Armed Forces TaoYuan General Hospital
Armed Forces TaoYuan General Hospital
Hsiao C.-J.,Armed Forces Taoyuan General Hospital |
Hsiao C.-J.,National Defense Medical Center
Journal of Internal Medicine of Taiwan | Year: 2016
Gastroesophageal varices are present in approximately 50% of patients with cirrhosis, and hemorrhage of the varices serves as an important factor of death in cirrhotic patients. Patients without varices develop them at a rate of 8% per year, and the strongest predictor for development of varices is a hepatic venous pressure gradient (HVPG) >10 mmHg. The predictors of variceal bleeding are: 1. Size of the varices. 2. Severity of cirrhosis. 3. Endoscopic presentation of red color signs. The gold standard in the diagnosis of varices is esophagogastroduodenoscopy (EGD). EGD should be performed once the diagnosis of cirrhosis is established. In patients with compensated cirrhosis who have no varices on screening endoscopy and whom the etiologic factors were removed, the EGD should be repeated in 3 years. In those who have small varices and whom the etiologic factors were removed, or in those without varices but are with ongoing liver injury, the EGD should be repeated in 2 years. In the presence of decompensated cirrhosis or large varices, EGD should be repeated at yearly intervals. Non-selective beta blockers therapy or prophylactic endoscopic variceal ligation (EVL) should be underwent to prevent first variceal bleeding in patients with small varices and decompensated cirrhosis, large varices or those with red color signs. In acute esophageal variceal hemorrhage, intravascular volume support and blood transfusion to keep hemoglobin around 7-8 g/dl are optimal. Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in any patient with cirrhosis and variceal hemorrhage. Pharmacological therapy (somatostatin or its analogues: octreotide and vapreotide; vasopressin or its analogue: terlipressin) should be initiated as soon as variceal hemorrhage is suspected and continued for 3-5 days after diagnosis is confirmed. EGD, performed within 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage, either with EVL or sclerotherapy. Transjugular intrahepatic portosystemic shunt (TIPS) and balloon tamponade could be used if combined pharmacological and endoscopic control fails.
Wu S.-L.,Chang Hua Christian Hospital |
Wu S.-L.,Da - Yeh University |
Wang W.-F.,Chang Hua Christian Hospital |
Shyu H.-Y.,Armed Forces Taoyuan General Hospital |
And 5 more authors.
Neuroscience Letters | Year: 2010
Hyperactivation of N-methyl-d-aspartate receptors (NMDARs) leads to neuronal excitotoxicity and is suggested to play a role in many brain disorders, including Alzheimer's disease and schizophrenia. However, the association between polymorphisms in the genes that code for NMDAR subunits, N-methyl-d-aspartate 1 and 2B (GRIN1 and GRIN2B) and Parkinson's disease (PD) remains unclear. In a hospital-based case-control study of PD, DNA samples were collected from 101 PD patients and 205 healthy controls. Genotyping assays were used to screen for polymorphisms in the GRIN1 (rs2301364 T>C, rs28489906 T>C, and rs4880213 T>C) and GRIN2B (C366G, C2664T, and rs1805476 T>G) genes, and logistic regression analysis was then used to assess the association between these single nucleotide polymorphisms (SNPs) and PD susceptibility. None of the 6 SNPs were significantly associated with PD risk on their own. However, in conjunction with putative low-risk genotypes for the GRIN1 gene, the GRIN2B C366G variant was significantly associated with reduced PD risk compared with the homozygous genotype 366CC (OR=0.38, 95%CI=0.17-0.93, P=0.033). A synergistic effect on risk reduction was observed in subjects who carried multiple polymorphisms of GRIN1 and the GRIN2B C366G polymorphism (OR=0.78, 95%CI=0.59-1.02, Ptrend=0.073). Our results suggest that polymorphisms in the GRIN1 and GRIN2B genes may serve as potential biomarkers for a reduced risk of PD among the Chinese population in Taiwan. © 2010 Elsevier Ireland Ltd.
