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PubMed2002

A role for DNA polymerase beta in mutagenic UV lesion bypass.

We report here that DNA polymerase beta (pol beta), the base excision repair polymerase, is highly expressed in human melanoma tissues, known to be associated with UV radiation exposure. To investigate the potential role of pol beta in UV-induced genetic instability, we analyzed the cellular and molecular effects of excess pol beta. We firstly demonstrated that mammalian cells overexpressing pol beta are resistant and hypermutagenic after UV irradiation and that replicative extracts from these cells are able to catalyze complete translesion replication of a thymine-thymine cyclobutane pyrimidine dimer (CPD). By using in vitro primer extension reactions with purified pol beta, we showed that CPD as well as, to a lesser extent, the thymine-thymine pyrimidine-pyrimidone (6-4) photoproduct, were bypassed. pol beta mostly incorporates the correct dATP opposite the 3'-terminus of both CPD and the (6-4) photoproduct but can also misinsert dCTP at a frequency of 32 and 26%, respectively. In the case of CPD, efficient and error-prone extension of the correct dATP was found. These data support a biological role of pol beta in UV lesion bypass and suggest that deregulated pol beta may enhance UV-induced genetic instability.

Adenosine Triphosphate↗
PubMed1983

Prevalence of contagious pustular dermatitis (orf) in six million lambs at slaughter: a three-year study.

In the three years from October 1979 to September 1982 over 6.3 million lambs were processed in two meat works and of these 0.5% had lesions of contagious pustular dermatitis (CPD). The proportion of lambs affected was highest in the months of December and January when up to 2.2% of the lambs slaughtered had lesions of CPD. On average 13.4% of a consignment (referred to as a line) of lambs showing evidence of CPD were affected. The total lambs in affected lines constituted 4.1% of the total slaughtered. If it was decided to reject for slaughter lines with CPD, approximately 1 1/4 million lambs would be returned to farms each year. It was concluded that such a policy would be unlikely to substantially reduce the level of infection in meat workers.

Journal Article↗
PubMed2003

Diabetic retinopathy screening.

As part of the Institute of Medical Illustrators' (IMI) scheme for continuing professional development (CPD), worksheets will be published at regular intervals in this Journal. These are designed to provide the members of IMI with a structured CPD activity that offers one way to earn credits. It is recognized that this worksheet requires some time spent obtaining and reading a number of publications. As a way of ensuring that the allocated time has been spent on the activities a number of self-assessment exercises (SAEs) have been included. Upon completion of this worksheet, you will be credited with 10 CPD points. The answers to the SAEs, along with any notes you make and other publications you find, should be kept in your CPD portfolio.

Diabetic Retinopathy↗
PubMed2004

Patient privacy.

As part of the Institute of Medical Illustrators' (IMI) scheme for continuing professional development (CPD), worksheets will be published at regular intervals in this Journal. These are designed to provide the members of IMI with a structured CPD activity that offers one way to earn credits. It is recognized that this worksheet requires some time spent obtaining and reading a number of publications. As a way of ensuring that the allocated time has been spent on the activities a number of self-assessment exercises (SAEs) have been included. Upon completion of this worksheet, you will be credited with 15 CPD points. The answers to the SAEs, along with any notes you make and other publications you find, should be kept in your CPD portfolio.

Confidentiality↗
PubMed2005

The influence of gender, race, and menthol content on tobacco exposure measures.

Research has suggested that race, gender, and menthol cigarette use influence tobacco-smoke exposure measures and smoking-related disease risk. For example, a high proportion of Black smokers prefer menthol cigarettes and, despite smoking fewer cigarettes per day (CPD) than do Whites, tend to have higher cotinine levels. Additionally, Black males are more at risk for smoking-related lung cancer. High cotinine levels and smoking menthol cigarettes may lead to higher toxin intake, which contributes to increased disease risk. We explored the relationship between tobacco exposure variables (i.e., cotinine, CPD, carbon monoxide [CO], nicotine content, and nicotine dependence) with respect to race, gender, and menthol content in a sample of 307 smokers recruited from the greater Boston area to participate in a smoking cessation treatment trial. The pattern of correlations between tobacco exposure measures and cotinine showed a consistently positive correlation between cotinine and CO in all smokers and a correlation between cotinine and CPD in those who smoked nonmenthol cigarettes. Cotinine and CPD correlations varied by gender and race among menthol cigarette smokers. Consistently, we found a significant gender x race x menthol interaction on salivary cotinine level as well as cotinine/CPD ratio. These findings suggest that the relationship between number of cigarettes consumed and salivary cotinine is more complex than previously believed. It is not sufficient to look at race alone; researchers and clinicians need to look at race and gender concurrently, as well as type of cigarette consumed.

