宋《本草图经》草木部所述植物药主要产地及药材集散地考略

1 宋代社会经济、医事制度与历史地理 1.1 宋代的社会经济 宋朝是我国历史上继唐朝之后,社会经济发展、科技文化进步的一个历史时期,后世有"治隆唐宋"之说.公元960年陈桥兵变,赵匡胤(宋太祖)"黄袍加身"以后,遂代周而自立,是为宋朝,史称北宋.当时的社会在经历了五代十国的战乱之后而趋于安定,经济逐渐恢复,科学也日益发达.     

利多卡因治疗外伤性蛛网膜下腔出血疗效分析

目的探讨早期静脉注射利多卡因对外伤性蛛网膜下腔出血（tsAH）继发性脑损伤的治疗作用。方法重度颅脑损伤后SAH患者60例（GCS评分≤8分）。随机分为治疗组（早期静脉注射利多卡因组）和对照组。在治疗前后对患者均进行GCS评分、颅内压（ICP）测定以及头部CT、发射计算机体层摄影（ECT）、经颅多普勒（TCD）检查。结果利多卡因治疗7d后即出现颅内压降低、挫伤脑组织血流供应改善、脑水肿减轻，与对照组比较，有明显差异（P〈0．01）；GCS评分在利多卡因治疗7d、14d后较对照组明显增加（P〈0．01）。结论早期静脉注射利多卡因能明显减轻颅脑损伤后SAH继发性脑组织损伤的程度，有利于神经功能的早期恢复。     

The effects of chymase on matrix metalloproteinase-2 activation in neointimal hyperplasia after balloon injury in dogs.

Chymase is known to generate angiotensin II in the vascular wall. In this study we investigated a novel role for chymase other than angiotensin II production in vascular proliferation after balloon injury. Chymase promoted the migration of vascular smooth muscle cells in the matrix-coated invasion chambers and activated promatrix metalloproteinase-2 obtained from the culture medium of vascular smooth muscle cells. Two weeks after balloon injury, significant neointimal formation was found in dog carotid arteries. After injury, active matrix metalloproteinase-2 was increased in parallel with the augmentation of chymase activity that was seen in the proliferating region of the vascular wall. The oral administration of NK3201 (1 mg/kg per day), a chymase inhibitor, prevented neointimal formation and significantly suppressed both active matrix metalloproteinase-2 and chymase activities 2 weeks after injury. These results suggest that chymase inhibitors can prevent the development of intimal hyperplasia via the inhibition of matrix metalloproteinase-2 activation in balloon-injured arteries.     

Fidgetin-like 1 gene inhibited by basic fibroblast growth factor regulates the proliferation and differentiation of osteoblasts.

The FIGNL1 gene was proven to be a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). In this in vitro study, the AAA proteins inhibited osteoblast proliferation and stimulated osteoblast differentiation. We showed that FIGNL1 may play some regulatory role in osteoblastogenesis. INTRODUCTION: The fidgetin-like 1 (FIGNL1) gene encodes a new subfamily member of ATPases associated with diverse cellular activities (AAA proteins). Although the FIGNL1 protein localizes to both the nucleus and cytoplasm, the function of FIGNL1 remains unknown. In a previous study, we identified several genes that mediate the anabolic effects of basic fibroblast growth factor (bFGF) on bone by using microarray data. FIGNL1 was one of the genes that downregulated >2-fold in MC3T3-E1 cells after treatment with bFGF. Therefore, this study was aimed to identify and confirm the function of FIGNL1 on osteoblastogenesis. MATERIALS AND METHODS: We examined the effect of the FIGNL1 gene on proliferation, differentiation, and apoptosis in mouse osteoblast cells (MC3T3-E1 and mouse primary calvarial cells) using flow cytometry, RT-PCR, cell proliferation assay, and cell death assay. MC3T3-E1 cells and mouse calvarial cells were transfected with small interfering RNA (siRNA) directed against the FIGNL1 or nontargeting control siRNA and examined by cell proliferation and cell death assays. Also, FIGNL1 was fused to enhance green fluorescent protein (EGFP), and the EGFP-fused protein was transiently expressed in MC3T3-E1 cells. RESULTS: Reduced expression of FIGNL1 by bFGF and TGF-beta1 treatment was verified by RT-PCR analysis. Overexpression of FIGNL1 reduced the proliferation of MC3T3-E1 and calvarial cells, more than the mock transfected control cells did. In contrast, siFIGNL1 transfection significantly increased the proliferation of osteoblasts, whereas overexpression of FIGNL1 did not seem to alter apoptosis in osteoblasts. Meanwhile, overexpression of FIGNL1 enhanced the mRNA expression of alkaline phosphatase (ALP) and osteocalcin (OCN) in osteoblasts. In contrast, siFIGNL1 decreased the expression of ALP and OCN. A pEGFP-FIGNL1 transfected into MCT3-E1 cells had an initially ubiquitous distribution and rapidly translocated to the nucleus 1 h after bFGF treatment. CONCLUSIONS: From these results, we proposed that FIGNL1, a subfamily member of the AAA family of proteins, might play some regulatory role in osteoblast proliferation and differentiation. Further analyses of FIGNL1 will be needed to better delineate the mechanisms contributing to the inhibition of proliferation and stimulation of osteoblast differentiation.     

Fontan conversion with arrhythmia surgery.

