Diabetes mellitus : frühes Eingreifen verhindert Folgeerkrankungen

Glukose ist ein zentrales Element des normalen Energiehaushalts im Körper. Seine Konzentration im Blut wird von Insulin, einem Hormon, das außerdem für Wachstums- und Entwicklungsprozesse mitverantwortlich ist, reguliert. Normale Glukosespiegel im Blut und in den Zellen sind die Folge einer fein abgestimmten Insulinwirkung am Insulinrezeptor, der in der Zelle eine nachgeschaltete Signalkette auslöst, bei der Glukose in die Zelle eingeschleust wird. Insulin bindet an den Insulinrezeptor nach dem Schlüssel-Schloss-Prinzip, wobei die Türöffnung hier den Eintritt von Glukose in die Zelle bedeutet. Gibt es zu wenig Insulin (Typ 1-Diabetes) oder ist die Wirkung von Insulin am Rezeptor oder in der nachgeschalteten Signalwirkung gestört, so resultieren Zuckerstoffwechselveränderungen bis hin zu Diabetes mellitus (Zuckerkrankheit). Für die häufigste Diabetes mellitus-Form (Typ 2) sind Störungen am Rezeptorsystem verantwortlich

Оптимизация системы материально-технического обеспечения как фактор повышения производительности производства

Объектом исследования является система материально-технического обеспечения ЗАО "Сибирская сервисная компания". Цель работы–анализ, оценка и оптимизация деятельности компании в сфере материально-технического обеспечения на примере ЗАО "Сибирская сервисная компания".The object of the research is the logistics system of the Siberian Service Company CJSC. The purpose of the work is the analysis, evaluation and optimization of the company's activities in the field of logistics through the example of CJSC Siberian Service Company

Der selektive Cyclooxygenase-2-Inhibitor Celecoxib ist ein sicheres Ausweichpraparat bei Intoleranz gegenuber nichtsteroidalen Antiphlogistika

BACKGROUND: Adverse reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) are frequent, and the need to identify a safe alternative drug is a common problem in clinical practice. We assessed the tolerability of the selective cyclooxygenase-2 inhibitor celecoxib in a group of NSAID-sensitive patients. PATIENTS AND METHODS: 77 patients (24 males, 53 females, age 31-80 years) with a history of adverse reactions to NSAIDs underwent standardized skin prick, scratch and patch tests along with oral, placebo-controlled blinded exposure to celecoxib (maximum single dose 200 mg, cumulative daily dose 350 mg). RESULTS: 21 patients had a history of cutaneous reactions only (urticaria), 25 had encountered respiratory symptoms (asthma), 18 reported cutaneous as well as respiratory symptoms, and in 13 patients an anaphylactoid shock occurred. Acetylsalicylic acid triggered symptoms in 38 patients. In 46 cases, several NSAIDs of different chemical groups caused symptoms. Oral challenge with celecoxib was tolerated by all 77 patients without adverse effects. CONCLUSION: This study demonstrates that celecoxib does not have cross-intolerance to NSAIDs. Celecoxib is a safe alternative in subjects with previous adverse reactions to NSAIDs

Correlation of Microsomal and TSH Receptor Antibodies with the Intensitiy of the Intrathyroidal Autoimmune Process in Graves' Disease

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Stimulation of proliferation and inhibition of function of xenotransplanted human thyroid tissue by epidermal growth factor

