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W Ahrens

Publications and source records attributed to W Ahrens.

At least 55 records · Page 3Linked to original sources
PubMed2000

Temporal expression of the chondrogenic and angiogenic growth factor CYR61 during fracture repair.

The repair of a fractured bone is a complex biological event that essentially recapitulates embryonic development and requires the activity of a number of different cell types undergoing proliferation, migration, adhesion, and differentiation, while at the same time expressing a host of different genes. To identify such genes, we employed differential display and compared messenger RNA (mRNA) populations isolated from postfracture (PF) day 5 calluses to those of intact rat femurs. One such gene in which expression was up-regulated at PF day 5 is identified as CYR61, a member of the CCN family of secreted regulatory proteins. CYR61 is a growth factor that stimulates chondrogenesis and angiogenesis. We show that its mRNA expression during fracture repair is regulated temporally, with elevated levels seen as early as PF day 3 and day 5, rising dramatically at PF day 7 and day 10, and finally declining at PF day 14 and day 21. At the highest peak of expression (PF day 7 and day 10, which correlates with chondrogenesis), CYR61 mRNA levels are approximately 10-fold higher than those detected in intact femurs. Similarly, high protein levels are detected throughout the reparative phase of the callus, particularly in fibrous tissue and periosteum, and in proliferating chondrocytes, osteoblasts, and immature osteocytes. The secreted form of CYR61 also was detected within the newly made osteoid. No labeling was detected in hypertrophic chondrocytes or in mature cortical osteocytes. These results suggest that CYR61 plays a significant role in cartilage and bone formation and may serve as an important regulator of fracture healing.

Animals↗
PubMed2000

Lung cancer risk in nonsmokers and GSTM1 and GSTT1 genetic polymorphism.

Glutathione S-transferase (GST) polymorphism may contribute to the individual variability in detoxifying lung carcinogens. This effect might be particularly relevant at low-level exposure to environmental carcinogens, such as in nonsmokers exposed to environmental tobacco smoke (ETS). We conducted a case-control study among 122 nonsmoking lung cancer cases and 121 nonsmoking controls from eight countries. Information on environmental exposures was obtained through a personal interview. The presence of GSTM1 and GSTT1 genes was determined using multiplex PCR. GSTM1-positive samples were then analyzed for *1A and *1B polymorphism using an allele-specific amplification-PCR method. GSTM1*2 (null) individuals had an odds ratio (OR) of lung cancer of 1.5 [95% confidence interval (CI), 0.9-2.7]; the risk associated with this genotype was higher for cases with squamous and small cell carcinomas (OR, 2.3; 95% CI, 0.9-6.1) than for cases with adenocarcinomas. It was also elevated in individuals with long-term exposure to indoor wood combustion (OR, 3.1; 95% CI, 0.9-9.9), in subjects who mainly lived in a rural setting (OR, 3.6; 95% CI, 1.0-13), and in cases exposed to occupational carcinogens (OR, 10.7; 96% CI, 0.4-260) but not in subjects exposed to ETS. GSTT1*2 subjects did not show a risk of lung cancer. Our study suggests that the effect of GSTM1 polymorphism in nonsmokers is similar to that found in smokers. It does not seem to interact with ETS exposure, although we cannot exclude that it does in association with exposure to other specific environmental carcinogens.

Adenocarcinoma↗
PubMed2000

Sorting the hype from the facts in testicular cancer: is testicular cancer related to trauma?