Chang C.-P.,National Central University |
Tseng Y.-K.,National Central University |
Ko C.-Y.,Armed Forces Taoyuan General Hospital |
Wang C.-C.,National Central University
Nucleic Acids Research | Year: 2012
In eukaryotes, the cytoplasmic and mitochondrial forms of a given aminoacyl-tRNA synthetase (aaRS) are typically encoded by two orthologous nuclear genes, one of eukaryotic origin and the other of mitochondrial origin. We herein report a novel scenario of aaRS evolution in yeast. While all other yeast species studied possess a single nuclear gene encoding both forms of alanyl-tRNA synthetase (AlaRS), Vanderwaltozyma polyspora, a yeast species descended from the same whole-genome duplication event as Saccharomyces cerevisiae, contains two distinct nuclear AlaRS genes, one specifying the cytoplasmic form and the other its mitochondrial counterpart. The protein sequences of these two isoforms are very similar to each other. The isoforms are actively expressed in vivo and are exclusively localized in their respective cellular compartments. Despite the presence of a promising AUG initiator candidate, the gene encoding the mitochondrial form is actually initiated from upstream non-AUG codons. A phylogenetic analysis further revealed that all yeast AlaRS genes, including those in V. polyspora, are of mitochondrial origin. These findings underscore the possibility that contemporary AlaRS genes in V. polyspora arose relatively recently from duplication of a dual-functional predecessor of mitochondrial origin. © 2011 The Author(s).
Tang Y.-C.,National Central University |
Liu C.-W.,National Central University |
Chang H.-H.,National Central University |
Juan C.-C.,National Yang Ming University |
And 4 more authors.
Endocrinology | Year: 2014
Resistin and endothelin (ET)-1 have been reported to inhibit adipogenesis and regulate adipocyte insulin resistance, respectively. Although both hormones interact with each other, the exact signaling pathway of ET-1 to act on resistin gene expression is still unknown. Using 3T3-L1 adipocytes, we investigated the signaling pathways involved in ET-1-stimulated resistin gene expression. The up-regulation of resistin mRNA expression by ET-1 depends on concentration and timing. The concentration of ET-1 that increased resistin mRNAlevels by 100%-250% was approximately 100nMfor a range of 0.25-12 hours of treatment. Treatment with actinomycin D blocked ET-1-increased resistin mRNA levels, suggesting that the effect of ET-1 requires new mRNA synthesis. Treatment with an inhibitor of the ET type-A receptor, such as N-[1-Formyl-N-[N-[(hexahydro-1H- azepin-1-yl)carbonyl]-L-leucyl]-D-tryptophyl]-D-tryptophan (BQ610), but not with the ET type-B receptor antagonist N-[(cis-2,6-Dimethyl-1-piperidinyl)carbonyl]- 4-methyl-L-leucyl-1-(methoxycarbonyl)-D-tryptophyl-D-norleucine (BQ788), blocked ET-1, increased the levels of resistin mRNA, and phosphorylated levels of downstream signaling molecules, such as ERK1/2, c-Jun N-terminal kinases (JNKs), protein kinase B (AKT), and signal transducer and activator of transcription 3 (STAT3). Moreover, pretreatment of specific inhibitors of either ERK1/2 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio] butadiene [U0126] and 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one [PD98059], two inhibitors of MEK1), JNKs (SP600125), phosphatidylinositol 3-kinase/AKT (LY294002 and Wortmannin), or Janus kinase 2 (JAK2)/STAT3 ((E)-2-Cyano-3-(3,4-dihydrophenyl)- N-(phenylmethyl)-2-propenamide, AG490) prevented ET-1-increased levels of resistin mRNA and reduced the ET-1-stimulated phosphorylation of ERK1/2, JNKs, AKT, and STAT3, respectively. However, the p38 kinase antagonist 4-[5-(4-Fluorophenyl)-2-[4-(methylsulfonyl)phenyl]-1H-imidazol-4-yl] pyridine(SB203580)did not alter the effect of ET-1.These result simply that ET type-Areceptor, ERK1/2, JNKs, AKT, and JAK2, but not ET type-Breceptor or p38, are necessary for the ET-1 stimulation of resistin gene expression. In vivo observations that ET-1 increased resist in mRNA and protein levels in sc and epididymal adipose tissues support the in vitro findings. Copyright © 2014 by the Endocrine Society.
