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The authors discuss the development and use of a digital tool for journalism. They mention how the tool called INJECT assists in creative thinking by journalists, its ability to visualize data and run discovery services, and report on the test of INJECT by several newspapers which included looking at the novelty of news stories.

A recent study conducted at Children's Mercy Hospitals in Kansas City, Missouri, focused on the development and validation of a frailty score for pediatric patients with congenital and acquired heart disease. The study found that children and adolescents with heart disease performed worse in various frailty domains compared to their peers without heart disease. The researchers created a composite frailty score based on measures such as slowness, weakness, fatigue, body composition, and physical activity. The study also identified correlations between the frailty score and various outcomes, such as NYHA class, medication use, and exercise capacity. However, the study was limited by a small sample size for longitudinal analyses. [Extracted from the article]

Birnbaum, Daniel. Dr. B Harper: HarperCollins. May 2022.256p. tr. from Swedish by Deborah Bragan-Tumer. ISBN 9780062939814. $27.99. F Birnbaum, the former director of Stockholm's Museum of Modern Art, was inspired [...]

This article presents a position highlighting the importance of combining artificial intelligence approaches with human intelligence, in other words, the involvement of humans. To do so, we specifically focus on [...]

A mentor is a person who takes a special interest in the professional development of a junior colleague and provides guidance and support. Mentoring can be beneficial for students, residents, junior colleagues and researchers and can be very rewarding for the physician who provides this guidance. Although mentoring is a well-recognized topic in academic medicine, relatively little has been written about mentoring in emergency medicine (EM). Consequently, we conducted a literature review on mentoring in EM and present our findings in this paper. We discuss different models of mentoring, factors that foster the development of strong mentorship programs, the responsibilities of mentors and mentees, and issues specific to mentorship of female, minority and research physicians. We also present several case scenarios as a basis for recommendations for teachers and learners in EM. Keywords: mentors, emergency medicine, literature review, education, research, medical student, resident faculty, female, minority Un mentor est une personne qui prend un interet particulier dans le developpement d'un collegue moins experimente et lui fournit des conseils et du soutien. Le mentorat peut etre benefique pour les etudiants et les residents ainsi que des collegues et des chercheurs en debut de carriere. Il peut aussi s'averer tres gratifiant pour le medecin mentor qui fournit cette orientation. Bien que le mentorat soit un sujet bien connu dans le milieu de la medecine universitaire, il existe relativement peu d'articles sur le mentorat en medecine d'urgence. Par consequent, nous avons effectue une revue de la litterature sur ce sujet et presentons nos conclusions dans cet article. Nous discutons de divers modeles de mentorat, des facteurs qui favorisent le developpement de programmes de mentorat solides, des responsabilites du mentor et du mentore, et d'enjeux propres au mentorat de femmes, de minorites et de medecins chercheurs. Nous presentons aussi plusieurs mises en situation servant de base aux recommandations a l'intention des enseignants et des apprenants en medecine d'urgence., CASE SCENARIOS Case scenario 1--medical student: After working together for a few shifts, a medical student asks a staff physician to be her mentor, as she is interested in pursuing [...]

OBJECTIVE--Abnormal expression of the hepatic gluconeogenic genes (glucose-6-phosphatase [G6Pase] and PEPCK) contributes to hyperglycemia. These genes are repressed by insulin, but this process is defective in diabetic subjects. Protein kinase [...]

Insulin and contraction increase GLUT4 translocation in skeletal muscle via distinct signaling mechanisms. Akt substrate of 160 kDa (AS160) mediates insulin-stimulated GLUT4 translocation in L6 myotubes, presumably through activation of Akt. Using in vivo, in vitro, and in situ methods, insulin, contraction, and the AMP-activated protein kinase (AMPK) activator AICAR all increased AS160 phosphorylation in mouse skeletal muscle. Insulin-stimulated AS160 phosphorylation was fully blunted by wortmannin in vitro and in Akt2 knockout (KO) mice in vivo. In contrast, contraction-stimulated AS160 phosphorylation was only partially decreased by wortmannin and unaffected in Akt2 KO mice, suggesting additional regulatory mechanisms. To determine if AMPK mediates AS160 signaling, we used AMPK α2-inactive (α2i) transgenic mice. AICAR-stimulated AS160 phosphorylation was fully inhibited, whereas contraction-stimulated AS160 phosphorylation was partially reduced in the AMPK α2i transgenic mice. Combined AMPK α2 and Akt inhibition by wortmannin treatment of AMPK α2 transgenic mice did not fully ablate contraction-stimulated AS160 phosphorylation. Maximal insulin, together with either AICAR or contraction, increased AS160 phosphorylation in an additive manner. In conclusion, AS160 may be a point of convergence linking insulin, contraction, and AICAR signaling. While Akt and AMPK α2 activities are essential for AS160 phosphorylation by insulin and AICAR, respectively, neither kinase is indispensable for the entire effects of contraction on AS160 phosphorylation., Insulin and exercise share the capacity to increase glucose uptake into skeletal muscle and positively regulate glucose homeostasis in healthy individuals and people with type 2 diabetes. Each stimulus, alone [...]