PURPOSE: The rate of testicular cancer is increasing. Trauma severe enough to cause testicular atrophy is a putative risk factor for testicular cancer but the epidemiological evidence is not conclusive. A population based, multicenter case-control study was performed from 1995 to 1997 to investigate potential risk factors for gonadal and extragonadal germ cell cancer. MATERIALS AND METHODS: The study was done in 5 German regions. Interviews were performed with 269 eligible male patients with a histologically verified diagnosis and 797 controls. Detailed information on medical and family history was collected at personal interviews. RESULTS: We identified a significantly elevated risk for testicular cancer in relation to testis and/or groin trauma (odds ratio 2.5, 95% confidence interval [CI] 1.51 to 4.20). After introducing a lag time by excluding reports of trauma within the last 12 months before diagnosis or interview the corresponding odds ratio was 2.1 (95% CI 1.24 to 3.61). Analysis of the circumstances and the reported types of injury allowed us to restrict the study to testis trauma specifically, which had an odds ratio of 3.49 (95% CI 1.78 to 6.81). To account for a potential reporting bias analysis was restricted to traumatic episodes for which medical attention was sought. This restriction resulted in an odds ratio of 0.70 (95% CI 0.19 to 2.63) after excluding from study trauma reports within the last 12 months. CONCLUSIONS: The results of our study do not support the hypothesis that testicular trauma is an important risk factor for testicular cancer. The possibility of recall bias should be considered.

Adolescent↗
PubMed1999

Exposure to environmental tobacco smoke and risk of adenocarcinoma of the lung.

We conducted a case-control study of adenocarcinoma of the lung and exposure to environmental tobacco smoke (ETS) in 7 countries. We interviewed 70 cases of adenocarcinoma of the lung and 178 population or hospital controls. All subjects had smoked fewer than 400 cigarettes in their lifetimes. Ever exposure to ETS from the parents during childhood was associated with a decreased risk [odds ratio (OR) 0.6, 95% confidence interval (CI) 0.3-1.2], and there was a suggestion of a decreasing trend in risk with increasing duration of exposure. Ever exposure to ETS from the spouse was not associated with an increased risk (OR 1.0, 95% CI 0.5-1.8), while the OR of ever exposure to ETS at the workplace was 1.5 (95% CI 0.8-3.0). For both exposure sources, an increased risk was observed among the highly exposed, and the OR among those with the highest duration of exposure to ETS from the spouse or at the workplace was 1.8 (95% CI 0.5-6.2). A similar risk was estimated for current exposure to ETS from either source. Our results confirm previous reports of a weak effect of adult ETS exposure on risk of adenocarcinoma of the lung. Bias and confounding cannot be excluded as explanations for the apparent decrease in risk from childhood exposure.

Adenocarcinoma↗
PubMed1999

Occupational risk factors for lung cancer in women: results of a case-control study in Germany.

BACKGROUND: To investigate the association between lung cancer and occupational factors in women. METHODS: Six hundred eighty-six women with lung cancer and 712 controls matched for age and region were interviewed to gather occupational histories and information about other risk factors and confounders. Odds ratios (OR) and 95%-confidence intervals (CI) were calculated. RESULTS: There were 11 cases and 2 controls who reported occupational asbestos exposure. Significantly elevated risks (P < 0.05, smoking-adjusted), were observed in the following industries: chemical, oil (OR 3.7), pottery, glass (OR 2.5), engine, vehicle building (OR 2.2), paper, wood, print (OR 1.9), cleaning service, hairdressing, housekeeping, waste disposal (OR 1.5); and occupations: assemblers, unskilled metal workers (OR 2.5), stock clerks, etc. (OR 1.6), restaurant owners and hoteliers (OR 2.7), as well as waitresses and travel attendants (OR 2.6). CONCLUSIONS: The study provides evidence that both occupations previously observed as hazardous in males, and occupations of particular significance for women only, play a role in the risk of lung cancer in women.

Adult↗
PubMed1999

Lung cancer risk in male workers occupationally exposed to diesel motor emissions in Germany.

