Tso-Hsiao Chen

Wan Fang Hospital, T’ai-pei, Taipei, Taiwan

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Publications (49)142.6 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Heat stroke is a life-threatening condition characterized by an increased core body temperature (over 40°C) and a systemic inflammatory response, which may lead to a syndrome of multiple organ dysfunction. Heat stroke may be due to either strenuous exercise or non-exercise-induced exposure to a high environmental temperature. Current management of heat stroke is mostly supportive, with an emphasis on cooling the core body temperature and preventing the development of multiple organ dysfunction. Prognosis of heat stroke depends on the severity of organ involvement. Here, we report a rare case of non-exercise-induced heat stroke in a 73-year-old male patient who was suffering from acute liver failure after prolonged exposure in a hot sauna room. We successfully managed this patient by administering high-volume plasma exchange, and the patient recovered completely after treatment. J. Clin. Apheresis, 2014. © 2014 Wiley Periodicals, Inc.
    Journal of Clinical Apheresis 02/2014; · 2.27 Impact Factor
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    ABSTRACT: Epithelial-mesenchymal transition (EMT) occurs in stressed tubular epithelial cells, contributing to renal fibrosis. Initial mechanisms promoting EMT are unknown. Pressure force is an important mechanism contributing to the induction and progression of renal fibrogenesis in ureteric obstruction. In our study of cultured rat renal tubular cells (NRK-52E) under 60 mmHg of pressure, we found that the epithelial marker E-cadherin decreased and mesenchymal markers, e.g., α-smooth muscle actin, fibronectin and Snail, increased. Pressure also induced the expression of connective tissue growth factor and transforming growth factor-β. MicroRNA array assays showed that pressure reduced miR-328 at the initial stage of pressurization. We identified a potential target sequence of miR-328 in rat CD44 3'-untranslated regions. In contrast with the miR-328 expression, CD44 expression was up-regulated at the initial pressurization stage. We also found that miR-328 expression decreased and CD44 increased in ureteric obstruction kidneys in the animal study. CD44 siRNA transfection significantly increased E-cadherin expression and inhibited pressure-induced EMT. Both hyaluronan binding peptide pep-1 and osteopontin neutralizing antibody inhibited pressure-induced EMT. Our results suggest that miR-328-mediated CD44 transient upregulation is an important trigger of the pressure-induced EMT in renal fibrosis.
    PLoS ONE 01/2014; 9(6):e99802. · 3.73 Impact Factor
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    ABSTRACT: Objective In this study, a Hemodialysis Eating Index (HDEI) suitable for hemodialysis (HD) patients in Taiwan was developed based on the dietary recommendations of the U.S. National Kidney Foundation for HD patients and the Taiwanese 2011 Daily Food Guide. The HDEI was used to explore HD-associated cardiovascular disease (CVD) risk factors. Methods In this prospective study, 108 HD patients from 2 HD centers in Taiwan were recruited as participants in 2010. All participants were older than 20 years. Patient CVD risk factor and 3-day dietary data were collected, and their HDEI scores were calculated. The HDEI scores comprise 12 food-related factors: the consumption of vegetables, fruits, total grains, whole grains, high-protein foods, high biological values, red and white meat, fish, oils, saturated fatty acids or trans fatty acids, nuts, and the duration of multivitamin use. The scores ranged from 5 to 100, and SAS software version 9.3 was used to perform statistical analyses. A P value less than .05 was considered statistically significant. Results The HDEI scores and serum albumin (Alb) levels were significantly and positively correlated. The participants were divided into 2 groups on the basis of the median HDEI score of 72.2. Two months after HDEI evaluation, the high-HDEI scoring group exhibited significantly decreased levels of serum total cholesterol and increased hemoglobin (Hb) levels. Conclusion The HDEI can be used to reflect selected nutritional status markers, such as Alb and Hb levels and CVD risk factors, for HD patients. The HDEI can also serve as an eating index for HD patients in Taiwan to facilitate CVD prevention.
