Dental education in Wuhan, China: challenges and changes

The aim of this article is to describe the innovations in the School of Stomatology at Wuhan University (WHUSS) that are likely to shape the future of dental education in the People's Republic of China. There are forty dental schools in China; the five most well known are located in Beijing, Chengdu, Shanghai, Xi'an, and Wuhan. Although patient-centered, comprehensive care has been recommended as the future of dental education, traditional dental education in China still faces many challenges to accomplish this goal. WHUSS, one of the more progressive dental schools in China, has implemented several educational innovations to traditional dental education by restructuring the curriculum through the introduction of problem-based learning (PBL) and other strategies in clinical training. Although implementation of educational innovations is still at an early stage throughout China, it is reasonable to speculate that many schools will develop similar strategies as those developed at Wuhan to improve dental education during the next several years. However, additional research is necessary to evaluate the efficacy of such educational strategies and to determine the appropriate implementation of a contemporary dental curriculum and pedagogic methodology. The curriculum modifications that have been achieved to date as well as the existing challenges are discussed to provide the reader with an understanding of contemporary dental education in China.     

毒性中药生川乌质量标准研究

目的:建立毒性中药生川乌的液质联用等质量检验方法。方法:采用显微、化学、液相色谱、液质联用方法进行定性鉴别、含量测定。结果:采用液相色谱质谱/质谱联用具有灵敏、专属性强等优点,适用于微量乌头生物碱的检测。结论:建立的方法可为其质量标准的提高提供参考。     

肌浆网钙泵的抑制不参与过氧化氢诱导的大鼠主动脉收缩

目的:研究肌浆网钙泵抑制是否参与H_2O_2诱导的大鼠主动脉收缩反应。方法:离体主动脉环张力实验比较H_2O_2及钙泵特异性抑制剂环匹阿尼酸(CPA)缩血管效应及其信号机制的差异。结果:H_2O_2和CPA均收缩去内皮主动脉环,但H_2O_2触发快速短暂相位相收缩,而CPA诱导缓慢持续的张力相收缩。在无钙液中,仅CPA30μmol/L而非H_2O_230μmol/L预处理取消苯肾上腺素10μmol/L缩血管效应。Thap-sigargin 30μmol/L诱导最大收缩反应时,仅H_2O_2能使血管环进一步收缩。另外,P_2受体拮抗剂suramin、RB-2(各100μmol/L)以及多种酶抑制剂包括PLC、PKC、PLA_2、COX和蛋白质酪氨酸激酶均能抑制H_2O_2而非CPA诱导的缩血管效应,但2-APB50μmol/L对两者都有抑制作用。结论:肌浆网钙泵抑制不是H_2O_2收缩大鼠去内皮主动脉的机制。     

FOERSTER'S OPERATION FOR SPASTIC PARAI,YSIS OF THE LOWER EXTREMITIES* REPORT OF A CASE

Ncurologist and surgeon alike are often confronted with the problem of treatment of spasticity of the extremities due to diseases of the brain or of the spinal cord. Among the various causes which may produre such spasticity are syphilis, acute infectious diseases, mechanical injury to the central nervous system, vascular disturbances, thcir sequelae, and other degenerative diseases. Of all tbc varieties of spasticity none has attracted more attention than Little''s diseasc-the spastic paralysjs of children, because here enough motor power of the extre- mities persists to warrant successful devclopment of control if the spasticity can be eliminatPd or diminished.     

心血管组织内的成纤维细胞之信息传递

Introduction In cardiovascular tissues, fibroblasts play a central and dynamic role in the remodeling process, which includes proliferation of fibroblasts, and changes in the extent and composition of the synthesis of extra-cellular matrix proteins.     

