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Biomedical subjects

T C Liu

Publications and source records attributed to T C Liu.

At least 145 records · Page 8Linked to original sources
PubMed1982

Histology of indeterminate leprosy.

Skin biopsies from 20 patients with indeterminate leprosy were studied histopathologically. The most common clinical manifestation of the disease was a hypopigmented macule. In most cases, 5% to 10% of the dermis was occupied by the infiltrate. Sweat glands were involved in two thirds of the cases, and approximately half the biopsies showed involvement of arrector pili muscle and pilosebaceous glands. Ninety-five percent of the cases had involvement of the dermal nerves, with perineural infiltration being the most common finding. Twenty-five percent of the cases showed lesions of the epithelium.

Adolescent↗
PubMed1981

Effects of GnRH and drugs that affect cAMP levels on LH synthesis and release.

We examined basal and gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release and synthesis in response to drugs that raise intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels. Anterior pituitaries from ovariectomized rats were incubated with or without drugs in the presence of GnRH and [3H]glucosamine. Neither 8-bromo-cAMP (8-Br-cAMP) (10 mM), cholera toxin (10 micrograms/ml), nor phosphodiesterase inhibitors [theophylline, 2 and 8 mM; 3-isobutyl-1-methylxanthine (MIX), 0.2 mM] had any detectable effect on release of immunoreactive LH (IR-LH) when used alone. However, 8-Br-cAMP and the inhibitors potentiated (P less than 0.01) GnRH-induced release of IR-LH. Total radiolabeled LH in the system was elevated (P less than 0.01) by either GnRH, 8-Br-cAMP for cholera toxin, but reduced (P less than 0.01) by 8 mM theophylline and unaffected by MIX or 2 mM theophylline. 8-Br-cAMP did not alter the effect of GnRH on radiolabeled LH in the total system, whereas MIX and 2 mM theophylline reduced (P less than 0.05) it. These results suggest that 1) cAMP does not effect LH release directly, but may interact with GnRH to potentiate it, 2) GnRH and cAMP have a similar mode of action on LH glycosylation, and 3) phosphodiesterase inhibitors have additional actions that interfere with LH glycosylation.

1-Methyl-3-isobutylxanthine↗
PubMed1981

Differential effects of cyclic nucleotide analogues and GnRH on LH synthesis and release.

We compared the effects of gonadotropin-releasing hormone (GnRH) and cyclic nucleotides on biosynthesis and release of luteinizing hormone (LH) by rat anterior pituitary glands (APs). APs from ovariectomized rats were incubated in the presence of test compounds, [3H]glucosamine, and [14C]alanine. GnRH significantly (P less than 0.01) increased both incorporation of [3H]glucosamine into LH (glycosylation) and release of immunoreactive LH (IR-LH) and [3H]LH. None of the cyclic nucleotides alone at 5 mM significantly stimulated release of IR-LH. Adenosine 3',5'-cyclic monophosphate (cAMP), N6,O2'-dibutyryl cAMP (DBcAMP), and 8-bromo-adenosine 3',5'-cyclic monophosphate (8-Br-cAMP) stimulated (P less than 0.01) glycosylation, whereas 8-Br-AMP, 8-bromoguanosine 5'-monophosphate (8-Br-GMP), cGMP, and 8-Br-cGMP had no detectable effect. Release of [3H]LH was increased by GnRH, 8-Br-cAMP, and DBcAMP, but not by other nucleotides. None of the cyclic nucleotides elevated [14C]LH, whereas GnRH elevated it (P less than 0.01) in the medium. Dose-response curves for glycosylation in response to 8-Br-cAMP and GnRH were parallel. In contrast, dose-response curves for release of both [3H]LH and IR-LH were nonparallel. It appears that cAMP can mimic the action of GnRH on LH glycosylation, but may have little direct effect on LH release.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1978

Modifications of luteinizing hormone biosynthesis and release by gonadotropin-releasing hormone, cycloheximide, and actinomycin D.