    Journal of Renal Nutrition 01/2014; · 1.75 Impact Factor
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    ABSTRACT: Urotensin II (U-II), an 11-amino acid peptide, exerts a wide range of actions in cardiovascular systems. Interleukin-8 (IL-8) is secreted by endothelial cells, thereby enhancing endothelial cell survival, proliferation, and angiogenesis. However, the interrelationship between U-II and IL-8 as well as the detailed intracellular mechanism of U-II in vascular endothelial cells remain unclear. The aim of this study was to investigate the effect of U-II on IL-8 expression and to explore its intracellular mechanism in human umbilical vein endothelial cells. Primary human umbilical vein endothelial cells were used. Expression of IL-8 was determined by real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, and luciferase reporter assay. Western blot analyses and experiments with specific inhibitors were performed to reveal the downstream signaling pathways as concerned. U-II increased the mRNA/protein levels of IL-8 in human umbilical vein endothelial cells. The U-II effects were significantly inhibited by its receptor antagonist [Orn(5)]-URP. Western blot analyses and experiments with specific inhibitors indicated the involvement of phosphorylation of p38 mitogen-activated protein kinase and extracellular signal-regulated kinase in U-II-induced IL-8 expression. Luciferase reporter assay further revealed that U-II induces the transcriptional activity of IL-8. The site-directed mutagenesis indicated that the mutation of AP-1 and NF-kB binding sites reduced U-II-increased IL-8 promoter activities. Proliferation of human umbilical vein endothelial cells induced by U-II could be inhibited significantly by IL-8 RNA interference. The results show that U-II induces IL-8 expression in human umbilical vein endothelial cells via p38 mitogen-activated protein kinase and extracellular signal-regulated kinase signaling pathways and IL-8 is involved in the U-II-induced proliferation of human umbilical vein endothelial cells.
    PLoS ONE 01/2014; 9(2):e90278. · 3.73 Impact Factor
  • Kidney International 12/2013; 84(6):1291-2. · 8.52 Impact Factor
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    ABSTRACT: An 85-year-old female presented with fever and consciousness disturbance for 3 days. The patient's blood culture subsequently revealed persistent methicillin-resistant Staphylococcus aureus (MRSA) bacteremia despite the administration of vancomycin or teicoplanin monotherapy. Gallium inflammation scan and magnetic resonance image of the spine disclosed osteomyelitis and discitis at the level of L4-5. Surgical debridement was not feasible in this debilitated patient. Because of the creeping minimal inhibitory concentration of vancomycin of the causative isolate (1.5 μg/mL) and clinical failure with glycopeptide monotherapy, we changed the antibiotic therapy to a fosfomycin and teicoplanin combination therapy. The patient showed improved clinical response in terms of her enhanced consciousness as well as subsidence of persisted bacteremia. Despite the potential side effects of fosfomycin (such as diarrhea and hypernatremia), it combined with a glycopeptide may be an alternative therapy for invasive refractory MRSA infections.
    Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi 11/2013; · 1.63 Impact Factor
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    ABSTRACT: Zhibai Dihuang Wan (ZDW) is an ancient traditional Chinese medicine composed of eight herbal ingredients and has been used to treat chronic kidney inflammation and diabetes for thousands of years. Nonetheless, the influence of ZDW on acute kidney injury is still unknown. We intended to identify the influence of ZDW on cell growth and gentamicin-induced apoptotic injury in renal tubular cells. We extracted ZDW with artificial intestinal fluid and treated rat renal tubular cells (NRK-52E) with various concentrations of the ZDW extraction. Cell proliferation and gentamicin-induced apoptosis of NRK-52E cells were evaluated using real-time proliferation monitoring and annexin V staining, respectively. Western blotting was used to evaluate the levels of Bcl-2 and caspase-3 expression. The effect of ZDW on gentamicin-induced kidney injury was also monitored in mice using the terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) assay, and the measurement of serum creatinine and blood urea nitrogen. We found that 30μg/ml of ZDW promoted cell proliferation of the rat renal tubular cells. ZDW also expressed a dose-dependent protective effect against gentamicin-induced apoptosis in the cells. Pretreatment with 3μg/ml or 30μg/ml of ZDW maximally increased Bcl-2 and decreased cleaved caspase-3 in the gentamicin-treated NRK-52E cells. Among the herbal ingredients of ZDW, only Phellodendron amurense Rupr., bark (Cortex Phellodendri), and Anemarrhena asphodeloides Bunge, rhizome inhibited both the gentamicin-induced Bcl-2 decrease and cleaved caspase-3 increase. Phellodendron amurense Rupr., bark and Anemarrhena asphodeloides Bunge, rhizome also inhibited gentamicin-induced apoptosis at particular concentrations; however, these two ingredients were less effective than ZDW. In the mouse model of gentamicin-induced nephropathy, the ZDW treatment significantly reduced apoptotic cells in the renal cortex and improved renal function. Our results suggest that ZDW at adequate doses attenuates gentamicin-induced apoptotic injury in renal tubular cells and also protects kidneys from gentamicin-induced injury in mice.
