PubMed Health⌕ Search

Biomedical subjects

C Riedel

Publications and source records attributed to C Riedel.

48 records · Page 3Linked to original sources
PubMed1991

Sequential cerebrospinal fluid and plasma sampling in humans: 24-hour melatonin measurements in normal subjects and after peripheral sympathectomy.

Simultaneous measurements of plasma and cerebrospinal fluid (CSF) melatonin and urinary excretion of 6-hydroxymelatonin were performed in four normal volunteers and one patient before and after upper thoracic sympathectomy for the control of essential hyperhidrosis. For normal individuals, hourly 24-h melatonin concentrations in plasma and CSF exhibited similar profiles, with low levels during the day and high levels at night. Peak plasma levels varied from 122-660 pmol/L, and the peak CSF levels from 94-355 pmol/L. The onset of the nocturnal increase in melatonin did not occur at the same time for each individual. Urinary 6-hydroxymelatonin levels also exhibited a daily rhythm, with peak excretion at night. The individual with the lowest nocturnal levels of circulating melatonin also had the lowest excretion of 6-hydroxymelatonin. In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.

Adult↗
PubMed1991

Cardiopulmonary responses to acute hypoxia, head-down tilt and fluid loading in anesthetized dogs.

The separate and combined acute effects of hypoxia (HY-11% O2), head-down tilt (HD-30 degrees) and fluid loading (FL-1.0 L saline) on hemodynamics and pulmonary gas exchange were determined in 17 anesthetized, mechanically ventilated dogs. Both during HY and normoxia (NO), the total respiratory compliance was decreased by HD, attributable to pulmonary vascular congestion. The reductions in compliance were twice as great with FL, indicating pulmonary interstitial edema, which was supported by histological observation of lung tissue. Pressure-flow relationships in the pulmonary circulation indicated that superimposing HD on HY doubled the increase in vascular resistance due to HY alone, while in the systemic circulation the resistance was returned to below NO by HD. A significant positive correlation between the changes in blood volume and pulmonary artery pressure for experimental transitions suggests that a shift in blood volume from systemic to pulmonary circulations and changes in total blood volume probably contributed substantially to these apparent changes in resistance. Pulmonary gas exchange efficiency, whether expressed in terms of shunt or ventilation/perfusion distribution from arterial-end-tidal PCO2 and PO2 differences, showed a significant inverse relationship with pulmonary driving pressure for the experimental conditions imposed. No clear synergistic effects of HY on HD were evident in contributing to pulmonary edema when superimposed prior to FL, but after FL this risk must be considered.

Acute Disease↗
PubMed1990

Autonomic regulation of cutaneous vascular resistance in the bullfrog Rana catesbeiana.

To gain a better understanding of the regulation of cutaneous blood flow in the bullfrog, the vascular innervation, vasoactivity and adrenoceptor types of the cutaneous vasculature were investigated using a pump-perfused skin preparation. Stimulation of cranial nerve I, the vagal ganglion, sympathetic ganglion 1 and sometimes sympathetic ganglion 2 caused cutaneous vascular resistance (CVR) to increase. Stimulation of cranial nerve IX and spinal nerves 1 and 2 had no effect on CVR. The response to stimulation of sympathetic ganglion 1 was antagonized by phentolamine but not by atropine. Phentolamine, atropine and alpha,beta-methylene ATP had no effect on the response to vagal stimulation. Both epinephrine (EPI) and norepinephrine (NE) increased CVR, with EPI being more potent than NE. The minimum concentrations of EPI and NE required for a significant change in CVR were much higher than plasma catecholamine levels reported for resting bullfrogs. Phentolamine antagonized, but propranolol had no effect on, the responses to the catecholamines. Isoproterenol caused small decreases in CVR which were abolished by propranolol. Acetylcholine was a weak vasodilator. The results indicate that the cutaneous vasculature has two types of vasomotor nerves: sympathetic nerves that are probably adrenergic, and other nerves that are non-adrenergic/non-cholinergic and which do not use ATP as a transmitter. Although catecholamines are vasoactive, the sensitivity of the cutaneous vasculature to EPI and NE is probably too low to allow a direct regulatory role of these hormones on CVR. There is no evidence for cholinergic regulation of CVR. Both alpha- and beta-adrenoceptors are present in the cutaneous vasculature. alpha-Adrenoceptors mediate the constrictor responses to sympathetic nerve stimulation and catecholamine administration. It is unlikely that beta-adrenoceptors play a significant role in regulating CVR.

Acetylcholine↗
PubMed1989

Sudden appearance of anti-protein IgG1-forming cell precursors early during primary immunization.

