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Biomedical subjects

A Mast

Publications and source records attributed to A Mast.

At least 19 recordsLinked to original sources
PubMed2002

Gastric emptying of solids in cirrhotic and peritoneal dialysis patients: influence of peritoneal volume load.

INTRODUCTION: A delay in gastric emptying rate has been reported in peritoneal dialysis patients, often normalizing after evacuation of the dialysate. To evaluate the effect of the intraperitoneal volume, we compared this finding with a cirrhotic model in which gastric emptying was studied before and after a large-volume paracentesis. METHODS AND DESIGN: We used the 13C-octanoic acid breath test to measure gastric half-emptying time (T1/2) for solids in patients with alcoholic cirrhosis, non-diabetic peritoneal dialysis patients, and a control population (asymptomatic volunteers). Cirrhotic patients underwent the test on two consecutive mornings before and after an evacuating paracentesis. Peritoneal dialysis patients were studied twice on consecutive days: once with the dialysate present intra-abdominally ("full"), and once with an emptied abdomen ("empty"). Biochemical analysis was carried out on blood samples before the first test. All cirrhotics underwent a 13C-aminopyrine breath test to assess residual liver function. RESULTS: Gastric emptying in cirrhotics showed no difference before or after paracentesis (median T1/2 108.0 min v. 117.9 min), but it was delayed significantly versus normal in both tests. There was no correlation with biochemical parameters, Child-Pugh score, or 13C-aminopyrine breath test results. Gastric half-emptying times of "full" peritoneal dialysis patients (median T1/2 103.1 min) were significantly higher than those of "empty" peritoneal dialysis patients (median T1/2 68.9 min) and asymptomatic volunteers (median T1/2 60.1 min). "Empty" peritoneal dialysis patients showed no gastroparesis. CONCLUSION: In alcoholic cirrhotic patients with ascites, gastric emptying of solids is delayed, independently of the volume of ascites. In peritoneal dialysis patients, gastric emptying was delayed when "full" and normalized after drainage of the dialysate.

Adult↗
PubMed2001

Molecular evolution of receptor-like kinase genes in hexaploid wheat. Independent evolution of orthologs after polyploidization and mechanisms of local rearrangements at paralogous loci.

Hexaploid wheat is a young polyploid species and represents a good model to study mechanisms of gene evolution after polyploidization. Recent studies at the scale of the whole genome have suggested rapid genomic changes after polyploidization but so far the rearrangements that have occurred in terms of gene content and organization have not been analyzed at the microlevel in wheat. Here, we have isolated members of a receptor kinase (Lrk) gene family in hexaploid and diploid wheat, Aegilops tauschii, and barley (Hordeum vulgare). Phylogenetic analysis has allowed us to establish evolutionary relationships (orthology versus paralogy) between the different members of this gene family in wheat as well as with Lrk genes from barley. It also demonstrated that the sequences of the homoeologous Lrk genes evolved independently after polyploidization. In addition, we found evidence for gene loss during the evolution of wheat and barley. Analysis of large genomic fragments isolated from nonorthologous Lrk loci showed a high conservation of the gene content and gene organization at these loci on the homoeologous group 1 chromosomes of wheat and barley. Finally, sequence comparison of two paralogous fragments of chromosome 1B showed a large number of local events (sequence duplications, deletions, and insertions), which reveal rearrangements and mechanisms for genome enlargement at the microlevel.

Base Sequence↗
PubMed1995

The carboxy terminus of tissue factor pathway inhibitor is required for interacting with hepatoma cells in vitro and in vivo.

Tissue factor pathway inhibitor (TFPI) is a plasma Kunitz-type serine protease inhibitor that directly inhibits coagulation Factor Xa and also inhibits tissue factor-initiated coagulation. Normal human plasma TFPI exists both as the full-length molecule and as variably carboxy-terminal truncated forms. We reported recently that the low density lipoprotein receptor-related protein mediates the cellular degradation of TFPI after TFPI binding to the hepatoma cell surface. To examine whether the carboxy terminus of TFPI was required for interacting with hepatoma cells, a mutant of TFPI lacking the third Kunitz-type domain and basic carboxy terminus was generated. We found that this mutant, TFPI-160, did not compete with full-length 125I-TFPI-160 for binding to hepatoma cells. We were also unable to demonstrate specific binding of 125I-TFPI-160 to hepatoma cells at 4 degrees C. At 37 degrees C, significantly less 125I-TFPI-160 was internalized and degraded via low density lipoprotein receptor-related protein than full-length 125I-TFPI. Full-length 125I-TFPI binding to hepatoma cells could be inhibited > 90% by heparin and other highly charged molecules. Since TFPI, but not TFPI-160, was capable of effectively binding to cultured hepatoma cells, the fates of TFPI and TFPI-160 in vivo were examined. Both 125I-TFPI and 125I-TFPI-160 disappeared rapidly from the circulation after their intravenous administration into rats. The initial plasma half-life of 125I-TFPI was approximately 30 s whereas the half-life of 125I-TFPI-160 was approximately 4 min. 125I-TFPI was cleared predominantly by the liver. In contrast, 125I-TFPI-160 accumulated in the outer cortex of the kidney. Using microscopic autoradiography, we demonstrate that 125I-TFPI clearance is largely hepatocellular, whereas 125I-TFPI-160 accumulates mainly in the cells of the kidney proximal tubules. Together our findings demonstrate that the carboxy-terminal region(s) distal to amino acid 160 of TFPI mediates TFPI binding to hepatoma cells both in vitro and in vivo.

