Incidència de la crisi econòmica sobre l'estructura de despesa dels pressupostos del Servei Catalá de la Salut (CatSalut)

Treballs Finals de Grau de Gestió i Administració Pública, Facultat de Dret, Universitat de Barcelona, Curs: 2014-2015, Tutora: Marina Solé i CatalaL'objectiu principal d'aquest treball serà analitzar i avaluar l'efecte de la crisi econòmica en l'atenció sanitària de cobertura pública i, amb aquesta finalitat, s'observarà la incidència d'aquesta crisi en el pressupost de despeses del Servei Català de la Salut (CatSalut) durant el període comprés des del 2008 al 2015. Aquesta anàlisi es realitzarà mitjançant una recerca descriptiva i analítica dels pressupostos de l'entitat en l'esmentat període, comparant les variacions que s'han pogut produir tant pel que fa als ingressos com a les despeses, per tal de conèixer i poder valorar de quina forma ha pogut incidir la crisi econòmica en les seves dotacions pressupostàries i en la seva estructura econòmica i funcional. El treball s'ha estructurat en quatre parts; en primer lloc es descriu el funcionament de l'entitat i quins són els seus objectius, en segon lloc es mostra el seu pressupost d'ingressos i l'evolució en la seva estructura, el tercer apartat exposa alguns indicadors sobre la situació de la despesa en sanitat a Catalunya, i en el quart i darrer punt es mostra i s'analitza com ha evolucionat el seu estat de despeses segons les classificacions econòmica i per programes

Força lumbar en jugadors d'hoquei sobre herba

Introducció: El dolor lumbar té una alta prevalença entre els esportistes, s’ha relacionat amb dèficits en la força extensora lumbar, i el fet de patir-ne representa un obstacle important per a la pràctica d’esports d’alta intensitat. Mètode: S'ha mesurat la força lumbar en dos grups de practicants d'hoquei sobre herba mitjançant màquina MedX® i un test de resistència isomètric lumbar. Resultats: Entre ambdós grups els resultats han estat molt homogenis. Els dos tests no presenten relació entre si, ni amb les característiques biomèdiques dels jugadors (edat, índex de massa corporal o VO2màx). Els nivells de força màxima i resistència isomètrica obtinguts han estat superiors als de referència entre sedentaris. D’una manera característica, entre els jugadors d'hoquei la relació entre la força extensora del tronc en flexió (M) respecte la força extensora del tronc en extensió (m) és més gran que en altres esportistes (ràtio M/m > 1,6, mentre que en la població normal és 1,4) a causa probablement de la posició en semiflexió pròpia de l'hoquei. Conclusió: Els resultats dels test de força extensora lumbar tenen unes característiques pròpies entre els jugadors d’hoquei

Fuerza lumbar en jugadores de hockey hierba

Introducción: El dolor lumbar tiene una alta prevalencia entre los deportistas, se ha relacionado con déficits en la fuerza extensora lumbar, y el hecho de padecerlo representa un obstáculo importante para la práctica de deportes de alta intensidad. Método: Se ha medido la fuerza lumbar en 2 grupos de practicantes de hockey hierba mediante máquina MedX® y un test de resistencia isométrico lumbar. Resultados: Entre ambos grupos los resultados han sido muy homogéneos. Los 2 tests no presentan relación entre sí ni con las características biomédicas de los jugadores (edad, índice de masa corporal o VO2máx). Los niveles de fuerza máxima y resistencia isométrica obtenidos han sido superiores a los de referencia entre sedentarios. Característicamente, entre los jugadores de hockey hierba la relación entre la fuerza extensora del tronco en flexión (M) respecto a la fuerza extensora del tronco en extensión (m) es mayor que en otros deportistas (ratio M/m > 1,6, mientras que en la población normal es 1,4) debido probablemente a la postura en semiflexión propia del hockey. Conclusión: Los resultados de los test de fuerza extensora lumbar tienen unas características propias entre los jugadores de hockey hierba

Indoor falls and number of previous falls are independent risk factors for long-term mortality after a hip fracture

Hip fractures are almost always the result of a fall. Causes and circumstances of falls may differ between frail and vigorous patients. To describe the circumstances of falls causing hip fractures, number of falls during the previous year, and their association with long-term mortality. The study is a retrospective review conducted in a tertiary university hospital serving a population of 425,000 inhabitants in Barcelona. All patients admitted with hip fractures with medical records describing the circumstances and number of previous falls were included. The number of falls in the previous 12 months was recorded, including the one causing the fracture. The circumstances of the index fall were dichotomized according to whether it was from the patient's own height or above; day or night; indoors or outdoors, due to intrinsic or extrinsic causes. Cumulative mortality was recorded for almost 5 years after hip fracture. Indoor falls were strongly associated with shorter survival. Falling more than once in the previous year was also a risk factor for long-term mortality (hazard ratio 1.461, p < 0.001 and hazard ratio 1.035, p = 0.008 respectively). Indoor falls and falling more than once in the previous year are long-term risk factors for mortality after hip fractures. It is always essential to take a careful patient history on admission to determine the number of falls and their circumstances, and special care should be taken to reduce mortality in patients at high risk