Biochemical abnormalities of venous plasma membrane fraction isolated from spontanously hypertensive rats

Alkaline phosphatase activity and Ca²⁺ accumulation were examined in the isolated plasma membrane fractions from small arteries and veins of spontaneously hypertensive (SHR) and normotensive (WKY). Increased Ca²⁺ binding by plasma membrane fractions from veins, decreased ATP-dependent Ca²⁺ accumulation by those from arteries and increased alkaline phosphatase activity in both fractions from SHR were observed. We conclude that biochemical abnormalities in vascular smooth muscle cell membrane cannot be explained solely as adaptive changes induced by elevated blood pressure.     

STUDIES OF SERUM LONG-ACTING THYROID STIMULATOR (LATS) IN RELATION TO EXOPHTHALMOS AFTER THERAPY FOR THYROTOXICOSIS

Observations have been made on a series of 30 thyrotoxic patients before and after therapy, with particular attention to exophthalmos (measured by the Hertel exophthalmometer) and serial determinations of serum levels of protein-bound iodine (PBI) and long-acting thyroid stimulator (LATS). In 14 cases in which there was an exacerbation of exophthalmos (mean maximal increase of 2·8 mm. Hg) there was a greater fall in serum PBI levels (7.3 µg. per 100 ml.) than in 16 cases in which there was no such exacerbation (3.5 µg. per 100 ml.), although initial serum levels of PBI were the same in the two groups. The serum LATS level was more likely to be initially elevated in the group showing exacerbation. and a further rise was observed more frequently in this group following therapy, whether with antithyroid drugs, surgery or radio-iodine. Suppression of serum levels of LATS with azathioprine or steroids did not significantly affect the exophthalmos which had already developed in two cases. These observations suggest that a determination of serum level of LATS could be carried out advantageously before therapy. If a high level is seen, then exacerbation of exophthalmos is more likely to occur. Immunosuppressive therapy may be indicated in addition to antithyroid drug therapy. surgery or the use of radio-iodine if exacerbation is to be prevented. Further studies are suggested to try to define more clearly the susceptible group of patients and to assess the value of immunosuppressive therapy in preventing exacerbations of exophthalmos.     

Pramanicin,an antifungal agent,raises cytosolic Ca2+ and causes cell death in vascular endothelial cells

The effects of a newly discovered antifungal agent, pramanicin, on cytosolic Ca(2+) and cell viability of cultured bovine pulmonary artery endothelial cells and on endothelium-dependent relaxation of dog carotid arterial rings were investigated by digital dynamic fluorescence ratio imaging and morphological and contractility studies, respectively. Pramanicin 100 microM, previously shown to cause maximal endothelium-dependent and NO-mediated vascular relaxation, induced a small transient elevation of cytosolic Ca(2+) concentration in Ca(2+)-free medium; subsequent introduction of 1 mM Ca(2+) caused a steady, nonsaturating increase of Ca(2+), which could be brought down to the basal level by the addition of EGTA. At the single cell level, the elevation of cytosolic Ca(2+) initiates from the cell periphery and progresses toward the central region. When added to the plateau phase of phenylephrine-induced contraction, pramanicin induced a slow endothelium-dependent relaxation, which could be reversed with the NO synthase inhibitor, L-NOARG. When preincubated with vascular tissue, pramanicin resulted in an irreversible loss of endothelial function characterized by the lack of carbachol-induced relaxation. Pramanicin caused cell injury characterized by plasmalemmal bleb formation, leading to cell death characterized by Trypan blue staining of the nuclei in cultured vascular endothelial cells in a concentration- and time-dependent manner. Such pramanicin-induced cell death was not associated with Ca(2+)-mediated or NO-mediated mechanisms. The time course of Ca(2+) elevation corresponds with that of pramanicin-induced relaxation of precontracted arterial rings, whereas the time course of endothelial cell death corresponds to that of pramanicin-induced loss of endothelial function as assessed by carbachol-induced relaxation. The pramanicin analogue, PMC-A, a by-product of the biosynthesis of pramanicin, in which the epoxy group is replaced by a CC bond, caused little endothelial-dependent relaxation, but it was able to cause endothelial cell dysfunction, albeit to a lesser extent compared to pramanicin, suggesting a role of the epoxy group in pramanicin for its vasorelaxant effect.