Animals↗
PubMed1994

[Cholestatic jaundice caused by amoxicillin-clavulanic acid in 4 patients].

In four patients, two men and two women aged 73, 68, 84 and 72 years respectively, reversible cholestatic liver injury was seen 28-35 days after the start of treatment with amoxycillin-clavulanic acid (Augmentin). This rare complication of amoxycillin-clavulanic acid treatment is characterized by a relatively long latent period before the onset of symptoms or biochemical abnormalities, which makes early recognition difficult. The mechanism responsible for this idiosyncratic cholestasis is unknown.

Aged↗
PubMed1993

A hinge region mutation in C1-inhibitor (Ala436-->Thr) results in nonsubstrate-like behavior and in polymerization of the molecule.

C1-inhibitor(Mo), a dysfunctional C1-inhibitor molecule produced in two kindred with type II hereditary angioedema, has a mutation at the P10 position (Ala436 to Thr). Like most serpins with hinge region mutations (P14, P12, P10), C1-inhibitor(Mo) loses its inhibitory activity. However, unlike the other hinge region mutations, this mutant is not converted to a substrate. As shown by nondenaturing gel electrophoresis, gel filtration, sucrose density gradient ultracentrifugation, and electron microscopy, C1-inhibitor(Mo) exists in both monomeric and multimeric forms. Polymerization probably results from reactive center loop insertion into the A sheet of an adjacent molecule. Native C1-inhibitor(Mo) was shown to have a thermal stability profile intermediate to those of intact and of cleaved normal C1-inhibitor. Native C1-inhibitor(Mo) did not bind to monoclonal antibody KII, which binds only to reactive center-cleaved normal C1-inhibitor. It did, however, react with monoclonal antibody KOK12, which recognizes complexed or cleaved C1-inhibitor but not intact normal C1-inhibitor. Native C1-inhibitor(Mo), therefore, exists in a conformation similar to the complexed form of normal C1-inhibitor.

Alanine↗
PubMed1993

Sulfasalazine-associated encephalopathy in a patient with Crohn's disease.

We report a case of acute encephalopathy in a patient with Crohn's disease who had taken sulfasalazine for 1 month. The development of a toxic hepatitis and dermatitis prompted interruption of the drug. Four days later, neurological symptoms became evident. These included acute monoparesis of the left arm, the development of stupor and coma, with endorotation of both arms and a left Babinski sign. CT and magnetic resonance imaging revealed multiple lesions in the white and gray brain matter, suggesting diffuse cerebral microangiitis. All cerebrospinal fluid examinations were negative. Methylprednisolone was given intravenously. Complete clinical normalization followed. Neurotoxicity secondary to sulfasalazine has seldom been reported in the literature. We found certain similarities between this case and two previous case reports suggesting a hypersensitivity reaction to sulfasalazine or one of its metabolites. For ethical reasons, no rechallenge was performed.

Acute Disease↗
PubMed1993

Sulfasalazine-associated encephalopathy in a patient with Crohn's disease.

We report a case of acute encephalopathy in a patient with Crohn's disease who had taken sulfasalazine for 1 month. The development of toxic hepatitis and dermatitis prompted interruption of the drug. Four days later, neurologic symptoms became evident. These included acute monoparesis of the left arm, the development of stupor and coma, with endorotation of both arms, and a left Babinski sign. CT and MR imaging revealed multiple lesions in the white and gray brain matter, suggesting diffuse cerebral microangiitis. All cerebrospinal fluid examinations were negative. Methylprednisolone was given intravenously. Complete clinical normalization followed. Neurotoxicity secondary to sulfasalazine has seldom been reported in the literature. We found certain similarities with two previous case reports suggesting a hypersensitivity reaction to sulfasalazine or one of its metabolites. For ethical reasons, no rechallenge was performed.