Adult↗
PubMed1996

Localization of DNA damage and its role in altered antigen-presenting cell function in ultraviolet-irradiated mice.

Prior ultraviolet (UV) irradiation of the site of application of hapten on murine skin reduces contact sensitization, impairs the ability of dendritic cells in the draining lymph nodes (DLN) to present antigen, and leads to development of hapten-specific suppressor T lymphocytes. We tested the hypothesis that UV-induced DNA damage plays a role in the impaired antigen-presenting activity of DLN cells. First, we assessed the location and persistence of cells containing DNA damage. A monoclonal antibody specific for cyclobutyl pyrimidine dimers (CPD) was used to identify UV-damaged cells in the skin and DLN of C3H mice exposed to UV radiation. Cells containing CPD were present in the epidermis, dermis, and DLN and persisted, particularly in the dermis, for at least 4 d after UV irradiation. When fluorescein isothiocyanate (FITC) was applied to UV-exposed skin, the DLN contained cells that were Ia+, FITC+, and CPD+; such cells from mice sensitized 3 d after UV irradiation exhibited reduced antigen-presenting function in vivo. We then assessed the role of DNA damage in UV-induced modulation of antigen-presenting cell (APC) function by using a novel method of increasing DNA repair in mouse skin in vivo. Liposomes containing T4 endonuclease V (T4N5) were applied to the site of UV exposure immediately after irradiation. This treatment prevented the impairment in APC function and reduced the number of CPD+ cells in the DLN of UV-irradiated mice. Treatment of unirradiated skin with T4N5 in liposomes or treatment of UV-irradiated skin with liposomes containing heat-inactivated T4N5 did not restore immune function. These studies demonstrate that cutaneous immune cells sustain DNA damage in vivo that persists for several days, and that FITC sensitization causes the migration of these to the DLN, which exhibits impaired APC function. Further, they support the hypothesis that DNA damage is an essential initiator of one or more of the steps involved in impaired APC function after UV irradiation.

Animals↗
PubMed1995

Substitution of equally carcinogenic UV-A for UV-B irradiations lowers epidermal thymine dimer levels during skin cancer induction in hairless mice.

Cyclobutane pyrimidine dimers (CPD) are the predominant DNA lesions induced by UV-B radiation, among these lesions thymine dimers are most frequent. Although UV-A radiation may also induce CPD, it has been found that equally cytotoxic or equally mutagenic UV-A and UV-B doses do not induce equal amounts of CPD, indicating that other DNA adducts contribute to the UV-A effects. Thus far it has not been established whether this finding can be extrapolated and also holds true for the more complex biological endpoint of skin cancer. Therefore, we compared thymine dimer levels during skin cancer induction by combined UV-A and UV-B daily exposures with the levels from equally carcinogenic daily UV-B exposures. From control experiments it was known that both groups would react similarly regarding the occurrences of carcinomas, with a median latency time of 170 +/- 10 days. After 50, 106 and 151 days of irradiation eight hairless mice (SKH:HR1) from both groups were euthanized and thymine dimers in epidermal cell suspensions were quantified by flow cytometry. Staining on DNA content enabled us to quantify thymine dimers in G0/G1-phase, in S-phase and in G2M-phase subpopulations. Both in total epidermal cell populations and in subpopulations of replicating epidermal cells thymine dimer levels were significantly lower in the UV-A/B combination group than in the UV-B group (0.010 < P < 0.025 and P < 0.005 respectively). This indicates that the carcinogenicity of UV-A relative to that of UV-B is not properly measured by thymine dimers and that other DNA lesions than CPD, for example, from reactive oxygen species, are likely to contribute to UV-A carcinogenicity.

