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Biomedical subjects

A Schmidt

Publications and source records attributed to A Schmidt.

At least 523 records · Page 29Linked to original sources
PubMed1989

Appearance and transient expression of oxytocin receptors in fetal, infant, and peripubertal rat brain studied by autoradiography and electrophysiology.

The development of oxytocin (OT) receptors in the rat brain and spinal cord was studied by in vitro light microscopic autoradiography and by electrophysiology. OT receptors were labeled using a monoiodinated OT antagonist in tissue sections from animals aged between embryonic day 12 (E12) and postnatal day 90 (PN90); the response of ongoing spike activity to the addition of OT was assessed in neurons located in the dorsal motor nucleus of the vagus nerve of the neonate. Specific binding was detected first at E14 in a region that later differentiated into the dorsal motor nucleus of the vagus nerve. Many other regions were progressively labeled between E20 and PN5. From PN5 to PN16, the distribution of binding sites remained essentially unchanged but differed markedly from that characteristic of the adult. The change-over from the "infant pattern" to the "adult pattern" occurred in 2 stages: the first change took place between PN16 and PN22, a time corresponding to the preweaning period; the second change occurred after PN35 and thus coincided with the onset of puberty. During the first transition period, binding was reduced or disappeared in several areas intensely labeled at earlier stages, in particular, in the cingulate cortex and the dorsal hippocampus. At the same time, binding sites appeared in the ventral hippocampus. At puberty, high densities of OT binding sites appeared in the ventromedial hypothalamic nucleus and the olfactory tubercle. Electrophysiological activity was recorded from vagal neurons in slices obtained from animals sacrificed at PN1-PN12. OT and a selective OT agonist reversibly increased the firing rate of these neurons in a concentration-dependent manner. The neuronal responsiveness was similar to that reported previously in the adult. These results suggest that OT binding sites detected by autoradiography in the developing rat brain represent, at least in some areas, functional neuronal receptors.

Animals↗
PubMed1989

[Reconstruction of the cranial vault and soft tissues of the skull after electrotrauma].

Of 550 patients treated in our burn unit 5.1% had electrical injuries. Injuries of the skull and scalp were caused by entry of electrical current. The classic reconstruction of the scalp and skull is performed after sequestration of the necrotic bone, a time-consuming process which frequently has complications. An alternative is to induce regeneration of the vitalized bone by covering it early with a vascular tissue flap. Skeletal scintigraphy has the advantage of allowing early and safe assessment of the vitality of the injured bone and helps to control vitalization.

Bone Regeneration↗
PubMed1989

[1 year's experience with the multifunctional lithotriptor Dornier MPL 9000].

From March 1988 until May 1989, 361 patients with 438 stones were treated with the Dornier multipurpose lithotripter MPL 9000. 64.8% of the stones were situated in the calyx, 32.6% in the renal pelvis, 1.1% in the upper and 1.4% in the distal ureter. 19.6% of the stones were radiolucent. Multiple MPL treatments were performed in 10.2%. In 4.3% fragments post-ESWL treatment were larger than 5 mm. In 95.7% of the cases complete disintegration was achieved. 63.5% of the treatments were performed without using analgesia or anesthesia. Intravenous anesthesia was used in 20.5%. Analgesia and sedation in 13.6%, general anesthesia in 1.7% and epidural anesthesia in 1.1%. After 3 months' follow up 74.3% were stone-free. Residual fragments were found in the upper calyx in 1%, in the middle calyx in 5%, in the lower calyx in 13%, in the renal pelvis in 5.6% and in the ureter in 1%. The MPL 9000 has been proven to be similarly effective for the treatment of renal stones, while difficulties in localizing ureteral stones, while difficulties in localizing ureteral stones were noted. The major number of treatment was performed without any analgesia or anesthesia. No major complications were encountered. Due to the small focal area and the ultrasound location system. Special advantages were found for the therapy of children.

Evaluation Studies as Topic↗
PubMed1989

Temporally different stimulation of TNF-alpha and PGE2 release from GM-CSF-primed macrophages.

Since granulocyte-macrophage colony-stimulating factor (GM-CSF) has previously been shown to activate macrophages, it was of particular interest to study its effect on synthesis and release of tumor necrosis factor-alpha (TNF-alpha). GM-CSF alone was incapable of activating murine peritoneal macrophages to TNF-alpha release. However, in response to lipopolysaccharide (LPS), GM-CSF was found to prime macrophages for enhanced TNF-alpha production. This priming effect was short-lived and was superseded by the contrary, an unresponsiveness to LPS. The suppressed response was due to a delayed production of prostaglandin E2 (PGE2) which did not affect GM-CSF-enhanced TNF-alpha gene transcription but blocked TNF-alpha production. When PGE2 synthesis was inhibited by indomethacin, the priming effect of GM-CSF was entirely reconstituted. Thus, GM-CSF initially primes for TNF-alpha and subsequently for PGE2 release which, taken together, may represent an autoregulatory feed-back system that could restrict macrophage activation.

Animals↗
PubMed1989

[Tumor-like courses in lung sarcoidosis (4 observations)].

