Mental and physical distress of field veterinarians during and soon after the 2010 foot and mouth disease outbreak in Miyazaki, Japan.

An outbreak of foot and mouth disease occurred in Miyazaki, Japan, in April 2010, and nearly 290,000 animals were culled to control the disease. This study was conducted to demonstrate the causes and intensity of mental distress felt by the field veterinarians participating in the control programme. A focus group discussion was conducted with ten veterinarians to understand their distress during the outbreak, and a questionnaire to quantify the degree of distress experienced each week was administered to 16 veterinarians. A detailed questionnaire was separately administered to 70 veterinarians six months after the outbreak was controlled, to assess mental distress status and to identify the risk factors for serious mental illness (SMI) using the six-item Kessler scale (K6). Overall, mental distress (mean 3.1) was significantly greater than physical distress (mean 1.9, p < 0.001). The risk factors for mental distress were categorised into three groups: culling, communication with farmers, and gender; each category was qualitatively described. Only two respondents (2.9%) had high K6 scores suggesting SMI. In the final generalised linear models with quasi-Poisson errors, the riskfactorsfor SMI that remained were: disinfecting vehicles (p = 0.01), distress (p <0.001), and increased alcohol consumption (p = 0.057), and a protective factor: participation in culling (p = 0.07), which suggested healthy worker bias. Sensitive individuals had been allocated to non-culling activities during disease control. In conclusion, human resource management was adequate during the outbreak from a public-health perspective. However, monitoring delayed symptoms of post-traumatic stress disorder is recommended.

Heavy overtime work and depressive disorder among male workers.

BACKGROUND: The association between overtime and depression is unclear and very few studies have examined the association between heavy overtime work, i.e. working more than 60 h per week, and depression. AIMS: To examine the association between heavy overtime work and the onset of depressive disorder among male workers. METHODS: A 1-year follow-up cohort study of male workers in a manufacturing company in Japan, between 2008 and 2009. Working hours, depressive disorder, assessed by the Center for Epidemiologic Studies Depression (CES-D) Scale (score ≥16 points), and covariates were measured at baseline and at follow-up. Participants who had depressive disorder at baseline were excluded. RESULTS: At follow-up, 1194 participants aged between 18 and 71 years were analysed. Multiple logistic regression analysis revealed that the odds ratio for the new onset of depressive disorder was 4.5 (95% CI 1.8-11.1) times higher for employees working >60 h per week than for those working ≤50 h per week, when adjusted for age, lifestyle factors, work-related characteristics and socio-demographic characteristics at baseline and working hours at follow-up. However, the correlation between working 50.1 to 60 h per week and depressive disorder was not significant. The trend test of depressive disorder among groups by working hours was significant (P < 0.01). CONCLUSIONS: Heavy overtime work is a risk factor for the new onset of depressive disorder in this population of male workers. Working >60 h per week may be the cut-off to screen for high-risk groups who need preventive action against depressive disorder.

Laser microdissection-based analysis of cytokine balance in the kidneys of patients with lupus nephritis.

To determine the cytokine balance in patients with lupus nephritis (LN), we analysed kidney-infiltrating T cells. Renal biopsy samples from 15 systemic lupus erythematosus (SLE) patients were used. In accordance with the classification of International Society of Nephrology/Renal Pathology Society, they were categorized into Class III, Class III+V (Class III-predominant group, n = 4), Class IV, Class IV+V (Class IV-predominant group, n = 7) and Class V (n = 4) groups. The single-cell samples of both the glomelular and interstitial infiltrating cells were captured by laser-microdissection. The glomerular and interstitial infiltrating T cells produced interleukin (IL)-2, IL-4, IL-10, IL-13 and IL-17 cytokines in the Class III-predominant, Class IV-predominant and Class V groups. Interferon-gamma was detected only in the glomeruli of the Class III-predominant and Class V group samples. The expression level of IL-17 was correlated closely with clinical parameters such as haematuria, blood urea nitrogen level, SLE Disease Activity Index scores in both glomeruli and interstitium, urine protein level in glomeruli and serum creatinine and creatinine clearance levels in interstitium. This suggests that the glomerular infiltrating T cells might act as T helper type 1 (Th1), Th2 and Th17 cells while the interstitial infiltrating T cells, act as Th2 and Th17 cells in the Class III-predominant and Class V groups. In contrast, both the glomerular and interstitial infiltrating T cells might act as Th2 and Th17 cells in the Class IV-predominant group. The cytokine balances may be dependent upon the classification of renal pathology, and IL-17 might play a critical role in SLE development.

