Comparison of the hollow fiber artificial kidney with the coil dialyzers.
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Biomedical subjects
Publications and source records attributed to M Schulz.
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An 8(10)/(12) year old girl with infantile cerebral paresis (ICP), severe mental retardation and seizure disorder was admitted to the intensive care unit (ICU) with clinical signs of aspiration and died ten days later. Final diagnosis was esophagobronchial fistula caused by a foreign body in the esophagus provoking aspiration pneumonia, mediastinitis and respiratory distress syndrome (ARDS). The foreign body was found to be part of a plastic toy. The clinical relevance of aspiration in mentally retarded children and the peculiar nature of the foreign body impacted in the esophagus in this case are discussed. We conclude that in cases of aspiration pneumonia in mentally retarded children the presence of unusual foreign bodies should be suspected.
Activation of the intracellular "death domain" (DD) of the 55kD-TNF alpha-receptor by TNF alpha initiates signal and effector cascades with pro- and anti-apoptotic function. Co-activation of the adjacent "NO-domain" is followed by induction of inducible nitric oxide-synthase (iNOS) and generation of nitric oxide radicals (NO.). Recently, we have shown NO.-generation to be essential for TNF alpha-induced apoptosis of various tumor cell lines. However, the impact of iNOS activation in relation to other promoters of apoptosis, such as the caspases, is still unclear. Caspase activation, iNOS induction and death rate were therefore investigated in TNF alpha-treated MCF-7 cells. Incubation with TNF alpha (+/- cycloheximide) led to activation of the caspase cascade and was followed by apoptosis. Simultaneously, TNF alpha stimulated induction of iNOS and generation of NO.. Caspase inhibitors DEVD-CHO, YVAD-cmk and YVAD-CHO effectively inhibited caspase activation and prevented apoptosis. Apoptotic cell death was decreased to a similar degree following inhibition of iNOS by L-nitro-arginine-methyl-ester (L-NAME). Cell death suppression by caspase inhibition did not result in reduced iNOS activity, as well as L-NAME-dependent prevention of apoptosis was not associated with caspase inactivation. Taken together, TNF alpha induces apoptosis in MCF-7 cells by initiating a two-sided effector pathway including iNOS-induction and activation of caspase 1- and 3-like proteases. Both mechanisms seem to be equally essential for the execution of the death program. The exact nature of their cooperation needs further clarification.
Lymphocytes of 36 patients with malignant Non-Hodgkin lymphomas (NHL) were characterized by electrophoretic mobility (EPM) and EAC-rosette and E-rosette formation. Unimodal cytopherograms found in patients with low-grade malignant NHL are compatible with a monoclonal origin of the proliferating lymphoid cells. Within the CLL subgroup, deviations from the general mean EPM value in the intermediumrange were not unequivocally related to the B- or T-cell origin of the lymphocytes and remain to be explained. Comparing distinct entities of low-grade malignant NHL characterized by lymphocyte arrest at a certain stage of differentiation (Kiel Classification) we found an increase of the mean EPM in the direction of CLL----lymphoplasmacytoid immunocytoma----polymorphic immunocytoma. This arrest of leukemic cells at a certain EPM level may support a cytogenetically oriented subclassification of NHL. The Limitations of the diagnostic value of cytopherograms and rosette formation in malignant NHL--especially in those of high malignancy--are outlined.
OBJECTIVES: A double-blind randomized study involving pregnant women undergoing cesarean section was conducted to compare the effectiveness of a single 100 micrograms intravenous injection of the long-acting oxytocin analog, carbetocin, with that of a standard infusion of oxytocin with respect to intraoperative blood loss. The two treatments also were compared for safety and ability to maintain adequate uterine tone. STUDY DESIGN: The study drug was administered to 57 women during elective cesarean section after placental delivery; blood was collected until abdominal closure. Intraoperative blood loss was calculated with a sensitive colorimetric method. Position, tone of the fundus, and vital signs were assessed up to 24 hours after the operation. The need for additional uterotonic agents was recorded. RESULTS: A single 100 micrograms intravenous injection of carbetocin was as effective as a continuous 16 hour infusion of oxytocin in controlling intraoperative blood loss after placental delivery. Mean blood loss after carbetocin administration was 29 ml less than after oxytocin administration (p = 0.3). Subset analysis deleting two patients who received oxytocic intervention in the operating room and one extreme outlier revealed a mean blood loss of 41 ml less in the carbetocin group (p = 0.14) with lower variances (p = 0.02). The percentage of patients with blood loss of 200 ml or less was greater with carbetocin (79% vs 53%; p = 0.041). Carbetocin enhanced early postpartum uterine involution. The fundus was below the umbilicus in more patients who received carbetocin at 0, 2, 3, and 24 hours on the ward (p < 0.05). There were no significant differences in uterine tone or type or amount of lochia. Additional oxytocin was used to treat three patients for postpartum hemorrhage or persistent uterine atony. All interventions were in the oxytocin group. Vital signs and hematologic values were comparable in each group, confirming similar safety profiles. CONCLUSIONS: A single 100 micrograms intravenous injection of carbetocin is as effective and more reliable than a standard continuous infusion of oxytocin in maintaining adequate uterine tone and preventing excessive intraoperative blood loss during cesarean section after delivery of the placenta. Patients receiving carbetocin required less intervention. Carbetocin was well tolerated.