Biomedical subjects

Kun Wang

Publications and source records attributed to Kun Wang.

At least 73 records · Page 4Linked to original sources

PubMed2004

Perioperative cimetidine administration promotes peripheral blood lymphocytes and tumor infiltrating lymphocytes in patients with gastrointestinal cancer: Results of a randomized controlled clinical trial.

AIM: To study the effects of perioperative administration of cimetidine (CIM) on peripheral blood lymphocytes, natural killer (NK) cells and tumor infiltrating lymphocytes (TIL) in patients with gastrointestinal (GI) cancer. METHODS: Forty-nine GI cancer patients were randomized into treatment group, who took CIM in perioperative period, and control group, who did not take the drug. The treatment was initiated 7 days before operation and continued for 10 days after surgery. At baseline examination before operation, on the 2nd and 10th postoperative days, total T lymphocytes, T helper cells, T suppressor cells, and NK cells in peripheral blood were measured respectively by immunocytochemical method using mouse-anti human CD(3), CD(4), CD(8) and CD(57) monoclonal antibodies. Blood samples from 20 healthy volunteers were treated in the same way as normal controls. Surgical specimens were examined during routine histopathological evaluation for the presence of TIL in tumor margin. Immunohistochemical study was performed to measure the proportion of T and B lymphocytes in TIL population. T and B lymphocytes were detected respectively using mouse-anti-human CD(3) and CD(20) monoclonal antibodies. RESULTS: In comparison with normal controls, both the treatment and control groups had decreased T cells, T helper cells and NK cells at baseline. In control group, total T cells, T helper cells and NK cells declined continuously with the disease progression and the decrease became more obvious after operation. From baseline to the 2nd postoperative day, the proportion of total T cells, T helper cells, and NK cells went down from 60.5+/-4.6% to 56.2+/-3.8%, 33.4+/-3.7% to 28.1+/-3.4%, and 15.0+/-2.8% to 14.2+/-2.2%, respectively. On the other hand, there were significant improvements in these parameters after CIM treatment. On the 10th postoperative day, the treatment group had significantly higher percentages of total T cells, T helper cells and NK cells than control group. Moreover, CIM treatment also boosted TIL response, as was reflected by findings that 68% (17/25) of the patients in treatment group had significant TIL responses and only 25% (6/24) of the cases had discernible TIL responses (P<0.01). CONCLUSION: Perioperative application of CIM to GI cancer patients could help restore the diminished cellular immunity induced by tumor burden and surgical maneuver. The drug could also boost TIL responses to tumor. These effects suggest that the drug be used as an immunomodulator for GI cancer patients.

Adjuvants, Immunologic↗

PubMed2004

Relationship between mutations of mitochondrial DNA ND1 gene and type 2 diabetes.

BACKGROUND: Recent studies have indicated that many mutations in mitochondrial (mt) DNA NDI gene region are related to diabetes mellitus. In this study we explored the relationship between various mtDNA ND1 gene mutations and type 2 diabetes mellitus (DM) among Chinese. METHODS: Using PCR restriction fragment length polymorphism (PCR-RFLP) analysis and gene sequencing, 4 spots of mtDNA (nt3243, nt3316, nt3394, nt3426) were screened in 478 diabetics and 430 non-diabetic subjects. RESULTS: In diabetic group, there were 13 carriers (2.72%) of 3316 G-->A mutation,12 (2.51%) of 3394 T-->C mutation and 2 (0.42%) of 3426A-->G mutation. In controls, only 3394 T-->C mutation was observed in 2 subjects (0.47%). There was significant difference in the frequency of 3316 and 3394 mutation between two groups (P < 0.05, respectively). More subjects with mitochondrial DNA ND1 gene mutations had DM family history and greater tendency of maternal inheritance when compared to those patients without mutation in diabetic group (P < 0.01). A 3426 mutation diabetic pedigree was studied, and we found 12 maternal members in the family had the same mutation. CONCLUSION: mtDNA ND1 gene mutations at nt3316 (G-->A), nt3394 (T-->C) and 3426 (A-->G) might contribute to the pathogenesis of DM with other genetic factors and environment factors.