Animals↗
PubMed2006

Epidermal stem and progenitor cells in murine epidermis accumulate UV damage despite NER proficiency.

Ultraviolet (UV) radiation induces cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts (6-4PPs) in DNA, which through gene mutations (e.g. in P53) may lead to skin carcinogenesis. Upon chronic low-level UV exposure, certain basal cells in mouse epidermis were reported to accumulate CPDs. These observations raised questions on whether these cells were fully DNA-repair deficient, and whether they were stem or progenitor cells, as suggested by their long residence time. We found that CPD-retaining basal cells (CRBCs) in SKH-1 hairless mice were repair proficient as accumulation of (6-4)PP, which is a hallmark for complete nucleotide excision repair-deficiency in rodents, was not observed. Accumulation of 6-4PP as well as CPD did, however, occur in basal cells in the epidermis of DNA repair-deficient Xpc-/- mice. Chronic UV exposure of DDB2 transgenic mice and DDB2 knockout mice revealed that the occurrence of CRBCs was inversely correlated with DDB2-expression, indicating that a boost in DNA repair lowered CPD accumulation. Stem cells are quiescent cells and can be identified as 5-bromo-2'-deoxyuridine-label retaining cells (BrdU-LRCs). Induction of BrdU-LRCs followed by chronic UV irradiation showed that all BrdU-label retaining stem cells were also CPD-retaining cells. As most CRBCs were not BrdU-labeled we surmized that these cells must include BrdU-negative stem cells and early progenitor cells. In confirmation of the latter, we found that CRBCs occurred among MTS24+ hair follicle progenitor cells. These findings provide the first evidence that epidermal stem and progenitor cells are prone to the accumulation of UV-induced DNA-damage and can be a prominent target in skin carcinogenesis.

Animals↗
PubMed2002

Enhanced repair of cyclobutane pyrimidine dimers and improved UV resistance in photolyase transgenic mice.

During evolution, placental mammals appear to have lost cyclobutane pyrimidine dimer (CPD) photolyase, an enzyme that efficiently removes UV-induced CPDs from DNA in a light-dependent manner. As a consequence, they have to rely solely on the more complex, and for this lesion less efficient, nucleotide excision repair pathway. To assess the contribution of poor repair of CPDs to various biological effects of UV, we generated mice expressing a marsupial CPD photolyase transgene. Expression from the ubiquitous beta-actin promoter allowed rapid repair of CPDs in epidermis and dermis. UV-exposed cultured dermal fibroblasts from these mice displayed superior survival when treated with photoreactivating light. Moreover, photoreactivation of CPDs in intact skin dramatically reduced acute UV effects like erythema (sunburn), hyperplasia and apoptosis. Mice expressing the photolyase from keratin 14 promoter photo reactivate CPDs in basal and early differentiating keratinocytes only. Strikingly, in these animals, the anti-apoptotic effect appears to extend to other skin compartments, suggesting the presence of intercellular apoptotic signals. Thus, providing mice with CPD photolyase significantly improves repair and uncovers the biological effects of CPD lesions.

Actins↗
PubMed2004

Continuing professional development of occupational medicine practitioners: a needs assessment.

OBJECTIVE: The aim of this study was to identify elements of occupational medicine practice used on a frequent basis which are considered to be of high priority for continuing professional development (CPD). METHODS: A postal questionnaire covering 28 areas of knowledge or practice was sent to all members of the Society of Occupational Medicine in September 2000. Respondents were asked to allocate scores to the 28 items for both CPD priority and frequency of use. RESULTS: The return rate for questionnaires was 29.5%. There was reasonable agreement between frequency of use and CPD priority ratings for the elements covered in the questionnaire. CONCLUSIONS: Despite the low return rate for questionnaires, this survey has helped identify themes which are important to physicians practising occupational medicine and has also highlighted those which are less important for inclusion in a CPD programme. Some differences in responses were identified between accredited specialists, specialist registrars and non-specialist practitioners of occupational medicine. The findings from this survey should be useful to providers of continuing medical education in planning courses, study days and electronic or distance learning educational packages.

