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Articles by Y. H Chen
Total Records ( 5 ) for Y. H Chen
  T. J Fang , H. Y Li , R. E Gliklich , Y. H Chen , P. C Wang and H. F. Chuang

Objective  To analyze outcomes following fat injection laryngoplasty in patients with unilateral vocal cord paralysis.

Design  Longitudinal outcomes evaluation study.

Setting  Tertiary referral voice center.

Patients  Thirty-three consecutive patients with unilateral vocal cord paralysis undergoing autologous fat injection laryngoplasty with preoperative and serial postoperative follow-up at Chang Gung Memorial Hospital, Taipei, Taiwan.

Intervention  Autologous fat injection laryngoplasty.

Main Outcome Measures  Voice laboratory measurements, Voice Outcome Survey, and 36-item Short Form Health Survey.

Results  Except for the physical functioning dimension of global health, voice-related subjective outcomes and acoustic variables of the patients significantly improved after surgery (P < .05). Compared with population norms, the mean (SD) scores of patients were inferior on the 36-item Short Form Health Survey dimensions of physical functioning (80.7 [22.3] vs 90.2 [17.4]) and role functioning–physical problems (65.0 [36.2] vs 80.2 [36.2]). Overall, 88.9% (24 of 27) of the patients were satisfied with their surgery.

Conclusions  Fat injection laryngoplasty seems to be effective in enhancing acoustic and quality of life outcomes in patients with unilateral vocal cord paralysis. The effect is sustainable over 12 months.

  S. H Wang , S. J Lin , Y. H Chen , F. Y Lin , J. C Shih , C. C Wu , H. L Wu and Y. L. Chen

Objectives— The number of endothelial progenitor cells (EPCs) that can be obtained from adult bone marrow and peripheral blood to treat cardiovascular diseases is limited. The goal was to examine the endothelial potential of Wharton jelly in human umbilical cord (WJC)-derived stem cells and evaluate their potential to affect neointimal formation after vascular injury.

Methods and Results— Mesenchymal cells (MCs) were isolated from WJC and cultured in endothelial growth medium. Differentiation into late outgrowth endothelial cells (WJC-OECs) was demonstrated by incorporation of acetylated low-density lipoprotein and expression of the endothelial-specific markers. Transplantation of these cells into wire-injured femoral arteries in mice led to rapid reendothelialization. At 4 weeks after injury, the neointima/media area ratio was reduced and strong expression of pigment epithelium-derived factor (PEDF) compared to saline-or MC- or cord blood-OEC-treated mice. WJC-OECs-conditioned medium has an extremely strong capacity to inhibit the migration and proliferation of smooth muscle cells. The effects were inhibited by neutralizing antibody for PEDF and by siRNA silencing of PEDF.

Conclusions— We firstly demonstrated the presence of a cell population within WJC that has the potential to differentiate into OECs. Transplantation of WJC-OECs may play a crucial role in reestablishing endothelial integrity in injured vessels, thereby inhibiting neointimal hyperplasia. These findings have implications for a novel and practical cell-based therapy for vascular diseases.

  Y. H Chen , T. G Yandle , A. M Richards and S. C. Palmer

Background: The sources of secretion and clearance of plasma urotensin II (UII) in the human circulation remain uncertain and may be relevant to understanding the role of UII in human physiology and cardiovascular disease.

Methods: In 94 subjects undergoing clinically indicated cardiac catheterization, we collected blood samples from arterial and multiple venous sites to measure transorgan gradients of plasma UII immunoreactivity.

Results: Net UII release occurred (in descending order of proportional transorgan gradient) across the heart, kidney, head and neck, liver, lower limb, and pulmonary circulations (P < 0.01). Although no specific clearance site was localized, the absence of an overall subdiaphragmatic aorto-caval peptide gradient indicated that there were lower body segment sites of UII clearance as well as secretion. The proportional increase in UII immunoreactivity was significantly correlated across all sites of net peptide release within an individual (P ≤ 0.05). In univariate analyses, mixed venous UII concentrations were correlated with diagnosis of acute coronary syndrome and femoral artery oxygen tension and inversely with systolic blood pressure and body mass index. Diagnosis of acute coronary syndrome and body mass index were independent predictors of mixed venous UII immunoreactivity in multivariate analysis. No correlates of net cardiac UII release were identified.

