Cytomegalovirus and Epstein-Barr virus infection in renal transplant recipients.
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Antibodies, Viral↗
Biomedical subjects
T Lin
Publications and source records attributed to T Lin.
Virologic and immunologic study on acquired immune deficiency syndrome.
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Acquired Immunodeficiency Syndrome↗
[A case of bilateral renal cell carcinoma].
A 69-year-old man visited our clinic with the chief complaint of macroscopic hematuria. On CT scanning and renal arteriography, a round tumor about 3 cm in diameter on the frontlateral phase of the left kidney and another tumor ranging from the upper pole to the center of the right kidney were recognized. Under the diagnosis of bilateral renal tumor, first in November 1980 left partial nephrectomy was performed to extirpate the tumor. Then, upon recovery from postoperative transient renal hypofunction, right nephrectomy was performed in January 1981. After the operation renal hypofunction was noted again, but in March of the same year he was discharged as his creatinine value was stabilized to 3 approximately 4 mg/dl. Histopathologically the tumor of the left kidney was clear cell subtype and that of the right kidney was granular cell subtype of renal cell carcinoma. He has been followed up under administration of PSK and CQ in the outpatient clinic. As of January, 1985 he is well without recurrence or metastasis.
Aged↗
Virologic, immunologic, and epidemiologic associations with AIDS among gay males in a low incidence area.
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Acquired Immunodeficiency Syndrome↗
Immune response to respiratory syncytial virus: prevention of syncytia formation by human serum during in vitro infection.
Human serum specimens containing respiratory syncytial virus (RSV)-specific neutralizing antibody were found to prevent the formation of syncytia when applied to HEp-2 tissue culture monolayers which had been infected with RSV 12 h previously. This was evidenced by the demonstration of RSV-infected cells without any syncytia formation in the monolayers treated with RSV antibody-positive serum. On the other hand, widespread syncytia formation was observed with antibody-negative control serum. The inhibitory effects of RSV antibody progressively declined when applied beyond 12 h after infection. Protection of the monolayer against syncytia formation occurred only in the presence of antibody and was quickly lost after the serum was removed. The titer of antisyncytial antibody correlated with the titer of neutralization antibody.
Adult↗
Adenosine 3',5'-monophosphate and testosterone responses of normal and desensitized Leydig cells to forskolin.
Forskolin has a potent stimulatory effect on both cyclic AMP and testosterone formation by purified Leydig cells. Forskolin also markedly enhanced hCG-induced cyclic AMP formation, but maximal testosterone production remained unaltered. Cyclic AMP and testosterone responses of desensitized Leydig cells to in vitro hCG stimulation were completely lost. Cholera toxin-induced cyclic AMP formation was also reduced. However, forskolin was able to stimulate a 3.4-fold increment in cyclic AMP formation and potentiate hCG-induced cyclic AMP response by desensitized Leydig cells. The absolute cyclic AMP levels were significantly lower than in normal control cells. These results suggest that the catalytic unit remains intact in desensitized Leydig cells and the coupling between N-protein and catalytic unit is impaired. The N-protein is required for full expression of maximal response of Leydig cells to forskolin.
Animals↗
Effect of inhibitors of microsomal enzymes on aflatoxin B1-induced cytotoxicity and inhibition of RNA synthesis in isolated rat hepatocytes.
Previous studies conducted in this laboratory demonstrated that AFB1 activation and deactivation was effectively inhibited by metyrapone and TCPO in isolated hepatocytes. The present study was undertaken to study the toxic effect of AFB1 on hepatocyte and RNA synthesis, and to assess the influence of the inhibitors on AFB1-induced cytotoxicity and AFB1-inhibited RNA synthesis. AFB1 at 50 microM was toxic and inhibited macromolecular synthesis by greater than 70% at 180 min of incubation whereas at lower concentrations of AFB1 (0.05-10 microM) dose-and time-dependent decreases in cell viability, protein and RNA synthesis were observed. Using [3H]-AFB1 (0.1.5 microM), the uptake and covalent binding of the toxin were also dose-and time-dependent. Initial rates of these processes to reach half-maximum was found to be 0.25 microM AFB1. In cells treated with AFB1 (5 microM) and metyrapone (1.0 mM) or SKF-525A (10 microM), the cell viability was similar to the control and [3H]-uridine incorporation was significantly higher than AFB1 treated cells. AFB1 and TCPO (0.5 mM) treated cells exhibited further decreases in cell viability and RNA synthesis. Results suggest that the binding of AFB1 to DNA and impairment of transcriptional activity may lead to cell death.
