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Biomedical subjects

T Lin

Publications and source records attributed to T Lin.

At least 37 records · Page 2Linked to original sources
PubMed1990

Use of a new mixture for embolization of intracranial vascular malformations. Preliminary experimental experience.

The internal carotid artery system in swine has a special anatomic configuration similar to a brain "arterial-arterial malformation." The internal carotid artery breaks up into a multitude of fine channels (rete mirabile) situated at the base of the skull on the side of the hypophysis. This anatomic arterial model was used to analyze acute and chronic angiographic and histological changes after occlusion of the rete mirabile with I) avitene, II) avitene, and 50% ethanol, III) avitene, 30% ethanol and Polyvinyl alcohol, IV) avitene 50% ethanol and Polyvinyl alcohol, V) IBCA and VI) silk. Histopathological changes observed in the rete mirabile six weeks following occlusion demonstrated that a mixture of avitene, 30% ethanol and Polyvinyl alcohol and IBCA produced the best anatomic results. Embolization with avitene, PVA and ethanol induced a more bland histological reaction than the one observed with IBCA. Preliminary clinical experience with this mixture is reassuring in those cases in which the AVM was surgically resected. The partially thrombosed AVM was easily depressed and compressed by the neurosurgeon allowing for satisfactory hemostasis in and around the nidus of the AVM.

Animals↗
PubMed1990

Inhibition of human cancer cell growth by periodate-oxidized 3-aminopyridine adenine dinucleotide phosphate.

1. Periodate-oxidized 3-aminopyridine-adenine dinucleotide phosphate inhibited the proliferation of oral epithelium cancer and breast cancer cell lines. 2. The fast growing less differentiated embryonic kidney cell was more affected by the reagent then the embryonic lung fibroblast cell. 3. Incorporation of [3H]leucine of the treated cancer cells was inhibited. Incorporation of [3H]uridine was increased. Incorporation of [3H]thymidine was first increased and then decreased. 4. Tumor malic enzyme activity was inhibited by the reagent; but the treated cells did not show any difference in malic enzyme or glucose-6-phosphate dehydrogenase levels.

Adenine Nucleotides↗
PubMed1990

Interleukin-2 is a potent inhibitor of Leydig cell steroidogenesis.

Interstitial tissue of the testis consists of Leydig cells, macrophages, lymphocytes, plasma cells, mast cells and fibroblasts. Previously we have reported that interleukin-1 (IL-1) inhibits Leydig cell androgen production. In the present study, the effect of IL-2 was investigated. Leydig cells (10(5) cells/ml) from adult Sprague-Dawley rats were cultured with or without IL-2 for 24 h. After medium changes, human CG (hCG), 8-bromo-cAMP, or forskolin was added with or without IL-2. Cultures were continued for an additional 24 h, and testosterone and cAMP levels were measured. IL-2 up to 100 U/ml had no effect on basal testosterone production. hCG-stimulated testosterone formation was inhibited in a dose-dependent manner by the addition of IL-2. IL-2 in a concentration of 100 U/ml decreased hCG-induced testosterone formation from 49.6 +/- 3.6 ng/ml (mean +/- SE) to 8.5 +/- 4.2 ng/ml. The hCG dose-response curve was shifted to the right by the addition of IL-2. Maximal testosterone production in response to hCG was reduced 40% in the presence of IL-2 (50 U/ml) without alteration of median effective dose (ED50). IL-2 also inhibited hCG-induced cAMP formation and 8-bromo cAMP- and forskolin-stimulated testosterone production. However, IL-2 did not alter the binding of [125I]hCG to purified Leydig cells. Furthermore, IL-2 significantly inhibited the conversion of 20-OH-cholesterol, 22-OH-cholesterol, pregnenolone, progesterone, 17 alpha-hydroxypregnenolone, and 17 alpha-hydroxyprogesterone to testosterone but did not alter the conversion of dehydroepiandrosterone and androstenedione to testosterone. Our results suggest that a T cell growth factor, IL-2, is a potent inhibitor of steroidogenesis. IL-2 may play a paracrine role in modulating Leydig cell function.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Zygosity in two cases of triplet.