Conclusions: UII is secreted from the heart and multiple other tissues into the circulation. Related increments in UII immunoreactivity across multiple tissue sites suggest that peptide release occurs via a shared mechanism. Increased UII immunoreactivity is observed in subjects with acute coronary syndrome.

  G Vlotides , Y. H Chen , T Eigler , S. G Ren and S. Melmed

To investigate paracrine regulation of pituitary cell growth, we tested fibroblast growth factor (FGF) regulation of TtT/GF folliculostellate (FS) cells. FGF-2, and FGF-4 markedly induced cell proliferation, evidenced by induction of pituitary tumor transforming gene-1 (Pttg1) mRNA expression and percentage of cells in S phase. Signaling for FGF-2-induced FS cell proliferation was explored by specific pharmacological inhibition. A potent inhibitory effect on FGF-2 action was observed by blocking of Src tyrosine kinase with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine (≥0.1 µm), followed by protein kinase C (PKC) inhibition with GF109203X. Treatment with FGF-2 (30 ng/ml; 10 min) activated phosphorylation of signal transducer and activator of transcription-3, ERK, stress-activated protein kinase/c-Jun N-terminal kinase, Akt, and focal adhesion kinase. Src inhibition with 4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d] pyrimidine suppressed FGF-2-induced Akt and focal adhesion kinase, indicating effects downstream of FGF-2-induced Src activation. FGF-2 also markedly induced its own mRNA expression, peaking at 2–4 h, and this effect was suppressed by Src tyrosine kinase inhibition. The PKC inhibitor GF109203X abolished FGF-2 autoinduction, indicating PKC as the primary pathway involved in FGF-2 autoregulation in these cells. In addition to pituitary FGF-2 paracrine activity on hormonally active cells, these results show an autofeedback mechanism for FGF-2 in non-hormone-secreting pituitary FS cells, inducing cell growth and its own gene expression, and mediated by Src/PKC signaling.

  T. M Yu , Y. H Chen , J. Y Hsu , C. S Sun , Y. W Chuang , C. H Chen , M. J Wu , C. H Cheng and K. H. Shu

Background. Pulmonary hypertension (PH) is an overlooked cardiovascular morbidity in patients undergoing haemodialysis. Inflammation has been demonstrated to play a significant role with certain types of PH in non-uraemic patients, but studies analysing the mechanisms in dialyzed patients with PH are rare. Hence, we investigated systemic and local inflammation biomarkers associated with PH in uraemia patients to elucidate the potential mechanism.

Methods. A cross-sectional study was conducted in which 97 haemodialysis patients were initially evaluated in our hospital. Twelve inflammatory cytokines were measured using a cytometric beads assay in patients with and without PH. FENO (fractional exhaled nitric oxide) was checked by a chemiluminescence analyser in patients with and without PH as well as by normal controls.

Results. Thirty-nine eligible patients were enrolled. Compared to patients without PH (group A), patients with PH (group B) had significantly higher serum levels of hs-CRP, IL-1β, TNF- and IL-6. FENO was also measured. Though the pre-dialysis FENO levels were elevated in both groups; group B patients had significantly higher pre-dialysis FENO levels than group A patients (39.9 ± 16.7 versus 31.8 ± 10.3, P = 0.045). The post-dialysis FENO levels returned to normal in group A while the remaining were significantly higher in group B (30.3 ± 10.3 versus 20.1 ± 10.9, P = 0.003).

Conclusions. Our study revealed that dialyzed patients with PH had a significantly higher level of airway FENO as well as serum levels of acute phase reactive protein and cytokines, including IL-1β, TNF- and IL-6. A chronic inflammation might play an important role in the pathogenesis of PH in patients undergoing haemodialysis.

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