Development of an international online learning platform for hepatopancreatobiliary surgical training: a needs assessment

BackgroundThe Americas Hepato-Pancreato-Biliary Association (AHPBA) and the Australian and New Zealand Hepatic, Pancreatic and Biliary Association (ANZHPBA) are developing an online distance learning curriculum to facilitate an interactive didactic experience for hepatopancreatobiliary (HPB) fellows in the operationalization of existing HPB fellow curricula. Two needs assessment surveys were carried out to identify the optimal structure and process for deployment in fellow education.MethodsA 22-question survey querying fellows'' learning styles and current and anticipated use of learning tools was disseminated electronically to 38 North American and Australasian HPB fellows. A follow-up 20-question survey was administered to assess fellows'' feelings regarding online content.ResultsResponse rates were 55% (n = 21) for the first survey and 42% for the second (n = 16). In the first survey, 67% of respondents claimed familiarity with the required HPB curriculum, and 43% indicated dissatisfaction with current personal study strategies. A total of 62% (n = 13) reported studying with focused clinical relevance versus using a prescribed curriculum (n = 1, 5%). Fellows anticipated participating using online tools once (n = 10, 48%) or two or three times (n = 5, 24%) per week. Most respondents (n = 18, 86%) would meaningfully follow one or two discussions per month. The second survey identified themes for improvement such as discussion topics of interest, avoidance of holiday timing and mandatory participation.ConclusionsAn international online distance learning format is an appealing mechanism for improved dissemination and operationalization of the established HPB fellow curricula. Fellows will engage in interactive discussions monthly. Controversial topics or those requiring complex decision making are best suited to this learning format.     

Patient selection and the volume effect in pancreatic surgery: unequal benefits?

Background

The volume effect in pancreatic surgery is well established. Regionalization to high-volume centres has been proposed. The effect of this proposal on practice patterns is unknown.

Methods

Retrospective review of pancreatectomy patients in the Nationwide Inpatient Sample 2004–2011. Inpatient mortality and complication rates were calculated. Patients were stratified by annual centre pancreatic resection volume (low <5, medium 5–18, high >18). Multivariable regression model evaluated predictors of resection at a high-volume centre.

Results

In total, 129 609 patients underwent a pancreatectomy. The crude inpatient mortality rate was 4.3%. 36.0% experienced complications. 66.5% underwent a resection at high-volume centres. In 2004, low-, medium- and high-volume centres resected 16.3%, 24.5% and 59.2% of patients, compared with 7.6%, 19.3% and 73.1% in 2011. High-volume centres had lower mortality (P < 0.001), fewer complications (P < 0.001) and a shorter median length of stay (P < 0.001). Patients at non-high-volume centres had more comorbidities (P = 0.001), lower rates of private insurance (P < 0.001) and more non-elective admissions (P < 0.001).

Discussion

In spite of a shift to high-volume hospitals, a substantial cohort still receives a resection outside of these centres. Patients receiving non-high-volume care demonstrate less favourable comorbidities, insurance and urgency of operation. The implications are twofold: already disadvantaged patients may not benefit from the high-volume effect; and patients predisposed to do well may contribute to observed superior outcomes at high-volume centres.     

Rankings versus reality in pancreatic cancer surgery: a real-world comparison

Background

Patients are increasingly confronted with systems for rating hospitals. However, the correlations between publicized ratings and actual outcomes after pancreatectomy are unknown.

Methods

The Massachusetts Division of Health Care Finance and Policy Hospital Inpatient Discharge Database was queried to identify pancreatic cancer resections carried out during 2005–2009. Hospitals performing fewer than 10 pancreatic resections in the 5-year period were excluded. Primary outcomes included mortality, complications, median length of stay (LoS) and a composite outcomes score (COS) combining primary outcomes. Ranks were determined and compared for: (i) volume, and (ii) ratings identified from consumer-directed hospital ratings including the US News & World Report (USN), Consumer Reports, Healthgrades and Hospital Compare. An inter-rater reliability analysis was performed and correlation coefficients (r) between outcomes and ratings, and between rating systems were calculated.

Results

Eleven hospitals in which a total of 804 pancreatectomies were conducted were identified. Surgical volume correlated with overall outcome, but was not the strongest indicator. The highest correlation referred to that between USN rank and overall outcome. Mortality was most strongly correlated with Healthgrades ratings (r = 0.50); however, Healthgrades ratings demonstrated poorer correlations with all other outcomes. Consumer Reports ratings showed inverse correlations.

