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Biomedical subjects

Y Chao

Publications and source records attributed to Y Chao.

At least 199 records · Page 11Linked to original sources
PubMed1993

Hepatic hemodynamic features in patients with esophageal or gastric varices.

One hundred and fifty cirrhotic patients with or without esophageal varices and/or gastric varices were investigated by endoscopy and hepatic venous catheterization to evaluate differences in the degree of portal hypertension, main portal venous diameter and frequency of portal systemic encephalopathy. Hemodynamic values were correlated with varices size as assessed by endoscopy. Patients with large gastric varices had wedged hepatic venous pressures and hepatic venous pressure gradients which were lower than patients with esophageal varices only, but similar to patients without varices. In addition, in patients with large gastric varices, a decrease in the diameter of the main portal vein and an increase in the incidence of chronic portal systemic encephalopathy were noted. Our results implied that patients with large gastric varices presented different hemodynamic features including the degree of portal hypertension and the incidence of portal systemic encephalopathy from patients with esophageal varices only.

Aged↗
PubMed1993

In vitro transcription of Drosophila rRNA genes shows stimulation by a phorbol ester and serum.

The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and serum both stimulate rapid increases in the transcription of Drosophila rRNA genes in vivo. Here we report that this stimulation is observed in in vitro transcription assays using nuclear extracts from cells treated with TPA or serum. Experiments in which extracts from TPA- or serum-treated cells were mixed with extracts from cells grown in serum-restricted medium showed that there was an increased RNA polymerase I (Pol I) activity present in the cell extracts from treated cells. We used a series of plasmids that had been deleted in the region 5' to the start site of rRNA transcription to determine which sequences were necessary to support the increased transcription seen in extracts from stimulated cells. DNA templates that contain sequences between -150 and +32 (with +1 as the Pol I transcription start site) show dramatic increases in transcription with TPA- and serum-stimulated cell extracts; however, templates that contain 5' sequences to -60 or -43 show at most one-third of the stimulation level of transcription in nuclear extracts from treated cells in comparison with untreated cell extracts. The 5' deletion to -34 abolishes the stimulation effect and drops the basal-level transcription by 20-fold. These results indicate that the regulation of Pol I transcription in Drosophila cells by serum and TPA requires two DNA elements, sequences from -150 to -60 (upstream control element) and sequences from -43 to -34 (a portion of the core promoter.

Animals↗
PubMed1993

[A cephalometric study on determining the orientation of occlusal plane].

A study of the parallel relationship between the occlusal plane and the line connecting nasal alar and tragus was made in 90 dentulous cases by using cephalometry. The results show that the line connecting the inferior point of nasal alar and the mid-point of tragus runs much more parallel with the occlusal plane. The regression equation reveals a "line of closest fitting". It was used in the prosthetic treatment for 50 edentulous patients with good clinical results. The line connecting the inferior point of nasal alar and the mid-point of tragus therefore represents a proper reference plane for determining occlusal plane and hence should be still a valuable index in clinical dentistry.

Adolescent↗
PubMed1993

Endoscopic examination in patients with acquired immunodeficiency syndrome: Taiwan experience.

Endoscopic experience in patients with acquired immunodeficiency syndrome (AIDS) has rarely been reported in Taiwan. We present our experience in 9 AIDS patients (8 male and 1 female, age from 26 to 63 years) with 12 examinations. The risk factor of these patients were bisexual in 3, homosexual in 2, hemophilia in 1, drug abuse in 1, and paid-sex in 2. Odynophagia or dysphagia was the major complaints. Oral ulcers or/and thrush were noted in 8 patients. Endoscopic findings included negative (6/12), candidiasis (3/12), erosions (1/12), ulcers (1/12) and ulcer scar (1/12) in esophagus; negative (8/12), gastritis (1/12), erosions (1/12), ulcers (1/12) and Kaposi's sarcoma (1/12) in stomach; and negative (11/12) and duodenitis (1/12) in duodenum. Patients with esophageal candidiasis always had oral thrush. Dysphagia was highly correlated with positive endoscopic findings in esophagus. It is important for an endoscopist to identify clinical symptoms and to examine patient's oral cavity before an endoscopic examination. The endoscopist must keep himself from being infected by exposure to contaminated blood and secretion and avoid dissemination of this horrible disease by undisinfected instruments.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Idiopathic portal hypertension: a case report.