B cells play a crucial role as antigen-presenting cells and collaborate with inflammatory cytokines in glucose-6-phosphate isomerase-induced arthritis.

Anti-glucose-6-phosphate isomerase (GPI) antibodies from K/BxN mice directly induce arthritis; however, the transfer of these antibodies from mice with GPI-induced arthritis does not induce arthritis. CD4(+) T cells play an important role in the induction and effector phase in this model; however, the roles of B cells and immunoglobulins (Igs) have not been elucidated. We investigated the roles of B cells and Igs in GPI-induced arthritis by using adoptive transfer system into SCID mice. Transfer of splenocytes of male DBA/1 mice immunized with GPI into SCID mice induced arthritis on day 6 in the latter, in association with the production of anti-GPI antibodies. Co-localization of C3 and IgG on the articular surface was identified in arthritic SCID mice. Inoculation of IgG (or anti-GPI antibodies) and CD19(+)-depleted splenocytes from arthritic DBA/1 mice induced arthritis in SCID mice, but not CD19(+)-depleted or CD4(+)-depleted splenocytes from DBA/1 mice. In vitro analysis of cytokine production by splenocytes from DBA/1 arthritic mice demonstrated production of large amounts of tumour necrosis factor (TNF)-alpha and interleukin (IL)-6 in an antigen-specific manner (P < 0.01), and production was dominated by CD19(+)-depleted than CD4(+)-depleted splenocytes (P < 0.05). Addition of IgG from DBA/1 arthritic mice to the culture enhanced TNF-alpha but not IL-6 production, and this effect was blocked by anti-Fcgamma receptor antibody. In vivo analysis of neutralization with TNF-alpha protected arthritis completely in SCID mice. Our results highlight the important role of B cells in GPI-induced arthritis as autoantibody producers, and these autoantibodies can trigger joint inflammation in orchestration with inflammatory cytokines, especially TNF-alpha.

School-based psychoeducation and storytelling: Associations with long-term mental health in adolescent survivors of the Wenchuan earthquake.

AIMS: We explored the factors promoting long-term mental health among adolescent survivors of the 2008 Wenchuan earthquake in China. We examined the associations of their long-term mental health with disaster-related storytelling and school-based psychoeducation, and of school-based psychoeducation with disaster-related storytelling. METHODS: A secondary school-based cross-sectional survey was conducted 6 years after the disaster. Participants with traumatic experiences such as injury, loss, witnessing someone's death/injury and home destruction (N = 1028, mean age 15, standard deviation 1.38, male 51%) were eligible. Mental health/disaster education (MHE/DE) was defined as taking one or more lessons in MHE and/or DE at school since the earthquake. Experiences of storytelling about the disaster involved expressing distressing memories and feelings regarding the earthquake since the disaster happened, according to four groups: never expressed distressing memories and feelings, expressed them through writing/drawing, expressed them through talking to lay supporters and expressed them through talking to health professionals. Analysis of covariance was used to compare mean scores on five selected subscales of the Symptom Checklist-90 (SCL-90), the Athens Insomnia Scale (AIS) and the Psychotic-Like Experiences (PLEs) scale among the four storytelling groups. Linear regression analysis was used to identify the relationships between MHE/DE and current mental health as measured by the SCL-90, AIS and PLEs. The relationship between education and storytelling was probed by χ2 test. RESULTS: The talked-to-lay-supporters group showed better mental health on the SCL-90 (p ⩽ 0.001), AIS (p < 0.001) and PLEs (p = 0.004), while the consulted-health-professionals group showed worse mental health on the three dimensions of the SCL-90: depression (p = 0.05), anxiety (p = 0.02) and fear (p = 0.04), and on PLEs (p = 0.02) compared with the never-expressed group. MHE and DE were inversely associated with SCL-90, AIS and PLE scores. Participants who received these forms of education talked about their disaster experiences to lay supporters more than those who did not. CONCLUSIONS: MHE and DE at school may promote adolescents' mental health after a disaster. Experience of storytelling about the disaster to lay supporters may be helpful for long-term psychological recovery, and may be a potential mediating factor for school-based education and better mental health. Because of the cross-sectional nature of this study, causality cannot be inferred; therefore, further prospective intervention studies are needed to elucidate the effect of these factors on adolescent survivors' mental health.

