You-Lin Tain

Chang Gung University, Taoyuan, Taiwan, Taiwan

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Publications (47)123.77 Total impact

  • Article: Sex Differences of Oxidative Stress to Cholestatic Liver and Kidney Injury in Young Rats.
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    ABSTRACT: BACKGROUND: Sexual dimorphism plays a role in the liver and in renal injuries. However, whether sex is a risk factor in bile duct ligation (BDL) in young rats has never been examined. METHODS: Six male and six female rats treated with BDL were sacrificed 2 weeks after surgery and were designated as BDL-M and BDL-F groups. The other six male and six female rats that received sham ligation were designated as sham-M and sham-F groups. Plasma biochemistry and liver and kidney asymmetric dimethylarginine (ADMA)-related molecules were examined. RESULTS: Both BDL-M and BDL-F groups had elevated plasma aspartate transaminase (AST), alanine transaminase (ALT), bilirubin, and transforming growth factor-β1 levels. The BDL-F group had lower plasma AST and ALT levels than the BDL-M group. The BDL-M and BDL-F groups had elevated plasma ADMA levels. The cationic amino acid transporter 1 (CAT1) level was increased in the BDL-F group as compared to the sham-F group, whereas the CAT2 level was reduced in the both BDL-M and BDL-F groups. CONCLUSION: We found that young male rats were prone to higher degrees of biochemical liver and kidney injury to cholestasis. Sex differences in modulation of oxidative stress markers, such as ADMA, may play a role. Our results support careful monitoring and optimal treatment of cholestatic disease, especially in young male patients.
    Pediatrics & Neonatology 04/2013; 54(2):95-101. · 0.75 Impact Factor
  • Article: Melatonin regulates L-arginine transport and NADPH oxidase in young rats with bile-duct ligation: role of protein kinase C.
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    ABSTRACT: Background:Bile duct ligation (BDL) is a commonly used cholestatic liver disease model. We recently found that L-arginine levels were significantly raised by melatonin in young rats with BDL. We hypothesized thatPKC-α is involved in the increases of L-arginine in melatonin-treated BDL rats. Additionally, we tested whether melatonin prevents NADPH oxidase-induced ROS production is through PKC in rats with BDL.Methods:Four groups of young male rats were studied, shams (N = 6), untreated BDL rats (N = 9), melatonin-treated shams (N=6, M), and melatonin-treated BDL rats (N = 6, BDL + M). Melatonin-treated rats received daily melatonin 1 mg/kg/day via intraperitoneal injection. All surviving rats were killed 14 days after surgery.Results:Melatonin prevented BDL-induced mortality and kidney injury. Melatonin additionally increases L-arginine concentrations in BDL liver, which is correlated with decreased PKC-α translocation. Next, melatonin increases L-arginine levels in BDL kidneys, which is correlated with decreased renal level of arginase II. In the BDL kidney, melatonin decreases PKC-β translocation, reduces p47phox translocation, and diminishes NADPH-dependent superoxide production.Conclusion:Melatonin inhibits PKC-α to increase CAT-1-mediated L-arginine uptake in BDL liver, while it inhibits PKC-β to reduce NADPH-dependent superoxide production.Pediatric Research (2013); doi:10.1038/pr.2012.203.
    Pediatric Research 01/2013; · 2.70 Impact Factor
  • Article: Asymmetric dimethylarginine is associated with developmental programming of adult kidney disease and hypertension in offspring of streptozotocin-treated mothers.
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    ABSTRACT: Diabetes mellitus complicates pregnancies, leading to diseases in adult life in the offspring. Asymmetric dimethylarginine (ADMA) is increased in diabetes mellitus, kidney disease, and hypertension. We tested whether maternal diabetes causes increased ADMA in rats, resulting in kidney disease and hypertension in the adult offspring, and whether these can be prevented by maternal citrulline supplementation. Newborn female and pregnant Sprague-Dawley rats were injected with streptozotocin (STZ), which made up the nSTZ and STZ models, respectively. For the STZ model, 4 groups of male offspring were killed at age 3 months: the control, STZ, and Cit and STZ+Cit (control and STZ rats treated with 0.25% l-citrulline solution, respectively) groups. The nSTZ rats had lower nephron numbers. The renal level of ADMA was higher in the nSTZ rats than in controls. The STZ group developed kidney injury, renal hypertrophy, and elevated blood pressure at the age of 12 weeks. These conditions were found to be associated with increased ADMA levels, decreased nitric oxide (NO) production, and decreased dimethylarginine dimethylaminohydrolase (DDAH) activity in the kidney. In addition, ADMA caused a nephron deficit in cultured rat metanephroi. Maternal citrulline supplementation prevented hypertension and kidney injury, increased the renal DDAH-2 protein level, and restored the levels of ADMA and NO in the STZ+Cit group. Reduced nephron number and increased ADMA contribute to adult kidney disease and hypertension in offspring of mothers with STZ-induced diabetes. Manipulation of the ADMA-NO pathway by citrulline supplementation may be a potential approach to prevent these conditions.
