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Biomedical subjects

B Wolf

Publications and source records attributed to B Wolf.

At least 253 records · Page 14Linked to original sources
PubMed1987

UDP-D-xylose: proteoglycan core protein beta-D-xylosyltransferase: a new marker of cartilage destruction in chronic joint diseases.

We investigated the diagnostic significance of UDP-D-xylose : proteoglycan core protein beta-D-xylosyltransferase (EC 2.4.2.26) in different chronic joint diseases. This enzyme is located almost exclusively within chondrocytes, where it initiates the formation of chondroitin sulphate during the biosynthesis of proteoglycans and from which it is easily released after damage of articular cartilage. Xylosyltransferase activity was determined in synovial fluid and serum by a radiochemical method, based on the incorporation of [14C]xylose from UDP-[14C]xylose into an exogenous acceptor protein. Serum has been shown to be the appropriate material for the determination of xylosyltransferase activity in blood, since in plasma fibrinogen causes an inhibition of enzyme activity of about 50%. The catalytic concentrations of xylosyltransferase in synovial fluids and sera of patients with chronic joint diseases (n = 131) ranged from 0.5 to 22.0 mU/l and from 0.8 to 5.6 mU/l, respectively. On most cases we found higher xylosyltransferase activities in synovial fluids than in the corresponding sera. The highest catalytic concentrations of the enzyme were observed in the synovial fluids of patients suffering from rheumatoid arthritis (median value: 5.56 mU/l, 90%-range: 3.2-22.0 mU/l). Synovial fluids of patients with arthritis urica, however, showing a comparable high degree of inflammation, contained lower enzyme catalytic concentrations (median value: 2.38 mU/l, 90%-range: 0.7-5.2 mU/l), which were in the range of those in osteoarthrosis (median value: 2.50 mU/l, 90%-range: 0.8-4.8 mU/l). The higher xylosyltransferase activities in rheumatoid synovial fluids seem to be attributed to an increased cartilage destruction during the course of this disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Is thyrotropin-releasing hormone receptor involved in thyrotrope adaptation to starvation?

The aim of the present study was to delineate the involvement of TRH receptors in the thyrotrope adaptation to starvation (i.e. plasma TSH and thyroid hormone decrease, increased sensitivity to T3) by measuring [3H]TRH binding in euthyroid, hypothyroid and T3-substituted rats (175 ng/100 g body weight). Our results show that in euthyroid rats, starvation does not significantly modify either the affinity or the number of pituitary binding sites. In hypothyroid and T3-substituted rats, starvation does not alter the negative control exerted by T3 on the number of TRH binding sites. Our data indicate that the adaptation of thyrotrope to starvation does not primarily result from alterations of TRH binding sites.

Adaptation, Physiological↗
PubMed1987

[Extraction and determination of prednisolone in drugs and excipients in ointments and creams and the uniformity of distribution in prednisolone ointment].

For the purpose of measuring the contents of prednisolone in low concentrated ointments and creams an instruction was elaborated that includes several steps of extraction, in the resulting solution of which the assay of the steroid by Blue Tetrazolium reaction will be done. The procedure permits the determination of prednisolone in presence of most of usual ingredients of ointment bases except wool alcohols. Also no influence is given by some remedies combined with prednisolone for topical application except coal tar solution. The results confirm a correct reflection of the steroid contents declared respectively the recovery of the steroid added to various ointment bases. Introducing discussion to content uniformity concerning low concentrated ointments is made, and some deviations are shown.

Drug Compounding↗
PubMed1987

[Peculiarities of labor in the apallic syndrome].

Pregnancy and delivery in neuropsychiatrically ill patients demand a special and individual procedure of Obstetrician. There ist reported about particularities in management of delivery a seventeen-year-old primipara, who catched a bad necritizing encephalomeningitis and a following rare apallic syndrome after 37 weeks of pregnancy. Beside bad disturbance of consciousness the missing registration of labour pains was striking above all. After a very short duration of delivery process there was an easy outsliding of the child from the complete relaxed birth canal. Pains as a cortical phenomenon depends on functionary condition of higher nervous centres and therefore it is subject of psychic control. In recent literature there were no sufficient clues to, that pregnancy and delivery are unfavourably influenced by encephalitic infection. Therefore we considered right an individual procedure of spontaneous management of delivery and worth to inform about the associated peculiarities.

Adolescent↗
PubMed1986

Equine leukocyte antigens: relationships with sarcoid tumors and laminitis in two pure breeds.

Frequencies of equine leukocyte antigen distribution were determined by complement-mediated cytotoxicity testing among populations of Thoroughbred and Standardbred horses, including animals affected with equine sarcoid and laminitis. A highly significant association is described between the presence or history of sarcoid lesions in Thoroughbreds and the expression of the major histocompatibility complex (MHC)-encoded antigens, W3 and B1. No association was found between antigenic expression frequencies and laminitis in either breed. These findings suggest that a strong relationship exists between the equine MHC and a predisposition to sarcoid.