Invariant NKT cells produce IL-17 through IL-23-dependent and -independent pathways with potential modulation of Th17 response in collagen-induced arthritis.

Invariant natural killer T (iNKT) cells play a protective role in the development of certain autoimmune diseases. However, their precise role in the pathogenesis of autoimmune arthritis remains unclear. In this study, we examined the possible contribution of iNKT cells in collagen-induced arthritis (CIA) by using iNKT cell-deficient mice (Jalpha281-/- mice). CIA in these mice was markedly suppressed and interleukin (IL)-17 production was reduced in a native type II collagen (CII)-specific T cell response. Draining lymph nodes of CII-immunized Jalpha281-/- mice contained a significantly low number of IL-17-producing T helper cells. To determine whether iNKT cells produce IL-17, we measured IL-17 by enzyme-linked immunosorbent assay in iNKT cells stimulated with the ligand, alpha-galactosylceramide (alpha-GalCer). Notably, splenocytes from Jalpha281-/- mice stimulated in this way were negative for IL-17, whereas those from C57BL/6 mice produced IL-17. Immunostaining for IL-17 in iNKT cells confirmed intracellular staining of the protein. RT-PCR analysis showed that iNKT cells expressed retinoid-related orphan receptor gammaT and IL-23 receptor. Moreover, cell sorting demonstrated that NK1.1- iNKT cells were the main producers of IL-17 compared with NK1.1+ iNKT cells. IL-17 production by iNKT cells was induced by IL-23-dependent and -independent pathways, since iNKT produced IL-17 when stimulated with either IL-23 or alpha-GalCer alone. Our findings indicate that iNKT cells are producers and activators of IL-17 via IL-23- dependent and -independent pathways, suggesting that they are key cells in the pathogenesis of CIA through IL-17.

Work-related psychosocial factors and metabolic syndrome onset among workers: a systematic review and meta-analysis.

BACKGROUND: Work-related psychosocial factors have been associated with metabolic syndrome. However, no systematic reviews or meta-analyses have evaluated this association. METHODS: A systematic literature search was conducted, using PubMed, Embase, PsycINFO, PsycARTICLES and the Japan Medical Abstracts Society. Eligible studies included those that examined the previously mentioned association; had a longitudinal or prospective cohort design; were conducted among workers; provided sufficient data for calculating odds ratios, relative risks or hazard ratios with 95% confidence intervals; were original articles in English or Japanese; and were published no later than 2016. Study characteristics, exposure and outcome variables and association measures of studies were extracted by the investigators independently. RESULTS: Among 4,664 identified studies, 8 were eligible for review and meta-analysis. The pooled risk of adverse work-related stress on metabolic syndrome onset was significant and positive (RR = 1.47; 95% CI, 1.22-1.78). Sensitivity analyses limiting only the effects of job strain and shift work also indicated a significant positive relationship (RR = 1.75; 95% CI, 1.09-2.79; and RR = 1.59; 95% CI, 1.00-2.54, P = 0.049 respectively). CONCLUSION: This study reveals a strong positive association between work-related psychosocial factors and an elevated risk of metabolic syndrome onset. The effects of job strain and shift work on metabolic syndrome appear to be significant.

Epidermal growth factor-like, corneal wound healing substance in mouse tears.