Aflatoxin B1↗
Discordant regulation by luteinizing hormone of ornithine decarboxylase activity and testosterone production in isolated rat testicular cells in vitro.
Possible functional relationship between luteinizing hormone-stimulated ornithine decarboxylase and testosterone production was examined in rat testicular interstitial cells in vitro. Although luteinizing hormone enhanced both ornithine decarboxylase activity and testosterone production at a similar physiological dose range, we found dissociation in the two responses in terms of their temporal aspect and the way they were affected by an irreversible inhibitor of ornithine decarboxylase, alpha-difluoromethylornithine, and protein synthesis inhibitor cycloheximide. The results suggest that there appears to be no causal coupling between luteinizing hormone-stimulated enzyme activity and testicular steroidogenesis.
Animals↗
Activation and deactivation of aflatoxin B1 in isolated rat hepatocytes.
Isolated rat hepatocytes took up [3H]-aflatoxin B1 during incubation with fifty percent of the aflatoxin B1 covalantly bound to cellular macromolecules. The amount of bound-aflatoxin B1 was proportional to the medium concentration of aflatoxin B1. The specific radioactivity (pmole/mg) of aflatoxin B1 found in the DNA fraction was 20 fold greater than that associated with protein. Metyrapone (0.75 mM) inhibited significantly the uptake and binding whereas 1,2-epoxy-3,3,3-trichloropropane (0.5 mM) enhanced 2-3 fold both the uptake and binding. Glutathione (0.25 mM) reduced these processes. Results indicate that a transformation of aflatoxin B1 is catalyzed by cytochrome P-450 mixed function oxidase and aflatoxin B1-2,3-epoxide so formed is primarily deactivated by epoxide hydrolase. In the isolated hepatocyte depletion of the epoxide by glutathione apparently has an insignificant role in aflatoxin detoxication.
Aflatoxin B1↗
Tamoxifen inhibits Leydig cell steroidogenesis: in vivo and in vitro studies.
Using isolated interstitial cells from testes of Sprague-Dawley rats, we have shown previously that tamoxifen inhibits LH and 8-bromo-cyclic AMP stimulated testosterone synthesis in a dose-dependent manner. The inhibitory effect of tamoxifen could not be reversed with 17 beta-estradiol. The present studies indicate that tamoxifen directly inhibits testosterone response to gonadotropin stimulation both in immature and mature hypophysectomized rats. When interstitial cells were incubated with pregnenolone (5 x 10(-7) M), testosterone levels in the incubation medium were 27.0 +/- 1.9 ng/10(6) cells. Tamoxifen (10(-5) M) significantly inhibited pregnenolone-induced testosterone formation. Tamoxifen also significantly diminished adenylate cyclase activity whereas the binding of hCG to receptor was not affected. These results indicated that several steps of steroidogenesis are inhibited by tamoxifen.
Animals↗
Protein kinase activity of purified Leydig cells: low protein kinase activity causes impaired steroidogenesis by band two cells.
Using a 0-32% continuous metrizamide density gradient, interstitial cells could be separated into five distinct bands. Cells localized in bands 1 (B1), 2 (B2), and 3 (B3) were isolated and incubated for 1h with or without human chorionic gonadotropin (hCG). Both B2 and B3 cells responded to hCG with increased cyclic AMP formation, but only B3 cells produced significantly more testosterone. Protein kinase activity of B2 cells was found to be extremely low compared with B1 and B3 cells. Additional treatment of B3 cells with collagenase did not cause any change in protein kinase activity. These results indicate that decreased protein kinase activity may be responsible for impaired testosterone synthesis in B2 cells.