Base Sequence↗

PubMed2003

Anomalous pancreatic duct anatomy, ectopic distal location of the papilla of Vater and congenital biliary dilatation: a new developmental triad?

BACKGROUND: The opening of the papilla of Vater represents the orifice of the embryonic hepatic diverticulum from which the ventral pancreas, common bile duct, and liver are derived. Recently, we found a strong association between congenital biliary dilatation (CBD), certain types of pancreatic ductal anatomy (PDA), and ectopic distal location of the papilla of Vater which prompted us to study the relationship between the location of the papilla of Vater and abnormal PDA. METHODS: A total of 118 patients with CBD were studied. Cholangiograms documented the presence of pancreaticobiliary malunion (PBMU), the location of the papilla of Vater, and the PDA. Eleven age-matched patients with intermittent jaundice were used as controls. RESULTS: In the control group, the papilla of Vater was located normally in the descending portion of the duodenum in all cases. In the 118 CBD patients, the papilla of Vater was located normally in 38 (32.2%), but in 80 (67.8%), the papilla was located distal to the descending portion of the duodenum. When the papilla was located distally, the incidences of the specific types of PDA studied were significantly higher than when the papilla was located normally (p<0.01). Pancreatic duct dilatation was also more frequent if the papilla was located distally (28.7%) compared with CBD patients with a normal papilla (7.9%) or normal controls (0%) (both p<0.01). PBMU was present in all CBD patients and absent in all controls. CONCLUSION: Our study strongly suggests that abnormalities occurring during early embryological development of the hepatic diverticulum are responsible for the association between abnormal PDA and ectopic distal location of the papilla of Vater in CBD.

Adolescent↗

PubMed2003

Experimental allogenic penile transplantation.

PURPOSE: The aim of this study was to assess the feasibility of allogenic penile transplantation (PTx) for creating a source of viable penile tissue for use in penile reconstruction. METHODS: The entire penis from an adult Brown-Norway rat was transplanted into a pouch created in the omentum of an adult Lewis rat (fully allogenic PTx, n = 23). Recipients were divided into 2 groups according to immunosuppressant (FK506) usage: in the FK+ group, FK506 (0.6 mg/kg/d) was administered intraperitoneally until a predetermined day (day 3, 5, 7, 10, 14, or 21) after PTx, and then the grafts were harvested. No FK506 was used in the FK- group. Syngeneic PTx (n = 8) patients were used as controls. All grafts were stained with H&E for histologic examination. RESULTS: At laparotomy, each successfully transplanted penis appeared as a cylindrical mass in the omentum. Grafts could be mobilized to the genital area because of a long omental pedicle. Graft survival in the control and FK+ groups was 100%. Rejection was minimal to moderate in FK+ grafts harvested on days 3 and 5 after PTx and minimal or absent in FK+ grafts harvested on days 7, 10, 14, and 21. Penile structure on H&E staining was normal in FK+ and control specimens. Rejection with massive cellular infiltration was observed in all FK- grafts. CONCLUSIONS: FK506 successfully prevented rejection in allogenic PTx, and the authors' technique has potential for creating viable penile tissue that could be used as an option for penile reconstruction.

Animals↗

PubMed2003

Living-related partial bladder transplantation for bladder augmentation in rats: an experimental study.

PURPOSE: To assess the feasibility of transplanting adult bladder tissue to its offspring as a source of neobladder tissue for bladder augmentation. METHODS: The dome of the bladder of an adult Lewis rat was excised and transplanted into the omentum of a 6-week-old offspring (living-related partial bladder transplant: n = 15). The bladder remnant of the donor rat was closed. Two weeks after transplantation, a laparotomy was performed to mobilize the bladder graft with its omental pedicle into the pelvis. Bladder augmentation (BA) was performed by anastomosing the graft to the recipient's bladder. Thirty days after BA, the entire neobladder was excised and histopathologically examined. RESULTS: At laparotomy, each bladder graft appeared macroscopically as a thin-walled cyst in the recipient's omentum. Each graft could be mobilized into the pelvis and anastomosed to the recipient's bladder. BA was successful in all 15 recipients, and histopathologic studies showed that the mucosa was normal throughout each neobladder. Postoperatively, donors and recipients were clinically well without any sign of urinary incontinence or obstruction. CONCLUSIONS: This is the first report of adult tissue being transplanted successfully into a recipient without vascular reconstruction in a rat. Living-related partial bladder transplantation for the purpose of BA is feasible using our technique and could have application as an alternative technique for BA in a rat.

