Biomedical subjects

H C Lin

Publications and source records attributed to H C Lin.

At least 271 records · Page 15Linked to original sources

PubMed1995

Adenosine and glutamate modulate the cardiovascular responses of angiotensins II and III in the area postrema of rats.

The purpose of this study was to determine the interactions of the renin-angiotensin system with adenosine and glutamate in the area postrema (AP) of rats. Male Sprague-Dawley rats were anesthetized with urethane. Adenosine, angiotensins (Ang) II, III and their antagonist 1,3-Dipropyl-8-p-sulfophenylxanthine (DPSPX), [Sar1Ile7]Ang III and glutamate antagonist, L-glutamic acid diethyl ester (GDEE) were microinjected into the AP of rats. Our results demonstrated that microinjection of DPSPX significantly attenuated the depressor and bradycardic effects of Ang II and III at low (9.6 pmol) and high dose (480 pmol) of Ang II in normotensive rats. To test the interaction of glutamate and renin-angiotensin system, we found that glutamate antagonist, GDEE, markedly lowered depressor and bradycardic responses of Ang II but did not influence Ang III in rats. On the other hand, microinjection of the Ang antagonist [Sar1Ile7]Ang III 10 min prior to the injection of adenosine significantly altered the cardiovascular effects of adenosine in the AP. In conclusion, the endogenous adenosine and glutamate may influence the renin-angiotensin system on cardiovascular responses in the AP of rats.

Adenosine↗

PubMed1995

Molecular characterization of galactosemia (type 1) mutations in Japanese.

We characterized two novel mutations of the galactose-1-phosphate uridyltransferase (GALT) gene in two Japanese patients with GALT deficiency and identified N314D and R333W mutations, previously found in Caucasians. One novel missense mutation was an G-to-A transition in exon 8, resulting in the substitution of arginine by histidine at the codon 231 (R231H). GALT activity of the R231H mutant construct was reduced to 15% of normal controls in a COS cell expression system. The other was a splicing mutation, an A-to-G transition at the 38th nucleotide in exon 3 (318A-->G), resulting in a 38-bp deletion in the GALT cDNA by activating a cryptic splice acceptor site. In seven Japanese families (14 alleles for classic form and one allele for Duarte variant) with GALT deficiency, the R231H and 318A-->G mutations were found only on both alleles of the proband. The N314D and R333W mutations were found on one allele each. The Q188R was prevalent in the United States but not in Japanese patients. The N314D mutation was associated with the Duarte variant in Japanese persons, as well as in the United States. We speculate that classic galactosemia mutations appear to differ between Japanese and Caucasian patients. Our limited data set on galactosemia mutations in Japanese suggests that the N314D GALT mutation encoding the Duarte variant arose before Asian and Caucasian people diverged and that classic galactosemia mutations arose and/or accumulated after the divergence of Asian and Caucasian populations.

Amino Acid Sequence↗

PubMed1995

Myelin- and microbe-specific antibodies in Guillain-Barré syndrome.

We surveyed the frequency of reported infections and target autoantigens in 56 Guillain Barré syndrome (GBS) patients by detecting antibodies to myelin and microbes. Sulfatide (43%), cardiolipin (48%), GD1a (15%), SGPG (11%), and GM3 (11%) antibodies were the most frequently detected heterogenous autoantibodies. A wide spectrum of antimicrobial IgG and IgM antibodies were also detected; mumps-specific IgG (66%), adenovirus-specific IgG (52%), varicella-zoster virus-specific IgG (46%), and S. pneumoniae serotype 7-specific IgG (45%) were the most prevalent. Our results indicate that polyclonal expansion of physiologic and pathologic antibodies and/or molecular mimicry likely occurs following infection and is related to other autoimmune factors in the etiology of GBS. Although no single definitive myelin-specific autoantibody was identified, our results suggest a unique pattern of reactivity against autoantigens.

Adolescent↗

PubMed1995

Multiple autoantibodies in patients with silicone breast implants.

