91 research outputs found
Effect of Different Combinations of Soybean and Wheat Bran on Enzyme Production from Aspergillus oryzae S
AbstractTo investigate the enzyme production from Aspergillus oryzae S. NPUST-FS-206-A1, different combinations of soybean and wheat bran (40%:60%, 50%:50%, and 60%:40% w/w) in koji were used as substrates in soybean koji fermentation. During cultivation period, pH change of various samples was similar. However, moisture content of koji obviously decreased. Koji with high content of soybean conducted high protease activity. After 48h of cultivation, koji containing 60% soybean showed the highest neutral protease activity of 84.38 U/g dry weight. Sample with high amount of wheat bran presented high amylase activity of 731.53 U/g dry weight. Reducing sugar content of koji was related to amylase activity. Moreover, different inoculum sizes of A. oryzae S. spore had no effect on the enzyme production
Persistent H. pylori colonization in early acquisition age of mice related with higher gastric sialylated Lewis x, IL-10, but lower interferon-γ expressions
<p>Abstract</p> <p>Background</p> <p><it>H. pylori </it>infection is less prevalent in childhood. This study validated whether the rates of <it>H. pylori </it>colonization depend on different acquisition ages, and correlate with the different gastric Lewis antigens or cytokine expressions after <it>H. pylori </it>acquisition.</p> <p>Methods</p> <p>We applied a young (7-day-old) C57BL/6 mice group (n = 50) and adult (6-week-old) C57BL/6 mice group (n = 50). In each group, 30 mice were challenged with <it>H. pylori </it>and 20 mice served as naïve control. The success of <it>H. pylori </it>colonization was assessed on the 2<sup>nd </sup>week and the 8<sup>th </sup>week, respectively. The intensity of the Lewis x, sialylated Lewis x<sup/>(sialyl-Le<sup>x</sup>), and cytokine expressions, including TNF-α, IFN-γ, IL-6, IL-10, and IL-1β, were immunochemically stained and graded.</p> <p>Results</p> <p>On the 2<sup>nd </sup>week after <it>H. pylori </it>challenge, the colonization rates of <it>H. pylori </it>were similar between the young mice group and the adult mice group (89% vs. 100%, <it>P </it>> 0.05). However, on the 8<sup>th </sup>week, the <it>H. pylori </it>colonization rate was significantly lower in the young mice group than in the adult mice group (53% vs. 95%, <it>P </it>= 0.003). On the 8<sup>th </sup>week, the young mice with a persistence of <it>H. pylori </it>colonization had higher sialyl-Le<sup>x</sup>, higher IL-10, and lower IFN-γ than those of the mice that lost colonization during the 2<sup>nd </sup>to the 8<sup>th </sup>week (<it>P </it>< 0.05).</p> <p>Conclusion</p> <p>The persistence of <it>H. pylori </it>colonization could be an acquisition-age determinant process. After <it>H. pylori </it>exposure at an early acquisition age, the host response with a higher sialyl-Le<sup>x </sup>and IL-10, but a lower IFN-γ correlates to the consequent persistence of <it>H. pylori </it>colonization.</p
Etiology and Treatment of Childhood Peptic Ulcer Disease in Taiwan: A Single Center 9-Year Experience
Background/PurposePeptic ulcer disease (PUD) in children is relatively rare as compared with adults. This study aimed to assess the etiology, clinical and histological characteristics, and treatment of PUD in children.MethodsAll children aged < 18 years with an endoscopic diagnosis of PUD were enrolled in a tertiary referral center. The demographic data, clinical, endoscopic, and histological findings were compared between patients with different causes of PUD.ResultsFrom 1234 endoscopic examinations, 67 (5.4%) children (median age, 11.4 years) with gastric ulcer (GU; n = 27) or duodenal ulcer (DU; n = 40) were included. Thirty-two (47.7%) of them had Helicobacter pylori infection and 11 (16.5%) had previous use of non-steroidal anti-inflammatory drugs (NSAIDs). Non-H. pylori, non-NSAID PUD was found in 24 (35.8%) patients. Children with H. pylori-related PUD had a significantly higher mean age, antral chronic inflammatory score, rate of familial PUD, and presence of DU and nodular gastritis than those with NSAID-related and non-H. pylori, non-NSAID PUD (p < 0.01). In contrast, children with NSAID-related PUD had a higher rate of upper gastrointestinal bleeding, associated with acute febrile disease, than those with H. pylori-related and non-H. pylori, non-NSAID PUD (p < 0.05). All but two patients with non-H. pylori, non-NSAID PUD were disease free after H. pylori eradication and proton pump inhibitor treatment for 1–2 months.ConclusionIn children, H. pylori-related PUD is associated with familial peptic ulcer and the presence of DU. However, short-term NSAID use is correlated highly with GU. The outcome of childhood PUD is good
