Critical Role of Nutrition in Improving Quality of Care

The current era of healthcare delivery, with its focus on providing high‐quality, affordable care, presents many challenges to hospital‐based health professionals. The prevention and treatment of hospital malnutrition offer a tremendous opportunity to optimize the overall quality of patient care, improve clinical outcomes, and reduce costs. Unfortunately, malnutrition continues to go unrecognized and untreated in many hospitalized patients. This article represents a call to action from the interdisciplinary Alliance to Advance Patient Nutrition to highlight the critical role of nutrition intervention in clinical care and to suggest practical ways to promptly diagnose and treat malnourished patients and those at risk for malnutrition. We underscore the importance of an interdisciplinary approach to addressing malnutrition both in the hospital and in the acute posthospital phase. It is well recognized that malnutrition is associated with adverse clinical outcomes. Although data vary across studies, available evidence shows that early nutrition intervention can reduce complication rates, length of hospital stay, readmission rates, mortality, and cost of care. The key is to systematically identify patients who are malnourished or at risk and to promptly intervene. We present a novel care model to drive improvement, emphasizing the following 6 principles: (1) create an institutional culture where all stakeholders value nutrition, (2) redefine clinicians’ roles to include nutrition care, (3) recognize and diagnose all malnourished patients and those at risk, (4) rapidly implement comprehensive nutrition interventions and continued monitoring, (5) communicate nutrition care plans, and (6) develop a comprehensive discharge nutrition care and education plan.     

左肺移植的实验研究

目的为临床肺移植积累经验。方法分析总结29例犬左肺移植的资料。其中15例的供体肺用Euro-Collings液在4℃下保存6h,14例用UW液保存22～25h,作同种异体移植,并阻断受体的右肺动脉,以测定移植左肺的功能。结果所有的移植左肺均能胜任气体交换,循环稳定。结击本左肺移植方法可靠,可供临床应用时参考。     

Human mesenchymal stem cells improve myocardial performance in a splenectomized rat model of chronic myocardial infarction.

BACKGROUND/PURPOSE: Cellular therapy has been applied to animal studies and clinical trials for acute or subacute myocardial infarction. Little is known about the effect of cell therapy on chronic myocardial infarction. The goal of this study was to investigate myocardial performance after human bone marrow-derived mesenchymal stem cell (hMSCs) transplantation in rats with chronic myocardial infarction. METHODS: The hMSCs were obtained from adult human bone marrow and expanded in vitro. The purity and characteristics of hMSCs were identified by flow cytometry and immunophenotyping. Splenectomy in male rats was performed to prevent immune reaction. One week after splenectomy, ligation of the left anterior descending coronary artery was performed to induce myocardial infarction. Four weeks after ligation of the coronary artery, culture-expanded hMSCs were injected intramyocardially at the left anterior free wall. Left ventricular function measured by echocardiography, infarct size and immunohistochemical stain were performed to evaluate the effect of the therapy. RESULTS: The engrafted hMSCs were positive for the cardiac marker troponin T. Infarct size (35.4 +/- 3.4% vs. 53.3 +/- 3.0%, p < 0.001) and fibrotic area (2.6 +/- 0.1% vs. 5.9 +/- 0.2%, p < 0.001) were significantly smaller in the hMSC-treated group than in the control group at 28 days after therapy. hMSC transplantation resulted in smaller left ventricular end-diastolic dimension (6.5 +/- 0.1 mm vs. 7.9 +/- 0.7 mm, p < 0.001) and better left ventricular ejection fraction (88.7 +/- 1.2% vs. 65.8 +/- 2.5%, p < 0.001) than in the control group. Capillary density was markedly increased after hMSC transplantation compared with the control group. CONCLUSION: This study demonstrates that intramyocardial transplantation of hMSCs improves cardiac function after chronic myocardial infarction through enhancement of angiogenesis and myogenesis in the ischemic myocardium. Transplantation of hMSCs for myocardial regeneration may become the future therapy for chronic myocardial infarction.     

Sympathetic and noradrenaline effects on C-fibre transmission: single-unit analysis

Single afferent unmyelinated fibres were dissected from the otherwise intact sural nerve in anesthetized rabbits. The sympathetic trunk could be stimulated via electrodes implanted through the abdomen. The response in single C fibres was elicited by electrical stimulation in the cutaneous innervation area of the fibre. Sympathetic stimulation (8 Hz, 1 ms pulses, 5 mA for 60 s) increased the latency in all tested C fibres (2.0% +/- 0.8%, mean +/- SD, n = 17). In 48% of the units the amplitude of the action potential decreased (26.4% +/- 12.3%) during sympathetic stimulation. Infusion of noradrenaline (5 micrograms min-1) increased (7.7% +/- 4.1%) the latency in all units and increased (36.9% +/- 29.8%) the amplitude of 25% of the units. The effects of sympathetic stimulation and noradrenaline infusion were blocked by pre-treatment with phentolamine (3 mg kg-1 i.v.). The results suggest that catecholamines change the membrane properties of unmyelinated fibres.     

Assessment of FMR1 Gene Mutation at-Risk Status in Young Children

Fragile X syndrome (FXS), caused by a mutation of the FMR1 gene, is the most commonly inherited cause of developmental disability. Fragile X syndrome occurs relatively equally in all racial and ethnic groups and is one of the few disorders affecting child behavior for which the exact gene is identified. Furthermore, from infancy, both males and females with this syndrome are predisposed for manifesting characteristic cognitive, emotional, and behavioral challenges. The purpose of this article is to illuminate the multisystemic and multifaceted phenotype of the FMR1 gene mutation by means of the parent response Biopsychosocial Screening Inventory for Fragile X, for which preliminary studies show promise.     

Pharmacokinetics of didanosine in patients with acquired immunodeficiency syndrome or acquired immunodeficiency syndrome-related complex

The pharmacokinetics of didanosine (2',3'-dideoxyinosine) after intravenous and oral administration were evaluated in an open, escalating-dose phase I study in patients with acquired immunodeficiency syndrome (AIDS) or severe AIDS-related complex. Didanosine was administered twice a day for 2 weeks as an intravenous infusion of 60 minutes duration at doses ranging from 0.4 to 16.5 mg/kg, followed by 4 weeks of oral treatment at twice the intravenous dose. Serial blood and urine samples were obtained on the first and final day of intravenous administration and after the first oral dose, as well as at steady state. Didanosine demonstrated linear pharmacokinetic behavior over the dose ranges of 0.4 to 16.5 mg/kg intravenously and 0.8 to 10.2 mg/kg orally. There was no indication of significant changes in pharmacokinetic parameters with repeated administration. The apparent elimination half-life after oral administration was approximately 1.4 hour. Renal clearance values exceeded the glomerular filtration rate, indicating that active tubular secretion of didanosine occurs. Bioavailability of didanosine when administered as a solution with an antacid was approximately 43% for doses from 0.8 to 10.2 mg/kg in patients with AIDS and advanced AIDS-related complex. Bioavailability of didanosine from the citrate-phosphate-buffered solution, the formulation currently used in phase II and expanded access studies, was comparable to the formulation used in the phase I trials.