Animals↗
PubMed1986

Rett syndrome revisited: a patient with biotin dependency.

A patient with Rett syndrome (cerebral atrophy associated with hyperammonemia) was studied. Primary defects of urea cycle enzymes were excluded as causes of the disorder. The analysis of urinary organic acids showed a moderate increase of lactate, methylcitrate, tiglyglycine and 3-hydroxisovalerate, indicating an abnormality of multiple carboxylases. Biotin supplementation reversed the urinary abnormalities. In fibroblasts grown with a low biotin medium propionylCoA and 3-methylcrotonylCoA carboxylase activities were reduced. Holocarboxylase synthetase activity was normal (Vmax and Km). Surprisingly the biotinidase in fibroblasts was not decreased. The data indicate that some patients with Rett syndrome might suffer from a biotin-dependent defect of unknown nature.

Amino Acids↗
PubMed1986

Lack of a lipoprotein-induced insulin resistance in hepatoma cells in culture.

A lipoprotein-induced resistance to the action of insulin has been postulated. To test this hypothesis, cultured rat-derived hepatoma cells, designated FAO, and human-derived hepatoma cells, designated HEP-G2, were incubated for 20 h in the presence or absence of lipoprotein; specific 125I-insulin receptor binding and labeled glucose incorporation into glycogen were then measured. Very low density lipoproteins (d less than 1.006 g/ml) in physiologic (0.5 mg/ml) or pathophysiologic (5 mg/ml) concentrations did not modify insulin receptor binding of FAO or HEP-G2 cells. This was true for very low density lipoproteins derived from normal human, diabetic human, and streptozotocin-diabetic rat plasma. Low density lipoproteins (d = 1.019 - 1.063 g/ml) isolated from normal human plasma similarly failed to modify insulin receptor binding. Concerning insulin action, the different very low density lipoprotein preparations did not modulate either basal or insulin-stimulated glucose incorporation into glycogen of the cells. Thus, very low density lipoproteins and low density lipoproteins did not induce insulin resistance in cultured hepatoma cells either at the insulin receptor level or at the post-receptor level.

Animals↗
PubMed1986

Preliminary investigations of a correlation between electron energy loss and morphometric analyses on ultrathin cryosections from normal and neoplastic gastric tissues.

Electron energy loss spectroscopy (EELS) has been used to measure the ratios of C, N, O, P and Ca in ultrathin cryosections from normal and neoplastic gastric tissues. First results show a correlation between the EELS, and morphometric data in cells from these tissues. We have found that ultrathin, freeze-dried cryosections, with an average thickness of up to 75 nm, are stable enough for EELS-analysis in a 200 KV electron microscope with an adapted Gatan-EELS-Spectrometer.

Adenocarcinoma↗
PubMed1986

Neonatal screening for biotinidase deficiency: results of a 1-year pilot study.

We screened 81,243 infants born in Virginia during the 1-year period beginning Jan. 24, 1984, for deficiency of the enzyme biotinidase. A simple colorimetric screening procedure was used to detect the presence or absence of biotinidase activity on the same blood-soaked filter paper cards that are currently used in most neonatal metabolic screening programs. Two newborn infants with biotinidase deficiency were identified during the 12-month pilot study. In addition, two affected siblings of one of the newborn infants were detected through secondary family screening. On the basis of these results, the disorder appears to be at least as frequent as several others for which newborn screening is currently conducted. There were no known false-negative test results, and only 0.09% false-positive results that necessitated requests for second blood samples. False-positive test results can be readily identified by the use of a quantitative assay, which can also be used to confirm the diagnosis and to detect heterozygous family members in the case of true positives. On the basis of currently recognized criteria, biotinidase deficiency should be considered for inclusion among the metabolic disorders for which screening is performed in the neonatal period.

Age Factors↗
PubMed1986

Effect of biotin deficiency and supplementation on lipid metabolism in rats: cholesterol and lipoproteins.

The effect of biotin deficiency and supplementation upon tissue cholesterol and serum lipoprotein profile in rats was investigated. Biotin-dependent carboxylases in liver of deficient animals were decreased to 12-27% of control activity. The brain carboxylase activities of deficient rats were reduced less than in liver. The total, free, and esterified cholesterol were decreased in the serum of deficient rats compared to those in control or supplemented rats. Deficient rats had increased serum low-density lipoprotein fractions and decreased very low-density lipoprotein fractions, but no change in the high-density lipoprotein fractions. No differences were found between groups in the cholesterol content of liver, cerebrum, or cerebellum. Pharmacologic doses of biotin had no effect on tissue cholesterol content or serum lipoprotein profile. These results suggest that the neurologic symptoms in biotin deficiency and in the inherited multiple carboxylase deficiencies are not due to alterations in the content of cholesterol or lipoproteins.

Acetyl-CoA Carboxylase↗
PubMed1986

Effect of biotin deficiency and supplementation on lipid metabolism in rats: saturated fatty acids.

