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Biomedical subjects

C M Huang

Publications and source records attributed to C M Huang.

At least 109 records · Page 6Linked to original sources
PubMed1982

New immunoglobulin IgG allotypes and haplotypes found in wild mice with monoclonal anti-allotope antibodies.

Sera from 156 wild mice (Mus musculus L.) collected from parts of Eurasia, Northern Africa, and the Americas were tested in solid-phase radioimmunoassays for reactivity with 20 monoclonal anti-allotope antibodies directed against gene products of the Igh-1, Igh-3, and Igh-4 loci. Most of the wild mice have Igh phenotypes similar to those of inbred strains or heterozygotes thereof, but frequently the wild mice showed unique combinations of allotypes on a given chromosome (haplotypes) not seen in inbred strains. We found new allotypes of the Igh-1 and Igh-4 loci. Mice from three regions (Poland, Taiwan, and Japan) possess combinations of allotypes indicating that recombination, gene conversion, or other gene duplication events have occurred in portions of the Igh constant region gene complex. Most interestingly, sera of three mice from Egypt possess immunoglobulin molecules appearing to result from an intragenic recombination event involving either Igh-1d or Igh-3d with Igh-1b. Two mice from Pakistan and one from Seychelles Island in the Indian Ocean also showed similar unusual phenotypes. These mice possess two CH2 IgH-1b and two CH2 Igh-1a/CH2 Igh-1d determinants, suggesting that these variant immunoglobulin arose from recombinations within the CH2 domain.

Animals↗
PubMed1981

Comparison of antihypertensive effects of captopril and propranolol in essential hypertension.

The antihypertensive effects of the oral converting enzyme inhibitor captopril and of propranolol were evaluated in a single-blind trial of 12 weeks in 19 ambulatory men with moderated essential hypertension (supine diastolic blood pressure [DPB], 100 to 120 mm Hg after receiving placebo for two weeks) whose sodium intake was unrestricted. The captopril group included 12 patients and the propranolol group seven. After the initial dose-finding period of four weeks, supine DBP was significantly reduced in eight patients receiving captopril and in four of the patients receiving propranolol. In these patients DBP decreased throughout the following eight weeks. In the remaining patients from each group, DBP was not reduced by either drug given alone at maximum allowable dosages during dose-finding periods, nor by combined administration in following weeks. No adverse side effects attributable to captopril were noted, except in one patient in whom proteinuria developed after seven weeks. Captopril has potential value in the treatment of moderate essential hypertension.

Adult↗
PubMed1981

Time constants of acoustic adaptation.

Evoked potentials were recorded from cochlear nuclei of intact, awake cats through chronically implanted electrodes during stimulation with 10,000 c/sec at 35 dB above the visual detection threshold of evoked potentials. The stimulus rate was varied from 0.5 to 100/sec and the stimulus duration was varied from 1 to 1800 msec but no overlap occurred between successive stimuli. A model was proposed to explain the amplitude of evoked potentials as a function of the stimulus duration and repetition rate. The time constant for the exponential decrease of evoked potential amplitude during stimulation is 8.9 msec, whereas the time constant for the exponential recovery of evoked potentials following the cessation of the tone is 39.5 msec.

Acoustic Stimulation↗
PubMed1981

Long-term treatment of hypertension with methyldopa. IV. Duration of methyldopa therapy.

Methyldopa was administered for an average of 3 years to 435 patients with essential hypertension who were included in this retrospective survey. In 73% of patients, methyldopa was added to prior diuretic therapy, and in 19%, methyldopa and a diuretic were started concurrently. The remaining patients (8%) started treatment with methyldopa alone. After the initiation of methyldopa administration, a diuretic and/or additional antihypertensive agent(s) was included in the treatment regimen of 167 (38%) of the 435 patients. Treatment was interrupted in 147 patients - 14 (3%) because of lack of response, 73 (17%) with adverse effects, and 60 (14%) because of other or unknown reasons. Two-thirds of the patients treated had been receiving methyldopa continuously up to the time these data were collected in early 1979.

Adolescent↗
PubMed1980

Murine antigen H-2.7: localization of its antigenic determinant to the Ss (C4) molecule.