The anti-keyhole limpet hemocyanin (KLH) B-cell repertoire of unimmunized adult mice was examined by culture of splenocytes (generally 100-3000) at limiting dilution. Cells were polyclonally stimulated with Escherichia coli lipopolysaccharide (LPS) and an interleukin-4-containing lymphokine mixture in the presence of 3T3 fibroblast filler cells. After 7 days of culture, supernatants were examined for their content of anti-KLH IgM and IgG1 antibody by an enzyme-linked immunosorbent assay (ELISA). Parallel cultures of smaller numbers (generally 1-15) of splenocytes were examined to determine the cloning efficiency of B cells in terms of total IgM and IgG1 production. Whereas one spleen cell in 370 produced clones secreting anti-KLH IgM, only 1% of these produced IgG1 that could bind to KLH, despite the fact that about half of the clones switched to IgG1 production with these stimuli. In mice immunized with KLH, this situation did not change until day 5, when there was a sudden, explosive emergence of B cells that could form clones secreting anti-KLH IgG1. The absolute number of such cells in the spleen was found to rise by a factor of 350 between days 3 and 7 of immunization. Moreover, the median amount of IgG1 antibody formed per clone and binding to KLH also rose markedly. In contrast, neither the numbers nor the median KLH-binding antibody content of anti-KLH IgM clones changed significantly after immunization. The results show that the repertoire of anti-protein B cells detected through IgM formation in ELISA consists chiefly of cells producing antibody of low avidity and of doubtful in vivo significance. Assuming that the small proportion of these cells making antibody that is of sufficient avidity to bind as the IgG1 isotype are the ancestors of the many such cells found on day 7 of the primary immune response, one would have to postulate a very high recruitment and/or division rate to account for the increase in numbers and avidity that occurs. It is possible that the anti-KLH IgG1 precursors that suddenly emerge are the results of early variable region gene (V) mutations in B cells. Moreover, it is not excluded that they represent products of a subset of B cells different from those that give rise to the primary in vitro anti-KLH IgM response. The findings have implications for theories of B-cell tolerance.

Animals↗
PubMed1988

A significant proportion of normal resting B cells are induced to secrete immunoglobulin through contact with anti-receptor antibody-activated helper T cells in clonal cultures.

This report describes single-cell techniques to address the nature of a cellular interaction in which activated T lymphocytes stimulate small resting B cells to develop into antibody-forming cell clones in the absence of any surface immunoglobulin ligand or an antigen bridge. The cloned T helper cell line E9.D4 was stimulated with the anti-V beta 8 antibody F23.1 bound to the plastic of Terasaki 10-ul culture wells. When an excess of T helper lymphocytes was used (1,000 X-irradiated or 600 unirradiated, stimulated E9.D4 cells), 10-25% of B cells responded by antibody formation as judged by an enzyme-linked immunosorbent assay performed after 5 days of culture. When one of a very small number of B cells were present, the rate-limiting step to antibody-forming cell formation was the number of T cells present. Far fewer T cells sufficed for stimulation when culture trays were tilted to force T and B cells into proximity at the sulcus formed at the bottom edge of the culture wells. When T cell numbers were limiting, unirradiated T cells out-performed irradiated T cells. Some cell clones held for 7 days switched to IgG antibody production. E9.D4 supernatants were virtually ineffective in causing B cell stimulation, even when 3T3 filler cells were added to support cultures. The results suggest that cell contact, and perhaps conjugate formation, with a strongly activated T cell can cause changes in the adjacent resting B cells akin to those of Ig receptor cross-linking, following which a lymphokine flux (even one not involving IL 4 and 5) promotes antibody-forming cell development.

Animals↗
PubMed1986

Fibrinolytic treatment by infusion of streptokinase-plasminogen-complex (activator): laboratory effects.

144 patients were treated with 50.000 or 100.000 fibrinolytic units (U) activator per hour over a period of up to 5 days. The drug is not yet available but in trial for the time being. We report on a survey of laboratory results in 32 of these patients. The plasminogen content of 100.000 U activator is comparable to the plasminogen content of 29 ml plasma. During activator infusion laboratory findings showed a moderate fall in plasminogen and fibrinogen. Plasmin activity was measurable during the whole period of treatment while antiplasmin was lowered considerably. There was a distinct hypocoagulabilty during activator infusion visible by a prolongation of the thrombin time and aPTT. Interestingly, no measurable activator or streptokinase activities appeared in the plasma during activator infusion. This is in contrast to findings with conventional streptokinase infusion schemes.

Aged↗
PubMed1980

[Primary malignant lymphoma of the central nervous system].

Clinical and morphological observation of 56-year-old man with a primary isolated malignant non-Hodgkin's lymphoma of the central nervous system in the hypothalamus, with the formation of metastases in the space of the cerebrospinal fluid and a solitary extraneural metastasis in the epicardium. No generalised lymphoma. The histological classification is discussed. The importance of the cytology of the cerebrospinal fluid to a climical diagnosis is pointed out.

Brain Neoplasms↗
PubMedDate not supplied

Relationship between microsatellite instability, response and survival in palliative patients with colorectal cancer undergoing first-line chemotherapy.

BACKGROUND AND AIMS: The aim of this work was to investigate the relationship between microsatellite instability (MSI), treatment response and survival in palliative patients with colorectal cancer (CRC) undergoing first-line treatment with weekly 24-hour infusion (24-h inf.) of high-dose 5-fluorouracil (5-FU) and folinic acid (FA). PATIENTS AND METHODS: Tumour material from the colorectal primary carcinomas was analysed for 43 patients. MSI analysis was carried out and immunohistochemistry was performed with hMLH1 and hMSH2. RESULTS: Tumours of 7 patients (16%) were highly instable (MSI-H). These patients had a better response rate (72% vs. 41%; p = 0.072) and a significantly better median survival (33 months, [95% CI 20-46] vs. 19 months, [95% CI 10-28]; p = 0.021) than microsatellite stable (MSS) patients (n = 36). Furthermore, MSI status was shown to be an independent predictive marker for survival (p = 0.037). CONCLUSION: These data provide further support for the hypothesis that MSI-H CRC might have a better response and survival than (MSS) CRC in palliative first-line treatment.

Adaptor Proteins, Signal Transducing↗