Solution to the dilemma of retrieving an endoscope from the esophagus.
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Biomedical subjects
Publications and source records attributed to T H Wang.
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On-line highflux hemodiafiltration (HDF) is a clinically interesting and effective mode of renal replacement therapy, which offers the possibility to obtain an increased removal of both small and large solutes. The fundamental role of urea kinetic monitoring to assess dialysis adequacy in conventional hemodialysis has been widely studied. Both direct measurement of the urea removed by the modified direct dialysate quantitation (mDDQ) based on partial dialysate collection (PDC) and dialysate-based urea kinetic modeling (DUKM) using urea monitor have been advocated. The validity of this assessment tool in the patients with on-line HDF remained unclear. The aims of this investigation were (1) to compare the delivered Kt/V, urea mass removal (UMR), solute removal index (SRI) and normalized protein catabolic rate (nPCR) between pre- and postdilutional high-flux HDF; (2) to verify and compare the efficiency of pre- and postdilutional HDF using DUKM with on-line dialysate urea sensor, and mDDQ with partial dialysate collection. During both mode of HDF, the paired analysis urea removed and Kt/V showed no significant difference. Using mDDQ, mean values for predilutional mode were as follows: Kt/V 1.53 +/- 0.01 UMR, 16.8 +/- 0.3 g/session; urea clearance 178 +/- 18 ml/min; SRI 75.5 +/- 7.7%; urea distribution volume (V) 28.3 +/- 1.2 liters; nPCR 1.34 +/- 0.18 g/kg/day; on the other hand, mean values for postdilutional mode were Kt/V 1.58 +/- 0.01; UMR 17.10 +/- 0.28 g/session; urea clearance 184 +/- 21 ml/min; SRI 77.2 +/- 3.5%; urea distribution volume, 27.8 +/- 1.5 liters; nPCR 1.34 +/- 0.19 g/kg/day. The mean value of urea generation rate was 5.82 +/- 1.12 mg/min during HDF. Our results showed that dialysis adequacy was achieved with both high-volume predilutional HDF and postdilutional HDF. These two modes of HDF provided similar and adequate small solute clearance. In addition, we found that on-line analysis of urea kinetics is a reliable tool for quantifying and assuring delivery of adequate dialysis.
HGF is a pulmotrophic factor in the regeneration of an injured lung. However, the physiological role of HGF in vivo remains largely unknown. We studied HGF in patients with inflammatory lung diseases to investigate the clinical significance of HGF and compared with C-reactive protein (CRP) in inflammatory lung diseases. Forty-seven patients with inflammatory lung diseases (16 tuberculosis, 18 pneumonia, and 13 chronic obstructive pulmonary disease (COPD)) were studied. Fifty normal, healthy individuals were analyzed as normal control subjects. Serum HGF levels were measured by enzyme-linked immunosorbent assays (ELISA). Serum CRP levels were also performed. The mean +/- SE numbers of serum HGF levels in the patients with inflammatory lung diseases (4.33 +/- 0.41 ng/ml) were significantly elevated when compared with those in normal control subjects (0.36 +/- 0.02 ng/ml) (p < 0.0001). Serum HGF levels in patients with COPD was significantly lower than those were with tuberculosis or pneumonia (p < 0.05). There was a significant correlation between serum HGF levels and CRP in inflammatory pulmonary diseases (r = 0.48, p = 0.00087). The significantly decreased serum HGF levels in patients with improved inflammatory lung diseases were also observed subsequently. Our results suggest that secreted HGF may play an important role in bronchial epithelium reconstruction during respiratory inflammation.
Cell division and cell death are the ultimate differential decisions made by the cell. Apoptosis is the most prevalent type of cell death. The machinery for apoptosis in all cell types is genetically encoded and readily expressed. All multicellular organisms employ apoptosis to achieve developmental plasticity and homeostasis, to select the fittest cells, to sculpt the body shape, and to defend themselves against invading viruses and their own deleterious cells. In this article, which is part of two related reviews, the historic identification of apoptosis and some key discoveries of the mechanistic components of the apoptotic process are reviewed, followed by discussions of the physiology, pathology, and clinical significance of apoptosis.