Case reports on 4 women operated on for suspected tumour. The diagnosis of sarcoidosis was confirmed histologically. The difficulties associated with the differential diagnosis are discussed and, the need for morphological clarification is emphasized.

Adult↗
PubMed1989

[Quantification of the myocardial scar with technetium-99m-isonitrile (MIBI) in emission computerized tomography (SPECT)--comparison with serial creatine kinase determinations and radionuclide ventriculography].

Estimation of the size of myocardial infarction is of major interest for clinical patient management and a simple and reliable method is still searched for. In this study the potential of the new myocardial perfusion tracer, Technetium-99m (Tc-99m) methoxy-isobutyl-isonitril (MIBI) combined with emission computertomography (SPECT), is tested vs. the standard procedures of serial plasma creatine kinase (CK) measurements and radionuclide ventriculography (RNV). In 10 patients with first myocardial infarction, integral values for CK were obtained during the acute phase. Following three weeks of uncomplicated recovery the patient was referred for both types of myocardial imaging within four days. 370 MBq Tc-99m-MIBI were injected with the patient supine and at rest. One hour later SPECT acquisition commenced. The reconstructed slices were rearranged to long and short axes slices, which served to calculate a functional "scar image" in polar coordinates. The color-coded areas of significantly reduced tracer uptake were expressed in percent of the total myocardial area. RNV was performed with the patient supine and at rest, the left anterior oblique angle being optimized for septum visualization. Infarct localizations were antero-apical (three), anterolateral (two), postero-lateral (one), and posterior (four).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Nuclear factors interacting with the mitogen-responsive regulatory region of the interleukin-2 gene.

We have investigated the interaction of nuclear factors with the regulatory region of the interleukin-2 (IL-2) growth factor gene, which is induced upon activation of T lymphocytes. The regulatory region of IL-2 has been defined previously on the basis of transient transfection experiments and DNase I hypersensitive site analyses. This region of about 275 base pairs contains both tissue-specific as well as activation-dependent elements. Here we demonstrate nuclear factors which bind in this region. Some of these interactions are cell type-specific and several depend on prior activation of cells. This suggests that multiple activation responsive elements reside in the IL-2 promoter region. The inducible DNA binding activity of one of the factors is dependent also on protein synthesis. We have established an in vitro transcription assay to assess functional requirements for these DNA binding proteins. The possible involvement of some of these factors in regulating other genes expressed in T cells is discussed.

Animals↗
PubMed1988

Release of tumor necrosis factor-alpha from macrophages. Enhancement and suppression are dose-dependently regulated by prostaglandin E2 and cyclic nucleotides.

PGE2 has previously been shown to suppress various leukocyte functions. In this study, we examined whether PGE2 would affect release of TNF-alpha from rat resident peritoneal macrophages. Two different, dose-dependent effects were observed: low PGE2 concentrations (0.1 to 10 ng/ml) stimulated, whereas higher concentrations (greater than 10 ng/ml) suppressed TNF-alpha release. PGE2-stimulated TNF-alpha production was dependent on de novo protein synthesis and was associated with an intracellular rise of cGMP. The importance of cGMP as an intracellular messenger for PGE2 was confirmed by the following evidence: (1) low PGE2 concentrations preferentially increased cGMP and not cAMP and (2) cGMP, either exogenously added or endogenously generated by sodium nitroprusside, were efficient stimulators of TNF-alpha production. In contrast, agents increasing intracellular cAMP concentrations such as PGE1, higher PGE2 doses, isoproterenol, and theophylline, all suppressed TNF-alpha synthesis. Only resident, but not casein-elicited or Corynebacterium parvum-activated macrophages, were stimulated by low PGE2 concentrations to increase TNF-alpha production. In tumor cytotoxicity assays, PGE2-activated macrophages were active only against TNF-alpha-sensitive target cells. These findings demonstrate that TNF-alpha synthesis in macrophages is up-regulated by cGMP and down-regulated by cAMP, which indicates that cyclic nucleotides act as intracellular messengers for extracellular signals of macrophage activation.

Adjuvants, Immunologic↗
PubMed1988

[Treatment with mexiletine. Clinical and pharmacokinetic studies].

Pharmacokinetics of the antiarrhythmic agent mexiletine were found to be highly variable. Ineffective or toxic doses can be avoided by monitoring mexiletine concentrations in patients plasma. However, the success of antiarrhythmic therapy is mainly determined by the severity of the underlying disease. Therefore, the efficacy of treatment with mexiletine should be controlled by Holter monitoring.

Adult↗
PubMed1988

Isolation and characterization of two proteoheparan sulfate species of calf arterial tissue.

