98 research outputs found

    Monsoon mixing cycles in the Bay of Bengal: A year-long subsurface mixing record

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    Based on the first year-long record of mixing collected in the eastern central Bay of Bengal, we quantify the role that subsurface turbulent heat fluxes play in upper-ocean cooling brought on by southwest (SW) and northeast (NE) monsoons. During the NE (dry, or winter) monsoon, atmospheric and subsurface turbulent heat fluxes each contribute about 50% of the net sea surface cooling. During the SW (wet, or summer) monsoon, the atmospheric heat flux varied widely due to “active” and “break” cycles of the monsoon intraseasonal oscillations, but had a net positive seasonal average. The subsurface turbulent heat flux during the SW monsoon led to surface cooling at rates more than three times greater than those measured during the NE monsoon. Since the seasonally averaged atmospheric heat flux was positive, subsurface mixing accounted for nearly all of the cooling during the SW monsoon. During the transition between the NE and SW monsoons, subsurface heat flux was near zero, and atmospheric heating rapidly warmed the sea surface. Following the SW monsoon, passage of Tropical Storm Hudhud led to O(1) m2 s–1 rates of turbulence diffusivity and strong subsurface heat flux, accounting for roughly half of the 1.4°C surface cooling that occurred over a 60-hour period

    Mixing to monsoons: Air-sea interactions in the bay of Bengal

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    More than 1 billion people depend on rainfall from the South Asian monsoon for their livelihoods. Summertime monsoonal precipitation is highly variable on intraseasonal time scales, with alternating "active" and "break" periods. These intraseasonal oscillations in large-scale atmospheric convection and winds are closely tied to 1°C-2°C variations of sea surface temperature in the Bay of Bengal

    Early efficacy of CABG care delivery in a low procedure-volume community hospital: operative and midterm results

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    BACKGROUND: The Leapfrog Group recommended that coronary artery bypass grafting (CABG) surgery should be done at high volume hospitals (>450 per year) without corresponding surgeon-volume criteria. The latter confounds procedure-volume effects substantially, and it is suggested that high surgeon-volume (>125 per year) rather than hospital-volume may be a more appropriate indicator of CABG quality. METHODS: We assessed 3-year isolated CABG morbidity and mortality outcomes at a low-volume hospital (LVH: 504 cases) and compared them to the corresponding Society of Thoracic Surgeons (STS) national data over the same period (2001–2003). All CABGs were performed by 5 high-volume surgeons (161–285 per year). "Best practice" care at LVH – including effective practice guidelines, protocols, data acquisition capabilities, case review process, dedicated facilities and support personnel – were closely modeled after a high-volume hospital served by the same surgeon-team. RESULTS: Operative mortality was similar for LVH and STS (OM: 2.38% vs. 2.53%), and the corresponding LVH observed-to-expected mortality (O/E = 0.81) indicated good quality relative to the STS risk model (O/E<1). Also, these results were consistent irrespective of risk category: O/E was 0, 0.9 and 1.03 for very-low risk (<1%), low risk (1–3%) and moderate-to-high risk category (>3%), respectively. Postoperative leg wound infections, ventilator hours, renal dysfunction (no dialysis), and atrial fibrillation were higher for LVH, but hospital stay was not. The unadjusted Kaplan-Meier survival for the LVH cohort was 96%, 94%, and 92% at one, two, and three years, respectively. CONCLUSION: Our results demonstrated that high quality CABG care can be achieved at LVH programs if 1) served by high volume surgeons and 2) patient care procedures similar to those of large programs are implemented. This approach may prove a useful paradigm to ensure high quality CABG care and early efficacy at low volume institutions that wish to comply with the Leapfrog standards

    Use of hierarchical models to evaluate performance of cardiac surgery centres in the Italian CABG outcome study

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    <p>Abstract</p> <p>Background</p> <p>Hierarchical modelling represents a statistical method used to analyze nested data, as those concerning patients afferent to different hospitals. Aim of this paper is to build a hierarchical regression model using data from the "Italian CABG outcome study" in order to evaluate the amount of differences in adjusted mortality rates attributable to differences between centres.</p> <p>Methods</p> <p>The study population consists of all adult patients undergoing an isolated CABG between 2002–2004 in the 64 participating cardiac surgery centres.</p> <p>A risk adjustment model was developed using a classical single-level regression. In the multilevel approach, the variable "clinical-centre" was employed as a group-level identifier. The intraclass correlation coefficient was used to estimate the proportion of variability in mortality between groups. Group-level residuals were adopted to evaluate the effect of clinical centre on mortality and to compare hospitals performance. Spearman correlation coefficient of ranks (<it>ρ</it>) was used to compare results from classical and hierarchical model.</p> <p>Results</p> <p>The study population was made of 34,310 subjects (mortality rate = 2.61%; range 0.33–7.63). The multilevel model estimated that 10.1% of total variability in mortality was explained by differences between centres. The analysis of group-level residuals highlighted 3 centres (VS 8 in the classical methodology) with estimated mortality rates lower than the mean and 11 centres (VS 7) with rates significantly higher. Results from the two methodologies were comparable (<it>ρ </it>= 0.99).</p> <p>Conclusion</p> <p>Despite known individual risk-factors were accounted for in the single-level model, the high variability explained by the variable "clinical-centre" states its importance in predicting 30-day mortality after CABG.</p

