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Biomedical subjects

W Rummel

Publications and source records attributed to W Rummel.

At least 73 records · Page 4Linked to original sources
PubMed1982

Independence of the activation of mucus and potassium secretion on the inhibition of sodium and water absorption by deoxycholate in rat colon.

The dose dependence of the influence of deoxycholic acid (DOC) on fluid and sodium absorption, transmural potential difference (PD), permeability of 14C-erythritol and secretion of potassium and mucus (protein bound hexoses) was measured in the in vivo perfused rat colon. The following results were obtained: 1. The threshold concentration for the inhibitory effect of DOC on fluid and sodium absorption is 2 mmol. In order to decrease PD and increase the colonic permeability for 14C-erythritol the same concentration was needed. 2. In contrast, DOC stimulated potassium and mucus secretion even in a fourfold lower concentration (0.5 mmol). No difference in the responsiveness of the descending and ascending colon was observed. 3. It is concluded that the identical dose dependency of the effect of DOC on fluid and sodium movement, PD, and permeability of the colonic mucosa is consistent with the interpretation that the secretagogue effect of DOC is mediated by an increase in permeability. However, because of their greater sensitivity, mucus and potassium secretion obviously are affected by a different mechanism. It is speculated that mucus and potassium are secreted together by the mucus producing cells of the colonic mucosa under the influence of DOC.

Animals↗
PubMed1982

Effect of deoxycholate on the perfused rat colon. Scanning and transmission electron microscopic study of the morphological alterations occurring during the secretagogue action of deoxycholate.

In parallel with the study on the correlation between increased mucosal permeability and the secretagogue effect of deoxycholate on the perfused rat colon, we examined the mucosal morphology by scanning and transmission electron microscopy. Dependent on concentration (2, 4, and 8 mmol/l), the treated mucosa showed structurally altered 'ballooned' absorptive cells, severely injured sloughing cells, and exfoliated cells lying on the surface. In spite of these changes, the continuity of the epithelial lining was maintained. Patchy defects exposing the lamina densa of the basement membrane could be observed only in specimens artificially altered by cell loss through vigorous rinsing. Clusters of extruded cells were still seen attached to the mucosal surface in the region between the openings of neighbouring crypts when net transfer of fluid and permeability after a period of recovery had returned to control levels. These findings support the hypothesis that fluid filtration during perfusion with deoxycholate occurs via a paracellular pathway through a leaky, damaged epithelium.

Animals↗
PubMed1980

Comparative study of the effect of cholera toxin and sodium deoxycholate on the paracellular permeability and on net fluid and electrolyte transfer in the rat colon.

1. The effect of deoxycholate and cholera toxin on the transfer of water, sodium, potassium and chloride and on mucosal permeability was studied in perfusion experiments on rat colon in vivo. The influence of both secretagogues on surface morphology was assessed by scanning electron microscopy. 2. Deoxycholate turned the absorption of water, sodium and chloride to secretion and enhanced potassium secretion. Cholera toxin induced water and sodium secretion, inhibited chloride absorption and enhanced potassium secretion. 3. Deoxycholate increased reversibly the mucosal permeability as measured by the colonic clearance of 51CrEDTA and glucose, whereas cholera toxin decreased the colonic 51CrEDTA clearance. 4. Deoxycholate caused protrusion of the luminal cell surface and an increase of exfoliation of epithelial cells. The epithelial continuity was preserved. The only change induced by cholera toxin was an enhanced mucus extrusion. 5. Our results are consistent with the view that deoxycholate causes fluid secretion by filtration whereas cholera toxin enhances the secretory activity of the epithelium.

Animals↗
PubMed1979

Early detection of ductal breast cancer: the diagnostic procedure for grouped microcalcifications.