Phosphorylation at Ser-181 of oncogenic KRAS is required for tumor growth

KRAS phosphorylation has been reported recently to modulate the activity of mutant KRAS protein in vitro. In this study, we defined S181 as a specific phosphorylation site required to license the oncogenic function of mutant KRAS in vivo. The phosphomutant S181A failed to induce tumors in mice, whereas the phosphomimetic mutant S181D exhibited an enhanced tumor formation capacity, compared with the wild-type KRAS protein. Reduced growth of tumors composed of cells expressing the nonphosphorylatable KRAS S181A mutant was correlated with increased apoptosis. Conversely, increased growth of tumors composed of cells expressing the phosphomimetic KRAS S181D mutant was correlated with increased activation of AKT and ERK, two major downstream effectors of KRAS. Pharmacologic treatment with PKC inhibitors impaired tumor growth associated with reduced levels of phosphorylated KRAS and reduced effector activation. In a panel of human tumor cell lines expressing various KRAS isoforms, we showed that KRAS phosphorylation was essential for survival and tumorigenic activity. Furthermore, we identified phosphorylated KRAS in a panel of primary human pancreatic tumors. Taken together, our findings establish that KRAS requires S181 phosphorylation to manifest its oncogenic properties, implying that its inhibition represents a relevant target to attack KRAS-driven tumors

Oncogenic K-Ras segregates at spatially distinct plasma membrane signaling platforms according to its phosphorylation status

Activating mutations in the K-Ras small GTPase are extensively found in human tumors. Although these mutations induce the generation of a constitutively GTP-loaded, active form of K-Ras, phosphorylation at Ser181 within the C-terminal hypervariable region can modulate oncogenic K-Ras function without affecting the in vitro affinity for its effector Raf-1. In striking contrast, K-Ras phosphorylated at Ser181 shows increased interaction in cells with the active form of Raf-1 and with p110α, the catalytic subunit of PI 3-kinase. Because the majority of phosphorylated K-Ras is located at the plasma membrane, different localization within this membrane according to the phosphorylation status was explored. Density-gradient fractionation of the plasma membrane in the absence of detergents showed segregation of K-Ras mutants that carry a phosphomimetic or unphosphorylatable serine residue (S181D or S181A, respectively). Moreover, statistical analysis of immunoelectron microscopy showed that both phosphorylation mutants form distinct nanoclusters that do not overlap. Finally, induction of oncogenic K-Ras phosphorylation - by activation of protein kinase C (PKC) - increased its co-clustering with the phosphomimetic K-Ras mutant, whereas (when PKC is inhibited) non-phosphorylated oncogenic K-Ras clusters with the non-phosphorylatable K-Ras mutant. Most interestingly, PI 3-kinase (p110α) was found in phosphorylated K-Ras nanoclusters but not in non-phosphorylated K-Ras nanoclusters. In conclusion, our data provide - for the first time - evidence that PKC-dependent phosphorylation of oncogenic K-Ras induced its segregation in spatially distinct nanoclusters at the plasma membrane that, in turn, favor activation of Raf-1 and PI 3-kinase

Effects of mindfulness-based interventions on biomarkers and low-grade inflammation in patients with psychiatric disorders: A meta-analytic review

Mindfulness-Based Interventions (MBIs) present positive effects on mental health in diverse populations. However, the detailed associations between MBIs and biomarkers in patients with psychiatric disorders remain poorly understood. The aim of this study was to examine the effects of MBIs on biomarkers in psychiatric illness used to summarise the effects of low-grade inflammation. A systematic review of PubMed, EMBASE, PsycINFO, and the Cochrane Library was conducted. Effect sizes (ESs) were determined by Hedges’ g and the number needed to treat (NNT). Heterogeneity was evaluated. A total of 10 trials with 998 participants were included. MBIs showed significant improvements in the event-related potential amplitudes in attention-deficit hyperactivity disorder, the methylation of serotonin transporter genes in post-traumatic stress disorder, the salivary levels of interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-a) in depression, and the blood levels of adrenocorticotropic hormone (ACTH), IL-6, and TNF-a in generalised anxiety disorder. MBIs showed low but significant effects on health status related to biomarkers of low-grade inflammation (g = -0.21; 95% confidence interval (CI) –0.41 to -0.01; NNT = 8.47), with no heterogeneity (I2 = 0; 95% CI 0 to 79). More trials are needed to establish the impact of MBIs on biomarkers in psychiatric illness

A randomized controlled trial: branched‐chain amino acid levels and glucose metabolism in patients with obesity and sleep apnea

