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Actualmente puede observarse altos niveles de desgaste profesional asociado a niveles bajos de desempeño y, por tanto, de productividad en diversos sectores empresariales. El objetivo formulado fue medir la relación existente entre desgaste profesional y job performance en entidades microfinancieras de la región Junín. La investigación estuvo enmarcada en los lineamientos del paradigma cuantitativo y en los criterios de un diseño no experimental-transversal, de tipo básico observacional y nivel relacional. La muestra lo conformaron 190 colaboradores de entidades microfinancieras de la región Junín. La técnica empleada fue la encuesta, se midió el desgaste profesional utilizando el inventario de agotamiento de Maslach y para medir job performance se utilizó la escala de desempeño laboral, los datos fueron analizados con el soporte del SPSS 25 para Windows. Los resultados muestran correlación negativa de -0,224 entre desgaste profesional y job performance con un p-valor de 0,027. Por tanto, se concluyó que existe correlación negativa significativa entre desgaste profesional y job performance en colaboradores de entidades microfinancieras de la región Junín.

Aging and the age-associated decline of the proteome is determined in part through neuronal control of evolutionarily conserved transcriptional effectors, which safeguard homeostasis under fluctuating metabolic and stress conditions by regulating an expansive proteostatic network. We have discovered theCaenorhabditis eleganshomeodomain-interactingproteinkinase (HPK-1) acts as a key transcriptional effector to preserve neuronal integrity, function, and proteostasis during aging. Loss ofhpk-1results in drastic dysregulation in expression of neuronal genes, including genes associated with neuronal aging. During normal aginghpk-1expression increases throughout the nervous system more broadly than any other kinase. Within the aging nervous system,hpk-1is co-expressed with key longevity transcription factors, includingdaf-16(FOXO),hlh-30(TFEB),skn-1(Nrf2), andhif-1, which suggestshpk-1expression mitigates natural age-associated physiological decline. Consistently, pan-neuronal overexpression ofhpk-1extends longevity, preserves proteostasis both within and outside of the nervous system, and improves stress resistance. Neuronal HPK-1 improves proteostasis through kinase activity. HPK-1 functions cell non-autonomously within serotonergic and GABAergic neurons to improve proteostasis in distal tissues by specifically regulating distinct components of the proteostatic network. Increased serotonergic HPK-1 enhances the heat shock response and survival to acute stress. In contrast, GABAergic HPK-1 induces basal autophagy and extends longevity. Our work establisheshpk-1as a key neuronal transcriptional regulator critical for preservation of neuronal function during aging. Further, these data provide novel insight as to how the nervous system partitions acute and chronic adaptive response pathways to delay aging by maintaining organismal homeostasis.

The nervous system systemically coordinates proteostasis to delay organismal aging. However, the neuronal regulatory mechanisms that coordinate cellular anti-aging programs across tissue and cell-types are relatively unknown. In this work, we identify the homeodomain-interacting protein kinase (HPK-1), a transcriptional cofactor, as a novel neuronal component of the proteostatic network: its overexpression produces a paracrine signal to hyper-induce molecular chaperones and a neuroendocrine signal to induce autophagy in peripheral tissues. Neuronal HPK-1 signaling improves proteostasis in distal tissues through neurotransmitters. These pro-longevity modalities are independently regulated within serotonergic and GABAergic neurons, respectively, through distinct adaptive responses, either of which improve proteostasis in a cell non-autonomous manner. Serotonergic HPK-1 activity amplifies the heat shock response and protects the proteome from acute stress, without altering longevity. Conversely, increased GABAergic HPK-1 activity is sufficient to induce autophagy and extend longevity, without altering acute stress survival. Consistently, GABAergic neurons, but not serotonin, is essential for the cell non-autonomous induction of autophagy by neuronal HPK-1. These findings provide novel insight into how the nervous system partitions and coordinates unique adaptive response pathways to delay organismal aging, and reveals a key role for neuronal HPK-1 in regulating the proteostatic network throughout an intact metazoan animal.Significance StatementAging and the age-associated decline of the proteome is determined in part through neuronal control of evolutionarily conserved transcriptional effectors, which safeguard homeostasis under fluctuating metabolic and stress conditions by regulating an expansive proteostatic network in peripheral tissues. How neuronal signaling mechanisms are primed, relayed through an organism, and specific responses are initiated in receiving cell types remain poorly understood. We have discovered that the Caenorhabditis elegans homeodomain-interacting protein kinase (HPK-1) is a novel transcriptional effector that functions within two distinct neuronal cell-types to non-autonomously regulate divergent components of the proteostatic network to enhance stress resistance, improve proteostasis and delay aging.

