山东省总费用分配下的公共卫生机构筹资研究

目的:了解山东省卫生总费用下的公共卫生机构筹资情况.方法:利用机构流向法测算1998-2012年山东省卫生总费用结果,结合山东卫生财务年报资料,采用定量和对比分析等方法,研究山东省公共卫生机构筹资情况,进而提出解决的方法和相关政策建议.结果:山东省公共卫生机构费用在总费用中的比例偏低;公共卫生筹资模式不合理;公共卫生资源的利用效率不高.结论:继续加强政府在优化卫生资源分配方面的主导作用;逐步改革和优化公共卫生筹资模式;重点提升政府卫生资金分配和绩效管理水平.     

医院临床科室盈余管理的探讨

2012年台州医院进行绩效奖金改革,将科室的收支结余与下拔科室的奖金总额相挂钩。因此如何规避新奖金核算制度的扣奖条款成为临床科室保持收入稳定的一项重要方面。但最近几个月出现了一些科室通过盈余管理,人为地调整收支结余,规避扣奖金的风险。虽然此类盈余管理并不违反现行的管理制度,但是会导致新奖金绩效方案流于形式,使原本激励效果大打折扣。     

政府卫生支出健康效率测算及分析

目的：测算和分析中国1990年、2000年和2010年政府卫生支出的健康效率及其影响因素。方法：运用DEA和Tobit测算政府卫生支出的健康效率,评估效率值的影响因素。结果：政府卫生支出的健康生产效率在波动中有所提高,不同年度处于前沿面的省份基本一致,远离前沿面的省份存在较大差别;该效率在各区域间的差异较显著,东部地区政府卫生支出的健康生产效率高于中、西部地区;财政分权与政府卫生支出健康效率存在显著负相关关系。结论：财政分权制度的改革与完善是提高政府卫生支出健康效率的重要途径。     

公立医院财政预算项目绩效管理制度设计、实施与研究进展

本文主要采取文献分析、专家咨询和调查研究等方法,了解公立医院财政预算项目绩效管理的研究进展、制度设计和实施情况,发现公立医院预算绩效管理仍处于起步阶段,管理制度体系不健全,指标体系、信息系统、人才队伍建设等相对滞后。建议学术界积极开展相关研究,政府特别是中央层面应组织对项目绩效评价试点情况开展基线调查,了解各试点医院工作进展、问题和需要改进的方向,设计分项目绩效评价指标,赋予各类评价指标科学合理权重、分值,明确评价标准,形成统一的预算绩效管理制度框架,指导各医院推进预算绩效管理。     

l-Leucine Supplementation Worsens the Adiposity of Already Obese Rats by Promoting a Hypothalamic Pattern of Gene Expression that Favors Fat Accumulation

Several studies showed that l-leucine supplementation reduces adiposity when provided before the onset of obesity. We studied rats that were exposed to a high-fat diet (HFD) for 10 weeks before they started to receive l-leucine supplementation. Fat mass was increased in l-leucine-supplemented rats consuming the HFD. Accordingly, l-leucine produced a hypothalamic pattern of gene expression that favors fat accumulation. In conclusion, l-leucine supplementation worsened the adiposity of rats previously exposed to HFD possibly by central mechanisms.     

Insulin-like growth factor-I in man enhances lipid mobilization and oxidation induced by a growth hormone pulse

Summary Growth hormone (GH) secretion is suppressed during insulin-like growth factor-I (IGF-I) administration. The aim of the study was to examine whether IGF-I alters the metabolic response to a GH pulse. Seven healthy male subjects (age 27±4 years, BMI 21.8±1.7 kg/m²) were treated with NaCl 0.9% (saline) or IGF-I (8 g · kg^–1 · h^–1) for 5 days by continuous subcutaneous infusion in a randomized, crossover fashion while receiving an isocaloric diet (30 kcal · kg^–1 · day^–1). On the third treatment day an intravenous bolus of 0.5 U GH was administered. Forearm muscle metabolism was examined by measuring arterialized and deep venous blood samples, forearm blood flow by occlusion plethysmography and substrate oxidation by indirect calorimetry. IGF-I treatment significantly reduced insulin concentrations by 80% (p<0.02) and C-peptide levels by 78% (p<0.02), as assessed by area under the curve. Non-esterified fatty acid (NEFA), glycerol and 3-OH-butyrate levels were elevated and alanine concentration decreased. Forearm blood flow rose from 2.10±0.43 (saline) to 2.79±0.37 ml · 100ml^–1 · min^–1 (IGF-I) (p<0.02). GH-pulse: 10 h after i.v. GH injection serum GH peaked at 40.9±7.4 ng/ml. GH did not influence circulating levels of total IGFI, C-peptide, insulin or glucose, but caused a further increase in NEFA, glycerol and 3-OH-butyrate levels, indicating enhanced lipolysis and ketogenesis. This effect of GH was much more pronounced during IGF-I: NEFA rose from 702±267 (saline) and 885±236 (IGF-I) to 963±215 (saline) (p<0.05) and 1815±586 mol/l (IGF-I) (p<0.02), respectively; after 5 h, 3-OH-butyrate rose from 242±234 (saline) and 340±280 (IGF-I) to 678±638 (saline) (p<0.02) and 1115±578 mol/l (IGF-I) (p<0.02) respectively. After injection of GH, forearm uptake of 3-OH-butyrate was markedly elevated only in the subjects treated with IGF-I: from 44±195 to 300±370 after 20 min (p<0.03) and to 287±91 nmol · 100 ml^–1 · min^–1after 120 min (p<0.02). In conclusion, the lipolytic and ketogenic response to GH was grossly enhanced during IGF-I treatment, and utilization of ketone bodies by skeletal muscle was increased.Abbreviations AUC Area under the curve - C-peptide connecting peptide - EE energy expenditure - FFM fat-free mass - GH growth hormone - IGF-I insulin-like growth factor-I - NEFA non-esterified fatty acid - Ra rate of glucose appearance - Rd rate of glucose disposal - FGU forearm glucose uptake - CV coefficient of variation     

