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Biomedical subjects

S Y Tan

Publications and source records attributed to S Y Tan.

At least 127 records · Page 7Linked to original sources
PubMed1989

Nucleotide sequence of bovine prochymosin cDNA and the mechanism of cDNA deletion.

A plasmid pTLC23 harbouring entire cDNA sequence coding for prochymosin was constructed from clones pCT5 and pCT15. The nucleotide sequence of the complete cDNA insert, determined by using dideoxy sequencing method, indicates that the cloned DNA apparently represents the coding sequence for prochymosin B. Based on the data presented here, the differences between the DNA sequences reported by Nishimori et al., Harris et al. and Moir et al. were discussed as well. DNA sequence analysis reveals that the deletion in pCT15 covers positions 862-960. The missing sequence is characterized as an entire exon between intron G and intron H of the prochymosin gene, and by ending with splicing signal AG, it is suggested that the deletion in middle region of coding sequence results from the incorrect splicing of pre-mRNA.

Amino Acid Sequence↗
PubMed1989

Pathohistogenetic approach on the etiology of Yunnan tin miner's lung cancer.

Pathological observation was made in 100 surgically resected lung cancers of Yunnan tin miners: peripheral type 44 including 9 scar cancers; central type 56, 27 of whom were early lung cancer, with limited initial loci in a well defined area. On the basis of dust retention in original sites of lung cancer and results of X-ray microanalysis, a scheme for calculating the relative probability of causation is formulated. The result of calculation shows that the contribution of exposure to radon daughters is about 7 times that of ore dust retention in the etiology of Yunnan tin miner's lung cancer.

Adenocarcinoma↗
PubMed1986

Psychosocial functioning of adult epileptic and MS patients and adult normal controls on the WPSI.

The psychosocial functioning of adult epileptic outpatients (N = 68) as assessed by the Washington Psychosocial Seizure Inventory (WPSI) was compared to that of control groups of adult MS outpatients (N = 37) and normal subjects (N = 42). When all WPSI profiles were considered, the epilepsy group showed distinct difficulties in Emotional Adjustment and Adjustment to Seizures, whereas the MS group had difficulties only in Emotional Adjustment. However, the MS group had significantly higher Lie Scale scores than did normal subjects. The epilepsy group had significantly more emotional problems than normal subjects and significantly more problems adjusting to their disorder than did the MS group. However, when only valid WPSI profiles were considered, the only significant finding was that the epilepsy group (N = 44) and the MS group (N = 20) had more emotional problems than normal subjects (N = 35). The epilepsy group showed distinct difficulties in Emotional Adjustment and Adjustment to Seizures, whereas the MS group had difficulties in Emotional Adjustment, Interpersonal Adjustment, and Overall Psychosocial Functioning. Implications are discussed.

Adaptation, Psychological↗
PubMed1984

Psychosocial problems in adults with epilepsy: comparison of findings from four countries.

Psychosocial problems in groups of adults with epilepsy from Canada, Finland, the German Democratic Republic, and the United States were evaluated by the Washington Psychosocial Seizure Inventory. A number of similarities in psychosocial concerns were found across the four countries. At the forefront for each group were emotional problems, followed by concerns pertaining to adjustment to the seizures themselves. Where far-reaching governmental support of a financial and vocational nature was lacking, difficulties in these areas were also noted. In all cases, few problems were found in matters pertaining to family relationships and to medical care. Hypotheses to account for differences between the groups were discussed.

Adolescent↗
PubMed1981

Hyporeninemic hypoaldosteronism. An overlooked cause of hyperkalemia.

To establish the frequency and clinical and biochemical characteristics of hyporeninemic hypoaldosteronism (HH), we reviewed 100 consecutive cases of hyperkalemia (potassium content > 5.3 mEq/L). The most common cause was end-stage renal failure (34%). Other causes included overzealous potassium replacement, spironolactone therapy, hemolysis, acute renal failure, acidosis, thrombocytosis, and Addison's disease. Ten of 19 patients with unexplained hyperkalemia showed suppressed renin (0.12 to 1.3 ng/mL/hr) and aldosterone (5.4 to 21.6 ng/dL) responses to furosemide-posture challenge. Cortisol reserve was normal in HH. Fludrocortisone acetate therapy corrected the hyperkalemia. Other features of HH include low serum bicarbonate content, mild renal insufficiency, diabetes, and advanced age. The use of indomethacin and ibuprofen was associated with one case of HH each. Results suggest that HH is an overlooked cause of hyperkalemia, especially in patients whose hyperkalemia is unexplained.

Adult↗
PubMed1981

The effect of biofeedback-assisted relaxation training on blood pressure and selected biochemical parameters in patients with essential hypertension.

