Search PubMed⌕ Search

Biomedical subjects

M Salaspuro

Publications and source records attributed to M Salaspuro.

At least 145 records · Page 8Linked to original sources
PubMed1981

Severe gastrointestinal bleeding due to carcinoid tumour of the ileum.

Repeated episodes of severe intestinal bleeding in a 55-year-old male were found to originate from multiple small carcinoid tumours of the ileum. Laparatomy was performed after extensive negative endoscopic and radiological investigation of the bleeding site, and five tumours, 6 to 15 mm in diameter, were found within a 40 cm bowel segment. The most distal tumour was situated 50 cm from the ileocaecal valve. The site of bleeding was erosion of the bowel mucosa at the largest tumour. The affected bowel was excised, including its mesentery with two lymph nodes containing small islands of metastatic carcinoid tumour. Otherwise no metastases were found.

Carcinoid Tumor↗
PubMed1980

Inhibition of the synthesis of macromolecules by ethanol in regenerating rat liver.

The effects of ethanol on DNA and protein synthesis of regenerating rat liver has been studied. A single dose of ethanol, when given either before, at the time or 1 h after the partial hepatectomy significantly inhibited the accelerated synthesis of ornithine decarboxylase protein which was used as a marker of protein synthesis. Ethanol seemed to inhibit the synthesis of ornithine decarboxylase at transcriptional level of protein synthesis and the inhibition appeared to be directly due to the presence of ethanol molecules. When rats were chronically fed with ethanol-containing liquid diet also the total protein synthesis was inhibited during the two first days of regeneration. In this experiment also the rate of DNA synthesis was greatly inhibited by ethanol treatment. The results show that the ethanol-induced inhibition of the synthesis of tissue macromolecules is ideally demonstrated in regenerating rat liver. Furthermore they suggest that this effect may be of importance in the progression of alcoholic liver injury.

Animals↗
PubMed1980

Low acetaldehyde levels in blood, breath and cerebrospinal fluid of intoxicated humans as assayed by improved methods.

A sensitive method for determination of human blood acetaldehyde (AcH), which avoids artefactual ethanol-derived Ach formation, was developed. AcH was trapped by collecting blood directly into isotonic semicarbazide, the plasma separated, AcH liberated by perchloric acid and analyzed by gas chromatography. Breath AcH was also trapped in semicarbazide and analyzed similarly. Using an experimentally determined blood:breath partition ratio of 190, calculated pulmonary blood and measured antecubital blood AcH were very similar at various concentrations. Blood AcH was found generally to be very low (< 10 microM) at moderate ethanol levels. Calcium carbimide (0.25 mg/kg) caused moderate flushing reactions and elevated AcH to 25-188 microM. 4-Methylpyrazole (5 mg/kg i.v.) rapidly attenuated AcH levels and symptoms, indicating its potential use in the treatment of disulfiram-ethanol reactions. AcH in the cerebrospinal fluid of 5 highly intoxicated patients was almost absent (0-5 microM). Blood AcH in occasional or chronic alcohol abusers were generally low (< 10 microM), elevated AcH levels being observed only in association with clinical abnormalities. The results indicate that in general, previously reported human blood AcH levels are erroneously high and that breath levels reflect blood levels. Blood AcH may play a lesser role in the actions of ethanol in humans than is often assumed.

Acetaldehyde↗
PubMed1980

Elevated blood acetaldehyde in alcoholics with accelerated ethanol elimination.

Alcoholics and controls given ethanol (1.2 g/kg body weight) were analyzed for blood and breath acetaldehyde using the more sensitive and reliable semicarbazide method. The acetaldehyde levels in controls were almost undetectable (less than 2 microM), but were found to be elevated (10--10 microM) in 6 of 8 alcoholics. Breath acetaldehyde and blood acetaldehyde co-fluctuated during the experiments. Fructose infusion transiently increased blood acetaldehyde, but only in 4 of the alcoholics. The apparent discrepancy between our finding and the simultaneously reported low acetaldehyde level in alcoholics (Eriksson and Peachy, this volume) may be explained by the different status of the alcoholics tested. Our alcoholics were tested on the day after hospital admission and eliminated ethanol 5% faster than controls. It is suggested that elevated blood acetaldehyde occurs regularly after interrupted drinking in heavy alcohol abusers with fast ethanol elimination, possibly combined with reduced liver aldehyde dehydrogenase activity, but that the phenomenon may rapidly disappear upon abstinence and hospital treatment, which reduces disturbances in hepatic functions and the ethanol elimination rate.

