麦冬类中药组织切片计算机三维重建图鉴

利用计算机技术实现麦冬类中药组织连续切片三维重建与动态显示,为计算机辅助生药学鉴定和教学提供了新的三维图像技术和研究资料。     

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...     

The impact of mitral valve morphology on the long-term outcome of mitral balloon valvuloplasty.

BACKGROUND: The effect of mitral valve morphology (MVM) on the long-term results of mitral balloon valvuloplasty (MBV) is not well established. The aim of the study was to evaluate the impact of MVM on long-term outcome of MBV. METHODS: Five hundred and eighteen consecutive patients (mean age, 31+/-11 years) who underwent successful MBV were followed up for 0.5-16.5 (mean, 6+/-4.5) years. Patients were divided into two groups according to their mitral echo score (MES) before MBV: group A (n=340; MES8). RESULTS: We report the immediate and long-term clinical and echocardiographic results of the above-mentioned 518 consecutive patients. The mitral valve area was significantly larger in group A than in group B, both immediately after MBV (2.0+/-0.3 vs. 1.82+/-0.3 cm2, respectively; P<0.0001) and also at the last follow-up (1.8+/-0.33 vs. 1.5+/-0.33 cm2, respectively; P<0.0001). Restenosis occurred in 38/340 (11%) in group A vs. 73/178 (41%) in group B (P<0.0001). Actuarial freedom from restenosis at 5, 10, 15 years were 92+/-2%, 85+/-3%, 65+/-6% for group A vs. 72+/-4%, 44+/-5%, 9+/-6% for group B (P<0.001). Event-free survival rates at 5, 10, 15 years for group A were 93+/-1%, 88+/-2%, 66+/-6% vs. 82+/-3%, 59+/-6%, 8+/-7% for group B (P<0.0001). Stepwise Cox multivariate regression analysis identified MES, preprocedure functional class, and postprocedure mitral valve area相似文献   

Hereditary deficiencies of antithrombin III, protein S, and the protein C pathway in Jordanian thrombosis patients.

Hereditary thrombophilia is caused by various inherited disorders. Most lead to a familial tendency to recurrent venous, not arterial, thrombosis, usually at a young age, and with spontaneous onset. Most of the genetic defects known today affect the function of natural anticoagulant pathways, in particular, the protein C system. In this study, 602 (265 female, 337 male) patients with suspected thrombosis, arterial or venous, were referred to King Hussein Medical Center in Amman, Jordan. The prevalence of hereditary deficiencies of antithrombin (AT), protein S (PS), and protein C (PC) were studied over a seven-year period (1993-2000). Activated protein C (APC-R) resistance subjects were studied over four years (1996-2000). The mean age was 30 years in females and 42 years in males. A diagnosis was established in 22.4% (n = 135) of the subjects (20.3% venous, 2.1% arterial). Protein C deficiency was found in 3.8%, protein S deficiency in 2.3% and antithrombin deficiency in 1.4% of our sample group. An APC-R problem was seen in 23.0% (n = 89) of the surveyed population. Out of the APC-R patients, 75.0% had the DNA analysis of a factor V Leiden mutation present. Of the subjects found to have the mutation 87.0% were heterozygous and 13.0% were homozygous. These results confirm that APC-R, as a result of factor V Leiden mutation, is the most prevalent cause of thrombosis, and thrombophilia is related to venous, not arterial, thrombosis.     

In situ saphenous vein bypass grafts: angiographic evaluation and interventional repair of complications

In situ saphenous vein grafts are being used with increasing frequency for bypass procedures involving the femoral and popliteal arteries. Complications of these procedures include anastomotic stenoses and persistent arteriovenous fistulae that may result in failure of the graft. Balloon angioplasty and embolotherapy with detachable balloons were employed successfully in three or four recent cases of patients with complications from in situ grafts. Tailored angiography is essential for evaluating in situ grafts, and interventional techniques are extremely useful for managing complications.     

In Vivo Effects of TRH, T3 and cGH on Antibody Production and T- and B-Lymphocytes Proliferation in Immature Male Chickens

Newly hatched White Leghorn male chicks were used in this study. Different doses of T₃ (O.1 or 1 ppm) or TRH (1 or 5 ppm) were administered in the feed for an 8-week period. Chicken growth hormone (cGH) (10 μg/kg BW) was injected (i.v.) into a different group of chicks twice daily for 1 week starting at 7 weeks of age. A different group received both T₃ (0.1 and 1 ppm) and cGH. Serum concentrations of T₄, T₃ and GH, antibody production against sheep red blood cells (SRBC) and Brucella Abortus (BA), and in vitro proliferative response of both T- and B-lymphocytes to mitogenic stimulation were measured. Supplementation of T₃ (1 ppm) significantly lowered T₄ and increased T₃ concentrations. No effect of any hormone treatment on antibody production was observed. T₃ supplementation and cGH injection alone or with T₃ (0.1 ppm) significantly increased blastogenic response of lymphocytes to either Con-A or LPS mitogenic stimulation. It was concluded that T₃ and GH are involved in lymphocyte activity of chickens.     

Plasma beta-endorphin level in cases of luteal phase defect

OBJECTIVE: To evaluate beta-endorphin secretion in euprolactinemic cases of luteal phase defect (LPD). DESIGN: Serial blood samples from the 18th to the 26th day of the menstrual cycle were assayed for beta-endorphin, progesterone (P), estradiol (E2), and prolactin (PRL) in cases of LPD and controls. Diagnosis of LPD was based on determinations of serum P and premenstrual endometrial biopsy. SETTING: From Cairo University Hospitals. PATIENT, PARTICIPANTS: Twenty-six women with LPD and 8 normal fertile women (controls) were chosen. INTERVENTIONS: None. MAIN OUTCOME MEASURES: beta-Endorphin, P, E2, and PRL concentrations were determined by the corresponding 125I radioimmunoassay. RESULTS: Plasma beta-endorphin level in cases of LPD varied from 2.58 to 9.14 pmol/L, whereas the level of controls varied from 2.41 to 5.57 pmol/L. The mean value of plasma beta-endorphin in cases of LPD was significantly higher than that of controls by 146% (P less than 0.0005). In spite of the significant decrease of serum P in cases of LPD, serum E2 level did not differ significantly from that of controls. CONCLUSION: The possible sources of beta-endorphin rise and its implication in the etiology of LPD are explained.