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Biomedical subjects

H J Lin

Publications and source records attributed to H J Lin.

At least 289 records · Page 16Linked to original sources

En bloc resection for extensive hepatocellular carcinoma: is it advisable?

When the adjacent organ is partially invaded by a hepatocellular carcinoma (HCC), whether to go on an aggressive resection is a difficult but challenging problem. To investigate the worth of en bloc resections, a retrospective controlled study was conducted. During a 9-year period, nine patients (seven men, two women: group I) who had HCC with invasions to extrahepatic adjacent organs had undergone en bloc resections. The adjacent organs included diaphragm (eight cases), adrenal gland (two cases), abdominal wall (one case), and spleen (one case). The patients selected for en bloc resections were those with a solitary tumor without evidence of vascular invasion or intravascular tumor thrombi, daughter nodule(s), or distant metastasis. The evidence was based on preoperative evaluation by ultrasonography, computed tomography, arteriography, and intraoperative ultrasonography. Eighteen matched patients with HCC but no involvement of neighboring organs were selected as controls (14 men, 4 women: group II). Though patients of group I had wider invasion of HCC and more extensive resection, their surgical morbidity, mortality, hospital mortality, disease-free interval, and survival time were similar to those of group II, who had more limited HCC and resections. Eighteen months after operation, the HCC recurrence rate was 44% and 41% in groups I and II, respectively, and the percent survivals were 71% and 63%, respectively. We suggest that in cases of large HCC with local invasion to neighboring organs, aggressive en bloc resection is recommended after appropriate patient selection.

Carcinoma, Hepatocellular↗

A controlled study of therapeutic endoscopy for peptic ulcer with non-bleeding visible vessel.

In a period of 14 months, a prospective, randomized, controlled trial was undertaken in 61 patients who had bled from peptic ulcers in which, at endoscopy, non-bleeding vessels were visible in the ulcer crater. The control group consisted of 31 patients in whom the procedure was limited to observation alone; in 30 patients the ulcer base was coagulated by means of a heat probe. There were no statistically significant differences between the two groups in the rate of rebleeding, the assurance of ultimate hemostasis, the volume of blood transfusion required, the duration of hospitalization, or eventual mortality. However, the need for emergency surgical intervention was less frequent in the heat probe group (2 of 30) than among the controls (9 of 31) (p = 0.0243). Moreover, in the treatment group, those patients of advanced age (greater than 60 years), in shock, requiring blood transfusion of greater than 500 ml, and in whom blood or coffee ground material was seen in the stomach, thermocoagulation achieved statistically more effective hemostasis than that observed in the control group. For these high-risk subsets of patients with non-bleeding visible vessels, we recommend heat probe coagulation rather than mere observation.

Blood Transfusion↗

Endoscopic injection for the arrest of peptic ulcer hemorrhage: final results of a prospective, randomized comparative trial.

A prospective, randomized comparative study was performed to compare the hemostatic effect of endoscopic injection with normal saline, 3% NaCl solution, 50% glucose/water solution, and pure alcohol during a period of 2 years. Only patients with peptic ulcers and active bleeding or nonbleeding visible vessels were considered. Each group comprised 50 patients. The four groups were matched at random for age, sex, location of bleeders, stigmata of recent hemorrhage, shock, hemoglobin, and concomitant illness. No statistically significant difference was observed among patients injected with normal saline, 3% NaCl solution, 50% glucose/water solution, or pure alcohol in achieving initial hemostasis (82%, 90%, 86%, and 92%, respectively); rebleeding rates (7.3%, 24.4%, 14%, and 10.9%, respectively); ultimate hemostasis (78%, 68%, 78%, and 84%, respectively); number of emergency operations (5, 7, 4, and 3, respectively); and average number of days in the hospital (6.7, 6.1, 6.1, and 5.8, respectively). A tendency toward a lower blood transfusion requirement was observed in the pure alcohol group, but this tendency failed to achieve statistical significance. One patient had a perforated ulcer develop 5 days after injection of 3 ml 50% glucose/water. Otherwise, no major complication was observed. We suggest that endoscopic injection with any of the above solutions can be used as the first-line modality for the arrest of peptic ulcer hemorrhage.

