Teaching behavioral medicine using individual coronary heart disease risk factors

Two hundred twenty-one first-year medical students participated in a voluntary coronary heart disease risk factor self-change project designed to teach the principles of behavioral change. Blood pressure, serum lipids, percentage body fat, cardiovascular fitness, and smoking status were measured prior to the project. Students designed their own programs of behavior modification and, after 8 weeks, repeat measurements were obtained in students whose projects related to coronary heart disease risk (56% of entire group). Despite generally low initial coronary heart disease risk factors, most risk factor groups successfully altered the targeted risk factors. The subgroup attempting to lower serum cholesterol (n = 49) reduced total cholesterol 15 +/- 24 mg/dl (mean +/- SD) and low-density lipoprotein cholesterol 11 +/- 20 mg/dl (P less than 0.001 for both). The blood pressure group (n = 9) decreased systolic blood pressure 8 +/- 10 mm Hg (P less than 0.05), and the weight-loss group (n = 33) lost 3.0 +/- 2.9 kg (P less than 0.001), reducing estimated percentage body fat 1.7 +/- 1.8 (P less than 0.001). The self-change project was well received by the students and appears to be a useful technique for introducing the principles of behavioral medicine to first-year medical students.     

Stimulation of β-adrenoceptors inhibits store-operated channel currents via a cAMP-dependent protein kinase mechanism in rabbit portal vein myocytes

Previously we have described the properties of store-operated channel currents (SOCs) in freshly dispersed rabbit portal vein smooth muscle cells. In addition to Ca²⁺ store depletion these SOCs could also be activated by α-adrenoceptor stimulation and diacylglycerol (DAG) via a protein kinase C (PKC)-dependent mechanism. In the present study we have investigated the effect of β-adrenoceptor stimulation on SOCs in rabbit portal vein myocytes. With whole-cell recording the selective β-adrenoceptor agonist isoprenaline reduced the current evoked by cyclopiazonic acid (CPA, sarcoplasmic/endoplasmic reticulum ATPase inhibitor) by over 85%. With cell-attached patch recording, bath application of isoprenaline produced a pronounced inhibition of SOC activity evoked by either CPA or the acetoxymethyl ester form of BAPTA (BAPTA-AM). SOC activity evoked by CPA, the DAG analogue, 1-oleoyl-acetyl- sn -glycerol (OAG) or the phorbol ester, phorbol-12,13-dibutyrate (PDBu) was also markedly inhibited by the adenylate cyclase activator, forskolin, and the cell-permeable non-hydrolysable analogue of cyclic adenosine monophosphate (cAMP), 8-Br-cAMP. With inside-out patches, bath application of PDBu evoked channel currents with similar properties to SOCs which were inhibited by over 90% by a catalytic subunit of protein kinase A (PKA) and by 8-Br-cAMP. Moreover bath application of PKA inhibitors, H-89, KT5720 and an inhibitory peptide to quiescent cell-attached or inside-out patches, activated channel currents with similar properties to SOCs. These data suggest that in rabbit portal vein myocytes, stimulation of β-adrenoceptors inhibits SOC activity via a cAMP-dependent protein kinase signal transduction cascade. In addition it is concluded that constitutive PKA activity has a profound inhibitory effect on SOC activity in this vascular preparation.     

The distribution of enzyme inhibitors in the joint in rheumatoid and experimental arthritis

The enzyme inhibitors alpha 2 macroglobulin (alpha 2M) and alpha antitrypsin (alpha 1AT) have been demonstrated previously in the pannus-cartilage junction area in 12 patients with rheumatoid arthritis (RA). These deposits were present in both inflammatory cells and in the cartilage matrix. As the tissue studied came from far advanced disease removed at the time of joint replacements, the initial phase of cartilage destruction was studied in a carrageenin-induced arthritis in rabbits. Sequential studies indicated that loss of proteoglycan from cartilage was necessary before alpha 2M penetrated the matrix. Explant cultures of synovial tissue from RA and osteoarthritis (OA) joints released an inhibitor of neutrophil elastase and plasminogen activator which was neither alpha 2M nor alpha 1AT. Synovial tissue (and cartilage) enzyme inhibitors may have important implications in relation to protective mechanisms within the joint in RA and OA over and above the effect of plasma inhibitors.     

凌晨3:00皮下注射短效胰岛素治疗2型糖尿病黎明现象

目的:观察应用凌晨3:00皮下注射短效胰岛素治疗2型糖尿病黎明现象的疗效。方法:对40例有黎明现象的2型糖尿病患者,使用短效胰岛素凌晨3:00注射4~6U。抽取肘静脉血测定空腹血糖(FPG)及早餐后2h血糖(2hPG),免疫比浊法测定糖化血红蛋白(HbA1c),比较治疗前后上述指标变化。结果:本组患者FPG从治疗前(9.5±1.6)mmol/L下降至(6.0±0.4)mmol/L,治疗2个月后仍保持为(5.6±0.4)mmol/L;2hPG从治疗前(13.8±0.8)mmol/L下降至(7.4±0.4)mmol/L,在治疗2个月后保持为(7.9±0.3)mmol/L;FPG和2hPG与治疗前比较,均具有显著性差异(P<0.01)。治疗2个月后,HbA1c从治疗前(8.3±0.6)%下降至(6.5±0.3)%,与治疗前比较,有显著性差异(P<0.01)。结论:短效胰岛素强化治疗黎明现象具有快速稳定的降血糖和降糖化血红蛋白作用。