Changes in movement patterns in relation to sun conditions and spatial scales in wild western gorillas.

For most primates living in tropical forests, food resources occur in patchworks of different habitats that vary seasonally in quality and quantity. Efficient navigation (i.e., spatial memory-based orientation) towards profitable food patches should enhance their foraging success. The mechanisms underpinning primate navigating ability remain nonetheless mostly unknown. Using GPS long-term tracking (596 days) of one group of wild western lowland gorillas (Gorilla gorilla gorilla), we investigated their ability to navigate at long distances, and tested for how the sun was used to navigate at any scale by improving landmark visibility and/or by acting as a compass. Long episodic movements ending at a distant swamp, a unique place in the home range where gorillas could find mineral-rich aquatic plants, were straighter and faster than their everyday foraging movements relying on spatial memory. This suggests intentional targeting of the swamp based on long-distance navigation skills, which can thus be efficient over a couple of kilometres. Interestingly, for both long-distance movements towards the swamp and everyday foraging movements, gorillas moved straighter under sunlight conditions even under a dense vegetation cover. By contrast, movement straightness was not markedly different when the sun elevation was low (the sun azimuth then being potentially usable as a compass) or high (so providing no directional information) and the sky was clear or overcast. This suggests that gorillas navigate their home range by relying on visual place recognition but do not use the sun azimuth as a compass. Like humans, who rely heavily on vision to navigate, gorillas should benefit from better lighting to help them identify landmarks as they move through shady forests. This study uncovers a neglected aspect of primate navigation. Spatial memory and vision might have played an important role in the evolutionary success of diurnal primate lineages.

Three-dimensional random walk models of individual animal movement and their application to trap counts modelling.

BACKGROUND: Random walks (RWs) have proved to be a powerful modelling tool in ecology, particularly in the study of animal movement. An application of RW concerns trapping which is the predominant sampling method to date in insect ecology and agricultural pest management. A lot of research effort has been directed towards modelling ground-dwelling insects by simulating their movement in 2D, and computing pitfall trap counts, but comparatively very little for flying insects with 3D elevated traps. METHODS: We introduce the mathematics behind 3D RWs and present key metrics such as the mean squared displacement (MSD) and path sinuosity, which are already well known in 2D. We develop the mathematical theory behind the 3D correlated random walk (CRW) which involves short-term directional persistence and the 3D Biased random walk (BRW) which introduces a long-term directional bias in the movement so that there is an overall preferred movement direction. In this study, we focus on the geometrical aspects of the 3D trap and thus consider three types of shape; a spheroidal trap, a cylindrical trap and a rectangular cuboidal trap. By simulating movement in 3D space, we investigated the effect of 3D trap shapes and sizes and of movement diffusion on trapping efficiency. RESULTS: We found that there is a non-linear dependence of trap counts on the trap surface area or volume, but the effect of volume appeared to be a simple consequence of changes in area. Nevertheless, there is a slight but clear hierarchy of trap shapes in terms of capture efficiency, with the spheroidal trap retaining more counts than a cylinder, followed by the cuboidal type for a given area. We also showed that there is no effect of short-term persistence when diffusion is kept constant, but trap counts significantly decrease with increasing diffusion. CONCLUSION: Our results provide a better understanding of the interplay between the movement pattern, trap geometry and impacts on trapping efficiency, which leads to improved trap count interpretations, and more broadly, has implications for spatial ecology and population dynamics.

Vicia sativa subsp. sativa native to the Middle East comprises Pea Albumin1 b-like homologs: A promising natural biopesticide.

The extensive and indiscriminate use of chemical pesticides in agriculture has led to adverse effects on human health, environmental pollution, and the emergence of pesticide-resistant pests. To mitigate these challenges, the development of environmentally friendly alternatives is crucial, with biopesticides emerging as promising solutions such as peptides. Legume seeds naturally contain diverse insecticidal peptides or proteins to combat pest attacks. One such peptide is PA1b (Pea Albumin 1, subunit b), a 37 amino acid extracted from pea seeds (Pisum sativum). PA1b has shown significant potential in controlling cereal weevils (Sitophilus spp.), a major pest of stored cereals. Here, we screened PA1b-like peptides in five wild seeds of vetches (Vicia sativa subsp. sativa) from the Middle East. Using a comprehensive set of biochemical, biological, and molecular techniques, we characterized different PA1b homologs and assessed their toxicity and expression profiles. Our results reveal that PA1b homolog from Vicia sativa subsp. sativa originating from turkey displays outstanding insecticidal activity against Sitophilus oryzae through binding to the receptor site found in the midgut of the insect. Moreover, it exhibits a strong cytotoxic effect against Sf9 cells. This cysteine-rich peptide shows sequence identity and the same hydrophobic pole as AG41, a tenfold more toxic isoform of PA1b from Medicago truncatula. Such observations pave the way for the development of bioinsecticides, with PA1b-like peptides as lead compounds.