Yang C.-P.,Armed Forces Taoyuan General Hospital |
Cherng C.-H.,Tri Service General Hospital |
Wu C.-T.,National Defense Medical Center |
Huang H.-Y.,Graduate Institute of Medical science |
And 3 more authors.
Anesthesia and Analgesia | Year: 2013
BACKGROUND:: Glutamate homeostasis and microglia activation play an important role in the development and maintenance of neuropathic pain. We designed this investigation to examine whether ultra-low dose naloxone administered alone or in combination with morphine could alter the concentration of the excitatory amino acids (EAAs) glutamate and aspartate, as well as the expression of tumor necrosis factor-α (TNF-α) and its receptors (TNFR1 and TNFR2) in the spinal cord dorsal horn of rats with partial sciatic nerve transection (PST). METHODS:: Male Wistar rats underwent intrathecal catheter implantation for drug delivery and were divided in 7 groups: sham-operated + saline (sham), PST + saline (S), PST + 15 ng naloxone (n), PST + 15 μg naloxone (N), PST + 10 μg morphine (M), PST + 15 ng naloxone + 10 μg morphine (Mn), PST + 15 μg naloxone + 10 μg morphine (MN). Thermal withdrawal latency and mechanical withdrawal threshold, TNF-α and TNFR expression in the spinal cord and dorsal root ganglia, and EAAs glutamate and aspartate concentration in cerebrospinal fluid dialysates were measured. RESULTS:: Ten days after PST, rats developed hyperalgesia (P < 0.0001) and allodynia (P < 0.0001), and increased TNF-α (P < 0.0001) and TNFR1 expression (P = 0.0009) were measured in the ipsilateral spinal cord dorsal horn. The antihyperalgesic and antiallodynic effects of morphine (10 μg) were abolished by high-dose naloxone (15 μg; P = 0.0031) but enhanced by ultra-low dose naloxone (15 ng; P = 0.0015), and this was associated with a reduction of TNF-α (P < 0.0001) and TNFR1 (P = 0.0009) expression in the spinal cord dorsal horn and EAAs concentration (glutamate: P = 0.0001; aspartate: P = 0.004) in cerebrospinal fluid dialysate. Analysis of variance (ANOVA) or Student t test with Bonferroni correction were used for statistical analysis. CONCLUSIONS:: Ultra-low dose naloxone enhances the antihyperalgesia and antiallodynia effects of morphine in PST rats, possibly by reducing TNF-α and TNFR1 expression, and EAAs concentrations in the spinal dorsal horn. Ultra-low dose naloxone may be a useful adjuvant for increasing the analgesic effect of morphine in neuropathic pain conditions. Copyright © 2013 International Anesthesia Research Society.
Wu C.-L.,A-Life Medical |
Ho J.-Y.,Tri Service General Hospital |
Chou S.-C.,Armed Forces Taoyuan General Hospital |
Yu D.-S.,A-Life Medical |
Yu D.-S.,Tri Service General Hospital
Oncotarget | Year: 2016
Epithelial-mesenchymal transition (EMT) accompanying loss of E-cadherin is important for invasiveness and metastasis of bladder cancer. MicroRNAs (miRs) had been associated with cancer progression and differentiation in several cancers. Our goal is to find out the specific miR which modulates EMT in bladder cancer. Real-time quantitative polymerase chain reaction was used to measure the miRs expression in urothelial cell carcinoma (UCC) cell lines. MiR or siRNA mimics was used to regulate miR and mRNA level respectively. Migration and scratch assays were used to determine the migratory ability. Zymography assay was used to confirm the metalloproteinase activity. Western blotting was used to elucidate the mechanism which regulated by specific miR. MiR-429 was highly expressed in low grade UCC cell lines. Exogenous mimic of miR-429 treatment dramatically inhibited the migratory ability of T24 cells. MiR-429 downstream target ZEB1 was decreased, E-cadherin was restored, and β-catenin was contrarily decreased by exogenous mimic of miR-429 treatment in T24 cells. Cell invasive ability was also inhibited by exogenous mimic of miR-429 treatment through inactivating the MMP-2 activity in T24 cells. E-cadherin protein expression level was inhibited by E-cadherin siRNA accompanied with increasing cell migratory ability when compared with control group in low grade TSGH8301 cells. MiR-429 decreased the cell migratory and invasive abilities through reducing ZEB1 and β-catenin, restoring the E-cadherin expression and inactivation of MMP-2 of UCC cells. MiR-429 might be used as a progression marker of bladder cancer.