BACKGROUND: Although in several epidemiological studies exposure to diesel motor emissions (DME) shows an elevated lung cancer risk, it is still controversial whether DME is a human carcinogen. METHODS: In a pooled analysis of two case-control studies on lung cancer in Germany a total of 3498 male cases with histologically or cytologically ascertained lung cancer and 3541 male population controls were included. Information about lifelong occupational and smoking history was obtained by questionnaire. Drivers of lorries, buses, taxies, diesel locomotives and forklift trucks, bulldozers, graders, excavators, and tractors, were considered as exposed to DME and their cumulative exposure was estimated. All odds ratios were adjusted for smoking and asbestos exposure. RESULTS: The evaluation of lung cancer risk for all jobs with DME-exposure combined showed an odds ratio of OR=1.43 (95%-CI: 1.23-1.67). Most pronounced was the increase in lung cancer risk in heavy equipment operators (OR=2. 31 95%-CI: 1.44-3.70). The risk of tractor drivers increased with length of employment and reached statistical significance for exposures longer than 30 years (OR=6.81, 95%-CI: 1.17-39.51). The group of professional drivers (e.g., trucks, buses, and taxies), showed an increased risk only in West Germany (OR=1.44, 95%-CI: 1. 18-1.76), but not in East Germany (OR=0.83, 95%-CI: 0.60-1.14). DME-exposure in other traffic related jobs (e.g., diesel engine locomotive drivers, switchmen, forklift operators) was associated with an odds ratio of OR=1.53 (95%-CI: 1.04-2.24). CONCLUSIONS: The study provides further evidence that occupational exposure to diesel motor emissions is associated with an increased lung cancer risk.

Aged↗
PubMed1999

Occupational risk factors for lung cancer among young men.

OBJECTIVES: This study evaluated whether occupational exposure plays a role for lung cancer at a very young age. METHODS: In a pooled analysis of 2 German case-referent studies including 3498 incident cases among men and 3541 male population referents, a group of men (187 cases and 202 referents) aged > or =45 years was compared with a group of 2186 cases and 2146 referents aged 55-69 years. Occupational exposure to known (A list) or suspected (B list) lung carcinogens was assessed using job and industry codes, and exposure to asbestos was assessed using job-specific supplementary questionnaires. A conditional logistic regression was used to calculate the odds ratios (OR) and to control for smoking. RESULTS: Asbestos exposure showed an odds ratio (OR) of 2.39 [95% confidence interval (95% CI) 1.41-4.04] for the younger group and 1.46 (95% CI 1.24-1.72) for the older group. Having ever worked in a job belonging to the A list as compared with never working in an A- or B-list job was associated with a significantly increased risk for the younger (OR 2.06, 95% CI 1.03-4.12) and older (OR 1.35, 95% CI 1.10-1.65) groups, adjusted for asbestos. Lung cancer risk for those working in A-list jobs at a very young age (under 16 years) was increased in the younger group (OR 6.14, 95% CI 1.41-28.01) in contrast to the older group (OR 1.19, 95% CI 0.91-1.63). CONCLUSION: Occupational risk factors play an important role for lung cancer among young men. Early age at first exposure may favor an early age of the onset of lung cancer.

Adult↗
PubMed1999

Control response proportions in population-based case-control studies in Germany.

We investigated the methods of recruitment, levels and determinants of response, and the calculation method of response proportions in population-based case-control studies in Germany. We identified 26 eligible studies. The pooled analysis showed that the response proportion was 68% among controls and 80% among cases. Response proportions among controls without telephones were about 50% lower than for controls with telephones. We propose a new measure that indicates the efficacy of the recruitment strategy.

Adult↗
PubMed1998

Multicenter case-control study of exposure to environmental tobacco smoke and lung cancer in Europe.

