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Biomedical subjects

T C Liu

Publications and source records attributed to T C Liu.

At least 127 records · Page 7Linked to original sources
PubMed1986

Bacterial and mycotic otological infections in Singapore.

This paper describes a microbiological study of 84 young adult men with clinical otitic infections. Gram-negative aerobic bacilli were frequently isolated from these patients diagnosed as having otitis externa or chronic suppurative otitis media, of which Pseudomonas species predominated. Staphylococcus aureus, S. epidermidis and aerobic Corynebacterium species (diphtheroids) were also found. About 40% of ear infections were attributed to otomycoses, chiefly from Aspergillus species and Candida parapsilosis. Antimicrobial susceptibility testing of the bacterial isolates revealed that Pseudomonas species were generally resistant to antibiotics commonly employed in general practice: ampicillin, erythromycin, co-trimoxazole, tetracycline and cephaloridine. However, polymyxin B, gentamicin and neomycin were active against some Pseudomonas isolates. Other Gram-negative bacilli were also mainly sensitive to gentamicin, neomycin as well as co-trimoxazole. Disc diffusion and minimum inhibitory concentration studies demonstrated good activity of ceftazidime, cefoperazone, tobramycin and carbenicillin against strains of Pseudomonas species and other Gram-negative rods. Cefotaxime and cefoxitin were active against Gram-negative bacilli other than Pseudomonas species. Beta-lactamase production did not appear to be the main mechanism of resistance in these community-acquired Gram-negative bacillary isolates. The antimicrobial therapy of otological infections is reviewed.

Adult↗
PubMed1986

Synthesis and release of luteinizing hormone by rat anterior pituitary cells: effects of cytochalasins B and D.

We determined the role of microfilaments in regulating LH synthesis (translation or glycosylation) and release from cultured rat anterior pituitary cells under basal and GnRH-stimulated conditions. Cells were pretreated for 2 h with microfilament-disrupting drugs, cytochalasin B (CB; 2 and 20 microM) or cytochalasin D (CD; 1 and 10 microM). LH synthesis and release were measured after 4 h of incubation with or without 1 nM GnRH and drugs. LH translation and glycosylation were monitored by measuring the incorporation of [14C]alanine and [3H]glucosamine, respectively, into total (cell and medium) immunoprecipitable LH. Immunoreactive LH (IRLH) in medium and cells was measured by RIA. GnRH at 1 nM significantly (P less than 0.01) increased the release of IRLH and total [3H]LH (glycosylation), but had no effect on total [14C]LH (translation), uptake, or incorporation of precursors into total protein. Neither CB (2 and 20 microM) nor CD (10 microM) altered basal or GnRH-stimulated IRHL release. Neither drug altered basal medium concentrations of [3H]LH or [14C]LH. In contrast, both CB and CD reduced (P less than 0.01) GnRH-stimulated [3H]LH in the medium and total system (LH glycosylation). CB reduced (P less than 0.01) [3H]glucosamine uptake, total [3H]protein synthesis, and basal level of total [3H]LH, while CD had no effects on these parameters. Thus, CD exerted a more specific inhibitory effect on GnRH-stimulated LH glycosylation than CB. CB (2 and 20 microM) increased (P less than 0.01), while CD (10 microM) decreased (P less than 0.01) [14C]alanine uptake, total [14C]LH, and [14C]protein under both basal and GnRH-stimulated conditions. These results demonstrated that while the cytochalasins did not inhibit either basal or GnRH-stimulated IRLH release, they did inhibit GnRH-stimulated LH glycosylation, although the effect of CB was due partially to reduced [3H]glucosamine uptake. Integrity of microfilaments appears to be important for GnRH-enhanced LH glycosylation, but not for GnRH-enhanced LH release.

Actin Cytoskeleton↗
PubMed1985

Synthesis and release of luteinizing hormone in vitro: manipulations of Ca2+ environment.