Role of medical history and medication use in the aetiology of upper aerodigestive tract cancers in Europe: the ARCAGE study.

BACKGROUND: The study aimed to investigate the role of medical history (skin warts, Candida albicans, herpetic lesions, heartburn, regurgitation) and medication use (for heartburn; for regurgitation; aspirin) in the aetiology of upper aerodigestive tract (UADT) cancer. METHODS: A multicentre (10 European countries) case-control study [Alcohol-Related CAncers and GEnetic susceptibility (ARCAGE) project]. RESULTS: There were 1779 cases of UADT cancer and 1993 controls. History of warts or C. albicans infection was associated with a reduced risk [odds ratio (OR) 0.80, 95% confidence interval (CI) 0.68-0.94 and OR 0.73, 95% CI 0.60-0.89, respectively] but there was no association with herpetic lesions, heartburn, regurgitation or medication for related symptoms. Regurgitation was associated with an increased risk for cancer of the oesophagus (OR 1.47, 95% CI 0.98-2.21). Regular aspirin use was not associated with risk of UADT cancer overall but was associated with a reduced risk for cancer of oesophagus (OR 0.51, 95% CI 0.28-0.96), hypopharynx (OR 0.53, 95% CI 0.28-1.02) and larynx (OR 0.74, 95% CI 0.54-1.01). CONCLUSIONS: A history of some infections appears to be a marker for decreased risk of UADT cancer. The role of medical history and medication use varied by UADT subsites with aspirin use associated with a decreased risk of oesophageal cancer and suggestive of a decreased risk of hypopharyngeal and laryngeal cancers.

Excess of cardiovascular mortality among node-negative breast cancer patients irradiated for inner-quadrant tumors.

BACKGROUND: Radiotherapy of the left breast is associated with higher cardiovascular mortality linked to cardiotoxic effect of irradiation. Radiotherapy of inner quadrants can be associated with greater heart irradiation, but no study has evaluated the effect of inner-quadrant irradiation on cardiovascular mortality. PATIENTS AND METHODS: We identified 1245 women, the majority with breast-conserving surgery, irradiated for primary node-negative breast cancer from 1980 to 2004 registered at the Geneva Cancer Registry. We compared breast cancer-specific and cardiovascular mortality between inner-quadrant (n = 393) versus outer-quadrant tumors (n = 852) by multivariate Cox regression analysis. RESULTS: After a mean follow-up of 7.7 years, 28 women died of cardiovascular disease and 91 of breast cancer. Patients with inner-quadrant tumors had a more than doubled risk of cardiovascular mortality compared with patients with outer-quadrant tumors (adjusted hazard ratio 2.5; 95% confidence interval 1.1-5.4). Risk was particularly increased in the period with higher boost irradiation. Patients with left-sided breast cancer had no excess of cardiovascular mortality compared with patients with right-sided tumors. CONCLUSIONS: Radiotherapy of inner-quadrant breast cancer is associated with an important increase of cardiovascular mortality, a possible result of higher irradiation of the heart. For patients with inner-quadrant tumors, the heart should be radioprotected.

Life course social mobility and risk of upper aerodigestive tract cancer in men.

The aim of this study was to explore associations between social mobility and tumours of the upper aero-digestive tract (UADT), focussing on life-course transitions in social prestige (SP) based on occupational history. 1,796 cases diagnosed between 1993 and 2005 in ten European countries were compared with 1585 controls. SP was classified by the Standard International Occupational Prestige Scale (SIOPS) based on job histories. SIOPS was categorised in high (H), medium (M) and low (L). Time weighted average achieved and transitions between SP with nine trajectories: H --> H, H --> M, H --> L, M --> H, M --> M, M --> L, L --> H, L --> M and L --> L were analysed. Odds ratios (ORs) and 95%-confidence intervals [95%-CIs] were estimated with logistic regression models including age, consumption of fruits/vegetables, study centre, smoking and alcohol consumption. The adjusted OR for the lowest versus the highest of three categories (time weighted average of SP) was 1.28 [1.04-1.56]. The distance of SP widened between cases and controls during working life. The downward trajectory H --> L gave an OR of 1.71 [0.75-3.87] as compared to H --> H. Subjects with M --> M and L --> L trajectories ORs were also elevated relative to subjects with H --> H trajectories. The association between SP and UADT is not fully explained by confounding factors. Downward social trajectory during the life course may be an independent risk factor for UADT cancers.