The importance of apoptosis has been increasingly appreciated during the last decade. Apoptosis and cell proliferation are two opposing and tightly-controlled events in physiology and pathology. In the 21st century, therapy through either enhancement or suppression of the apoptotic process, depending on the type of disease, will be one important task in medicine. Learning methods to document and quantify apoptotic events is the first step in embracing the approaching era in which modulation of apoptosis may become a goal of clinical treatment. In this article, the second part of two related reviews (first review, J Formos Med. Assoc. 1999; 98:381-93), characteristics of apoptosis, including morphology, biochemistry, and the efficient elimination of apoptotic cells by tissues are discussed with a special emphasis on the quantitative analyses of apoptosis in biomedical research.
We report a case of a 30-year-old man who suffered from epigastralgia for 1 month. During an upper gastrointestinal endoscopic examination, a small nodule with a smooth surface was found at the greater curvature of the gastric antrum. Endoscopic ultrasonography showed focal thickening of the second and third layers of the stomach with slightly hypoechoic echotexture in the submucosa. The tumor was excised by means of endoscopic mucosal resection, with a cap-fitted panendoscope. Pathologic examination of the resected tissue revealed a heterotopic pancreas, which was subsequently removed. Heterotopic pancreas is often difficult to diagnose preoperatively. This is the first reported case in which endoscopic mucosal resection was used for both diagnosis and treatment heterotopic pancreas.
BACKGROUND: In the skin, the expression of androgen action is dependent on the reduction of testosterone to dihydrotestosterone mediated by the enzyme 5 alpha-reductase. Additionally, an exaggeration of this peripheral metabolism has been associated with acne in women. METHODS: Fifty-two women with acne vulgaris but without hirsutism were recruited in this study, including 42 with oligomenorrhea or amenorrhea (Group 1) and 10 with regular menstrual cycles (Group 2). As a control, another 15 oligomenorrheic women without acne were also studied (Group 3). Flutamide combined with sequential estrogen-progestogen preparations was given to patients in Group 1. In Group 2, flutamide alone was administered. In Group 3, the women were treated with sequential estrogen-progestogen. RESULTS: In Groups 1 and 2, a significant decrease in the number of inflammatory lesions was found at the end of 3 and 6 months of treatment, and even after discontinuation of therapy for 6 months. Before treatment, patients in Group 1 showed signs of biochemical hyperandrogenism, including elevated levels of serum testosterone (T), androstenedione (A), and dehydroepiandrosterone sulfate (DHEA-S), as well as a decreased level of sex hormone-binding globulin (SHBG). A decrease in circulating T and A, and an elevation in serum SHBG were found 3 and 6 months after treatment in Group 1. In Group 2, clinical improvement of acne was achieved by flutamide alone without alteration in circulating androgens (including T, A, and DHEA-S). Similarly, no change in serum androgens was observed in the women of Group 3 after treatment. CONCLUSION: A low dose of flutamide (250 mg/day) in association with or without estrogen-progestogen is effective for the clinical improvement of acne vulgaris in women with or without oligomenorrhea or amenorrhea. However, the effectiveness on hyperandrogenic symptoms by antiandrogens may or may not be reflected by the suppression of serum androgens.
