用混合粘合剂碳糊电极测定丁螺环酮

用混合粘合剂碳糊电极测定丁螺环酮张正奇，曾鸽鸣，刘传桂，黎艳飞（湖南大学化学化工系，长沙４１００８２）碳糊电极无毒，制作方便，表面更新容易，应用电位范围广，在药物分析中已有应用［１～５］。我们在液体石腊中加入添加剂，组成混合粘合剂，可显著改善电极的检...     

Effects of alpha 2-adrenergic blockade on renal hemodynamics in patients with insulin dependent diabetes mellitus.

The role of renal alpha 2-adrenoceptors in the regulation of glomerular filtration and renal perfusion is unknown. We studied the effects of alpha 2-adrenergic blockade on renal hemodynamics in six patients with insulin-dependent diabetes mellitus (IDDM) and in six healthy subjects. At the basal state, glomerular filtration rate (GFR) was higher in IDDM although the difference from control levels was not statistically significant. Volume expansion, achieved by infusion of isotonic sodium chloride solution, during placebo infusion induced a significant drop in GFR in healthy subjects but not in IDDM patients. Infusion of the alpha 2-adrenoceptor antagonist idazoxan did not further modify the effect of volume expansion on GFR. Renal plasma and blood flow as well as filtration fraction were not significantly changed by volume expansion or idazoxan infusion. Plasma renin activity and plasma aldosterone levels decreased during volume expansion in both IDDM and control subjects. In conclusion, volume expansion induced decreased GFR in healthy controls but not in IDDM patients. Since infusion of idazoxan did not affect GFR or other parameters of renal hemodynamics, renal alpha 2-adrenoceptors do not seem to be involved in the regulation of renal function. Hence, enhanced renal alpha 2-adrenoceptor activity is not likely to underlie hyperfiltration as seen in IDDM.     

The intestinal peptide PEC-60 inhibits insulin secretion in the mouse and the rat.

The newly discovered 60-amino-acid porcine intestinal peptide, PEC-60, shows a structural similarity to pancreatic secretory trypsin inhibitor. PEC-60 was recently demonstrated to inhibit glucose-stimulated insulin secretion from the perfused rat pancreas. We examined in this study whether the peptide affects basal and stimulated insulin secretion in vivo. Purified porcine PEC-60 was injected intravenously in mice at 1 or 8 nmol/kg alone or together with glucose (2.8 mmol/kg) or the cholinergic agonist carbachol (0.16 mumol/kg). PEC-60 was found to inhibit glucose- and carbachol-induced insulin secretion (p less than 0.01 and p less than 0.05, respectively) at 8 nmol/kg, whereas at 1 nmol/kg, the peptide had no effect. In contrast, basal plasma insulin levels were not affected by PEC-60. In a second experimental series, PEC-60 was infused intravenously in rats at 17 or 68 pmol/min alone or together with glucose (56 mumol/min). At 68 pmol/min (p less than 0.01), but not at 17 pmol/min, PEC-60 inhibited glucose-stimulated insulin secretion. The peptide had no influence on basal plasma insulin levels. It is concluded that the newly isolated intestinal peptide, PEC-60, inhibits stimulated insulin secretion under in vivo conditions both in the mouse and in the rat without affecting basal insulin secretion.     

Viral infections in the mouth

Oral hairy leukoplakia (OHL) and Kaposi's sarcoma (KS) are commonly encountered in the HIV-infected patient. A unique feature of OHL is non-cytolytic high level of replication of Epstein–Barr virus (EBV) in the glossal epithelium. The expression of viral-encoded anti-apoptotic proteins concomitant to replicative proteins probably underlies this phenomenon. The question of whether OHL arises from activation of EBV latent in the tongue, or from superinfection by endogenous EBV shed via non-glossal sites or by exogenous EBV remains unresolved. Human herpesvirus 8 (HHV8) is now seen as necessary but not sufficient cause of KS. Expression of HHV8-encoded oncogenic proteins in endothelial cells probably explains the aberrant proliferation of these cells in KS lesions. Studies into why KS is so commonly observed at the palate in HIV-infected patients may provide important clues to its pathogenesis.     

Thrombin activatable fibrinolysis inhibitor and hemostatic changes in patients with type I diabetes mellitus with and without microvascular complications.