We have identified the presence of a putative corneal wound healing substance in mouse tears, which has a molecular size and immunological properties similar to those of epidermal growth factor (EGF). The substance was capable of binding to EGF receptors in mouse parenchymal cells and this binding was inhibited by anti-EGF serum. The concentration of the EGF-like substance in the tears of male and female mice was estimated to be 79.3 +/- 7.0 (SD) ng/ml and 76.5 +/- 8.1 (SD) ng/ml, respectively, by EGF radioimmunoassay. Removal of the submandibular glands, which produce large amounts of EGF, reduced plasma EGF to an undetectable level and also decreased the concentration of the EGF-like substance in tears to 27.3 +/- 3.9 (SD) ng/ml in male mice and 25.8 +/- 3.7 (SD) ng/ml in female mice. Approximately 50% of sialoadenectomized (submandibular glands removed) male mice with deep corneal wounds developed severe ocular lesions or loss of sight whereas none of normal male mice with similar wounds did. Topical application of EGF to deeply wounded eyes of sialoadenectomized mice eliminated the various complications and restored the healing rate and incidence of recovery to virtually normal levels.

Importance of epidermal growth factor in implantation and growth of mouse mammary tumor in female nude mice.

In female nude mice, epidermal growth factor (EGF) was present at a mean concentration of 42.8 +/- 16.9 (SD) ng/mg wet tissue in the submandibular gland and 0.28 +/- 0.13 ng/ml in the plasma. Sialoadenectomy (removal of the submandibular glands) decreased circulating EGF to undetectable levels (less than 0.1 ng/ml). The possible role of EGF in transplantation and growth of mouse mammary tumors in nude mice was examined by sialoadenectomy, anti-EGF treatment, and EGF replacement therapy. The success rate of transplantation of a spontaneous mouse mammary tumor into nude mice was 55% in normal females and 17% in sialoadenectomized animals. Anti-EGF treatment of sialoadenectomized mice completely abolished the implantation of the tumor. Daily administration of EGF at a dose of 5 micrograms per mouse to both normal and sialoadenectomized animals enhanced the success rate of tumor implantation to more than 80%. Sialoadenectomy and/or anti-EGF treatment of tumor-bearing nude mice reduced the growth of implanted mammary tumors. These results suggest that EGF is important for implantation and growth of spontaneous mouse mammary tumor in female nude mice.

Characterization of melanogenesis and morphogenesis of melanosomes by physicochemical properties of melanin and melanosomes in malignant melanoma.

This study elucidates the nature of melanogenesis in B16 and Harding-Passey (HP) mouse melanomas producing melanin and melanosomes of different color and fine structure, i.e., brown-black eumelanosome-like B16 granules and reddish brown pheomelanosome-like HP granules, and compares them with "typical" 3,4-dihydroxyphenylalanine (DOPA) and sepia eumelanins and sepia eumelanosomes. The melanin content of B16 melanosomes was more than three times higher than that of HP melanosomes. The content of free and protein-bound DOPA and 5-S-cysteinyldopa varied greatly in B16, HP, and sepia melanosomes and was unrelated to melanin content. Chemical analysis of the eumelanin: pheomelanin ratio in melanosomes and elemental analysis of isolated melanin showed that B16 and HP melanins are primarily eumelanic, with a higher ratio of pheomelanic component in HP melanin. The spectra of electron spin resonance and IR and X-ray small-angle scattering of B16 and HP melanins were basically similar to those of sepia and DOPA melanins. B16, HP, and DOPA melanins were dissolved in aqueous NH3, while sepia melanin was dissolved to a far lesser extent. It was concluded that both B16 and HP melanomas are primarily involved in eumelanogenesis, although the fine structure of their melanosomes is entirely different, and that the marked color difference in the two melanosomes is related to a difference in the absolute content of eumelanin, the presence of a small amount of pheomelanin, and the mode of chemical bindings of melanin to structural proteins. In contrast to normal skin and hair, melanosome morphogenesis may not directly correspond to melanogenesis type in malignant melanoma.

Nutritional and mental health status of Afghan refugee children in Peshawar, Pakistan: a descriptive study.

The study sought to ascertain and describe the physical and mental health states of Afghan refugee children after the terrorist attack on September 11, 2001 in the US and the aerial bombing of Afghanistan that followed. A cross-sectional survey was carried out in four refugee camps in Peshawar, Pakistan from February to March 2002, and comparisons among camps were made. A total of 70 males (mean age SD = 9.81 +/- 1.98 years old) and 30 females (7.94 +/- 2.07) answered a self-developed questionnaire on demographic data, traumatic events experience, living environment in the camps, and physical and mental health, through interviews. Anthropometric measures were measured and physical symptoms including anaemia and edema were assessed. Severe malnutrition was not shown and there were no significant differences in most nutritional and physical states among the camps. Nevertheless, in the newer camps more children experienced war related traumatic events. Mental symptoms were prevalent in all camps, though the characteristics of the symptoms differed among the camps.

