Chromogranin peptides in brain diseases

Synaptic disturbances may play a key role in the pathophysiology of neuropsychiatric diseases. In this article, we review immunohistological findings of chromogranin peptides in neurodegenerative and neurodevelopmental disorders, with particular emphasis on Alzheimer’s disease, the disorder chromogranins have been studied most extensively. Data was collected from existing and new experimental data and medline research. This review focuses on synaptic changes elicited by chromogranin peptides immunoreactivity in Alzheimer’s disease, as well in schizophrenia and amyotrophic lateral sclerosis (ALS). An imbalanced availability of chromogranin peptides may be responsible for impaired neurotransmission and a reduced functioning of dense core vesicles. Since chromogranin A was postulated as a potent proinflammatory agent, we focused on chromogranin A in neuroinflammation in Alzheimer’s disease and ALS. Further understanding of role and function of chromogranin peptides in neuropathological conditions is still required.     

CCL17-expressing dendritic cells drive atherosclerosis by restraining regulatory T cell homeostasis in mice

Immune mechanisms are known to control the pathogenesis of atherosclerosis. However, the exact role of DCs, which are essential for priming of immune responses, remains elusive. We have shown here that the DC-derived chemokine CCL17 is present in advanced human and mouse atherosclerosis and that CCL17+ DCs accumulate in atherosclerotic lesions. In atherosclerosis-prone mice, Ccl17 deficiency entailed a reduction of atherosclerosis, which was dependent on Tregs. Expression of CCL17 by DCs limited the expansion of Tregs by restricting their maintenance and precipitated atherosclerosis in a mechanism conferred by T cells. Conversely, a blocking antibody specific for CCL17 expanded Tregs and reduced atheroprogression. Our data identify DC-derived CCL17 as a central regulator of Treg homeostasis, implicate DCs and their effector functions in atherogenesis, and suggest that CCL17 might be a target for vascular therapy.     

Rapid spoligotyping of Mycobacterium tuberculosis complex bacteria by use of a microarray system with automatic data processing and assignment

Membrane-based spoligotyping has been converted to DNA microarray format to qualify it for high-throughput testing. We have shown the assay's validity and suitability for direct typing from tissue and detecting new spoligotypes. Advantages of the microarray methodology include rapidity, ease of operation, automatic data processing, and affordability.     

Immunohistochemically detectable dickkopf-3 expression in tumor vessels predicts survival in gastric cancer

Dickkopf-3 (Dkk-3) may act as a tumor suppressor as it is downregulated in various types of cancer. Moreover, a putative role in tumor neovascularization is discussed. Here, we investigated the expression of Dkk-3 protein in gastric cancer and its potential value as a prognostic marker. Dkk-3 expression was analyzed by immunohistochemistry in 136 tumor samples and was correlated with microvessel density (MVD), tumor stage, and grading as well as the clinical outcome of the patients. Dkk-3 expression was detected in endothelial cells of the tumor vessels in 129/136 (94.9%) and in tumor cells in 85/136 (62.5%) samples. MVD was high and low in 57 (42.9%) and 76 (57.1%) specimens respectively. In tumor cells, overexpression of Dkk-3 was found in 41 (30.1%) of all cases and was correlated significantly to pT-stage (p < 0.05) and UICC stage (p < 0.05). Survival analysis regarding Dkk-3 expression in tumor endothelial cells showed that Dkk-3 is an independent predictor of disease-free survival (p < 0.05). Dkk-3 expression in tumor vessels of patients with gastric cancer identifies a population of patients with relatively favorable prognosis.     

Fetal microchimerism is not involved in the pathogenesis of lichen sclerosus of the vulva

OBJECTIVES: The aim of this study was to investigate a possible relationship between fetal cell microchimerism and lichen sclerosus of the vulva. We searched for the presence of male cells and DNA in vulval tissue samples. METHODS: Paraffin-embedded skin biopsy samples from 15 women affected with vulval lichen sclerosus who gave birth to at least one son were analyzed for the presence of microchimeric male cells using fluorescence in situ hybridization (FISH) and fluorescent PCR. We included three lichen sclerosus samples originating from women without male offspring, six vulval specimens without pathological finding originating from autopsies and seven male gingival specimens as controls. RESULTS: Nucleated cells containing Y-chromosome specific sequences were neither detected at any site of the lesions nor in normal vulval specimens by using FISH. These results were confirmed by the use of PCR amplification demonstrating only DNA sequences specific for the X chromosome. No female microchimerism was detected in the male gingival samples. CONCLUSION: Despite the limited number and size of the samples, we conclude that persistent male fetal cells are not involved in the pathogenesis of lichen sclerosus of the vulva, since we consistently could not detect Y-chromosome specific sequences by using two molecular techniques.     

Sexual behavior, knowledge of STI prevention, and prevalence of serum markers for STI among tour guides in Cuzco/Peru

BACKGROUND: Sexual behavior during travel has increasingly become a focus of travel medicine research. The perceived freedom when away from home can lead to increased casual sexual activities, often unprotected. Local sexual partners, particularly those who are in close contact with tourists due to their occupation, need to be considered more in research. The purpose of this study was to explore the sexual behavior, knowledge of STI prevention, and prevalence of serum markers of selected STIs in tour guides in Cuzco/Peru. METHODS: In this cross-sectional study, 161 tour guides completed a questionnaire consisting of information on demographics, sexual behavior, and knowledge about STI prevention. Blood samples of the participants were tested for antibodies against HSV2, Chlamydia trachomatis, and Treponema pallidum using commercial enzyme-linked immunosorbent assay kits. RESULTS: The majority of guides (65%) were sexually active during the year prior to the study and 10% had foreign partners. Consistent condom use was reported by 38.1%, but almost 42% did not use condoms. In total, 27.6% reported symptoms compatible with STI. Three quarters of the participants had previously received information on STI prevention, predominantly from health professionals. In total, 22% considered themselves at high risk for STI. Antibodies against C trachomatis were prevalent in 15%, while 88.2% were against HSV2. None had antibodies against T pallidum. CONCLUSIONS: There is an inconsistency in reported sexual behavior and reported knowledge about STI prevention. Because of the tour guides' bridging position between potential STI carriers in tourists and the local population, the reported nonuse of condoms is of concern. The prevalence of serum markers supports this concern, which is aggravated by the potential of noncurable infections. Current sexual health education strategies seem unsatisfactory, and major modifications are highly recommended.