Anastomosis, Surgical↗

PubMed2003

Translocation of annexin I from cellular membrane to the nuclear membrane in human esophageal squamous cell carcinoma.

AIM: To investigate the alteration of the annexin I subcellular localization in esophageal squamous cell carcinoma (ESCC) and the correlation between the translocation and the tumorigenesis of ESCC. METHODS: The protein localization of annexin I was detected in both human ESCC tissues and cell line via the indirect immunofluorescence strategy. RESULTS: In the normal esophageal epithelia the annexin I was mainly located on the plasma membrane and formed a consecutive typical trammels net. Annexin I protein also expressed dispersively in cytoplasm and the nuclei without specific localization on the nuclear membrane. In esophageal cancer annexin I decreased very sharply with scattered disappearance on the cellular membrane, however it translocated and highly expressed on the nuclear membrane, which was never found in normal esophageal epithelia. In cultured esophageal cancer cell line annexin I protein was also focused on the nuclear membrane, which was consistent with the result from esophageal cancer tissues. CONCLUSION: This observation suggests that the translocation of annexin I protein in ESCC may correlate with the tumorigenesis of the esophageal cancer.

Annexin A1↗

PubMed2003

Loss of clusterin both in serum and tissue correlates with the tumorigenesis of esophageal squamous cell carcinoma via proteomics approaches.

AIM: To identify the differentially secreted proteins or polypeptides associated with tumorigenesis of esophageal squamous cell carcinoma (ESCC) from serum and to find potential tumor secreted biomarkers. METHODS: Proteins from human ESCC tissue and its matched adjacent normal tissue; pre-surgery and post-surgery serum; and pre-surgery and normal control serum were separated by two-dimensional electrophoresis (2-DE) to identify differentially expressed proteins. The silver-stained 2-DE were scanned with digital ImageScanner and analyzed with ImageMaster 2D Elite 3.10 software. A cluster of protein spots differentially expressed were selected and identified with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). One of the differentially expressed proteins, clusterin, was down-regulated in cancer tissue and pre-surgery serum, but it was reversed in post-surgery serum. The results were confirmed by semi-quantitative reverse-transcription (RT)-PCR and western blot. RESULTS: Comparisons of the protein spots identified on the 2-DE maps from human matched sera showed that some proteins were differentially expressed, with most of them showing no differences in composition, shape or density. Being analyzed by MALDI-TOF-MS and database searching, clusterin was differentially expressed and down-regulated in both cancer tissue and pre-surgery serum compared with their counterparts. The results were also validated by RT-PCR and western blot. CONCLUSION: The differentially expressed clusterin may play a key role during tumorigenesis of ESCC. The 2DE-MS based proteomic approach is one of the powerful tools for discovery of secreted markers from peripheral.

Aged↗

PubMed2003

[Functional characterization of recombinant myostatin and its inhibitory role to chicken muscle development].

Myostatin is a recently discovered member of transforming growth factor beta (TGFbeta) superfamily and shares similar structure features with other members of TGFbeta superfamily. For a better understanding of molecular mechanism of myostatin function, the production of C-terminal truncated form of recombinant myostatin protein (rMSTN) in E. coli was previously reported. Herein, the functional role of the recombinant myostatin in regulating myogenesis in a chicken embryonic myoblasts (CEMs) system was determined. By using flow cytometric analysis, the myostatin was found to inhibit cell cycle transition from G1 to S phase and result in a cell cycle arrest at G1. In addition, myostatin blocked the multi-nucleus myotube formation and caused a decreased expression of the muscle cell differentiation markers (myogenin and MHC) in CEMs. In this study, a rabbit polyclonal antibody against myostatin was produced and high affinity and specificity of this anti-myostatin antibody to recombinant and endogenous myostatin were assayed by Western blot analysis. Further studies showed that the antibody could also recognize the tissue endogenous myostatin of human, mouse and rat. A specific 40 kD band was detected in chicken muscle, which suggested that chicken myostatin might have different splicing pattern. Immunofluorescence assay indicated that myostatin predominantly existed in the cytosol in C2C12 cells. Taken together, the results show that myostatin inhibits chicken muscle cells proliferation and differentiation and down-regulates expression of two differentiation marker gene in CEMs. Remarkably, production of functional recombinant myostatin protein and its specific antibody provides important reagents for unraveling molecular mechanisms underlying myostatin action during myogenesis.