Adolescent↗

Bcl-2 and M-Myc coexpression increases IGF-IR and features of malignant growth in neuroblastoma cell lines.

The bcl-2 and c-myc oncogenes cooperate to transform multiple cell types. In the pediatric malignancy NB(2), Bcl-2 is highly expressed. In tumors with a poor prognosis, N-Myc, a protein homologous to c-Myc, is overexpressed as a result of gene amplification. The present study was designed to determine whether Bcl-2 cooperates with N-Myc to bestow a tumorigenic phenotype to neuroblastoma (NB) cells. NB cell lines that at baseline express neither Bcl-2 nor N-Myc were stably transfected to express these gene products. In this model, we found Bcl-2 rescues N-Myc-expressing cells from apoptosis induced by serum withdrawal. Coexpression of Bcl-2 and N-Myc supports growth in low serum conditions and anchorage-independent growth in soft agar. Similarly, in vivo tumorigenic and angiogenic activity was dependent on coexpression. Our data further suggests that the mechanism underlying these changes involves the receptor for insulin growth factor type I (IGF-IR).

Animals↗

A prospective evaluation of biopsy site in the diagnosis of gastric malignancy: the margin or the base?

The diagnostic value of endoscopic biopsy from the ulcer margin (six specimens) and the base (six specimens) in 46 cases of gastric malignancy was evaluated. The biopsy positive rates for malignancy from the ulcer margin and the base were 42 of 46 (91.3%) and 37 of 46 (80.4%), respectively (P = 0.2312). The diagnostic positive rate was increased to 95.6% (44 of 46) when the results of 12 biopsy specimens obtained from the ulcer margin and the base were combined. The diagnostic positive rate was not statistically different when the morphology or the location of the gastric malignancy was considered. No complication of massive bleeding or perforation was found after both sites had been biopsied. It is concluded that the margin and the base of a gastric malignant ulcer are both suitable and diagnostically effective for endoscopic biopsy. If the ulcer margin of the gastric malignancy is difficult to approach, the ulcer base appears to be a satisfactory alternative site for endoscopic biopsy.

Adenocarcinoma↗

Comparison of two plasma-derived hepatitis B vaccines: long-term report of a prospective, randomized trial.

Subjects at high risks for hepatitis B virus (HBV) infection were allocated randomly (n = 591) to receive one of the two plasma-derived hepatitis B vaccines produced by the Institut Pasteur Production, Paris (HEVAC B) or the Green Cross Corporation, Osaka (GCC VAC). There are differences in the production of these two vaccines, with an added step of heat inactivation and longer formaldehyde treatment for the GCC VAC. Three doses of vaccines were given at 0, 1, and 5 months for both vaccines. Antibody to hepatitis B surfaces antigen (anti-HBs) titres were tested at 1, 3, 6, 9, 12, 18, 24 months. Antibody to hepatitis B core antigen (anti-HBc) was tested at 6 and 24 months. A fourth dose was given after 12 months to subjects who did not develop an anti-HBs titre of 10 miu/mL at month 6. Two hundred and seventy-four subjects received HEVAC B. Excluding nine subjects (3.4%) who became positive for anti-HBc, the immunogenicity was 87.2%. For the 317 subjects receiving GCC VAC, excluding 17 subjects (5.4%) who became positive for anti-HBc, the immunogenicity was 83.7% (the difference was not statistically significant). The anti-HBs titres were significantly higher in those who received HEVAC B in the 3, 6, 9, 12 and 18 months but the anti-HBs levels for GCC VAC recipients were still well above the 'protective' level of 10 miu/mL. Most hypo/non-responders did not respond to the fourth dose of vaccine. The side-effects were transient and mild, and occurred in 1.5% of subjects for both vaccines.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Benign recurrent intrahepatic cholestasis in a Chinese girl.

