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Biomedical subjects

M C Kao

Publications and source records attributed to M C Kao.

At least 19 recordsLinked to original sources
PubMed2004

Prediction of the distance from skin to epidural space for low-thoracic epidural catheter insertion by computed tomography.

BACKGROUND: It may be clinically useful to predict the depth of the epidural space. METHODS: To investigate the accuracy of preoperative abdominal computed tomography (CT) in prediction of the distance for low-thoracic epidural insertion, a single group observational study was conducted in 30 male patients undergoing elective major abdominal surgery requiring epidural analgesia for postoperative pain relief. Using the paramedian approach, low-thoracic epidural insertion at T10-11 interspace was performed with a standardized procedure to obtain an actual insertion length (AIL). According to the principles of trigonometry, an estimated insertion length (EIL) was calculated as 1.26 times the distance from skin to epidural space measured from the preoperative abdominal CT. RESULTS: The mean (SD) EIL and AIL were 5.5 (0.7) and 5.1 (0.6) cm, respectively, with a significant correlation (r=0.899, P<0.01). The EIL tended to have a higher value than the AIL (0.4 (0.3) cm). There were significant correlations of both EIL and AIL with weight (P<0.01), BMI (P<0.01), and body fat percentage (P<0.01), but not with height (P>0.05). CONCLUSIONS: We conclude that the preoperative abdominal CT is helpful in prediction of the distance for low-thoracic epidural insertion using the paramedian approach.

Abdomen↗
PubMed2002

Sympathectomy.

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Foot↗
PubMed2001

Modulation of NO and cytokines in microglial cells by Cu/Zn-superoxide dismutase.

The activation of microglial cells in response to neuropathological stimuli is one of the prominent features of human neurodegenerative diseases. Cytokines such as IL-1 beta and TNF-alpha and inflammation-related enzymes such as inducible nitric oxide synthase are usually induced during the activation of microglial cells. We investigated the modulation of the activation of microglial cell by transfecting a Cu/Zn-SOD cDNA into BV-2 cells. Parental and transfected BV-2 cells were then subjected to LPS stimulation. The results showed that in Cu/Zn-SOD-transfected BV-2 cells, the expression and activity of Cu/Zn-SOD increased. On the other hand, upon activation by LPS, these cells produced less NO, IL-1 beta, and TNF-alpha than the parental microglial cells. This finding suggests that superoxide may be an early signal triggering the induction of cytokines and that the transfected Cu/Zn-SOD may provide a neuroprotective function via suppression of microglial activation. In addition, this approach may provide a rationale for the development of treatments for neurodegenerative diseases.

Animals↗
PubMed2001

NADH dehydrogenases: from basic science to biomedicine.

This review article is concerned with two on-going research projects in our laboratory, both of which are related to the study of the NADH dehydrogenase enzyme complexes in the respiratory chain. The goal of the first project is to decipher the structure and mechanism of action of the proton-translocating NADH-quinone oxidoreductase (NDH-1) from two bacteria, Paracoccus denitrificans and Thermus thermophilus HB-8. These microorganisms are of particular interest because of the close resemblance of the former (P. denitrificans) to a mammalian mitochondria, and because of the thermostability of the enzymes of the latter (T. thermophilus). The NDH-1 enzyme complex of these and other bacteria is composed of 13 to 14 unlike subunits and has a relatively simple structure relative to the mitochondrial proton-translocating NADH-quinone oxidoreductase (complex I), which is composed of at least 42 different subunits. Therefore, the bacterial NDH-I is believed to be a useful model for studying the mitochondrial complex I, which is understood to have the most intricate structure of all the membrane-associated enzyme complexes. Recently, the study of the NADH dehydrogenase complex has taken on new urgency as a result of reports that complex I defects are involved in many human mitochondrial diseases. Thus the goal of the second project is to develop possible gene therapies for mitochondrial diseases caused by complex I defects. This project involves attempting to repair complex I defects in the mammalian system using Saccharomyces cerevisiae NDI1 genes, which code for the internal, rotenone-insensitive NADH-quinone oxidoreductase. In this review, we will discuss our progress and the data generated by these two projects to date. In addition, background information and the significance of various approaches employed to pursue these research objectives will be described.

Animals↗
PubMed2000

Heat shock modulates prion protein expression in human NT-2 cells.

The pathological hallmarks of Prion disease are cortical spongiform changes and neuronal loss, which are induced by the accumulation of the scrapie-isoform prion protein (PrP(Sc)). PrP(Sc) is derived from a post-translational modification of the cellular form of prion protein (PrP(C)). Heat-shock proteins, a group of molecular chaperones, are involved in the degradation of denatured proteins and post-translational folding of newly synthesized polypeptides. In an attempt to examine any possible relationship between heat shock stress and an induction of prion protein (PrP), human NT-2 cells were treated with heat shock at 42 degrees C for 30 min. After heat-shock treatment, both the level of mRNA and PrP(C) protein were analyzed at various time points by Northern and Western blot, respectively. There was a 1.5- to 2.5-fold increase in PrP mRNA levels 1 and 3h following heat shock. In addition, a two-fold increase in protein level of PrP was found 3 h after heat-shock treatment. These results suggest that cellular stress induces the elevation of both PrP mRNA and protein synthesis. The up-regulation of prion-protein mRNA and protein, implies that PrP may play a role in cellular stress.

Gene Expression Regulation↗
PubMed2000

Creutzfeldt-Jakob disease: heat shock protein 70 mRNA levels in mononuclear blood cells and clinical study.

Prion diseases such as Creutzfeldt-Jakob disease (CJD) are associated in most cases with the accumulation of an unusual isoform of prion protein (PrPSC). PrPSC is derived from the abnormal folding of the cellular isoform of prion protein (PrPC). On the other hand, heat shock protein is known to ensure proper protein assembly and folding and to facilitate proteolytic digestion of abnormal or denatured proteins. Many studies have therefore hypothesized that heat shock protein is linked to prion disease. We examined the relationship between heat shock protein HSP70 and prion disease in CJD patients. HSP70 mRNA levels in mononuclear blood cells (MBCs) were compared in 14 CJD patients (10 confirmed by histo-pathological study), 12 vascular dementia (VD) patients, 16 patients with Parkinson's disease and dementia (PD) and 14 nondemented control subjects. The possible correlation between HSP70 mRNA expression levels and clinical findings was also evaluated. HSP70 mRNA expression levels in MBCs were measured by northern blotting. HSP70 mRNA levels in MBCs from patients with CJD were significantly higher than those from patients with VD or PD and in nondemented controls. Age at symptom onset, dementia severity, disease duration and neuroimaging grade of CJD patients were not correlated with relative HSP70 mRNA levels. No significant relationship between HSP70 mRNA levels and ageing was found. These results suggest that measurement of HSP70 mRNA in MBCs might provide an auxiliary tool for the diagnosis of CJD.

Aged↗