There is evidence that changes in branched‐chain amino acid (BCAA) levels may correlate with the efficacy of therapeutic interventions for affecting improvement in metabolic control. The objective of this study was to evaluate whether serum concentrations of BCAAs (leucine, isoleucine, valine) could mediate in insulin sensitivity and glucose tolerance after continuous positive airway pressure (CPAP) treatment in patients with obstructive sleep apnea (OSA). A prospective randomized controlled trial of OSA patients with morbid obesity was conducted. Eighty patients were randomized into two groups: 38 received conservative treatment and 42 received CPAP treatment for 12 weeks. Plasma levels of BCAA, glucose tolerance and insulin resistance were evaluated at baseline and after treatment. After treatment, significant decreases of leucine levels were observed in both groups when compared with baseline levels (P < 0.005). With respect to patients with normal glucose tolerance (NGT), patients with impaired glucose tolerance (IGT) had higher baseline levels of isoleucine (78 ± 16 versus 70 ± 13 μmol L−1, P = 0.014) and valine (286 ± 36 versus 268 ± 41 μmol L−1, P = 0.049), respectively. Changes in levels of leucine and isoleucine after treatment were related negatively to changes in fasting plasma glucose and glycosylated haemoglobin values only in the conservative group (P < 0.05). In summary, we found that the treatment with CPAP for 12 weeks caused similar changes in circulating BCAAs concentrations to conservative treatment and a differential metabolic response of CPAP and conservative treatment was observed between the relationship of BCAAs and glucose homeostasis. Additional studies are needed to determine the interplay between branched‐chain amino acids and glucose metabolism in patients with sleep apnea

Tumor necrosis factor system activity is associated with insulin resistance and dyslipidemia in myotonic dystrophy

Myotonic dystrophy (MyD) is a multisystem autosomal dominant disorder associated with progressive muscle wasting and weakness. The striking metabolic abnormality in MyD is insulin resistance. The mechanism by which target tissues are insensitive to insulin action remains uncertain. In a recent study, plasma soluble tumor necrosis factor receptor (sTNFR)2 levels were found to be associated with muscle tissue mass and insulin resistance. Given these associations, we speculated that disorders of the muscle cell membrane could lead simultaneously to insulin insensitivity and sTNFR2 leakage in MyD. To test this hypothesis, we measured the levels of circulating sTNFR1 and sTNFR2 and insulin resistance in MyD patients. We studied 22 MyD patients and 24 age-, BMI-, and fat mass-matched control subjects. Both MyD men and women showed higher plasma insulin levels in the presence of comparable glucose concentrations than did control subjects. sTNFR2, but not sTNFR1, levels were approximately 1.5-fold higher in MyD patients. In parallel with these findings, the fasting insulin resistance index (FIRI) was also higher in MyD patients. In fact, in the whole population, fasting insulin and FIRI strongly correlated with sTNFR2 in both men (r = 0.77 and r = 0.81, P<0.0001, respectively) and women (r = 0.67 and r = 0.64, P = 0.001, respectively). sTNFR2 levels were also associated with the insulin sensitivity index (S(I)), calculated from an oral glucose tolerance test (OGTT) according to the method by Cederholm and Wibell (r = -0.43, P = 0.006). We constructed a multiple linear regression to predict FIRI, with BMI, waist-to-hip ratio, and sTNFR2 as independent variables. In this model, both BMI (P = 0.0014) and sTNFR2 (P = 0.0048) levels contributed independently to 46% of the variance of FIRI. In another model, in which FIRI was substituted for S(I) from the OGTT, both BMI (P = 0.0001) and sTNFR2 (P = 0.04) levels contributed independently to 48% of the variance of S(I) from the OGTT. Plasma cholesterol and triglyceride concentrations were significantly increased in MyD patients. sTNFR1 and sTNFR2 levels were found to be strongly associated with plasma cholesterol, LDL cholesterol, and triglycerides. sTNFR1 and sTNFR2 also correlated with serum creatine kinase activity in MyD patients (r = 0.57, P = 0.006; r = 0.75, P<0.0001, respectively). In conclusion, here we describe, for the first time to our knowledge, a relationship between insulin action and plasma sTNFR2 concentration in MyD patients. We have also found increased concentrations of plasma triglycerides and cholesterol levels in parallel with sTNFR1 and sTNFR2 concentrations in MyD patients. We speculate that the latter associations are dependent on, and secondary to, increased tumor necrosis factor (TNF)-alpha action. Whether TNF action is implicated in the pathogenesis of MyD or is a simple marker of disease activity awaits further studies

IAA : Información y actualidad astronómica (20)

Sumario : ¿Cómo se forma un Sol?.-- El observatorio virtual.-DECONSTRUCCIÓN Y otros ENSAYOS Estrellas peculiares.-- ACTUALIDAD.-- ENTRE BASTIDORES.-- CIENCIA: PILARES E INCERTIDUMBRES.-- HISTORIAS DE ASTRONOMÍA. Pero, ¿quién inventó el telescopio?.-- ACTIVIDADES IAA.Esta revista se publica con la ayuda de la Accion Complementaria CCT003-05-00325 del Programa Nacional de Fomento de la Cultura Cientifica y Tecnologica.N