Stem cell factor prevents Fas-mediated apoptosis of human erythroid precursor cells with Src-family kinase dependency.

The Fas ligand (Fas-L) expressed on mature erythroblasts may induce apoptosis of more immature erythroid cells that express Fas, whereas stem cell factor (SCF) may prevent Fas-mediated cell death in hematopoietic progenitor cells. The manner in which SCF prevents Fas-mediated cell death still is unclear. Given the essential role of SCF and the potentially important involvement of the Fas/Fas-L system in the development of erythrocytes, we studied mechanisms related to SCF prevention of Fas-mediated apoptosis. We used primary cultured human erythroid colony-forming cells (ECFC) derived from CD34+ cells and enriched glycophorin A positive (GPA+) c-kit+ cells in ECFC. Apoptosis of ECFC was induced by an Fas-L mimetic monoclonal antibody CH11. DNA fragmentation and the activation of caspase-3 and caspase-8 were measured using commercially available kits. Characterization of expanded cells was performed using multiparameter flow cytometry. Lyn kinase activity was measured by enolase kinase assays. SCF inhibited the CH11-induced DNA fragmentation of ECFC as well as enriched GPA+ c-kit+ cells in ECFC, but not those of GPA+ c-kit- cells. SCF also inhibited the activation of caspase-3 and caspase-8, without downregulation of the surface expression of Fas, suggesting that SCF prevents apoptosis through uncoupling of Fas ligation from subsequent caspase activation. PP2, a specific inhibitor of Src-family kinases, antagonized the effects of SCF in preventing Fas-mediated apoptosis. We propose that SCF prevents Fas-mediated apoptosis of erythroid progenitor cells in a manner dependent on the activity of Src-family tyrosine kinases. We also identified active Lyn in erythroid cells. These data suggest the presence of a novel Src-family-dependent function of SCF in the development of erythrocytes.

Infrared studies of interaction between metal ions and Ca(2+)-binding proteins. Marker bands for identifying the types of coordination of the side-chain COO- groups to metal ions in pike parvalbumin (pI = 4.10).

Metal-ligand interactions in the Ca(2+)-binding sites of pike parvalbumin (pI = 4.10) have been examined by Fourier-transform infrared spectroscopy. The region of the COO- antisymmetric stretch provides useful information on the types of coordination of the COO- groups to the metal ions in the Mg(2+)-, Mn(2+)-, and Ca(2+)-bound forms. In the spectrum of the Ca(2+)-bound form, two bands are observed at 1,582 and 1,553 cm-1, whereas, in the spectra of the Mg(2+)- and Mn(2+)-bound forms, bands are observed only in the region around 1,582 cm-1 and no band is found in the region around 1,553 cm-1. The 1,553-cm-1 band of the Ca(2+)-bound form reflects the bidentate coordination of the COO- groups of both Glu-62 in the CD site and Glu-101 in the EF site to the Ca2+ ions, which has been made clear by X-ray analysis as a feature of the Ca(2+)-bound form. Absence of such a band in the spectrum of the Mn(2+)-bound form is consistent with the X-ray structure of this form where both of the two COO- groups are unidentate. These unidentate COO- groups of Glu-62 and Glu-101 in the Mn(2+)-bound form seem to give rise to a band at 1,577-1,574 cm-1. The spectrum of the Mg(2+)-bound form is also consistent with the 'pseudo-bridging' coordination of the COO- group of Glu-101 reported in the X-ray structure of a form where the Mg2+ ion occupies only the EF site, and the same spectrum is further indicative of the 'pseudo-bridging' coordination of the COO- group of Glu-62.

In vivo transfer of hepatocyte growth factor gene accelerates proliferation of hepatic oval cells in a 2-acetylaminofluorene/partial hepatectomy model in rats.

