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Biomedical subjects

S J Lan

Publications and source records attributed to S J Lan.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Frequency distribution of birth weight and gestational age in Taiwan].

Perinatal mortality rate is closely related to birth weight. We collected data on 35919 single liveborn babies at a teaching hospital in central Taiwan between 1977 and 1987, excluding 1980. The average birth weights of the two sexes combined, and of male and female live births separately, were 3163 +/- 486 gm, 3211 +/- 499 gm (N = 18865) and 3110 +/- 466 gm (N = 17054), respectively. The average gestational age of these live births was 39.7 +/- 2.1 weeks. The skewness and kurtosis of birth weight and gestational age distribution were -0.86 and 3.13, and -2.11 and 10.29, respectively. The two distributions indicated high kurtosis and left skewness, and were approximately normally distributed. Because birth weight and gestational age are highly associated, the skew-to-left residual distribution of birth weight might have been induced by low gestational age. Babies of low gestational age might not be able to develop mature organs and tissues, which, thus, results in high perinatal mortality. The distribution of birth weight intersects the normal curve within the region between 1500 gm and 2000 gm, which means that we may divide it into a predominant part and a residual part. Many articles have shown that the residual part is highly correlated to perinatal mortality rate and deserves further analysis. The average birth weight with gestational age at 40 weeks was 3239 +/- 385 gm, skewness and kurtosis were 0.16 and 0.75, respectively. The birth-weight distribution for a given number of gestational weeks is closer to the normal distribution. This paper provides standard figures and tables of birth weight with specific gestational age as a norm for related medical research.

Birth Weight↗
PubMed1990

An increased risk of hepatitis B virus infection from tattooing in Taiwan.

From among 2,375 young men, examined by doctors, 111 tattooed subjects were found. Twenty one subjects reported engaging in promiscuous sexual behavior or being intravenous drug abusers, and so were excluded. The other 90 were evaluated. To make up the control group, 180 non-tattooed subjects from the remaining 2,264, who neither engaged in promiscuous sexual activity nor were intravenous drug abusers, were matched from household registry reports by age, sex, education, occupation, and geographic origin from Mainland China, where their parents were born. IgG antibody of hepatitis A (anti-HAV) and markers of hepatitis B were tested in serum with radioimmunoassay. In the prevalence rate of hepatitis A and carrier rate of HBsAg there were no differences between the tattooed and the non-tattooed groups. However, the prevalence odds ratio of hepatitis B virus (HBV) infection for the tattooed group was 8.1 (95% CI 1.9-34.8) as compared to the non-tattooed groups. Moreover, there was a trend correlation when the prevalence rates of hepatitis B were compared for the group with multiple sites of tattoos, for the group with one site of tattoos, and for the non-tattooed group (p = 0.002). These findings suggested an association between HBV infection and tattooing. Tattoo exposure, with improper or no sterilization of the needle, seems to appear to increase the risk of HBV infection in the already high risk endemic area in question.

Adolescent↗
PubMed1989

Female to male transmission of hepatitis B virus between Chinese spouses.

Three hundred thirty-seven community-based spouses were tested for the presence of hepatitis B virus (HBV) markers to assess the direction of HBV transmission between couples. The prevalence rate of HBV infection among husbands whose wives were hepatitis B surface antigen (HBsAg)-positive was higher compared with those whose wives were HBsAg-negative. Moreover, the frequency of HBV seropositivity among husbands was 100% if their wives carried HBeAg and showed a trend correlation (P = .009). The prevalence difference was 13.8%, and the 95% confidence interval (95% Cl) was 7.9-19.7% after adjusting for spouses' age. In contrast, HBV infection rate of wives did not show an association with the husbands' HBsAg or HBeAg carrier status. The prevalence difference was 7.1%, but 95% Cl was -2.5-16.8% after adjusting for spouses' age. Female to male transmission of HBV between spouses appears to be more efficient.

Adolescent↗
PubMed1988

Rapid metabolic inactivation of tipredane, a structurally novel topical steroid.

