected in its miscoding properties. Primer extension reactions catalyzed by DNA polymerases show that dAMP and dCMP can be incorporated on DNA templates during tranlesional synthesis and readily extended from the 3{prime} terminus. In contrast Fapy lesions block the progression of DNA polymerase. Plasmid vectors containing a single lesion were used to establish the mutational frequency and specificity of 9oxodG in bacteria and mammalian cells. 9-OxodG is weakly mutagenic in both systems G C{l_arrow}T A transversions are targeted to the site of the lesion . Mutagenic properties have not been reported for Fapy. Energy Technology Data Exchange ETDEWEB 166 Is it clinically relevant to repair focal multiple sclerosis lesions Comi G. 2008-01-01 Multiple sclerosis MS is an inflammatory disease of the central nervous system predominantly but not exclusively involving the normal appearing white matter. Until very recently we believed that nervous dysfunction in MS was completely depending on the accumulation of lesions in the white matter of the CNS. As a consequence lesions seen by magnetic resonance imaging MRI have been considered a potential surrogate end point in clinical trials assessing new MS treatments. More recently this concept have been challenged by the emerging evidences mostly from pathological and MRI studies that lesions may be located also in grey matter and that the white and grey matter not affected by lesions is abnormal. The causes of this normal appearing grey and white matter damage are still debat... Electronic Table of Contents ETOC United Kingdom 167 Effectiveness of external rotation immobilization in highly active young men with traumatic primary anterior shoulder dislocation or subluxation. Yoshitaka Tanaka We treated 15 highly active young men 16 shoulders with traumatic primary anterior shoulder dislocation or subluxation using 3-week external rotation immobilization. Fourteen patients 14 shoulders were members of the Self-Defense Force and the other patient 2 shoulders was a high school student who played club-level rugby. Average patient age at the time of the primary injury was 21.3 years range 17-26 years . Magnetic resonance imaging MRI was performed on 14 of 16 shoulders after the 3-week external rotation immobilization and showed that the anteroinferior labrum was reduced on the glenoid rim in 11 shoulders but remained medially displaced on the glenoid neck in 3 shoulders. Five shoulders including these 3 shoulders underwent arthroscopic Bankart repair after 3-week external rotation immobilization. Eleven shoulders continued nonoperative treatment after the immobilization. Four of 11 shoulders had no recurrence of symptoms for gt 2 years and these patients were able to return to their preinjury activities. However 7 shoulders experienced recurrence within 2 years.We concluded that external rotation immobilization may not be as effective as mentioned previously in highly active young men with primary traumatic anterior shoulder dislocation or subluxation. Whether a patient has instability symptom recurrence after external rotation immobilization depends on more than the fact that the anteroinferior labrum is not reduced on MRI. Science.gov United States 168 Excision repair of UV radiation-induced DNA damage in Caenorhabditis elegans Hartman P.S. Hevelone J. Radioimmunoassays were used to monitor the removal of antibody-binding sites associated with the two major UV radiation-induced DNA photoproducts cyclobutane dimers and 6-4 photoproducts . Unlike with cultured human cells where 6-4 photoproducts are removed more rapidly than cyclobutane dimers the kinetics of repair were similar for both lesions . Repair capacity in wild type diminished throughout development. The radioimmunoassays were also employed to confirm the absence of photoreactivation in C. elegans. In addition three radiation-sensitive mutants rad-1 rad-2 rad-7 displayed normal repair capacities. An excision defect was much more pronounced in larvae than embryos in the fourth mutant tested rad-3 . This correlates with the hypersensitivity pattern of this mutant and suggests that DNA repair may be developmentally regulated in C. elegans. The mechanism of DNA repair in C. elegans as well as the relationship between the repair of specific photoproducts and UV radiation sensitivity during development are discussed. Science.gov United States 169 Excision repair of UV radiation-induced DNA damage in Caenorhabditis elegans Hartman P. S. Hevelone J. Dwarakanath V. Mitchell D.L. Texas Christian Univ. Fort Worth USA 1989-06-01 Radioimmunoassays were used to monitor the removal of antibody-binding sites associated with the two major UV radiation-induced DNA photoproducts cyclobutane dimers and 6-4 photoproducts . Unlike with cultured human cells where 6-4 photoproducts are removed more rapidly than cyclobutane dimers the kinetics of repair were similar for both lesions . Repair capacity in wild type diminished throughout development. The radioimmunoassays were also employed to confirm the absence of photoreactivation in C. elegans. In addition three radiation-sensitive mutants rad-1 rad-2 rad-7 displayed normal repair capacities. An excision defect was much more pronounced in larvae than embryos in the fourth mutant tested rad-3 . This correlates with the hypersensitivity pattern of this mutant and suggests that DNA repair may be developmentally regulated in C. elegans. The mechanism of DNA repair in C. elegans as well as the relationship between the repair of specific photoproducts and UV radiation