Diverse immunologic abnormalities have been described in women who received silicone breast implants. However, most studies have focused on either a limited number of patients or a small panel of autoantibodies. We report the analysis of 20 autoantibodies in 116 women with implants and 134 controls. The patients ranged from 26- to 66-years-old, with a mean of 45.7 +/- 8.3 years; breast prostheses were in place for a mean of 15 +/- 5.6 years, with a range of 4 to 30, the chief complaints of the 116 patients included polyarthralgias, fatigue, myalgias, morning stiffness, and decreased memory. All 250 sera were tested blindly using a panel of 20 autoantigens including SS-A, SS-B, RNP, cardiolipin (CL), collagen types I, II and IV, phosphatidylserine (PS), myeloperoxidase (MPO), sulfatides (sulf), thyroglobulin (TG), gangliosides (GDIa;GM2), proteinase-3 (PR3), Jo-1, Sm, HPRPP-ribosomal phosphate, histones (H2AH2B), Scl-70 and glomerular basement membrane (NC-1). Values from individual patients were considered positive only when greater than 3 SD above the control mean. There was a statistically significant greater frequency of autoantibodies in women with implants for 15 of the 20 autoantigens; these were particularly striking for anti-H2AH2B, HPRPP, SS-A, SS-B, Scl-70, CL, PS, GM2, and NC-1. Many patients harbored several autoantibodies; 20% had four autoantibodies; 8% had six autoantibodies. The association of autoantibodies and implants suggests an adjuvant action of silicon/silicone byproducts.

Adjuvants, Immunologic↗

PubMed1995

Autoantibody profile in the sera of women with hyperprolactinemia.

Prolactin (PRL) has been implicated as an important in vivo modulator of cellular and humoral immunity. In order to elucidate the impact of elevated serum PRL levels on the immune system, we measured circulating autoantibodies in the serum of 33 hyperprolactinemic (HPRL) women and in 19 healthy women with normal PRL levels. All sera were examined for the presence of autoantibodies against 15 different antigens, including: ssDNA, dsDNA, histones (H2AH2B), Sm, RNP, SS-A/Ro, SS-B/La, cardiolipin, Scl-70, Jo1, collagen, glomerular basement membrane (GBM), pyruvate dehydrogenase (PDH), proteinase-3 (PR3) and MPO. Twenty-five of 33 (75.7%) HPRL women were found to have at least one autoantibody, while none of the 19 women with normal PRL had any. Eight HPRL women had seven or more (up to nine) different autoantibodies. Some of the autoantibodies were more frequently expressed than others, namely: anti-ss-DNA, anti-dsDNA, anti-Sm, anti-PDH and anti-SS-A/Ro. Autoantibodies to the autoantigens tested are common in a variety of autoimmune and rheumatic disorders including systemic lupus erythematosus (SLE), Sjögren's syndrome, mixed connective tissue disease (MCTD), scleroderma, primary biliary cirrhosis (PBC), polymyositis/dermatomyositis and vasculitis. Yet none of the HPRL women whose serum was found to contain high titers of autoantibodies presented with symptoms related to the respective autoimmune disorders. Our results support the role of PRL in the regulation of immune responses in man.

Adult↗

PubMed1995

Linkage disequilibrium between a SacI restriction fragment length polymorphism and two galactosemia mutations.

We have identified a novel SacI restriction fragment length polymorphism (RFLP) in the human galactose-1-phosphate uridyl transferase (GALT) gene. This RFLP can be readily typed by the polymerase chain reaction (PCR). The polymorphic allele is found on about 11% of normal chromosomes and is in linkage disequilibrium with the two most common mutations identified in GALT thus far: Q188R and N314D. Q188R is found exclusively on chromosomes with the SacI restriction site, whereas N314D is found only on chromosomes lacking this site. This suggests that these two mutations arose independently in evolution on different chromosomal backgrounds. Galactosemia patients without the Q188R mutation have a frequency of the SacI polymorphism similar to normal controls suggesting that several different galactosemia mutations must be present in them. The SacI RFLP may also be useful in the prenatal diagnosis of galactosemia.

DNA Mutational Analysis↗

PubMed1995

Plasma endothelin levels in patients with cirrhosis and their relationships to the severity of cirrhosis and renal function.

