None.

This review considers the epidemiologic evidence of an increasing incidence of type 2 diabetes in youth, the classification and diagnostic issues related to diabetes in young populations, pathophysiologic mechanisms relevant to the increasing incidence, the role of genetics and environment, and the community challenge for prevention and treatment. Type 2 diabetes in youth has been recognized to be frequent in populations of native North Americans and to comprise some 30 percent of new cases of diabetes in the 2nd decade of life, largely accounted for by minority populations and associated with obesity. Among Japanese schoolchildren, type 2 diabetes is seven times more common than type 1, and its incidence has increased more than 30-fold over the past 20 years, concomitant with changing food patterns and increasing obesity rates. The forms of diabetes seen in children and youth include typical type 1, occurring in all races; type 2, seen predominantly in minority youth; atypical diabetes, seen as an autosomal dominantly transmitted disorder in African-American populations; and maturity-onset diabetes of the young (MODY), seen rarely and only in Caucasians. Of the nonautoimmune forms of diabetes seen in youth, only type 2 diabetes is increasing in incidence. Proper classification requires consideration of onset (acute/severe versus insidious), ethnicity, family history, presence of obesity, and if necessary, studies of diabetes related autoimmunity. Insulin resistance predicts the development of diabetes in Pima Indians, in offspring of parents with type 2 diabetes, and in other high-risk populations. African-American children and youth have greater insulin responses during glucose tolerance testing and during hyperglycemic clamp study than do whites. There is also evidence of altered beta-cell function preceding the development of hyperglycemia. Of particular interest is the evidence that abnormal fetal and infantile nutrition is associated with the development of type 2 diabetes in adulthood. The thrifty phenotype hypothesis states that poor nutrition in fetal and infant life is detrimental to the development and function of the beta-cells and insulin sensitive tissues, leading to insulin resistance under the stress of obesity. The thrifty genotype hypothesis proposes that defective insulin action in utero results in decreased fetal growth as a conservation mechanism, but at the cost of obesity-induced diabetes in later childhood or adulthood. The vast majority of type 2 diabetes in adults is polygenic and associated with obesity. Monogenic forms (MODY, maternally transmitted mitochondrial mutations) are rare, but are more likely to appear in childhood. Linkage studies of the common polygenic type 2 diabetes have emphasized the heterogeneity of the disorder. The prevention and treatment of type 2 diabetes in children and youth is a daunting challenge because of the enormous behavioral influence, difficulty in reversing obesity, and typical nonadherence in this age-group. The emerging epidemic of type 2 diabetes i...

ospital medicine is the fastest growing medical specialty in the United States. 1,2 A major driver of this growth has been empirical evidence suggesting that hospitalists provide inpatient care that is more efficient, less costly, and of equal or higher quality than traditional models of care. 3,4 Currently, hospitalist programs face growing pressure to increase productivity to compensate for declining revenue or to meet operational demands resulting from policy and practice changes, such as limitations on resident work hours, specialty comanagement, and decreased presence of primary care physicians in the hospital. [5][6][7] Increased workloads for nurses and resident physicians have been associated 6,8 with adverse events, leading to mandated workload reductions, but there is little empirical evidence illuminating the association of hospitalist workload and clinical outcomes.Historically, benchmark recommendations for US hospitalist workload range from 10 to 15 patient encounters per day, but these figures lack empirical support. 9 In a recent national survey of hospitalists, 10 40% of respondents reported exceeding what they perceived as a safe workload at least monthly and that increased workload led to delays in care, poor communication between physicians and patients, delivery of unnecessary care, medication errors, and complications of care, including death. Although the correlations between these physician perceptions and patient outcomes are not known, increasing productivity requirements for hospitalists could un-IMPORTANCE Hospitalist physicians face increasing pressure to maximize productivity, which may undermine the efficiency and quality of care.OBJECTIVE To determine the association between hospitalist workload and the efficiency and quality of inpatient care. DESIGN, SETTING, AND PARTICIPANTSWe conducted a retrospective cohort study of 20 241 admissions of inpatients cared for by a private hospitalist group at a large academic community hospital system between February 1, 2008, and January 31, 2011.EXPOSURES Daily hospitalist workload as measured by relative value units and patient encounters from the hospitalist billing records. MAIN OUTCOMES AND MEASURESThe main outcomes were length of stay (LOS), cost, rapid response team activation, in-hospital mortality, patient satisfaction, and 30-day readmission rates. Key covariates included hospital occupancy and patient-level characteristics. RESULTSThe LOS increased as workload increased, particularly at lower hospital occupancy. For hospital occupancies less than 75%, LOS increased from 5.5 to 7.5 days as workload increased. For occupancies of 75% to 85%, LOS increased exponentially above a daily relative value unit of approximately 25 and a census value of approximately 15. At high occupancy (>85%), LOS was J-shaped, with significant increases at higher ranges of workload. After controlling for LOS, cost increased by $111 for each 1-unit increase in relative value unit and $205 for each 1-unit increase in census across the range of values. Changes i...

The Hospital Readmissions Reduction Program (HRRP), a part of the US Patient Protection and Affordable Care Act, requires the Centers for Medicare and Medicaid Services to penalize hospitals with excess readmissions. We take an economic and operational (patient flow) perspective to analyze the effectiveness of this policy in encouraging hospitals to reduce readmissions. We introduce a single-hospital model to capture the dependence of a hospital's readmission-reduction decision on various hospital characteristics. We derive comparative statics that predict how changes in hospital characteristics impact the hospital's readmissionreduction decision. We then proceed to develop a game-theoretic model that captures the competition between hospitals introduced by the HRRP policy's benchmarking mechanism. We provide bounds that apply to any equilibrium of the game and show that the comparative statics derived from the single-hospital model remain valid after the introduction of competition. Importantly, the comparison of the single-hospitals and multi-hospital models shows that, while the competition among hospitals often encourages more hospitals to reduce readmissions, it can only increase the number of "worst offenders," which are hospitals that prefer paying penalties over reducing readmissions in any equilibrium. We calibrate our model with a dataset of hospitals in California which allows us to quantify the results and insights derived from the model. Last, we validate our model with recent hospitals' performance data collected since the policy was implemented.

The behavioral performance of rats subjected in the neonatal period to hypoxia-ischemia at either 37 degrees C or 21 degrees C was compared to that of sham-ligated animals. Performance on complex motor tests was significantly delayed only in the hypoxic-ischemic 37 degrees C rats. However, cognitive testing disclosed significant delay of spatial learning in animals subjected to hypoxia-ischemia at 21 degrees C and those with gross infarction at 37 degrees C. There was enhanced avoidance learning in the animals with gross infarction in the hypoxia-ischemia 37 degrees C group. Hypoxic-ischemic damage in the neonatal rat at 37 degrees C results in transient delay of complex motor skills, but longer lasting cognitive changes. Hypoxia-ischemia during hypothermia produces no motor deficits, although there may be similar alterations in learning.