The effects of biotin deficiency and supplementation upon saturated fatty acids in serum, liver, cerebrum, and cerebellum of rats were investigated. Serum total fatty acids were reduced in deficient animals to 29% of normal. The percentage composition of some odd-chain fatty acids was increased in the serum and liver of deficient rats. The relative composition of most saturated fatty acids with carbon-chain lengths greater than or equal to 22 were increased in serum and liver of deficient rats. In contrast, there were no differences in the brain saturated fatty acids of deficient animals compared to those of normal and supplemented animals. These results may indicate that alterations in saturated fatty acids do not play a major role in the neurologic abnormalities in human biotin or inherited multiple-carboxylase deficiencies.

Animals↗
PubMed1986

Enzymatic degradation of thyrotropin releasing hormone by pancreatic homogenates. Failure to detect His-Pro-diketopiperazine as TRH metabolite.

Characteristics of pancreatic TRH-degrading activity were determined using [L-proline-2,3-3H] TRH and [L-histidine-2,5-3H] TRH as tracers and thin-layer chromatography to detect, identify and quantify TRH metabolites following incubation of tritiated TRH with pancreatic homogenates. The apparent Km of pancreatic enzymes was 2.2 10(-5) M, the V, 45 pmol/min, and the apparent specific activity, 62.3 +/- 3.45 pmol/min/mg total protein. In conditions of enzyme saturation, the percent of TRH degraded was found to be similar to the sum of degraded products formed (TRH-OH and His-Pro). Based on the chromatographic identification of metabolites, the presence of a deamidase pathway and a nondeamidase pathway in the TRH-degradation process of the pancreas was postulated. To better characterize the corresponding pancreatic enzymes, active site-directed inhibitors were then used and metabolites yielded were compared to those obtained in the same experimental conditions using plasma as enzyme source. The detection of His-Pro diketopiperazine among the metabolites was of special interest since this biologically active metabolite was also found in the pancreas as an endogenous peptide and reported to be either a TRH degradation product or derived from sources other than just TRH. However, in presence of inhibitors, His-Pro diketopiperazine was only detected using plasma as enzyme source. Nevertheless, a pancreatic contribution to plasma TRH-degrading activity cannot be discarded.

Animals↗
PubMed1986

Development of rheumatoid factors and anti-F(ab')2 antibodies in guinea pigs immunized with type II bovine collagen.

The purpose of this report is to present results demonstrating for the first time the development of rheumatoid factors to rabbit IgG-Fc as well as antirabbit F(ab')2 antibodies in guinea pigs after chronic sensitization with purified native type II bovine collagen. The sensitized animals also developed antibodies to guinea pig Ig. Antibodies to rabbit Ig arose as early as 3 weeks after bovine type II collagen injection and persisted for as long as 80 weeks when the experiment was terminated. The anti-Ig antibodies did not cross-react with the type II bovine collagen. Despite development and persistence of higher titers of RF and anti-F(ab')2 antibodies in the immunized animals, the animals failed to show clinical evidence of inflammatory polyarthritis. These results indicate that rheumatoid factors as well as antibodies to F(ab')2 arise independently of the clinical expression of disease.

Animals↗
PubMed1986

The spectrum of neurologic disorder from vitamin E deficiency.

We describe nine patients with fat malabsorption in whom a spectrum of vitamin E deficiency was present. Early deficiency was generally asymptomatic, and intermediate deficiency produced some impairment. Ataxia, weakness, reflex changes, impaired vision, and pigment retinopathy were associated with chronic, advanced deficiency. In the last group, delayed central somatosensory conduction and amplitude reduction of the electroretinogram were present. In adults, a severe vitamin E deficiency state existed for more than 5 years before producing measurable neurologic damage. The clinical picture is less homogeneous than previously suggested, and electrophysiologic abnormalities need not predate clinical dysfunction.

Adult↗
PubMed1986

Biotinidase deficiency: accumulation of lactate in the brain and response to physiologic doses of biotin.

Biotinidase deficiency is the most common cause of late onset, biotin-responsive multiple carboxylase deficiency (MCD). We studied the two oldest known boys with this disorder who had high CSF content of lactate that could have contributed to the clinical disorder. The symptoms of these patients implied that near physiologic, rather than pharmacologic, doses of biotin may be sufficient for treatment.

Amidohydrolases↗
PubMed1986

Haematological study in Cabo Delgado province, Mozambique; sickle cell trait and G6PD deficiency.

A haematological study was done in several villages in the northern province of Cabo Delgado in Mozambique. The prevalence of sickle cell trait (HbAS) was found to be about 4%. The prevalence of G6PD deficiency in males was about 18%. No significant differences were found in haemoglobin values between HbAA and HbAS individuals and between G6PD deficient and G6PD normal individuals. The number of males with both HbAS and G6PD deficiency was not significantly greater than expected.

Adolescent↗