    PLoS ONE 01/2013; 8(2):e55420. · 4.09 Impact Factor
  • Article: Roles of melatonin in fetal programming in compromised pregnancies.
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    ABSTRACT: Compromised pregnancies such as those associated with gestational diabetes mellitus, intrauterine growth retardation, preeclampsia, maternal undernutrition, and maternal stress may negatively affect fetal development. Such pregnancies may induce oxidative stress to the fetus and alter fetal development through the epigenetic process that may affect development at a later stage. Melatonin is an oxidant scavenger that reverses oxidative stress during the prenatal period. Moreover, the role of melatonin in epigenetic modifications in the field of developmental programming has been studied extensively. Here, we describe the physiological function of melatonin in pregnancy and discuss the roles of melatonin in fetal programming in compromised pregnancies, focusing on its involvement in redox and epigenetic mechanisms.
    International Journal of Molecular Sciences 01/2013; 14(3):5380-401. · 2.60 Impact Factor
  • Article: Fish Omega-3 Fatty Acids Induce Liver Fibrosis in the Treatment of Bile Duct-Ligated Rats.
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    ABSTRACT: BACKGROUND: Biliary atresia-induced cholestasis increases hepatic oxidative stress with eventual progression to cirrhosis and liver failure. Omega-3 fatty acids play a possible role in the regulation of oxidative stress and the improvement of cholestasis. AIM: The goal of the present study is to investigate the role of dietary supplementation of fish omega-3 fatty acids in the reduction of hepatocellular damage by using a rat common bile duct ligation model. METHODS: Sprague-Dawley rats received either sham or bile duct ligation (BDL) and were divided into four study groups: Sham+saline (Sham+sal) group, Sham+Fish oil (Sham+FO) group, BDL+saline (BDL+sal) group, and BDL+Fish oil (BDL+FO) group. Rats from each group were assigned to receive, besides regular chow, once daily with either normal saline or fish omega-3 fatty acids (0.4 % of its own body weight) via gavage for 10 days. Samples of blood, liver tissue homogenates, and histological studies from different groups were analyzed at the end of the study. RESULTS: Rats from BDL+FO had significantly impaired liver function as compared to other study groups (p < 0.05 is of significant difference). Ishak scores and the TGF-b1 contents were significantly higher in rats that received BDL+FO, p < 0.05. Contrary to TGF-b1 liver content, rats from the BDL+FO group had the lowest glutathione levels among the study groups, p < 0.05. CONCLUSIONS: Fish omega-3 fatty acids supplementation, albeit increased tissue content of DHA, tended to increase liver fibrosis in BDL rats, decrease liver glutathione level, and compromise hepatic function; fish oil supplementation to subjects with biliary atresia might be of potential hazard and should be used with caution.
    Digestive Diseases and Sciences 12/2012; · 2.12 Impact Factor
  • Article: Alterations in NADPH oxidase expression and blood-brain barrier in bile duct ligation-treated young rats: effects of melatonin.
