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Biomedical subjects

P N Hsu

Publications and source records attributed to P N Hsu.

15 recordsLinked to original sources
PubMed2003

Double-blind, randomised, comparative trial of etodolac SR versus diclofenac in the treatment of osteoarthritis of the knee.

A multi-centre, double-blind, randomised parallel-group study was conducted to compare the efficacy and safety between etodolac SR and diclofenac in treating patients with osteoarthritis of the knee. Thirty-two patients receiving etodolac SR (400 mg/day) and 32 patients receiving diclofenac (100 mg/day) were included for analyses. After receiving the study treatment, etodolac SR and diclofenac were shown to produce comparable improvement in pain relief as measured by a 10-cm visual analogue scale. There was no statistically significant difference observed between groups for the degree of functional impairment or the amount of paracetamol taken. The etodolac SR treatment group showed fewer incidents of adverse event. In addition, fewer gastrointestinal symptoms were observed in the etodolac SR treatment group. A statistically higher percentage of etodolac SR-treated patients were better tolerated to the study treatment compared with the diclofenac-treated patients. Etodolac SR-treated patients also took fewer antacids than the diclofenac-treated patients during the treatment period. In conclusion, etodolac SR is an effective treatment with fewer side-effects than diclofenac for patients with osteoarthritis of the knee.

Abdominal Pain↗
PubMed2001

Enhanced proliferation and increased IFN-gamma production in T cells by signal transduced through TNF-related apoptosis-inducing ligand.

TNF-related apoptosis-inducing ligand (TRAIL, also called Apo2L), a novel member of TNF superfamily, induces apoptosis in transformed cell lines of diverse origin. TRAIL is expressed in most of the cells, and the expression is up-regulated in activated T cells. Four receptors for TRAIL have been identified, and there is complex interplay between TRAIL and TRAIL receptors in vivo. The actual biological function of TRAIL/TRAIL receptor is still not clear. Growing evidence has demonstrated that members of TNF superfamily transduce signals after engagement with their receptors. Cross-linking of TRAIL by plate-bound rTRAIL receptor, death receptor 4-Fc fusion protein enhanced T cell proliferation and increased IFN-gamma production in conjunction with immobilized suboptimal anti-CD3 stimulation in mouse splenocytes. The increase of T cell proliferation by death receptor 4-Fc was dose dependent, and this effect could be blocked by soluble rTRAIL proteins, indicating the occurrence of reverse signaling through TRAIL on T cell. The enhanced secretion of IFN-gamma mediated via TRAIL could be blocked by SB203580, a p38 mitogen-activated protein kinase-specific inhibitor. Thus, in addition to its role in inducing apoptosis by binding to the death receptors, TRAIL itself can enhance T cell proliferation after TCR engagement and signal the augmentation of IFN-gamma secretion via a p38-dependent pathway. This provides another example of reverse signaling by a member of TNF superfamily. In conclusion, our data suggest that TRAIL can itself transduce a reverse signal, and this may shed light on the biological function of TRAIL.

Animals↗
PubMed2001

Association of mouse mammary tumor virus superantigen with MHC class II during biosynthesis.

Mouse mammary tumor viruses encode superantigens that interact with MHC class II proteins and stimulate T cells. We show here that presentation of mouse mammary tumor virus superantigen does not require DM. Furthermore, we have identified a strong class II peptide binding motif in the Mtv-7 superantigen, and we show that this motif is necessary for association with class II molecules in in vitro translation and in vivo functional assays. Our results suggest that endogenously synthesized viral superantigen can bind to MHC class II heterodimers during biosynthesis in the endoplasmic reticulum in a manner analogous to that used by the class II-associated invariant chain.

Amino Acid Motifs↗
PubMed2001

Eradication of Helicobacter pylori prevents ulcer development in patients with ulcer-like functional dyspepsia.

