Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Einzelreferate und Buchbesprechungen

Journal of Molecular Medicine -     

Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Psychiatric Inferences from Data on Psychologic/Psychiatric Symptoms in Multiple Chemical Sensitivities Syndrome

When abnormal psychologic/psychiatric symptom data are obtained on personality tests or psychiatric interviews administered to patients who report symptoms of Multiple Chemical Sensitivities Syndrome, investigators typically attribute these to either psychiatric traits or to psychogenic origins of illness. The primary purpose of these studies was the evaluation of the plausibility of nonpsychiatric explanations of psychologic/psychiatric symptom data. In Study 1, patients with Multiple Chemical Sensitivities Syndrome used the Minnesota Multiphasic Personality Inventory 2 (MMPI-2) to describe which items had changed after they developed the condition. In Study 2, three diverse groups of professionals predicted which items on the MMPI-2 might change after a mentally healthy person developed the Syndrome or a condition resembling it. In Study 3, a second sample of Multiple Chemical Sensitivities Syndrome patients completed the MMPI-2 and other questionnaires by mail, which allowed the authors to ascertain whether these patients showed more or different psychopathology than was described by patients and hypothesized by professionals. Data from Study 1 patient informants indicated that developing the syndrome might result in a psychopathological MMPI-2 profile, characterized by abnormal Hypochondriasis and Hysteria scale scores. Professionals in Study 2 showed a consensus about hypothesized MMPI-2 changes following the development of the syndrome. These changes likely elevated the Hypochondriasis, Hysteria, Psychasthenia, Depression, and Schizophrenia scale scores. In Study 3, the patients taking the MMPI-2 showed elevations on the Hypochondriasis, Hysteria, Depression (women only), and Schizophrenia scales. Abnormal scores were associated closely with greater severity of illness and greater adjustment to illness. The strategy of administering psychometric tests to ill populations for the purposes of evaluating psychiatric illness or traits, and/or psychogenic origins of illness was shown to be potentially misleading.     

Regional differences in responses of rabbit detrusor to electrical and adrenergic stimulation: influence of outlet obstruction

OBJECTIVE: To examine regional responses of control and obstructed rabbit detrusor strips to electrical and adrenergic stimulation, and determine whether outlet obstruction causes regional variations in blood flow throughout the detrusor, as the detrusor smooth muscle of the bladder body has previously been considered homogeneous in its pharmacological properties. MATERIALS AND METHODS: Fourteen male rabbits had the bladder outlet surgically obstructed for 2 weeks and were compared with 10 unoperated control rabbits. Blood flow was measured with the bladder empty and at capacity, using fluorescent microspheres. Paired dorsal and ventral strips were harvested from the midline equatorial detrusor and electrically and adrenergically stimulated. RESULTS: Obstructed rabbits had significantly higher bladder capacities and bladder weights than control rabbits. Dorsal strips from both control and obstructed rabbits contracted in response to noradrenaline, whereas ventral strips relaxed. The addition of prazosin, a nonselective alpha1-adrenergic-receptor blocker, completely blocked the contraction in dorsal strips, but had no effect on responses of ventral strips. There was also a regional difference in response to electrical stimulation, with ventral strips generating significantly more tension than dorsal strips in both control and obstructed rabbits. There were no regional differences in detrusor blood flow. Obstruction resulted in significantly lower responses to all forms of stimulation, and significantly less blood flow throughout the detrusor. CONCLUSION: There are regional differences in adrenergic receptor function and response to electrical-field stimulation throughout control and obstructed rabbit detrusor, a region that was previously thought to be functionally homogeneous. These differences must be recognized and acknowledged to obtain accurate and reproducible data from in vitro studies of the bladder.     

Tumour necrosis factor receptor type II 196M/R genotype correlates with circulating soluble receptor levels in normal subjects and with graft-versus-host disease after sibling allogeneic bone marrow transplantation

BACKGROUND: A single nucleotide polymorphism in the tumor necrosis factor type II receptor (TNFRII) gene, codon 196, results in the substitution of arginine (R allele) for methionine (M allele). The 196R allele is reportedly associated with an increased susceptibility to autoimmune disease, and donor 196R allele carriage correlates with increased severity of acute graft-versus-host disease (GVHD) after matched unrelated bone marrow transplantation (BMT). METHODS: We investigated the impact of donor and recipient TNFRII genotype on GVHD incidence and severity among 104 adult recipients of myeloablative sibling BMTs. RESULTS: 196R allele frequency was 0.28 among recipients, donors, and controls. There was an increased incidence of acute GVHD among 196R-positive recipients (odds ratio [OR] 3.6, P=0.05). This association was confirmed in multivariate analysis (relative risk 4, P=0.04), correcting for previously established clinical and genetic risk factors. Donor 196R homozygosity was associated with an increased incidence of extensive chronic GVHD (OR 18.5, P=0.02). This association was also confirmed in multivariate analysis (OR 11, P=0.02). To investigate the functional impact of the TNFRII 196 M/R polymorphism, 79 volunteer blood donors were genotyped at this locus, by polymerase chain reaction and single-strand conformational polymorphism analysis, and plasma soluble TNFRII (sTNFRII) levels were measured by ELISA. Mean plasma sTNFRII levels (pg/mL: +/-SEM) were 1224 (+/-26) and 1063 (+/-65) for 196M-postive (196 M homozygous or heterozygous) individuals and 196R homozygotes, respectively (P=0.02). CONCLUSIONS: Because sTNFRIIs can act as TNF antagonists, the association between recipient and donor TNFRII 196R allele status and acute or extensive chronic GVHD incidence, respectively, may reflect reduced circulating sTNFRII.     

Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes

Protein kinase C (PKC) beta isoform activity is increased in myocardium of diabetic rodents and heart failure patients. Transgenic mice overexpressing PKCbeta2 (PKCbeta2Tg) in the myocardium exhibit cardiomyopathy and cardiac fibrosis. In this study, we characterized the expression of connective tissue growth factor (CTGF) and transforming growth factor beta (TGFbeta) with the development of fibrosis in heart from PKCbeta2Tg mice at 4-16 weeks of age. Heart-to-body weight ratios of transgenic mice increased at 8 and 12 weeks, indicating hypertrophy, and ratios did not differ at 16 weeks. Collagen VI and fibronectin mRNA expression increased in PKCbeta2Tg hearts at 4-12 weeks. Histological examination revealed myocyte hypertrophy and fibrosis in 4- to 16-week PKCbeta2Tg hearts. CTGF expression increased in PKCbeta2Tg hearts at all ages, whereas TGFbeta increased only at 8 and 12 weeks. In 8-week diabetic mouse heart, CTGF and TGFbeta expression increased two- and fourfold, respectively. Similarly, CTGF expression increased in rat hearts at 2-8 weeks of diabetes. This is the first report of increased CTGF expression in myocardium of diabetic rodents suggesting that cardiac injury associated with PKCbeta2 activation, diabetes, or heart failure is marked by increased CTGF expression. CTGF could act independently or together with other cytokines to induce cardiac fibrosis and dysfunction.