[3H]Tipredane ([3H]TP), [3H]triamcinolone acetonide ([ 3H]TAAC), [3H]hydrocortisone ([3H]HC), and [3H]betamethasone-17 alpha-valerate ([3H]BMV), each at a concentration of 1 microM, were separately incubated with the 10,000 g supernatant fraction of the liver and skin homogenates of humans, rats and mice (BMV was studied only in human liver). Sequential samples were taken for up to 1 h during each incubation. The radioactivity in each sample was extracted with methanol, and the methanolic extracts were analyzed by high performance liquid chromatography. Among the four compounds studied, [3H]TP was most rapidly biotransformed by the liver preparations of the three species. The rates of in vitro biotransformation of TP were 2.5-30 times faster than those of TAAC, HC and BMV. In the human liver preparation, the rates of biotransformation were in the order of: TP greater than TAAC greater than HC = BMV. In the mouse and rat liver preparations, the orders were: TP greater than TAAC greater than HC and TP greater than HC greater than TAAC, respectively. In the skin preparations, little, if any, biotransformation of [3H]TP and [3H]TAAC was observed in any of the species studied; however, [3H]HC underwent a slow, steady biotransformation in the skin preparations of humans and rats but not of mice. [3H]TP was biotransformed by the liver preparations of all three species to numerous metabolites, thirteen of which have been identified. The biotransformation reactions included: (1) sulfoxidation; (2) elimination of either one or both alkylthio groups; and (3) hydroxylation of the steroid nucleus. Some metabolites were synthesized and tested for glucocorticoid receptor binding and anti-inflammatory activities; all were found to be much less potent than TP. The observed separation of local anti-inflammatory activity from systemic side effects of TP is most probably due to its rapid metabolic inactivation; the liver, rather than the skin, is mainly responsible for the metabolic inactivation of TP.

Androstadienes↗
PubMed1984

Captopril: pharmacology, metabolism and disposition.

By inhibiting ACE, captopril blocks the conversion of AI or AII and augments the effects of bradykinin both in vitro and in vivo. In rats, dogs, and monkeys with 2-kidney renal hypertension, orally administered captopril rapidly and markedly reduces blood pressure; this antihypertensive effect apparently occurs via a renin-dependent mechanism; that is, the inhibition of ACE. In 1-kidney renal hypertension studies in rats and dogs, it was determined that oral doses of captopril markedly lowered blood pressure, but only after several days of dosing; the mechanism is thought to be non-renin dependent. In SHR, daily oral doses of captopril progressively lowered blood pressure; normal levels were attained by the sixth month. In all species studied, the reduction in blood pressure resulted from a reduction in total peripheral resistance; cardiac output remained unchanged or increased. In humans, captopril reduces blood pressure in patients with essential hypertension with low, normal, and high renin levels, and in patients with renovascular hypertension and hypertension associated with chronic renal failure. In hypertensive patients with high plasma renin activity, captopril apparently exerts most of its pharmacologic effects through inhibition of ACE. The means by which captopril reduces high blood pressure associated with low or normal PRA is not known, but it is clear that captopril does not act on an overactive plasma renin-angiotensin system in these cases. The antihypertensive effect of captopril is enhanced when it is given in combination with a diuretic or after salt depletion. Captopril was rapidly and well absorbed in all species tested, including man. Studies in rodents indicated that ingestion of food caused a reduction in the extent of absorption and bioavailability of captopril. Captopril and/or its metabolites were distributed extensively and rapidly throughout most tissues of normal rats; no radioactivity was detected in the brain. In vitro and in vivo, captopril formed disulfide bonds with albumin and other proteins. This binding was reversible in nature. In vitro studies in blood indicates that the disulfide dimer of captopril and mixed disulfides of captopril with L-cysteine and glutathione were formed. In intact blood cells, captopril remained in the reduced form (sulfhydryl), whereas in whole blood or plasma, captopril was converted to its disulfide dimer and other oxidative products. Biotransformation of captopril may involve both enzymatic and nonenzymatic processes.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Induction of hepatic drug-metabolizing enzymes in rats, dogs, and monkeys after repeated administration of an anti-inflammatory hexahydroindazole.

The effect of repeated administration of an anti-inflammatory hexahydroindazole, (+/-)-3,3 alpha,4,5,6,7-hexahydro-2-[3-(4-morpholinyl)-propyl]-3-phenyl-7-(phenylmethylene)-2H-indazole (HMPPI), on hepatic microsomal drug-metabolizing enzymes in rats, dogs and monkeys was studied. Dose-dependent increases in the ratio of liver weight to body weight were observed in all three species. Microsomal protein concentration increased in rats and monkeys but not in dogs. Cytochrome P-450 concentration and aminopyrine N-demethylase activity increased in all species. Aniline hydroxylase activity increased only in dogs. In all three species, the largest increase in all parameters, except for the liver weight/body weight ratio, was observed in animals on the intermediate dose (50 mg/kg per d) of the hexahydroindazole, probably of the toxicity of the hexahydroindazole at the high dose (250 mg/kg per d).

Aminopyrine N-Demethylase↗
PubMed1978

Metabolism of alpha-methylfluorene-2-acetic acid (cicloprofen): isolation and identification of metabolites from rat urine.