BACKGROUND: Although the eradication of Helicobacter pylori infection benefits patients with gastric or duodenal ulcers, the value of eradicating the infection in the patients with functional dyspepsia (FD) remains controversial. AIMS: To determine whether eradicating H. pylori can prevent the subsequent development of ulcers or relieve the symptoms of functional dyspepsia patients. METHODS: In a double-blind, placebo-controlled trial, 161 patients infected with H. pylori who had functional dyspepsia were randomly assigned to 7 days of treatment with a lansoprazole-based triple therapy or placebo and then followed for 1 year. The main outcome measures were the development of peptic ulcers and the resolution of symptoms. RESULTS: H. pylori was eradicated in 63 out of 81 patients (78%) in the treatment group and none of the 80 patients (0%) in the placebo group. During the follow-up period, two patients in the treatment group and six patients in the placebo group developed peptic ulcers at repeat endoscopy (2.5% vs. 7.5%; 95% CI: -12 to 2). The reduction in ulcer rates was statistically significant in the 'ulcer-like' sub-group (0% vs. 16.7%; 95% CI: -32 to -2), but not in the 'dysmotility-like' and 'unclassifiable' sub-groups. Regarding symptom response, the resolution rates of symptoms were similar between the treatment and placebo groups (58.0% vs. 55.0%, 95% CI: -12 to 18). Additionally, no significant differences existed in the symptom responses between the treatment and control arms in each of the dyspepsia sub-groups. CONCLUSIONS: Eradicating H. pylori can prevent the subsequent development of peptic ulcers in the patients with 'ulcer-like' functional dyspepsia. However, this approach does not significantly reduce the symptoms of functional dyspepsia patients.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

HLA DPB1*0201 allele is negatively associated with immunoglobulin E responsiveness specific for house dust mite allergens in Taiwan.

BACKGROUND: House dust mite (HDM) Dermatophagoides pteronyssinus is the most important source of indoor allergens that cause allergic diseases in Taiwan. We prepared purified HDM allergens (Der p 1, Der p 2 and Der p 5) to detect allergen-specific immunoglobulin (Ig) E responsiveness among a large number of test subjects. The robust genetic typing system for HLA class II genes also facilitated the study on association of HLA and allergic response toward HDM. OBJECTIVE: This study intended to investigate the association between HLA class II alleles and the IgE responsiveness to the major allergens from HDM, D. pteronyssinus. METHODS: Two hundred and forty-eight subjects were selected for HLA association study. Plasma HDM allergen (Der p 1, Der p 2, Der p 5) -specific IgE and Der p 2-specific IgG antibodies were detected by ELISA, while HLA class II -DRB1, -DQA1, -DQB1, -DPB1 genetic polymorphism was determined by polymerase chain reaction/sequence-specific oligonucleotide probe hybridization (PCR/SSOPH). Statistical comparison of the allelic distribution of each HLA class II genes among the individuals with/without HDM allergen-specific IgE and IgG antibodies were performed. RESULTS: There was no significant association between HLA DRB1, DQB1, DQA1 alleles and HDM-specific IgE responsiveness noted. Only DRB1*0803 and the linked DQA1*0103 alleles showed positive association with Der p 5-specific IgE responsiveness. However, we found that HLA-DPB1*1301 predisposed subjects to IgE responsiveness to HDM Der p 5. HLA DPB1*0501 was weakly associated with the IgE responsiveness to HDM Der p 1 and Der p 5. There was a strong negative association between the HLA-DPB1*0201 allele with IgE responsiveness to Der p 1 (OR: 0.30, P </= 0.0001, P </= 0.0007, Pc </= 0.010). CONCLUSION: We clearly observed the association between HLA DPB1 alleles and specific IgE responsiveness to HDM major allergens. The molecular mechanism of HLA-DPB1*0201 involvement in protecting subjects from HDM-specific IgE responsiveness awaits further investigation.

Adult↗
PubMed2000

Risk factors for presentation with bleeding in patients with Helicobacter pylori-related peptic ulcer diseases.