sensitivity during development are discussed. Energy Technology Data Exchange ETDEWEB 170 Enhancement of DNA strand break repair by hyperexpression of recombinant human poly ADP-ribose polymerase Bhatia K. Giri C. Pommier Y. Chernev B. Dritschilo Chen D. Alkhatib H. Smulson M. 1987-05-01 The eukaryotic nuclear enzyme poly ADP-Rib polymerase is believed to be important in altering chromatin structure around DNA strand breaks to facilitate various steps in DNA repair . They have recently isolated the full-length cDNA for this enzyme from the Okayama-Berg expression vector. However its direct role in DNA repair has not until now been experimentally accessible. Experiments to be presented show that the transient hyperexpression of functional poly ADP-Rib polymerase in the Cos cells to levels 15 times that of endogenous cellular levels significantly increases the ability of these cells to repair DNA lesions caused by gamma irradiation as measured by the alkaline elution method. Incubation of transfected cells with minimal amounts of the poly ADP-Rib polymerase inhibitor 3-aminobenzamide prevents the increased DNA repair induced by the expressed polymerase. The transient hyperexpression of polymerase and concomitant enhanced initial rate of DNA repair did not influence Cos cell survival to radiation damage. These results suggest that the cDNA for poly ADP-Rib polymerase encodes a protein that is functionally involved in DNA repair and possibly DNA synthesis in eukaryotic cells. Energy Technology Data Exchange ETDEWEB 171 Computational studies of radiation and oxidative damage to DNA and its recognition by repair enzyme Pinak M. Center for Promotion of Computational Science and Engineering Tokai Research Establishment Japan Atomic Energy Research Inst. Tokai Ibaraki Japan 2000-03-01 Molecular dynamics MD simulation is used to study the time evolution of the recognition processes and to construct a model of the specific DNA- repair enzyme apos complexes. MD simulations of the following molecules were performed DNA dodecamer with thymine dimer TD DNA 30-mer with thymine glycol TG and respective specific repair enzymes T4 Endonuclease V and Endonuclease III. Both DNA lesions are experimentally suggested to be mutagenic and carcinogenic unless properly recognized and repaired by repair enzymes. In the case of TD there is detected a strong kink around the TD site that is not observed in native DNA. In addition there is observed a different value of electrostatic energy at the TD site - negative apos -9 kcal/mol apos in contrast to the nearly neutral value of the native thymine site. These two factors - structural changes and specific electrostatic energy - seem to be important for proper recognition of a TD damaged site and for formation of DNA-enzyme complex. Formation of this complex is the onset of the repair of DNA. In the case of TG damaged DNA the structural characteristics of the TG were calculated charges bond lengths bond angles etc. . The formed TG was used to replace the native thymine and then submitted to the simulation in the system with a repair enzyme with Endonuclease III for the purpose of the study of the formation of the DNA-enzyme complex. author Energy Technology Data Exchange ETDEWEB 172 Genetics of x-ray induced double strand break repair in Saccharomyces cerevisiae Budd M. E. 1982-01-01 This thesis examined the possible fates of x-ray induced double strand breaks in Saccharomyces cerevisiae. One possible pathway which breaks can follow is the repair pathway and this pathway was studied by assaying strains with mutations in RAD51 RAD54 and RAD57 loci for double strand break repair using neutral sucrose sedimentation. Rad54-3 strains were sensitive to x-ray at 36/sup 0/ and resistant at 23/sup 0/ while rad57-1 strains are sensitive to radiation at 23/sup 0/ and resistant at 36/sup 0/. In order of increasing radiation sensitivity one finds rad57-1 23/sup 0/ gt rad51-1 30/sup 0/ gt rad54-3 36/sup 0/ . At the restrictive temperature 36/sup 0/ rad54-3 cells are unaable to repair double strand breaks while at the permissive temperature 23/sup 0/ these strains are able to repair double strand breaks. On the other hand strains with the rad57-1 mutation appear to be able to rejoin broken chromosomes at both the permissive and restrictive temperature. However the low assay is not distinguishing large DNA fragments which allow cell survival from large DNA fragments which cause cell death. A rad51-1 strain also appeared able to rejoin broken chromosomes and is thus capable of incomplete repair . The data can be explained with the hypotheses that rad54-3 cells are blocked in a later step of repair . The fate of double strand breaks when they are left unrepaired was also investigated with the temperature conditional rad54-3 mutation. If breaks are prevented from entering the RAD54 repair pathway they are modified and become uncommitted lesions . The rate these uncommitted lesions are repaired is slower than the rate the original breaks are repaired . Energy Technology Data Exchange ETDEWEB 173 DNA repair and radiation sensitivity in mammalian cells Chen D.J.C. Stackhouse M. Los Alamos National Lab. NM United States Ionizing radiation induces various types of damage in mammalian cells including DNA single-strand breaks DNA double-strand breaks DSB DNA-protein cross links and altered DNA bases. Although human cells can repair many of these lesions there is little detailed knowledge of the nature of the genes and the encoded enzymes that control these repair processes. We report here on the