Discoveries made in the nematode Caenorhabditis elegans revealed that aging is under genetic control. Since these transformative initial studies, C. elegans has become a premier model system for aging research. Critically, the genes, pathways, and processes that have fundamental roles in organismal aging are deeply conserved throughout evolution. This conservation has led to a wealth of knowledge regarding both the processes that influence aging and the identification of molecular and cellular hallmarks that play a causative role in the physiological decline of organisms. One key feature of age-associated decline is the failure of mechanisms that maintain proper function of the proteome (proteostasis). Here we highlight components of the proteostatic network that act to maintain the proteome and how this network integrates into major longevity signaling pathways. We focus in depth on the heat shock transcription factor 1 (HSF1), the central regulator of gene expression for proteins that maintain the cytosolic and nuclear proteomes, and a key effector of longevity signals.

The ability to maintain proper function and folding of the proteome (protein homeostasis) declines during normal aging, facilitating the onset of a growing number of age-associated diseases. For instance, proteins with polyglutamine expansions are prone to aggregation, as exemplified with the huntingtin protein and concomitant onset of Huntington’s disease. The age-associated deterioration of the proteome has been widely studied through the use of transgenic Caenorhabditis elegans expressing polyQ repeats fused to a yellow fluorescent protein (YFP). This polyQ::YFP transgenic animal model facilitates the direct quantification of the age-associated decline of the proteome through imaging the progressive formation of fluorescent foci (i.e., protein aggregates) and subsequent onset of locomotion defects that develop as a result of the collapse of the proteome. Further, the expression of the polyQ::YFP transgene can be driven by tissue-specific promoters, allowing the assessment of proteostasis across tissues in the context of an intact multicellular organism. This model is highly amenable to genetic analysis, thus providing an approach to quantify aging that is complementary to lifespan assays. We describe how to accurately measure polyQ::YFP foci formation within either neurons or body wall muscle during aging, and the subsequent onset of behavioral defects. Next, we highlight how these approaches can be adapted for higher throughput, and potential future applications using other emerging strategies for C. elegans genetic analysis.

Determinar la capacidad antioxidante y el Indice glicemico de frutos promisorios amazonicos del Peru. La Capacidad antioxidante de los jugos de frutos amazonicos diluidos al 1/100, se determino mediante el metodo DPPH expresado como el porcentaje de inhibicion, tomando como referencia el jugo de Limon diluido al 1/100. El indice glicemico expresado en porcentaje fue determinado por el area bajo la curva del alimento en prueba y de la glucosa, considerando el area de la curva de glucosa como el 100 % Se utilizaron 12 ratas albinas machos con peso aproximado de 250 g, a los cuales se determino la glicemia (en ayunas) basal (tiempo cero) posteriormente se administro glucosa (estandar) por via orogastrica a la dosis de 50 mg/70 g de peso, determinando la glicemia a diferentes tiempos (15, 30, 45, 60, 90, 120, 150 min). Dias posteriores se administro el alimento de prueba por via orogastrica a la dosis equivalente a la de la glucosa dependiendo del contenido de carbohidratos del alimento, determinando la glicemia a los diferentes tiempos. La capacidad antioxidante expresado como porcentaje de inhibicion fueron: caju 76%, caja 201%, araza 268%, caimito 302%, mango ciruela 353% y pitujaya 524% y los IG fueron: caju 75,8 %, caja 74%, caimito 71,6 %, mango ciruela 59,7%, pitujaya 51,8% y araza 43,8%. Los frutos estudiados tienen alta capacidad