To clarify the effect of hepatocyte growth factor (HGF) on proliferation of hepatic oval cells, we transferred HGF gene into liver of the Solt-Farber rat model. Male Fisher 344 rats were infected with a recombinant adenovirus carrying the cDNA for HGF (pAxCAHGF) from tail vein. HGF mRNA showed its peak at 4 days, and diminished thereafter. The total and proliferating cell nuclear antigen-positive hepatic oval cells were significantly elevated in HGF-transferred rats, in which stem cell factor and c-kit mRNA increased at each time point. Our results suggest that in vivo transfer of the HGF gene into liver accelerates proliferation of hepatic oval cells in the Solt-Farber model in rats.

Intravenous recombinant tissue plasminogen activator in acute carotid artery territory stroke.

To determine the effect of intravenous recombinant tissue plasminogen activator (rt-PA) on vascular and neurologic outcomes, we enrolled 31 patients with acute carotid artery-territory ischemic stroke within 6 hours from symptom onset in a randomized, double-blind, placebo-controlled study. We gave either rt-PA (duteplase at the dose of 20 or 30 mega-international units [MIU]) or placebo intravenously for 60 minutes in patients randomly assigned to the three groups. A comparison between the baseline and postinfusion angiograms showed that complete or partial reperfusion occurred in 50% (5/10) of patients treated with 30 MIU rt-PA, 44% (4/9) of those treated with 20 MIU rt-PA, and 17% (2/12) in the control group. In patients with middle cerebral artery occlusions, reperfusion occurred in 71% (5/7) of the 30-MIU group, in 67% (4/6) of the 20-MIU group, and in 13% (1/8) of the control group. Patients treated with 30 MIU rt-PA showed a significantly early and better clinical improvement, as measured by the neurologic scale, than did those treated with placebo. Parenchymal hemorrhage occurred in one patient in each group, and frequency of clinically insignificant hemorrhagic infarction was comparable among the treatment groups. No major systemic complications occurred in any group. These results support the efficacy of intravenous infusion of rt-PA soon after the onset of stroke in producing rapid thrombolysis and neurologic recovery; it may be of particular value in patients with thromboembolic occlusion in the middle cerebral artery.

beta(2)-glycoprotein I deficiency: prevalence, genetic background and effects on plasma lipoprotein metabolism and hemostasis.

beta(2)-glycoprotein I (beta(2)-GPI=apolipoprotein H) is an important autoantigen in patients with the antiphospholipid syndrome. It also plays a role in lipoprotein metabolism, such as anti-atherogenic property, triglyceride removal, and enhancement of lipoprotein lipase. Serum beta(2)-GPI concentration of 812 apparently healthy Japanese individuals was measured by sandwich EIA. Two families with complete beta(2)-GPI deficiency were identified. In one family, all affected had increased serum LDL-cholesterol levels or smaller particle sizes of LDL, while the other had no apparent abnormality in lipid metabolism. Individuals investigated had no history of thrombosis or overt abnormalities in hemostatic tests. A thymine corresponding to position 379 of the beta(2)-GPI cDNA was deleted in every beta(2)-GPI deficient individual. The incidence of this heterozygous deficiency determined by RFLP was 6. 3% in Japanese and none in Caucasians. Heterozygotes had significantly lower concentrations of serum beta(2)-GPI than did those without the mutation, yet no significantly different lipid profiles, such as total cholesterol, triglyceride, HDL-cholesterol, LDL-cholesterol, apoA-I, apoB and Lp(a), were observed. A low concentration of beta(2)-GPI seemed not to be associated with apparent abnormality in lipoprotein metabolism.

Genetic determinants of plasma factor VII activity in the Japanese.

We investigated the frequency of the factor VII Gln353 (FVII Gln353) allele in Japan, where coronary artery disease is much less common and factor VII coagulant activity (FVIIc) is lower than in Western countries. Japanese males (n = 144) aged 40-59 years living in 2 different districts were studied, and the FVIIc and activated factor VII (FVIIa) levels were measured with human (FVIIa Hum) and bovine soluble tissue factor (FVIIa Bov). The frequency of the FVII Gln353 allele in the 2 districts was 0.026 and 0.052 (combined: 0.034), which was about one third of that in a European population. Thus, the lower FVIIc level in Japanese is not due to the effect of FVII Gln353 allele. Ten individuals with the Gln353 allele showed a 39% decrease of FVIIa Hum levels and a 29% decrease of the FVIIa Bov level compared with 134 individuals homozygous for the FVII Arg353 allele. These decreases of FVIIa were greater than the decrease of FVIIc (17%), suggesting that FVII Gln353 may be difficult to activate in vivo. The marked decrease of FVIIa levels in individuals with the FVII Gln353 allele suggests that they are genetically protected against cardiovascular disease irrespective of ethnic background, by virtue of their decreased FVIIa level.

