Emotion Management Training (EMT) in persons with treatment-resistant schizophrenia: first results.
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The primary reaction of the macrophage electrophoretic mobility test (MEM) and its modifications (viz. the interaction of myelin basic protein (MBP) and mononuclear cells) has been investigated. The binding of MBP to mononuclear cells is rather weak, and on incubation with mononuclear cells the MBP is proteolytically degraded. A fast process leads to fragments with mol. wts in the range 9000-14,000, followed by a slower process leading to peptides smaller than 5000. Both binding and proteolytic degradation are the same for mononuclear cells from cancer patients and from control individuals.
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OBJECTIVE: To compare the initial emergency medical services (EMS) prehospital assessment of medical and traumatic cardiopulmonary arrest in the pediatric patient with that of the Office of the Medical Investigator (OMI) and assess differences and implications for EMS training and prevention. DESIGN: Retrospective review of ambulance run forms with the OMI autopsy confirmations. SETTING: An urban EMS system and the state Office of the Medical Investigator. PARTICIPANTS: Patients 15 years of age or less who were treated by prehospital personnel from November 1, 1990, to October 31, 1991, for a medical or traumatic arrest. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: Ambulance runs were reported for 2,586 pediatric patients. Of these, 42 (1.6%) had suffered arrests, with 32 (76%) medical arrests and ten (24%) traumatic arrests. Children 1 year of age or less accounted for 75% of the medical arrests, while children more than 1 year of age accounted for 80% of the traumatic arrests (p = 0.003). Overall mortality was 81%. When EMS prehospital assessments of medical and traumatic arrests were compared with autopsy reports, there was good agreement for sudden infant death syndrome (SIDS) (kappa = 0.70), but poor agreement for child abuse (kappa = 0.37). CONCLUSION: The authors found good agreement between EMS prehospital assessments and autopsy diagnoses for identifying pediatric SIDS, but child abuse was not well identified prior to autopsy.
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The extraneuronal monoamine transporter plays an important role in the inactivation of monoamine transmitters. A basal extraneuronal tissue expression of this transporter has been reported, but it is also expressed in CNS glia. As little is known about the expression pattern and the function of the extraneuronal monoamine transporter in the brain, we performed a detailed investigation. Firstly, a northern blot analysis of different rat organs revealed that the transporter is strongly expressed in placenta, lung and heart and less prominently in the whole brain, brain stem, intestine, testis, epididymis, stomach, kidney and skeletal muscle. It was not expressed in cerebellum, liver and embryo. Using an in situ hybridization to the rat brain, we detected a marked and highly confined expression of the extraneuronal monoamine transporter in the area postrema, but in no other brain areas. These findings were confirmed by polyclonal antibodies against rat extraneuronal monoamine transporter showing an intensive signal in the area postrema, although a few cells in the cerebellum and the brain stem also showed a signal. Additionally, a partly overlapping expression pattern of the monoamine oxidase-B was detected. Summarizing, we firstly describe a marked and highly confined expression of the extraneuronal monoamine transporter in the rat area postrema by in situ hybridisation which may play a role in physiological functions of this circumventricular organ such as emesis, food intake and the regulation of cardiovascular functions.
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Enhancement of tumor cell growth and invasiveness by transforming growth factor-beta (TGF-beta) requires constitutive activation of the ras/MAPK pathway. Here we have investigated how MEK activation by epidermal growth factor (EGF) influences the response of fully differentiated and growth-arrested pig thyroid epithelial cells in primary culture to TGF-beta1. The epithelial tightness was maintained after single stimulation with EGF or TGF-beta1 (both 10 ng/ml) for 48 hours. In contrast, co-stimulation abolished the transepithelial resistance and increased the paracellular flux of [(3)H]inulin within 24 hours. Reduced levels of the tight junction proteins claudin-1 and occludin accompanied the loss of barrier function. N-cadherin, expressed only in few cells of untreated or single-stimulated cultures, was at the same time increased 30-fold and co-localised with E-cadherin at adherens junctions in all cells. After 48 hours of co-stimulation, both E- and N-cadherin were downregulated and the cells attained a fibroblast-like morphology and formed multilayers. TGF-beta1 only partially inhibited EGF-induced Erk phosphorylation. The MEK inhibitor U0126 prevented residual Erk phosphorylation and abrogated the synergistic responses to TGF-beta1 and EGF. The observations indicate that concomitant growth factor-induced MEK activation is necessary for TGF-beta1 to convert normal thyroid epithelial cells to a mesenchymal phenotype.
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