Echinoderms possess an incredible regenerative capacity. Within this phylum, holothurians, better known as sea cucumbers, can regenerate most of their internal and external organs. While regeneration has been studied in several species, the most recent and extensive studies have been done in the species Holothuria glaberrima, the focus of most of our discussion. This chapter presents the model system and integrates the work that has been done to determine the major steps that take place, during regeneration of the intestinal and nervous system, from wound healing to the reestablishment of original function. We describe the cellular and molecular events associated with the regeneration processes and also describe the techniques that have been used, discuss the results, and explain the gaps in our knowledge that remain. We expect that the information provided here paves the road for new and young investigators to continue the study of the amazing potential of regeneration in members of the Echinodermata and how these studies will shed some light into the mechanisms that are common to many regenerative processes.

Interleukin 3-dependent bone marrow and Ba/F3 cells present constitutive Fas expression. A dose dependent increase in Fas surface expression was induced in these cells by X-ray irradiation. Using primary cell cultures and established cell lines derived from p53-null mice (p53-/-), we demonstrated that the increase in Fas expression upon X-ray irradiation is dependent on the presence of at least one wild-type p53 allele. Fas induction by X-ray irradiation was negatively modulated by IL-3; an earlier Fas induction was observed in the absence of IL-3 or at low IL-3 concentrations. However, IL-3 withdrawal in non-irradiated cells did not induce an increase in Fas expression. X-ray irradiation of Ba/F3 cells induced the expression of functional Fas receptors. Therefore, in IL-3-dependent cells, IL-3 regulates the rate of Fas expression, which is correlated with the degree of apoptosis observed in X-irradiated cells. Finally, we demonstrate that IL-3 controls the degree of Fas expression induced by irradiation through a p53-mediated pathway.

El pdf del artículo es la versión de autor., Both prolactin (PRL) and estrogen (E2) are involved in the pathogenesis and progression of mammary neoplasia, but the mechanisms by which these hormones interact to exert their effects in breast cancer cells are not well understood. We show here that PRL is able to activate the unliganded estrogen receptor (ER). In breast cancer cells, PRL activates a reporter plasmid containing estrogen response elements (EREs) and induces the ER target gene pS2. These actions are blocked by the antagonist ICI 182,780, showing that ER is required for the PRL-mediated effect. Moreover, PRL leads to phosphorylation of ERα in serine-118 (P-ERα), a modification related to the potentiation of ligand-independent transcriptional activation. In addition, PRL mimics the effect of E2 on target gene expression by inducing cyclical recruitment of ERα and P-ERα to ERE-containing promoters, resulting in recruitment of co-activators and acetylation of histone H3. Finally, PRL induces expression of c-Myc and Cyclin D1 and leads to increased cell proliferation, which is specifically antagonized by ICI 182,780 or ERα depletion. These results show that ligand-independent ERα activation appears to be an important component of the proliferative and transcriptional actions of PRL in breast cancer cells., This work was supported by grants SAF2006-00371 and BFU2007-62402 from the Ministerio de Educación y Ciencia, RD06/0020/0036 and PIO40682 from the Fondo de Investigaciones Sanitarias, by a grant from the Fundación MMA and by the EU Project CRESCENDO (FP6-018652).

