The Effect of Casein Protein Prior to Sleep on Fat Metabolism in Obese Men

We have previously shown that ingesting protein at night before sleep is either beneficial or non-detrimental to metabolism, health, and body composition in obese women. However, the overnight protein-induced lipolytic actions and mechanism for improved metabolism and body composition have not been fully established. Therefore, in a crossover design, twelve obese men (age, 27.0 ˘ 2.2 years) were randomly assigned to ingest (within 30 min of sleep) casein protein (CAS, 120 kcal) or a non-nutritive placebo (PLA) before going to sleep. Markers of fat metabolism (lipolysis, substrate utilization, growth hormone), insulin, glucose, resting energy expenditure (REE), and appetite (questionnaire and ghrelin) were measured. During sleep and the next morning, interstitial glycerol from the subcutaneous abdominal adipose tissue (SCAAT) was measured using microdialysis. There were no differences in SCAAT glycerol (overnight: CAS, 177.4 ˘ 26.7; PLA, 183.8 ˘ 20.2 µmol/L; morning: CAS, 171.6 ˘ 19.1; PLA, 161.5 ˘ 18.6 µmol/L), substrate utilization, REE, or any blood markers between CAS and PLA. Desire to eat was greater for CAS compared to baseline (p = 0.03), but not different from PLA (baseline: 39 ˘ 6, CAS: 62 ˘ 8, PLA: 55 ˘ 5 mm). CAS consumption before sleep did not affect fat or glucose metabolism, REE, or suppress appetite in hyperinsulemic obese men. CAS may be consumed before sleep without impeding overnight or morning fat metabolism in young, obese men

Gentamicin Rapidly Inhibits Mitochondrial Metabolism in High-Frequency Cochlear Outer Hair Cells

Aminoglycosides (AG), including gentamicin (GM), are the most frequently used antibiotics in the world and are proposed to cause irreversible cochlear damage and hearing loss (HL) in 1/4 of the patients receiving these life-saving drugs. Akin to the results of AG ototoxicity studies, high-frequency, basal turn outer hair cells (OHCs) preferentially succumb to multiple HL pathologies while inner hair cells (IHCs) are much more resilient. To determine if endogenous differences in IHC and OHC mitochondrial metabolism dictate differential sensitivities to AG-induced HL, IHC- and OHC-specific changes in mitochondrial reduced nicotinamide adenine dinucleotide (NADH) fluorescence during acute (1 h) GM treatment were compared. GM-mediated decreases in NADH fluorescence and succinate dehydrogenase activity were observed shortly after GM application. High-frequency basal turn OHCs were found to be metabolically biased to rapidly respond to alterations in their microenvironment including GM and elevated glucose exposures. These metabolic biases may predispose high-frequency OHCs to preferentially produce cell-damaging reactive oxygen species during traumatic challenge. Noise-induced and age-related HL pathologies share key characteristics with AG ototoxicity, including preferential OHC loss and reactive oxygen species production. Data from this report highlight the need to address the role of mitochondrial metabolism in regulating AG ototoxicity and the need to illuminate how fundamental differences in IHC and OHC metabolism may dictate differences in HC fate during multiple HL pathologies

MILLER'S ANESTHESIA

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Family medicine and psychosocial knowledge: How many hats can the family doctor wear?

The paper examines the impact of teaching family physicians psychosocial skills and knowledge during their residency training in family medicine. The idea put forth by the family practice profession that family physicians are trained to treat their patients' biological, as well as psychosocial problems, is important to the social work profession since social workers have had primary responsibility in treating patients' psychosocial problems in the health care arena in the United States from 1904 until now. In order to learn about the effect of adding psychosocial knowledge to the family practitioner's training curricula, the author conducted an exploratory and comparative study to see if family practitioners had any more psychosocial knowledge than other primary care physicians. No significant differences were found. Implications of the study for family medicine and social work, primary health care, and social/health policy are discussed.family practice education psychosocial knowledge social work primary care

An analysis of near misses identified by anesthesia providers in the intensive care unit

© 2015 Lipshutz et al. Background: Learning from adverse events and near misses may reduce the incidence of preventable errors. Current literature on adverse events and near misses in the ICU focuses on errors reported by nurses and intensivists. ICU nea

Predicting mortality in acute respiratory distress syndrome: circulatory system knows best.

peer reviewe

Transfusion-related acute lung injury: a review. Chest

Transfusion-related acute lung injury (TRALI) is an underreported complication of transfusion therapy, and it is the third most common cause of transfusion-associated death. TRALI is defined as noncardiogenic pulmonary edema temporally related to transfusion therapy. The diagnosis of TRALI relies on excluding other diagnoses such as sepsis, volume overload, and cardiogenic pulmonary edema. Supportive diagnostic evidence includes identifying neutrophil or human leukocyte antigen (HLA) antibodies in the donor or recipient plasma. All plasma-containing blood products have been implicated in TRALI, with the majority of cases linked to whole blood, packed RBCs, platelets, and fresh-frozen plasma. The pathogenesis of TRALI may be explained by a "two-hit" hypothesis, with the first "hit" being a predisposing inflammatory condition commonly present in the operating room or ICU. The second hit may involve the passive transfer of neutrophil or HLA antibodies from the donor or the transfusion of biologically active lipids from older, cellular blood products. Treatment is supportive, with a prognosis substantially better than most causes of clinical acute lung injury. ( CHEST 2004; 126:249 -258) Key words: ARDS; lung injury; pulmonary edema; transfusion; transfusion-related acute lung injury Abbreviations: ALI ϭ acute lung injury; FDA ϭ Food and Drug Administration; Fio 2 ϭ fraction of inspired oxygen; HLA ϭ human leukocyte antigen; PRBC ϭ packed RBC; TRALI ϭ transfusion-related acute lung injury T ransfusion-related acute lung injury (TRALI) was first coined by Popovsky et al 1 in 1983 to refer to noncardiogenic pulmonary edema complicating transfusion therapy. The syndrome had previously been referred to as pulmonary hypersensitivity reaction, 2,3 allergic pulmonary edema, 4 noncardiogenic pulmonary edema, 5-7 and pulmonary leukoagglutinin reaction. 8 Barnard 9 in 1951 described the first case of fatal pulmonary edema accompanying transfusion therapy. Brittingham 10 in 1957 was the first to initially shed light on the pathogenesis of TRALI. He transfused a strong leukoagglutinin to a volunteer who developed bilateral pulmonary infiltrates. This review will summarize the clinical features of TRALI and highlight potential mechanisms that may precipitate acute lung injury (ALI) and the ARDS. Definition and Clinical Presentation TRALI is defined as noncardiogenic pulmonary edema temporally related to the transfusion of blood products. The development of TRALI has been associated with all plasma-containing blood products, but most commonly involves whole blood, packed RBCs (PRBCs), fresh-frozen plasma, and platelets. TRALI has also occurred after the transfusion of cryoprecipitate and IV Ig. 11