Animals↗

PubMed2003

[Preliminary research of the relationship between overexpression of facilitative glucose transporter-1 and fluorodeoxyglucose uptake in primary human lung squamous cell carcinoma].

OBJECTIVE: To assess the relationship between the overexpression of facilitative glucose transporter-1 (Glut1) and fluorine-18 fluorodeoxyglucose (FDG) uptake in patients with primary lung squamous cell carcinoma. METHODS: From April 1999 to March 2001, 23 patients with lung squamous cell carcinoma were imaged using FDG positron emission tomography (PET) before surgery. Their maximum and mean standard uptake values (SUVmax and SUVmean) of tumor and SUV of the normal lung (SUVlung) were measured. The expression of Glut1 of all the 23 cases was analysed in paraffin sections using SP immunohistochemistry. RESULTS: All the 23 tumors tested were Glut1 positive (69 +/- 18)% of tumor cell area was positive and staining intensity was 4.6 +/- 0.7. All tumors of the patients could be detected by FDG-PET. FDG uptake of tumor was higher than that of normal lung (P < 0.01). SUVmax, SUVmean and SUVlung were 8.33 +/- 4.14, 6.10 +/- 3.00 and 0.38 +/- 0.13 respectively. Correlations were found among Glut1 expression and FDG uptake and tumor size (P < 0.01). CONCLUSIONS: (1) Glut1 overexpression is universal in the lung squamous cell carcinoma. (2) SUV was higher in the lung squamous cell carcinoma than that of the normal lung tissue. (3) Glut1 expression and FDG uptake and tumor size appear to be correlated with each other in patients with lung squamous cell carcinoma.

Aged↗

PubMed2002

Compromised ATP binding as a mechanism of phosphoinositide modulation of ATP-sensitive K+ channels.

Inhibition of ATP-sensitive K(+) (K(ATP)) channels by ATP, a process presumably initiated by binding of ATP to the pore-forming subunit, Kir6.2, is reduced in the presence of phosphoinositides (PPIs). Previous studies led to the hypothesis that PPIs compromise ATP binding. Here, this hypothesis was tested using purified Kir6.2. We show that PPIs bind purified Kir6.2 in an isomer-specific manner, that biotinylated ATP analogs photoaffinity label purified Kir6.2, and that this labeling is weakened in the presence of PPIs. Patch-clamp measurements confirmed that these ATP analogs inhibited Kir6.2 channels, and that PPIs decreased the level of inhibition. These results indicate that interaction of PPIs with Kir6.2 impedes ATP-binding activity. The PPI regulation of ATP binding revealed in this study provides a putative molecular mechanism that is potentially pivotal to the nucleotide sensitivity of K(ATP) channels.

Adenosine Triphosphate↗

PubMed2002

Intrasplenic transplantation of syngenic hepatocytes modified by IFN-gamma gene ameliorates hepatic fibrosis in rats.