Clinically, idiopathic portal hypertension (IPH) is characterized by overt splenomegaly with pancytopenia, portal hypertension and relatively mild abnormalities in liver function tests. Although its etiology is still undetermined, the liver pathology is characterized by occlusive changes of the intrahepatic portal radicles, portal and periportal fibrosis, irregularly distributed parenchyma atrophies and absent of regeneration nodules. The disease is relatively benign and does not progress to cirrhosis. Differential diagnosis between IPH and liver cirrhosis is mandatory. We now report a case with histologically proven IPH, including clinical course, laboratory data, roentgenographic findings of hepatic venogram and celiac angiogram, hepatic hemodynamic features and intravariceal pressure of esophageal varix which has never been reported in Taiwan.

Adult↗
PubMed1991

A randomized controlled trial of quinidine in the treatment of cirrhotic patients with muscle cramps.

In an attempt to evaluate the effect of quinidine in the treatment of patients with cirrhosis and muscle cramps, 31 cirrhotic patients with muscle cramps were randomly divided into two groups and given orally 400 mg of quinidine sulfate per day or placebo, respectively. Baseline clinical and laboratory data for these two groups were similar. Four weeks after oral administration of quinidine, the number of cramps significantly decreased from 14.4 +/- 1.7 (mean +/- S.E.) to 4.4 +/- 1.1 episodes (p less than 0.0001), but it remained unchanged in the placebo group (from 11.8 +/- 1.0 to 11.5 +/- 1.5 episodes, p greater than 0.05). In addition, 88% of the 16 patients on quinidine and 13% of the 15 patients on a placebo showed a greater than 50% reduction in the number of cramps during a 4-week treatment period (p less than 0.0001). The peak and trough serum levels of quinidine in patients having received quinidine for 2 weeks were 1.3 +/- 0.1 and 0.7 +/- 0.1 mg/l, respectively. There was a significant relationship between serum quinidine concentrations and attenuation of cramps. No significant adverse effect was observed during the study, except for five (31%) patients who developed mild diarrhea after quinidine therapy. Diarrhea subsided spontaneously or was controlled by medications without the interruption of quinidine therapy. It was concluded that quinidine is a safe and effective drug for the treatment of cirrhotic patients with muscle cramps.

Aged↗
PubMed1991

Lowering of plasma cholesterol levels in animals by lovastatin and simvastatin.

Lovastatin and simvastatin are potent competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Key inhibit the synthesis of cholesterol in cultured HepG23 cells, rat hepatocytes and in rats. The primary target organ of cholesterol synthesis inhibition by lovastatin and simvastatin is the liver. Lovastating and simvastatin lower levels of plasma cholesterol in rats, dogs and rabbits by inhibition the endogenous cholesterol synthesis and induction of LDL receptor in the liver.

Animals↗
PubMed1987

Hepatitis type B virus DNA in patients receiving hemodialysis: correlation with other HBV serological markers.

Possible presence of hepatitis type B virus (HBV) was assessed in 239 end-stage renal failure patients who were receiving long-term maintenance hemodialysis (average 30.8 months; duration: 1-94 months), and who had not shown any other symptom of HBV infection. Their HBV serological markers, including HBV DNA, were evaluated together with those of normal control individuals. HBV surface antigen (HBsAg) was detected in 42 of the 239 dialysis patients, 15 of whom also positive for HBV DNA (mean +/- SD = 56.2 +/- 23.7 pg/100 microliters of serum). HBV DNA was also found in 22 of the 197 (11.2%) dialysis patients who were negative for HBsAg, with an average of 36.2 +/- 19.0 pg/100 microliters of serum. This rate of detecting HBV DNA in HBV seronegative dialysis individuals was significantly higher than the rate of 1.83% found among healthy HBsAg(-) individuals. Among these 22 dialysis patients who were HBsAg(-) but HBV DNA(+), 15 were found to possess antibodies against HBsAg (anti-HBs) and/or antibody against HBV e antigen (anti-HBe). These data suggested that the absence of serum HBV antigen or the presence of antibodies against HBV markers might not be sufficient to identify possible HBV infection in immunocompromised hosts such as hemodialysis patients.

Adult↗
PubMed1982

Effects of cholestyramine on low density lipoprotein binding sites on liver membranes from rabbits with endogenous hypercholesterolemia induced by a wheat starch-casein diet.