A stimulation of thyroid epithelial cell proliferation by epidermal growth factor (EGF) has been repeatedly reported in different in vitro systems. Furthermore, a suppression of thyroid epithelial cell function by EGF has been described in vitro. In order to investigate the effects of EGF on the thyroid in vivo, human Graves' disease tissue was transplanted to 59 nu/nu mice. EGF was given once, and over a period of 7 days 7 times intermittently or continuously by osmotic mini pumps to mice. 3-H-thymidine histoautoradiography of transplants showed an increased 3-H-thymidine incorporation of thyroid epithelial cells and mesenchymal cells, following each form of EGF application, Thyroid epithelial cell nuclear volume, which has previously been shown to be a parameter for thyroid epithelial cell function showed a decrease following EGF application, There was a tendency to a more intensive proliferation and dedifferentiation following intermittent EGF application compared to continuous stimulation. These results demonstrate that EGF does stimulate proliferation of thyroid epithelial as well as mesenchymal cells in vivo. The growth stimulating effect of EGF is linked with a concomitant decrease of thyroid function in vivo. The latter is most likely due to the dedifferentiating action of EGF previously shown in in vitro systems.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Correlation of microsomal antibodies with the intensity of the intrathyroidal autoimmune process in Graves' disease

Graves' disease is an organ-specific autoimmune disease, and intrathyroidal lymphocytes seem to be the major source of thyroid autoantibodies. Consequently, the intensity of the intrathyroidal lymphocytic infiltration is generally believed to reflect the activity of the autoimmune process. We, therefore, investigated the correlation of microsomal (enzyme immunoassay), thyroglobulin (RIA), and TSH receptor antibodies (RRA) with the degree of intrathyroidal infiltration by immunoglobulin G-producing plasma cells, activated T-cells, antigen-presenting cells, and the total number of lymphocytes. The immunocompetent cells were identified immunohistologically with monoclonal antibodies for immunoglobulins κ and λ, UCHL1, and the S100 antibody, respectively, in 26 thyroid glands of patients suffering from Graves' disease. The intensity of lymphocytic infiltration was determined by the point-counting method and by counting all lymphocytes and the labeled lymphocytes in 3 x 51 visual fields or 3 slides/thyroid gland. Microsomal antibodies correlated significantly (P = 0.001) with the total number of lymphocytes (r = 0.86), κ (r = 0.71), λ (r = 0.71), UCHL1 (r = 0.9), and S100 (r = 0.9) positive cells. These correlations were also significant for thyroglobulin antibodies. However, TSH receptor antibodies showed no significant correlations with any of the populations of immunocompetent cells. Patients with preoperatively undetectable TSH receptor or microsomal antibodies showed a broad variation of intrathyroidal infiltration by the immunocompetent cells investigated. Microsomal antibody titers, therefore, seem to reflect the intensity of the intrathyroidal autoimmune process in Graves' disease better than TSH receptor antibodies. However, the broad baseline variation in intrathyroidal infiltration observed with nondetectable thyroid antibodies will not always allow determination of the intensity of the intrathyroidal autoimmune process from microsomal or thyroglobulin antibody titers.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Mechanisms of hepatotoxicity caused by dacarbazine in rats

Possible risks of fatal dacarbazine hepatotoxicity have not been studied systematically. We therefore asked whether dacarbazine hepatotoxicity is influenced by the dose or mode of application, by dacarbazine light-decay products, by prior liver damage or by an induction of dacarbazine metabolism. 22 Sprague-Dawley rats were treated with 4.5 mg and 200 mg dacarbazine/kg bodyweight i.p. and i.v. with dacarbazine light-decay products and with 4.5 mg and 200 mg dacarbazine/kg bodymass after previous galactosamine and ethanol treatment. Serum alanine amino-transferase, cholinesterase and white blood cell and platlet numbers were measured and liver histology was evaluated. Dose-dependent dacarbazine hepatotoxicity could be demonstrated by histology. The mode of application, dacarbazine light-decay products and acute liver damage did not influence dacarbazine hepatotoxicity. However 200 mg dacarbazine/kg bodymass after ethanol pretreatment caused significant serological changes and a significant leucodepression. The increased hepato-and myelotoxicity after induction of hepatic microsomal enzymes should be reason to exclude ethanol and drugs that induce hepatic microsomal enzymes prior to treatment with dacarbazine. © 1993 Springer-Verlag.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Relapse of Graves' disease following development of a pheochromocytoma

SCOPUS: ar.jinfo:eu-repo/semantics/publishe