Adult↗
PubMed1992

Successful plasmapheresis in corticosteroid-resistant hemolysis in infectious mononucleosis: role of autoantibodies against triosephosphate isomerase.

A 19-year-old girl fell ill with a high temperature and cervical lymphadenopathy. The detection of heterophile antibodies as well as Epstein-Barr-virus-specific antibodies confirmed the diagnosis of infectious mononucleosis. In the course of the infection, the patient developed severe hemolytic anemia with her hemoglobin falling from 14 to 8 g/dl. High-dose corticosteroid therapy did not stop hemolysis; this could only be achieved by seven plasmapheresis sessions. Antibodies against triosephosphate isomerase (TPI) and the blood group marker 'i' were found in the patient's serum. Anti-i cold agglutinins were not active at 37 degrees C, whereas antibodies against TPI caused increased 51Cr release from marked patient's erythrocytes in vitro. Plasmapheresis removed the autoantibodies effectively and stopped the hemolysis. After 8 weeks, the patient gradually recovered.

Adrenal Cortex Hormones↗
PubMed1991

Proteolytic inactivation of alpha-1-anti-chymotrypsin. Sites of cleavage and generation of chemotactic activity.

The effect of several microbial and mammalian proteinases on the inhibitory activity of human plasma alpha-1-anti-chymotrypsin (alpha-1-Achy) has been tested. Most of these enzymes caused rapid inactivation of the inhibitor by cleavage at single sites within the reactive-site loop between P5 Lys and P3' Leu, with additional cleavages also being detected in some cases near the NH2 terminus of the native protein. In contrast, two of the enzymes tested failed to inactivate alpha-1-Achy, although they could cause removal of peptides near the NH2 terminus. Studies of neutrophil chemotaxis revealed that native or NH2-terminally truncated alpha-1-Achy was not stimulatory. However, testing of two enzymatically inactivated forms of the inhibitor (alpha-1-Achy), cleaved at widely different positions within the reactive-site loop, indicated that they had become potent chemoattractants at concentrations within the nanomolar range. Competition studies using proteolytically inactivated alpha-1-proteinase inhibitor suggested that the chemotactic activity of the two inactivated serpins was probably mediated by the same mechanism. The physiological relevance of this chemotactic activity is underscored by the results of plasma elimination studies which indicate that alpha-1-Achy is eliminated at approximately the same rate as native alpha-1-Achy, thus prolonging chemotactic stimuli within the tissues.

Amino Acid Sequence↗
PubMed1976

Congenital enzymopenic methaemoglobinaemia. Clinical and biochemical study of a family with three homozygotes.

Three brothers with congenital recessive methaemoglobinaemia without mental retardation were found to be homozygous for NADH diaphorase deficiency. Twelve family members were heterozygous. One of the probands had marked digital clubbing, an unusual feature in this disease. In the probands, the red-cell NADH diaphorase was very low and unstable, whereas in the leucocytes this enzyme was present at a normal level. Isoelectric focusing of haemoglobin in the three probands showed that the alpha-chain was preferentially oxidized spontaneously. This confirms the greater oxidizability of this chain, as already described on isolated chains.

Adolescent↗
PubMed1976

Gastric xanthoma.

Gastric xanthoma (GX) consists of a small yellowish lesion of the gastric mucosa, frequently of multiple occurrence; histologically, there is an accumulation of lipid-laden histiocytes in the lamina propria. Seven cases are reported. One patient also had jejunal localizations. There is no correlation with hypercholesterolemia but in four cases a slight hypertriglyceridemia was found. A control gastroscopy, performed in four cases, revealed no changes in the first patient but a decrease in size in a second and the disappearance of GX in two other patients.

Aged↗
PubMedDate not supplied

Giant cell (temporal) arteritis diagnosed following upper limb claudication.

Giant cell arteritis or temporal arteritis occurs almost exclusively in people over 50 years of age. It classically presents with new onset temporal headache, scalp tenderness and jaw claudication. Proximal muscle pain and stiffness is often present because of frequent association with polymyalgia rheumatica. In most cases, the erythrocyte sedimentation rate is markedly elevated. Uncommon presentations include systemic symptoms and symptoms related to large artery involvement. We report a case of giant cell arteritis without symptoms related to the temporal artery, diagnosed angiographically following upper limb claudication and confirmed by temporal artery biopsy.

Aged↗