Acetaldehyde↗
PubMed1979

Alcoholic liver damage is provoked by 4-methylpyrazole, which prolongs the influence of ethanol but reduces acetaldehyde levels.

Rats chronically fed ethanol developed liver injury only if they also received low doses of the alcohol dehydrogenase inhibitor, 4-methylpyrazole, suggesting that the consistency of the influence of ethanol and its metabolism, rather than the level of acetaldehyde or the degree of the metabolic effects, contributes to the pathogenesis of alcoholic liver damage.

Acetaldehyde↗
PubMed1979

Effects of ethanol on liver microtubules and Golgi apparatus. Possible role in altered hepatic secretion of plasma proteins.

A combined morphometric and biochemical approach was used to study the effects of alcohol on hepatic microtubules. Feeding of ethanol-containing diets to rats decreased the amount of polymerized tubulin and the number of visible microtubules, and it also produced morphologic alterations of this organelle. These microtubular alterations were reproduced in isolated hepatocytes after incubation with ethanol. Pyrazole, an inhibitor of alcohol dehydrogenase, prevented these effects. Two oxidation products of ethanol, acetaldehyde and acetate, in concentrations likely to occur "in vivo" also reproduced the effects of ethanol on microtubules. The alterations of microtubules, induced by either ethanol or its metabolites, were associated with significant increases in the volume and surface densities of the Golgi complex. Moreover, both the microtubular and the Golgi alterations were prevented by inhibiting the oxidation of ethanol with pyrazole, an inhibitor of alcohol dehydrogenase. These findings indicate that ethanol oxidation alters liver microtubules; as a likely result, delayed secretion of export proteins ensues with early retention in the Golgi vesicles. After chronic alcohol feeding, there was also a significant increase in the volume of the cytoplasm, which could reflect retention of soluble proteins and water.

Animals↗
PubMed1978

A new cause of increased serum aspartate aminotransferase activity.

Two healthy young women had an unexplained persistent elevation of aspartate aminotransferase (ASAT) activity. In both cases electrophoresis of serum ASAT isoenzymes displayed an abnormally moving fraction that comprised the whole serum activity, while liver and muscle revealed the normal cytoplasmic and mitochondrial isoenzymes. In the first case serum ASAT was found to be bound by serum IgG, in the second case the binding protein remained unidentified.

Adult↗
PubMed1977

Rectal mucosal adrenergic innervation and enterochromaffin cells in ulcerative colitis and irritable colon.

Rectal mucosal biopsies of 13 patients suffering from ulcerative colitis, 7 patients presenting symptomatology typical of irritable colon, and 7 control persons were studied by the recently introduced glyoxylic-acid-induced fluorescence histochemical method. In ulcerative colitis, compared to control specimens: 1) the density of the adrenergic nerve network was significantly pronounced; 2) the mean diameter of the varicosities and the proportional share of large varicosities were increased, as well as the number of varicosities per a given length of an axon; 3) the intensity of the fluorescence of varicosities of comparable size was significantly increased; 4) the number of enterochromaffin cells was significantly decreased. In irritable colon, compared to control specimens, the number of enterochromaffin cells was significantly increased. These findings suggest that biogenic amines are somehow involved in both ulcerative colitis and irritable colon. The fluorescence histochemical method used was found sensitive, specific, and suitable for comparative studies on human clinical material.

Cell Count↗
PubMed1976

Demonstration of an intracellular copper-binding protein by orcein staining in long-standing cholestatic liver diseases.

Liver biopsies from eight patients with primary biliary cirrhosis, two with chronic active hepatitis of a cholestatic form, three with long-standing alcoholic liver cirrhosis, and one with extrahepatic biliary obstruction were studied. In each case dark brown cytoplasmic material was seen after staining of the tissue sections with Shikata's orcein method. In exactly the same cellular and subcellular locations as the orcein-positive material, and with morphologically equal granules, two different ordinary staining methods for copper (rubeanic acid and Mallory-Parker's haematoxylin) gave positive reactions. The earlier histochemical findings have revealed the protein nature and high sulphydryl content of the orcein-positive material. Its close association with copper in liver sections suggests its copper-binding nature and indicates that a common copper-protein complex accumulates in the cytoplasm of liver cells during longstanding cholestasis in biliary diseases of various pathogenetic origin.

Cholestasis↗