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Articles by Y. T Shih
Total Records ( 2 ) for Y. T Shih
  W. C Lin , C. H Lu , Y. C Lee , H. C Wang , C. C Lui , Y. F Cheng , H. W Chang , Y. T Shih and C. P. Lin

BACKGROUND AND PURPOSE: White matter (WM) injury in carbon monoxide (CO) intoxication is thought to be related to delayed cognitive sequelae. To determine if microstructural changes in WM are responsible for the delayed onset of cognitive symptoms, we performed diffusion tensor imaging (DTI) in patients with CO intoxication.

MATERIALS AND METHODS: DTI was performed in 14 patients with delayed sequelae after CO intoxication and in 16 sex- and age-matched healthy volunteers. The fractional anisotropy (FA) and apparent diffusion coefficient (ADC) of several WM regions were measured. We also determined the correlation between FA of the selected WM and neuropsychological rating scores for the CO intoxication group.

RESULTS: FA of patients with CO intoxication decreased in the corpus callosum, orbitofrontal WM, high frontal WM, parietal WM, and temporal lobes in comparison with the corresponding regions of healthy controls. FA of the WM in the occipital lobe and internal capsule of patients was not significantly different from that in controls. ADCs of all measured WM increased significantly in patients exposed to CO. High correlations were found between the FA of all selected WM and the Mini-Mental State Examination score ( = 0.631, P = .016) and the digit span backward task ( = 0.759, P = .001).

CONCLUSIONS: CO intoxication may cause FA decline in associated cortical areas. This observation indicates microstructural WM pathology in CO intoxication, which is related to delayed cognitive encephalopathy.

  M. C Tsai , L Chen , J Zhou , Z Tang , T. F Hsu , Y Wang , Y. T Shih , H. H Peng , N Wang , Y Guan , S Chien and J. J. Chiu

Rationale: Phenotypic modulation of smooth muscle cells (SMCs), which are located in close proximity to endothelial cells (ECs), is critical in regulating vascular function. The role of flow-induced shear stress in the modulation of SMC phenotype has not been well defined.

Objective: The objective was to elucidate the role of shear stress on ECs in modulating SMC phenotype and its underlying mechanism.

Methods and Results: Application of shear stress (12 dyn/cm2) to ECs cocultured with SMCs modulated SMC phenotype from synthetic to contractile state, with upregulation of contractile markers, downregulation of proinflammatory genes, and decreased percentage of cells in the synthetic phase. Treating SMCs with media from sheared ECs induced peroxisome proliferator-activated receptor (PPAR)-, -, and - ligand binding activities; transfecting SMCs with specific small interfering (si)RNAs of PPAR- and -, but not -, inhibited shear induction of contractile markers. ECs exposed to shear stress released prostacyclin (PGI2). Transfecting ECs with PGI2 synthase-specific siRNA inhibited shear-induced activation of PPAR-/, upregulation of contractile markers, downregulation of proinflammatory genes, and decrease in percentage of SMCs in synthetic phase. Mice with PPAR- deficiency (compared with control littermates) showed altered SMC phenotype toward a synthetic state, with increased arterial contractility in response to angiotensin II.

Conclusions: These results indicate that laminar shear stress induces synthetic-to-contractile phenotypic modulation in SMCs through the activation of PPAR-/ by the EC-released PGI2. Our findings provide insights into the mechanisms underlying the EC-SMC interplays and the protective homeostatic function of laminar shear stress in modulating SMC phenotype.

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