cellular and genetic analyses of DNA double-strand break repair deficient mammalian cells. It has been well established that the DNA double-strand break is one of the major lesions induced by ionizing radiation. Utilizing rodent repair -deficient mutant we have shown that the genes responsible for DNA double-strand break repair are also responsible for the cellular expression of radiation sensitivity. The molecular genetic analysis of DSB repair in rodent/human hybrid cells indicate that at least 6 different genes in mammalian cells are responsible for the repair of radiation-induced DNA double-strand breaks. Mapping and the prospect of cloning of human radiation repair genes are reviewed. Understanding the molecular and genetic basis of radiation sensitivity and DNA repair in man will provide a rational foundation to predict the individual risk associated with radiation exposure and to prevent radiation-induced genetic damage in the human population. Science.gov United States 174 DNA repair and radiation sensitivity in mammalian cells Chen D. J. Stackhouse M. Los Alamos National Lab. NM United States Chen D.S. Rochester Univ. NY United States . Dept. of Radiation Oncology 1993-01-01 Ionizing radiation induces various types of damage in mammalian cells including DNA single-strand breaks DNA double-strand breaks DSB DNA-protein cross links and altered DNA bases. Although human cells can repair many of these lesions there is little detailed knowledge of the nature of the genes and the encoded enzymes that control these repair processes. We report here on the cellular and genetic analyses of DNA double-strand break repair deficient mammalian cells. It has been well established that the DNA double-strand break is one of the major lesions induced by ionizing radiation. Utilizing rodent repair -deficient mutant we have shown that the genes responsible for DNA double-strand break repair are also responsible for the cellular expression of radiation sensitivity. The molecular genetic analysis of DSB repair in rodent/human hybrid cells indicate that at least 6 different genes in mammalian cells are responsible for the repair of radiation-induced DNA double-strand breaks. Mapping and the prospect of cloning of human radiation repair genes are reviewed. Understanding the molecular and genetic basis of radiation sensitivity and DNA repair in man will provide a rational foundation to predict the individual risk associated with radiation exposure and to prevent radiation-induced genetic damage in the human population. Energy Technology Data Exchange ETDEWEB 175 DNA repair and radiation sensitivity in mammalian cells Chen D. J. Stackhouse M. Los Alamos National Lab. NM United States Chen D.S. Rochester Univ. NY United States . Dept. of Radiation Oncology 1993-02-01 Ionizing radiation induces various types of damage in mammalian cells including DNA single-strand breaks DNA double-strand breaks DSB DNA-protein cross links and altered DNA bases. Although human cells can repair many of these lesions there is little detailed knowledge of the nature of the genes and the encoded enzymes that control these repair processes. We report here on the cellular and genetic analyses of DNA double-strand break repair deficient mammalian cells. It has been well established that the DNA double-strand break is one of the major lesions induced by ionizing radiation. Utilizing rodent repair -deficient mutant we have shown that the genes responsible for DNA double-strand break repair are also responsible for the cellular expression of radiation sensitivity. The molecular genetic analysis of DSB repair in rodent/human hybrid cells indicate that at least 6 different genes in mammalian cells are responsible for the repair of radiation-induced DNA double-strand breaks. Mapping and the prospect of cloning of human radiation repair genes are reviewed. Understanding the molecular and genetic basis of radiation sensitivity and DNA repair in man will provide a rational foundation to predict the individual risk associated with radiation exposure and to prevent radiation-induced genetic damage in the human population. Energy Technology Data Exchange ETDEWEB 176 Sister chromatid exchange DNA repair and single-gene mutation Carrano A. V. Thompson L. H. 1981-04-13 Sister chromatid exchange SCE has been studied in cultured mammalian cells with regard to the nature of the inducing lesion mutation induction and factors that modify the observed frequency following mutagen exposure. SCEs can be induced by a wide spectrum of DNA lesions and for nine agents examined the frequency of induced SCE is linearly related to induced single-gene mutation. Further a deficiency in DNA repair may alter the expression of both SCE and mutation in a qualitatively similar manner. The frequency of SCE induced by mitomycin-C is suppressed in heterochromatin relative to euchromatin and in non-dividing lymphocytes the lesions leading to the formation of SCEs may persist for several months. Energy Technology Data Exchange ETDEWEB 177 Avulsion fractures of the anterior inferior iliac spine spectrum of imaging findings Avulsao da espinha iliaca antero-inferior espectro dos achados de imagem Fernandes Joao Luiz Hospital Santa Lucia Brasilia DF Brazil . Dept. de Ressonancia Magnetica Viana Sergio L. Mendonca Jose L. Freitas Flavia M. Lima Gylse-Anne D. Vila Ana F. Ribeiro Nelmar Clinica Radiologica Vila Rica Brasilia DF Brazil . Dept. de Ressonancia Magnetica . E-mail radiolog@uol .br 2005-07-15 Avulsive injuries of the pelvic aphophyses are relatively common among 13-18 