Conclusions

The plethora of publicly available hospital ratings systems demonstrates heterogeneity. Volume remains a good but imperfect indicator of surgical outcomes. Further systematic investigation into which measures predict quality outcomes in pancreatic cancer surgery will benefit both patients and providers.     

The systems biology of mitochondrial fission and fusion and implications for disease and aging

Mitochondria organize themselves as dynamic populations within a cell, by undergoing continuous cycles of fission and fusion. The spatio-temporal distribution and abundance of mitochondria determines the cell’s energy budget and is thus intimately linked to the cell’s response to environmental stimuli during aging. The dynamic balance of mitochondrial fission and fusion can be studied in terms of antagonistic subpopulations that regulate the mitochondrial responses in space and time. The dynamic nature of these processes motivates mathematical modelling and the simulation of such complex process. In several neurodegenerative and metabolic diseases the dynamic balance of fission and fusion is disturbed. However, how this dynamics plays a role in the progression of diseases is largely unclear. Fission and fusion help mitochondria to regulate cellular energy (ATP) levels, and minimize accumulation of harmful oxidized material called reactive oxygen species which accelerate mutations in mitochondrial DNA (mtDNA) during aging. We discuss how systems biology approaches can be used to investigate the mechanisms controlling the fission–fusion dynamics under two categories: dissecting the design of its molecular regulatory motifs, and understanding complex mitochondrial responses through their population level interactions. This will help us to understand how different regulatory mechanisms regulate the ATP and mutation (mtDNA) landscape of mitochondria to a variety of environmental stimuli in order to maintain their function during aging.     

MyD88 Is Dispensable for Cerebral Amyloidosis and Neuroinflammation in APP/PS1 Transgenic Mice

Activated microglia are associated with amyloid plaques in transgenic mouse models of cerebral amyloidosis and in human Alzheimer disease; yet, their implication in Alzheimer disease pathogenesis remains unclear. It has been suggested that microglia play dual roles depending on the context of activation, contributing negatively to disease pathogenesis by secreting proinflammatory innate cytokines or performing a beneficial role via phagocytosis of amyloid beta (Aβ) deposits. Toll-like receptors, most of which signal through the adaptor protein myeloid differentiation factor 88 (MyD88), have been suggested as candidate Aβ innate pattern recognition receptors. It was recently reported that MyD88 deficiency reduced brain amyloid pathology and microglial activation. To assess a putative role of MyD88 in cerebral amyloidosis and glial activation in APPswe/PS1ΔE9 (APP/PS1) mice, we crossed MyD88-deficient (MyD88^−/−) mice with APP/PS1 mice, interbred first filial offspring, and studied APP/PS1 MyD88^+/+, APP/PS1 MyD88^+/−, and APP/PS1 MyD88^−/− cohorts. Biochemical analysis of detergent-soluble and detergent-insoluble Aβ_1-40 or Aβ_1-42 in brain homogenates did not reveal significant between-group differences. Furthermore, no significant differences were observed on amyloid plaque load or soluble fibrillar Aβ by quantitative immunohistochemical analysis. In addition, neither activated microglia nor astrocytes differed among the three groups. These data suggest that MyD88 signaling is dispensable for Aβ-induced glial activation and does not significantly affect the nature or extent of cerebral β-amyloidosis in APP/PS1 mice.Alzheimer disease (AD) is an insidious public health threat characterized by deposition of β-amyloid as senile plaques, formation of neurofibrillary tangles, and large-scale cortical neuronal loss leading to dementia. In addition to these pathognomonic features of the disease, AD patients exhibit low-level chronic neuroinflammation. This is hallmarked by the spatial and temporal occurrence of activated microglia with amyloid beta (Aβ) deposits. Yet, the mechanisms by which microglia recognize and respond to Aβ accumulation remain unclear. Current evidence suggests that there are varied forms of activated microglia in AD, some of which are detrimental and others beneficial.¹ Because microglial activation is a complex continuum of varied responses,² it stands to reason that a wide array of immune molecules may orchestrate microglial responses to Aβ. Ultimately, a clearer understanding of the pathways leading to beneficial microglial responses and clearance of misfolded proteins could open new avenues for AD treatment.Numerous recent studies have proposed that Toll-like receptors (TLRs) play a role in the microglial response to Aβ and, more specifically, that aggregated Aβ can activate microglia via TLRs.^3–11 Most TLRs (except TLR3) signal through the adaptor protein myeloid differentiation factor 88 (MyD88), suggesting that it may play an important role in microglial activation in response to cerebral amyloid accumulation. To test this possibility, two recent studies crossed MyD88 knockout mice with APP/PS1 mouse models of cerebral amyloid deposition and examined effects on cognitive deficits and AD-like pathology. In one study, it was reported that MyD88 deficiency of the doubly transgenic APPswe/PS1dE9 mouse reduced cerebral amyloid pathology and microglial activation and decreased expression of CX3CR1 in 10-month-old animals.¹² Lim and coworkers¹² suggested that inhibiting MyD88-associated TLR signaling would alter the microglial activation state, and they reported less cerebral amyloid deposition in this cross. However, their findings were perplexing given previous reports showing that activation of TLRs leads to decreased amyloid load and increased Aβ phagocytosis, leading to the hypothesis that MyD88 deficiency would either cause buildup of amyloid or have no effect on amyloid levels in APP/PS1 mice.^{4,6,11,13–15} Another recent study published findings more consistent with this hypothesis, demonstrating that APPswe/PS1A246E mice heterozygous for MyD88 had accelerated spatial learning and memory deficits and increased levels of soluble Aβ oligomers. These results led the authors to conclude that MyD88-mediated activation of microglia was protective in the context of cerebral amyloid deposition.¹⁶ In an attempt to clarify the uncertainty surrounding this critical question, we crossed APPswe/PS1dE9 (APP/PS1) mice with MyD88 knockout (MyD88^−/−) mice (both on a C57BL/6 background) and analyzed APP/PS1 MyD88^+/+, APP/PS1 MyD88^+/−, and APP/PS1 MyD88^−/− cohorts for Alzheimer-like pathology at 15 months of age.     

