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H Louie

Publications and source records attributed to H Louie.

23 records · Page 2Linked to original sources
PubMed1991

Mitochondrial ultrastructural and molecular changes induced by zidovudine in rat hearts.

Zidovudine (azidothymidine (AZT)) inhibits human immunodeficiency virus replication, prolongs survival, and delays progression of acquired immune deficiency syndrome. We determined AZT-induced molecular and ultrastructural changes in the rat heart. Rats (3 per group) were given drinking water with or without AZT (0.2 to 1.0 mg/ml; 29 to 102 mg/kg/day). After 21, 35, or 49 days, hearts were glutaraldehyde-fixed by abdominal aortic perfusion, processed, and examined by transmission electron microscopy. In parallel, myocardial RNA was extracted from hearts (AZT dose: 1 mg/ml; 35 days) and subjected to Northern analysis using cDNA probes for: alpha c-actin, troponin C, mitochondrial creatine kinase and malate dehydrogenase, a portion of the mitochondrial genome containing cytochrome b coding region (pMM26), and glyceraldehyde-3-phosphate dehydrogenase. Results showed marked and widespread cardiac mitochondrial swelling with fractured and disrupted cristae after 35 days of 1 mg/ml AZT. After a 14-day recovery, these ultrastructural defects did not reverse. Changes were not present in myocardium after 21 days of AZT nor after 35 days of lower dose AZT (0.2 mg/ml). Mitochondrial cytochrome b mRNA expression was depressed in AZT-treated rat hearts (35 days; 1 mg/ml AZT). mRNAs encoding glyceraldehyde-3-phosphate dehydrogenase, alpha c-actin, troponin C, mitochondrial creatine kinase, malate dehydrogenase, and mitochondrial ribosomal RNAs remained unchanged. AZT disrupts cardiac mitochondrial ultrastructure and expression of mitochondrial cytochrome b mRNA in a dose- and time-dependent fashion. The mechanism of AZT cardiotoxicity may relate to inhibition of mitochondrial DNA replication (at the level of DNA polymerase gamma) as postulated by others.

Animals↗
PubMed1986

Testosterone removal in rats results in a decrease in social aggression and a loss of social dominance.

Alpha male rats from mixed sex colony groups were tested for aggressiveness toward nonaggressive male intruders. Afterward, they were castrated and implanted with testosterone filled Silastic tubes, castrated and implanted with empty tubes, or sham castrated and implanted with empty tubes. There were significant declines in the aggressiveness (lateral attacks, bites, and piloerection but not on-top) of castrated rats without testosterone replacement but not in castrated rats with testosterone replacement. At a second operation, castrated animals had their testosterone capsules removed or had their empty capsules replaced with testosterone filled capsules. When tested for aggression toward nonaggressive intruders, those alpha males which had testosterone removed declined in aggressiveness while those which had it implanted returned to a level of aggressiveness close to that emitted by sham castrated control animals. Subordinate males became dominant when alpha males were castrated and not given testosterone replacement. In a final series of observations, sham castrated males were found to be more aggressive than castrated males when pitted against one another. It is argued that testosterone plays a primary role in intermale social aggression and that the decline in aggressiveness following castration is typically accompanied by a loss of social dominance.

Aggression↗
PubMed1986

Spontaneous mouse killing rats: gentling and food deprivation result in killing behavior almost identical to that of rats with medial hypothalamic lesions.

Rats that were found to kill a mouse spontaneously were divided into two groups. One group was left untreated and allowed free access to food while the other was gentled for 15 min/day and given only 15 g of food/day. Nonkilling rats were induced to kill mice by lesions of the medial hypothalamus. Seven to ten days after being divided into groups or subjected to brain lesions, each rat's behavior toward a series of stimuli was observed. The stimuli were a live mouse, a second live mouse, a freshly killed mouse, and a cotton wad. Food-deprived/gentled spontaneous killers and rats induced to kill by medial hypothalamic lesions each tended to attack with higher intensities and lower latencies than control spontaneous killers. The food-deprived/gentled spontaneous killers and lesion-induced killers (but not the control spontaneous killers) also attacked a dead prey moved vertically and then held onto the prey with sufficient intensity that their feet would leave the floor of the cage before they would release their grip on the prey. It is argued that the behavior of food-deprived spontaneous killers may constitute a more valid model of spontaneous mouse killing than that of sated spontaneous killers. The close correspondence between behavior toward a prey by lesion-induced killers and food-deprived spontaneous killers suggests that the lesion-induced killers fit this model of mouse killing remarkably well.

Aggression↗