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Biomedical subjects

G S Liu

Publications and source records attributed to G S Liu.

66 records · Page 4Linked to original sources

Measures for improving therapeutic results of esophageal carcinoma in stage III: preoperative radiotherapy.

Surgical therapeutic results of esophageal carcinoma stage III in 245 cases admitted to our hospital from 1966 to 1982 are reported in this paper. In this series, 171 cases were treated by surgery alone and 74 cases treated with a combination of preoperative radiotherapy and surgery. Of the entire group, 184 cases underwent gastroesophagostomy or colon interposition for esophageal reconstruction preceded by resection of the cancerous esophageal segment. The resectability rate was 75.1%, and the resection operative mortality rate was 7.1%. The 5- and 10-year survival rates were 30.0 and 25.8%, respectively. In the group of 171 cases treated by surgery alone, the resectability rate was 73.1% (125/171), and the resectability in the middle third esophageal carcinoma was only 64.7% (44/68), while in the group of 74 cases treated by combination treatment, the resectability increased to 79.7% (59/74) and the resectability in the middle third esophageal carcinoma increased to 79.3% (46/58). The 5-year survival rate in the combination-therapy group (60.1%) was 42.9% higher than that of the group treated by surgery alone (17.2%) (p less than 0.01). However, the differences in the rates of resection operative mortality and operative complications between these two groups were not significant. Therefore, we think that preoperative radiotherapy for esophageal carcinoma in stage III is an effective measure for improving resectability and survival rate.

Adenocarcinoma↗

Effects of lidoflazine and mioflazine against potassium and veratrine induced shape changes in isolated rat cardiac myocytes.

The protective effects of lidoflazine and mioflazine against shape changes in isolated rat cardiac myocytes induced by depolarizing concentrations of potassium and veratrine have been examined. Myocardial cells, isolated from adult rat hearts and plated in Petri-dishes, yielded a population of nearly 100% rod-shaped calcium-tolerant myocytes. Addition of veratrine or potassium resulted in a calcium-dependent cell shortening and finally rounding up of nearly all cells. Ultrastructurally, the shape changes were accompanied by a complete loss of calcium associated with the sarcolemmal and T-tubular bilayer. Calcium deposits accumulated in the mitochondria, indicating intracellular calcium overload. Pretreatment of the myocytes with lidoflazine or mioflazine (10(-7)-10(-5) M) dose-dependently increased the number of remaining rod-shaped cells after potassium or veratrine addition. Such rod-shaped cells retained a normal pattern of calcium distribution along the sarcolemma and T-tubuli with no evidence of mitochondrial calcium overload. The protective effects of lidoflazine and mioflazine are explained in terms of preserving sarcolemmal integrity, whereby excessive calcium influx and subsequent cytosolic calcium overload could be prevented.

Animals↗

Structural changes of atrial myocardium during chronic atrial fibrillation.

Of all known arrhythmia's, atrial fibrillation (AF) is the most often met in the clinical setting and it is associated with an increase in mortality risk. Several risk factors for AF have been described and several mechanisms of induction and maintenance have been proposed. Studies in patients with AF have shown that structural changes occur in the atria, but the relationship between the structural remodelling and the chronicity of the arrhythmia are not well understood. The changes mainly concern adaptive (dedifferentiation of cardiomyocytes) and maladaptive (degeneration of cells with replacement fibrosis) features. In order to characterise the time course of the structural remodelling the need for animal models which adequately mimic chronic atrial fibrillation in humans is felt essential. In this review, the structural changes that are observed during prolonged sustained AF in patients and animal models, are described. Furthermore, the time course and potential mechanisms of structural remodelling are discussed and methods for elucidation of the underlying molecular mechanisms are presented.

Actins↗