Murine blood group antigen H-2.7 is encoded by a locus mapping in the vicinity of the S locus which codes for the Ss antigen carried by the fourth component of the complement pathway (C4). Normal mouse serum of H-2.7-positive strains contains a substance which inhibits anti-H-2.7 hemagglutination. This substance cannot be removed by passage of the serum through an anti-Ss immunoabsorbent column indicating that the Ss and H-2.7 antigens are present on separate molecules or molecular fragments in the serum. In contrast, fresh plasma either does not contain the H-2.7-bearing substance at all or it contains it at a far lower concentration than normal serum, although it has a normal level of the Ss-antigen-bearing substance. However, the H-2.7-positive substance appears when the plasma is allowed to stand for several hours, or when it is dialyzed and treated subsequently in a manner favoring spontaneous degradation of complement components. Removal of the Ss substance from the fresh plasma prevents the appearance of the H-2.7 antigen at any time thereafter. These findings indicate that the Ss and H-2.7 antigens are carried by the same molecule or molecular complex. The intact molecule expresses only the Ss antigen; the H-2.7 antigen is either hidden or masked so that it is inaccessible or poorly accessible to H-2.7 antibodies. Degradation of these molecules results in the generation of two fragments, a large fragment carrying the Ss antigen and a smaller H-2.7-positive fragment. The data are consistent with the interpretation that the H-2.7 antigen is encoded by the S locus, and that it is carried by that portion of the C4 molecule split off during complement activation.

Animals↗
PubMed1980

Changes of acoustic nerve and cochlear nucleus evoked potentials due to repetitive stimulation.

Evoked potential recordings were studied in the acoustic nerve and cochlear nucleus of adult decerebrate cats as a function of the tone duration (1-1500 msec) and the tone repetition rate (0.5/sec-200/sec). Response decrements due to repetitive tonal stimulation were primarily a function of the inter-tone interval. At inter-tone intervals longer than 100 msec, no response decrements were observed in the acoustic nerve or the cochlear nucleus. With shorter inter-tone intervals, reversible response decrements of identical magnitudes ocurred in both the acoustic nerve and the cochlear nucleus evoked potentials. The mechanism of response decrement may be due to depression at the hair cell-acoustic nerve junction.

Acoustic Stimulation↗
PubMed1978

Factors that affect the amplitudes and latencies of the vertex short latency acoustic responses in the cat.

The latencies and amplitude of the short latency (less than 10 msec) acoustic evoked responses recorded from the vertex of the cat have been studied as a function of acoustic stimulus parameters. A change in the stimulus intensity, duration, or rate of repetition resulted in parallel changes in the first 5 evoked responses, i.e., the latencies shifted the same amount and the amplitudes were modified in the same proportion. Comparison of responses to monaural versus binaural stimuli indicated an occlusive effect of binaural stimulation only in potential 4.

Acoustic Stimulation↗
PubMed1977

Sudden fatal pulmonary calcification following renal transplantation.

A 42-year-old male was hemodialyzed for 2 years with excellent control of calcium-phosphate metabolism. He received a cadaveric renal transplant but experienced a prolonged episode of acute tubular necrosis during which he could not tolerate phosphate-binding antacids. His calcium X phosphate product became markedly elevated for 20 days. Following a brief period of function, the homograft was removed on the 45th post-transplant day after severe rejection and subsequent infection. Chest X-ray was normal. Six days after graft nephrectomy, he became acutely dyspneic and markedly hypoxemic. Diffuse, flocculent pulmonary infiltrates appeared on the chest film. The patient expired 1 day later. At postmortem examination, there was severe, diffuse pulmonary alveolar calcification demonstrated by chemical and histologic examination. Although unlikely, the prolonged post-transplant period characterized by elevated calcium X phosphate product may have played a pathogenetic role. Calciphylaxis may have occurred, with hyperparathyroidism as the sensitizing agent and any of several drugs acting as challenger.

Adult↗
PubMed1976

Hemodialysis for severe procainamide toxicity: clinical and pharmacokinetic observations.

A 67-yr-old woman who ingested approximately 7 gm procainamide developed severe hypotension, renal insufficiency, and life-threatening cardiac toxicity. Hemodialysis doubled the rate of procainamide elimination and increased fourfold the clearance of NAPA, the N-acetylated metabolite of procainamide. Observations of procainamide and N-acetylprocainamide (NAPA) plasma levels during the patient's recovery suggest that lethargy and profound hypotension can be expected when these levels total 60 mug/ml and that severe cardiac toxicity should be anticipated with levels totaling 42 mug/ml or more. Hemodialysis also permitted investigation of the effects of hypotension on the pharmacokinetics of these compounds. The apparent volume of procainamide distribution was reduced from a normal value of 2 L/kg to 0.76 L/kg, and that of NAPA from 1.4 L/kg to 0.63 L/kg. The elimination + 1/2 of procainamide was prolonged from the normal of 3 hr to 10.5 hr, and that of NAPA from 6 to 35.9 hr. Procainamide absorption was also slowed in this clinical setting, causing procainamide plasma levels to continue rising for some time after toxicity was first recognized.

Acetylation↗