BACKGROUND: An association between exposure to environmental tobacco smoke (ETS) and lung cancer risk has been suggested. To evaluate this possible association better, researchers need more precise estimates of risk, the relative contribution of different sources of ETS, and the effect of ETS exposure on different histologic types of lung cancer. To address these issues, we have conducted a case-control study of lung cancer and exposure to ETS in 12 centers from seven European countries. METHODS: A total of 650 patients with lung cancer and 1542 control subjects up to 74 years of age were interviewed about exposure to ETS. Neither case subjects nor control subjects had smoked more than 400 cigarettes in their lifetime. RESULTS: ETS exposure during childhood was not associated with an increased risk of lung cancer (odds ratio [OR] for ever exposure = 0.78; 95% confidence interval [CI] = 0.64-0.96). The OR for ever exposure to spousal ETS was 1.16 (95% CI = 0.93-1.44). No clear dose-response relationship could be demonstrated for cumulative spousal ETS exposure. The OR for ever exposure to workplace ETS was 1.17 (95% CI = 0.94-1.45), with possible evidence of increasing risk for increasing duration of exposure. No increase in risk was detected in subjects whose exposure to spousal or workplace ETS ended more than 15 years earlier. Ever exposure to ETS from other sources was not associated with lung cancer risk. Risks from combined exposure to spousal and workplace ETS were higher for squamous cell carcinoma and small-cell carcinoma than for adenocarcinoma, but the differences were not statistically significant. CONCLUSIONS: Our results indicate no association between childhood exposure to ETS and lung cancer risk. We did find weak evidence of a dose-response relationship between risk of lung cancer and exposure to spousal and workplace ETS. There was no detectable risk after cessation of exposure.

Aged↗
PubMed1998

Cloning of a novel cDNA expressed during the early stages of fracture healing.

Using differential mRNA display (DD-PCR), a novel cDNA, FxC1 (Fracture Callus 1) was isolated from the early stages of a healing fractured femur. Utilizing 5' RACE PCR, a 598-bp full-length cDNA was obtained for FxC1 that contains an open reading frame (ORF) of 243 bp, encoding for an 80 amino acid protein. Within this ORF, a leucine zipper motif was present. In vitro transcription/translation of the full-length cDNA generated the expected 9-kDa protein. Northern analysis reveals that this gene is expressed in calluses harvested from post-fracture day 5, 7 and 10, as well as in several other tissues and bone-derived cell lines. During the differentiation of MC3T3 cells along the osteoblast lineage, FxC1 expression increases 3- to 4-fold during the production and deposition of matrix proteins, suggesting a possible role for this protein in cell differentiation.

Amino Acid Sequence↗
PubMed1998

Lung cancer risk and welding: results from a case-control study in Germany.

In a case-control study, 839 male hospital-based cases of primary lung cancer and the same number of population-based controls--matched by sex, age, and region of residence--were personally interviewed for their job and smoking histories. The study allows to quantify occupational asbestos exposure that was thought to be a welding-associated risk: 6% of cases and 2% of controls were classified into the occupational category "welders or burners# (odds ratio [OR] = 2.65). This OR was reduced to 1.93 (95% confidence limit [CL]: 1.03-3.61) after adjustment for smoking and asbestos. In contrast, a history of welding in general for at least a half-year is 28% among cases and 23% among controls, yielding an OR of 1.25 (95% CL: 0.94-1.65) after adjustment for both confounders. The OR of welding for more than 6,000 hr is 1.45 (95% CL = 1.04-2.02), reduced to 1.10 after adjustment for smoking and asbestos. Oxyacetylene welding for more than 6,000 hr lifelong is associated with an OR of 1.86 (95% CL = 1.01-3.43) reduced to 1.46 (n.s.) after adjustment for smoking and asbestos. The risk of oxyacetylene welding seems to be highest for oat cell carcinoma with an adjusted OR for ever-exposure of 1.46 (95% CL = 0.69-3.10). Therefore, the present study supports the hypothesis that some, but not all, of the excess risk of welders observed in the literature may be due to a history of cigarette smoking and occupational asbestos exposure. The elevated risk for the subgroup of employees in the aircraft industry reported for the midterm evaluation of the study still prevails, though no longer statistically significant. However, employees in this industry who ever welded show an OR of 2.29 (95% CL = 1.19-4.42) after adjustment for smoking and asbestos.

Adult↗
PubMed1998

Occupational risk factors for lung cancer: a case-control study in West Germany.