Skeletal muscle contraction stimulates multiple signaling cascades that govern a variety of metabolic and transcriptional events. Akt/protein kinase B regulates metabolism and growth/muscle hypertrophy, but contraction effects on this target and its substrates are varied and may depend on the mode of the contractile stimulus. Accordingly, we determined the effects of endurance or resistance exercise on phosphorylation of Akt and downstream substrates in six trained cyclists who performed a single bout of endurance or resistance exercise separated by ~7 days. Muscle biopsies were taken from the vastus lateralis at rest and immediately after exercise. Akt [Ser.sup.473] phosphorylation was increased (1.8-fold; P = 0.011) after endurance but was unchanged after resistance exercise. Conversely, Akt [Thr.sup.308] phosphorylation was unaltered after either bout of exercise. Several exercise-responsive phosphoproteins were detected by immunoblot analysis with a phospho-Akt substrate antibody, pp160 and pp300 were identified as AS160 and filamin A, respectively, with increased phosphorylation (2.0- and 4.9-fold, respectively; P < 0.05) after endurance but not resistance exercise. In conclusion, AS160 and filamin A may provide an important link to mediate endurance exercise-induced bioeffects in skeletal muscle., Skeletal muscle contractile activity stimulates multiple signaling molecules known to regulate metabolic and transcriptional events (rev. in 1,2). Akt/protein kinase B regulates metabolism, growth/muscle hypertrophy, and cell survival (3-6) and [...]

Insulin resistance is predominantly characterized by decreased insulin-stimulated glucose uptake into skeletal muscle. In the current study, we have assessed various aspects of the phosphatidylinositol (PI) 3-kinase pathway in skeletal muscle biopsies obtained from normal, obese nondiabetic, and type 2 diabetic subjects, before and after a 5-h insulin infusion. We found a highly significant inverse correlation between in vivo insulin sensitivity (as measured by the glucose infusion rate) and increased protein expression of p85/55/50, protein kinase C (PKC)-θ activity, levels of p[Ser.sup.307] insulin receptor substrate (IRS)-1 and p-Jun N[H.sub.2]-terminal kinase (JNK)-1, and myosin heavy chain IIx fibers. Increased basal phosphorylation of [Ser.sup.307] IRS-1 in the obese and type 2 diabetic subjects corresponds with decrease in insulin-stimulated IRS-1 tyrosine phosphorylation, PI 3-kinase activity, and insulin-induced activation of Akt and, more prominently, PKC-θ/λ. In summary, increased expression of the PI 3-kinase adaptor subunits p85/55/50, as well as increased activity of the proinflammatory kinases JNK-1, PKC-θ, and, to a lesser extent, inhibitor of κB kinase-β, are associated with increased basal [Ser.sup.307] IRS-1 phosphorylation and decreased PI 3-kinase activity and may follow a common pathway to attenuate in vivo insulin sensitivity in insulin-resistant subjects. These findings demonstrate interacting mechanisms that can lead to impaired insulin-stimulated PI 3-kinase activity in skeletal muscle from obese and type 2 diabetic subjects. Diabetes 54:2351-2359, 2005, Insulin resistance is a characteristic feature of type 2 diabetes, obesity, syndrome X, and a number of other human disorders (1-3). Insulin resistance refers to a decreased ability of insulin [...]

Phosphatidylinositol (PI) 4,5-bisphosphate (PI[P.sub.2]) plays a pivotal role in insulin-stimulated glucose transport as an important precursor to PI 3,4,5-trisphosphate (PI[P.sub.3]) and a key regulator of actin polymerization. Since endothelin (ET)-1 impairs insulin sensitivity and PI[P.sub.2] is a target of ET-1-induced signaling, we tested whether a change in insulin-stimulated PIPS generation and signaling, PI[P.sub.2]-regulated actin polymerization, or a combination of both accounted for ET-1-induced insulin resistance. Concomitant with a time-dependent loss of insulin sensitivity, ET-1 caused a parallel reduction in plasma membrane PI[P.sub.2]. Despite decreased insulin-stimulated PI 3-kinase activity and PI[P.sub.3] generation, ET-1 did not diminish downstream signaling to Akt-2. Furthermore, addition of exogenous PI[P.sub.2], but not PI[P.sub.3], restored insulin-regulated GLUT4 translocation and glucose transport impaired by ET-1. Microscopic and biochemical analyses revealed a PI[P.sub.2]-dependent loss of cortical filamentous actin (F-actin) in ET-1-treated cells. Restoration of insulin sensitivity by PI[P.sub.2] add-back occurred concomitant with a reestablishment of cortical F-actin. The corrective effect of exogenous PI[P.sub.2] in ET-1-induced insulin-resistant cells was not present in cells where cortical F-actin remained experimentally depolymerized. These data suggest that ET-1-induced insulin resistance results from reversible changes in PI[P.sub.2]-regulated actin polymerization and not PI[P.sub.2]-dependent signaling., In muscle and adipose tissues, insulin stimulates glucose transport by increasing the level of the glucose transporter protein GLUT4 (1) at the plasma membrane (1,2). Extensive study demonstrates that insulin [...]