    Journal of ethnopharmacology 11/2013; · 2.32 Impact Factor
  • Chung-Te Liu, Tso-Hsiao Chen, Chung-Yi Cheng
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    ABSTRACT: We report two patients with drug-induced liver injury (DILI)-related acute liver failure (ALF) who were successfully treated with high-volume plasma exchange without liver transplantation. The first patient was a 66-year-old man admitted because of a perforated duodenal ulcer complicated with peritonitis and septic shock. After treatment with multiple antibiotics, the patient developed DILI and ALF. Grade 3 hepatic encephalopathy and profound jaundice were present. Symptoms and signs of ALF improved dramatically after initiation of plasma exchange. The patient was discharged uneventfully. The second patient was a 94-year-old man admitted for treatment of newly diagnosed pulmonary tuberculosis. DILI and ALF developed 5 days after initiation of anti-tuberculosis treatment. Grade 4 hepatic encephalopathy was present. After plasma exchange, the patient's level of consciousness improved dramatically, and he recovered from ALF. These 2 cases show the potential of plasma exchange in the treatment of DILI despite occurrence acute liver failure. J. Clin. Apheresis, 2013. © 2013 Wiley Periodicals, Inc.
    Journal of Clinical Apheresis 08/2013; · 2.27 Impact Factor
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    ABSTRACT: Urotensin II (UII) is a cyclic vasoactive peptide which is mainly expressed in kidneys. Although elevated plasma UII levels are associated with renal impairment, the influence of UII on renal injury is unclear. In this study, we monitored the influence of UII on gentamicin-induced apoptosis in rat tubular cells (NRK-52E). We found that UII significantly reduced gentamicin-induced apoptosis and apoptotic signals. Blocking endogenous UII secretion caused cells to be more susceptible to gentamicin. In gentamicin-treated mice, UII also expressed protective effect on renal tubular cells. UII was also found to induce prostacyclin (PGI2) production, which caused peroxisomal proliferator-activated receptor α (PPARα) activation as revealed by both PGI2 synthase siRNA transfection and piroxicam treatment. Blockage of PPARα by siRNA transfection inhibited UII-induced Akt phosphorylation and the antiapoptotic effect of UII. Our results suggest that UII can protect renal tubular cells from gentamicin-induced apoptosis through PGI2-mediated PPARα and Akt activation.
    Molecular and Cellular Endocrinology 08/2013; · 4.04 Impact Factor
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    ABSTRACT: AIMS: Heart failure is among the most frequent complications of patients on long-term haemodialysis. The benefits of renin-angiotensin system (RAS) blockade on the outcomes of these patients have yet to be determined. METHODS AND RESULTS: We conducted a nationwide observational study using data from the Taiwan National Health Insurance claims database, between 1999 and 2010. We enrolled patients aged ≥35 years with new-onset heart failure [diagnosed by International Classification of Diseases, 9th revision, clinical modification (ICD-9-CM) codes] under treatment with medications. New users of a RAS blocker (RASB; i.e. an ACE inhibitor or an ARB used as monotherapy or dual therapy) were selected to compare with non-RASB users. We used Cox proportional hazards regression with and without propensity score adjustment to compare the risk of 3-year all-cause and cardiovascular mortality. Stratified analyses and RASB therapy duration as a time-dependent covariate were also performed. In all, 4771 were treated with an RASB (n = 3024) or without an RASB (n = 1747). RASB users had a higher prevalence of hypertension and diabetes, and a higher number of hospitalization. Among RASB users, 1148 deaths (38.0%) occurred during 5272 person-years of follow-up compared with 734 deaths (42.0%) among non-RASB users during 2683 person-years of follow-up. Three-year mortality rates were 45.4% and 49.1% for patients receiving and those not receiving an RASB, respectively (log-rank test, P < 0.001). Adjusted hazard analysis revealed that RASB therapeutic effects remained significant on all-cause [hazard ratio (HR) 0.8; 95% confidence interval (CI) 0.72-0.89; P < 0.001] and cardiovascular mortality (HR 0.76; 95% CI 0.64-0.90; P < 0.01). CONCLUSIONS: RASB therapy reduced all-cause and cardiovascular mortality in heart failure patients on long-term haemodialysis.