Transplanted hepatocytes are ideal carriers for exogenous genes in liver gene therapy. The present study investigated the anti-fibrogenic effects of intrasplenically transplanted hepatocytes modified with interferon gamma (IFN-gamma) gene on cirrhotic rats. Hepatocytes isolated from normal Sprague-Dawley (SD) rats were transfected with an adenoviral vector encoding human IFN-gamma gene (AdCMVhIFN-gamma) and transplanted into the spleens of syngenic recipients with ongoing liver fibrosis induced by carbon tetrachloride (CCl(4)). Histology was assessed, and liver hydroxyproline was detected. Additionally, serum procollagen type III (PIIINP) levels and hepatic collagenase activity were measured to determine hepatic collagen synthesis and degradation. Transplantation with AdCMVhIFN-gamma transfected hepatocytes ameliorated the histological outcome of liver fibrosis by reducing liver collagen content and decreasing hepatic hydroxyproline. Additionally, IFN-gamma transfected hepatocytes reduced serum PIIINP levels and increased hepatic collagenase activity. Our data suggest that transplantation of IFN-gamma transfected hepatocytes may reduce the pace of liver fibrosis by inhibiting the synthesis and enhancing the degradation of hepatic collagen.

Adenoviridae↗

PubMed2002

Hydrocarbon oxidation by Bis-mu-oxo manganese dimers: electron transfer, hydride transfer, and hydrogen atom transfer mechanisms.

Described here are oxidations of alkylaromatic compounds by dimanganese mu-oxo and mu-hydroxo dimers [(phen)(2)Mn(IV)(mu-O)(2)Mn(IV)(phen)(2)](4+) ([Mn(2)(O)(2)](4+)), [(phen)(2)Mn(IV)(mu-O)(2)Mn(III)(phen)(2)](3+) ([Mn(2)(O)(2)](3+)), and [(phen)(2)Mn(III)(mu-O)(mu-OH)Mn(III)(phen)(2)](3+) ([Mn(2)(O)(OH)](3+)). Dihydroanthracene, xanthene, and fluorene are oxidized by [Mn(2)(O)(2)](3+) to give anthracene, bixanthenyl, and bifluorenyl, respectively. The manganese product is the bis(hydroxide) dimer, [(phen)(2)Mn(III)(mu-OH)(2)Mn(II)(phen)(2)](3+) ([Mn(2)(OH)(2)](3+)). Global analysis of the UV/vis spectral kinetic data shows a consecutive reaction with buildup and decay of [Mn(2)(O)(OH)](3+) as an intermediate. The kinetics and products indicate a mechanism of hydrogen atom transfers from the substrates to oxo groups of [Mn(2)(O)(2)](3+) and [Mn(2)(O)(OH)](3+). [Mn(2)(O)(2)](4+) is a much stronger oxidant, converting toluene to tolyl-phenylmethanes and naphthalene to binaphthyl. Kinetic and mechanistic data indicate a mechanism of initial preequilibrium electron transfer for p-methoxytoluene and naphthalenes because, for instance, the reactions are inhibited by addition of [Mn(2)(O)(2)](3+). The oxidation of toluene by [Mn(2)(O)(2)](4+), however, is not inhibited by [Mn(2)(O)(2)](3+). Oxidation of a mixture of C(6)H(5)CH(3) and C(6)H(5)CD(3) shows a kinetic isotope effect of 4.3 +/- 0.8, consistent with C-H bond cleavage in the rate-determining step. The data indicate a mechanism of initial hydride transfer from toluene to [Mn(2)(O)(2)](4+). Thus, oxidations by manganese oxo dimers occur by three different mechanisms: hydrogen atom transfer, electron transfer, and hydride transfer. The thermodynamics of e(-), H(*), and H(-) transfers have been determined from redox potential and pK(a) measurements. For a particular oxidant and a particular substrate, the choice of mechanism is influenced both by the thermochemistry and by the intrinsic barriers. Rate constants for hydrogen atom abstraction by [Mn(2)(O)(2)](3+) and [Mn(2)(O)(OH)](3+) are consistent with their 79 and 75 kcal mol(-)(1) affinities for H(*). In the oxidation of p-methoxytoluene by [Mn(2)(O)(2)](4+), hydride transfer is thermochemically 24 kcal mol(-)(1) more facile than electron transfer; yet the latter mechanism is preferred. Thus, electron transfer has a substantially smaller intrinsic barrier than does hydride transfer in this system.

Anthracenes↗

PubMed2002

A novel member of a zinc transporter family is defective in acrodermatitis enteropathica.