At present, there is no study that simultaneously addresses the apparent differences between bacterial and host factors in patients with bleeding and nonbleeding Helicobacter pylori-related ulcer diseases. Therefore, we designed this prospective study to evaluate whether there are identifiable differences between the two groups of patients whose H. pylori-related peptic ulcer diseases present with bleeding or dyspepsia. From July 1996 to November 1996, consecutive patients presenting with upper gastrointestinal bleeding or dyspepsia were enrolled if H. pylori-related ulcer diseases were confirmed. Fifteen clinical, endoscopic, histologic, and serologic factors were tested for association with ulcer bleeding by a logistic regression analysis. In the study period, bleeding occurred in 39 out of 119 patients with H. pylori-related peptic ulcer diseases. Multivariate analysis showed that ingestion of nonsteroidal antiinflammatory drugs (NSAIDs; p = 0.0156; odds ratio = 5:4), ulcer size > or = 1 cm (p = 0.0033; odds ratio = 4:2), and low bacterial density (p = 0.0030; odds ratio = 4:1) were independent factors associated with the risk of bleeding. There were no associations between ulcer bleeding and age, sex, smoking, alcohol consumption, the histologic grade of gastritis, location and number of ulcers, and the cytotoxin-associated gene (CagA) status of H. pylori strain. Therefore, we concluded that H. pylori-related ulcer patients who use NSAIDs or have large ulcers are more likely to present with upper gastrointestinal bleeding; that the CagA-bearing strains are not associated with the development of bleeding complication in patients with peptic ulcer diseases; and that the exact reason concerning the association between low bacterial density and ulcer bleeding merits further investigation.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Impact of Helicobacter pylori eradication on the development of MALT, gland atrophy and intestinal metaplasia of the antrum.

BACKGROUND: Chronic Helicobacter pylori infection leads to the development of mucosa-associated lymphoid tissue (MALT), gland atrophy, intestinal metaplasia, and in certain individuals, gastric lymphoma and adenocarcinoma. We conducted a prospective study to determine the effect of H pylori eradication on the development of MALT, gland atrophy and intestinal metaplasia. METHODS: From July 1995 to October 1996, 63 consecutive patients with H pylori-associated peptic ulcer disease were enrolled in a bacterial eradication trial. The grade of MALT and the degree of gastritis of the antrum were assessed using Wotherspoon's scale and the Sydney system before treatment, and at eight weeks and one year after H pylori eradication therapy. RESULTS: During the study period, 43 patients received complete follow-up. In the patient group with eradication failure (n = 22), MALT score was significantly decreased at the end of the eighth week (p < 0.05) but returned to the initial level by one year of follow-up. There were no changes in the scores for inflammation, neutrophil activity, gland atrophy or intestinal metaplasia at the end of the eighth week and at one year following H pylori eradication therapy. In contrast, there was a marked reduction in the MALT, inflammation, and activity scores at eight weeks (p < 0.01, < 0.05 and < 0.05, respectively) and one year after treatment (p < 0.05, < 0.001 and < 0.001, respectively) in the patient group with successful eradication (n = 21). However, no significant changes in gland atrophy and intestinal metaplasia were observed during the follow-up period. CONCLUSIONS: Eradication of H pylori leads to regression of MALT in the stomach, but the degrees of gland atrophy and intestinal metaplasia remain unchanged, even after one-year of follow-up.

Adult↗
PubMed1997

Correlation of serum immunoglobulin G Helicobacter pylori antibody titers with histologic and endoscopic findings in patients with dyspepsia.