Impact of a positive family history on diagnosis, management, and survival of breast cancer: different effects across socio-economic groups.

BACKGROUND: This study aims to investigate whether increased awareness of breast cancer, due to a positive family history (FH), reduces diagnostic, therapeutic, and survival differences between women of low versus high socio-economic status (SES). METHODS: All breast cancer patients registered between 1990 and 2005 at the population-based Geneva Cancer Registry were included. With multivariate logistic and Cox regression analysis, we estimated the impact of SES and FH on method of detection, treatment, and mortality from breast cancer. RESULTS: SES discrepancies in method of detection and suboptimal treatment, as seen among women without a FH, disappeared in the presence of a positive FH. SES differences in stage and survival remained regardless of the presence of a positive FH. Overall, positive FH was associated with better survival. This effect was the strongest in women of high SES (age-adjusted Hazard Ratio [HR(ageadj)] 0.54 [0.3-1.0]) but less pronounced in women of middle (0.77 [0.6-1.0]), and absent in women of low SES (0.80 [0.5-1.2]). CONCLUSION: A positive FH of breast cancer may reduce SES differences in access to screening and optimal treatment. However, even with better access to early detection and optimal treatment, women of low SES have higher risks of death from their disease than those of high SES.

Lung cancer and use of cigarettes: a French case-control study.

A case-control study of 1,625 cases and 3,091 controls was conducted in France from 1976 to 1980 to compare the effects of different smoking habits, especially the use of filter cigarettes, tobacco types (light or dark), and the use of hand-rolled or manufactured cigarettes on the occurrence of lung cancer. All cases had histologically confirmed lung cancer; the controls were matched by sex, age, hospital of admission, and interviewer. The reported results concern only male nonsmokers and males who smoked (or had smoked) cigarettes exclusively, i.e., a total of 1,217 Kreyberg I and Kreyberg II cancer cases and 1,915 controls. Cigarette smoking was associated with both Kreyberg I and Kreyberg II cell categories although with different relative risks (RR) (17.2 and 3.6, resp.). Within the Kreyberg I category, RR were significantly increased (P less than .0001) with certain indices of duration and intensity of cigarette exposure, such as early age at first cigarette smoked, daily consumption, depth of inhalation, and duration of smoking. A significant difference in risk was found within the Kreyberg I category for nonfilter versus filter cigarette smokers (RR = 18.1 and 10.9, resp.) and dark versus light tobacco smokers (RR = 18.1 and 4.9, resp.) but not for hand-rolled versus manufactured cigarette smokers (RR = 19.8 and 16.0, resp.). When all the covariates were taken into account in a matched logistic regression, lung cancer risks for nonfilter versus filter cigarette smokers was RR = 1.23, for hand-rolled versus manufactured cigarette users RR = 1.22, and for dark versus light tobacco users RR = 1.94.

Prophylactic cranial irradiation for patients with small-cell lung cancer in complete remission.