Animals↗
The aging Leydig cell V. Diurnal rhythms in aged men.
Basal circulating levels of progesterone, 17 alpha-OH-progesterone, dehydroepiandrosterone, androstenedione, testosterone and oestradiol-17 beta were measured in 'young' (median age 34 years) and 'old' (median age 73 years) normal males between 08.30 and 17.00 h. Diurnal rhythms for 17 alpha-OH-progesterone, dehydroepiandrosterone, androstenedione and testosterone were observed in both young and old men. No rhythms were discernible for progesterone or oestradiol-17 beta in both age groups.
Adult↗
The aging Leydig cell: VI. Response of testosterone precursors to gonadotrophin in men.
The effects of a single im injection of human chorionic gonadotrophin (hCG) on circulating testosterone precursor levels at 0, 1-6, 24, 48 and 72 h were examined in normal young adult (mean age 34 years) and normal aged men (mean age 74 years) Basal 08.30- 09.00 h concentrations of androstenedione and dehydroepiandrosterone were lower in aged men while progesterone levels were not significantly different from young men. A significant biphasic increase of circulating progesterone was observed in young men, characterized by an early peak at 2 h (33% above basal) and a secondary peak at 24 h (49% above basal). In old men there were no increases in circulating progesterone levels following hCG treatment during the early (1-6 h) or late (24-72 h) periods. There were not discernable increases in circulating dehydroepiandrosterone levels following hCG administration in both groups of men. Androstenedione levels in young men. Androstenedione levels in young men did not change during the first 6 h following hCG but increased significantly at 48 and 72 h, while in old men there was a small peak at 4 h (which was not statistically significant) and a secondary significant rise at 48 and 72 h. However, early and late stimulated absolute levels for androstenedione were lower in the aged population. Thus, there are differences in precursor concentrations in the basal state and in response to hCG in aged men.
Age Factors↗
Direct inhibition of rat leydig cell function by tamoxifen.
The effects of tamoxifen on rat testicular steroidogenesis were studied using dispersed interstitial cells. Tamoxifen significantly inhibited LH-, and 8-bromo-adenosine 3',5'-monophosphate (8-bromo-cyclic AMP)-stimulated testosterone synthesis in a dose-dependent manner. Tamoxifen (10(-5)M) also reduced LH-stimulated cyclic AMP formation. The addition of equimolar concentrations of 17 beta-estradiol or tamoxifen separately to interstitial cells resulted in similar inhibition of LH-stimulated testosterone synthesis. When equimolar concentrations of 17 beta-estradiol and tamoxifen were added concomitantly to interstitial cells, the inhibition was additive. Present studies demonstrate that tamoxifen has direct inhibitory effects on testicular steroidogenesis: both at the plasma membrane resulting in decreased cyclic AMP formation and also at steps subsequent to cyclic AMP.
Animals↗
The aging Leydig cell: 2. Two distinct populations of Leydig cells and the possible site of defective steroidogenesis.
Using metrizamide gradient centrifugation two populations of Leydig cells were found in both 60-90 day-old and 24 month-old rats. Cells from both Band 2 (B2) and Band 3 (B3) responded to LH stimulation with increased cyclic AMP formation; however, only B3 cells produced significant amounts of testosterone. Cells from both B2 and B3 of the old rats synthesized less cyclic AMP and testosterone than cells from their younger counterparts. In response to LH stimulation, 0.01 - 1.0 mIU/ml, no appreciable difference of cyclic AMP formation could be detected between young and old Leydig cells. Maximal testosterone production occurred when 1 mIU/ml LH was used. Only when LH concentration was increased to 10 and 100 mIU/ml, did young Leydig cells produce significantly more cyclic AMP than old Leydig cells. After addition of 5X10(-7)M of pregnenolone or progesterone to the incubation medium, both young and old Leydig cells produced comparable amounts of testosterone. These results demonstrate no impairment of old rat Leydig cells to synthesize testosterone from pregnenolone and progesterone.
Aging↗
Regulation of cyclic guanosine 3',5'-monophosphate in interstitial cells of the rat testis.