Brief calorie restriction (CR; 20 days of 60% of ad libitum [AL] intake) improves insulin-stimulated glucose transport, concomitant with enhanced phosphorylation of Akt2. The purpose of this study was to determine whether Akt2 is essential for the calorie restriction-induced enhancement in skeletal muscle insulin sensitivity. We measured insulin-stimulated 2-deoxyglucose (2DG) uptake in isolated extensor digitorum longus (EDL) and soleus muscles from male and female wild-type (WT) and Akt2-null (knockout [KO]) mice after ad libitum or calorie-restricted (20 days at 60% of AL) feeding. In WT mice, calorie restriction significantly enhanced insulin-stimulated 2DG uptake in both muscles regardless of sex. However, in KO mice, calorie restriction did not enhance insulin-stimulated 2DG in male or female EDL or in female soleus. Only in male KO soleus did calorie restriction significantly increase insulin-stimulated 2DG through an Akt2-independent mechanism, although 2DG uptake of the KO-CR group was reduced compared with the WT-CR soleus group. Akt2 serine phosphorylation was enhanced approximately two- to threefold in insulin-stimulated WT-CR versus WT-AL muscles. Calorie restriction induced an ~1.5- to 2-fold elevation in Akt1 phosphorylation of insulin-treated muscles, regardless of genotype, but this increase was insufficient to replace Akt2 for insulin-stimulated 2DG in Akt2-deficient muscles. These results indicate that Akt2 is essential for the full effect of brief calorie restriction on insulin-stimulated glucose uptake in skeletal muscle with physiologic insulin., Moderate calorie restriction (25-40% reduction below ad libitum intake) is an effective treatment for improving insulin sensitivity in many species (1-4). Improved insulin sensitivity occurs rapidly (manifested within 20 days [...]

Thiazolidinediones (TZDs), agonists of peroxisome proliferator-activated receptor-γ (PPARγ), improve insulin sensitivity in vivo, and the mechanism remains largely unknown. In this study, we showed that, in Zucker obese (fa/fa) rats, acute (1-day) treatment with both rosiglitazone (a TZD) and a non-TZD PPARγ agonist (nTZD) reduced plasma free fatty acid and insulin levels and, concomitantly, potentiated insulin-stimulated Akt phosphorylation at threonine 308 (Akt-pT308) in adipose and muscle tissues. A similar effect on Akt was observed in liver after a 7-day treatment. The increase in Akt-pT308 was correlated with an increase in Akt phosphorylation at serine 473 (Akt-pS473), tyrosine phosphorylation of insulin receptor β subunit and insulin receptor substrate-1, and serine phosphorylation of glycogen synthase kinase-3α/β. The agonists appeared to potentiate Akt1 phosphorylation in muscle and liver and both Akt1 and Akt2 in adipose. Finally, potentiation of insulin signaling was also observed in isolated adipose tissue ex vivo and differentiated 3T3 L1 adipocytes in vitro, but not in rat primary hepatocytes in vitro. These results suggest that 1) PPARγ agonists acutely potentiate insulin signaling in adipose and muscle tissues and such regulation may be physiologically relevant to insulin sensitization in vivo; 2) the agonists directly target adipose tissues; and 3) the metabolic and signaling effects of the agonists are mediated by structurally distinct PPARγ agonists., Thiazolidinediones (TZDs) (e.g., troglitazone, pioglitazone, and rosiglitazone) are a class of antidiabetic, drugs that act as insulin sensitizers by decreasing insulin resistance in human and animal models (1,2). TZDs decrease [...]

This review focuses on genes other than the high penetrance genes BRCA 1 and BRCA2 that are involved in breast cancer susceptibility. The goal of this review is the discovery [...]

A AAAA Benefits Inc. 8305 University Executive Park, Suite 320, Charlotte, N.C. 28262-3354; 704-594-6270; fax: 704-594-6290 Staff Total 15 Involved in 401(k) plan services 13 Clients Total 150 Average participants/plan [...]