Circulatory response to muscle trauma following denervation and hemorrhage in dogs.
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Biomedical subjects
Publications and source records attributed to C T Liu.
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We have determined the comparative activities of peroxisomal proliferators, ciprofibrate and clofibric acid on various hepatic parameters associated with endoplasmic reticulum, mitochondria and peroxisomes in primary cultures of rat hepatocytes. We have measured the activities of carnitine acetyltransferase and fatty acylCoA oxidase, and the amount of 60 and 80 kD polypeptides as biochemical markers of the peroxisomal function; laurate hydroxylase and cytochrome P-450 as markers of the endoplasmic reticulum; and carnitine palmitoyltransferase as a marker of mitochondria in primary cultures of hepatocytes. Ciprofibrate (0.01 to 0.3 mM) and clofibric acid (0.1 to 3 mM) produced similar changes in several components of cultured hepatocytes within 72 hr. Increases of protein (18 and 11%), carnitine palmitoyltransferase (23 and 97%), cytochrome P-450 (37 and 49%), carnitine acetyltransferase (484 and 614%), fatty acylCoA oxidase (529 and 931%) and laurate hydroxylase (624 and 671%) were obtained in hepatocytes after a 72-hr exposure to 0.1 mM ciprofibrate and 1.0 mM clofibric acid, respectively. In cultured hepatocytes, ciprofibrate was about 30-fold more active than clofibric acid for the stimulation of carnitine acetyltransferase, laurate hydroxylase and fatty acylCoA oxidase activities. Ciprofibrate was also more potent than clofibric acid as an inducer of the 60 and 80 kD proteins in hepatocytes. The maximal drug-induced increases in carnitine acetyltransferase activity were not additive, and the induction of carnitine acetyltransferase by ciprofibrate was blocked by addition (1 micrograms per ml) of cycloheximide or actinomycin D. Changes in protein and RNA synthesis preceded the drug-induced increases of carnitine acetyltransferase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.
The effects of lung surgery on respiratory function were investigated in 80 patients; 17 patients were submitted to left pneumonectomy (LPN); 11 patients were submitted to right pneumonectomy (RPN); 7 patients underwent a left upper lobectomy (LUL); 16 patients a left lower lobectomy (LLL); 17 patients were submitted to right upper lobectomy (RUL); 12 patients underwent right lower lobectomy (RLL). All patients were submitted to spirometry and arterial blood gas analysis. The effects of lung surgery on respiratory function depends upon the extent of the resected tissue.
Pulmonary function was studied in sixty patients with pleural effusion and seventy patients with fibrothorax. The patients with pleural effusion were divided into three groups according to the extent of the effusion. The patients were submitted to spirometry and arterial blood gas analysis. The effects of pleural effusion on pulmonary function is evaluated with regards to the size of effusion. Small-size pleural effusion little affects arterial oxygen tension. Pleural effusion and fibrothorax have a similar pattern of pulmonary function.
From July 1987 to December 1988, 19,625 children in Taiwan were measured for their body weights and heights. They were 9,564 boys and 10,061 girls and were seen either in a well baby clinic of a large community hospital or in the local kindergartens. We divided these children into 64 groups according to their sex and ages. The mean values and standard deviation of body weight and height were tried to correlate with those from children of school age reported for 1987 by the Ministry of Education. Furthermore, body weight and height growth curves were drawn for these children, aged from 1 month to 18 years.