The present studies were performed to evaluate the role of luteinizing hormone (LH) and calcium on cyclic guanosine 3',5'-monophosphate (cyclic GMP) formation in rat testicular interstitial cells. Dose related increases were observed in both intra-and extra-cellular cyclic GMP when various concentrations of LH (1, 10, 100 mlU/ml) were added to the purified Leydig cells. Cyclic GMP was also increased significantly with calcium ionophore A23187 at concentrations of 0.1, 1 and 10 microgram/ml. Adding LH concomitantly with A23187 resulted in a synergistic response and greatly enhanced cyclic GMP formation. When interstitial cells were incubated in calcium-free medium with 1 mM EGTA, the effects of LH and 123187 on cyclic GMP formation were abolished. These data suggest that LH and A23187 can increase cyclic GMP formation in interstitial cells and this response requires extracellular calcium.
Animals↗
The effects of cytochalasin B on testosterone synthesis by interstitial cells of rat testis.
The present study examined the effects of cytochalasin B on various steps in the luteinizing hormone (LH)-stimulated increase in testosterone synthesis by collagenase-dispersed interstitial cells of adult rat testis. Cytochalasin B at a concentration range of 0.1--50 microM inhibited the LH-stimulated increase in testosterone synthesis in a dose-dependent manner. Both intracellular and medium (released) testosterone levels were reduced, thus indicating that the decrease was not due to the accumulation of testosterone inside the cell as a result of cytochalasin B treatment. Cytochalasin B also inhibited the 8-bromocyclic AMP and pregnenolone-stimulated testosterone synthesis in a similar dose-dependent manner. Cytochalasin B at the two higher doses (10 and 50 microM) also inhibited the LH-stimulated generation of cyclic AMP by interstitial cells. However, this drug had no effect on basal testosterone synthesis except at the highest concentration added. Previous studies on adrenocorticotropic hormone (ACTH)- and LH-stimulated increase in glucocorticoid and testosterone synthesis in adrenal and Leydig cells, respectively, demonstrated that cytochalasin B or anti-actin inhibited the transport of cholesterol into mitochondria. The present studies suggest that cytochalasin B inhibits at least two additional steps in the LH-stimulated increase in testosterone synthesis: (1) the generation of cyclic AMP at the level of the plasma membrane, and (2) the conversion of pregnenolone to testosterone at the level of the smooth endoplasmic reticulum. It remains to be established whether these are direct effects of cytochalasin B, or whether they are mediated by disruption of microfilaments by cytochalasin B.
8-Bromo Cyclic Adenosine Monophosphate↗
The effects of calcium ionophore A23187 on interstitial cell steroidogenesis.
The present study was performed to evaluate the effects of calcium ionophore A23187 on adenosine 3',5'-monophosphate (cyclic AMP) and testosterone production in rat interstitial cells. Interstitial cells were incubated in Krebs-Ringer solution with varying amounts of luteinizing hormone, pregnenolone, or A23187. Cyclic AMP and testosterone were measured in the incubation medium after 4 h incubation. A23187 (0.01--10 microgram/ml) caused progressive increases of cyclic AMP formation (from 0.18 +/- 0.02 (S.E.) pmol/10(6) cells for the control of 0.42 +/- 0.02 pmol/10(6) cells, P less than 0.025), while testosterone production remained unaltered. When varying amounts of A23187 were added concomitantly with luteinizing hormone (5 IU/l), A23187 inhibited luteinizing hormone-induced steroidogenesis in a dose-dependent manner, but it had no effect on luteinizing hormone-induced cyclic AMP formation. When pregnenolone (10(-6) M) was added to the cells, testosterone formation increased from 1.50 +/- 0.22 to 8.46 +/- 1.65 ng/10(6) cells. A23187 (1 microgram/ml) had no discernable effect on the conversion of pregnenolone to testosterone. The main effect of increased cytosol calcium on steroidogenesis seems to be at the steps beyond adenylate cyclase-cyclic AMP. These results suggest that calcium is important for the conversion of cholesterol to pregnenolone, while the steps beyond pregnenolone are relatively independent of Ca2+.
Animals↗