Síndrome de pseudo-Meigs secundario a leiomioma uterino

Pseudo-Meigs syndrome is a condition characterised by the presence of ascites and pleural effusion associated with pelvic tumours other than fibroid-type ovarian tumours. Although the clinical picture simulates a neoplastic process, it is, however, a benign pathology that resolves after the removal of the tumour. Pseudo-Meigs syndrome secondary to uterine leiomyoma is a very rare combination, with less than 40 cases published in the literature.The case is presented of a 28 year-old woman attending the emergency department due to ascites and pleural effusion, with an elevated Ca-125 in the context of pseudo-Meigs syndrome that resolved after myomectomy.     

Is the mealtime experience in nursing homes understood? A qualitative study

Aim: The aim of the present study was to explore the significance of the mealtime experience among residents of nursing homes in Spain. Methods: A qualitative phenomenological approach was followed. An initial purposeful sampling of Spanish residents in for‐profit nursing homes in the southern area of Madrid was carried out. A theoretical sampling was also implemented in order to gain a more in‐depth understanding of dependence. Inclusion criteria for nursing home residents were: age (60 years or older) and lack of any cognitive impairment. Data were collected using unstructured and semistructured interviews. Data collection was concluded once theoretical saturation was reached, and the data were analysed using the Giorgi proposal. Results: A total of 26 residents with a mean age of 83 years were included. Three main themes that describe the significance of meals in nursing homes emerged from the data: (i) timing of the meals – mealtimes serve as a point of reference for organizing activities in the nursing home and orient the residents during the day; (ii) table allocation – table allocation depends on the judgment of the personnel, the behavior of each resident and on the input from the residents that use a table; and (iii) the meals themselves – food is experienced as a privilege, as a sign of autonomy and normality, and as an indicator of personal identity. Conclusion: Understanding the social significance of meals for residents in nursing homes would provide deeper insight into resident expectations. This will in turn help to improve service and quality of life for residents. Geriatr Gerontol Int 2013; 13: 482–489 .     