Crosstalk between adipokines and myokines in fat browning

Skeletal muscle is the largest organ determining whole‐body insulin sensitivity and metabolic homoeostasis. Adaptive changes of skeletal muscle in response to physical activity include adjustments in the production and secretion of muscle‐derived bioactive factors, known as myokines, such as myostatin, IL‐4, IL‐6, IL‐7 and IL‐15, myonectin, follistatin‐like 1 or leukaemia inhibitory factor. These myokines not only act locally in the muscle in an autocrine/paracrine manner, but also are released to the bloodstream as endocrine factors to regulate physiological processes in other tissues. Irisin, derived from the cleavage of FNDC5 protein, constitutes a myokine that induces myogenesis and fat browning (switch of white adipocytes to brown fat‐like cells) together with a concomitant increase in energy expenditure. Besides being a target for irisin actions, the adipose tissue also constitutes a production site of FNDC5. Interestingly, irisin secretion from subcutaneous and visceral fat depots is decreased by long‐term exercise training and fasting, suggesting a discordant regulation of FNDC5/irisin in skeletal muscle and adipose tissue. Accordingly, our group has recently reported that the adipokine leptin differentially regulates FNDC5/irisin expression in skeletal muscle and fat, confirming the crosstalk between both tissues. Moreover, irisin secretion and function are regulated by other myokines, such as follistatin or myostatin, as well as by other adipokines, including fibroblast growth factor 21 and leptin. Taken together, myokines have emerged as novel molecular mediators of fat browning and their activity can be modulated by adipokines, confirming the crosstalk between skeletal muscle and adipose tissue to regulate thermogenesis and energy expenditure.     

Twenty-four-hour energy expenditure in Pima Indians with Type 2 (non-insulin-dependent) diabetes mellitus

Summary To assess the impact of Type 2 (non-insulin-dependent) diabetes mellitus on energy metabolism, 24-h energy expenditure, basal metabolic rate and sleeping metabolic rate were measured in a respiratory chamber in 151 Pima Indians, 102 with normal glucose tolerance (67 male/35 female, (mean ± SD) 28±7 years, 99±24 kg, 32±9% body fat) and in 49 with Type 2 diabetes (22 male/27 female, 35±11 years, 107±33 kg, 39±7% body fat), after at least 3 days on a weight maintaining diet. After adjustment for differences in fat-free mass, fat mass, age and sex, 24-h energy expenditure, basal metabolic rate and sleeping metabolic rate were significantly higher in diabetic patients than in control subjects (72 kcal/day, p<0.05; 99 kcal/day, p<0.005; 99 kcal/day, p<0.001 respectively). Spontaneous physical activity was similar in both groups whereas the thermic effect of food, calculated as the mean energy expenditure corrected for activity throughout the day above sleeping metabolic rate and expressed as a percentage of energy intake, was significantly lower in Type 2 diabetic patients (17.1±7.1 vs 19.8±5.6%, p<0.05). Adjusted values of 24-h energy expenditure, basal metabolic rate and sleeping metabolic rate were correlated with hepatic endogenous glucose production (r=0.22, p<0.05; r=0.22, p<0.05; r=0.31, p<0.01 respectively). Therefore, increased basal and sleeping metabolic rates, resulting in increased 24-h sedentary energy expenditure may play a role in the weight loss so often observed in Type 2 diabetic subjects in addition to the energy loss from glycosuria.