BACKGROUND: The aim of this study is to evaluate carcinogens and occupations suspected to cause lung cancer and to generate new hypotheses about occupational risks. METHODS: In a hospital-based study 1004 incident lung cancer cases and the same number of population controls matched for region, sex and age were interviewed between 1988 and 1993 for their smoking and occupational history. Exposure assessment was based on 33 job-specific supplementary questionnaires. Conditional logistic regression was used to calculate odds ratios (OR) and to control for smoking and occupational asbestos exposure. RESULTS: Lifelong prevalence of exposure to asbestos was 20.5% for exposure of more than 940 lifetime working hours among controls, corresponding to an OR of 1.62 (95% confidence interval [CI] : 1.28-2.05) that was reduced to 1.45 after adjustment for smoking (P < 5%). Statistically elevated risks after adjustment for smoking and asbestos were seen in metal production and processing workers, transportation workers and freight handlers, in the rubber and plastics industry, in metal production, in engine and vehicle building, and installation. Significantly increased OR after adjustment for smoking and asbestos that deserve further attention were seen in plastics processing workers (OR = 3.49), and sheet and structural metal workers (OR = 2.01 and 2.37, respectively). CONCLUSIONS: The results of the study confirm previously described occupational risks. Because of the possibility of controlling for occupational asbestos exposure, the study gives clear indications for prevention and further research.

Adult↗
PubMed1998

4-Hydroxy-1-(3-pyridyl)-1-butanone-hemoglobin adducts as biomarkers of exposure to tobacco smoke: validation of a method to be used in multicenter studies.

Hemoglobin (Hb) adducts of 4-hydroxy-1-(3-pyridyl)-1-butanone (HPB), a metabolite of two tobacco-specific nitrosamines [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N'-nitrosonornicotine], were measured as biomarkers of exposure to tobacco smoke as part of a study on genetic alterations and susceptibility to lung cancer among nonsmokers. HPB-Hb adducts were measured after collection of RBCs by Ficoll gradient in six collaborating centers, release of HPB by alkaline hydrolysis from Hb, clean-up by solid-phase extraction, and analysis of an electron-capturing derivative by gas chromatography-electron capture mass spectrometry. Prior to analysis of samples from study subjects, the reproducibility of this approach was validated in blood from donors. The coefficient of variation of reproducibility of paired aliquots from five samples ranged from 7 to 25%; the within-sample reproducibilities of four and eight aliquots were 4 and 16%, respectively. The study subjects consisted of 18 smokers and 52 never-smokers. HPB-Hb adduct levels were significantly higher (P = 0.02) in smokers (26 +/- 13 fmol HPB/g Hb) than in never-smokers (20 +/- 8 fmol HPB/g Hb). There was no difference between sexes. These results suggest that the level of HPB-Hb adducts, measured using a method modified to facilitate use in multicenter studies, can be a useful biomarker of exposure to tobacco smoke.

Biomarkers↗
PubMed1998

Environmental tobacco smoke and lung cancer.

In a case-control study of 1,004 lung cancer cases and 1,004 population controls, all nonsmokers (71 cases, 236 controls) were interviewed for their exposure to environmental tobacco smoke. On the basis of indices of duration, we separated intermediate and high exposures from low or no exposure. The odds ratio for high exposure was 2.09 (95% confidence interval = 1.02-4.28). Exposure from the spouse was only weakly associated with lung cancer risk. We found little association for exposure during childhood. High exposure at the work place showed an odds ratio of 1.91. There was little indication of confounding by dietary habits.

Adult↗
PubMed1997

[Occupationally-induced lung cancer--a quantitative evaluation for the North Germany area].