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    ABSTRACT: Bile duct ligation (BDL)-treated rats exhibit cholestasis and increased systemic and brain oxidative stress. Activation of NADPH (nicotinamide adenine dinucleotide phosphate) oxidase and disruption of the blood-brain barrier (BBB) are implicated as the pathogenetic mechanisms of brain dysfunction in BDL-treated adult rats. Young rats underwent sham ligation or BDL at day 17 for 2 or 4weeks. Treatment group rats were administered melatonin between day 17 and 45. We found a progressive increase in prefrontal cortex NADPH-dependent superoxide anion (O(2)(-)) production and increased expression of NADPH oxidase subunits in either the prefrontal cortex or the hippocampus in BDL-treated young rats. In addition, expression of intercellular adhesion molecule-1 (ICAM) and tissue plasminogen activator (t-PA) genes were increased in either the prefrontal cortex or the hippocampus. Prefrontal cortex capillary junctional complex proteins expressions including occludin, claudin-5, platelet endothelial cell adhesion molecule-1 and vascular endothelial cadherin were not altered. Melatonin lowered the prefrontal cortex NADPH-dependent O(2)(-) production and t-PA gene expression. We conclude that alterations in NADPH oxidase expression and BBB are involved in brain dysfunction in BDL-treated young rats. In addition, melatonin regulates NADPH oxidase activity and t-PA gene expression.
    Neurochemistry International 06/2012; 60(8):751-8. · 2.86 Impact Factor
  • Article: Neonatal seizures: dialogues between clinic and bench.
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    ABSTRACT: Neonatal seizures are common and often reflect a severe underlying neurologic dysfunction in neonates. Phenobarbital remains the mainstay of treatment of neonatal seizures, however, but it is ineffective in many patients and has adverse profiles in cognition. Furthermore, gamma-aminobutyric acid is excitatory early in brain development; therefore, treatment of neonatal seizures with phenobarbital must be cautious. In this review, we highlight the substantial progress that has been made in animal studies, and translate these results to the treatment of seizures in human neonates.
    Journal of the Formosan Medical Association 05/2012; 111(5):239-44. · 1.13 Impact Factor
  • Article: The combined ratios of L-arginine and asymmetric and symmetric dimethylarginine as biomarkers in spontaneously hypertensive rats.
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    ABSTRACT: Hypertension and hypertensive end-organ damage have been associated with decreased nitric oxide (NO) bioavailability. Asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) both can inhibit NO availability by competition with L-arginine (L-Arg). However, whether a combined analysis of these 3 parameters can serve as an ideal biomarker of hypertension remains unclear. We measured the plasma and renal levels of L-Arg, ADMA, and SDMA in spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) control rats at 3 stages: 4 weeks old (prehypertensive), 12 weeks old (hypertensive), and 24 weeks old (end-organ damage). The plasma and renal L-Arg/ADMA ratio (AAR) and the ADMA/SDMA ratio (ASR) were computed for all 3 age stages. Our results revealed an ADMA level increase, and an AAR decrease in plasma and kidneys may develop early on, even before the onset of hypertension in 4-week-old SHRs. The renal ADMA level and AAR were restored in SHRs at 24 weeks of age, which might protect SHRs against kidney injury. We found that the plasma AAR is superior to the levels of L-Arg and ADMA in plasma, and it predicted blood pressure and urinary NOx levels. Renal AAR is a strong independent marker of renal dimethylarginine dimethylaminohydrolase (DDAH) activity. The plasma ASR was correlated strongly to blood pressure. However, renal DDAH activity was related to the renal ASR but not the plasma ASR. In conclusion, the AAR and ASR may serve as better markers for disease activity and progression than each individual parameter. Clinical use of these ratios to elucidate the role of ADMA in hypertension awaits further validation.
    Translational research : the journal of laboratory and clinical medicine. 02/2012; 159(2):90-8.
  • Article: Melatonin utility in neonates and children.
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    ABSTRACT: Melatonin (N-acetyl-5-methoxytryptamine) is an endogenously produced indoleamine secreted by the pineal gland and the secretion is suppressed by light. Melatonin is a highly effective antioxidant, free radical scavenger, and has anti-inflammatory effect. Plenty of evidence supports the utility of melatonin in adults for cancer, neurodegenerative disorders, and aging. In children and neonates, melatonin has been used widely, including for respiratory distress syndrome, bronchopulmonary dysplasia, periventricular leukomalacia (PVL), hypoxia-ischemia encephalopathy and sepsis. In addition, melatonin can be used in childhood sleep and seizure disorders, and in neonates and children receiving surgery. This review article discusses the utility of melatonin in neonates and children.
    Journal of the Formosan Medical Association 02/2012; 111(2):57-66. · 1.13 Impact Factor
  • Article: Roles of nitric oxide and asymmetric dimethylarginine in pregnancy and fetal programming.