A total of 11 techniques including 57 items for zygosity diagnosis was employed in two sets of triplet. Namely, placenta-fetal membrane, LDH isoenzymes, etc. The authors made an investigation in detail on the pedigree history of polyembryony and systematic analysis of two sets of male triplets. The conclusion was that the first triplet came from a single ovum, whereas the second triplet developed from double ova. Different methods for the zygosity diagnosis were discussed. It was considered that there was hereditary influence in the occurrence of triplets developing either from a single ovum or from multiple ova.

Adult↗
PubMed1989

Neurovascular lesions and endovascular therapy: the role of MR.

Magnetic resonance imaging (MRI) studies were performed on 27 patients with vascular lesions of the central nervous system before and after embolization with either IBCA, polyvinyl alcohol foam particles, Avitene (microfibrillar collagen) or balloons. Thirteen pial brain arteriovenous malformations (AVMs), 3 brain AV fistulas, 2 giant aneurysms, 5 dural AVMs, 1 vertebro-vertebral fistula and 3 meningiomas were studied. The pre-embolization MR demonstrated the nidus and venous drainage of all pial AVMs. MR failed to detect 3 out of 5 dural AVMs using only spin echo sequences. A draining vein alone was seen in the remaining two cases. MR was superior to CT in detecting contiguous parenchymal changes such as atrophy, reversible ischemia, and mass effect in the pre-embolization studies. Following embolization, MR demonstrated partial or complete obliteration of the vascular nidus in all 13 pial AVMs. The embolized area was seen as an area of increased signal consistent with thrombus where previously there had been signal void. Ischemic or edematous changes in the brain parenchyma following embolization were seen on MR more easily than on CT scans. MR was accurate in the assessment of aneurysm patency, degree of thrombosis and balloon position in both giant aneurysms, and AV fistulae. These MR findings had an impact on patient management. MR will be an increasingly useful tool in the diagnosis and management of a number of neurovascular diseases requiring endovascular intervention.

Arteriovenous Malformations↗
PubMed1989

Hypercalcemia of immobilization in an adult patient with peripheral neuropathy.

A 48-year-old man developed a marked and persistent hypercalcemia 3 months after admission for paraplegia resulting from severe peripheral neuropathy most likely of alcoholic etiology. Serum ionized calcium was elevated, and parathyroid hormone levels were low normal by the two separate radioimmunoassays. Urinary calcium excretion was markedly elevated, and serum 1,25-dihydroxyvitamin D level was decreased. An extensive clinical evaluation for possible occult malignancy, myeloma, and sarcoidosis as a cause of hypercalcemia produced no positive findings. Treatment with calcitonin caused prompt normalization of serum calcium, and its discontinuation resulted in recurrence of hypercalcemia. With improvement of neuropathy, the patient started active physical therapy. We gradually discontinued calcitonin, and the patient's serum calcium remained normal during the following 11 months. We discuss difficulties in both clinical and laboratory diagnosis of hypercalcemia of immobilization in the adult patient because no specific laboratory test is available.

Alcoholism↗
PubMed1989

Regulation of Leydig cell function in primary culture by inhibin and activin.

Inhibin and activin are gonadal glycoproteins that selectively inhibit and stimulate FSH release, respectively. Previously we have reported that transforming growth factor-beta inhibited hCG-stimulated testosterone formation in mature Leydig cells. In the present study we evaluated the effects of other members of the transforming growth factor-beta family, inhibin and activin, on Leydig cell function. We found that activin (0.1-10 ng/ml) had no effect on basal testosterone formation, but inhibited hCG-stimulated testosterone formation in a dose-dependent manner. Activin (10 ng/ml) inhibited hCG-stimulated testosterone formation by 42%. Activin also inhibited hCG-stimulated cAMP formation. In the presence of activin (5 ng/ml), forskolin (10 microM)- and 8-bromo-cAMP (0.1 mM)-induced testosterone formation were reduced about one third. Conversions of pregnenolone and progesterone to testosterone were also blocked by activin. Interestingly, [125I]hCG binding to Leydig cells and forskolin-induced cAMP formation were not affected by the addition of activin. In contrast to activin, inhibin (0.1-10 ng/ml) had no effect on hCG-induced testosterone formation at any concentration used. However, the inhibitory effects of activin on Leydig cell function were reversed by the concomitant addition of inhibin. Our results suggest that activin inhibits testosterone formation by the Leydig cells derived from normal mature rats. Multiple steps of the steroidogenic pathway are affected by testosterone. Inhibin alone has no effect, but reverses the inhibitory action of activin.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

2(3)-tert-butyl-4-hydroxyanisole inhibits oxidative metabolism of aflatoxin B1 in isolated rat hepatocytes.