BACKGROUND/AIMS: Increased plasma endothelin levels have been reported in patients with cirrhosis. However, the relationship between plasma endothelin concentrations and hyperdynamic circulation or renal functions has not been documented. METHODS: We measured the plasma endothelin-1 and endothelin-3 concentrations using radioimmunoassay in 96 patients with cirrhosis (Pugh's A in 26, Pugh's B in 45 and Pugh's C in 25) and compared these values to 56 age- and sex-matched healthy subjects. Systemic and portal hemodynamic measurements, effective renal plasma flow, creatinine clearance, plasma aldosterone concentration and plasma renin activity were recorded for each patient. RESULTS: Plasma endothelin-1 and endothelin-3 levels were significantly increased in patients with cirrhosis compared to healthy subjects. Additionally, plasma endothelin-1 and endothelin-3 values were higher in patients with cirrhosis and ascites than in those without ascites. Moreover, plasma endothelin-1 levels increased in relation to the severity of cirrhosis. On the other hand, modest negative correlations were found between endothelin-1 and creatinine clearance or effective renal plasma flow. CONCLUSIONS: Plasma endothelin-1 and endothelin-3 levels are increased in patients with cirrhosis compared to healthy subjects. The increase in plasma endothelin-1 levels is related at least in part to the severity of cirrhosis. Increased endothelin-1 levels may possibly contribute to renal dysfunction in patients with cirrhosis.

Adult↗

PubMed1995

Endotoxemia in patients with chronic liver diseases: relationship to severity of liver diseases, presence of esophageal varices, and hyperdynamic circulation.

Plasma endotoxin levels were investigated using a quantitative Limulus assay in patients with chronic liver diseases and correlated with the severity of liver diseases, the presence of esophageal varices, and hemodynamic parameters. The plasma endotoxin levels were significantly higher in chronic hepatitis patients with acute exacerbation (10.1 +/- 1.3 pg/ml, n = 13, p < 0.05) and patients with cirrhosis (7.0 +/- 0.7 pg/ml, n = 126, p < 0.05) than in healthy subjects (2.9 +/- 0.2 pg/ml, n = 45). Chronic hepatitis patients (n = 30) had plasma endotoxin levels which were similar to those in healthy subjects (4.6 +/- 0.5 vs. 2.9 +/- 0.2 pg/ml, p > 0.05) but lower than those in chronic hepatitis patients with acute exacerbation (4.6 +/- 0.5 vs. 10.1 +/- 1.3 pg/ml, p < 0.05). Endotoxemia (plasma endotoxin level > 5.7 pg/ml) was found in 27%, 85% and 41% of patients with chronic hepatitis, chronic hepatitis with acute exacerbation, and cirrhosis, respectively. In patients with cirrhosis, the plasma endotoxin levels progressively increased in relation to the severity of liver dysfunction (Pugh's class A/B/C = 4.9 +/- 0.5/7.9 +/- 1.4/10.2 +/- 2.0 pg/ml, p < 0.05). In contrast, plasma endotoxin levels were comparable between patients with cirrhosis with and without esophageal varices (p > 0.05). Chronic hepatitis patients with acute exacerbation (no collaterization) had much higher plasma endotoxin levels than those in patients with cirrhosis and large varices (p < 0.05), whereas compensated patients with cirrhosis and large esophageal varices had plasma endotoxin levels similar to those seen in chronic hepatitis patients (no collaterization) (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Circulation↗

PubMed1995

Epidemiology of hypertension in Kin-Hu, Kinmen.

Data on the prevalence and predictors of hypertension in Kinmen, an island very close to southern mainland China but under Republic of China administration, would be very helpful to understand the effect of environmental and psychosocial factors on hypertension in a specific ethnic group. In 1991, Kin-Hu residents > or = 30 years of age, living in the second largest township of Kinmen, were invited to participate in this survey incorporating face-to-face interviews with a structured questionnaire, collection of fasting blood samples and oral glucose tolerance test. The response rate for subjects with complete data was 80.3% (3289 of 4097). The prevalence rates for definite hypertension (> or = 160/95 mm Hg and/or under antihypertensive treatment) were 20.1, 14.0, and 16.9% for men, women, and the total population, respectively. Overall awareness, treatment, and control rates of definite hypertension were 46.9, 25.0, and 4.7%, respectively. According to the final logistic regression model, after controlling for all other covariates, the significant predictors for current-definite hypertension were old age, male sex, nonsmoking, obesity, alcohol intake, high waist-to-hip ratio, high serum triglyceride and high serum uric acid levels. In comparison with Chinese in Taiwan and mainland China, the unexpectedly high prevalence of hypertension and distinct set of its predictors in Kin-Hu form the basis for future study.