Lactobacillus acidophilus ameliorates H. pylori-induced gastric inflammation by inactivating the Smad7 and NFκB pathways
<p>Abstract</p> <p>Background</p> <p><it>H. pylori </it>infection may trigger Smad7 and NFκB expression in the stomach, whereas probiotics promote gastrointestinal health and improve intestinal inflammation caused by pathogens. This study examines if probiotics can improve <it>H. pylori</it>-induced gastric inflammation by inactivating the Smad7 and NFκB pathways.</p> <p>Results</p> <p>Challenge with <it>H. pylori </it>increased IL-8 and TNF-α expressions but not TGF-β1 in MKN45 cells. The RNA levels of Smad7 in AGS cells increased after <it>H. pylori </it>infection in a dose-dependent manner. A higher dose (MOI 100) of <it>L. acidophilus </it>pre-treatment attenuated the <it>H. pylori</it>-induced IL-8 expressions, but not TGF-β1. Such anti-inflammatory effect was mediated via increased cytoplasmic IκBα and depletion of nuclear NFκB. <it>L. acidophilus </it>also inhibited <it>H. pylori</it>-induced Smad7 transcription by inactivating the Jak1 and Stat1 pathways, which might activate the TGF-β1/Smad pathway. <it>L. acidophilus </it>pre-treatment ameliorated IFN-γ-induced Smad7 translation level and subsequently reduced nuclear NF-κB production, as detected by western blotting.</p> <p>Conclusions</p> <p><it>H. pylori </it>infection induces Smad7, NFκB, IL-8, and TNF-α production <it>in vitro</it>. Higher doses of <it>L. acidophilus </it>pre-treatment reduce <it>H. pylori</it>-induced inflammation through the inactivation of the Smad7 and NFκB pathways.</p
Matrix metalloproteinase-3 promoter polymorphisms but not dupA-H. pylori correlate to duodenal ulcers in H. pylori-infected females
<p>Abstract</p> <p>Background</p> <p>This study investigated if the <it>H. pylori dupA </it>genotype and certain host single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), including MMP-3, MMP-7, MMP-9, TIMP-1 and TIMP-2, might correlate with ulcer risk of <it>H. pylori-</it>infected Taiwanese patients.</p> <p>Results</p> <p>Of the 549 <it>H. pylori-</it>infected patients enrolled, 470 patients (265 with gastritis, 118 with duodenal ulcer, and 87 with gastric ulcer) received SNPs analysis of MMP-3<sub>-1612 6A > 5A</sub>, MMP-7<sub>-181 A > G</sub>, MMP-9<sub>exon 6 A > G</sub>, TIMP-1<sub>372 T > C </sub>and TIMP-2<sub>-418 G > C </sub>by PCR-RFLP. The 181 collected <it>H. pylori </it>isolates were detected for the <it>dupA </it>genotype by PCR. The rates of <it>dupA</it>-positive <it>H. pylori </it>infection were similar among patients with duodenal ulcer (22.8%), gastric ulcer (20.0%), and gastritis (25.5%) (<it>p </it>> 0.05). Males had higher rates of duodenal ulcer and gastric ulcer than females (<it>p </it>< 0.01). Of <it>H. pylori</it>-infected patients, the MMP-3 6A6A genotype were more common in patients with duodenal ulcers than in those with gastritis (87.7% <it>vs</it>. 74.9%, <it>p </it>< 0.05) in females. This genotype had a 2.4-fold (95% CI: 1.02-5.66) increased risk of duodenal ulcer, compared to those with the 5A carrier. Combining the MMP-3/TIMP-1 genotype as 6A6A/CC, the risk of duodenal ulcer increased up to 3.6 fold (<it>p </it>< 0.05) in <it>H. pylori-</it>infected females.</p> <p>Conclusions</p> <p>The MMP-3 promoter polymorphism, but not the <it>dupA</it>-status, may correlate with susceptibility to duodenal ulcer after <it>H. pylori </it>infection in Taiwanese females.</p
Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer
<p>Abstract</p> <p>Background</p> <p>Nearly all Taiwanese <it>H. pylori </it>stains are <it>cagA</it>-genopositive and encode CagA protein. In this study, we evaluated whether different intensity of tyrosine phosphorylated-CagA (p-CagA) had an impact on the clinical diseases and histological outcomes in this area.</p> <p>Results</p> <p>We enrolled 469 dyspeptic patients and prospectively obtained the gastric biopsy specimens and the <it>H. pylori </it>isolates. These patients were categorized according to the clinical diseases, such as duodenal ulcer, gastric ulcer, gastric cancer, and gastritis with or without intestinal metaplasia. Their gastric specimens were reviewed by the updated Sydney's system. Furthermore, a total of 146 patients were randomly selected from each clinical category for evaluation of their isolates' p-CagA intensity by <it>in vitro </it>AGS cells co-culture. The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates. The isolates from the patients of gastric cancer or gastritis with intestinal metaplasia had stronger p-CagA intensity than those of gastritis without intestinal metaplasia (<it>p </it>≤ 0.002). Moreover, the patients infected with isolates with strong or weak p-CagA intensity had a higher risk of gastric intestinal metaplasia (<it>p </it>< 0.05, odds ratio 3.09~15.26) than those infected with sparse p-CagA isolates.</p> <p>Conclusions</p> <p>Infection with <it>H. pylori </it>stains with stronger p-CagA intensity may lead to an increased risk of gastric intestinal metaplasia and cancer.</p
