OBJECTIVE: To investigate the relationship of job stress and scores on the Minnesota Multiphasic Personality Inventory (MMPI) clinical scales in firefighters. METHOD: A total of 648 firefighters from Daegu Metropolitan City were given 2 sets of questionnaires, the Korean Occupational Stress Scales (KOSS) and the MMPI. The results of 428 qualifying questionnaires were analyzed using ANOVA, correlation, and multiple regression. RESULTS: The study demonstrated that job stress differed by age, department, amount of exercise, and duty period. MMPI clinical scales differed by age, smoking, and amount of exercise. Job stress correlated with MMPI clinical scales and in particular with 2 MMPI clinical scales, -Depression and Social introversion-. In addition, job stress subscales were related. On multiple regression analysis, some MMPI clinical scales were affected by job stress subscales. CONCLUSION: This study suggests that job stress is associated with psychogenic factors in firefighters. The effective management for job stress might be helpful for the overall mental health of firefighters. Further study is required to determine which psychogenic factors are related to job stress.
Firefighters ; Humans ; Mental Health ; Minnesota ; MMPI ; Questionnaires ; Smoke ; Smoking ; Weights and Measures

OBJECTIVE: It is well established that manganese neurotoxicity is associated with clinical symptoms similar to those of idiopathic Parkinson's disease. Recent research has shown that the exposure to manganese (MnCl2) leads to induction of iNOS in BV2 microglial cells via iNOS transcriptional up-regulation and activation of both MAPKs and PI3K/Akt signaling pathways. Here, we further investigated the effect and the action mechanism of MnCl2 on iNOS expression in C6 glioma cells. METHODS: Western blot analyses demonstrated that treatment with MnCl2 at 250 micronmeter was sufficient to induce iNOS at both the protein and mRNA levels in C6 cells. RESULTS: These studies demonstrated that the induction of iNOS protein and mRNA was visible after 4h- and 2 h-treatment with MnCl2, respectively. MnCl2 treatment led to strong phosphorylation of JNKs and ERKs, members of MAP kinases (MAPKs), and Akt, a PI3-kinase (PI3K) downstream effector, in C6 cells. MnCl2 treatment had no effect on I kappa B-alpha in C6 cells. Notably, pretreatment with LY294002 (a PI3K inhibitor), which inhibited phosphorylation of Akt by MnCl2, caused strong suppression of MnCl2- induced iNOS protein and mRNA expression in C6 cells. Moreover, pretreatment with SP600125 (an inhibitor of JNKs) and PD98050 (an inhibitor of ERKs), which respectively interfered with MnCl2-mediated phosphorylation of JNKs and ERKs, led to the partial suppression of MnCl2-induced iNOS protein. Interestingly, pretreatment with LY294002 inhibited phosphorylation of not only Akt, but also ERKs and JNKs, in response to MnCl2. Moreover, there was an effective suppression of MnCl2-mediated phosphorylation of AKT by SP600125. CONCLUSION: These results collectively suggest that MnCl2 induces iNOS expression in C6 glioma cells via activation of PI3K/Akt and JNK-ERK MAPK signaling proteins, whose activations seem to be mutually interconnected in response to MnCl2.
Anthracenes ; Blotting, Western ; Chlorides ; Chromones ; Glioma ; Manganese ; Manganese Compounds ; Morpholines ; Nitric Oxide Synthase Type II ; Parkinson Disease ; Phosphatidylinositol 3-Kinases ; Phosphorylation ; Phosphotransferases ; Proteins ; RNA, Messenger ; Up-Regulation

BACKGROUND: Infections and vascular disorders are the two most widely accepted probable causes of sudden hearing loss. Tumor necrosis factor alpha (TNF-alpha) is major pro-inflammatory cytokine that is thought to be important in the pathogenesis of sudden deafness. However, the functions of genetic polymorphism in this cytokine have not been throughly examined in the context of sudden deafness pathology. In an effort to discover polymorphism in genes whose variants have been implicated in sudden deafness phenotypes, we examined the genetic effects of TNF-alpha polymorphisms in Koreans with sudden deafness. METHODS: Two common single nucleotide polymorphism (SNP) in TNF-alpha gene were genotyped in a Korean sudden deafness. Ninety nine patients with sudden deafness (45 males and 54 females) were selected from Keimyung University Dongsan Medical Center. The control subjects consisted of healthy 285 males and 319 females. RESULTS: Human genomic DNA was extracted from peripheral blood sample. The SNP at position -863 C/A and -857 C/T of TNF-alpha promoter were analyzed by PCR and pyrosequencing. Genotype distribution and allele frquencies in subjects were in Hardy-Weinberg equilibrium (p>0.05). No significant association was found between TNF-alpha -863 C/A and -857 C/T polymorphism and sudden deafness. We examined whether the relation between TNF-alpha polymorphism and sudden deafness varied according to tinnitus. Statistical analysis of TNF-alpha polymorphism at -857 C/T showed that there was a significant difference between SD without tinnitus and the control in both genotype distribution (p<0.05) and allele frequency [OR (95% CI)=2.63 (1.29-5.34)], but not between SD with tinnitus. CONCLUSION: These findings suggest TNF-alpha polymorphisms at -863C/A, -857 C/T are likely to play a role in SD.
Alleles ; DNA ; Female ; Gene Frequency ; Genotype ; Hearing Loss, Sudden* ; Humans ; Male ; Pathology ; Phenotype ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Polymorphism, Single Nucleotide* ; Tinnitus ; Tumor Necrosis Factor-alpha*