Adult↗

PubMed1995

Effect of nasal continuous positive airway pressure on methacholine-induced bronchoconstriction.

Bronchial hyper-responsiveness is a cardinal feature of asthma. To determine whether nasal continuous positive airway pressure (NCPAP) influences airway smooth muscle in response to exogenous stimuli, we examined the effect of NCPAP on aerosolized methacholine-induced bronchoconstriction in 16 stable asthmatic patients. The dose-response curve for each subject was measured by a log transformation and linear regression analysis as well as a formula fitted to the data points to obtain values for a (slope) and b (position). The PD20FEV1 significantly increased in patients receiving 8 cmH2O of NCPAP by one doubling dose compared with that in patients using sham pressure. NCPAP shifted the dose-response curves to be flatter, deviated upwards and to the right. The coefficient a, indicating bronchial reactivity, was significantly lower in patients receiving NCPAP. The coefficient b, indicating the bronchial sensitive threshold, was higher after applying NCPAP. In contrast, coefficients a and b did not change in subjects with sham pressure. NCPAP also significantly enhanced the bronchodilator effect of inhaled salbutamol in response to methacholine-induced bronchoconstriction. In summary, we have shown that NCPAP therapy improves bronchial smooth reactivity with an increase in PD20FEV1 and a reduction in the bronchial reactivity and bronchial sensitivity. Therefore, NCPAP may provide an adjuvant therapy in patients with acute bronchial asthma.

Acute Disease↗

PubMed1995

Changes in portal hypertensive gastropathy after endoscopic variceal sclerotherapy or ligation: an endoscopic observation.

To determine the effect of endoscopic variceal sclerotherapy or ligation on portal hypertensive gastropathy, 90 cirrhotic patients with esophageal variceal bleeding were randomized to receive sclerotherapy (n = 44) or ligation (n = 46). Follow-up endoscopic observations of the gastric mucosa were recorded at 3-month intervals after variceal eradication. Clinical characteristics in both groups were similar. Probability for a change in the severity of portal hypertensive gastropathy was not related to method of eradication. Most cases of portal hypertensive gastropathy that changed in severity returned to baseline status with time, but the return was faster after ligation than after sclerotherapy. According to the results of multivariate analyses, sclerosant volume was the only factor associated with a significant difference between the group with static gastropathy (n = 15) and that with dynamic change in gastropathy (n = 23) after sclerotherapy. No relevant factors were found in the patients receiving ligation. We conclude that changes in the severity of portal hypertensive gastropathy after endoscopic variceal sclerotherapy or ligation are reversible. Most cases of gastropathy return to baseline status sooner or later.

Esophageal and Gastric Varices↗

PubMed1995

Novel antiplatelet naphthalene from Rhamnus nakaharai.

A new naphthalene derivative, isotorachrysone [1], was isolated from the stem bark of Rhamnus nakaharai along with several known compounds. The antiplatelet effects of isotorachrysone [1], isotorachrysone peracetate [2], 6-methoxysorigenin [3], quercetin 3-O-methyl ether [4], and quercetin 3-O-methyl ether peracetate [5] were studied using washed rabbit platelets. Of the compounds tested, 1, 2, 4, and 5 showed potent antiplatelet effects on arachidonic acid (AA-) and collagen-induced platelet aggregation. Compound 5 also showed potent antiplatelet effects on platelet-activating factor-(PAF-) induced platelet aggregation. Isotorachrysone [1] and its peracetate [2] were also studied for antiplatelet activity in human platelet-rich plasma (PRP) and both showed potent inhibition of the secondary aggregation induced by epinephrine. The antiplatelet effects of 1 and 2 are due partially to an inhibitory effect on thromboxane formation.

Animals↗

PubMed1995

Synthesis and antiplatelet effects of omega-aminoalkoxylxanthones.