Shyu H.-Y.,Armed Forces Taoyuan General Hospital |
Shyu H.-Y.,Institute of Biology and Anatomy |
Shieh J.-C.,Chung Shan Medical University |
Lin J.-H.,Taipei General Hospital |
And 2 more authors.
Journal of Atherosclerosis and Thrombosis | Year: 2012
Aim: Cigarette-smoking induced oxidative DNA damage to endothelial cells has been reported to play an etiological role in atherosclerosis development. Individual vulnerability to oxidative stress through smoking exposure and the ability to repair DNA damage, which plays a critical role in modifying the risk susceptibility of large artery atherosclerotic (LAA) stroke, is hypothesized. Thus, we examined the effect of genetic polymorphisms of DNA repair pathway genes and cigarette smoking in relation to risk susceptibility of LAA stroke. Methods: We enrolled 116 LAA stroke patients and 315 healthy controls from the Armed Forces Taoyuan General Hospital, Taoyuan, Taiwan. Genotyping of polymorphisms of the OGG1 (Ser326Cys), XRCC1 (Arg399Gln), ERCC2 (Lys751Gln), and ERCC5 (Asp1104His) genes was performed and used to evaluate LAA stroke susceptibility. Results: Of those non-synonymous polymorphisms, the ERCC2 Lys751Gln variant was found to be associated with LAA stroke risk (OR: 1.69, 95%CI: 1.02-2.86), and this association was more pronounced in smokers, manifesting a 2.73-fold increased risk of LAA stroke (p = 0.027). A joint effect on risk elevation of LAA stroke was seen in those patients with OGG1 and ERCC2 polymorphisms (OR: 2.75, 95%CI: 1.26-6.00). Moreover, among smokers carrying the OGG1 Ser326Cys polymorphism, there was a tendency toward an increased risk of LAA stroke in those patients who had a greater number of high-risk genotypes of XRCC1, ERCC2, and ERCC5 polymorphisms (p trend = 0.010). Conclusion: The susceptible polymorphisms of DNA repair pathway genes may have a modifying effect on the elevated risk of LAA stroke in smokers among ethnic Chinese in Taiwan.
Yang C.-P.,Armed Forces Taoyuan General Hospital |
Yang C.-P.,Graduate Institute of Medical science |
Cherng C.-H.,Tri Service General Hospital |
Wu C.-T.,Tri Service General Hospital |
And 4 more authors.
Anesthesia and Analgesia | Year: 2011
Background: In this study, we examined the effects of ultra-low dose naloxone on the antinociceptive effect of morphine and on spinal cord dorsal horn glutamate transporter expression in rats with neuropathic pain. Methods: Neuropathic pain was induced in male Wistar rats by partial transection of the left sciatic nerve and an intrathecal catheter was implanted for drug administration; in some rats, an intrathecal microdialysis probe for cerebrospinal fluid (CSF) dialysate collection was also implanted. Nociception was assessed using the plantar test, a Hargreaves radiant heat apparatus, and by the von Frey test, using a dynamic plantar anesthesiometer. Glutamate transporter protein expression in the left spinal cord dorsal horn was examined by Western blotting and immunohistochemistry. Levels of the excitatory amino acids (EAAs) glutamate and aspartate in the CSF dialysate were measured using high-performance liquid chromatography. Results: Reduced astrocyte expression of glutamate transporters (GLT-1 and GLAST levels were 55% and 53%, respectively, of that in sham-operated rats) in laminae I and II of the spinal cord dorsal horn ipsilateral to the partial sciatic nerve transection (PST), and hyperalgesia and allodynia in the PST hindlimb were observed. High-dose naloxone (15 μg) attenuated the antihyperalgesia and antiallodynia effects of the morphine (10 μg). In contrast, ultra-low dose (15 ng) naloxone enhanced the antinociceptive effect of morphine (10 μg), with an increase in the paw withdrawal threshold to thermal stimulus (from 19% to 35%) and to tactile stimulus (from 33% to 55%) compared with morphine treatment alone, and this was associated with restoration of GLAST and GLT-1 expression to control levels (102% and 114%, respectively) in the astrocytes of laminae I and II in the spinal cord dorsal horn ipsilateral to the PST hindlimb and a decrease in EAA levels in the CSF dialysate (glutamate: 10.0 μM; aspartate: 1.1 μM). Conclusions: Ultra-low dose naloxone enhanced the antinociceptive effect of morphine in PST rats, possibly by restoration of GLAST and GLT-1 expression in astrocytes, which inhibited the accumulation of EAAs in the synapses, resulting in a neuroprotective effect. Copyright © 2011 International Anesthesia Research Society.