Mammography and xeroradiography for grouped microcalcifications are considered the most effective diagnostic methods to detect occult breast carcinoma. Radiography must direct the surgeon to excise the nonpalpable area. The removal of the tissue with grouped microcalcifications must be confirmed by intraoperative radiological control. The histologic preparation must be guided by radiographic controls. Tissue with calcific deposits is examined by step sections. The diagnostic success depends upon the cooperation between the radiologist, the surgeon, and the pathologist. Our results from 1964 to 1977 have shown a frequency of 14.4% of occult carcinoma. Ductal or lobular carcinomata in situ have been diagnosed in 8.9%. In 9.9% of the patients, cystic disease with severe and atypical proliferations has been encountered.

Biopsy↗
PubMed1979

Early detection of ductal breast cancer: the diagnostic procedure for pathological discharge from the nipple.

Pathologic discharge from the nipple may be the only symptom of an early stage of carcinoma. Galactography is then the diagnostic method of choice to locate intraductal, nonpalpable lesions. The technique of galactography, the adequate surgical approach of pathologic galactographs (milk-duct segment resection), and the appropriate histological work-up of the surgical specimen are demonstrated. We report on 1918 galactographies in 1363 women with pathological discharge. In only 427 cases was a milk duct segment resection necessary (31.4%). In 8.5%, we found invasive intraductal cancer and in 2.9% ductal carcinomata in situ. Only 1 patient with breast cancer had axillary metastases. Extensive intraductal solid, papillary or adenomatous proliferations were found in 11.9% of the patients with excision. In 46.7% of the patients, papillomas were excised, a definitive treatment for this process. The supposition for success in the early diagnosis of cancer is close teamwork among the radiology, surgery and pathology services: the diagnostic result depends upon this. We attribute our yield of exact diagnosis to a very sophisticated histological work-up. We believe that this is necessary to avoid diagnostic failures.

Biopsy↗
PubMed1979

Binding of copper to mucosal transferrin and inhibition of intestinal iron absorption in rats.

1. The chromatographic elution patterns on Sepharose 6B of the supernatant from mucosal homogenates prepared 10 min after administration of copper into duodenal segments in vivo, indicate that copper is bound preferentially in the fraction of mucosal transferrin. 2. In iron deficiency the amount of 64Cu-copper taken up into the duodenal mucosa is more than two times higher and the amount bound to proteins of the supernatant is also increased to approximately the same degree whereas the amount transferred into the body is diminished to one fourth. 3. In the iron deficient group 64Cu-copper was also bound to a fraction which contains probably metallothionein. 4. The distribution of copper in the supernatant was changed due to a simultaneous administration of iron; the amount of copper bound in the transferrin fraction decreased in favor of the metallothionein fraction and another copper binding fraction was eluted between the transferrin and the metallothionein fraction. 5. Copper in a tenfold molar excess inhibited the iron absorption; simultaneously, the iron bound in the iron binding fractions of the supernatant was remarkably diminished. 6. The results suggest that the affinity of copper to two mucosal iron binding proteins, transferrin and metallothionein, is at least partly responsible for the inhibitory effect of copper on iron absorption in iron deficiency.

Animals↗
PubMed1979

Intestinal absorption of cobalt and iron: mode of interaction and subcellular distribution.

1. The absorption kinetic of 59Fe-(FeCl3) and 60CO-(CoCl2) 10 min after administration of increasing doses (0.5--1,000 nmoles metal) into tied-off duodenal segments of normal and iron-deficient rats shows saturation characteristic for both metals; in iron-deficient rats the absorption of both metals was enhanced. 2. The addition of increasing amounts of cobalt to the 59Fe-containing test solutions caused a decrease of the absorption of iron. 3. The study of the time dependence of this interaction in iron-deficient rats revealed, that cobalt inhibits the release of iron from mucosal cells into the blood, whereas the uptake of iron from the lumen into the mucosal cells did not differ from the controls without administration of cobalt. 4. The subcellular distribution of 59Fe and 60 Co in mucosal cell homogenates of iron-deficient rats after ultracentrifugation on a polyvinylpyrrolidone-CsCl solution shows a similar pattern for both metals; in the presence of cobalt the subcellular distribution of 59Fe is not changed. 5. From these results the conclusion is drawn that cobalt inhibits iron absorption not by an interference with iron binding sites on or in the luminal membranes of the mucosal cells but by an interaction with the releasing process at the contraluminal side.