Noncanonical GPCR signaling arising from a PTH receptor–arrestin–Gβγ complex

G protein-coupled receptors (GPCRs) participate in ubiquitous transmembrane signal transduction processes by activating heterotrimeric G proteins. In the current “canonical” model of GPCR signaling, arrestins terminate receptor signaling by impairing receptor–G-protein coupling and promoting receptor internalization. However, parathyroid hormone receptor type 1 (PTHR), an essential GPCR involved in bone and mineral metabolism, does not follow this conventional desensitization paradigm. β-Arrestins prolong G protein (G_S)-mediated cAMP generation triggered by PTH, a process that correlates with the persistence of arrestin–PTHR complexes on endosomes and which is thought to be associated with prolonged physiological calcemic and phosphate responses. This presents an inescapable paradox for the current model of arrestin-mediated receptor–G-protein decoupling. Here we show that PTHR forms a ternary complex that includes arrestin and the Gβγ dimer in response to PTH stimulation, which in turn causes an accelerated rate of G_S activation and increases the steady-state levels of activated G_S, leading to prolonged generation of cAMP. This work provides the mechanistic basis for an alternative model of GPCR signaling in which arrestins contribute to sustaining the effect of an agonist hormone on the receptor.According to the current model for activation and signaling of G protein-coupled receptors (GPCRs), receptor (R) signaling begins when the binding of an agonist ligand (L) stabilizes the active form of the receptor (R*), allowing its coupling to heterotrimeric G proteins (Gαβγ) through a diffusion-controlled process (1–3). The L–R*–G complex catalyzes GDP–GTP exchange on the Gα subunit, promoting the dissociation of the activated G protein into GTP-bound Gα (Gα-GTP) and Gβγ dimers from the receptor. Dissociated Gα-GTP and Gβγ proteins in turn activate specific downstream effectors, such as adenylyl cyclases in the case of Gα_S (Fig. 1A). Activated adenylyl cyclases catalyze a few rounds of cAMP production, the number of which is determined by the rate of GTP hydrolysis of the Gα_S-bound GTP. In order for subsequent rounds of adenylyl cyclase activation to occur, inactive GDP-bound Gα must encounter a Gβγ dimer and then reform an L–R*–G complex (Fig. 1A). In this classical model, arrestin plays a dual role: On one hand, it desensitizes the receptor by preventing further rounds of L–R* and G coupling; on the other, it promotes receptor endocytosis, thus reducing receptor availability on the cell surface. In either case, the classical model predicts that arrestin negatively regulates the levels of the L–R*–G complex, providing the main mechanism by which the signal of a GPCR system is turned off (4, 5). This model, primarily derived from the analysis of the behavior of the β₂-adrenergic receptor (β₂-AR) (4, 5) and many other class 1 GPCRs (6–12), is taken to be universal for GPCR biology (13). Recent findings have challenged this view. We recently showed that parathyroid hormone receptor type 1 (PTHR)–arrestin complexes contribute to prolonging cAMP signaling mediated by PTH or its fully functional N-terminal synthetic analog, PTH(1–34), in cells as diverse as human embryonic kidney (HEK)293 cells expressing recombinant receptor and osteoblastic ROS17/2.8 cells (2, 14) that natively express PTHR. PTH rapidly recruits β-arrestin 1 or β-arrestin 2 to PTHR and stabilizes a persistent ternary PTH–PTHR–arrestin complex that continues signaling via adenylyl cyclases for a considerable time (>30 min) after exposure to a short “pulse” of agonist ligand (14). Because prolonged PTH-induced signaling requires persistent activation of G_S by coupling with PTHR in its L–R* state, this raises the intriguing question of how G_S can bind and be activated by a PTHR that is already associated with arrestin. We reasoned that a long-lived PTH–PTHR–arrestin complex could contribute to sustained cAMP signaling by stabilizing an interaction with the active state of G_S (Fig. 1B, model 1). Alternatively, complexes formed through interactions between β-arrestins and the Gβγ dimer, known to scaffold some signaling complexes (15–17), could promote sustained PTH-induced cAMP signaling by maintaining multiple rounds of Gα_S association with and dissociation from a PTHR–arrestin–Gβγ complex that generates a high level of active Gα_S (Fig. 1B, model 2). Here we tested these hypotheses by using a series of diverse biochemical and biophysical approaches.Open in a separate windowFig. 1.Signaling models of GPCR. (A) Classical model. A ligand binds the inactive state of a GPCR and stabilizes its active form, which then couples with heterotrimeric G proteins (Gαβγ) through a diffusion-controlled process (step 1). The L–R*–G complex in turn catalyzes GDP–GTP exchange on Gα, leading to dissociation of the GTP-bound Gα (Gα-GTP) along with the Gβγ dimer from the receptor (step 2). In the case of G_S, Gα-GTP activates specific effectors such as adenylyl cyclases (AC), which catalyze the synthesis of cAMP from ATP (step 3). The hydrolysis of GTP to GDP causes the dissociation of Gα_S from adenylyl cyclases, shutting down cAMP production and its reassociation to Gβγ subunits (step 4). In this model, the recruitment of β-arrestin mediates desensitization of G-protein signaling. (B) Noncanonical model. (1) A long-lived PTH–PTHR–arrestin complex could contribute to sustained cAMP signaling by stabilizing an interaction with the active state of G_S. (2) Alternatively, the interaction between the activated PTHR and G_S is stabilized by β-arrestins. After the first round of activation, step 1 is bypassed, such that free Gα-GDP directly reassociates with PTHR–Gβγ complexes to initiate a new cycle of G-protein activation. Arrestin stabilizes the G-protein cycle, resulting in prolonged cAMP production.     

Correlates of Perinatal Post-Traumatic Stress among Culturally Diverse Women with Depressive Symptomatology

Post-traumatic stress disorder (PTSD) is an important and often neglected comorbidity of pregnancy; left untreated, it can lead to serious health complications for the mother and developing fetus. Structured interviews were conducted to identify risk factors of PTSD among culturally diverse women with depressive symptomatology receiving perinatal services at community obstetric/gynecologic clinics. Women abused as adults, with two or more instances of trauma, greater trauma severity, insomnia, and low social support were more likely to present perinatal PTSD symptoms. Perinatal PTSD is prevalent and has the potential for chronicity. It is imperative healthcare providers recognize salient risk factors and integrate culturally sensitive screening, appropriate referral, and treatment services for perinatal PTSD.     

Economical saving due to prophylaxis in the prevention of surgical wound infection

The objective was to know the principal risk factors that influence in the development of surgical would infection, and the economical saving achieved with the control of a single variable, that is, right prophylaxis. A prospective study was carried out at the Traumatology Department of La Paz Hospital. A total of 5260 patients operated during 1990–1993 are included. Active epidemiological surveillance was used to check patients; logistic regression was used in the multivariant analysis. The principal risk factors found were: immunodeficiency (OR = 8.67), incorrect healing (OR = 14.42), re-operated patient (patients who needed more than one surgical procedure while they are admitted; reoperations) (OR = 3.57), type of surgery (OR = 4.71) and wrong prophylaxis (OR = 6.36). Making constant all the variables except for prophylaxis, we calculated the percentage of infections prevented by a right prophylaxis, and the cost was calculated starting from the number of extra days of infection. The number of infections prevented during the four years was 310, saving a total of 194 million pesetas (1.5 million dollars), due to right prophylaxis. Cost-benefice ratio = 1/17. We consider of special importance to control this manipulable risk factor, in order to avoid the development of infections.