Attitude of Health Personnel↗
PubMed2001

Public health physicians' knowledge of core skills and current policy: clinical audit by questionnaire.

BACKGROUND: The aim of this study was to facilitate the assessment of the knowledge of general public health physicians on a range of topics relating to everyday areas of work and core skills, and to encourage learning in the process, by means of an educational clinical audit exercise. METHODS: A group of experts in different aspects of public health were asked to contribute multiple-choice questions. These were developed into a questionnaire that could be marked by computer. The questionnaire was circulated to all members of the Faculty registered for Continuing Professional Development (CPD) and to specialist registrar members, but participation was voluntary. The experts marked answers according to a marking scheme against model answers agreed. RESULTS: A total of 499 public health doctors returned answer sheets. There was no 'pass mark' as this was a learning exercise, not an examination. However, although the negative marking system meant that the possible range of scores was -100 per cent to 100 per cent, no one had a negative score. The median uncorrected result was 44 out of 80. Questions on communicable disease and critical appraisal had the highest scores, and one on Primary Care Trusts the lowest. Participants thought the most interesting questions were those on epidemiology and evidence-based medicine, whereas the most unpopular was on Personal Medical Services pilots. Most comments were favourable to the approach but several commented that the whole exercise was too general and questions outside their current area of specialization were irrelevant. CONCLUSION: The general public health physicians who took part in this audit appeared to be mainly competent in their knowledge of core skills and up to date with current health policy issues. However, the audit raises a debate about what 'core' knowledge is required in the post-training period. The place of UK-wide CPD initiatives over national or regional, or local approaches needs consideration, as do potential regional or national variations in CPD. This will receive further impetus because of revalidation and the need to demonstrate valid CPD activities in public health medicine.

Attitude of Health Personnel↗
PubMed1997

Efficient protein production using a Bombyx mori nuclear polyhedrosis virus lacking the cysteine proteinase gene.

Infection by a baculovirus (Bombyx mori nuclear polyhedrosis virus, BmNPV) in silkworm (Bombyx mori) larvae is highly efficient as an expression system for the production of useful proteins. However, the amount of the protein of interest expressed tends to decrease in the later stages of infection presumably due, in part, to a proteinase produced in the larval haemolymph. The N-terminal amino acid sequence of a proteinase purified from the haemolymph of BmNPV-infected larvae was identical to the internal amino acid sequence of the viral cysteine proteinase gene of BmNPV, suggesting that the cysteine proteinase in the haemolymph originated from the BmNPV gene. We constructed a mutant virus (CPd) which had a deletion in the cysteine proteinase gene. No proteinase activity corresponding to this proteinase was detected in the haemolymph of silkworm larvae infected with CPd. The firefly luciferase and the human growth hormone genes were separately introduced into CPd under control of the polyhedrin promoter. These constructs produced these proteins very efficiently, because of a greatly reduced degree of degradation of these proteins. A BmNPV vector system using CPd enhances the stability of foreign expressed proteins, especially for those that are cysteine proteinase-sensitive.

Animals↗
PubMed1993

Effects of sunscreens and a DNA excision repair enzyme on ultraviolet radiation-induced inflammation, immune suppression, and cyclobutane pyrimidine dimer formation in mice.

Exposure of skin to ultraviolet (UV) radiation inhibits the induction of delayed-type hypersensitivity (DTH) responses initiated at a distant, unirradiated site. Recent studies attributed this form of immune suppression to DNA damage in the form of cyclobutane pyrimidine dimers (CPD). In the present study, we investigated the protective defects of sunscreens on UV-induced systemic suppression of DTH to Candida albicans, inflammation, and DNA damage. The photoprotective effects of sunscreen preparations containing 8% octyl-N-dimethyl-p-aminobenzoate, 7.5% 2-ethylhexyl-p-methoxycinnamate, or 6% benzophenone-3 were studied in C3H mice exposed to a single dose of 500 mJ/cm2 UVB radiation from FS40 sunlamps. Inflammation was determined by the amount of skin edema at the site of UV irradiation, and DNA damage was assessed by measuring the frequency of endonuclease-sensitive sites in the epidermis. Application of the sunscreens before UV irradiation gave 75-97% protection against UV-induced edema, 67-91% protection against formation of CPD, but only 30-54% protection against suppression of DTH. In contrast, the topical application of liposomes containing a CPD-specific DNA repair enzyme immediately after UV irradiation resulted in 82% protection against suppression of DTH, but at best, 39% protection against skin edema. These findings demonstrate that sunscreens give less protection against UV-induced immune suppression than against skin edema and CPD formation. Furthermore, they suggest that less DNA damage is required to cause UV-induced immune suppression than to cause sunburn.