In the first experiment, the influence of synthetic gonadotropin-releasing hormone (GnRH) on the time course of [3H]glucosamine ([3H]GA) and [14C]alanine ([14C]A) incorporation into LH by quartered rat anterior pituitary glands and the sequence of release of radiolabeled and total immunoreactive LH (IR-LH) was investigated. Radiolabeled LH was measured by immunoprecipitation and total IR-LH was measured by RIA. After lag periods of 5 and 20 min, respectively, incorporation of [14C]A and [3H]GA into tissue LH increased linearly for 4 h. GnRH stimulated incorporation of [3H]GA only. The ratio of [14C]A-LH to [3H]GA-LH (14C:3H ratio) in the tissue decreased significantly with time and with GnRH treatment. In the second experiment, replenishment of GnRH in the medium every 0.5 h elevated the release rate (release during each sequential 0.5 h) of both [3H]GA and [14C]A-labeled LH within 1.5 h. The release rate of radiolabeled LH increased linearly until 3.5 h. The 14C:3H ratio in LH released during each time interval was reduced by GnRH. The release rate of IR-LH increased linearly with time, plateaued by 1.5-3 h, and started to decline. In other experiments, cycloheximide blocked synthesis of [14C]A-LH and greatly reduced the GnRH-induced synthesis and release of [3H]GA-LH, but reduced release of IR-LH by only 25%. Actinomycin D had no effect on GnRH-induced synthesis and release of LH at 2 h, but significantly reduced both at 4 h. These data suggest that 1) the time course for the release of preexisting IR-LH differs from that for newly synthesized LH, 2) the newly synthesized LH released in response to high levels of GnRH has more sugar residues than that released under basal conditions, 3) the GnRH-induced LH release can occur under conditions in which LH synthesis has been blocked, and 4) synthesis of messenger RNA is not required for GnRH-induced LH release or short term LH synthesis but seems to be required for continued synthesis and subsequent release of LH.

Alanine↗
PubMed1977

Effect of in vivo treatment with estrogen on luteinizing hormone synthesis and release by rat pituitaries in vitro.

The influence of estrogen on uptake of [3H]glucosamine and [14C]alanine and their incorporation into LH and total protein was investigated. Ovariectomized rats were sacrificed 22 h after injection with either oil or estradiol benzoate (EB, 50 microng/rat). Quartered anterior pituitary glands were incubated for 4 h with radioactive precursors in the presence or absence of 3.6 X 10-8M synthetic gonadotropin-releasing hormone (GnRH). Labeled LH was isolated by immunoprecipitation with specific anti-LH-beta serum. Both EB and GnRH significantly elevated the amount of [3H]glucosamine-LH appearing in the medium, the tissue, and the total system (medium + tissue), but they increased the amount of [14C]alanine-LH only in the medium. There was a significant positive interaction between EB and GnRH on the amounts of [3H]glucosamine-LH and [14C]alanine-LH in the medium and of [3H]glucosamine-LH in the tissue and total system. EB enhanced [3H]glucosamine uptake and incorporation into total protein, but GnRH had little or no effect on these parameters. In time course studies rats were injected with either oil or EB at 22, 11, or 5.5 h prior to sacrifice. At all times EB significantly increased synthesis and release of [3H]-glucosamine-LH and release of total immunoreactive LH (IR-LH) by pituitaries incubated with GnRH. The amounts of labeled and IR-LH released into the medium increased linearly with time after EB injection, but the amount of labeled LH in the total system plateaued at 5.5 h after EB injection. In another study, estradiol (E2, 5 microng/rat) dissolved in 1% ethanol-saline was injected at 0.5, 1.0, 2.0, or 4 h prior to sacrifice. Incorporation of [3H]glucosamine into tissue protein and release of [3H]glucosamine-LH was stimulated within 2 h after E2 injection. However, incorporation of [3H]glucosamine into LH was not stimulated until 4 h after E2 injection. These results suggest that estrogen and GnRH regulate LH synthesis at different sites, and that the effect of estrogen is non-specific compared to that of GnRH. The synthesis of the carbohydrate moiety of LH appears to be subjected to hormonal regulation more readily than the synthesis of the polypeptide moiety.

Alanine↗
PubMed1976

Effects of synthetic gonadotropin-releasing hormone on incorporation of radioactive glucosamine and amino acids into luteinizing hormone and total protein by rat pituitaries in vitro.