Chang T.-C.,Armed Forces Taoyuan General Hospital |
Shih J.-T.,Armed Forces Taoyuan General Hospital
Formosan Journal of Musculoskeletal Disorders | Year: 2012
We report the case of a 76-year-old right-hand dominant man with hypertension and type 2 diabetes mellitus who presented with numbness of the right ring and little fingers for 8 months and a palpable mass lesion in the right forearm for 3 months before his hospital visit. The patient exhibited grip power weakness and atrophy of intrinsic muscles. Magnetic resonance imaging confirmed a well-defined oval mass of 1.5 × 0.6 × 0.6 cm3 between the ulnar bone and nerve. This lesion was hyperintense on T2-weighted images and isointense on T1-weighted images. A zigzag incision was made for ulnar nerve exposure, and the tumor lesion was identified and carefully excised with minimal damage of ulnar nerve. A cystic mass invaded ulnar nerve extending approximately 1.5 cm was resected and reconstructed by sural nerve grafting. The patient was examined 6 months after surgery. His grip power and muscle strength increased, and no numbness or pain was detected. The outcome of this case suggests a potential surgical benefit exists even in cases of apparent chronic or severe denervation atrophy and that ganglion excision and nerve grafting should be considered. © 2012.
Hsieh Y.-H.,Armed Forces Taoyuan General Hospital |
Shih J.-T.,Armed Forces Taoyuan General Hospital |
Lee H.-M.,Armed Forces Taoyuan General Hospital |
Ho Y.-J.,Armed Forces Taoyuan General Hospital
Formosan Journal of Musculoskeletal Disorders | Year: 2010
Background: Few studies on median nerve mobility in carpal tunnel were reported. The purpose of this study was to observe median nerve mobility in the carpal tunnel dynamically with ultrasound during wrist and fingers flexion and extension and define the abnormality between normal people and patients with carpal tunnel syndrome. Materials and Methods: Thirty-two persons without symptoms of carpal tunnel syndrome and 18 patients with symptoms of carpal tunnel syndrome (10 patients confirmed by nerve conduction velocity/electromyography) were evaluated by high-resolution ultrasound (the SonoSite Titan high-resolution ultrasound; transducer: 5-10 MHz, 38-mm broadband linear array) with wrist and fingers in flexion and extension positions. The motions of median nerve and flexor tendons were observed. Result: In our observation, median nerve will move from the volar side of the flexor tendons to the dorsal side of the flexor tendons smoothly through the tract between flexor pollicis longus and flexor digitorum superficialis of index when wrist and fingers flexed. In patients with carpal tunnel syndrome, the normal mobility of median nerve was absent. In 18 patients with carpal tunnel syndrome symptoms, there were 17 patients (94%) with positive findings in ultrasound examination. In 32 persons without the symptom of carpal tunnel syndrome, there were four cases with positive findings. Conclusions: Median nerve has mobility in the carpal tunnel. In patients with carpal tunnel syndrome, the mobility was absent. Ultrasonography of median nerve mobility is helpful in diagnosing carpal tunnel syndrome. Its reliability and sensitivity should be further evaluated. © 2010, Taiwan Orthopaedic Association.