We determined if luteinizing hormone (LH) synthesis is Ca2+ dependent and coupled to LH release. We monitored LH synthesis when LH release was stimulated either by specific [gonadotropin-releasing hormone (GnRH)] or nonspecific stimuli (50 mM K+ and 2 or 20 microM Ca2+ ionophore A23187) and inhibited by Ca2+-reduced medium. LH synthesis was estimated by measuring incorporation of [3H]glucosamine (glycosylation) and [14C]alanine (translation) into total (cell and medium) immunoprecipitable LH by cultured rat anterior pituitary cells. Both GnRH (1 nM) and 50 mM K+ significantly stimulated LH release and glycosylation, but had no effect on LH translation. A23187 also stimulated LH release, but significantly depressed glycosylation of LH and total protein and [14C]alanine uptake. Deletion of Ca2+ from the medium depressed both GnRH-induced LH release and glycosylation. Addition of 0.1 mM EGTA to Ca2+-free medium not only inhibited GnRH-induced release and glycosylation of LH but also uptake of precursors and glycosylation and translation of total protein. Thus glycosylation and release of LH are Ca2+ dependent. Whether parallel changes in LH release and glycosylation reflect a cause and effect relationship remains to be determined.

Alanine↗
PubMed1985

Synthesis and release of luteinizing hormone in vitro by rat anterior pituitary cells: effects of gallopamil hydrochloride (D600) and pimozide.

We compared the role of Ca2+ in regulating GnRH-induced LH synthesis and release from cultured rat pituitary cells. LH synthesis and release were measured after a 4-h treatment of cells with gallopamil hydrochloride (D600; 1 and 100 microM), a Ca2+ channel blocker, or pimozide (0.5 and 5.0 microM), a calmodulin inhibitor, with or without 1 nM GnRH. LH translation and glycosylation were monitored by measuring incorporation of [14C]alanine and [3H]glucosamine, respectively, into total (cell and medium) immunoprecipitable LH. GnRH significantly (P less than 0.01) increased total [3H]LH (glycosylation), but had no effect on total [14C]LH (translation). D600 significantly (P less than 0.01) depressed (1 microM) and completely blocked (100 microM) GnRH-induced LH glycosylation and release of [3H]LH, [14C]LH, and immunoreactive LH. D600 (100 microM) also reduced (P less than 0.05) total basal synthesis of [14C]LH. Neither dose of D600 altered uptake of [3H]glucosamine, but 100 microM D600 significantly (P less than 0.01) depressed its incorporation into total protein. D600 (100 microM) significantly (P less than 0.01) depressed [14C]alanine uptake and incorporation into total protein. Pimozide significantly (P less than 0.01) reduced, in a dose-related manner, GnRH-induced LH glycosylation, and release of immunoreactive LH, [3H]LH, and [14C]LH. Pimozide did not alter LH translation or uptake of radiolabeled precursors or their incorporation into total protein. These results demonstrate that D600 and pimozide inhibit both GnRH-induced LH glycosylation and release. Thus, the actions of GnRH on LH glycosylation and release are both mediated by similar Ca2+-dependent pathways.

Alanine↗
PubMed1984

Long term superfusion of rat anterior pituitary cells: effects of repeated pulses of gonadotropin-releasing hormone at different doses, durations, and frequencies.

We investigated the temporal release of LH by rat pituitary cells superfused with repeated pulses of GnRH at different doses (amplitudes), frequencies, and pulse durations. Anterior pituitary (AP) cells prepared from ovariectomized rats were cultured on bio-beads and then placed in columns and superfused. The cells were stimulated intermittently for 24 h with synthetic GnRH given as pulses of 6-, 10-, or 15-min duration at frequencies of one pulse per 30, 60, or 90 min. In the first experiment we tested the temporal response of cells exposed to different doses of GnRH. At all doses, the first pulse of GnRH stimulated greater LH release than subsequent pulses. The response to subsequent pulses varied with dose. At low doses (1 and 5 X 10(-10)M) of GnRH, the AP cells stabilized and released similar amounts of LH in response to each sequential identical GnRH pulse for up to 24 h. In contrast, at high doses (10(-8) and 10(-6)M) of GnRH, the AP cells gradually released less LH with each pulse. During the initial pulses, the dose-response curves of LH release were linear between doses of 5 X 10(-10) to 1 X 10(-6) M GnRH. Thereafter, the maximum response was diminished, and the slope of the dose-response curve was reduced. In subsequent experiments we found that the decline in responsiveness with time was not due to either degradation of GnRH in the medium or loss of cell viability. The low responsiveness to high GnRH pulses at the end of the superfusion period could be overcome temporarily by further increasing the dose of GnRH. In the presence of high doses, changing GnRH pulse frequency from one 6-min pulse per h to one 6-min pulse per 1.5 h or changing duration from one repeated 10-min pulse per h to one repeated 6-min pulse per h had no detectable effect on the temporal pattern of LH release. These results suggest that, similar to constant infusion, pulsatile delivery of GnRH at high doses to AP cells can induce cell refractoriness to GnRH. This loss of responsiveness probably involves factors in addition to depletion of GnRH receptors and the releasable LH pool. In contrast, pulsatile delivery of low doses of GnRH appears to maintain LH release at a relatively constant level for up to 24 h.

