AIDS in Poland.
Explore the source record for details and available documents.
Acquired Immunodeficiency Syndrome↗
Biomedical subjects
H Seyfried
Publications and source records attributed to H Seyfried.
[Prostaglandin I2 (PG I2; prostacyclin) synthesis by human gastric mucosa (author's transl)].
The human gastric mucosa generates prostacyclin (22 +/- 6 ng PG I2/g). There is no age or sex difference in PG I2 formation by normal gastric mucosa. The properties of the substance are the same as reported in other tissues.
Adenosine Diphosphate↗
[Anti-HBs immunoglobulin].
Explore the source record for details and available documents.
Antibodies, Viral↗
Rectal mucosa prostacyclin formation in ulcerative colitis.
Explore the source record for details and available documents.
Adult↗
[Physiopathology of prostaglandin I2 synthesis in the human gastrointestinal mucosa].
1. PGI2 is synthetized in human gastrointestinal mucosa. 2. PGI2 seems to be responsible for pathophysiological conditions. 3. Disorders caused by an enhanced or diminished PGI2-synthesis could be treated in the future by inhibition of prostacyclin synthetase or exogenous synthetic PGI2 respectively. 4. In order to remove the problems with the unstable PGI2, synthetic analogs could be used for the treatment.
Adult↗
Human rectal mucosa generates prostacyclin.
Explore the source record for details and available documents.
Adult↗
[Serum concentrations of thyroid hormones in severe non-thyroidal illnesses (author's transl)].
Pathologically low serum total triiodothyronine (T3) concentrations are a characteristic finding in patients with severe non-thyroidal illnesses. No adequate explanation has yet been offered for this phenomenon. We have, therefore, investigated the serum concentrations of total thyroxine (T4), total T3 and total 3,3',5'-triiodothyronine (reverse T3)--the metabolically-inactive metabolite of thyroxine--and of TSH in 13 patients with acute myocardial infarction, in 12 patients with compensated liver cirrhosis, in 9 patients with decompensated liver cirrhosis and in 15 patients with chronic renal failure on chronic intermittent haemodialysis by radioimmunoassay. The values obtained were compared to corresponding values of a normal control group (n - 23). According to our results the decrease in serum T3 combined with normal T4 concentrations in severe non-thyroidal illnesses seems to be a consequence of an alteration in thyroxine degradation. Two different possibilities of alteration can be considered: 1. inhibition of the overall deiodinationof T4, leading to low total T3 serum concentrations with concomitant normal to low reverse T3 serum concentrations (chronic uraemia), 2. a shift in the monodeiodination of T4 towards enhanced reverse T3 production, leading also to low total T3 concentrations, but with a concomitant increase in reverse T3 serum concentrations (myocardial infarction, liver cirrhosis). The results obtained in our patients with liver cirrhosis show, moreover, that this alteration of T4 metabolism depends on the severity of the illness.
Humans↗
Automated screening of red cells for the detection of autoantibodies.
The AutoAnalyser Technicon II system was adapted for screening red cells for the presence of warm-type autoantibodies. A significant decrease in optical density was recorded when the red cells of 38 patients with autoimmune haemolytic anaemia were tested using the bromelin-methylcellulose method. This was never seen with the red cells of 226 patients with other diseases or of healthy blood donors. The method is very simple and more sensitive than the manual direct antiglobulin test.
Anemia, Hemolytic, Autoimmune↗
Sensitivity of automated red cell antibody detection.
The principle of detecting red cell antibodies by automated technique using the two-channel Technicon Auto-Analyser with some modification is described. The sensitivity of automated methods in detecting antibodies of different specificities was determined. The study was carried out with 76 diagnostic human sera produced by the Institute of Hematology, Transfusion Centers and commercial firms: anti-RhD, -C, -E, -CW, -c, -e, anti-K, -k, Kpa, anti-Fya, -Fyb, anti-Jka, -Jkb, anti-M, -S, -s, anti-P1, anti-Lua, anti-Lea, -Leb, anti-H, -A1, anti-I, anti-Lua and anti-Vel. A majority of the antibodies were detected by both automated methods with greater sensitivity than by manual methods. Greatest sensitivity was observed in the detection of anti-S, -Vel and antibodies of the Rh system. Anti-Leb and anti A1 antibodies were not detected. The studies are the basis for introduction of the automated technique into routine use for antibodies in blood donors and recipients.
Antibody Specificity↗
[Bilirubin metabolism (author's transl)].
The degradation of haemoglobin haeme of senescent red blood cells - involving NADPH-dependent haeme oxygenase and biliverdin reductase - in the reticuloendothelial cells of the spleen, bone marrow and liver accounts for 80 to 90% of the 250 to 300 mg of bilirubin formed in 24 hours. The remaining 10 to 20% derive from catabolism of other haemoproteins and from the destruction of maturing red blood cells in the marrow. In studies with isotopically-labelled metabolic precursors of haeme this fraction can be found in the early-labelled peak. In plasma virtually all the bilirubin is tightly bound to plasma proteins, largely albumin, because it is only sparingly soluble in aqueous solutions at physiological pH. In the sinusoids unconjugated bilirubin dissocates from albumin, enters the liver cells across the cell membrane through non-ionic diffusion and is bound by the two cytoplasmic proteins Y (or ligandin) and Z. Little is known about the transfer of unconjugated bilirubin from these binding proteins to the smooth endoplasmatic reticulum, where it is converted to a water-soluble ester glucuronide by bilirubin UDP-glucuronyl transferase. The physiological significance of non-glucoronide conjugates (sulphate, disaccharides) is only of minor importance. Following conjugation, bilirubin is transferred rapidly across the canalicular membrane into the bile canaliculi. This process is energy-dependent and occurs against a concentration gradient. The epithelial lining of the intestine and of the gall bladder, which can easily reabsorb lipid-soluble unconjugated bilirubin, is virtually impermeable to organic anions of the size and charge of conjugated bilirubin, thereby ensuring efficient excretion of this pigment. In the intestinal tract bilirubin is reduced to urobilinogen, which is subsequently reabsorbed to some extent into the enterohepatic circulation, removed from plasma by the liver and excreted unchanged in the bile. This rapid bacterial reduction of bilirubin makes it unlikely that unconjugated bilirubin is formed and absorbed to an appreciable degree. The residual part of urobilinogen is further reduced to urobilin, stercobilin and dipyrrolmethenes and excreted in the faeces.