This study was conducted using roxatidine acetate or Mylanta combined with metronidazole and amoxicillin to evaluate the role of acid and Helicobacter pylori in the natural course of the duodenal ulcer. Eighty-three patients with H. pylori positive duodenal ulcers were randomly allocated into one of four treatment groups. Group A: roxatidine 75 mg hs for 8 weeks; Group B: the same as group A + metronidazole 250 mg and amoxicillin 250 mg qid for 1 week on the 3rd week; Group C: Mylanta (combined hydroxide of magnesium and aluminum) 20 ml qid for 8 weeks; Group D: the same as group C + metronidazole 250 mg and amoxicillin 250 mg qid for 1 week on the 3rd week. Repeated endoscopies were performed on the 8th week post the initial treatment and the sixth and 12th month post the termination of treatment, or, at the earliest recurrence of symptoms. Eradication of H. pylori was considered to be successful if the culture, histology and CLO test all showed negative. The ulcer healing rates of Groups A, B, C and D were 95%, 100%, 61% and 86%, respectively, with a significant difference between A and C. The eradication rates of groups B and D were 81% and 62%, respectively, without any significant difference. The 12 months cumulative ulcer recurrence rates were 72%, 15%, 80% and 22%, respectively, with a significant difference between each paired groups with and without antibiotics. In conclusions, roxatidine is effective in the healing of duodenal ulcer. One-week roxatidine-based triple therapy is powerful in the eradication of H. pylori. Potent acid suppression is sufficient to heal the duodenal ulcer. Eradication of H. pylori can potentiate ulcer healing under insufficient acid suppression. A causal role for H. pylori in recurrent duodenal ulcer is strongly supported by a much lower recurrence of ulcer in H. pylori free patients.
The purpose of this study was to determine the role of nitric oxide (NO) in the angiotensin II-induced hypertrophic response in cultured neonatal rat cardiac myocytes. Angiotensin II induced significant increase of protein content, decrease of NOS activity in cultured neonatal rat cardiomyocytes and decrease of NO concentration in the culture medium. Angiotensin II decreased significantly the eNOS mRNA level of cardiomyocytes. Saralasin and PTX inhibited significantly the increased protein content, the decreased NOS activity and the decreaseed NO production of cardiomyocytes induced by angiotensin II. Sodium nitroprusside increased significantly NO concentration in the culture medium and inhibited significantly the increased protein content of cardiomyocytes induced by angiotensin II. The results suggest that angiotensin II may induce hypertrophy of cultured neonatal rat cardiomyocytes. The effect of angiotensin II is mediated by receptors which are coupled with PTX-sensitive G protein and may be related to the decreased eNOS gene expression, NOS activity and NO production. Exogenous NO can prevent the hypertrophy of cardiomyocytes induced by angiotensin II.
In this present study, the effects of ET-1 on intracellular free calcium concentration ([Ca2+]i) and the underlying mechanisms were investigated in cultured neonatal rat myocardial cells loaded with fura-2/AM. The results are as follows. ET-1 induced an increase of [Ca2+]i in a dose-dependent manner, which consisted of a transient and sustained phase. BQ123, a selective ETA receptor antagonist, blocked the ET-1 induced [Ca2+]i responses, suggesting that these responses were mediated by ETA receptors. After removal of extracellular Ca2+, ET-1 induced the transient increase of [Ca2+]i without the sustained change. Protein kinase C (PKC) agonist PMA attenuated the ET-1 induced transient [Ca2+]i increase. Amiloride and nifedipine did not block the [Ca2+]i change induced by ET-1. After pretreatment of myocardial cells with pertussis toxin, ET-1 also induced the transient increase of [Ca2+]i but did not affect the sustained increase. These results suggest that the transient [Ca2+]i increase may involve pertussis toxin-insensitive G protein and the sustained one may be caused by extracellular calcium influx, in which pertussis toxin sensitive G protein is involved. Furthermore, PKC, but not Na+/H+ exchange, plays an important role in these effects.
The aim of this prospective randomized multicenter study was to find out if there is one or several promising regimens containing lansoprazole with various combinations of antibiotics which have a high eradication rate of Helicobacter pylori, few side-effects, good patient compliance, and relative low cost if possible. Two hundred and ninety-seven patients with H. pylori positive duodenal ulcer were enrolled and randomly allocated into one of the five treatment groups: 1) group A: received lansoprazole 30 mg once daily for 2 weeks plus amoxicillin (AM) 500 mg and metronidazole (MZ) 500 mg twice daily for one week in the first week; 2) group B: the AM in group A was replaced by clarithromycin (CM) 250 mg; 3) group C: the MZ in group A was replaced by CM 250 mg; 4) group D: the AM and CM in group C was used for 2 wk; 5) group E: the CM in group D was doubled to 500 mg twice daily. All patients received endoscopies pre- and 4-6 weeks post termination of treatment. H. pylori was detected by culture, histology and rapid urease test (CLO test). 13C-urea breath test was performed if the patients refused the second endoscopy. The E-test was adopted to evaluate the MZ and CM resistance of H. pylori. Totally, 253 patients completed the study. The eradication rate of groups A, B, C, D and E were 75%, 80%, 78%, 92%, and 96%, respectively. The eradication rate of group E was significantly higher than that of groups A, B, or C. There were no significant differences of eradication rates between the groups D and E. Sixty-seven cases (28.8%) were MZ-resistant. The difference of eradication rates between MZ-S and MZ-R patients was significant in group A (85.3% vs. 42.9%) and in the combination of groups A and B (83.8% vs. 59.4%). Good compliance (defined as taking > 90% of medications) was seen in more than 90% of cases in each group. Triple therapy containing lansoprazole 30 mg once daily, AM 500 mg and CM 250 mg twice daily for two weeks is a promising regimen which reaches a high eradication rate, avoids MZ resistance, and has very good patient compliance at an acceptable cost.