The rare inherited condition acrodermatitis enteropathica (AE) results from a defect in the absorption of dietary zinc. Recently, we used homozygosity mapping in consanguineous Middle Eastern kindreds to localize the AE gene to an approximately 3.5-cM region on 8q24. In this article, we identify a gene, SLC39A4, located in the candidate region and, in patients with AE, document mutations that likely lead to the disease. The gene encodes a histidine-rich protein, which we refer to as "hZIP4," which is a member of a large family of transmembrane proteins, some of which are known to serve as zinc-uptake proteins. We show that Slc39A4 is abundantly expressed in mouse enterocytes and that the protein resides in the apical membrane of these cells. These findings suggest that the hZIP4 transporter is responsible for intestinal absorption of zinc.

Acrodermatitis↗

PubMed2002

Advantages of in vitro cytotoxicity testing by using primary rat hepatocytes in comparison with established cell lines.

We investigated and compared the cytotoxicity of 16 reference compounds in four in vitro systems: primary cultured rat hepatocytes, hepatoma HepG2 cell line, non-hepatic HeLa and Balb/c 3T3 cell lines. After 24 hr of exposure to the test compounds, the water-soluble tetrazolium salts WST-1 assay was used as an endpoint to evaluate cytotoxicity. Acetaminophen, diclofenac sodium cyclophosphamide and disulfiram displayed from 2 to more than 10 times higher IC50 values in three cell lines than in rat primary cultured hepatocytes. The cytotoxic effects of aspirin, amiodarone, clorfibiric acid, chlorpromazine, erythomycin, lithocholic acid, cisplatin and quinidine in rat hepatocytes were similar or 2 times stronger than those observed in cell lines. Ketoconazole resulted in the lowest IC50 value in the HeLa cell line. The data suggested that the compounds which are known to be metabolism-mediated liver toxicants have a differential hepatotoxicity in vitro and that primary cultured rat hepatocytes could represent a valuable tool for both screening and study of the effects of bio-transformation on the cytotoxicity of new chemical entities and xenobiotics in vitro.

3T3 Cells↗

PubMed1998

Study on the causes of local recurrence of rectal cancer after curative resection:analysis of 213 cases.

AIM:To study the local recurrent rate and the causes of rectal cancer after surgery.METHODS:The clinicopathological data of 213 rectal cancer patients and the follow-up information were analyzed. The overall recurrent rate and the recurrent rates from different surgical appreaches were calculated. The main causes of recurrence were investigated.RESULTS:Among the 213 cases, 73 (34.27%) had local recurrence. The recurrent time ranged from 3 months to 62 months after the first operation. Most of the recurrence (65/73, 89.04%) occurred within 3 years after operation.CONCLUSION:Local recurrence had no significant correlation with surgical methods or pathological types, but closely related to Dukes' stages, location of primary tumors and the length of the distal rectum resected. Early resection and a wide tumor free resection margin are key factors to prevent local recurrence.

Journal Article↗

PubMed1997

Oxidation of Isopropylcyclopropane by Chromyl Chloride: Ring-Opened Products Support a Hydrogen Atom Abstraction Mechanism.

Chromyl chloride (CrO(2)Cl(2)) reacts with neat isopropylcyclopropane at 65 degrees C to give a dark precipitate along with at least 20 organic products. Both cyclopropyl products and ring-opened products are observed: 2-cyclopropyl-2-chloropropane (1, 0.4% yield based on chromium), 2-cyclopropyl-2-propanol (2, 0.2%), 5-chloro-2-methyl-2-pentene (3, 0.3%), and 4-methyl-3-penten-1-ol (4, 0.5%) as well as other ring-opened products. Authentic samples of 1-4 were synthesized, and their GC and GC/MS data were compared with the reaction mixture. Other organic products (5-10) were tentatively assigned by GC/MS on the basis of their m/z and fragmentation patterns. The ratio of (1 + 2) vs (3 + 4) increases by a factor of 2 when the initial concentration of CrO(2)Cl(2) increases from 0.3 to 1.12 M. The reaction was also carried out in the gas phase, and essentially all the products from the liquid phase reaction were observed. The products are explained by a mechanism involving initial hydrogen atom abstraction from the substrate. The resulting dimethylcyclopropylcarbinyl radical can either be trapped by CrO(2)Cl(2) (to form 1 and 2) or ring-open to give 4-methyl-3-pentenyl radical, which reacts with CrO(2)Cl(2) to form 3 and 4 as well as further oxidized products. The oxidation of isopropylcyclopropane by MnO(4)(-) in pyridine was also examined. Acetone, an expected ring-opened product, was the only product observed by our analytical techniques. Me(2)C(18)O is produced from (18)O-labeled MnO(4)(-). These results suggest that the reactions of CrO(2)Cl(2) and MnO(4)(-) with isopropylcyclopropane proceed by hydrogen atom transfer to form organic radical intermediates.