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    ABSTRACT: Nitric oxide (NO) regulates placental blood flow and actively participates in trophoblast invasion and placental development. Asymmetric dimethylarginine (ADMA) can inhibit NO synthase, which generates NO. ADMA has been associated with uterine artery flow disturbances such as preeclampsia. Substantial experimental evidence has reliably supported the hypothesis that an adverse in utero environment plays a role in postnatal physiological and pathophysiological programming. Growing evidence suggests that the placental nitrergic system is involved in epigenetic fetal programming. In this review, we discuss the roles of NO and ADMA in normal and compromised pregnancies as well as the link between placental insufficiency and epigenetic fetal programming.
    International Journal of Molecular Sciences 01/2012; 13(11):14606-22. · 2.60 Impact Factor
  • Article: Endotoxemia exacerbates kidney injury and increases asymmetric dimethylarginine in young bile duct-ligated rats.
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    ABSTRACT: Cirrhosis increases the risk of kidney injury and sepsis, leading to increased mortality. Elevated levels of plasma asymmetric dimethylarginine (ADMA) occur in patients critically ill with cirrhosis, renal failure, and sepsis. We used a rat model of cirrhosis with superimposed sepsis to assess the relationship of plasma and tissue ADMA profiles with acute kidney injury and survival. Seventeen-day-old male Sprague-Dawley rats (n = 37) were randomly assigned to four groups: (1) sham operation plus diet control (n = 6); (2) bile duct ligation (BDL, n = 8); (3) sham operation plus lipopolysaccharide (LPS, n = 9); and (4) BDL plus LPS (n = 14). Lipopolysaccharide was given by intraperitoneal injection (1 mg/kg in saline) 3 h before sacrifice. All rats were sacrificed 14 days after surgery. Lipopolysaccharide increased the rate of BDL-associated death and dysfunction of the liver and kidneys. These results were supported by increased levels of plasma ADMA and a decreased L-arginine/ADMA ratio (AAR). Plasma and tissue levels of ADMA and AAR were not correlated. Lipopolysaccharide restored BDL-induced ADMA level elevation in the liver but increased ADMA level in the kidneys. Lipopolysaccharide increased hepatic AAR, decreased renal AAR, and paradoxically mediated the expression of neuronal nitric oxide synthase-β in the liver and kidneys. A novel mechanism underlies the LPS-mediated L-arginine-ADMA-nitric oxide pathway activation and exacerbation of kidney injury and mortality in our BDL model. In the presence of cirrhosis with superimposed sepsis, simultaneous lowering of ADMA levels and enhancement of L-arginine levels to restore plasma and renal AARs may be an optimal strategy for the treatment of kidney injury.
    Shock (Augusta, Ga.) 12/2011; 37(4):441-8. · 2.87 Impact Factor
  • Article: Arginine and asymmetric dimethylarginine in puromycin aminonucleoside-induced chronic kidney disease in the rat.
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    ABSTRACT: Reduced renal L-arginine (L-Arg) synthesis/transport, induction of arginases and increased endogenous NOS inhibitor, asymmetric dimethylarginine (ADMA) will inhibit NO production. This study investigated pathways of L-Arg synthesis/uptake/utilization, ADMA degradation and oxidant/antioxidants in puromycin aminonucleoside (PAN) chronic kidney disease (CKD). Rats were given low- (LD) or high-dose (HD) PAN and followed for 11 weeks for proteinuria. BP was measured and blood and tissues were harvested and analyzed for abundance of argininosuccinate synthase (ASS) and lyase (ASL), arginase, cationic amino acid transporter (CAT1) and dimethylargininedimethylaminohydrolase (DDAH) in kidney, cortex, aorta and liver. Arginase and DDAH activity, plasma L-Arg and ADMA, renal pathology and creatinine clearances were also measured. PAN caused dose-dependent kidney damage and hypertension and creatinine clearance fell in HD-PAN. Renal ASS fell in HD-PAN, renal cortex and aortic ASL and membrane CAT1 fell in both PAN groups. There was no activation of renal arginase, but aortic arginase increased in LD-PAN. Renal DDAH activity fell moderately in LD-PAN and markedly in HD-PAN where hepatic DDAH activity also fell. Plasma L-Arg was unchanged while ADMA rose moderately and dose-dependently with PAN. There were several indices of oxidative stress which was most prominent in HD-PAN. Reduction in renal ASS/ASL and loss of renal cortex CAT1 compromises renal L-Arg synthesis and release. Loss of aortic CAT1 impairs L-Arg uptake. Increased plasma ADMA was associated with progressive loss of renal DDAH activity. However, loss of renal clearance and falls in hepatic DDAH activity in HD-PAN did not have additive effects on plasma ADMA.