Identification of the NLS and NES motifs of VP2 from chicken anemia virus and the interaction of VP2 with mini-chromosome maintenance protein 3
<p>Abstract</p> <p>Background</p> <p>VP2 of chicken anemia virus (CAV) is a dual-specificity phosphatase required for virus infection, assembly and replication. The functions of the nuclear localization signal (NLS) and nuclear export signal (NES) of VP2 in the cell, however, are poorly understood. Our study identified the presence of a NLS in VP2 and showed that the protein interacted significantly with mini-chromosome maintenance protein 3 (MCM3) in the cell.</p> <p>Results</p> <p>An arginine-lysine rich NLS could be predicted by software and spanned from amino acids 133 to 138 of VP2. The critical amino acids residues between positions 136 and 138, and either residue 133 or 134 are important for nuclear import in mammalian cells based on systematic mutagenesis. A NES is also predicted in VP2; however the results suggest that no functional NES is present and that this protein is CRM1 independent. It was also shown that VP2 is a chromatin binding protein and, notably, using a co-immunoprecipitation assay, it was found that VP2 association with MCM3 and that this interaction does not require DSP activity.</p> <p>Conclusions</p> <p>VP2 contains a NLS that span from amino acids 133 to 138. VP2 is a CRM1 independent protein during nuclear export and associates with MCM3 in cells.</p
Pin1 positively affects tumorigenesis of esophageal squamous cell carcinoma and correlates with poor survival of patients
Induction of cyclooxygenase-2 overexpression in human gastric epithelial cells by Helicobacter pylori involves TLR2/TLR9 and c-Srcdependent nuclear factor-
ABSTRACT Gastric epithelial cells were incubated with a panel of clinical isolates of Helicobacter pylori, including nonulcer dyspepsia with gastritis (HS, n ϭ 20), gastric ulcer (HU, n ϭ 20), duodenal ulcer (HD, n ϭ 21), and gastric cancer (HC, n ϭ 20). HC strains induced a higher cyclooxygenase-2 (COX-2) expression than those from HS, HD, and HU. The bacterial virulence factors and the host cellular pathways were investigated. Virulence genes of iceA, vacA, babA2, cagA 3Ј repeat region, and hrgA failed to show any association with the disease status and COX-2 expression. Methylation-specific polymerase chain reaction revealed HC strains not affecting the methylation status of COX-2 promoter. Nuclear factor (NF)-B, NF-interleukin 6, and cAMP response element were found to be involved in COX-2 induction. We explored a novel NF-B activation pathway. The mutants of TLR2 and TLR9, but not TLR4, inhibited H. pyloriinduced COX-2 promoter activity, and neutralizing antibodies for TLR2 and TLR9 abolished H. pylori-induced COX-2 expression
Weak up-regulation of serum response factor in gastric ulcers in patients with co-morbidities is associated with increased risk of recurrent bleeding
<p>Abstract</p> <p>Background</p> <p>Serum response factor (SRF) is crucial for gastric ulcer healing process. The study determined if gastric ulcer tissues up-regulate SRF and if such up-regulation correlated with co-morbidities and the risk of recurrent bleeding.</p> <p>Methods</p> <p>Ulcer and non-ulcer tissues were obtained from 142 patients with active gastric ulcers for SRF expression assessed by immunohistochemistry. Based on the degree of SRF expression between these two tissue types, SRF up-regulation was classified as strong, intermediate, and weak patterns. The patients were followed-up to determine if SRF up-regulation correlated to recurrent bleeding.</p> <p>Results</p> <p>Gastric ulcer tissues had higher SRF expression than non-ulcer tissues (<it>p </it>< 0.05). Patients with strong SRF up-regulation had lower rates of stigmata of recent hemorrhage (SRH) on the ulcer base than the others (<it>p </it>< 0.05). Multivariate logistic regression confirmed that co-morbidities and weak SRF up-regulation were two independent factors of recurrent gastric ulcer bleeding (<it>p </it>< 0.05). Combining both factors, there was an 8.29-fold (95% CI, 1.31~52.62; <it>p </it>= 0.03) higher risk of recurrent gastric ulcer bleeding.</p> <p>Conclusions</p> <p>SRF expression is higher in gastric ulcer tissues than in non-ulcer tissues. Weak SRF up-regulation, combined with the presence of co-morbidities, increase the risk of the recurrent gastric ulcer bleeding.</p
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