BACKGROUND: Prophylactic cranial irradiation in patients with small-cell lung cancer decreases the overall rate of brain metastases without an effect on overall survival. It has been suggested that this treatment may increase neuropsychological syndromes and brain abnormalities indicated by computed tomography scans. However, other retrospective data suggested a beneficial effect on overall survival for patients in complete remission. PURPOSE: Our purpose was to evaluate the effects of prophylactic cranial irradiation on brain metastasis, overall survival, and late-occurring toxic effects in patients with small-cell lung cancer in complete remission. METHODS: We conducted a prospective study of 300 patients who had small-cell lung cancer that was in complete remission. The patients were randomly assigned to receive either prophylactic cranial irradiation delivering 24 Gy in eight fractions during 12 days (treatment group) or no prophylactic cranial irradiation (control group). A neuropsychological examination and a computed tomography scan of the brain were performed at the time of random assignment and repeatedly assessed at 6, 18, 30, and 48 months. Patterns of failure were analyzed according to total event rates and also according to an isolated first site of relapse, using a competing-risk approach. RESULTS: Two hundred ninety-four patients who did not have brain metastases at the time of random assignment were analyzed. The 2-year cumulative rate of brain metastasis as an isolated first site of relapse was 45% in the control group and 19% in the treatment group (P < 10(-6)). The total 2-year rate of brain metastasis was 67% and 40%, respectively (relative risk = 0.35; P < 10(-13)). The 2-year overall survival rate was 21.5% in the control group and 29% in the treatment group (relative risk = 0.83; P = .14). There were no significant differences between the two groups in terms of neuropsychological function or abnormalities indicated by computed tomography brain scans. CONCLUSIONS: Prophylactic cranial irradiation given to patients with small-cell lung cancer in complete remission decreases the risk of brain metastasis threefold without a significant increase in complications. A possible beneficial effect on overall survival should be tested with a higher statistical power. IMPLICATIONS: The results of the trial favor, at present, the indication of prophylactic cranial irradiation for patients who are in complete remission. A longer follow-up and confirmatory trials are needed to fully assess late-occurring toxic effects. The possible effect on overall survival needs to be evaluated with a larger number of patients in complete remission, and a meta-analysis of similar trials is recommended.

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.

The effect of tobacco on lung cancer risk depends on CYP2D6 activity.

The genetically determined P450 CYP2D6 activity is suspected to be involved in lung carcinogenesis by activating carcinogens contained in tobacco smoke. Therefore, lung cancer risk should depend on both smoking exposure and CYP2D6 activity. The extent to which CYP2D6 activity, determined by using dextromethorphan, could modify the effect of tobacco was evaluated from a study on 128 lung cancers and 157 controls. A strong interaction was observed; the effect of tobacco on lung cancer risk rose with increasing CYP2D6 activity (P < 0.001). Increasing levels of smoking increased lung cancer risk only among smokers with the highest CYP2D6 activity, and CYP2D6 was a risk factor only among heavy smokers. Smokers with both the highest CYP2D6 activity and daily tobacco consumption were at very high risk for lung cancer. These results may explain discrepant results of previous studies on the association between CYP2D6 activity and lung cancer.

Association between DNA repair-deficiency and high level of p53 mutations in melanoma of Xeroderma pigmentosum.

Xeroderma pigmentosum (XP) is an inheritable disease characterized by sun-sensitivity and a high frequency of skin cancers including melanoma. We have analyzed two different groups of XP: the XP complementation group C (XP-C), deficient in global nucleotide excision repair but proficient in transcription-coupled repair and associated with a very early onset of skin cancers; and the XP variant (XPV), deficient in the bypass of DNA photoproducts. To get new insights into the biology of melanoma in XP patients, we studied 20 melanomas from four XP-C and two XPV patients in terms of pathology, immunohistochemistry of p53, mutations in exons 4-9 of the p53 gene, and polymorphisms of the p53 gene at codon 72. All statistical tests were two-sided. The majority of the XP melanomas were of the lentigo maligna melanoma (LMM) type, as found in the elderly. p53 point mutations were found in 60% of XP-C melanomas and in only 10% of XPV melanomas, this latter frequency being similar to what has been reported in the general population. Mutations show the specific UV-signature because the majority were CC to tandem and C to T transitions located at the bipyrimidine sites known to be hotspots of UV-induced DNA lesions. All DNA lesions giving rise to mutations in XP-C melanomas were located on the nontranscribed strand of the p53 gene, demonstrating that these patients' cells were able to carry out preferential repair in vivo. The LMMs found in XP-C are associated with an accumulation of unrepaired DNA lesions and may represent a good model for the LMM induction in the elderly.

Association between lung cancer and microsomal epoxide hydrolase genotypes.

Microsomal epoxide hydrolase (mEH) is involved in the metabolism of tobacco-derived carcinogens. Polymorphisms in exons 3 and 4 of the EPHX gene have been reported to be associated with variations in mEH activity. We examined whether the predicted mEH activity modified the lung cancer risk among 150 cases and 172 controls, all French Caucasian smokers. A significant association was found between predicted mEH activity and lung cancer (P < 0.02), with a dose-effect relationship (P < 0.005). The risks associated with intermediate and high activities, compared to low activity, were 1.65 (95% CI, 0.95-2.86) and 2.66 (95% CI, 1.33-5.33), respectively. The effect of mEH activity on lung cancer risk was not significantly modified by smoking exposure, CYP1A1 genotype, or GSTM1 genotype. mEH may thus be an important genetic determinant of smoking-induced lung cancer.

