A study on betel quid chewing behavior among Kaohsiung residents aged 15 years and above.

A telephone survey was used to study betel quid chewing behavior of Kaohsiung residents aged 15 and above in early 1991. Among the 1,162 subjects, 154 (13.3%) reported that they chewed betel quids and most of them (145/154) were men. Among the chewers, 33 (21.4%) indicated that they chewed it daily; all were men. Age distribution of the chewing behavior suggested that more young people chewed it at the time of the survey than had been the case in the past. The demographic distributions of betel quid chewing behavior were similar to the characteristics of tobacco smoking in Taiwan. The degree of concurrence of these two behaviors was very high. Nearly 90% of the subjects believed that betel quid chewing would cause more harm than good, or it would cause only harm, to their health. Discriminant analyses indicated that smoking behavior and attitude toward the health effect of chewing betel quids were the two most significant and meaningful variables in prediction of the chewing behavior. Strategies for prevention are recommended.

Growth hormone therapy initiated before starvation ameliorates the catabolic state and enhances the protein-sparing effect of total parenteral nutrition.

The effect of 7 days of subcutaneously administered bovine growth hormone (bGH) (0.2 mg kg-1 day-1; n = 4) or an equivalent volume of 0.15 mol l-1 saline (n = 3) on protein metabolism was assessed in lambs. The catabolic response to 48 h of starvation and subsequent hypocaloric total parenteral nutrition (TPN) was measured using primed constant intravenous infusions of [15N]urea and [14C]leucine. Following 48 h of starvation and 7 h of TPN, bGH-treated animals had a significantly decreased rate of net protein catabolism compared with controls (mean(s.e.m.) 2.4(0.2) versus 3.2(0.3) g kg-1 day-1, P < 0.01). The mean(s.e.m.) rate of whole-body protein catabolism was also significantly decreased in bGH-treated animals at 10.9(0.3) g kg-1 day-1 compared with 12.9(0.7) g kg-1 day-1 in saline-treated controls (P < 0.05). In addition, the rates of net and whole-body protein catabolism decreased significantly (P < 0.05) during the period of hypocaloric parenteral feeding to mean(s.e.m.) values of 2.3(0.2) and 8.6(0.6) g kg-1 day-1 respectively in bGH-treated animals. By contrast, in saline-treated controls net and whole-body protein catabolism continued to increase during hypocaloric parenteral feeding. There was a significant decrease (P < 0.05) in the rate of [14C]leucine uptake in tissues of the gastrointestinal tract, heart and diaphragm in bGH-treated animals compared with controls. These results demonstrate that daily administration of growth hormone decreases the catabolic response to a metabolic stress, resulting in the conservation of protein in the heart, diaphragm, gastrointestinal tract and musculoskeletal system by a primary anticatabolic action. In addition, growth hormone therapy initiated before induction of the catabolic state enhances the protein-sparing effects of TPN. Further study is justified to determine whether growth hormone therapy initiated before elective or urgent surgery in the nutritionally depleted patient may have a role in reducing the severity of the postoperative catabolic state, particularly in the patient in whom a complicated course is anticipated.

Preservation of regional and global left ventricular function by intracoronary infusion with oxygenated fluorocarbon emulsion Therox in dogs.

We tested the oxygen transport and delivery capacity of the novel perfluorocarbon emulsion, Therox (F44E, 1,2-bis-perfluorobutyl-ethylene) by comparing left ventricular regional and global function in dogs during perfusion of the left anterior descending coronary artery (LAD) with oxygenated Krebs buffer and oxygenated Therox emulsion (20% w/v) at 20 ml/min for two separate 3 min periods. During LAD perfusion with oxygenated Krebs buffer, complete loss of systolic wall thickening in the LAD perfusion area was observed, dP/dt was significantly reduced and left ventricular end-diastolic pressure (LVEDP) was increased. In contrast, LAD perfusion with oxygenated Therox maintained regional wall thickening at 60-70% of control and completely preserved global function as measured by dP/dt and LVEDP. Thus, Therox is an effective oxygen carrier in this animal model.

Leucine kinetics in patients with benign disease, non-weight-losing cancer, and cancer cachexia: studies at the whole-body and tissue level and the response to nutritional support.

We have performed intraoperative isotopic infusions of carbon 14-labeled leucine in 65 patients to define the abnormalities in protein metabolism at both the whole-body and tissue level in patients with weight-losing and non-weight-losing cancer. Eighteen patients had benign disease, 26 had non-weight-losing cancer, and 21 had cancer cachexia. Samples of plasma and expired breath were taken to determine rates of whole-body protein synthesis (WBPS), whole-body protein catabolism (WBPC), net protein catabolism, and albumin fractional synthetic rates. Tissue samples were taken to determine the fractional synthetic rates (FSR) of protein in muscle, liver, cancer, and the tissue in which the cancer arose. In addition, in 14 patients the effect of nutritional support on protein metabolism was assessed. In all parameters examined we were unable to detect any significant differences between patients with no cancer and the patients with non-weight-losing cancer. In contrast, patients with cancer cachexia had a significant elevation (p less than 0.005) in WBPC compared with the other two groups. WBPS was also elevated (to a lesser extent) in the patients with cancer cachexia, and the rate of net protein catabolism was increased significantly (p less than 0.05). Patients with cancer cachexia also had significantly higher values of FSR of protein in muscle (p less than 0.05), liver (p less than 0.05), and albumin (p less than 0.01) compared with the other two groups. In addition, the protein FSR in the cancer rose progressively when the values for the primary cancer were compared with those for nodal and systemic metastases. Further, although nutritional support resulted in an increase in host muscle protein synthesis (p less than 0.04), there was no promotion of FSR of protein in cancer. We conclude that patients with cancer cachexia are actively losing protein as a result of an increase in WBPC that is only partially compensated for by an increase in WBPS. There are compensatory increases in protein synthesis in muscle and liver, but these increases in host protein synthesis are insufficient to keep pace with the combined effect of the accelerated rate of protein synthesis in the cancer per se and the accelerated rate of net protein catabolism at the whole-body level. In response to nutritional support, there is a significant increase in the muscle protein synthesis, but we could not demonstrate any increase in cancer protein synthesis.