    American Journal of Nephrology 12/2011; 35(1):40-8. · 2.54 Impact Factor
  • Article: Apocynin attenuates oxidative stress and hypertension in young spontaneously hypertensive rats independent of ADMA/NO pathway.
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    ABSTRACT: Both NADPH oxidase-derived reactive oxygen species (ROS) and asymmetric dimethylarginine (ADMA) are increased in hypertension. Apocynin, an NADPH oxidase inhibitor, could inhibit ROS, thus we tested whether apocynin can block NADPH oxidase and prevent increases of ADMA and blood pressure (BP) in spontaneously hypertensive rats (SHRs). SHRs and Wistar Kyoto (WKY) rats, aged 4 weeks, were assigned to four groups: untreated SHRs and WKY rats, SHRs and WKY rats that received 2.5 mM apocynin for 8 weeks. BP was significantly higher in SHRs compared to WKY rats, which was attenuated by apocynin. Apocynin prevented p47phox translocation in SHR kidneys, but not the increase of superoxide and H(2)O(2). Additionally, apocynin did not protect SHRs against increased ADMA. Apocynin blocks NADPH oxidase to attenuate hypertension, but has little effect on the ADMA/nitric oxide (NO) pathway in young SHRs. The reduction of ROS and the preservation of NO simultaneously might be a better approach to restoring ROS-NO balance to prevent hypertension.
    Free radical research 11/2011; 46(1):68-76. · 2.22 Impact Factor
  • Article: Aliskiren prevents hypertension and reduces asymmetric dimethylarginine in young spontaneously hypertensive rats.
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    ABSTRACT: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS, decreases NO synthesis. Plasma ADMA concentrations increase markedly in hypertension. We tested whether the development of hypertension and the increases in ADMA in spontaneously hypertensive rats (SHR) are prevented by aliskiren, a renin inhibitor. Male SHRs and normotensive Wistar Kyoto (WKY) control rats, aged 4 weeks (pre-hypertensive stage), were assigned to 4 groups: untreated SHRs and WKY rats, and SHRs that received oral aliskiren 10 and 30 mg/kg/day for 6 weeks. All rats were sacrificed at age 10 weeks. Blood pressure decreased at age 6, 8, and 10 weeks in SHRs that received high-dose aliskiren. Aliskiren mitigated the increases in plasma ADMA in SHRs. Renal ADMA levels were lower in SHRs that received high-dose aliskiren versus SHRs. SHRs experienced decreased plasma and kidney l-Arg-to-ADMA ratios versus control rats, which were reverted by 30 mg/kg aliskiren. Renal cortical neuronal NOS-α and -β levels increased in SHRs fed with high-dose aliskiren. Early aliskiren treatment mitigates increases in ADMA, restores l-Arg-to-ADMA ratios, enhances neuronal NOS-α, prevents decreased nNOS-β levels in the kidney-which might restore NO bioavailability and contribute to the decrease of blood pressure in young SHRs. Our findings suggest that aliskiren is a therapeutic agent for prehypertension that regulates the ADMA/NO pathway.
    European journal of pharmacology 09/2011; 670(2-3):561-5. · 2.59 Impact Factor
  • Article: Identification of immunodeficient molecules in neonatal mononuclear cells by proteomic differential displays.