year old athletes particularly among soccer players in Brazil. Diagnosis is made upon clinical and imaging findings. These lesions show three distinct phases acute repair and consolidation phases. Although acute and consolidation phases usually represent no diagnostic challenge the repair phase may appear as an aggressive process on diagnostic images simulating neoplasic lesions . In this paper the authors present the imaging findings of patients with avulsion of the anterior inferior iliac spine on plain radiographs computerized tomography and magnetic resonance imaging emphasizing the typical features of the three evolutive phases of these lesions . author Energy Technology Data Exchange ETDEWEB 178 Avulsion fractures of the anterior inferior iliac spine spectrum of imaging findings Avulsao da espinha iliaca antero-inferior espectro dos achados de imagem Fernandes Joao L. Viana Sergio L. Mendonca Jose L. Freitas Flavia M. Lima Gylse-Anne D. Vila Ana F. Ribeiro Nelmar 2005-01-01 Avulsive injuries of the pelvic aphophyses are relatively common among 13-18 year old athletes particularly among soccer players in Brazil. Diagnosis is made upon clinical and imaging findings. These lesions show three distinct phases acute repair and consolidation phases. Although acute and consolidation phases usually represent no diagnostic challenge the repair phase may appear as an aggressive process on diagnostic images simulating neoplasic lesions . In this paper the authors present the imaging findings of patients with avulsion of the anterior inferior iliac spine on plain radiographs computerized tomography and magnetic resonance imaging emphasizing the typical features of the three evolutive phases of these lesions . author International Nuclear Information System INIS 179 A saccharomyces cerevisiae phleomycin-sensitive mutant phl40 is defective in the RAD6 DNA repair gene He Chuan H. Masson J-Y. Ramotar D. 1996-01-01 The antibiotic bleomycin is used as an anticancer agent for treating a variety of tumours. The anti tumour effect of bleomycin is related to its ability to produce lesions such as apurinic/apyrimidinic sites and single-and double-strand breaks in the cellular DNA. Phleomyein is a structurally related form of bleomycin but it is not used as an anticancer agent. While Phleomyein can also damage DNA neither the exact nature of these DNA lesions nor the cellular process that repairs phleomyein-induced DNA lesions is known. As a first step to understand how eukaryotic cells provide resistance to phleomyein we used the yeast Saccharomyces cerevisiae as a model system. Several phleomyein-sensitive mutants were generated following gamma-radiation treatment and among these mutants phl40 was found to be the most sensitive to phleomyein. Molecular analysis ... International Nuclear Information System INIS 180 A Two-tiered compensatory response to loss of DNA repair modulates aging and stress response pathways Kassahun Henok Full Text Available. Activation of oxidative stress-responses and downregulation of insulin-like signaling ILS is seen in Nucleotide Excision Repair NER deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage although the relevant lesions have not been identified. Here we show that loss of NTH-1 the only Base Excision Repair BER enzyme known to initiate repair of oxidative DNA damage inC. elegans restores normal lifespan of the short-lived NER deficient xpa-1 mutant. Loss of NTH-1 leads to oxidative stress and global expression profile changes that involve upregulation of genes responding to endogenous stress and downregulation of ILS. A similar but more extensive transcriptomic shift is observed in the xpa-1 mutant whereas loss of both NTH-1 and XPA-1 elicits a different profile with downregulation of Aurora-B and Polo-like kinase 1 signaling networks as well as DNA repair and DNA damage response genes. The restoration of normal lifespan and absence oxidative stress responses in nth-1 xpa-1 indicate that BER contributes to generate transcription blocking lesions from oxidative DNA damage. Hence our data strongly suggests that the DNA lesions relevant for aging are repair intermediates resulting from aberrant or attempted processing by BER of lesions normally repaired by NER. Scientific Electronic Library Online Colombia 181 UV Damage in DNA Promotes Nucleosome Unwrapping* Smerdon Michael J. 2010-08-20 Full Text Available.The association of DNA with histones in chromatin impedes DNA repair enzymes from accessing DNA lesions . Nucleosomes exist in a dynamic equilibrium in which portions of the DNA molecule spontaneously unwrap transiently exposing buried DNA sites. Thus nucleosome dynamics in certain regions of chromatin may provide the exposure time and space needed for efficient repair of buried DNA lesions . We have used FRET and restriction enzyme accessibility to study nucleosome dynamics following DNA damage by UV radiation. We find that FRET efficiency is reduced in a dose-dependent manner showing that the presence of UV photoproducts enhances spontaneous unwrapping of DNA from histones. Furthermore this UV-induced shift in unwrapping dynamics is associated with increased restriction enzyme accessibility of histone-bound DNA after UV treatment. Surprisingly the increased unwrapping dynamics is even observed in nucleosome core particles containing a single UV lesion at a specific site. These results highlight the potential for increased #x0201c intrinsic exposure #x0201d of nucleosome-associated DNA lesions in chromatin to repair proteins. Scientific Electronic Library