Serum immunoglobulin G (IgG) antibody tests are used extensively. We attempted to find out whether the titers of anti-Helicobacter pylori IgG antibody correlated with the degree of macroscopic gastrointestinal damage, the severity of antral gastritis, and the density of antral H. pylori colonization in symptomatic patients. Peripyloric antral biopsy specimens were obtained from 50 consecutive patients with dyspepsia undergoing upper gastrointestinal endoscopy. The macroscopic gastrointestinal damage and the histologic grades of antral gastritis were scored by a modified Lanza scale and Sydney system, respectively. In addition, the densities of antral H. pylori colonization were graded semiquantitatively. Serum IgG antibodies to H. pylori were measured by enzyme-linked immunosorbent assay. Thirty-six (M/F = 29/7) of the 50 patients had H. pylori infection documented by histologic examination or rapid urease test or both. Among the subjects, the IgG antibody titers to H. pylori correlated significantly with the grades of antral polymorphonuclear cell infiltration (p = 0.002) and antral bacterial density (p = 0.01) but not with endoscopic scores, the grades of mononuclear cell infiltration, mucosal atrophy, or intestinal metaplasia (p > 0.05). In addition, endoscopic scores also were found to be significantly correlated with antral bacterial density (p = 0.049) and the grade of polymorphonuclear cell infiltration (p = 0.012). We therefore conclude that high titers of IgG antibody to H. pylori in patients with dyspepsia indicate dense H. pylori colonization and severe antral polymorphonuclear cell infiltration. However, it cannot replace endoscopic examination to evaluate the degree of macroscopic gastrointestinal damage.

Aged↗
PubMed1996

Virus-encoded superantigens.

Superantigens are microbial agents that have a strong effect on the immune response of the host. Their initial target is the T lymphocyte, but a whole cascade of immunological reactions ensues. It is thought that the microbe engages the immune system of the host to its own advantage, to facilitate persistent infection and/or transmission. In this review, we discuss in detail the structure and function of the superantigen encoded by the murine mammary tumor virus, a B-type retrovirus which is the causative agent of mammary carcinoma. We will also outline what has more recently become known about superantigen activity associated with two human herpesviruses, cytomegalovirus and Epstein-Barr virus. It is likely that we have only uncovered the tip of the iceberg in our discovery of microbial superantigens, and we predict a flood of new information on this topic shortly.

Animals↗
PubMed1995

Superantigens. Gazing into the crystal ball.

The recently determined crystal structures of complexes between bacterial toxin 'superantigens' and MHC class II molecules shed light on the nature of the interactions between these two molecules.

Bacterial Toxins↗
PubMed1995

Direct binding of the Mtv7 superantigen (Mls-1) to soluble MHC class II molecules.

The superantigen encoded by the mouse mammary tumor virus (MMTV) is a potent stimulator of T cells when bound to MHC class II molecules. Recent data from this laboratory have shown that the Mtv7 superantigen, Mls-1, elicits a strong T cell response when presented by HLA-DR. To expand these observations further, we have produced the 28 kDa extracellular domain and the 18 kDa carboxy-terminal subfragment of the Mls-1 protein in E. coli and studied their interaction with human MHC class II molecules in vitro. In this report, we demonstrate direct binding of these recombinant forms of the Mls-1 protein to soluble HLA-DR1 and HLA-DR4, but not to HLA-A2. Our data imply a unique class II interaction site of retroviral superantigens that is not shared with bacterial superantigens.

Animals↗
PubMed1991

A subset of acute lymphoblastic leukemia with co-expression of myeloid antigens: prevalence and clinical significance.

In order to evaluate the biological features and clinical significance of myeloid antigen expression in acute lymphoblastic leukemia (ALL), immunophenotype analysis was performed on leukemic cells from 160 patients diagnosed as ALL by the French, American and British (FAB) criteria using a comprehensive panel of monoclonal antibodies to lymphoid and myeloid associated antigens. Expression of myeloid antigens was found in 32 cases (20%), including 11 out of 49 adults (22.4%) and 21 out of 111 children (18.9%). CD33 was positive in 18 patients (11.3% of the total cases), CD13 in 15 patients (9.4%), CD 11b in 12 patients (7.5%) and CD14 in 1 patient (0.6%). Nine patients expressed two or more myeloid antigens. There were no significant differences in clinical manifestations and hematological pictures between the ALL patients with myeloid antigen expression (My+ ALL) and those without (My- ALL). No consistent chromosomal abnormality was found in My+ ALL. Eighty percent of the childhood and 44.4% of the adult My+ ALL patients achieved complete remission, compared with 87% and 80%, respectively, for childhood and adult My- ALL, but the differences were not statistically significant. After a median follow-up of 2.1 years, there were also no statistically significant associations between myeloid antigen expression and shorter duration of remission or poorer survival rate for patients with both adult and childhood ALL.