A 15 year old Chinese girl presented with features of benign recurrent intrahepatic cholestasis, confirmed by liver biopsies performed during attack and remission. Her only younger brother also has features of this syndrome. Serial biochemistry monitoring during a recent attack demonstrated that a rise in the serum bile acids preceded the clinical onset of symptoms and the rise in serum bilirubin and ductal enzymes by 8 weeks. Whether this earlier rise in serum bile acids is related to the pathogenetic mechanism of this syndrome remains to be elucidated.

Adolescent↗

Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.

Adolescent↗

The influence of intravenous omeprazole on intragastric pH and outcomes in patients with peptic ulcer bleeding after successful endoscopic therapy--a prospective randomized comparative trial.

BACKGROUND/AIMS: The role of omeprazole in preventing rebleeding in patients with peptic ulcer bleeding after successful endoscopic therapy has been controversial. In this study, we used 3 different formulas of intravenous omeprazole in the above patients. We wished to compare the intragastric pH and outcomes among them. METHODOLOGY: Between July 1996 and May 1997, after having obtained initial hemostasis with endoscopic therapy, a total of 20 patients with peptic ulcer bleeding (spurting/oozing/non-bleeding visible vessel: 6/4/10) received intravenous bolus of omeprazole 20 mg every 3 hours; 20 patients (3/5/12) received intravenous bolus of omeprazole 40 mg every 6 hours; and, 20 patients (5/4/11) received intravenous bolus of omeprazole 80 mg every 12 hours for 3 days. One intragastric pH meter (Gastrograph Mark III, Medical Instruments Corp. Switzerland) was used to record 24-hour intragastic pH. RESULTS: The intragastric pH in the patients receiving omeprazole 20 mg every 3 hours was 6.1, 6.0-6.2 (mean: 95% CI); in patients receiving omeprazole 40 mg every 6 hours it was 6.4, 6.2-6.5; and, in patients receiving omeprazole 80 mg every 12 hours it was 5.8, 5.7-5.9. The duration of intragastric pH > 6.0 in omeprazole 20 mg every 3 hours was 70.9%, 57.3%-84.4% (mean: 95% CI); in omeprazole 40 mg every 6 hours it was 83.1%, 73.1%-93.1%; and, in omeprazole 80 mg every 12 hours it was 66%, 51.5%-80.4%. Patients with peptic ulcers receiving omeprazole 40 mg intravenous bolus every 6 hours had the highest intragastric pH as compared with the other 2 groups (p < 0.0001). There were no significant differences concerning rebleeding rates, volume of blood transfusion, hospital stay, numbers of operation and mortality among the 3 groups. CONCLUSIONS: After initial hemostasis had been obtained, patients with peptic ulcer bleeding receiving 40 mg intravenous bolus every 6 hours had the highest intragastric pH. However, they had similar outcomes with the other 2 groups.

Adult↗

Overexpression of Akt/AKT can modulate chemotherapy-induced apoptosis.

The AKT oncogenes are amplified or AKT kinase activity is constitutively elevated in several types of human malignancy. We sought to determine whether AKT might play a role in the development of resistance to apoptosis induced by chemotherapy. We showed that ovarian cancer cells either overexpressing constitutively active Akt/AKT1 or containing AKT2 gene amplification were highly resistant to paclitaxel than cancer cells express low AKT levels. The Akt/AKT1 clones also contained higher levels of phospho-Bad protein than parental cells. Further, the complexes between the endogenous proapoptotic protein, Bad, and the anti-apoptotic protein, BC1-XL were undetectable in Akt/AKT1 clones. These results suggest that Akt/AKT1 expressed in these clones can phosphorylate Bad and prevent it from binding to Bcl-XL. Furthermore, overexpression of Akt/AKT1 can inhibit the release of cytochrome c induced by paclitaxel. Therefore, our findings provide evidence that aberrant expression or activation of AKT in cancer cells may confer resistance to paclitaxel.

Adenocarcinoma↗