The effect of EMG biofeedback-assisted relaxation on blood pressure and selected biochemical parameters was evaluated in 38 patients with essential hypertension. Training consisted of 8 weeks of biofeedback and home practice of relaxation exercises. Mean blood pressure decreased in the experimental group from 144/90 to 133/84 mm Hg while the control group remained unchanged. Statistically significant decreases in the experimental group also occurred in muscle tension levels, in plasma aldosterone, and in urinary cortisol. Both aldosterone and cortisol are secreted by the adrenal cortex. It was concluded that the technique taught to the experimental group produced a reduction in skeletal muscle tension and a decrease in stress responding mediated by the adrenal cortex.

Adrenal Cortex↗
PubMed1981

Effects of indomethacin on plasma renin activity in the conscious rat.

The role of prostaglandins in the control of renin release in vivo was evaluated in the conscious rat. Indomethacin suppressed urinary prostaglandin E2 (PGE2) excretion from 5.3 +/- 0.5 to 2.6 +/- 0.5 ng/3 h (P less than 0.001). Basal plasma renin activity (PRA) fell from 6.20 +/- 1.07 to 2.98 +/- 0.45 ng . ml-1 . h-1 (P less than 0.02). Indomethacin suppressed PRA stimulated by furosemide, insulin-induced hypoglycemia, hydralazine, isoproterenol, arachidonic acid, and sodium-free diet, whereas PRA stimulated by PGE2 was not suppressed by indomethacin. The suppression of PRA by indomethacin in the sodium-deplete state rules out sodium retention as the mechanism of action of indomethacin. These results indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the renin response to several of the known stimulators, suggesting that prostaglandins may play a pivotal role in the control of renin release.

Animals↗
PubMed1981

Cortisol production by testicular tumors in a patient with congenital adrenal hyperplasia (21-hydroxylase deficiency).

Bilateral testicular tumors are known to occur in congenital adrenal hyperplasia, but their steroidogenic properties are not well studied. We have recently demonstrated steroid 11 beta-hydroxylase activity in these tumors from a 27-yr-old patient with documented salt-losing congenital hyperplasia (21-hydroxylase deficiency). Spermatic venous blood obtained at operation contained 3.6-5 ng/ml cortisol, as measured by specific RIA after Sephadex LH-20 chromatography. In contrast, the peripheral venous cortisol level was 0.64 ng/ml. The presence of 11 beta-hydroxylase activity was demonstrated by the in vitro conversion of [3H]deoxycorticosterone to [3H]corticosterone in tumor tissue. The conversion ratio of deoxycorticosterone to corticosterone was 4.3% and 7.07%/mg tissue in the tumor tissue, whereas in normal testicular tissue, it was less than 1%. The radiochemical identity of corticosterone was confirmed by rechromatography on Sephadex LH-20, coelution with added [14C]corticosterone, and a constant 3H to 14C ratio after acetylation and thin layer chromatography. The tumor cells grown in primary culture produced steroids and responded to ACTH and hCG. Electron microscopy of the tumor revealed a large number of mitochondria containing electron dense granules. Light microscopy was compatible with Leydig cell tumor. In conclusion, testicular tumors in association with congenital adrenal hyperplasia have morphological features of Leydig cells but have the capability of 11 beta-hydroxylation and cortisol production, properties which are unique to adrenocortical tissue. These findings suggest that they originate from pluripotential cells in the testicles. Regression of these tumors has been reported with optimal biochemical control of the disease.

Adrenal Hyperplasia, Congenital↗
PubMed1981

Active and inactive renin in low renin states: studies in human plasma.

Low PRA and active renin (AR) may be accompanied by low inactive renin (IR), indicating impaired renin production, or by normal or elevated IR, suggesting defective conversion to AR. To explore these possibilities, plasma AR and IR (acid activation method) were measured in normal volunteers and in patients with low PRA. All low renin states showed significant low PRA and AR when compared to normals; on the other hand, IR was 11.8 +/- 1.1 ng/ml.h in normals; low in primary aldosteronism (2.1 +/- 0.5 ng/ml.h) and anephric subjects; normal in low renin essential hypertension (7.5 +/- 1.3 ng/ml.h), nondiabetic hyporeninemic hypoaldosteronism (9.4 +/- 1.6 ng/ml.h) and diabetic hyporeninemic hypoaldosteronism (17.3 +/- 2.5 ng/ml.h); and significantly elevated in diabetics with nephropathy (21.0 +/- 1.6 ng/ml.h). The acute iv infusion of 2 liters saline in normal subjects did not decrease IR (11.8 +/- 2.0 vs. 13.0 +/- 1.8 ng/ml.h) despite a reduction in PRA and AR of 50-75%. These data indicate that in cases of primary aldosteronism and in anephric subjects both AR and IR are decreased, suggesting a decrease in total renal synthesis or release, whereas in low renin essential hypertension, nondiabetic hyporeninemic hypoaldosteronism, diabetic hyporeninemic aldosteronism, and diabetics with nephropathy AR is low and IR is normal or high, suggesting the possibility of impaired conversion to AR.