Bilirubin↗
[Myocardial infarct after gastroscopy. Case report and pathogenetic considerations].
Three cases are reported of myocardial infarction and severe myocardial ischemia following gastroscopy in patients with coronary heart disease. These cases demonstrate the high risk of endoscopy in such patients. It is assumed that the main pathogenetic factors are catecholamine-mediated tachycardia and the close vicinity of the lower esophagus to the right coronary artery, with its tendency to coronary spasmus.
Aged↗
[The genetics of Gilbert syndrome].
Investigation of 19 unrelated patients with Gilbert's syndrome and family studies in 21 first degree relatives of 7 of these patients are in agreement with an autosomal-dominant mode of inheritance with incomplete penetrance. The calculated penetrance in our study is 57%. HLA typing (locus A, B, C) showed a slight, insignificant increase in antigens A11 and BW35. Furthermore, this syndrome did not segregate in parallel with certain haplotypes within families.
Bilirubin↗
[Liver scanning in diffuse liver disease (author's transl)].
The results of liver scans performed with 99mTc-sulphur colloid in 169 patients suffering from diffuse liver diseases and in 48 normal controls were evaluated. The patients with reactive hepatitis, acute hepatitis, chronic persistent hepatitis, fatty liver and fibrosis of the liver show only minimal deviations from the scintigraphic pattern. On the contrary, highly increased colloid uptake in the spleen is found in cases of chronic aggressive hepatitis, whilst the intrahepatic distribution of the colloid is approximately normal. In cases of liver cirrhosis, increased colloid uptake is found in the left lobe of the liver as well as in the spleen and in the bone marrow. Either normal findings or cirrhosis-like changes of the colloid distribution are observed in patients with alcoholic hepatitis.
Bone Marrow↗
Biochemical, serological and family studies in individuals with Cis AB phenotypes.
Pedigree studies and serological characterization of three cis AB families are presented. Serums of these persons exhibit strongly reduced activities of A gene-specified alpha-acetylgalactosaminyltransferase and only trace activities of B gene-dependent alpha-galactosyltransferase.
ABO Blood-Group System↗
Serological classification of anti-I sera.
Twelve anti-I sera were examined by means of broad panel of cells: OI, BI, OhI, Oicord, Oiadult, BI-F. Titration, fixation-elution, and haemagglutination-inhibition tests, and comparison of agglutination of untreated and neuraminidase-treated erythrocytes allowed to establish the specificity of the sera. For some sera the serological heterogeneity was revealed, which consisted in the following combinations of two or more kinds of specificity: anti-I-D plus anti-I-F, anti-I-D plus anti-i, anti-I-D plus anti-I-S, anti-I-D plus anti-I-F plus anti-I-S. Methodical problems of classification of anti-I sera are discussed.
Absorption↗
Reactions of erythrocyte glycoproteins and their degradation products with various anti-I sera.
Three fractions of erythrocyte glycoproteins obtained from Sepharose 4-B chromatography were tested for I activity with ten serologically differentiated anti-I sera. The most active was fraction I, eluted at the void volume and containing the lowest amount of alkali-labile oligosaccharide chains. The desialization of glycoproteins increased their activity toward anti-I-s and anti-I-D sera, and did not change or decreased the activity toward anti-I-F sera. The most abundant fraction II (major sialoglycoprotein of erythrocyte membranes) showed no or only a very weak I activity, but I-active glycopeptides were isolated from products of digestion of fraction II with trypsin. The major product of digestion, sialoglycopeptide IIT-2 showed I activity only after alkaline elimination of alkali-labile oligosaccharide chains. The results indicate that I receptors are present in hindered form on apparently I-inactive components of erythrocyte membrane.
Alkalies↗
Gilbert's syndrome and HL-A. Preliminary report.
HL-A antigens were determined in 18 unrelated patients with Gilbert's syndrome and 3 families where this condition occurred in 2 generations. The data obtained do not point out an association between HL-A antigens and Gilbert's syndrome.
Gilbert Disease↗
[Detection of light chains of warm-type autoantibodies in autoimmune hemolytic anemia with the aid of an autoanalyzer].
A method was evolved for detection of light chains of erythrocyte autoantibodies using a Technicon II AutoAnalyser with properly selected dilutions of bromelin and methylcellulose and anti-kappa and anti-lambda sera. It was demonstrated that the method is superior to the direct Coombs test because it made possible detection of one or both light chains in warm autoantibodies coating the erythrocytes of 20 patients with autoimmunohaemolytic anaemias in whom they could not have been detected by the manual method. It was found that in warm-type autoantibodies light chains can be detected always and that in some cases only one light chain is found.
Anemia, Hemolytic, Autoimmune↗