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Biomedical subjects

S R Lin

Publications and source records attributed to S R Lin.

141 records · Page 8Linked to original sources
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Cerebral water content, blood flow and EEG changes after cardiac arrest in the dog.

Changes of cerebral water content, blood flow and cortical EEG following cardiac arrest (8-14 minutes) were studied in 14 mongrel dogs. With five hours of maintenance, changes in the water content both in grey and white matter were found to be insignificant. (Grey matter: control 78.68 +/- 2.62%; arrest 79.91 +/- 1.76%. White matter: control 66.66 +/- 4.10%; arrest 67.76 +/- 1.88%). Blood flow was measured using 15 micron microspheres labeled with Sr, 85 Ce141 and Yb.169 Flow in grey matter was decreased to 47% at 3 hours and 53% at 5 hours; while in white matter it was 67% at 3 hours and 75% at 5 hours from baseline. Deterioration of the cortical electrical activity was observed in all animals having an arrest of more than 8 minutes. In aminals having arrest of longer than 12 minutes there is either no return (isoelectric) or marked slowing of cortical electrical activity. From this and previous studies, it is concluded that with more than 8 minutes of cardiac arrest and up to 5 hours of maintenance there is impairment of cortical perfusion which is not associated with a significant increase in total water content. The lack of increase in total water content, however, does not mean there is no local swelling or edema such as in endothelial cells.

Animals↗
PubMedDate not supplied

Effect of dextran on cerebral function and blood after cardiac arrest. An experimental study on the dog.

EEG activity and regional cerebral blood flow were monitored during 5 hour survival following cardiac arrest in 32 pentobarbital anesthetized mongrel dogs. The animals were mechanically ventilated and blood gases were maintained at physiologic levels. Regional cerebral blood flow and cardiac output were measured using 15 mu microspheres. EEG was recorded from 6 epidural electrodes using bipolar techniques. The animals were divided into 3 groups. The animals in Group I had an arrest of 8-11 minutes and those in Group II and III had an arrest of 12-16 minutes. Group II animals received no treatment. Group III animals were given 1 g/kg of dextran 40 at a concentration of 10% in normal saline following the arrest and maintained with 10 mg/kg/min during the 5 hours of recovery. In Groups I and III there was shorter duration of a flat EEG and 5 hours after the arrest the EEG activity was closer to normal than in Group II. After 5 hours the EEG scores of Group III were significantly greater than Group II (p less than 0.03). The cortical grey matter and hippocampus had the greatest reduction of blood flow following cardiac arrest. The mean cortical grey matter blood flow in Group II was less than in Groups I and III at 3 hours. After 5 hours the grey matter blood flow was greater in Group III than in Group II (p less than 0.09). The findings of this study are consistent with the hypothesis that after cardiac arrest perfusion abnormalities persist or develop after return of blood pressure and that these can be corrected or prevented with improved functional survival by treatment with dextran 40 after the arrest.

Animals↗
PubMedDate not supplied

Cerebral circulation after cardiac arrest. Microangiographic and protein tracer studies.

The effects of ventricular fibrillation and subsequent resuscitation on the microcirculation of the verebral cortex were studied with microangiographic and fluorescent protein tracer techniques. Immediately after revival, a transient period of impaired cerebral perfusion occurred before complete recovery from circulatory arrest was obtained. A circulatory arrest of longer than ten minutes, followed by four to six hours of resuscitation, caused defects of cortical capillary filling in both microangiography and Trypan blue fluorescence. This was considered to represent impairment of cortical perfusion, most likely due to edema. Cardiac arrest up to 12 minutes and subsequent resuscitation per se caused no blood-brain barrier damage. Minimal blood-brain barrier damage occurred in one dog following uncomplicated revival from a 14-minute arrest and in animals with prolonged hypertension post-resuscitation. Up to three consecutive carotid angiographies did not cause blood-brain barrier damage in the postischemic brain.

Angiography↗
PubMedDate not supplied

Mutations of p53 gene in gastric carcinoma in Taiwan.