OBJECTIVE: Hemodynamic abnormalities and refractory atrial arrhythmias in patients late after the Fontan operation result in significant morbidity and mortality. We reviewed our experience with Fontan conversion and concomitant arrhythmia surgery. METHODS: Between January 1996 and February 2004, 16 patients underwent Fontan conversion and arrhythmia surgery. Mean age at the initial Fontan operation was 5.1+/-3.5 (range: 2-15) years and mean age at Fontan conversion was 17.0+/-5.8 (range: 6-30). The initial Fontan operations were atriopulmonary connections in 14 patients, extracardiac lateral tunnel in 1, and intracardiac lateral tunnel in 1. The types of arrhythmia included atrial flutter in 10 patients and atrial fibrillation in 3. Fontan conversion operation was performed with intracardiac lateral tunnel in 5 patients and extracardiac conduit in 11. Arrhythmia surgery included isthmus cryoablation in 10 patients and right-sided maze in 3. RESULTS: There has been no mortality. At Fontan conversion operation, 7 patients required permanent pacemaker. All patients have improved to New York Heart Association class I or II. With a mean follow-up of 26.9+/-30.6 (range:1-87) months, 16 patients had sinus rhythm, 2 patients had transient atrial flutter which was well controlled, and 2 patients required permanent pacemaker during follow-up. CONCLUSIONS: Fontan conversion with concomitant arrhythmia surgery and permanent pacemaker placement is safe, improves New York Heart Association functional class, and has a low incidence of recurrent arrhythmias. In most patients, concomitant permanent pacemakers are needed.     

Association of the GNAS1 gene variant with hypertension is dependent on alcohol consumption.

The beta-adrenoceptor (beta-AR)-stimulatory guanine nucleotide-binding (Gs) protein system has been shown to play important roles in the cardiovascular system. The gene encoding the alpha-subunit of Gs proteins (GNAS1) is a candidate genetic determinant for hypertension. Because alcohol consumption is known to affect blood pressure partly through the beta-AR-Gs protein system, we examined the possible interaction between GNAS1 T393C polymorphism and drinking status in the association with hypertension in the present study. As a result, a non-significant but reasonable trend supporting the presence of an interaction was shown (p = 0.076). In line with this trend, the T393C polymorphism significantly interacted with drinking status in the association with systolic blood pressure (p = 0.028). Moreover, supporting the presence of an interaction, T allele carriers consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than CC homozygotes in non-drinkers and light drinkers. In contrast, CC homozygotes consistently had a higher probability of hypertension, higher systolic blood pressure, and higher diastolic blood pressure than T allele carriers in moderate to heavy drinkers. The present study also showed a significant interaction between the T393C polymorphism and drinking status in the association with pulse pressure (p = 0.026), reflected by a significant association between the T393C polymorphism and pulse pressure in moderate to heavy drinkers (p = 0.026). These findings may be helpful in conducting further molecular and biological studies on the relationship among the effects of alcohol, the beta-AR-Gs protein system, and hypertension.     

慢性肾功能不全患者血管活性物质测定在血液净化中的临床研究

目的 评价血管紧张素Ⅱ、氨甲酰血红蛋白、醛固酮及甲状旁腺激素等在血液净化充分性中的意义。方法 120例慢性肾功能衰竭患者，按采用不同的透析膜分为3组：即聚砜膜、醋酸膜、铜仿膜。用放射免疫法测定其血管紧张素Ⅱ（AngⅡ）及醛固酮（ALD）浓度，化学发光法测甲状旁腺激素（PTH）。采用不同的血流量200ml／min及250ml／min比较。结果 对体内中、小分子物质清除率，聚砜膜〉醋酸膜〉铜仿膜。结论 高血流量、高通透性人工合成聚砜膜，对治疗慢性肾功能衰竭，提高肾功能不全患者的身心健康及生活质量、延长患者生命有很重要的临床意义。     

416例甲状腺肿瘤临床病理分析

目的了解本地区甲状腺肿瘤的发病情况，探讨甲状腺肿瘤的诊断与鉴别诊断6方法对416例甲状腺肿瘤病理资料进行回顾性分析。结果甲状腺肿瘤以良性多见，良恶性之比为8．2：1。各类型肿瘤均以女性明显多于男性，男女之比为1：5．4，好发年龄为21～50岁，肿瘤发生于甲状腺右侧多见。结论本组甲状腺肿瘤的发生率、好发年龄、性别差异、良恶之比与文献报道基本一致。乳头状腺瘤与乳头状癌的鉴别有一定难度，对可疑标本要多处取材，连续切片，仔细观察，找出其特征，提高诊断的准确性。     

葛根素对家兔肢体缺血再灌注后心脏功能的保护作用

目的:观察葛根素对家兔肢体缺血再灌注所致心脏损伤的保护作用并探讨其机制.方法:家兔40只,随机分4组:Ⅰ组为假手术对照组、Ⅱ组为缺血再灌注组、Ⅲ组为葛根素低剂量治疗组、Ⅳ组为葛根素高剂量治疗组.免疫组化法检测心肌组织Bcl-2和Bax蛋白表达;原位缺口末端标记法(TUNEL)检测心肌细胞凋亡;比色法测定心肌组织超氧化物岐化酶(SOD)和髓过氧化物酶(MPO)活性,丙二醛(MDA)含量,测定血清乳酸脱氢酶(LDH)活性;通过生理记录仪观察心功能指标.结果:与Ⅱ组比较,Ⅲ、Ⅳ组左心室功能增强,且Ⅳ组的左心室收缩功能比Ⅲ组增强,同时,Ⅲ、Ⅳ组心肌组织MDA含量和血清LDH活性减少,Bax蛋白表达减少,Ⅳ组的心肌凋亡指数低于Ⅱ组,心肌Bcl-2表达高于Ⅱ组.结论:葛根素促进肢体缺血再灌注后心脏功能的恢复,表现为剂量依赖效应,其作用机制与抗氧化损伤和抗细胞凋亡有关.