The aim of the study was to estimate the proportion of occupation-related lung cancer for males and females in Northern Germany. 1004 lung cancer cases (839 males, 165 females) were enrolled into an epidemiological case-control study in the study areas Bremen, the surroundings of Bremen and the Frankfurt/Main area. Population controls were matched for sex and region of residence. All patients born after 1913 of German nationality and with a histologically or cytologically verified carcinoma of the lung, the diagnosis not older than 3 months at the date of interview, were eligible. All individuals were personally interviewed with respect to their smoking and job history. Based on a published list of all jobs and branches of industries with sufficient evidence for lung carcinogenity (based on the reviews by IARC), the so called A-List, all individuals were classified regarding their lifelong occupational history. The same procedure was applied with regard to jobs and branches of industries with a suspected risk of lung cancer (List-B). The statistical analysis used conditional logistic regression, controlled for smoking. Being employed in a job of List-A for at least half a year was associated with a statistically significant odds ratio (OR) of 1.63 (p < 0.0001) and resulting attributable risk (AR) of 16% in males. For the B-List an OR of 1.34 and an AR of 10% resulted in males. The estimates of the attributable risk for jobs and branches of industry with a sufficient evidence of lung cancer risk is comparable to the estimates obtained by Doll and Peto for the US. If additionally jobs and branches of industries with a suspected risk for lung cancer is considered, it must be anticipated that approximately one quarter of all newly diagnosed male lung cancer cases in the study region may be caused by occupational risk factors. This should prompt to minimise occupational exposure.

Adult↗
PubMed1994

Lung cancer risk and welding--preliminary results from an ongoing case-control study.

In a hospital-based case-control study, 391 male cases or primary lung cancer and the same number of controls--matched by sex, age, and region--were personally interviewed for their job and smoking histories. The data reported reflect the midpoint of a study aiming at a total of 1,000 cases. One objective of the study was to assess confounding by asbestos exposure in what was thought to be a welding-associated risk. While the odds ratios (OR) increased steeply with cumulative exposure to tobacco smoke and were raised also for lifelong asbestos exposure of over 4,100 working hours (OR = 1.91), the effect of welding exposure was reduced after adjustment for smoking and exposure to asbestos. Furthermore, no consistent dose-response relationship could be shown in relation to welding hours. Therefore the present study supports the hypothesis that some, if not all, of the excess risk of welders observed in the literature may be due to the exposure to asbestos. The finding that the subgroup of employees in the aircraft industry showed an increased odds ratio of 2.14 after adjustment for smoking and exposure to asbestos deserves further attention. This suggests the need for further research on the role of berryllium-containing alloys, which has been suggested by other authors.

Aged↗
PubMed1993

Retrospective assessment of asbestos exposure--I. Case-control analysis in a study of lung cancer: efficiency of job-specific questionnaires and job exposure matrices.

Retrospective assessment of asbestos exposure--I. Case-control analysis in a study of lung cancer: efficiency of job-specific questionnaires and job exposure matrices. International Journal of Epidemiology 1993; 22 (Suppl. 2): S83-S95. In a lung cancer study in Northern Germany the asbestos exposure assessment obtained from detailed supplementary questionnaires (SQ) was compared to the assessment obtained by the application of two job exposure matrices (JEM) to the job history. The study includes 391 incident male cases and the same number of controls from the general population, matched by sex, age, and region. Almost 16% of the subjects are considered as never having been exposed to asbestos and 24% are classified as certainly exposed according to both of the JEM, the corresponding percentages of the SQ-method being 68% and 32%. Sixty percent are considered by the JEM as having an intermediate probability of exposure. In general, the agreement between the different methods is better when the exposure definition is restricted to definite exposures, the corresponding Kappa statistic being 0.67 for the comparison between both JEM and 0.44/0.39 between the JEM and the SQ. The positive agreement between SQ and JEM (reference) increases from 12% and 17% for subjects with low probability of exposure to 61% and 69% for those with definite exposures. A ranking according to cumulative exposure shows some dose-response relationship for each of the three methods with a smoking-adjusted OR in the highest category of 1.85 (95% CI: 1.01-3.38) for the SQ method and 2.47 (95% CI: 1.40-4.37) and 2.94 (95% CI: 1.73-4.99) for the two JEM. The results are discussed with reference to the conceptual differences between the methods and their potential scope in future studies.

Asbestos↗