Previous studies indicate that dietary administration of phenolic antioxidants, 2(3)-tert-butyl-4-hydroxyanisole (BHA) and 3,5-di-tert-butyl-4-hydroxytoluene, inhibits the carcinogenic effect of a number of chemical carcinogens including aflatoxin B1 (AFB1). Induction of hepatic enzymes, such as glutathione S-transferase, UDP-glucuronyltransferase, and epoxide hydrolase, has been shown to be responsible for the reduction of AFB1 cytotoxic and carcinogenic effects. The effect of BHA on AFB1 activation was examined in vitro utilizing isolated rat hepatocytes and liver microsomes. In hepatocytes, the total AFB1 content and bound form of AFB1 were 3.4 and 1.4 pmol/10(6) cells, respectively. In the cell-free microsomal activating system, 2.2 pmol were activated per mg of microsomal protein during 60 min of incubation. BHA (0.1-0.5 mM) inhibited AFB1 activation and binding in both systems in a dose-dependent manner; in hepatocytes, 90% inhibition was observed at 0.5 mM. Analyzing various AFB1 adducts, BHA (0.25 mM)-treated hepatocytes contained a significantly reduced amount of AFB1 macromolecular adducts. The antioxidant neither stimulated nor inhibited the cytosolic glutathione S-transferase and microsomal UDP-glucuronyltransferase activities. Analysis of various hydroxylated (aflatoxins M1 and Q1 (AFM1 and AFQ1] and demethylated (aflatoxin P1 (AFP1] metabolites of AFB1 in both the conjugated and unconjugated form indicated that there was a 30-50% reduction of unconjugated AFP1, AFQ1, and AFM1, whereas AFB1 was increased 3-fold. There was no significant change of conjugated metabolites. The effect of BHA on AFB1 activation in hepatocytes was compared with that of other cytochrome P-450 inhibitors; the ED50 values of SKF 525A, BHA, and metyrapone were 9 microM, 40 microM, and 280 microM, respectively. In the cell-free microsomal system, biotransformation of AFB1 to AFP1, AFM1, and AFQ1 was also inhibited. Kinetic analysis of p-nitroanisole O-demethylase activity of rat liver microsomes demonstrated that BHA inhibited noncompetitively with an apparent Ki of 90 microM. In the absence of enzyme induction, the phenolic antioxidant, BHA, blocks the oxidative biotransformation of AFB1 in isolated hepatocytes.

Aflatoxin B1↗
PubMed1985

The effects of homogeneous human prealbumin on in vitro and in vivo immune responses in the mouse.

A highly purified preparation of human prealbumin was shown to potentiate the sensitivity of rosette spleen forming cells of adult thymectomized mice to azathioprine in vitro and in vivo and to induce the appearance of the Thy 1, 2 antigen in vitro on spleen cells of adult thymectomized mice. Prealbumin also enhanced IgM antibody synthesis to sheep red blood cells (SRBC) in vitro in 12 week old mice and in vivo in aged (45 - 58 week old) and nude (nu/nu) mice. In vivo administration, to mice that had been pre-treated with hydrocortisone, resulted in a decrease in the specific activity of thymocyte terminal deoxynucleotidyl transferase. The data indicate that the prealbumin molecule possesses immunopotentiating properties in a number of in vitro and in vivo immunocompromised murine models and that the immuno-enhancing properties of the partially purified preparation previously described were in fact due to the prealbumin component and not to other contaminating proteins.

Adjuvants, Immunologic↗
PubMed1979

In vitro studies of the testis: the effect of LH on cyclic nucleotides.