Animals↗
PubMed1997

Moraxella (Branhamella) catarrhalis adherence to human bronchial and oropharyngeal cells: the role of adherence in lower respiratory tract infections.

To study the role of Moraxella (subgenus Branhamella) catarrhalis (B. catarrhalis) adherence to airway cells in lower respiratory tract infections, the in vitro attachments of B. catarrhalis to upper airway (oropharyngeal) and lower airway (bronchial) epithelial cells were compared. The adherence of 4 strains (1 nonfimbriated and 3 fimbriated) of B. catarrhalis to respiratory tract epithelial cells collected from 11 patients with chronic pulmonary disease (CPD) and 11 healthy individuals was evaluated. Both the fimbriated and nonfimbriated strains showed increased attachment to oropharyngeal cells in the CPD patients (mean +/- SEM; 25.0 +/- 3.2/cell; P < 0.01) when compared to the control subjects (12.1 +/- 1.1/cell). On the average, the attachment to bronchial cells was 6.1 to 13.6 times greater per surface area (bacteria/micron2) than the attachment to oropharyngeal cells. The fimbriated strains tended to adhere in higher numbers to bronchial cells (19.0 +/- 1.8/cell) than the nonfimbriated strain (8.7 +/- 1.2/cell), although there was no difference between the CPD and control groups. In conclusion, the attachment of B. catarrhalis to oropharyngeal cells may be an enhancing factor for colonization in the upper respiratory tract in patients with CPD, and elevated adherence of the bacteria to bronchial cells may suggest pathogenic importance when mucociliary function is impaired.

Adult↗
PubMed2005

ATX-S10(Na)-photodynamic therapy is less carcinogenic for mouse skin compared with ultraviolet B irradiation.

BACKGROUND: Photodynamic therapy (PDT) is available for the treatment of various skin tumours and other skin diseases. Ultraviolet (UV) irradiation induces DNA damage, cyclobutane pyrimidine dimers (CPD) (6-4) photoproducts (6-4PP) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), all of which are carcinogenic for the skin. However, effects of PDT on DNA damage and carcinogenesis are unclear. OBJECTIVES: To compare the production of photoproducts and the induction of skin tumours in mouse epidermis treated with UVB or PDT. METHODS: We performed UVB irradiation or ATX-S10(Na)-PDT on the skin of 20 hairless mice, in each case, and analysed DNA damage and tumour induction. RESULTS: After a single irradiation of UVB on mouse skin, CPD, 6-4PP and 8-OHdG were detected in the nuclei of keratinocytes. In contrast, PDT-treated mouse keratinocytes showed induction of 8-OHdG, but not of CPD or 6-4PP. Skin tumours induced by UVB irradiation (3 kJ m(-2) three times weekly) were observed following 15 weeks of irradiation (mean +/- SEM tumour incidence 3.2 +/- 1.8%; tumour number 3.2 +/- 1.6 per mouse) and increased depending on irradiation times and doses. Following 30 weeks of UVB irradiation (3 kJ m(-2) three times weekly), mean +/- SEM tumour incidence and tumour number were 28.7 +/- 4.8% and 14.2 +/- 2.8% per mouse, respectively. Although skin tumours were also detected in PDT-treated mouse skin following 80 weeks of treatment (mean +/- SEM tumour incidence 9.1 +/- 1.8%; tumour number 12.2 +/- 2.3 per mouse), the number of tumours was not statistically different from untreated mouse skin (mean +/- SEM tumour incidence 4.1 +/- 3.8%; tumour number 5.2 +/- 3.3 per mouse). CONCLUSIONS: PDT induced 8-OHDG but not CPD or 6-4PP, and was shown to be a relatively safe modality following multiple applications to mouse skin.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1990

Zinc ions inhibit factor I-mediated release of CR1-bound immune complexes and degradation of cell-bound complement factors C3b and C4b.