Animals↗
PubMed1984

Long-term superfusion of rat pituitary cells: interaction of 17 beta-estradiol with pulses of gonadotropin-releasing hormone on luteinizing hormone release.

In a series of four experiments, the temporal development of acute inhibitory and delayed stimulatory effects of 17 beta-estradiol (E) on luteinizing hormone (LH) release by superfused rat anterior pituitary cells pulsed with gonadotropin-releasing hormone (GnRH) was studied. Dispersed anterior pituitary cells from ovariectomized rats were cultured on Bio-Beads for 3 days and then placed in columns and superfused for up to 24 hr. During superfusion, the cells were exposed to GnRH pulses (3 X 10(-9) M, one 6-min pulse/hr). Cells treated with E (3 X 10(-10) M) either before (only 24 hr prior to superfusion) or before and during superfusion released significantly (P less than 0.05) more LH in response to the first few pulses of GnRH than cells treated with diluent. In contrast, cells treated with E only during superfusion initially released less GnRH-induced LH than cells treated with diluent. In a subsequent experiment, the inhibitory effect of E reached a maximum by 1.5 hr (P less than 0.01), and then gradually disappeared after 4.5 hr. Cells superfused simultaneously with E and fixed "low"-dose GnRH (5 X 10(-10) M) pulses did not exhibit enhanced LH responses with time to that dose of GnRH. However, E-superfused cells responded more than diluent-superfused cells to subsequent stimulation with a higher-dose GnRH pulse. Superfusion of cells with E for 16.5 hr in the absence of GnRH pulses also did not increase release of LH to low-dose (5 X 10(-10) M) pulses of GnRH, yet did cause a transitory increase to subsequent high-dose (10(-8) M) GnRH pulses. In conclusion, these results demonstrate the direct biphasic inhibitory then stimulatory effects of E on GnRH-induced LH release by superfused rat anterior pituitary cells. Expression of the stimulatory effect of E is related to the dose of GnRH.

Animals↗
PubMed1984

Pathological findings on peripheral nerves, lymph nodes, and visceral organs of leprosy.

Pathological findings in a) 103 autopsies, b) biopsy material of peripheral nerve tissue from 210 tuberculoid patients, and c) inguinal lymph nodes from 106 leprosy cases are presented. Overall, lesions in peripheral nerves were most common in the ulnar (85.7% in the TT type, 98.3% in LL), peroneal (77.8% in TT, 97.9% in LL), median (80% in TT, 90.2% in LL), radial (66.6% in TT, 82% in LL), and the great auricular, tibial and supraorbital nerves. The ratio of bilateral nerve involvement in the same nerve was higher than unilateral involvement (approximately 5:1). Lesions of the peripheral nerve ganglion were seen in the LL type (22 cases, 61.1%) and the TT type (8 cases, 53.3%). These have seldom been mentioned in past literature. Superficial lymph nodes were most commonly affected in all types of leprosy. Lymph nodes in the hepatic and splenic portal areas were sometimes involved in lepromatous or borderline cases. Between the two polar types of leprosy, the lesions in the lymph nodes showed gradual transitions in a spectrum-like pattern which were similar to the changes in the lesions in the skin. In lepromatous leprosy, lesions could be found in 85.3% of the cases in the liver, 41.1% in the spleen, 86.7% in the testes, approximately 50% in the upper respiratory tract (including 36.4% in the nasopharynx), and 34.4% in the adrenal gland. Three cases had ophthalmologic lesions. In borderline leprosy, biphasic lesions of leprosy were found in various internal organs.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