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    ABSTRACT: Human newborns are known to be susceptible to microbial infection. This susceptibility is generally attributed to immaturity of the newborn immune system. However, the mechanisms for impaired immunity in newborns are still incompletely defined. In this study, we sought to elucidate the protein differential display between adult and neonatal mononuclear cells (MNC) using a proteomic approach. MNC samples from cord blood and adult peripheral blood were subjected to 2-D PAGE analysis. Differential protein displays between cord blood and adult MNC were determined and validated. There were 34 differentially expressed proteins between cord blood and adult MNC identified by 2-D PAGE. The differentially displayed proteins were clustered into two major signal pathways, cellular processing and purine metabolism. After validation by Western blot, we found more abundant arginase-1 (ARG1) and Rho GDP-dissociation inhibitor 2 (RhoGDI2), while less adenosine deaminase (ADA) and β-actin in cord blood MNC. In functional validation, we found that lower ADA was proven to enhance the TNF-α production by cord blood monocytes. The results from this study discovered the proteomic displays for altered immunity between adult and neonatal MNC that support a understanding of the correction of impaired immune response in newborns.
    Proteomics 09/2011; 11(17):3491-500. · 4.43 Impact Factor
  • Article: Reciprocal changes of renal neuronal nitric oxide synthase-α and -β associated with renal progression in a neonatal 5/6 nephrectomized rat model.
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    ABSTRACT: Nitric oxide (NO) deficiency contributes to chronic kidney disease progression. NO deficiency could occur for many reasons, one of which is decreased NO synthase (NOS) abundance and/or activity. In these experiments, we studied two groups of male Sprague Dawley rats given sham or surgical excision of both poles of the left kidney (at 2 days of age) followed by sham or surgical removal of the right kidney at 10 days. Rats were sacrificed at 9 weeks of age and the kidneys examined for abundance of neuronal NOS (nNOS)-α and -β, endothelial NOS, arginase II, argininosuccinate synthase and lysate, protein arginine methyltransferase 1, dimethylarginine dimethylamino-hydrolase 1 and 2, as well as renal pathology. The 5/6 nephrectomy (NX) group showed renal dysfunction, severe rapidly progressing glomerulosclerosis, and hypertension. Renal cortical nNOSα abundance was significantly reduced, whereas nNOSβ abundance was increased in the 5/6 NX group versus sham. Renal endothelial NOS was unchanged. Next, renal protein arginine methyltransferase 1 abundance was higher, whereas dimethylarginine dimethylamino-hydrolase 2 expression was lower in the 5/6 NX group versus sham. Renal arginase II, argininosuccinate synthase, and argininosuccinate lysate abundances were significantly decreased in 5/6 NX rats than those in sham. The neonatal kidney is very susceptible to 5/6 NX-induced injury, and, as in adults, reciprocal changes in the nNOSα and nNOSβ in renal cortex occur during progression of chronic kidney disease and may contribute to the injury.
    Pediatrics & Neonatology 04/2011; 52(2):66-72. · 0.75 Impact Factor
  • Article: Ectopic pelvic kidney with urinary tract infection presenting as lower abdominal pain in a child.
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    ABSTRACT: Ectopic pelvic kidney is a rare developmental anomaly. Ectopic pelvic kidney can present without the characteristic symptoms associated with the urinary tract pathology. Ectopic pelvic kidney is usually unknown, and nonspecific vague abdominal comfort maybe the only symptom. Early detection and recognition of an ectopic kidney can prevent long-term complications. We report a 3-year-5-month-old girl with ectopic pelvic kidney who experienced intermittent episodes of lower abdominal pain for about 1 month. Abdominal ultrasound, computed tomography, and intravenous pyelography demonstrated a pelvic kidney. Thereafter, the urinalysis showed pyuria (white blood cell 20/high power field), and urine culture grew Escherichia coli. We emphasize that pelvic kidney should be considered in patients presenting unexplained vague abdominal pain, especially in pediatric patients who had intermittent recurrent episodes.
    Pediatrics & Neonatology 04/2011; 52(2):117-20. · 0.75 Impact Factor
  • Article: Carbon dioxide pneumoperitoneum induces anti-inflammatory response and hepatic oxidative stress in young rats with bacterial peritonitis.