ZnCl2 exerted a dose-dependent inhibition of citrate-phosphate-dextrose (CPD) plasma-induced release of 125I-labelled BSA-anti-BSA immune complexes (IC) bound to complement receptor type 1 (CR1, CD35) in human whole blood. Maximal inhibition was observed at 10 mM of ZnCl2. Furthermore, the release of IC bound to erythrocyte (E)-CR1 by purified factor I, factor I-deficient serum plus purified factor I, or normal human serum was reduced by approximately 90%, 64%, and 52%, respectively, in the presence of 10 mM ZnCl2. The effect of ZnCl2 on factor I-mediated degradation of cell-bound C3b/C4b was also investigated employing CPD blood or E from a factor I-deficient donor. These cells expressed covalently bound C3b and C4b as demonstrated by a simple agglutination technique. Upon incubation of CPD whole blood with purified factor I, or of E with purified factor I or normal CPD plasma, the C-fragments were cleaved and the cells were no longer agglutinated by antibodies to C3c and C4c. The presence of ZnCl2 prevented this factor I-mediated degradation of C3b and C4b, as evidenced by the unaffected agglutination of the cells by the antibodies. We conclude that ZnCl2 inhibited factor I activity since: (1) release of complement-preopsonized IC from E-CR1 by purified factor I was markedly inhibited (90%) in the presence of ZnCl2, (2) preincubation of the cells with ZnCl2 caused only a moderate inhibition (32-38%) of the IC release, and (3) degradation by purified factor I of covalently cell-bound C3b and C4b was abrogated in the presence of 10 mM ZnCl2.

Animals↗
PubMed1975

A clinical evaluation of citrate-phosphate-dextrose-adenine blood.

(1) Blood was stored in polyvinyl-chloride bags containing citrate-phosphate-dextrose (CPD) with adenine in a final concentration of 0.25 mM. (2) Red cell ATP was well maintained (greater than 70% of original) for 4 weeks in whole blood as well as in red cell concentrate (PCV 85 plus or minus 2%). After 5 weeks the ATP level was about 70% in whole blood and about 40% in red cell concentrate. (3) Red cell 2,3-diphosphoglycerate (DPG) was about 60% of the original after 2 weeks and about 30% after 3 weeks of storage when stored both as whole blood and as red cell concentrate. (4) The red cell 24-hour post-transfusion viability was about 80% after 4 weeks of storage both as whole blood and as red cell concentrate. After 5 weeks of storage the 24-hour viability was 78.7 plus or minus 3.5% in whole blood and 76.5 plus or minus 6.7% in red cell concentrate. (5) 820 patients received 3,238 units of CPD-adenine blood, and 761 patients serving as controls received 2,807 units of acid-citrate-dextrose (ACD) blood. The frequency of transfusion reactions was 3.5% for patients receiving CPD-adenine blood and 4.1% for the control group. (6) The maximum storage time was set at 5 weeks for the CPD-adenine blood and 3 weeks for the ACD blood. The longer preservation time decreased out-dating by at least 50%.

ABO Blood-Group System↗
PubMed1979

Improved yields of factor VIII from heparinized plasma.

The Factor VIII procoagulant activity in plasma, cryoprecipitate, and their polyethylene glycol (PEG) precipitates is markedly increased if blood is collected into heparin rather than into citrate phosphate dextrose (CPD). There is a 34% increase in the initial level of the Factor VIII activity in the heparinized plasma with 78% of this initial activity (184 U) recovered in the cryoprecipitated. As well, the stability of the Factor VIII activity is improved: after 24 h of incubation at 22 degrees C, 99% of the initial activity is retained in heparinized plasma whereas only 64% remains in CPD plasma. The cryoprecipitate prepared from heparinized plasma is equally stable after 24 h. The PEG concentrate prepared from the cryoprecipitate of heparinized plasma is increased to 128 U compared to only 54 U from CPD plasma. Relative recoveries were 531 U/l for heparinized plasma versus 215 U/l for CPD plasma. This represents a 147% increase in yield.

Anticoagulants↗