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Noxious digital nerve stimulation during isometric contraction of hand muscles leads to transient suppression of the electromyographic activity, the so-called cutaneous silent period (CSP), which is mostly due to a spinal reflex mediated by A-delta fibers. We investigated two patients with carpal tunnel syndrome (CTS) and two patients with ulnar entrapment at the elbow (UNE), in whom routine sensory conduction studies failed to document afferent fiber continuity across the lesion site. In three patients, motor nerve conduction studies and electromyography failed to demonstrate intact efferent fibers. Noxious stimulation of digit II elicited distinct CSPs in ulnar-innervated hand muscles in both patients with CTS, and stimulation of digit V evoked CSPs in median-innervated hand muscles in both UNE patients. The presence of a CSP can only be explained by preserved A-delta fibers crossing the respective lesion site. Thus, preserved CSPs may serve to document residual nerve continuity in severe entrapment neuropathies when fast-conducting fibers are so compromised that their continuity cannot be detected by standard electrodiagnostic techniques.  相似文献   
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Hippocampal cytoarchitectural abnormalities may be part of the cerebral substrate of schizophrenia. Amongst the chemical components being abnormal in brains of schizophrenics are altered calcium concentrations and reduced expression of the neurotrophin receptor, trkB. We studied by immunohistochemical methods the distribution of visinin-like protein-1 (VILIP-1), which is a calcium sensor protein and at the same time a trkB mRNA binding protein, in hippocampi of nine schizophrenic patients and nine matched control subjects. In normal hippocampi VILIP-1 immunoreactivity was found in multiple pyramidal cells and interneurons. A portion of VILIP-1 immunoreactive interneurons co-express calretinin (60%) and parvalbumin (<10%). In schizophrenics fewer pyramidal cells but more interneurons were immunostained. Our data point to an involvement of the protein in the altered hippocampal circuitry in schizophrenia.  相似文献   
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In 19 patients, who suffered from severe spinal spasticity of different etiologies and did not respond sufficiently to oral antispastic therapy, intrathecal Baclofen test boli were administered. In 11 patients a DAD (Drug Administration Device) [SynchroMedR Model 8611 H, Medtronic Inc. Minneapolis, USA] was implanted. Catheter dislocation or torsion was the most common complication to be observed in these 11 patients. Long term intrathecal Baclofen application was effective in all patients, as reducing spasticity, flexor spasms and spasm induced pain. In some cases the motor performance ameliorated.  相似文献   
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Zusammenfassung Nach Aufgliederung der prim?ren epithelialen Nierenparenchymtumoren aus pathologisch-anatomischer Sicht in 1. hypernephroide Karzinome, 2. papill?re Adenokarzinome, 3. übergangsformen von 1 und 2, werden Nierenveneneinbruch und Einbruch in das Nierenholsystem im Hinblick auf überlebenszeit bzw. H?maturie untersucht. Altersverteilung, Inivialsymptome und Laboratoriumsbefunde werden in Tabellen aufgeführt. In der R?ntgendiagnostik wird die überragende Bedeutung der Aortographie hervorgehoben und ihre Grenzen besprochen. Schlie?lich erfolgt die Darstellung der überlebensrate nach verschiedenen Einteilungsprinzipien: Tumor auf die Niere beschr?nkt, perirenale Infiltration, Veneneinbruch, makroskopisch radikal operiert und die Ergebnisse aller operierten Patienten.
Summary Classification of the primary epithelial tumors of the kidney parenchyma from a patho-anatomical standpoint in 1. hypernephroid carcinoma, 2. papillary adenocarcinoma, 3. transition of 1 to 2, invasion to renal vene and to calyx-pelvic system in relation to survival rate and haematuria is examinated. Age distribution, initial symptoms and laboratory findings are summarized in tables. The importance of aortography in the roentgenologic diagnostic of renal is emphasized. Discussion of survival rate according to: intraparenchymal tumor, perirenal and vene invasion, nephrectomy macroscopic radical and results of all operated patients.


Mit Unterstützung aus dem Felix-Mandl-Fonds zur F?rderung wissenschaftlicher Arbeiten an den St?dtischen Krankenanstalten der Gemeinde Wien und aus der Ludwig-Boltzmann-Gesellschaft zur F?rderung der wissenschaftlichen Forschung in ?sterreich.  相似文献   
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BACKGROUND: RhoE/Rnd3, a recently described novel member of the Rho GTPases family, was discussed as a possible antagonist of the RhoA protein that stimulates cell cycle progression and is overexpressed and/or overactivated in prostate cancer. We investigated the expression of RhoE and its role in cell cycle regulation and apoptosis in the human prostate. METHODS: RhoE expression in cell lines and tissue specimens was assessed by immunoblot analysis, real-time PCR (RT-PCR), and immunohistochemistry. To elucidate RhoE effects on the prostate, RhoE was cloned and overexpressed in DU-145 prostate cancer. Cell cycle modulation and apoptosis was investigated by immunoblot and FACS analysis. RESULTS: Immunoblot analysis showed a strong RhoE signal in both, benign epithelial and stromal cells. In contrast, almost no protein was detected in various prostate cancer cells. On RT-PCR and microarray analysis, RhoE mRNA expression was significantly reduced in malignant tissue when compared to benign samples. RhoE immunostaining was strong in benign tissue, especially in prostate epithelial cells, whereas it was minimal or absent in malignant tissue. Forced RhoE overexpression in a prostate cancer cell line inhibits the expression of two proteins essential for G2/M transition, namely CDC2 and cyclin B1, and induces G2/M arrest. In addition, apoptotic cell death as measured by a cleavage product of caspase 3 is significantly increased in RhoE-overexpressing cells. CONCLUSION: In conclusion, our findings suggest RhoE as a tumor suppressor gene that is downregulated early in the development of prostate cancer.  相似文献   
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Complex cellular and inflammatory interactions are involved in the progress of vascular diseases. Endothelial cells, upon exposure to cytokines, undergo profound alterations of function that involve gene expression and de novo protein synthesis. The functional reprogramming of endothelial cells by cytokines is of importance especially in patients with chronic vascular inflammation. The intercellular network of dendritic cells, T-lymphocytes, macrophages and smooth muscle cells generates a variety of stimulatory cytokines [e.g. TNF-alpha (tumour necrosis factor-alpha), IL (interleukin)-1, IL-6 and IFN-gamma (interferon-gamma)] and growth factors that promote the development of functional and structural vascular changes. High concentrations of proinflammatory cytokines increase oxidative stress, down-regulate eNOS (endothelial nitric oxide synthase) bioactivity and induce endothelial cell apoptosis. Chemoattractant cytokines [e.g. VEGF (vascular endothelial growth factor), TGF-beta1 (transforming growth factor-beta1) and IL-8] are important regulators of inflammation-induced angiogenesis and are directly modulated by nitric oxide. This review will focus on the vascular mechanisms orchestrated by cytokines and summarizes the current knowledge concerning the contribution of cytokines to cardiovascular diseases.  相似文献   
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