基于RBRVS的薪酬改革政策回顾、进展与常模设计

通过对我国自2009年以来的薪酬改革政策进行回顾,分析薪酬改革的主要脉络,介绍美国的量化支付模式的基本原理及在我国的应用现况,并设计应用常模,以期为公立医院薪酬改革建言献策。     

公立医院临床医生薪酬体系结构研究

临床医生是医疗服务的提供者，其行为直接影响医院医疗服务的质量和水平。文章在分析公立医院临床医生薪酬体系现状及问题的基础上，构建了基于闭环控制的动态薪酬体系，使薪酬体系更加科学地服务于临床医生，可以有效激励临床医生的医疗服务行为，更好地提高公立医院的医疗服务质量。     

基于云式薪酬的公立医院薪酬体系优化研究

介绍了云式薪酬理论及其优化层次。通过云式薪酬理论对公立医院的薪酬体系进行优化,使得薪酬体系能够覆盖到医院内每一名员工,并将医疗服务和对医院的战略性贡献进行量化,使其与薪酬有机切合,实现薪酬的柔性化,对于医疗行业的薪酬激励制度创新具有一定的借鉴意义。     

山东省县级公立医院医保支付方式改革实施现状研究

目的 分析县级公立医院医保支付方式改革实施现状，发现问题并提出对策。方法 通过邮寄问卷与实地调研的方法收集数据，采用SPSS19.0对数据进行运算处理与分析。结果 参与山东省第一、二批县级公立医院改革的医疗机构中160家（92.5%）进行了医保支付方式改革，但支付方式仍较单一；开展按病种限价付费与按病种定额付费的医院中，病种数量超过50种的分别占26.2%、11.4%；63.8%的医疗机构考核结果与医保支付挂钩等。结论 应推行复合型付费方式，增加按病种付费的病种数量，克服医保支付方式改革推行过程中来自“医、保、患”三方的阻力，发挥支付方式对医疗机构的正向引导作用。     

公立医院付费制度改革对医疗质量管理的影响探讨

首都医科大学附属北京友谊医院从2011年开始实施医保总额预付费制度改革、按病种分组（DRGs） 付费试点改革、医药分开改革等一系列支付制度改革,对医院的运行带来较大影响。付费制度改革对医疗质量的提高带来很大的挑战。医院采取了抓基础质量、抓环节质量、抓终末评价等一系列措施提高医疗服务质量和技术水平。在付费制度改革后,医院医疗服务量、DRGs评价、合理用药等数据均优于改革前,在保证医疗质量的前提下完成了付费制度改革,达到了医疗费用可控、医疗质量不降的双向目标。     

江苏省三种基本医疗保险支付方式改革与探索

对江苏省3种基本医疗保险支付方式改革探索作出分析,分别介绍了在城镇职工基本医疗保险支付方式上,淮安市实行的"病种分值结算办法"、镇江市实行的"总额预算、弹性结算、部分疾病按病种付费";在城镇居民基本医疗保险支付方式上,南京市实行的部分病种定额指标结算,住院医疗费用控制指标结算、连云港实行的问题控制结算办法;在新型农村合作医疗支付方式上,积极探索单病种定额付费等,并对支付方式改革取得的效果作了比较深入的分析。     

按病种付费下医生的隐藏特征问题分析

按病种付费作为控制医疗费用过快上涨的一项支付方式改革,在我国的进展较为缓慢且改革效果未及预期,主要原因之一是来自医生的阻力。本研究借用委托代理理论分析医生作为代理方在执行按病种付费改革过程中,如何利用自己的信息优势而采取机会主义行为,产生隐藏特征问题如何对改革的进展和效果起到阻碍作用,为进一步完善按病种付费制度提供参考建议。     

医疗保险费用支付方式改革对医院管理的影响

医疗保险支付方式是医疗保险制度的核心内容之一，它涉及医、患、保三方，是医疗保险过程中涉及各方经济利益的最直接、最敏感的环节。随着医疗保险制度的普及、医疗费用的快速增长，改革医疗保险支付方式已势在必行。疾病诊断相关组预付法是医疗保险支付方式改革的趋势，其实施将对医院的经营管理有重大影响，涉及到医院管理的重点、医保支付相关科室的结构与职能的调整以及相关人员的培训等方面。     

华东某省三级公立医院员工薪酬现状调查

目的 分析华东某省三级公立医院薪酬结构和薪酬水平并提出合理化建议,为公立医院薪酬制度改革和补偿机制改革提供决策依据。方法 以某省58家三级公立医院为研究对象,运用描述性分析、t检验和方差分析等方法,对薪酬结构和薪酬水平进行统计分析。结果 财政补助收入仅占总收入的4%;薪酬支出占总支出的26.6%,无地域差异;医务员工年人均收入9.47万元,存在地域差异;医务员工薪酬水平是非私营单位在岗职工的1.76倍。结论 政府应加大对公立医院的财政补助力度,放宽对医疗行业薪酬总量管控,提升医务员工薪酬水平和社会薪酬地位;公立医院迫切需要建立一套科学、合理的薪酬分配体系。     

手机支付在医院服务流程中的应用探讨

第三方手机支付平台正在打造的“未来医院计划”项目有望使患者可以在手机上完成挂号、候诊、缴费等环节，为患者就医提供便利。但与此同时，第三方手机支付平台也存在着如何克服支付主体资格不合法、支付安全无法保障以及患者隐私可能受到侵害等缺陷的难题。本文通过对第三方手机支付系统在医疗体系中应运的优缺点进行分析，旨在针对其在运作中存在的问题提出完善建议。     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.