This study evaluated the relationship between LH, cyclic AMP, cyclic GMP, and testosterone using in vitro incubation of decapsulated rat testes and sampling incubation medium. With added LH (1.0, 5.0, 100, and 500 mIU/ml) there were statistically significant increases in cyclic AMP at 5 mIU/ml or more LH, and progressively greater titers of this nucleotide were produced as LH was increased. For cyclic GMP all levels of added LH caused significant increments in titers of nucleotide; however, peak cyclic GMP concentrations occurred with 5 mIU/ml of LH. The addition of 10(-3) and 10-(4)M 8-bromo-cyclic AMP caused significant increases in testosterone production, while no changes in production of this androgen were found with 10(-3), 10(-4), or 10(-5)M 8-bromo-cyclic GMP. Neither cyclic AMP nor cyclic GMP titers were altered by the addition of 1 to 50 micrograms/ml of testosterone to medium bathing the rat testes. The dose response curves of cyclic AMP and cyclic GMP to LH are different. Progressive increments in added LH cause parallel increases of cyclic AMP and a biphasic change of cyclic GMP, 8-bromo-cyclic GMP does not cause testosterone generation, suggesting that cyclic GMP does not result in androgen synthesis. However, cyclic GMP may be involved in other Leydig cell functions.

Animals↗
PubMed1979

Plasma cyclic nucleotide levels in hyperthyroidism.

Plasma cyclic AMP and cyclic GMP levels were studied in a group of normal subjects and 10 subjects with hyperthyroidism. In the control group, mean plasma cyclic AMP levels were 15.3 +/- 1.3 nmol/l (SEM), and plasma cyclic GMP levels were 9.4 +/- 0.58 nmol/l (SEM). In untreated hyperthyroid subjects, both plasma cyclic AMP and cyclic GMP levels were significantly elevated above normal with mean values of 35.0 +/- 2.4 nmol/l (SEM) (P less than 0.001) and 14.7 +/- 0.2 nmol/l (SEM), (P less than 0.001), respectively. Six of the hyperthyroid subjects were re-studied when they became euthyroid; plasma cyclic nucleotide concentrations all fell within the normal range. To evaluate the relative contribution of triiodothyronine and thyroxine to elevated plasma cyclic nucleotide levels, two hyperthyroid subjects were treated with propylthiouracil and iodide. Plasma cyclic nucleotide levels were normalized when plasma triiodothyronine levels declined to normal range, at the time when plasma thyroxine levels were still elevated. These preliminary data suggest that increased triiodothyronine production is responsible for the increased cyclic nucleotide levels in hyperthyroidism.

Adult↗
PubMed1978

Effect of treadmill exercise on plasma and urinary cyclic adenosine 3'5'-monophosphate.

The effect of treadmill exercise on plasma and urinary cyclic adenosine 3'5' monophosphate levels (cyclic AMP) was studied in twelve healthy subjects. Plasma cyclic AMP levels were found to be markedly elevated without significant changes in urinary cyclic AMP or cyclic AMP/creatine ratio. Most likely altered plasma glucagon and catecholamine levels were responsible for these changes.

Adult↗
PubMed1977

Circadian rhythms in the urinary excretion of cyclic 3',5'-adenosine monophosphate (cyclic AMP) and cyclic 3',5'-guanosine monophosphate (cyclic GMP) in human subjects.

Significant circadian rhythns in urinary excretion of cyclic AMP, cyclic GMP, creatinine, 17-hydroxycorticosteroids and inorganic phosphorus were demonstrated in three normal subjects (two males and one post-menopausal female) who collected serial 4-h specimens for periods of 33, 22, and 14 days, respectively. Peak excretion of the above substances occurred, respectively, at approximately 1500-1700, 2300-0200, 1700-1800, 1100-1300, and 1800-2200 h. The estimated amplitudes of the rhythms expressed as a percentage of the mean 4-h excretion rate were 12-13%, 9-13%, 9-15%, 30-78% and 22-26%, respectively. With the possible exception of cyclic GMP, all of the observed rhythms appeared to be sinusoidal, with normal periods of 24 h. The rhythms in both cyclic AMP and creatinine excretion, but not in the remaining substances may be explained largely in terms of the known rhythm in glomerular filtration rate. The factors responsible for the rhythm in cyclic GMP excretion are unknown.

17-Hydroxycorticosteroids↗
PubMed1977

Construction of outcome scales measuring addicts' community functioning.

The current status of research in chemical abuse has depended heavily on unreliable cure rate as a criterion measure. This study was designed to construct reliable and valid quantitative outcome scales. One hundred and eighteen true-false items, all indicating changeable criterion behaviors, were written and administered to 154 hospitalized chemical abusers and 93 staff members. Clinical and factorial manipulation were employed to delete unwanted items. Tentatively, three scales of 41 items were derived, namely, Personal/Economic Independence, Chemical Use, and Job Satisfaction.

Economics↗