In the present study, the effect of endothelin-1 (ET-1) on the expression of proto-oncogene c-fos in cultured neonatal rat myocardial cells was investigated. The results are as follows: ET-1 induced c-fos expression in a dose-dependent manner. Selective ET(A) receptor antagonist blocked ET-1-induced responses. Protein kinase C(PKC) agonist PMA induced c-fos expression.PKC inhibitor staurosporine blocked ET-1 induced c-fos expression. Calcium channel blocker, nifedipine did not significantly affect the expression of c-fos induced by ET-1. These results suggest that in cultured neonatal cardiomyocytes, ET-1 induced c-fos gene expression is mediated by ET(A) receptor with the participation of protein kinase C, while the voltage-dependent L-type Ca(2+) channel is not involved.
This study attempted to identify a possible antibody response to Helicobacter pylori, which is associated with patients with adeno-carcinoma of the stomach. By using proteins of H. pylori as the antigen, pooled sera from gastric cancer and non-cancer patients were used as the first antibody for Western blot analysis. Antibody responses to a 26 kD secreted protein were observed in pooled cancer sera, but not in pooled sera from non-cancer patients. The protein was purified, while amino acid sequences revealed that it was a H. pylori species specific protein. The gene of this protein was cloned and a recombinant protein was expressed in E. coli. In addition, an antibody to the recombinant protein was tested in each individual patient using Western blot analysis. None of the forty non-gastric cancer patients were positive for the antibody to the recombinantly expressed 26 kD species specific protein. Meanwhile, six of the twenty four cancer patients tested positive (0/40 vs 6/24, p < 0.01). Results presented herein demonstrate that the species specific protein of H. pylori can be useful in detecting H. pylori associated with adenocarcinoma of the stomach.
The essential cellular functions associated with microtubules have led to a wide use of microtubule-interfering agents in cancer chemotherapy with promising results. Although the most well studied action of microtubule-interfering agents is an arrest of cells at the G2/M phase of the cell cycle, other effects may also exist. We have observed that paclitaxel (Taxol), docetaxel (Taxotere), vinblastine, vincristine, nocodazole, and colchicine activate the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pathway in a variety of human cells. Activation of JNK/SAPK by microtubule-interfering agents is dose-dependent and time-dependent and requires interactions with microtubules. Functional activation of the JNKK/SEK1-JNK/SAPK-c-Jun cascade (where JNKK/SEK1 is JNK kinase/SAPK kinase) was demonstrated by activation of a 12-O-tetradecanoylphorbol-13-acetate response element (TRE) reporter construct in a c-Jun dependent fashion. Microtubule-interfering agents also activated both Ras and apoptosis signal-regulating kinase (ASK1) and coexpression of dominant negative Ras and dominant negative apoptosis signal-regulating kinase exerted individual and additive inhibition of JNK/SAPK activation by microtubule-interfering agents. These findings suggest that multiple signal transduction pathways are involved with cellular detection of microtubular disarray and subsequent activation of JNK/SAPK.