Rabbits fed a wheat starch-casein diet develop a marked hypercholesterolemia with a lipoprotein distribution similar to that of humans. Approximately 76% of the total cholesterol is carried in the low density lipoprotein (LDL) fraction (1.006 less than d less than 1.063 g/ml). Inclusion of 1% cholestyramine in the diet prevents the increase in plasma cholesterol. The cholestyramine effect is mediated through an increased fractional catabolic rate of 125I-LDL. In order to determine the potential role of hepatic LDL receptors in the removal of LDL from the plasma, binding of 125I-LDL and 125I-beta-VLDL (beta-migrating very low density lipoproteins) to hepatic membranes prepared from livers of rabbits fed the wheat starch-casein diet with or without cholestyramine supplementation was investigated. Membranes from livers of the cholestyramine-supplemented animals exhibit high levels of specific EDTA-sensitive binding of either of the 125I-labeled lipoproteins. Very little EDTA-sensitive binding occurs on liver membranes from wheat starch-casein-fed rabbits that have not been treated with cholestyramine. These results indicate that the hypercholesterolemia in rabbits associated with the wheat starch-casein diet is wholly or partially the result of a decreased number of specific hepatic LDL receptors and thus a decreased catabolism of plasma cholesterol. The response of the liver to the inclusion in the diet of the bile acid sequestrant, cholestyramine, is to maintain or increase the number of specific LDL binding sites, thus promoting catabolism of plasma cholesterol.

Animals↗
PubMed1980

Determinants of hepatic uptake of triglyceride-rich lipoproteins and their remnants in the rat.

The uptake and metabolism of lymphatic large chylomicrons from fat-fed rats, lymphatic small chylomicrons from glucose-fed rats, and hepatic very low density lipoproteins from perfusates of isolated livers, and of remnants produced from these lipoproteins in functionally eviscerated rats were studied in the isolated perfused rat liver. All lipoproteins were labeled isotopically in their cholesteryl ester and triglyceride moieties. Uptake of the labeled lipids or large chylomicrons was slow and limited, but these lipids in small chylomicrons and hepatic very low density lipoproteins were taken up and metabolized progressively and at equal rates. Incubation with very low density lipoprotein-free plasma increased the content of C apolipoproteins in small chylomicrons and hepatic very low density lipoproteins and greatly retarded the hepatic uptake of their labeled lipids. In remnants from all sources, which are depleted of C apolipoproteins but not of apolipoprotein E, the labeled lipids were rapidly taken up and metabolized. Neither extensive hydrolysis of core triglycerides nor the production of monoglycerides was required for this rapid hepatic uptake. These results are consistent with the hypothesis that one or more of the C apolipoproteins opposes and apolipoprotein E promotes recognition of triglyceride-rich lipoproteins by a hepatic receptor.

Animals↗
PubMed1980

Isoprotein specificity in the hepatic uptake of apolipoprotein E and the pathogenesis of familial dysbetalipoproteinemia.

The uptake and catabolism of lamellar complexes of rat 125I-labeled apolipoprotein (apo) E with egg lecithin were increased severalfold in perfused livers of rats given large amounts of 17 alpha-ethynylestradiol for 5 days. Estrogen-stimulated uptake of lamellar complexes of human apo E that contained all of the major normally occurring "isoforms" of the protein (apo E-1, E-2, E-3, and E-4) was comparable to that of rat apo E. By contrast, uptake of complexes containing apo E from individuals with familial dysbetalipoproteinemia (dys beta LP; characterized by a lack of apo E-3 and E-4) was stimualted to a much smaller extent. With complexes containing individual isoforms of human apo E, it was shown that estrogen-stimulated hepatic uptake was largely confined to apo E-3 and E-4; uptake of apo E-2 from normolipoproteinemic or dys beta LP individuals, or of apo E-1 from the latter, was stimulated little or not at all. When considered in the light of available information about the hepatic uptake of lipoproteins and the metabolic defect in familial dys beta LP, these results are consistent with the following hypothesis: (i) apo E comprises an essential component of the site for normal recognition of remnants of triglyceride-rich lipoproteins by a specific hepatic receptor; (ii) accumulation of remnant lipoproteins in familial dys beta LP is caused by lack of apo E-3 and E-4, which are the forms of this protein that are primarily recognized by the receptor; and (iii) the normal conversion of remnants of very low density lipoproteins to low density lipoproteins is mediated by the hepatic remnant receptor.

Abetalipoproteinemia↗