High-activity microsomal epoxide hydrolase genotypes and the risk of oral, pharynx, and larynx cancers.

Human microsomal epoxide hydrolase (mEH), encoded by the EPHX1 gene, is involved in the metabolism of tobacco carcinogens. We investigated the effect of exon 3 and 4 polymorphisms of the EPHX1 gene in 121 patients with cancers of the oral cavity/pharynx, 129 patients with cancer of the larynx, and 172 non-cancer controls, all Caucasian regular smokers. The potential modifying role of previously analyzed GSTM1, GSTM3, and GSTP1 genotypes was also examined. Compared with the putative low-activity genotypes, odds ratios (ORs) associated with predicted intermediate and high mEH activity genotypes were significantly increased for oropharyngeal cancers [OR = 1.8; 95% confidence interval (CI) = 1.0-3.3; and OR = 2.1; 95% CI = 1.0-4.5, respectively; P(trend) = 0.03] and laryngeal cancers (OR = 1.7; 95% CI = 1.0-3.1; and OR = 2.4; 95% CI = 1.1-5.1, respectively; P(trend) = 0.02). Moreover, a positive interaction was found between mEH activity and GSTM3 genotype for laryngeal cancer. The combined EPHX1 high activity-associated genotype and GSTM3 (AB or BB) genotype conferred a 13.1-fold risk (95% CI = 3.5-48.4) compared with the concurrent presence of the EPHX1 low activity-associated genotype and the GSTM3 AA genotype. Thus, EPHX1 polymorphisms may be one of the factors of importance in susceptibility to smoking-related cancers of the upper aerodigestive tract.

p53 mutations and exposure to environmental tobacco smoke in a multicenter study on lung cancer.

Biomarker data may provide a way to strengthen the link between environmental tobacco smoke (ETS) exposure and lung cancer shown in epidemiological studies. We conducted a multicenter case-control study to investigate the association between ETS exposure and lung cancer in never-smokers using p53 mutations as a biomarker of tobacco-related carcinogenesis. Paraffin-embedded tissue or fresh tissue samples from 91 never-smokers and 66 smokers with histologically confirmed lung cancer and interview data about smoking habits and ETS exposure were analyzed for mutations in the p53 gene. Statistical analysis was performed using multivariate logistic regression. Among the lifelong nonsmokers, the overall mutation prevalence was 10% (nine cases). Among 48 never-smokers ever exposed to spousal ETS, 13% (six cases) showed mutations. Smokers exhibited 17 (26%) mutations. A 3-fold [odds ratio, 2.9; 95% confidence interval (CI), 1.2-7.2] increased risk of p53 mutation was observed for smokers as compared with all never-smokers combined (i.e., irrespective of ETS exposure). The increase was 4.4-fold (95% CI, 1.2-16.2) when compared with never-smokers without ETS exposure. Among never-smokers, the risk of mutation was doubled (odds ratio, 2.0; 95% CI, 0.5-8.7) for exposure to spousal ETS only, based on 6 exposed cases with mutation and 42 exposed cases without mutation. The risk was 1.5 (95% CI, 0.2-8.8) for those ever exposed to spousal or workplace ETS as compared with those never exposed to spousal or workplace ETS. For smokers, the most common mutation type was G:C to T:A transversion (31%), whereas G:C to A:T transitions were predominant among never smokers (57%). In conclusion, our study indicates a significant 3-4-fold increased risk of p53 mutation in smoking lung cancer cases, and it suggests that mechanisms of lung carcinogenesis in ETS-exposed never-smokers include mutations in the p53 gene, similar to that seen in smokers. However, the mutation patterns observed also suggest a difference between smokers and never-smokers. Clearly, additional investigations of the role of p53 mutation as a biomarker for tobacco-related carcinogenesis, including that related to ETS, are indicated.

Characteristics of UV-induced mutation spectra in human XP-D/ERCC2 gene-mutated xeroderma pigmentosum and trichothiodystrophy cells.