A series of omega-aminoalkoxylxanthones were synthesized and tested in-vitro for their ability to inhibit aggregation of rabbit washed platelets and human platelet-rich plasma (PRP) induced by various inducers. Nine of these compounds showed more potent antiplatelet effects than natural norathyriol tetraacetate on collagen-induced aggregation. The various omega-aminoalkoxyl side chains of the synthesized compounds modified the antiplatelet effects. All the compounds tested in human PRP showed significant inhibition of secondary aggregation induced by adrenaline, suggesting that the antiplatelet effects of these compounds is mainly due to an inhibitory effect on thromboxane formation. These compounds at high concentration also cause vasorelaxing action in rat thoracic aorta.

Animals↗

PubMed1995

Selective infection of human T-lymphotropic virus type 1 (HTLV-1)-infected cells by chimeric human immunodeficiency viruses containing HTLV-1 tax response elements in the long terminal repeat.

Previous studies have suggested that the human immunodeficiency virus long terminal repeat (HIV LTR) enhancer/promoter sequences contribute to the replication ability of HIV in different T-cell lines; mutation of these sequences can alter HIV tropism. We have utilized site-specific mutagenesis to generate variants of HIV that exhibit specific tropism for human T-lymphotropic virus type 1 (HTLV-1) Tax-expressing CD4+ T cells. The wild-type HIV LTR NF-kappa B and Sp1 sites in an infectious molecular clone of HIV type 1 were replaced with sequences derived from the 21-bp Tax response elements (TRE) from the HTLV-1 LTR to generate TRE-containing chimeric HIVs (TRE-HIVs). The TRE-HIVs exhibit selective replication and cell killing in HTLV-infected human CD4+ T cells, but not in HTLV-negative T cells. Transient transfections suggested that Tax-TRE interactions could account for the observed replication specificity. The TRE-containing HIV LTRs were synergistically activated by the HIV Tat and HTLV-1 Tax transactivators. These results demonstrate that it is possible to specifically target HIV replication and cytotoxicity to HTLV-1+, CD4+ human T cells, on the basis of Tax-TRE interactions, and provide a model for the development of specific, cytotoxic, retroviral gene therapy vectors for HTLV-1-infected cells based on alterations of the LTR transcriptional regulatory elements. They also suggest that HIV Tat can cooperate with heterologous transcriptional activators, such as Tax, which act through upstream binding sites without directly binding to DNA.

Base Sequence↗

PubMed1995

Relation of bronchoalveolar lavage T lymphocyte subpopulations to rate of regression of active pulmonary tuberculosis.

BACKGROUND: Effective host defence against mycobacterial infection chiefly depends on the interactions between macrophages and T lymphocytes. This study investigated the relation of cellular components and their activity of cells obtained by bronchoalveolar lavage (BAL) from the lower respiratory tract to disease regression in patients with active pulmonary tuberculosis without HIV infection. METHODS: Clinical indices including age, sex, the presence of diabetes, fever, the presence of resistant strains of mycobacteria, the bacterial load in sputum, and disease extent on chest radiography at presentation were assessed before commencing four-drug antituberculous therapy. Twenty two patients with active pulmonary tuberculosis were divided into rapid, intermediate, and slow regression groups. Subpopulations of alveolar macrophages separated using discontinuous Percoll density gradient centrifugation and T lymphocytes (with CD3, CD4, CD8, and CD25 monoclonal antibodies) were quantified. RESULTS: There were no differences among rapid, intermediate, and slow regression groups in terms of age, sex, the presence of diabetes, the presence of resistant strains of mycobacteria, or the bacterial load in sputum. No differences were found between the groups in terms of subpopulations of alveolar macrophages or numbers of CD3 and CD4 lymphocytes. By contrast, an increase in CD8 cells was shown in the slow regression group compared with the rapid and intermediate regression groups. CD25 cell numbers were increased in the rapid regression group compared with the slow regression group. The CD4/CD8 ratio was decreased in the slow regression group compared with the rapid and intermediate regression groups and the relation between the proportion of CD25 cells and the CD4/CD8 ratio in BAL fluid was significant. CONCLUSIONS: A decreased CD4/CD8 ratio with an increase in CD8 cells in the alveolar spaces was associated with slow disease regression in patients with active pulmonary tuberculosis without HIV infection, suggesting that the balance of T lymphocyte subsets may play a central part in the modulation of host defence against mycobacterial infection.