Factor VII and fibrinogen levels examined by age, sex, and other atherosclerotic risk factors in a Japanese population. The Jichi Medical School Cohort Study.

Factor VII coagulant activity (FVIIc) and fibrinogen (Fbg) levels have been investigated as cardiovascular risk factors. We studied these two factors with stratification for age, sex and blood pressure, and the relation with other atherosclerotic risk factors in a Japanese general population. The subjects were 3,139 Japanese (1,315 males and 1,824 females) aged 30 to 89 in 1992 and 1993. A linear increase with age was observed in the levels of Fbg in both men and women, but no differences were observed between men and women in each age group. A linear increase with age was also seen in the levels of FVIIc in women, but the levels of FVIIc in men were significantly higher for the age group 40-49 years than for any other age group. The levels of FVIIc in women were significantly higher than in men at age > or = 60 years. As concerning the effect of alcohol intake status, Fbg had a tendency to decrease with alcohol intake. Fbg and FVIIc levels were associated with an increase in smoking status in men, but no association was seen in women in either Fbg or FVIIc. FVIIc was positively correlated with age, body mass index, total cholesterol, triglycerides and fasting insulin level. Fbg was positively correlated with age, systolic blood pressure, diastolic blood pressure, total cholesterol, LDL-cholesterol and triglycerides in women, but Fbg had few positive correlations with risk factors in men. A comparison with previous Western studies showed that the Fbg levels of our Japanese population were lower than those of the Caucasians studied, but the present FVIIc levels were nearly the same level or slightly higher than theirs. The association of Fbg and FVIIc and with other cardiovascular risk factors in Japanese was similar to those observed in Caucasians.

Association between job characteristics and plasma fibrinogen in a normal working population: a cross sectional analysis in referents of the SHEEP Study. Stockholm Heart Epidemiology Program.

STUDY OBJECTIVE: To explore the association between job characteristics and plasma fibrinogen concentrations. DESIGN: Cross sectional design. SETTING: The Greater Stockholm area. SUBJECTS: A total of 1018 men and 490 women aged 45-70 who were randomly selected from the general population during 1992-1994. They were all employed and had no history of myocardial infarction. MAIN RESULTS: The self reported job characteristics were measured by a Swedish version of the Karasek demand-control questionnaire. For inferred scoring of job characteristics, psychosocial exposure categories (job control and psychological demands) were assigned by linking each subject's occupational history with a work organisation exposure matrix. Job strain was defined as the ratio between demands and control. In univariate analyses, expected linear trends were found in three of four tests of association between high plasma fibrinogen and low control (the self reported score for women and the inferred score for both sexes), in one of four tests of association between high plasma fibrinogen and high demands (the inferred score for women) and in two of four tests of association between high plasma fibrinogen and job strain (the inferred score for both sexes). Multiple logistic regression analyses showed that men in the inferred job strain group have an increased risk of falling into the increased plasma fibrinogen concentration group (above median level of the distribution) (odds ratio (OR) 1.2; 95% CI 1.0, 1.5) after adjustment for the variables that were associated with plasma fibrinogen in the univariate analyses. In women, low self reported control, high inferred demand, and inferred job strain were significantly associated with increased plasma fibrinogen concentration (OR 1.3; 95% CI 1.0, 1.8, OR 1.5; 95% CI 1.0, 2.2, OR 1.5; 95% CI 1.1, 2.2, respectively). CONCLUSIONS: These results indicate that adverse job characteristics may be related to plasma fibrinogen concentrations and this relation is more relevant in female workers. The clearest evidence for psychosocial effects on plasma fibrinogen seems to be with job control and the associations are clearer for the objective than for the self report variables.