Adolescent↗
PubMed1980

Effects of prostaglandins on adrenal steroidogenesis in the rat.

To elucidate the role of prostaglandins in adrenal steroidogenesis, we studied aldosterone and corticosterone responses to 3 x 10(-8) M--3 x 10(-4) M of prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), prostacyclin (PGI2), and arachidonic acid (AA) in collagenase dispersed rat adrenal capsular and decapsular cells. Whereas adrenocorticotrophic hormone (ACTH) and angiotensin II (AII) stimulated aldosterone production in capsular cells and ACTH stimulated corticosterone production in decapsular cells in a dose dependent fashion, aldosterone and corticosterone production were not stimulated significantly by PGE2, PGF2 alpha, PGI2, and AA. Although preincubation of dispersed adrenal cells with indomethacin (3 x 10(-5) M) markedly inhibited PGE2 synthesis, ACTH- and AII-stimulated aldosterone production and ACTH-stimulated corticosterone production were not attenuated despite prostaglandin blockade. These results indicate that prostaglandins are unlikely to play an important role in adrenal steroidogenesis.

Adrenal Glands↗
PubMed1980

Urinary prostaglandin E2 excretion in chronic renal disease.

To ascertain whether renal prostaglandin E2 production is impaired in chronic renal disease we measured urinary prostaglandin E2 in 25 female renal patiens, and in 38 female noirmal volunteers. Prostaglandin E2 averaged 337 +/- 63 ng/24 hr in 25 female renal patients, which was significantly higher (P < 0.01) than values in normal female subjects (166 +/- 17 ng/24 hr). None of the renal patients excreted less than 50 ng/24 hr, whereas normals when treated with indomethacin averaged 30 +/- 10 ng/24 hr (n=8). There were no significant correlations between prostaglandin E2 and creatinine clearance, or urine volume. No difference in prostaglandin E2 was encountered between hypertensive and normotensive renal patients. Our results indicate that renal prostaglandin E2 production is increased rather than decreased in renal disease. The failure to demonstrate decreased urinary prostaglandin E2 excretion in renal hypertension sharply contrasts with the situation in essential hypertension.

Chronic Disease↗
PubMed1980

Sodium intake as a determinant of urinary prostaglandin E2 excretion.

The effect of salt-loading on urinary prostaglandin D2 (PGE2) was studied in the rat. PGE2 doubled after 4 days of gavage with 40 ml 0.9% saline. Control animals receiving 5% glucose or tap water did not show this increase. When rats were allowed ad lib saline, PGE2 increased after 2 weeks, but returned to normal at 5 weeks. This same phenomenon of increased PGE2 early in the course of salt-loading was also observed in Dahl salt-sensitive and salt-resistant rats fed an 8% salt diet. Inhibition of prostaglandin biosynthesis by meclofenamate or indomethacin did not attenuate the natriuretic effect of saline loading. We conclude: 1) Salt-related changes in PGE2 is a time-dependent phenomenon, and 2) PGE2 is not the natriuretic factor since levels normalize despite continued salt-loading, and natriuresis was unaffected by prostaglandin blockade.

Administration, Oral↗
PubMed1980

Direct action of rat urinary kallikrein on rat kidney to release renin.

To study the effect of kallikrein on renal renin release, we superfused rat renal cortical slices with 3.5 to 140 milliesterase units (mEU)/ml of purified rat urinary kallikrein. Kallikrein was a potent stimulus of renin release. Renin rose in a dose-dependent fashion from 70 mEU/ml to 140 mEU/ml. The response to 140 mEU/ml was greater than that seen with maximal doses of prostaglandin E2 (170 +/- 43%, P < 0.05) and at least the same as isoproterenol (242 +/- 49% increase), or dibutyryl cyclic AMP (272 +/- 40%). Trypsin was ineffective under these experimental conditions. Kallikrein-stimulated renin release was completely abolished by trasylol, whereas bradykinin did not increase renin production, indicating that kallikrein's effect is not mediated via kinin generation. There was no demonstrable acid activation or kallikrein activation of the superfusate and chromatography on Sephacryl S-200 revealed a single renin peak of -40,000 mol wt, suggesting that all of the renin release was in the active form. The data suggests that urinary kallikrein acts directly on the rat kidney to release renin, possibly via proteolytic conversion of prorenin to active renin. Our results support the concept that kallikrein may be an endogenous activator of prorenin in the kidney.

Animals↗