Icteric type hepatocellular carcinoma is rare, and a poor prognosis has been demonstrated in the past. We performed this study to re-evaluate prognosis since the availability of modern diagnostic modalities. Of 3921 patients with hepatocellular carcinoma in our hospital, 9 patients who presented with tumor fragments in common bile duct and had a patent portal vein were submitted for analysis. Cholangiocarcinoma was suspected in 7 patients before the study was completed, and icteric type hepatocellular carcinoma was diagnosed in all 9 patients after serial studies that included serum alpha-fetoprotein levels, computed tomography, angiography, and histology. The prognosis was better in the 4 resectable patients (survival time 16, 31, 33, and 63 months, respectively), and was extremely poor for the 5 patients who received palliative treatment only (mean survival time, 4.5 months). Because of the apparently discrepant outcomes, this specific type of hepatocellular carcinoma should be kept in mind in areas where hepatocellular carcinomas are prevalent, and the suspected cases should be thoroughly investigated, because prognosis may be improved when resection is done at an earlier stage.
OBJECTIVES: Adequate vascular development of the placental bed is essential for normal pregnancy. We assessed serum levels of placenta growth factor, an angiogenic factor, throughout normal pregnancy and determined its association with preeclampsia. STUDY DESIGN: Serum samples were collected from (1) 308 healthy pregnant women throughout normal gestation, (2) at delivery from 30 each gestational age-matched patients with normal pregnancy and preeclampsia, and (3) maternal and cord blood samples from normal deliveries with and without labor (n = 37 each). Placenta growth factor levels were determined with an antigen-capture enzyme-linked immunosorbent assay. RESULTS: Maternal placenta growth factor levels during normal pregnancy increased from the first trimester to the late second trimester; they subsequently declined from 30 weeks' gestation to delivery. Significantly less maternal placenta growth factor (P <.0001) was found in pregnancies complicated by preeclampsia, and labor significantly lowered placenta growth factor levels in both maternal (P =.0189) and cord serum samples (P <.0001). CONCLUSION: Decreased levels of placenta growth factor during preeclampsia could influence endothelial cell and trophoblast function, thereby contributing to the pathogenesis of the disease.
A direct in situ polymerase chain reaction (IS-PCR) assay is described for the detection of HIV-1 proviral DNA in formalin fixed paraffin embedded brain tissue. Biotin-16-dUTP is incorporated during the PCR process and microwave pretreatment of tissue sections ensures that no non-specific incorporation into damaged or nicked genomic DNA occurs. Two methods are compared to detect the biotinylated amplified product, the use of an avidin-biotin-alkaline phosphatase complex (ABC) and the application of tyramide signal amplification (TSA) which allows both chromogenic and fluorescence detection. TSA detection enhances the sensitivity of IS-PCR, permitting fewer PCR cycles and preserving tissue morphology.
BACKGROUND: The prevalence of hepatitis G virus (HGV) and its strain variant, the GB agent (GBV-C) is high in non-virus-inactivated plasma products, but, persistent infection in recipients is relatively low. STUDY DESIGN AND METHODS: Stored samples from transfusion donors and recipients in a prospective study of posttransfusion hepatitis were tested for HGV RNA and antibody to the E2 protein (anti-E2). RESULTS: Thirty-two (2.1%) of the 1500 qualified donors were positive for HGV RNA. Twenty-four persons had received a transfusion of blood from one of these 32 viremic donors. Of these 24 recipients, 3 were positive for HGV RNA before transfusion. Of the remaining 21 recipients, 8 became viremic after transfusion, while the other 13 were not infected. Four of the eight infected recipients were persistently positive for HGV RNA, while four became negative in 1 to 3 years. Three of the four patients with HGV clearance seroconverted to anti-E2 positivity. Comparison of the viral titer, viral sequences at E2, storage period of blood donations, and clinical data in the infected and noninfected recipients revealed no significant differences. However, the noninfected recipients seemed to have a higher prevalence of anti-E2 before transfusion. CONCLUSION: The prevalence of HGV viremia in volunteer blood donors in Taiwan is 2.1 percent, and blood from 0.6 percent of them actually causes HGV infection in the recipients. In half of infected recipients, clearance of HGV occurs. Anti-E2 appears in most recipients whose viremia is cleared.