    European Journal of Heart Failure 05/2013; · 5.25 Impact Factor
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    ABSTRACT: End-stage renal disease represents a risk complex that complicates surgical results. The surgical outcomes of dialysis patients have been studied in specific fields, but the global features of postoperative adverse outcomes in dialysis patients receiving non-cardiac surgeries have not been examined. Taiwan's National Health Insurance Research Database was used to study 8,937 patients under regular dialysis with 8,937 propensity-score matched-pair controls receiving non-cardiac surgery between 2004 and 2007. We investigated the influence of hemodialysis and peritoneal dialysis, effects of hypertension and diabetes, and impact of additional comorbidities on postoperative adverse outcomes. Postoperative mortality in dialysis patients was higher than in controls (odds ratio [OR] 3.33, 95% confidence interval [CI] 2.56 to 4.33) when receiving non-cardiac surgeries. Complications such as acute myocardial infarction, pneumonia, bleeding, and septicemia were significantly increased. Postoperative mortality was significantly increased among peritoneal dialysis patients (OR 2.71, 95% CI 1.70 to 4.31) and hemodialysis patients (OR 3.42, 95% CI 2.62 to 4.47) than in controls. Dialysis patients with both hypertension and diabetes had the highest risk of postoperative complications; these risks increased with number of preoperative medical conditions. Patients under dialysis also showed significantly increased length of hospitalization, more ICU stays and higher medical expenditures. Surgical patients under dialysis encountered significantly higher postoperative complications and mortality than controls when receiving non-cardiac surgeries. Different dialysis techniques, pre-existing hypertension/diabetes, and various comorbidities had complication-specific impacts on surgical adverse outcomes. These findings can help surgical teams provide better risk assessment and postoperative care for dialysis patients.
    PLoS ONE 01/2013; 8(3):e58942. · 3.73 Impact Factor
  • Journal of Experimental & Clinical Medicine. 01/2013; 5(5):196–197.
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    ABSTRACT: Statins are reported to alleviate renal fibrosis in animal models with ureteral obstruction. However, the molecular mechanism of this antifibrotic effect is still unclear. Pressure force is an important mechanism contributing to induction and progression of tubulointerstitial fibrogenesis in ureteric obstruction. In this study, we investigated the influence of rosuvastatin on pressure-induced fibrotic responses in rat renal tubular cells (NRK-52E). We established an in vitro pressure culture system to study pressure-induced fibrotic responses in NRK-52E cells. When NRK-52E cells were cultured in the pressure culture system, 60mmHg of pressure induced the expression of connective tissue growth factor (CTGF), transforming growth factor (TGF)-β, fibronectin, Smad3, and phospho-Smad3. Rosuvastatin significantly reduced these pressure-induced fibrotic responses at concentrations above 10μM. Rosuvastatin also reduced the TGF-β-induced expression of fibronectin and CTGF in NRK-52E cells. Pretreatment with rosuvastatin significantly induced prostacyclin (PGI(2)) generation, but reduced pressure-induced prostaglandin E(2) (PGE(2)). PGI(2) synthase small interfering RNA (siRNA) transfection significantly inhibited rosuvastatin-induced peroxisome proliferator-activated receptor α activation. The blockage of peroxisome proliferator-activated receptor α by siRNA transfection reduced the inhibitory effect of rosuvastatin on pressure-induced fibrotic responses. N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide (NS398), a specific inhibitor of cyclooxygenase-2, diminished pressure-induced PGE(2) generation, and also reduced pressure-induced fibrotic responses. Additionally, PGE(2) decreased the antifibrotic effect of rosuvastatin. In conclusion, rosuvastatin reduces pressure-induced fibrotic responses in renal tubular cells by enhancing the PGI(2)- peroxisome proliferator-activated receptor α pathway and reducing PGE(2) generation.
    European journal of pharmacology 12/2012; · 2.59 Impact Factor
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    ABSTRACT: A 94-year-old female with end-stage renal disease presents with fever, fatigue, and hematochezia. She had previously resided in Hunan Province, China, and Myanmar, and she immigrated to Taiwan 30 years ago. Colonoscopy revealed a colonic ulcer. Biopsy of the colonic ulcer showed ulceration of the colonic mucosa, and many Paragonimus westermani-like eggs were noted. Serum IgG antibody levels showed strong reactivity with P. westermani excretory-secretory antigens by ELISA. Intestinal paragonimiasis was thus diagnosed according to the morphology of the eggs and serologic finding. After treatment with praziquantel, hematochezia resolved. The present case illustrates the extreme manifestations encountered in severe intestinal paragonimiasis.