1. Four metabolites of alpha-methylfluorene-2-acetic acid (cicloprofen) have been isolated from rat urine and identified as the 7-hydroxy, 9-hydroxy, 7,9-dihydroxy and 9-hydroxy-9-methoxy derivatives of cicloprofen. 2. 7-Hydroxy cicloprofen was the major metabolite, contributing 47% of the total radioactivity excreted in rat urine. The other three metabolites each contributed approx. 10% of the radioactivity in urine. There was little unchanged drug excreted in urine (2-6%); at least three other minor metabolites have not been identified. 3. A metabolic pathway for the formation of the 9-hydroxy-9-methoxy metabolite of cicloprofen is proposed.

Animals↗
PubMed1977

Metabolism of the (+)-, (+/-)-, and (-)-enantiomers of alpha-methylfluorene-2-acetic acid (cicloprofen) in rats.

1. After oral or intraperitoneal administration of (+/-)-[14C]cicloprofen to rats, the peak plasma concentrations of radioactivity and the areas under the plasma concentration/time curves did not increase proportionally with dose; total urinary and faecal excretions of radioactivity did increase with dose, suggesting saturation of plasma protein binding of drug and faster elimination of unbound drug at higher doses. 2. [14C]Cicloprofen and its metabolites were eliminated mainly via biliary excretion. Ratios of faecal to urinary excretion ranged from 2 to 3 and depended on dose administered. 3. Rats with cannulated bile ducts excreted the drug almost exclusively in bile, whereas intact rats excreted up to 32% of the dose in urine in 6 days, suggesting that [14C]cicloprofen or its metabolites or both undergo extensive enterohepatic recirculation in the rats. 4. The major metabolites of [14C]cicloprofen excreted in urine or bile were the 7-hydroxy, 9-hydroxy-, 7,9-dihydroxy-, and 9-hydroxy-9-methoxy-derivatives and their glucuronide or sulphate conjugates. 5. The (+)-enantiomer of [14C]cicloprofen was hydroxylated and excreted by rats at a faster rate than its (-)-antipode; no qualitative stereoselective metabolism of the individual enantiomers of [14C]cicloprofen was observed.

Administration, Oral↗
PubMed1976

Metabolism of a benzothiazine compound (SQ 11,579) by the intact rat, isolated perfused rat liver, and rat-liver microsomes.

1. The metabolic dispositions of a benzothiazine compound (SQ 11,579) by the intact rat, isolated perfused rat liver, and rat-liver microsomes have been investigated, and the results compared. 2. The drug was well absorbed after oral administration to rats and was widely distributed in all tissues, which, with the exception of brain, had higher concentrations of the drug, its metabolites, or both, than did plasma. 3. Metabolism by rat-liver microsomes included N-oxidation, N-demethylation, S-oxidation and aryl hydroxylation. Metabolites hydroxylated in the aromatic ring were excreted only in bile, both by the isolated perfused rat livers and by anaesthetized bile-duct-cannulated rats. 4. Liver perfusion of the benzothiazine or its monodesmethyl analogue (V) resulted in temporary cessation of the flow of perfusate through the organ. The benzothiazine sulphoxide (IV) had only a slight effect on the flow of liver perfusate, but IV followed by I caused the flow of perfusate to cease.

Administration, Oral↗
PubMed1976

Autoradiographic and tissue distribution studies on a nitrovinylfuran derivative (SQ 18506 14C) in S. mansoni infected mice.

Autoradiographic and tissue distribution studies of SQ 18506 14C were carried out on 13 Swiss albino mice. Infection was done by I.P. route with 50 to 60 cercaria of S. mansoni (puerto Rican strain) per animal. The safe single i.v. dose of a solution containing one mg of SQ 18506 dissolved in 0.06 ml dimethylsulfoxide was 0.003 ml/g b.w. of mice. Schistosome autoradiograms were clearly demonstrated one day after that dose injected in each mouse 50 days post-infection. However, hepatic autoradiograms were visible 14 days after 2 doses of our drug to each infected mouse. The higher the concentration of SQ 18506 14C in the culture medium the darker were the schistosomes in the autoradiograms and the greater their total d.p.m/mg. Tissue distribution studies after 2 1/2 doses of our drug/mouse revealed that schistosome total d.p.m/mg dry-weight was 50 times more than that of its liver. The latter d.p.m/g wet-weight was slightly higher than that of one ml of mouse blood.

5-Amino-3-((5-nitro-2-furyl)vinyl)-1,2,4-oxadiazol↗