13 páginas, 7 figuras -- PAGS nros. 3598-3610, Mesenchymal stem cells (MSC) have been extensively studied and gained wide popularity due to their therapeutic potential. Spontaneous transformation of MSC, from both human and murine origin, has been reported in many studies. MSC transformation depends on the culture conditions, the origin of the cells and the time on culture; however, the precise biological characteristics involved in this process have not been fully defined yet. In this study, we investigated the role of p53 in the biology and transformation of murine bone marrow (BM)-derived MSC. We demonstrate that the MSC derived from p53KO mice showed an augmented proliferation rate, a shorter doubling time and also morphologic and phenotypic changes, as compared to MSC derived from wild-type animals. Furthermore, the MSC devoid of p53 had an increased number of cells able to generate colonies. In addition, not only proliferation but also MSC differentiation is controlled by p53 since its absence modifies the speed of the process. Moreover, genomic instability, changes in the expression of c-myc and anchorage independent growth were also observed in p53KO MSC. In addition, the absence of p53 implicates the spontaneous transformation of MSC in long-term cultures. Our results reveal that p53 plays a central role in the biology of MSC, The work in the laboratory was supported by SAF2006-4628, RD06TEMP/01566, P-2006/BIO-204 and #2006 20F 0041 from the Ministry of Education and Science, Ministry of Health, Comunidad de Madrid and CSIC

To determine the effects of estrogen deprivation on bone mass in young women in whom large bone mass increases are known to occur.Over 2 years, nine amenorrheic and 21 normal women were studied, classified into exercising (dancers) and sedentary subjects. An integrated estrogen exposure score was used to determine estrogen response during the 2 years of study. Bone mineral density was measured by single and dual photon absorptiometry in the spine, wrist, and foot (metatarsus).Hypoestrogenism was present in all amenorrheic women in the first year, and mean estrogen exposure scores were lower in these subjects during the 2 years. Mean spine, wrist, and metatarsal bone mineral density measurements were lower in the amenorrheic women and remained below the levels in controls, despite changing clinical indices and return of menses in some of the subjects. Amenorrheic dancers showed the greatest increase in spine bone mineral density, gaining 9.65% in the first year, 4.49% in the second, and an increase of 14.43% (P.05) over the total period. Their bone mineral density values, however, remained significantly below those of normal controls during the duration of the study. The most significant gains were seen in two subjects with weight gain and return of irregular periods (three periods in 12 months).Young amenorrheic exercising women appear to increase bone mass before the return of normal menses; however, bone mass remained below control values during 2 years of study, possibly because of long-term adolescent hypoestrogenism.

Soluble class I antigens (sHLA) are secreted by lymphocytes upon activation in vitro. The intrathecal synthesis (ITS) of these molecules has been studied in patients with the varicella-zoster virus (VZV) meningitis. In this paper we describe a sHLA index IH = (CSF sHLA/serum sHLA): (CSF albumin/serum albumin) which is expected to increase only when sHLA is synthesised within the central nervous system (CNS). The IH is elevated in the first week of meningitis, when antibody synthesis is still low, and decreases thereafter. We think IH is an index of early lymphocyte activation within the CNS. The relation of these findings with previous in vitro studies is also discussed.

Soluble major histocompatibility complex class I molecules (sHLA) present in human serum can be resolved by gel filtration into two different peaks with an apparent molecular mass of about 200 kDa (30% of the total) and 50-60 kDa (60%-70%). The serological analysis of the peaks shows that A or B specificities can only be detected in the 200 kDa peak while both are recognized by the monomorphic W6/32 monoclonal antibody (mAb) and anti-beta 2-microglobulin mAb. Such sHLA (non HLA-A or -B) molecules are released from human spleen membranes upon incubation at 37 degrees C and have been purified by affinity chromatography with mAb W6/32 bound to Sepharose. The molecular mass analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the sHLA (non HLA-A or -B) and of the classical HLA-A or -B antigens still bound to the membranes and purified from the same membranes after detergent solubilization does not show a significant difference, indicating that sHLA do not represent proteolytic fragments of the classical HLA-A or -B antigens. The presence of sHLA (non HLA-A or -B) has also been detected in the supernatants of lymphocyte cultures and increases dramatically upon stimulation by mitogens. The effect of pokeweed mitogen, phytohemagglutinin, Staphylococcus aureus Cowan strain and phorbol 12-myristate 13-acetate on the secretion of sHLA has been studied. The molecular mass of the secreted sHLA (detected using [14C]leucine) is compared with the classical transmembrane proteins.