Online Colombia 182 Association of thymine glycol lesioned DNA with repair enzyme endonuclease III-molecular dynamics study Pinak Miroslav Japan Atomic Energy Research Inst. Tokai Ibaraki Japan . Tokai Research Establishment 2001-07-01 The 2 nanoseconds molecular dynamics MD simulation has been performed for the system consisting of repair enzyme and DNA 30-mer with native thymine at position 16 replaced by thymine glycol TG solvated in water environment. After 950 picoseconds of MD the enzyme and DNA associated together to form complex that lasted stable up to 2 ns when simulation was terminated. At the contact area of enzyme and DNA there is glutamic acid located as close as 1.6 A to the C3 apos atom of phosphodiester bond of TG. Initial B-DNA molecule was bent and kinked at the TG during MD. This distortion caused that phosphodiester bond was easier accessible by amino acids of enzyme. The negative value of electrostatic energy -26 kcal/mol discriminates TG from nearly neutral native thymine and contributes to the specific recognition of this lesion . Higher number of close water molecules at TG site before formation of complex compared with other nucleotides indicates that glycosyl bond of the lesion is easily approached by repair enzyme during scanning of DNA surface and suggests the importance of specific hydration at the lesion during recognition process. author Energy Technology Data Exchange ETDEWEB 183 DNA damage as the primary cause of aging Gensler H. L. Bernstein H. 1981-09-01 DNA damage appears to be ubiquitous in the biological world as judged by the variety of organisms which have evolved DNA- repair systems. Previously it was proposed that germ-line DNA of multicellular organisms may be protected from damage and consequently from aging by efficient recombinational repair during meiosis. The somatic line however may be vulnerable to the accumulation of DNA damage and hence undergo aging owing to relatively less repair . Although the DNA lesions most important in aging are not known yet there is evidence for serveral types of endogenous damage. DNA lesions have been shown to interfere with transcription and replication and so lead to loss of cell function and death. In mammals there is a progressive decline of function in many different tissues with increasing age. Deterioration of central nervous system functions appears to be a critical part of the aging process. This may be due to the low DNA repair capacity which is found in postmitotic brain tissue and which could result in the accumulation of DNA lesions in this tissue. Also reviewed is evidence that species longevity is directly related to tissue DNA- repair capacity and that aging may be accelerated by treatment with DNA-damaging agents or in individuals with genetically defective repair . Although it has been frequently postulated that somatic mutation may be cause of aging current evidence suggests that it is probably less important than DNA damage. A prominent theory on the evolution of aging which attributes special importance to genes that are advantagous in youth but are deleterious later on is discussed in terms of regulatory genes that reduce DNA repair as cells differentiate to the postmitotic state. Finally we hypothesize that the factors which determine maximum longevity of individuals in a population are the rate of occurrence of DNA damage the rate of DNA repair the degree of cellular redundancy and the extent of exposure to stress. Energy Technology Data Exchange ETDEWEB 184 Multiple effects of fluorescent light on repair of ultraviolet-induced DNA lesions in cultured goldfish cells Uchida Nobuhiro Mitani Hiroshi Shima Akihiro Tokyo Univ. Japan . Lab. of Radiation Biology 1995-01-01 It is known that fluorescent light illumination prior to UV irradiation FL preillumination of cultured fish cells increases photorepair PR ability. In the present study it was found that FL preillumination also enhanced UV resistance of logarithmically growing cells in the dark. This enhancement of UV resistance differs from induction of PR because it was not suppressed by cyclohexamide CH and it occurred immediately after FL preillumination. The effects of FL preillumination on repair of UV-induced DNA lesions in the dark were examined by an endonuclease-sensitive site assay to measure the repair of cyclobutyl pyrimidine dimers and by enzyme-linked immunosorbent assay to quantitate the repair of 6-4 photoproducts. It was found that excision repair ability for 6-4 photoproducts in the genome overall was increased by FL preillumination. Moreover a decrease in 6-4 photoproducts by FL illumination immediately after UV irradiation of the cells was found the decrement being enhanced by FL preillumination with or without CH. author . Energy Technology Data Exchange ETDEWEB 185 Clinical genetic and DNA repair studies on a consecutive series of patients with xeroderma pigmentosum Pawsey S. A. Magnus I. A. Ramsay C. A. Benson P. F. Giannelli F. 1979-04-01 We report clinical genetic and biochemical findings in 13 families with the photosensitive genodermatosis xeroderma pigmentosum. All patients had a defect in repair of DNA damage provoked by ultraviolet radiation. Some patients apos parents showed slightly reduced repair of UVR induced DNA damage. In xeroderma pigmentosum XP the defect in the excision of DNA lesions appears to be due to ions and homozygosity for one of at least seven different mutations and accordingly XP patients can be assigned to seven so-called complementation groups A to G. It was shown that mutations of