Adult↗
PubMedDate not supplied

Expression of human Fas ligand on mouse beta islet cells does not induce insulitis but is insufficient to confer immune privilege for islet grafts.

Fas (CD95) and Fas ligand (FasL/CD95L) are involved in programmed cell death and the regulation of host immune responses. FasL has been shown to provide immune privilege, thus prolonging the survival of unmatched grafts in a variety of tissues, such as eyes and testis. In murine FasL (mFasL) transgenic mice, FasL provoked granulocyte infiltration and insulitis in the pancreas. We intended to study whether the expression of human FasL, instead of mFasL, on mouse beta islet cells could avoid granulocyte infiltration, and whether islet cells transgenic for FasL could be used in islet transplantation. We produced transgenic mice in which the human FasL transgene was driven by rat insulin promoter and was expressed exclusively in the pancreas islet cells in ICR mice. In contrast to mFasL transgenic mice, histochemical staining showed that the pancreas was intact in human FasL transgenic ICR mice. However, when human FasL transgenic islet cells were transplanted into allogeneic mice with streptozotocin-induced diabetes, human FasL appeared not to prolong graft survival. Intensive granulocyte infiltration into the islet grafts was observed in recipients (Balb/c mice) which received islet grafts from human FasL transgenic mice, but not from nontransgenic, allogeneic ICR mice on day 31. Our observations suggest that FasL alone is insufficient to confer immune protection, and that other environmental factors might contribute to the formation of immune privilege sites in vivo

Animals↗
PubMedDate not supplied

Impact of bacterial eradication on the cell proliferation and p53 protein accumulation in Helicobacter pylori-associated gastritis.

BACKGROUND: This study investigates the cell proliferation and the expression of p53 protein in Helicobacter pylori (H. pylori)-associated gastritis and assesses the effect of bacterial eradication on these epithelial factors. MATERIAL AND METHODS: Seventy-nine patients with H. pylori-associated gastritis were randomized into the control group (n = 38) and anti-H. pylori group (n = 41). Each patient received endoscopic examinations with gastric biopsy before and 8 weeks after the treatment. The specimens from gastric antrum were immunostained for monoclonal antibodies against the proliferating cell nuclear antigen (PCNA) and p53 protein. RESULTS: In the control group, the total labeling index (L.I.) of PCNA and the positive index (P.I.) of p53 in the whole foveolar epithelium were unchanged after treatment. In the anti-H. pylori group, 35 of 41 cases (85.3%) achieved eradication of H. pylori. Amongst the H. pylori-eradicated cases, the total L.I. of PCNA in the whole foveolar epithelium did not meaningfully alter after H. pylori elimination (p > 0.05). However, a significant reduction of L.I. was observed in the middle compartments of the gastric pits (before vs. after treatment: 14.0 vs. 7.3, p < 0.05). With regard to the p53 expression, the P.I.s were significantly decreased in the whole foveolar epithelium (before vs. after treatment: 0.57 vs. 0.17, p < 0.05) and in each compartment of the gastric pits (before vs. after treatment: [upper compartment]: 0.34 vs. 0.15, p < 0.05; [middle compartment]: 0.67 vs. 0.23, p < 0.05; [lower compartment]: 0.71 vs. 0.20, p < 0.05) after eradication of H. pylori. CONCLUSIONS: Bacterial eradication reverses the hyperproliferating status of the foveolar epithelium in patients with H. pylori gastritis and leads to a decrease in p53 accumulation in the epithelial cells.

2-Pyridinylmethylsulfinylbenzimidazoles↗