Animals↗
PubMed1978

The role of mucosal iron binding proteins in adaptation of iron absorption during protein deficiency and rehabilitation.

1. A state of protein deficiency has been produced in rats by feeding a low protein diet, thereafter a period of rehabilitation with a normal protein but a low iron supply followed. 2. For characterization of the iron metabolism during both periods haemoglobin, total iron binding capacity, liver non-haemin iron, intestinal iron absorption and the uptake of 59Fe in the liver was determined. 3. Under these conditions the amount of 59Fe incorporated into the mucosal transferrin and the ferritin fractions has been measured. Both fractions were obtained from the supernatant of a mucosal homogenate after chromatography on sepharose 6B. 4. In anemia due to protein deficiency the typical increase of 59Fe incorporation into the fraction of mucosal transferrin--usually occuring in iron deficiency--could not be observed. This coincides with the absence of an increased iron absorption. Moreover a decrease of iron absorption is observed, which is associated with a decreased 59Fe ratio of transferrin/ferritin-fraction. 5. After normalization of the protein supply the ratio of 59Fe incorporated into the mucosal transferrin and ferritin fractions was changed remarkably in favor to transferrin together with a several fold increase of the intestinal iron absorption. 6. The conclusion is drawn that mucosal transferrin and ferritin enable the body not only to adapt the absorption to a higher but also to a lower requirement as it is the case in protein deficiency.

Adaptation, Physiological↗
PubMed1978

[Optically active barbiturates. Synthesis, configuration and pharmacological effects (author's transl)].

Optically active N-alkylated barbiturates are synthesized from disubstituted cyanoacetates. The configuration of the synthesized compounds is determined by chemical and chiroptical procedures and by X-ray analysis. In animals the barbiturates show a different anesthetic activity, in some cases the CNS activity is opposed, one enantiomer is anesthetically active, the other is a convulsive agent. In their pharmacokinetic behaviour the enantiomers show remarkable differences.

Anesthetics↗
PubMed1978

[The fluoroscopic detection of micro-calcifications of the breast during the operation in the excisional biopsy material (author's transl)].

In 101 excisional biopsies of the breast the biopsy material was examined fluoroscopically in the operating room for micro-calcifications with a specially constructed X-ray machine. This method of operation and control has the advantage of shortening the operative time and avoiding additional radiation to the breast. The surgeon becomes independent of a radiologist for control. Very accurate excisional biopsies of clinical obscure lesions in the breast become possible.

Adult↗
PubMed1977

Mucosal transferrin and ferritin factors in the regulation of iron absorption.

1. A standardized decompensation and recompensation of iron homeostasis has been produced by a change-over from normal to iron deficiency and back. 2. Under these conditions the 59Fe uptake into transferrin and ferritin of the mucosal "cytosol" and SDS treated "membrane" fraction has been measured together with the 59Fe amount transferred into the body. 3. The increase of the intestinal 59Fe absorption due to a progressive iron deficiency is associated with an increase of the 59Fe uptake into the mucosal transferrin of the "cytosol" and the "membrane" fraction; the reverse is observed with regard to mucosal ferritin. 4. Three days after the re-establishment of normal conditions the 59Fe absorption was lowered to normal values, while the 59Fe uptake into mucosal ferritin achieved again normally high values. 5. The high apparent rate of absorption in iron deficient animals decreased during the last 50 min after injection of the 59Fe labelled test dose. The 59Fe content in the ferritin fraction increased simultaneously, whereas the 59Fe content in the transferrin fraction remained the same. 6. The conclusion is drawn that the intestinal iron absorption is regulated by both mucosal iron binding proteins. Mucosal transferrin is responsible for the increase of absorption in iron deficiency while mucosal ferritin is responsible for the inhibition of iron absorption when the iron homeostasis recompensats.

Animals↗