    The Korean Journal of Parasitology 12/2012; 50(4):349-52. · 0.88 Impact Factor
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    ABSTRACT: Background Sitagliptin, a dipeptidyl peptidase-IV inhibitor, is widely used as an oral hypoglycemic agent. It may induce hemodynamic effects when interacting with angiotensin II receptor blockers. Methods The study was conducted in an outpatient setting at Taipei Medical University Hospital. Diabetic patients who had already received angiotensin II receptor blockers for more than 6 months and then had add-on sitagliptin for another 6 months were enrolled. The blood pressures and serum creatinine levels during the 6-month period before and after onset of concomitant use of the two agents were obtained by chart reviewing. Results Elevation of serum creatinine levels and reduction of estimated glomerular filtration rates were present after the addition of sitagliptin (p < 0.05). Moreover, a trend of reduction in diastolic blood pressure was also noted. Patients with chronic kidney disease and coronary artery disease were prone to have decreased diastolic blood pressures after combined use of valsartan and sitagliptin. Patients with chronic kidney disease alone were prone to have elevation of serum creatinine levels after combined treatment of valsartan and sitagliptin. Conclusion The addition of sitagliptin produced a trend of blood pressure lowering effects and decreased the glomerular filtration rate and HbA1c in diabetic patients using an angiotensin II receptor blocker, especially in those with chronic kidney disease.
    Journal of Experimental & Clinical Medicine. 12/2012; 4(6):334–337.
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    ABSTRACT: Klotho was identified as the responsible gene in a mutant mouse line whose disruption results in a variety of premature aging-related phenotypes. Nonetheless, the related mechanisms were still unknown. Many studies report that dietary phosphate restriction and genetic ablation of vitamin D pathways indirectly reverse premature aging processes in these mice. Furthermore, transgenic overexpression of klotho in mice extends their life span through inhibition of insulin and IGF1 signaling. We found that intraperitoneal injection of recombinant soluble Klotho protein at dose of 0.02mg/kg every other day effectively extends the life span of kl/kl mice by 17.4%. Soluble Klotho administration also ameliorated premature aging-related phenotype, such as growth retardation, premature thymus involution and vascular calcification, and effectively enhanced urinary phosphate excretion in kl/kl mice. Klotho treatment attenuated renal fibrosis through down-regulation of transforming growth factor-β signaling as well as reduced cellular senescence through down-regulation of p21-cip1 mRNA levels. In addition, soluble Klotho treatment significantly reduced both renal and aorta calcium deposits. In conclusion, our study shows the therapeutic potential of soluble Klotho protein to treat age-related disorders in mice.
    European journal of pharmacology 10/2012; · 2.59 Impact Factor
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    ABSTRACT: Adipokine leptin reportedly acts on the kidney in pathophysiological states. However, the influence of leptin on renal tubular epithelial cells is still unclear. Gentamicin, a widely used antibiotic for the treatment of bacterial infection, can cause nephrotoxicity. This study aims to investigate the influence of long-term leptin treatment on gentamicin-induced apoptosis in rat renal tubular cells (NRK-52E) and mice. We monitored apoptosis and molecular mechanisms using annexin V/ propidium iodide staining and small interfering RNA transfection. In NRK-52E cells, leptin reduced gentamicin-induced apoptosis at 24h, but significantly increased apoptosis at 48 h. Long-term treatment of leptin decreased Bcl-x(L) expression and increased caspase activity in gentamicin-treated NRK-52E cells. Leptin also increased the expression of cyclooxygenase-2 (COX-2) and its product, prostaglandin E(2) (PGE(2)), in a dose-dependent manner. The COX-2 inhibitor, NS398 (N-[2-(Cyclohexyloxy)-4- nitrophenyl]methanesulfonamide), blocked PGE(2) augmentation and the pro-apoptotic effects of leptin. The addition of PGE(2) recovered the pro-apoptotic effect of leptin in NS398-treated NRK-52E cells. In a mouse animal model, a 10 day leptin treatment significantly increased gentamicin-induced apoptotic cells in proximal tubules. NS398 treatment inhibited this in vivo pro-apoptotic effect of leptin. Results reveal that long-term elevation of leptin induces COX-2-mediated PGE(2) augmentation in renal tubular cells, and then increases these cells' susceptibility to gentamicin-induced apoptosis.