The influence of synthetic gonadotropin-releasing hormone (GnRH) on incorporation of glucosamine and amino acids into LH and total protein was investigated. Rat pituitaries were incubated in vitro with radioactive precursors for 4 h at 37 C. Labeled LH was isolated by immunoprecipitation with specific anti-LH-beta serum. Total LH in the medium and pituitary glands was measured by radioimmunoassay. GnRH significantly stimulated incorporation of [3H]glucosamine into LH in pituitaries from immature male, intact female, and ovariectomized rats. Pituitaries from ovariectomized rats synthesized more [3H]glucosamine-labeled LH than those from intact adult rats. GnRH enhanced release of [3H]glucosamine-LH into medium in pituitaries of both adult intact and ovariectomized rats. The response to GnRH was greatly reduced when pituitaries were exposed to cold shock before the 4 h incorporation period. In contrast to its effect on incorporation of [3H]glucosamine into LH, GnRH had either no or little effect, depending on experimental conditions, on uptake of [3H]glucosamine by pituitaries. Incorporation of [3H]glucosamine into total protein was not affected by GnRH treatment. GnRH increased release of either [3H]leucine- or [3H]alanine-labeled LH into medium, but had no significant effect on incorporation of labeled amino acids into total LH in the system. GnRH modified neither uptake nor incorporation of amino acids into total protein. GnRH significantly stimulated the release of cold LH into medium under all conditions, but the total amount of immunoassayable LH in the system was not detectably modified by GnRH treatment.

Age Factors↗
PubMedDate not supplied

Estrogenic and antiestrogenic actions of PCBs in the female rat: in vitro and in vivo studies.

A series of studies were performed to examine the effects of various PCB congeners [3,4,3',4'-TCB (PCB77), 2,5,2',5'-TCB (PCB52), 4' OH-2,4,6-TCB (OHPCB)] and a complex PCB mixture (Aroclor 1242; A1242) on the weights and patterns of cell proliferation of immature rat uteri in vivo and the effects of A1242 on gonadotropin release by dispersed anterior pituitary cells in vitro. Immature (20-day) rats were treated ip with corn oil (vehicle), PCBs, or 17 beta-estradiol (E2) once or daily for two consecutive days. Except for PCB77, all PCBs and E2 produced significant increases in uterine weights (P < 0.01) and increases in uterine 3H-thymidine labeling. PCB77 attenuated (P < 0.01) the increase in uterine weight due to either A1242 or E2 treatment. Cultured anterior pituitary cells exposed to varying concentrations of A1242 (0.1 to 50 ppm) exhibited enhanced gonadotropin responses to gonadotropin-releasing hormone (GnRH) similar to that of E2. These results demonstrate that PCBs can produce either estrogenic or antiestrogenic effects.

Animals↗
PubMedDate not supplied

Probe-tube microphone measures in patients with open-mastoid surgery: real-ear-to-coupler differences and real-ear unaided responses.

Real-ear-to-coupler differences (RECDs) and real-ear unaided responses (REURs) were measured using a probe-tube microphone system in 15 patients who underwent open mastoid surgery. The results show that RECDs are significantly smaller at higher frequencies (1.5, 2.0, 3.0, 4.0 and 6.0 kHz) in mastoid ears. The intrasubject variability of RECDs measures in these patients is on average 2.6 dB larger than for controls. For REURs, mastoid surgery significantly reduced the mean peak resonant frequency without affecting the amplitude and bandwidth. In operated ears, mean resonant frequency is by a factor of 1.4 lower than that for normal ears. Reduced responses (negative gains) at frequencies above the resonance peak occurred in 7 out of the 15 patients. These reduced responses corresponded to the smaller RECD at the middle and high frequencies. The results support the need for individual RECD measures to be made in operated ears instead of using average values from normal subjects. Otherwise, real-ear measures of the aided response should be made for each patient with open-mastoid cavity and the fitting should be done in terms of the target response at the eardrum rather than by defining a target insertion gain.

Adolescent↗
PubMedDate not supplied

Effect of acoustic trauma on cytochrome oxidase activity in stria vascularis.

The present study was undertaken to determine the role of metabolic disturbance in noise-induced hearing loss by histochemical studies of cytochrome oxidase activity. Adult normal albino guinea pigs were used. The experimental animals were exposed to broad-band noise at 105 dB SPL for 24 h. The control animals were not exposed to the noise. The thresholds of the auditory brainstem response (ABR) of all guinea pigs were measured 3 times: before noise exposure, 1 day and 1 month later. The difference between the ABR thresholds before and after noise exposure was statistically significant. Vibratome sections of decalcified cochleae of the noise-exposed (n = 8) and control groups (n = 4) were incubated with Spector's medium and embedded with Epon. Thin sections (2 microm) and ultrathin sections (100 nm) were cut to observe cytochrome oxidase activity in the stria vascularis under light and electron microscopes, respectively. A decreased activity of cytochrome oxidase was consistently shown in the normal-appearing stria vascularis of most noise-exposed ears. Acoustic trauma has an adverse effect on cytochrome oxidase activity in the stria vascularis as well as on hearing. A decrease in the activity of cytochrome oxidase implicates that metabolic damage may play a role in noise-induced hearing loss.

Animals↗