different genes play a role in XP and genes interact to secure repair of DNA lesions in normal cells. We discuss the phenotype of XP from different complementation groups in relation to the severe neurological abnormalities which may develop. We also discuss the biochemical anomalies of XP. Lastly we review the relationship between DNA repair and skin cancer in XP. Energy Technology Data Exchange ETDEWEB 186 DNA excision repair in cell extracts from human cell lines exhibiting hypersensitivity to DNA-damaging agents Hansson J. Keyse S. M. Lindahl T. Wood R.D. Imperial Cancer Research Fund South Mimms United Kingdom 1991-07-01 Whole cell extracts from human lymphoid cell lines can perform in vitro DNA repair synthesis in plasmids damaged by agents including UV or cis-diamminedichloroplatinum II cis-DDP . Extracts from xeroderma pigmentosum XP cells are defective in repair synthesis. We have now studied in vitro DNA repair synthesis using extracts from lymphoblastoid cell lines representing four human hereditary syndromes with increased sensitivity to DNA-damaging agents. Extracts of cell lines from individuals with the sunlight-sensitive disorders dysplastic nevus syndrome or Cockayne apos s syndrome complementation groups A and B showed normal DNA repair synthesis in plasmids with UV photoproducts. This is consistent with in vivo measurements of the overall DNA repair capacity in such cell lines. A number of extracts were prepared from two cell lines representing the variant form of XP XP-V . Half of the extracts prepared showed normal levels of in vitro DNA repair synthesis in plasmids containing UV lesions but the remainder of the extracts from the same cell lines showed deficient repair synthesis suggesting the possibility of an unusually labile excision repair protein in XP-V. Fanconi apos s anemia FA cells show cellular hypersensitivity to cross-linking agents including cis-DDP. Extracts from cell lines belonging to two different complementation groups of FA showed normal DNA repair synthesis in plasmids containing cis-DDP or UV adducts. Thus there does not appear to be an overall excision repair defect in FA but the data do not exclude a defect in the repair of interstrand DNA cross-links. Energy Technology Data Exchange ETDEWEB 187 Primary repair versus conservative treatment of first-time traumatic anterior dislocation of the shoulder a randomized study with 10-year follow-up. Wulff Jakobsen B. PURPOSE The purpose of this study was to compare long-term results after surgical and conservative primary treatment of first-time traumatic anterior shoulder dislocation. Methods Arthroscopic diagnosis after first-time traumatic anterior shoulder dislocation was performed and in cases of a Baker type 1 2 or 3 lesion patients were randomized either to conservative treatment with a fixed sling for 1 week followed by a rehabilitation program or to open repair with a similar rehabilitation program. RESULTS In this study 76 patients 14 female and 62 male patients aged 15 to 39 years were randomized to surgical repair n = 37 or conservative treatment n = 39 . Of the patients 6.6% had Baker type 1 lesions 13.2% had type 2 lesions and 80.3% had type 3 lesions . After a minimum of 2 years' follow-up 56% had recurrence after conservative treatment and 3% after open repair P lt .005 . Among nondislocators 39% in the conservative group and 7% in the repair group had a positive apprehension test. When evaluated after 10 years by use of the Oxford self-assessment score 72% of patients in the surgical group had good or excellent results. Of the conservatively treated patients 75% had unsatisfactory results because of recurrence instability and pain or stiffness. CONCLUSIONS Arthroscopic evaluation after first-time anterior shoulder dislocation revealed a Baker type 2 or 3 lesion in 93.5% of patients. At 2 years' follow-up 21 54% of the conservatively treated patients had recurrence as compared with 1 patient with recurrence 3% after open surgical repair . After 8 years a further 3 patients in the conservatively treated group had redislocations 1 had subjective instability and 4 had pain or stiffness resulting in 74% having unsatisfactory results according to the Oxford score. Of the patients who had surgical repair 72% had good or excellent results after 10 years. Because open repair produces superior results compared with conservative treatment we recommend that the surgeon consider performing primary repair in active patients to reduce the risk of recurrence. LEVEL OF EVIDENCE Level I high-quality prospective randomized controlled trial. Science.gov United States 188 The Roles of Several Residues of Escherichia coli DNA Photolyase in the Highly Efficient Photo- Repair of Cyclobutane Pyrimidine Dimers Zhu Guoping Full Text Available. Escherichia coli DNA photolyase is an enzyme that repairs the major kind of UV-induced lesions cyclobutane pyrimidine dimer CPD in DNA utilizing 350 #x02013 450 #x02009 nm light as energy source. The enzyme has very high photo- repair efficiency the quantum yield of the reaction is ~0.85 which is significantly greater than many model compounds that mimic photolyase. This suggests that some residues of the protein play important roles in the photo- repair of CPD. In this paper we have focused on several residues discussed their roles in catalysis by reviewing the existing literature and some hypotheses. Scientific Electronic Library Online Colombia 189 Modulation of DNA double-strand break repair activity in cell-free extracts of gamma-irradiated mouse testicular cells