Journal Article↗

PubMedDate not supplied

Poor responders to intravenous omeprazole in patients with peptic ulcer bleeding.

BACKGROUND/AIMS: Although proton pump inhibitors are highly effective in raising intragastric pH, there still remains a small group of patients who resist acid suppression. A high dose of omeprazole has been shown to reduce rebleeding rate in patients with bleeding peptic ulcers after endoscopic therapy. The primary objective of this study was to assess the incidence of peptic ulcer bleeding patients who were resistant to intravenous omeprazole. The secondary objective was to evaluate the relationship between intragastric pH and rebleeding rate in studied patients after successful endoscopic therapy. METHODOLOGY: Between Oct. 1996 and Aug. 1999, 88 bleeding peptic ulcer patients who had obtained initial hemostasis with endoscopic therapy were enrolled in this study. In these patients, 40 mg of omeprazole was given as intravenous bolus followed by 40 mg intravenously every 6 h for 3 days. Thereafter, omeprazole was given 20 mg orally once daily for 2 months. The intragastric pH was recorded for 24 hours after the first dose of omeprazole. The occurrence of rebleeding was observed for 14 days. RESULTS: The mean intragastric pH value of these 88 patients was 6.07, (95% CI: 5.91-6.23). Four patients (5%) were found to have omeprazole resistance (pH < 4.0, 50% of the time). By the 3rd days after entering the study, more patients with a mean pH < 6 rebled (5/25 vs. 3/63, p<0.05). CONCLUSIONS: About five percent of patients with peptic ulcer bleeding respond poorly to intravenous omeprazole. Rebleeding rate is higher in patients with a mean intragastric pH of less than 6.

Aged↗

PubMedDate not supplied

The effect of H2-receptor antagonist and proton pump inhibitor on microbial proliferation in the stomach.

BACKGROUND/AIMS: Intra-gastric bacterial proliferation is frequent in patients with hypochlohydria. However, status of gastric bacterial infection in patients receiving proton pump inhibitor or H2-receptor antagonist remains controversial. The purpose of this study was to investigate the microbial condition of the stomach in patients who received H2-receptor antagonist or proton pump inhibitor. METHODOLOGY: Between November 2000 and January 2002, 102 patients were enrolled in this study. Of these, 52 did not receive any treatment (group I), 26 received H2-receptor antagonist (group II), and 24 received proton pump inhibitor (group III). Ten mL of gastric juice were aspirated for culture during endoscopic examination. The aerobic and anaerobic bacterial and fungal cultures were performed immediately. A glass pH meter measured the pH of the gastric juice. RESULTS: The intra-gastric pH was 2.91+/-2.06 (mean +/- SD), 4.12+/-2.83, and 5.11+/-2.47 for groups I, II, and III, respectively (p=0.001 between groups I and III, p>0.05 between groups I and II, and groups II and III). The positive bacterial culture rates were 66.7% (16/24) in group III, 46.2% (12/26) in group II, and 28.8% (15/52) in group I (p=0.007 between groups III and I,p>0.05 between groups I and II, and groups II and III). The positive candidal culture rates were 12.5% (3/24) in group III, 11.5% (3/26) in group II, and 17.3% (9/52) in group I (p>0.05). CONCLUSIONS: Patients who received proton pump inhibitor had more acid suppression and intra-gastric bacterial infection than those of the control group. The intra-gastric candidal infection was not related to intra-gastric pH or anti-secretory medication in this study.

Adult↗