We investigated thrombin activatable fibrinolysis inhibitor (TAFI) and its influence on fibrinolysis by measuring pro-TAFI activity and total TAFI antigen in 38 patients with type I diabetes mellitus (18 with and 20 without microvascular complications), as well as in 20 healthy controls. The pro-TAFI levels in the two groups of patients did not differ from those in the control group. Total TAFI antigen [i.e. pro-TAFI, TAFI and inactive carboxypeptidase U (TAFIi)] tended to decrease in both the patient groups (59.7 +/- 7.2 and 73.4 +/- 8.9% with and without microvascular complications, respectively) compared with controls (91.9 +/- 12.2%) (P = 0.12). We also assessed the overall hemostatic potential (OHP) in plasma, the clot lysis time and the overall fibrinolytic potential. The OHP was significantly higher in patients with complications compared with controls (8.9 +/- 0.9 versus 6.7 +/- 0.4; P < 0.05) and also higher in the diabetics without complications (7.8 +/- 0.6), although the latter difference did not reach statistical significance. Levels of clot lysis time and overall fibrinolytic potential were similar in the two groups of patients and the controls. The increased OHP in plasma from diabetic patients with microvascular complications indicates an imbalance of the hemostatic system towards a prothrombotic state. No signs of impaired fibrinolysis were observed in patients with diabetes. Using the OHP method for estimation of overall hemostasis, it seems that TAFI does not influence either fibrinolysis or the increased thrombotic potential observed in patients with type I diabetes mellitus.     

Determination of functional kidney volume by single-photon emission computed tomography in patients with insulin-dependent diabetes mellitus.

Functional parenchymal kidney volume was determined by single-photon emission computed tomography (SPECT) for 99mTc-dimercaptosuccinic acid (DMSA) using a rotating gamma camera in phantom experiments and in patients with insulin-dependent diabetes mellitus (IDDM). The results from the patient examinations were corrected according to the phantom studies and were thereafter set in relation to renal haemodynamics, blood pressure, and urinary albumin excretion. Functional parenchymal kidney volume was significantly greater in diabetic patients compared to that of 11 healthy controls (P < 0.003). Urinary albumin excretion was increased and glomerular filtration rate (GFR) per renal parenchymal volume significantly less in patients with a duration of diabetic disease of more than 15 years compared to patients with shorter duration of disease (P < 0.03 and P < 0.05 respectively). Diabetic patients with a GFR of more than 120 ml/min had greater renal parenchymal volume than patients with lower GFR (P < 0.02). Patients with increased GFR, renal plasma flow (RPF), renal blood flow, or filtration fraction had significantly greater functional parenchymal volume than the healthy subjects (P < 0.01 for all comparisons). We conclude that by application of SPECT for DMSA we were able to show that IDDM patients have greater renal parenchymal volumes than healthy subjects. GFR/kidney volume was increased in IDDM patients with a duration of disease of < 15 years compared to patients with long-standing diabetes. The SPECT technique seems suitable for prospective long-term follow-up studies of functional kidney volume in IDDM patients.     

In vitro differences in lymphocyte subpopulation reactivity in lung cancer patients: purified protein derivative-specific suppressor T lymphocytes in patients who have received Bacillus Calmette-Guerin

Antigen-specific responses of lymphocyte to purified protein derivative (PPD) were studied in seven patients with non-small cell lung cancer who had undergone complete resection and received postoperative intrapleural Bacillus Calmette-Guerin. In addition, one patient with unresected lung cancer and reactive tuberculin skin test (PPD +) and five normal PPD- individuals were also studied. Lung cancer patients had significantly fewer responsive peripheral blood lymphocytes, unfractionated T cells, and T cells bearing Fc-IgG receptors (TG + populations) than normal controls. These deficits were most pronounced in the group who had received intrapleural Bacillus Calmette-Guerin but who had failed to develop reactive tuberculin skin tests. In contrast, the TG-populations (FC-IgG receptor-negative T cells) from all patients responded to PPD. TG + cells specifically inhibited TG- -cell responses to PPD in both proliferation and immunoglobulin secretion. Radiosensitive suppressor monocytes were found in other patients. This study shows interesting immune deficits in early lung cancer patients. These patients appear to have PPD-specific suppressor TG + cells which may contribute to the immune deficits in these patients.