Srivastava Niloo Raman Mercy J. Pradhan Satyajit 2004-01-01 DNA double-strand breaks DSBs are potentially mutagenic lesions demanding effective damage recognition and repair . Even a single DSB can be detrimental if left unrepaired or misrepaired and if present in gamete it can cause foetal wastage or malformations/congenital defects in the offspring. The threats posed by DSBs have triggered the evolution of two major pathways of DSB repair homologous recombination-mediated repair HRR and non-homologous end-joining NHEJ conserved from bacteria to mammals. Though HRR is more predominant in bacteria and yeast NHEJ is more efficient in mammalian somatic cells. Studies in our laboratory have shown that both the pathways are equally efficient in mammalian male germ cells International Nuclear Information System INIS 190 Local changes of higher-order chromatin structure during DSB- repair Falk M. Lukasova E. Gabrielova B. Ondrej V. Kozubek S. 2008-01-01 We show that double-strand breaks DSBs induced in DNA of human cells by gamma-radiation arise mainly in active gene-rich decondensed chromatin. We demonstrate that DSBs show limited movement in living cells occasionally resulting in their permanent clustering which poses a risk of incorrect DNA rejoining. In addition some DSBs remain unrepaired for several days after irradiation forming lesions repairable only with difficulty which are hazardous for genome stability. These 'late' DSBs colocalize with heterochromatin markers dimethylated histone H3 at lysine 9 HP1 and CENP-A proteins despite the low density of the surrounding chromatin. This indicates that there is epigenetic silencing of loci close to unrepaired DSBs and/or stabilization of damaged decondensed chromatin loops during repair and post- repair reconstitution of chromatin ... International Nuclear Information System INIS 191 Early and Midterm Results of an Alternative Procedure to Homografts in Primary Repair of Truncus Arteriosus Communis Curi-Curi P. Cervantes J. Soule M. Erdmenger J. Calderon-Colmenero J. Ramirez S. 2010-01-01 ABSTRACT Background. Repair of truncus arteriosus communis TAC in the neonatal and early infant period has become a standard practice. We report our experience on primary repair of TAC with a bovine pericardial-valved woven Dacron conduit as an alternative procedure to homografts with a focus on early and midterm results. Methods. From January 2001 to December 2007 15 patients with mean age 1.5 years range 3 months to 8 years underwent primary repair of simple TAC. Cases with cardiogenic shock complex-associated cardiac lesions or adverse anatomy of the truncal valve were excluded. The Collett and Edwards anatomical type classification of TAC was as follows type I 13 87% and type II 2 13% . Right ventricular outflow tract was reconstructed in all the cases with a bovine per... Electronic Table of Contents ETOC United Kingdom 192 Arthroscopic Anterior and Posterior Labral Repair After Traumatic Hip Dislocation Case Report and Review of the Literature Cross M. B. Shindle M. K. Kelly B. T. 2010-01-01 With the improvements in flexible instrumentation hip arthroscopy is being increasingly used to treat a variety of hip pathology including labral tears. However up to this point there has not been a case report of an anterior and a posterior labral tear successfully repaired arthroscopically. We present a case report of a 27-year-old male firefighter who presented to our institution with an anterior and posterior labral tear as well as a cam lesion and loose body following a traumatic hip dislocation. The purpose of this case report is to illustrate that both anterior and posterior labral tears can be repaired using hip arthroscopy. Anterior and posterior labral tears can be caused by a traumatic hip dislocation and both can be successfully repaired using arthroscopic techniques. Electronic Table of Contents ETOC United Kingdom 193 Archaeal DNA uracil repair via direct strand incision A minimal system reconstituted from purified components Schomacher L. Schurer K. A. Ciirdaeva E. McDermott P. Chong J. P. Kramer W. Fritz H. J. 2010-01-01 Hydrolytic deamination of DNA cytosine residues results in U/G mispairs pre-mutagenic lesions threatening long-term genetic stability. Hence DNA uracil repair is ubiquitous throughout all extant life forms and base excision repair triggered by a uracil DNA glycosylase UDG is the mechanistic paradigm adopted as it seems by all bacteria and eukaryotes and a large fraction of archaea. However members of the UDG superfamily of enzymes are absent from the extremely thermophilic archaeon Methanothermobacter thermautotrophicus DH. This organism as a hitherto unique case initiates repair by direct strand incision next to the DNA-U residue a reaction catalyzed by the DNA uridine endonuclease Mth212 an ExoIII homologue. To elucidate the detailed mechanism in particular to identify the ... Electronic Table of Contents ETOC United Kingdom Website Policies and Important Links Comments WorldWideScience.org is maintained by the U.S. Department of Energy's Office of Scientific and Technical Information as the Operating Agent for the WorldWideScience Alliance . 