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    ABSTRACT: The aim of this study was to investigate the effects of carbon dioxide (CO(2)) pneumoperitoneum on the intra-abdominal spread of bacteria, the local and systemic cytokine expression, and oxidant/antioxidant status in young rats with bacterial peritonitis. Young Sprague-Dawley rats, aging 20-27 days and weighing around 50 g, were allocated to six groups of six to nine animals in each. Intra-abdominal infection model was developed by intraperitoneal injection with 1 cc of Escherichia coli (E. coli) (10(8) CFU/mL, ATCC25922 strain) via right lower abdominal wall. Carbon dioxide (CO(2)) pneumoperitoneum was applied to the rats via umbilical pit insufflation with 20 cc CO(2) for 30 min. All survived rats underwent laparotomy and were killed 24 h or 3 days later. Serum levels of CO(2) and CRP were measured. Left lower abdomen peritoneum, peritoneal fluid, mesenteric lymph node of terminal ileum, and liver were taken for bacterial culture. Liver and plasma levels of TNF-α, IL-1β, and IL-6 were examined for the level of local and systemic immunologic response. Oxidant/antioxidant status in liver and plasma were assessed by measuring malondialdehyde (MDA), and reduced to oxidized glutathione ratio (GSH/GSSG). Carbon dioxide (CO(2)) pneumoperitoneum does not facilitate E. coli dissemination to other intra-abdominal organs in rats with localized E. coli peritonitis. Peritonitis rats that underwent abdominal CO(2) insufflation have insignificantly higher CRP or lower CO(2) levels. Plasma and liver TNF-α, IL-1β concentrations were not significantly different among the four groups, but plasma IL-6 was significantly increased in rats with E. coli peritonitis and CO(2) pneumoperitoneum that were killed 3 days later as compared with that of rats that were killed 24 h later. In rats with E. coli peritonitis, CO(2) pneumoperitoneum was significantly associated with decreased hepatic GSH/GSSG ratio. However, plasma and liver MDA levels were not altered after CO(2) pneumoperitoneum. Carbon dioxide (CO(2)) pneumoperitoneum is not associated with E. coli dissemination in the presence of local intra-abdominal infection. CO(2) pneumoperitoneum elicited systemic anti-inflammatory response at a specific time period and decreased hepatic antioxidant status in young rats with E. coli peritonitis.
    Pediatric Surgery International 03/2011; 27(3):289-94. · 1.25 Impact Factor
  • Article: Urachal catheter provides new choice for long-term urinary diversion in prune belly syndrome.
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    ABSTRACT: Prune belly syndrome has been identified as a clinical triad of abdominal muscle deficiency, bilateral cryptorchidism, and urologic abnormalities. We present the case of a discordant monozygotic twin with prune belly syndrome and voiding dysfunction that was relieved by long-term urinary catheterization by way of the urachus. To the best of our knowledge, this alternative method has not been previously reported. We suggest that for newborn infants with long-term voiding dysfunction, if the urachus retains patency, urinary catheterization through the urachus could be a choice for urine drainage instead of cystostomy, providing a better cosmetic appearance and quality of life.
    Urology 02/2011; 77(2):466-8. · 2.43 Impact Factor
  • Article: Asymmetric dimethylarginine: clinical applications in pediatric medicine.
    You-Lin Tain, Li-Tung Huang
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    ABSTRACT: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS). Growing evidence indicates that ADMA plays an important role in the initiation and progression of a variety of adulthood diseases, especially in the cardiovascular and renal systems. However, the study of ADMA in pediatric diseases has just begun. This review provides an overview of potential clinical applications of ADMA in pediatric practice, with an emphasis on the following areas: the biochemistry and pathophysiology of ADMA; clinical ramifications of elevated ADMA levels in pediatric population; age-related normal reference ranges of ADMA; methodology for measuring ADMA; current and potential agents to reduce ADMA; and the problems that must be addressed before use of ADMA in pediatric medicine. ADMA will soon be available for use as a biomarker and therapeutic target in the pediatric population.
    Journal of the Formosan Medical Association 02/2011; 110(2):70-7. · 1.13 Impact Factor

Institutions

  • 2008–2013
    • Chang Gung University
      • • Department of Anesthesiology
      • • Department of Pediatrics
      • • College of Medicine
      Taoyuan, Taiwan, Taiwan
  • 2002–2013
    • Chang Gung Memorial Hospital
      • • Department of Pharmacy
      • • Division of Pediatric Nephrology
      Taipei, Taipei, Taiwan
  • 2006–2011
    • University of Florida
      • Department of Physiology and Functional Genomics
      Gainesville, FL, USA
  • 2008–2010
    • Semmelweis University
      • Department of Pulmonology
      Budapest, Budapest fovaros, Hungary
  • 2007
    • West Virginia University
      • Department of Physiology & Pharmacology
      Morgantown, WV, USA