Antitubercular Agents↗

PubMed1995

Decreased vascular contractile and inositol phosphate responses in portal hypertensive rats.

The purpose of this study was to investigate the vascular contractile and inositol phosphate responses in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Sham-operated rats served as controls. Pressures, vasoconstrictor responses, and inositol phosphate responses were determined at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower, in PVL rats. Dose-dependent contractile responses were observed for both norepinephrine (1 x 10(-8) - 3 x 10(-6) M) and vasopressin (3 x 10(-10) - 3 x 10(-8) M) in the tail artery of both groups. The contractile response to norepinephrine was significantly decreased in PVL rats compared with controls at all doses. The contractile response to vasopressin was significantly decreased in PVL rats at higher doses. After myo-[3H]inositol incorporation in tail artery, the levels of 3H-labelled phosphatidylinositols (cpm/mg) were similar between the two groups. Norepinephrine (10(-7) - 10(-5) M) and vasopressin (10(-10) - 10(-8) M) dose dependently stimulated the 3H-labelled inositol phosphate production in the tail artery of both PVL and sham-operated rats. However, the response was significantly lower in PVL rats. The results suggested that the attenuation of vascular contractile responses in portal hypertension was reflected in the phosphoinositide messenger system.

Animals↗

PubMed1995

Bile salt-dependent inhibition of gallbladder emptying.

Little is known about the inhibitory controls of gallbladder emptying. Since cholestyramine, a binding agent that reduces luminal concentration of bile salt, has been reported to accelerate gallbladder emptying, suggesting that bile salt is inhibitory, we hypothesized that fat-stimulated gallbladder emptying is inhibited by a bile salt-dependent mechanism. To test this idea, we compared gallbladder emptying in 10 dogs equipped with duodenal and jejunal fistulas that allowed for complete diversion of the native bile while varying concentrations of bile salt were perfused into the small intestine. In six dogs, 30 mM oleate and 5, 10, or 20 mM sodium taurocholate was perfused into the whole intestine. Since bile salt availability alters fat absorption, in a separate experiment in seven dogs we also compared gallbladder emptying while 30 mM oleate and 5 mM taurocholate were perfused between fistula and 0, 5, 10, or 20 mM taurocholate were perfused beyond jejunal fistula to separate fat from varying concentrations of bile salt. We found that intestinal taurocholate inhibited fat-stimulated gallbladder emptying in a dose-dependent fashion (P < 0.01; analysis of variance, significant linear dose effect) and that the inhibitory effect of bile salt persisted when 5-20 mM taurocholate was perfused beyond the jejunal fistula (0 vs. average of 5-20 mM taurocholate, P < 0.05, paired t-test). We conclude that fat-stimulated gallbladder emptying is inhibited by a bile salt-dependent inhibitory mechanism.

Anastomosis, Surgical↗

PubMed1995

Change in vascular cAMP and cGMP contents in portal hypertensive rats.

The purpose of this study was to investigate the possible changes of cyclic nucleotide contents in portal hypertensive rats. Portal hypertension was induced by partial portal vein ligation (PVL) in Sprague-Dawley rats. Sham-operated rats served as controls. Hemodynamic and cyclic nucleotide measurements were performed at 14 days after surgery. The portal venous pressure was significantly higher, while systemic arterial pressure and heart rate were lower in PVL rats than those in controls. Basal cAMP (PVL, 10.91 +/- 0.98, vs. sham, 8.08 +/- 0.81 pmol/mg protein) and cGMP (PVL, 0.91 +/- 0.12, vs. sham, 0.59 +/- 0.05 pmol/mg protein) contents in the tail artery were significantly higher in PVL rats. Isobutyryl methylxanthine (10(-5) M), a nonspecific phosphodiesterase inhibitor, exerted similarly stimulating effects on the tissue cGMP (PVL, 158 +/- 10, vs. sham, 178 +/- 20%) and cGMP (295 +/- 28 vs. 316 +/- 71%) levels in both PVL and control rats; so did forskolin (10(-6) M) on the cAMP (184 +/- 20 vs. 197 +/- 66%) content in both groups. Our results showed that the arterial cAMP and cGMP contents were higher in PVL rats, which may contribute to the reduction of peripheral resistance in portal hypertension.

1-Methyl-3-isobutylxanthine↗