1.800.417.2035 Email Us Home ASC Review Current Issue Past Issues Subscribe Advertise About Conferences 18th Annual Ambulatory Surgery Centers Conference Conferences and Events Exhibiting Sponsorship E-Weekly Latest Issue Issue Archives Advertise About Becker's Operating Room Clinical Quality Infection Control Resources Webinars Upcoming Webinars Past Webinars About Us About Becker's ASC Review Advertising Contact Us 100 Best Places to Work ASC Coding Billing and Collections-News and Analysis Sponsored by AdvantEdge Healthcare Solutions bgilbert@ahsrcm 877 501-1611 Bankart Lesion Repair By Paul Cadorette CPC CPC-H CPC-P CEDC COSC CASCC November 18 2009 Editor's Note This article by Paul Cadorette director of education for mdStrategies originally appeared in The Coding Advocate mdStrategies free monthly newsletter. Sign-up to receive this newsletter by clicking here . CPT copyright 2008 American Medical Association. All rights reserved. CPT is a registered trademark of the American Medical Association. One type of labral tear is known as a Bankart lesion. Within the shoulder capsule there are a number of ligaments that act as restraints reinforcing the shoulder joint holding the humeral head in the glenolabral cup or socket. At the front lower portion of the shoulder anteroinferior you will find the inferior glenohumeral ligament. When this ligament fails during a dislocation injury the humeral head will push down towards the front of the shoulder tearing the labrum resulting in a Bankart lesion. Typical symptoms of a Bankart lesion include joint instability or repeat dislocations with a popping sound and/or mechanical catching within the joint. Repair of a Bankart lesion can be accomplished by either an open procedure or arthroscopic technique. The CPT codes are as follows 23455 – Capsulorrhaphy anterior with labral repair Bankart procedure . There are parenthetical notes under this CPT code that instruct a coder to report 29806 for the arthroscopic procedure. 29806 – Arthroscopy shoulder surgical capsulorrhaphy The information provided should be utilized for educational purposes only. Facilities are ultimately responsible for verifying the reporting policies of individual commercial and MAC/FI carriers prior to claim submissions. To receive the latest ASC news and feature stories from Becker's ASC Review sign-up for the free Becker's ASC Review E-weekly by clicking here . 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All Rights Reserved. rebound Orthopedic Physical Therapy Bankart Repair The shoulder joint is made up of numerous bones muscles ligaments and other tissues. All of these must work together in good rhythm for the shoulder to function correctly. Even a well functioning shoulder can develop problems if not cared for properly or if overused. Also there is always the risk for injury. A relatively common injury to the shoulder is a Bankart lesion. To better understand this condition a working knowledge of the anatomy involved the cause and potential problems associated with a Bankart lesion and the surgery and rehabilitation process is helpful. The shoulder joint is actually a combination of many joints working together but for now we will only discuss the glenohumeral joint the main joint that most would consider the shoulder joint. The glenohumeral joint is where the upper bone of the arm the humerus attaches to the body at the scapula . The specific area of the scapula where the humerus attaches is the socket called the glenoid fossa. Running along the rim of the glenoid fossa is a band of cartilage called the labrum . The role of the labrum is to deepen the socket to allow greater congruency between the humerus and the glenoid fossa during movements of the arm. A Bankart lesion is when the anterior/inferior portion of the labrum is torn away from the glenoid fossa. This is usually caused by a dislocation of the glenohumeral joint anteriorly or forward. The main problem that can result from a Bankart lesion is recurrent anterior shoulder dislocations. If the shoulder continues to repetitively dislocate it can potentially cause further damage to different areas of the shoulder. For those individuals that continue to experience dislocations surgery is often a good decision. Where the tear occurs with a Bankart Lesion. The surgical technique used to correct a Bankart lesion is simply called a Bankart repair. The goal of the surgery is to reconnect the torn labrum to the glenoid fossa thus repairing and stabilizing the joint to prevent further dislocations. It is not within the scope of this paper to discuss the different surgical techniques. The rehabilitation process following a Bankart repair begins almost immediately. Within the first few days following surgery passive range of motion of the shoulder is begun. The patient should be properly instructed by their physical therapist and doctor as to what motions and activities are appropriate to do for regaining range of motion of the shoulder as some motions are contraindicated. For the first four-to-six weeks following surgery the focus of the rehabilitation will be on regaining as much range of motion as possible while continuing to protect surgical repair. During that time the strength of the shoulder will also improve and the symptoms of pain should decrease. At the four-to-six week timeline depending on the progress the focus of the rehabilitation will begin to focus more on increasing the strength of the shoulder. As the strength of the shoulder improves the functional level of the patient will also improve. B y continuing with the proper strengthening program the patient should expect to return to their full level of activity as before the injury without the risk of dislocation. recurrent bone the August many and but 515 Shoulder greatly i anterior 11 . or To the for of single the stabilization. or anterior of for lesions cuff Elbow found and

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