To study the relationships between mutagenesis and carcinogenesis, we compared the mutations and their frequency induced by ultraviolet irradiation at 254 nm (UV-C) in XP-D (GM-08207B/XP6BE), TTD/XP-D (TTD1VI-LAS-KMT11) and wild-type (MRC-5V1) human cells. XP-D and TTD/XP-D cells, mutated in the same XP-D/ERCC2 gene, are deficient in nucleotide excision repair. Whereas XP-D patients develop early skin tumors, TTD patients do not exhibit abnormal levels of cancers. After verification of UV hypersensitivity and DNA repair defect of the immortalized cell lines XP-D and TTD compared with a wild-type cell line, UV-induced mutagenesis was studied with a new shuttle vector pR2, carrying the target lacZ' gene. The UV-mutation frequencies in XP-D and TTD cells were similar and significantly increased compared with normal cells. Sequence analysis of 312 independent mutant plasmids revealed that more rearrangements were induced in TTD cells (16%) than in XP-D (5%) and normal cells (1%), while XP-D cells exhibited a twofold higher rate of tandem mutations compared with TTD and normal cells. In the three cell lines, a predominance of G:C to A:T transitions was found, especially in chiefly on the cytosine at 5'-TC-3' sites. The types of UV-induced point mutations in TTD cells were, however, more similar to those in normal cells than those found in XP-D cells. XP-D mutations were preferentially located in 5'-TCPur-3' sites, while mutations in normal and TTD cells were mostly at 5'-TCC-3' sites. Analysis of mutation spectra revealed differences in the location of the mutational hotspots between the three lines. Although the mutation frequency of the UV-irradiated pR2 vector is much higher in TTD and XP-D cells than in normal cells, the mutation spectrum is closer between TTD and normal cells as compared with XP-D cells. These dissimilarities could contribute to an explanation of some of the differences between the two syndromes.

Orientation in the wandering albatross: interfering with magnetic perception does not affect orientation performance.

After making foraging flights of several thousands of kilometers, wandering albatrosses (Diomedea exulans) are able to pinpoint a specific remote island where their nests are located. This impressive navigation ability is highly precise but its nature is mysterious. Here we examined whether albatrosses rely on the perception of the Earth's magnetic field to accomplish this task. We disturbed the perception of the magnetic field using mobile magnets glued to the head of nine albatrosses and compared their performances with those of 11 control birds. We then used satellite telemetry to monitor their behavior. We found that the ability of birds to home specific nest sites was unimpaired by this manipulation. In particular, experimental and control birds did not show significant differences with respect to either foraging trip duration, or length, or with respect to homing straightness index. Our data suggest that wandering albatrosses do not require magnetic cues to navigate back to their nesting birds.

Role of glutathione S-transferase GSTM1, GSTM3, GSTP1 and GSTT1 genotypes in modulating susceptibility to smoking-related lung cancer.

Glutathione S-transferases GSTM1, GSTM3, GSTP1 and GSTT1 are involved in the detoxification of active metabolites of several carcinogens in tobacco smoke. We studied the potential role of GSTM3 and GSTP1 gene polymorphisms either separately, or in combination with GSTM1 and GSTT1 gene polymorphisms, in susceptibility to lung cancer using peripheral blood DNA from 150 lung cancer patients and 172 control individuals, all regular smokers. The frequencies of GSTM3, AA, AB and BB genotypes were 70.7%, 24.0% and 5.3% in cases and 72.7%, 24.4% and 2.9% in control individuals respectively. The frequencies of GSTP1, AA, AG and GG genotypes were 44.7%, 44.0% and 11.3% in cases and 50.0%, 37.2% and 12.8% in control individuals respectively. When studied separately, neither GSTM3 nor GSTP1 genotypes contributed significantly to the risk of lung cancer. Although failing to reach statistical significance, the combined GSTM3 AA and GSTP1 (AG or GG) genotype conferred a nearly threefold risk when the GSTM1 gene was concurrently lacking (odds ratio 2.9, 95% confidence interval 0.7-12.1). Significant interactions were observed between pack-years of smoking and the combined GSTM3 AA and GSTP1 (AG or GG) genotype, or the combined GSTM3 AA, GSTP1 (AG or GG) and GSTM1 null genotype. The combination of these three a priori at risk genotypes conferred an increased risk of lung cancer among smokers with a history of at least 35 pack-years (odds ratio 2.7, 95% confidence interval 1.2-6.0), but not in lighter smokers, probable because of the lower average number of pack-years of smoking found among control individuals with this genotype combination.