信息不对称下公立医院过度医疗的治理

过度医疗作为医疗实践中的不良现象,是引发医疗纠纷和“看病贵”的重要原因。文章从信息不对称的角度,通过分析我国公立医院过度医疗治理现状,找出当前我国公立医院过度医疗治理存在的问题,提出信息不对称下公立医院过度医疗的治理模式,以期从根本上遏制公立医院过度医疗问题的发生。     

基于多层感知器网络的过度医疗防治绩效评价研究

目的 通过多层感知器网络的构建评价过度医疗防治的效果,为进一步完善过度医疗防治体系提供参考。方法 基于多层感知器网络,构建了具有三层神经网络、9个隐含层节点数的过度医疗绩效评价模型。结果 多层感知器网络的训练结果与专家评价（期望结果）两者评价是完全一致的。 结论 该多层神经网络及其评价指标的选取能够很好的应用于医疗服务中的过度医疗防治绩效评价。     

一体化智慧医疗体系的构建与发展策略研究

将一体化智慧医疗系统应用于医院管理中主要是为了医疗资源分配的合理化,协调医院、患者和卫生计生管理部门之间的关系,提升医院自身管理水平。但是当前在发展智慧医疗的过程中仍然存在着功能原始单一、过度重视硬件投入、未形成统一的智慧医疗网络等诸多问题。未来一体化智慧医疗系统需要在建设智慧医院、构建全社会智慧医疗网络、合理利用智慧医疗云和卫生信息系统的同时健全和完善医院的各项管理制度,真正实现医院管理质的飞跃。     

经济社会新常态下的过度医疗再探讨

过度医疗作为新医改进程中亟待解决的社会热点和难点问题,是导致“看病贵、看病难”、“恶性医疗事件频发”的重要原因。本文重新探讨经济社会新常态下过度医疗的现状、表现形式和新特点,提出防治过度医疗的措施建议,以期从根本上解决“看病贵、看病难”问题,推进健康中国建设。     

基于体域网的家庭健康监护及远程急诊分诊模式

随着社会急诊医疗需求的快速增长,大量患者涌入医院,造成急诊室过度拥挤、医疗服务质量下降、医疗费用升高和住院时间延长等问题。基于体域网技术的家庭健康监护及远程急诊分诊模式通过加强对特殊人群的健康监护,起到疾病早期积极干预的作用,将急诊患者的分诊平台延伸到院前阶段,有效分流急诊患者到各级医疗机构,缓解急诊室过度拥挤,提高优质急诊医疗资源的利用效率。     

三级甲等公立医院过度医疗形成影响因素研究

目的 分析医方以及患方对过度医疗形成的影响因素,探讨过度医疗的形成机理。方法 随机抽调某省5所三级甲等医院进行问卷调查。运用结构方程模型,通过软件SPSS19.0和AMOS17.0进行数据分析处理。结果 医患之间的信息不对称以及医务人员自身薪酬待遇不足等因素对过度医疗的形成产生重要影响。结论 提高医务人员的薪酬待遇和消除医患之间的信息不对称是解决过度医疗问题的关键。     

公立医院过度医疗根源及对策浅析

“小病大治，大病豪治”的过度医疗现象屡见不鲜，不仅没有提高医疗效果，反而给患者及其家庭带来了沉重的负担。针对过度医疗一直是公立医院难以解决的顽疾，尝试探讨过度医疗产生的根源，并提出相应的解决办法。     

移动医疗服务热潮中的几点冷思考

通过阐述国内外移动医疗服务的形成与发展,介绍了移动医疗的主要应用领域,同时也分析了当前我国移动医疗服务中存在的不足,如健康数据可靠性问题、网络诊疗安全性问题、网络行医医师资质认定问题、移动医疗中医患法律责任界定问题等,并从监管、法律、政策等层面探讨了相应的解决对策。     

我国台湾地区医疗服务审查制度研究

医疗保险在成为医疗服务的最主要付费者后,为避免医务工作者因道德风险产生过度医疗,确保医疗服务的必要性与合理性,建立了医疗服务审查制度,以达到费用控制和质量保障两大作用。但成本降低和质量提高是一对矛盾体,加上审查标准不一致、相关规范不全面、审核过程不够透明等问题使得台湾医疗服务审查制度饱受医疗机构的不满和诟病,尽管如此台湾在此方面还是积累了比较丰富的经验。了解台湾地区医疗服务审查制的历史、现状及存在问题对于大陆相应制度的制订有一定的启示和借鉴意义。     

自由现金流量与公立医院过度投资关系研究 ——以B地区公立医院为例

基于自由现金流量假说理论,结合公立医院所面临的融资、盈余分配制度、医疗费用的支付方式以及公立医院面临的市场风险等,提出自由现金流量对公立医院过度投资影响的理论假设;然后,以固定资产过度投资为因变量,自由现金流量以及医院等级等为自变量,并控制医院的规模、现金存量以及上期资本支出因素,构建多元回归模型,以B地区公立医院的实际数据对研究假设进行实证检验。研究结果表明：自由现金流量是公立医院过度投资的重要诱因之一,且三级医院比二级医院更容易发生自由现金流量过度投资。     

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.     

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.     

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.     

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.