Comprehensive Biomarker Testing of Glycemia,Insulin Resistance,and Beta Cell Function Has Greater Sensitivity to Detect Diabetes Risk Than Fasting Glucose and HbA1c and Is Associated with Improved Glycemic Control in Clinical Practice

Blood-based biomarker testing of insulin resistance (IR) and beta cell dysfunction may identify diabetes risk earlier than current glycemia-based approaches. This retrospective cohort study assessed 1,687 US patients at risk for cardiovascular disease (CVD) under routine clinical care with a comprehensive panel of 19 biomarkers and derived factors related to IR, beta cell function, and glycemic control. The mean age was 53?±?15, 42 % were male, and 25 % had glycemic indicators consistent with prediabetes. An additional 45 % of the patients who had normal glycemic indicators were identified with IR or beta cell abnormalities. After 5.3 months of median follow-up, significantly more patients had improved than worsened their glycemic status in the prediabetic category (35 vs. 9 %; P?HbA1c values of 5.5–5.6; 56 vs. 18 %, p?相似文献   

A cross-sectional study on factors associated with health seeking behaviour of Malawians aged 15+ years in 2016

IntroductionHealth seeking behaviour (HSB) refers to actions taken by individuals who are ill in order to find appropriate remedy. Most studies on HSB have only examined one symptom or covered only a specific geographical location within a country. In this study, we used a representative sample of adults to explore the factors associated with HSB in response to 30 symptoms reported by adult Malawians in 2016.MethodsWe used the 2016 Malawi Integrated Household Survey dataset. We fitted a multilevel logistic regression model of likelihood of ‘seeking care at a health facility’ using a forward step-wise selection method, with age, sex and reported symptoms entered as a priori variables. We calculated the odds ratios (ORs) and their associated 95% confidence intervals (95% CI). We set the level of statistical significance at P < 0.05.ResultsOf 6909 adults included in the survey, 1907 (29%) reported symptoms during the 2 weeks preceding the survey. Of these, 937 (57%) sought care at a health facility. Adults in urban areas were more likely to seek health care at a health facility than those in rural areas (AOR = 1.65, 95% CI: 1.19–2.30, P = 0.003). Females had a higher likelihood of seeking care from health facilities than males (AOR = 1.26, 95% CI: 1.03–1.59, P = 0.029). Being of higher wealth status was associated with a higher likelihood of seeking care from a health facility (AOR = 1.58, 95% CI: 1.16–2.16, P = 0.004). Having fever and eye problems were associated with higher likelihood of seeking care at a health facility, while having headache, stomach ache and respiratory tract infections were associated with lower likelihood of seeking care at a health facility.ConclusionThis study has shown that there is a need to understand and address individual, socioeconomic and geographical barriers to health seeking to increase access and appropriate use of health care and fast-track progress towards Universal Health Coverage among the adult population.