    European journal of pharmacology 06/2012; 689(1-3):65-71. · 2.59 Impact Factor
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    ABSTRACT: Necrotizing fasciitis is a lethal soft tissue infection for its rapid progression to septic shock. We present a 59-year-old male on chronic hemodialysis (HD). We made the diagnosis of necrotizing fasciitis of the right thigh due to the crepitus from physical examination and subcutaneous emphysema from an X film. He was successfully treated with antibiotics and surgical debridement. The blood and surgical drainage cultures showed Escherichia coli, which is less commonly seen in cutaneous infection. The colonoscopic finding revealed adenomatous polyps. Necrotizing fasciitis in patients on HD requires early diagnosis and aggressive treatment to ensure the favorable clinical outcomes.
    Hemodialysis International 02/2012; · 1.44 Impact Factor
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    ABSTRACT: Many studies suggest that far-infrared (FIR) therapy can reduce the frequency of some vascular-related diseases. The non-thermal effect of FIR was recently found to play a role in the long-term protective effect on vascular function, but its molecular mechanism is still unknown. In the present study, we evaluated the biological effect of FIR on vascular endothelial growth factor (VEGF)-induced proliferation in human umbilical vein endothelial cells (HUVECs). We found that FIR ranging 3∼10 µm significantly inhibited VEGF-induced proliferation in HUVECs. According to intensity and time course analyses, the inhibitory effect of FIR peaked at an effective intensity of 0.13 mW/cm(2) at 30 min. On the other hand, a thermal effect did not inhibit VEGF-induced proliferation in HUVECs. FIR exposure also inhibited the VEGF-induced phosphorylation of extracellular signal-regulated kinases in HUVECs. FIR exposure further induced the phosphorylation of endothelial nitric oxide (NO) synthase (eNOS) and NO generation in VEGF-treated HUVECs. Both VEGF-induced NO and reactive oxygen species generation was involved in the inhibitory effect of FIR. Nitrotyrosine formation significantly increased in HUVECs treated with VEGF and FIR together. Inhibition of phosphoinositide 3-kinase (PI3K) by wortmannin abolished the FIR-induced phosphorylation of eNOS and Akt in HUVECs. FIR exposure upregulated the expression of PI3K p85 at the transcriptional level. We further found that FIR exposure induced the nuclear translocation of promyelocytic leukemia zinc finger protein (PLZF) in HUVECs. This induction was independent of a thermal effect. The small interfering RNA transfection of PLZF blocked FIR-increased PI3K levels and the inhibitory effect of FIR. These data suggest that FIR induces the nuclear translocation of PLZF which inhibits VEGF-induced proliferation in HUVECs.
    PLoS ONE 01/2012; 7(1):e30674. · 3.73 Impact Factor
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    ABSTRACT: Vancomycin and teicoplanin are the two most used glycopeptides for the treatment of methicillin-resistant Staphylococcus aureus (MRSA). Vancomycin is suspected to have more nephrotoxicity but this has not been clearly established. The aim of this study was to assess its nephrotoxicity by a consensus definition of acute kidney injury (AKI): the risk (R), injury (I), failure (F), loss and end-stage renal disease (RIFLE) classification. Patients with MRSA bacteraemia who were prescribed either vancomycin or teicoplanin between 2003 and 2008 were classified. Patients who developed AKI were classified by RIFLE criteria. Variables such as comorbidities, laboratory data and medical cost information were also obtained from the database. Outcomes determined were: (i) the rate of nephrotoxicity and mortality; and (ii) the association of nephrotoxicity with the length of hospital stay and costs. The study included 190 patients (vancomycin 33, teicoplanin 157). Fifteen patients on vancomycin and 27 patients on teicoplanin developed AKI (P = 0.0004). In the vancomycin group, four, eight and three patients were classified to RIFLE criteria R, I and F, respectively. In the teicoplanin group, 17, nine and one patient were classified to RIFLE criteria R, I and F, respectively. Kaplan-Meier analysis showed significant difference in time to nephrotoxicity for the vancomycin group compared to the teicoplanin group. No significant differences were found between the groups in terms of total mortality, length of hospital stay and costs. The study data suggest that vancomycin is associated with a higher likelihood of nephrotoxicity using the RIFLE classification.
    Nephrology 06/2011; 16(8):697-703. · 1.69 Impact Factor