When calf aortic tissue, preincubated under organ culture conditions in the presence of [35S]sulfate, was submitted to a sequential collagenase and elastase digestion and guanidinium chloride extraction, the bulk of proteoheparan sulfate was obtained in the elastase fraction. Ion-exchange chromatography on DEAE-cellulose of the elastase digest under dissociative conditions yielded a proteoglycan fraction that contained heparan sulfate as the sole glycosaminoglycan. The proteoheparan sulfate fraction was resolved into a high-molecular-mass (P-HS 1) and a low-molecular-mass (P-HS 2) fraction by gel filtration on Sephacryl S-400. P-HS 1 has a Mr of 175,000 and possesses four heparan sulfate side-chains (Mr 32,000) covalently bound to the protein core via a galactose- and xylose-containing polysaccharide-protein binding region. The protein core (Mr 38,000), which was obtained after deglycosylation of PG-HS 1 with trifluormethane sulfonic acid, contained in addition a few N-glycosidically linked oligosaccharide units representing a complex type with terminal neuraminic acid residues. P-HS 2 is a single-chain peptidoheparan sulfate of Mr of 38,000 containing one heparan sulfate chain (Mr 32,000) linked to a polypeptide (Mr 6000). The ratio of specific radioactivities of P-HS 1 and P-HS 2 was 1:0.66.

Amino Acids↗
PubMed1988

Efficacy and safety of intravenous amiodarone in acute refractory arrhythmias.

Few data are available on intravenous amiodarone therapy in refractory arrhythmias. This retrospective study in 50 patients (14 with supraventricular and 36 with ventricular tachyarrhythmias) revealed a favorable effect of intravenous amiodarone in the treatment of life-threatening arrhythmias with an overall success rate of 76%. In the subgroup of patients with ventricular fibrillation and concomitant severe congestive heart failure success rate was low (25%, 2/8), whereas effectiveness in patients with ventricular tachycardias was high (greater than 90%) and proved to be independent of left ventricular function. If patients with recurrent ventricular fibrillation were excluded from the analysis, successful treatment with intravenous amiodarone was achieved in 90%, even in those patients with severely compromised myocardium.

Acute Disease↗
PubMed1988

Pathophysiological aspects of predominant preload lowering on pulmonary circulation, gas exchange, and the biventricular function in patients with chronic obstructive lung disease.

A group of 21 patients with various degrees of chronic obstructive pulmonary disease underwent radionuclide ventriculography with hemodynamic monitoring to assess the extent to which pulmonary artery pressures and pulmonary vascular resistance can be lowered by the vasodilator molsidomine. Molsidomine (N-carboxy-3-morpholino-sydnonimin-ethylester) is similar to nitroglycerin in its mode of action. After hemodynamic and radionuclide data acquisition, at rest and during submaximal exercise in the steady state, 2 mg molsidomine was injected intravenously. Rest and exercise measurements were repeated 45 min after molsidomine injection. In patients with mild to moderate disease (group 1), pulmonary artery resting pressures decreased by 12% (p less than 0.05) at rest by 22% (p less than 0.01) during exercise after the administration of the drug. Total pulmonary resistance during exercise decreased significantly (p less than 0.01) as a result of marked decrease of pulmonary artery pressure (PAP) compared with a minimal decrease in cardiac index (CI). In patients with severe disease (group 2), only the resting values of PAP decreased while the relationship between pressure and flow was unchanged. During the exercise period, the preload parameters of the right and left ventricles decreased by an average of 30%. With regard to gas exchange, only the arterial PO2 at rest decreased slightly but significantly (p less than 0.05) after molsidomine, while the coefficient of oxygen delivery was not affected by the drug. However, in four patients arterial PO2 was markedly reduced by the drug. Right ventricular ejection fraction increased significantly (p less than 0.01) both at rest and during exercise in group 1 and during exercise in group 2 after administration of molsidomine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Biological activities of EGF-receptor mutants with individually altered autophosphorylation sites.

In vitro site-directed mutagenesis was used to replace individually the three known autophosphorylation sites of the epidermal growth factor (EGF)-receptor (i.e. Tyr1173, Tyr1148 and Tyr1068) by phenylalanine, a residue which cannot serve as a phosphate acceptor site. In another mutant, Tyr1173 was substituted by a serine residue. The cDNA constructs encoding either mutant or wild-type EGF-receptors were transfected into NIH-3T3 cells devoid of endogenous EGF-receptors. The mutant receptors were expressed on the cell surface and displayed typical high- and low-affinity binding sites for [125I]EGF. Phorbol ester (PMA) modulated the binding affinity of wild-type and mutant receptors in a similar manner. Mutant EGF-receptors exhibited EGF-dependent tyrosine kinase activity leading to self-phosphorylation and phosphorylation of exogenous substrates both in vitro and in living cells. The internalization and degradation of EGF-receptors were not affected by the mutations. Cells expressing mutant EGF-receptors became mitogenically responsive to EGF, indicating that none of the vital functions of the EGF-receptor were critically impaired by the loss of individual autophosphorylation sites. Maximal mitogenic stimulation correlated with the number of wild-type or mutant receptors per cell, highly expressing cells showing higher maximal stimulation. However, the dose-response curves of cells expressing mutant receptors were slightly shifted to lower concentrations of EGF, rendering the cells mitogenically responsive to lower doses of EGF than cells expressing normal EGF-receptor at similar expression levels. Basal [3H]thymidine incorporation in the presence of 0.5% calf serum was consistently higher for cells expressing mutant receptors, while the response to stimulation with 10% calf serum was not affected.

Animals↗