    Utilizing Risk Scores in Determining the Optimal Revascularization Strategy for Complex Coronary Artery Disease

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    Percutaneous coronary intervention (PCI) of multivessel and/or left main stem disease have been shown to be potentially legitimate revascularization alternatives in appropriately selected patients. Risk stratification is an important component in guiding patients to identify the most appropriate revascularization modality (PCI or coronary artery bypass grafting [CABG]) in conjunction with the Heart Team. The aim of this paper is to give the clinician a concise overview of the important established and evolving contemporary risk models in aiding this decision-making process. Risk models, based on clinical and anatomical variables alone, the novel concept of functional anatomical risk scores, and risk models combining aspects from both clinical and anatomical scores, are all discussed. The emerging concepts of the patient-empowered risk/benefit tradeoff between PCI and CABG to help personalize the choice of revascularization modality are also explored

    Progression and regression of incident cervical HPV 6, 11, 16 and 18 infections in young women

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    <p>Abstract</p> <p>Background</p> <p>We describe type-specific progression, regression and persistence of incident human papillomavirus (HPV)-6-11-16 and -18 infections, along with type distribution in cervical intra-epithelial neoplasia (CIN) lesions.</p> <p>Methods</p> <p>The study population consisted of 16–23 year-old women undergoing Pap testing and cervical swab polymerase chain reaction testing for HPV DNA at approximate 6 month intervals for up to 4 years in the placebo arm of a clinical trial of an HPV 16-vaccine. HPV types in incident infections were correlated with types in lesion biopsy specimens.</p> <p>Results</p> <p>56.7% of CIN-1 and nearly one-third of CIN-2/3 lesions following incident HPV-6-11-16 or -18 infections did not correlate with the incident infection HPV type. Cumulative 36-month progression rates to CIN-2/3 testing positive for the relevant HPV type were highest for HPV-16 infections (16.5%), followed by HPV-18 (8.2%). Overall, 26.0% of CIN-1, 50.0% of CIN-2 and 70.6% of CIN-3 biopsies tested positive for HPV-6-11-16-18 infections.</p> <p>Conclusion</p> <p>Women with a given HPV type may often be co-infected or subsequently infected with other types which may lead to subsequent cervical lesions. This issue has been addressed in this study reporting data for the natural history of HPV-6-11-16 and -18 infections and is a relevant consideration in designing future studies to evaluate the incidence/risk of CIN following other type-specific HPV infections.</p

    A Key Role for E-cadherin in Intestinal Homeostasis and Paneth Cell Maturation

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    E-cadherin is a major component of adherens junctions. Impaired expression of E-cadherin in the small intestine and colon has been linked to a disturbed intestinal homeostasis and barrier function. Down-regulation of E-cadherin is associated with the pathogenesis of infections with enteropathogenic bacteria and Crohn's disease. To genetically clarify the function of E-cadherin in intestinal homeostasis and maintenance of the epithelial defense line, the Cdh1 gene was conditionally inactivated in the mouse intestinal epithelium. Inactivation of the Cdh1 gene in the small intestine and colon resulted in bloody diarrhea associated with enhanced apoptosis and cell shedding, causing life-threatening disease within 6 days. Loss of E-cadherin led cells migrate faster along the crypt-villus axis and perturbed cellular differentiation. Maturation and positioning of goblet cells and Paneth cells, the main cell lineage of the intestinal innate immune system, was severely disturbed. The expression of anti-bacterial cryptidins was reduced and mice showed a deficiency in clearing enteropathogenic bacteria from the intestinal lumen. These results highlight the central function of E-cadherin in the maintenance of two components of the intestinal epithelial defense: E-cadherin is required for the proper function of the intestinal epithelial lining by providing mechanical integrity and is a prerequisite for the proper maturation of Paneth and goblet cells
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