BACKGROUND: p53 gene mutation and p53 protein accumulation is the most common event in human cancers. The present study was conducted to investigate the occurrence of p53 mutations in patients with gastric carcinoma in Taiwan. MATERIALS AND METHODS: Tumor samples from 36 patients with primary gastric carcinoma undergoing radical gastrectomy were evaluated. The mutational status of the p53 (exons 5 to 8) was screened by polymerase chain reaction/single strand conformation polymorphism (PCR-SSCP) analysis followed by direct sequencing. These results were compared with p53 protein expression as assessed by immunohistochemical staining. RESULTS: Of all 36 gastric carcinomas, mutations of the p53 gene were found in 7 cases (19.4%). These results from direct sequencing indicated that mutations consisted of five missence mutations, one silent mutation and one mutation within the splice donor site of intron 5. Mutations were found at codon 145 in exon 5 (1 case), intron 5 (1 case), codon 248 in exon 7 (1 case), codon 251 in exon 7 (2 cases), codon 285 in exon 8 (1 case) and codon 287 in exon 8 (1 case). The mutation hot spot at codon 251 in gastric cancer has not been observed previously. Over-expression of p53 oncoprotein was observed in 10 patients (27.8%) immunohistochemically. CONCLUSIONS: p53 gene mutation might contribute to the pathogenesis of human gastric carcinoma. However, the suggestion awaits further investigation for confirmation.

Adenocarcinoma↗
PubMedDate not supplied

Evaluation of an office-based urine test for detecting Helicobacter pylori: a Prospective Pilot Study.

BACKGROUND/AIMS: To ascertain the reliability of a newly developed office-based urine test, the RAPIRUN test, used for detection of H. pylori infection. METHODOLOGY: Urine specimens from 142 consecutive patients undergoing gastroendoscopy (77 men, 65 women; mean 52.0 years) were tested with RAPIRUN at the same time. The total reaction time for the urine test is 20 min. None of the patients had received any H. pylori eradicating treatment. The H. pylori status was evaluated based on 5 different tests: culture, histology, biopsy urease test, 13C-urea breath test, and the RAPIRUN test. A commercial office-based kit using an immunochromatographic technique was used to examine urine samples for H. pylori antibody. H. pylori status was defined as positive when the culture was positive or if 2 of the other 3 tests (histology, biopsy urease test, and 13C-urea breath test were positive. RESULTS: Of 93 patients with H. pylori infection, 88 were tested as positive by RAPIRUN (sensitivity 94.6%). Of 48 patients without infection, 43 were found to be negative by RAPIRUN (specificity 89.6%). One case with an invalid urine test was excluded. CONCLUSIONS: This urine test is a rapid, inexpensive, reliable and easy-to-use tool for the diagnosis of H. pylori infection in untreated patients. It can be used for mass screening of patients' H. pylori status, particularly in children, postgastrectomy patients, uncooperative patients, and patients undergoing bismuth or proton pump inhibitor treatment.

Adenocarcinoma↗
PubMedDate not supplied

The effect of portal hypertension on expression of gastric mucin mRNA in rats.

BACKGROUND/AIMS: Gastric mucin, a principal component of gastric mucus, is thought to play an important role in protecting gastric mucosa and maintaining the homeostasis of the gastric mucosa. Our previous studies have demonstrated that the contents of gastric mucin were decreased in rats with portal hypertension. Thus, the purpose of this present study was designed to confirm the effect of portal hypertension on the expression of gastric mucin mRNA and to localize gastric mucin mRNA production site in rats. METHODOLOGY: Portal hypertension was induced experimentally by partial ligation of the portal vein in Wistar rats. The severity of gastric mucosal lesions was evaluated macroscopically by a gross ulcer index. We simultaneously measured the levels of mRNA in the gastric tissues of control and portal hypertension rats by reverse transcription-polymerase chain reaction, Southern blot hybridization, and in situ hybridization. RESULTS: The damage to gastric mucosa was found to be prominently greater in the portal hypertension rats compared to the control (P < 0.01). The expression of mucin mRNA was significantly reduced in portal hypertension rats compared to the control using the reverse transcription-polymerase chain reaction and Southern blot hybridization (both P < 0.01). In situ hybridization showed that mucin mRNA was localized primarily in the gastric submucosa and mucosa, particularly in the surface mucous and the gland mucous cells. CONCLUSIONS: Our results reveal that portal hypertension would cause a decrease in mucin mRNA, and it would be helpful in understanding the mechanism of gastric mucosal mucin alteration in portal hypertension and the pathogenesis of portal hypertension gastropathy. Furthermore, it may provide the strategy in the prevention and therapy of portal hypertension gastropathy.

Animals↗