Hardness and approximation for the geodetic set problem in some graph classes

In this paper, we study the computational complexity of finding the \emph{geodetic number} of graphs. A set of vertices $S$ of a graph $G$ is a \emph{geodetic set} if any vertex of $G$ lies in some shortest path between some pair of vertices from $S$. The \textsc{Minimum Geodetic Set (MGS)} problem is to find a geodetic set with minimum cardinality. In this paper, we prove that solving the \textsc{MGS} problem is NP-hard on planar graphs with a maximum degree six and line graphs. We also show that unless $P=NP$, there is no polynomial time algorithm to solve the \textsc{MGS} problem with sublogarithmic approximation factor (in terms of the number of vertices) even on graphs with diameter $2$. On the positive side, we give an $O\left(\sqrt[3]{n}\log n\right)$-approximation algorithm for the \textsc{MGS} problem on general graphs of order $n$. We also give a $3$-approximation algorithm for the \textsc{MGS} problem on the family of solid grid graphs which is a subclass of planar graphs

Validation of persuasive messages for the promotion of physical activity among people with coronary heart disease

OBJECTIVE: to validate the content of persuasive messages for promoting walking among patients with coronary heart disease (CHD). The messages were constructed to strengthen or change patients' attitudes to walking. METHOD: the selection of persuasive arguments was based on behavioral beliefs (determinants of attitude) related to walking. The messages were constructed based in the Elaboration Likelihood Model and were submitted to content validation. RESULTS: the data was analyzed with the content validity index and by the importance which the patients attributed to the messages' persuasive arguments. Positive behavioral beliefs (i.e. positive and negative reinforcement) and self-efficacy were the appeals which the patients considered important. The messages with validation evidence will be tested in an intervention study for the promotion of the practice of physical activity among patients with CHD.OBJETIVO: validar el contenido de mensajes persuasivos para promover la caminata entre pacientes con enfermedad arterial coronaria (DAC). Los mensajes fueron construidos objetivando al fortalecimiento/cambio de la actitud del paciente con relación a la caminata. MÉTODO: la selección de los argumentos persuasivos fue basada en las creencias comportamentales (determinantes de la actitud) relacionadas a la caminata. Los mensajes fueron construidos con base en el Modelo de Probabilidad de Elaboración y sometidos a la validez de contenido. RESULTADOS: los datos fueron analizados por medio del índice de validez de contenido y por la importancia atribuida por los pacientes a los argumentos persuasivos de los mensajes. Las creencias comportamentales positivas (ejemplo: refuerzo positivo y negativo) y la autoeficacia fueron los reclamos considerados importantes por los pacientes. Los mensajes con evidencias de validación serán testadas en estudio de intervención para promoción de la práctica de actividad física entre pacientes con DAC.OBJETIVO: validar o conteúdo de mensagens persuasivas para promover a caminhada entre pacientes com doença arterial coronária (DAC). As mensagens foram construídas com vistas ao fortalecimento/mudança da atitude do paciente em relação à caminhada. MÉTODO: a seleção dos argumentos persuasivos foi baseada nas crenças comportamentais (determinantes da atitude), relacionadas à caminhada. As mensagens foram construídas com base no Modelo de Probabilidade de Elaboração e submetidas à validade de conteúdo. RESULTADOS: os dados foram analisados por meio do índice de validade de conteúdo e pela importância atribuída pelos pacientes aos argumentos persuasivos das mensagens. As crenças comportamentais positivas (i.e. reforço positivo e negativo) e a autoeficácia foram os apelos considerados importantes pelos pacientes. As mensagens com evidências de validação serão testadas em estudo de intervenção para promoção da prática de atividade física entre pacientes com DAC

Raphe-mediated signals control the hippocampal response to SRI antidepressants via miR-16

Serotonin reuptake inhibitor (SRI) antidepressants such as fluoxetine (Prozac), promote hippocampal neurogenesis. They also increase the levels of the bcl-2 protein, whose overexpression in transgenic mice enhances adult hippocampal neurogenesis. However, the mechanisms underlying SRI-mediated neurogenesis are unclear. Recently, we identified the microRNA miR-16 as an important effector of SRI antidepressant action in serotonergic raphe and noradrenergic locus coeruleus (LC). We show here that miR-16 mediates adult neurogenesis in the mouse hippocampus. Fluoxetine, acting on serotonergic raphe neurons, decreases the amount of miR-16 in the hippocampus, which in turn increases the levels of the serotonin transporter (SERT), the target of SRI, and that of bcl-2 and the number of cells positive for Doublecortin, a marker of neuronal maturation. Neutralization of miR-16 in the hippocampus further exerts an antidepressant-like effect in behavioral tests. The fluoxetine-induced hippocampal response is relayed, in part, by the neurotrophic factor S100β, secreted by raphe and acting via the LC. Fluoxetine-exposed serotonergic neurons also secrete brain-derived neurotrophic factor, Wnt2 and 15-Deoxy-delta12,14-prostaglandin J2. These molecules are unable to mimic on their own the action of fluoxetine and we show that they act synergistically to regulate miR-16 at the hippocampus. Of note, these signaling molecules are increased in the cerebrospinal fluid of depressed patients upon fluoxetine treatment. Thus, our results demonstrate that miR-16 mediates the action of fluoxetine by acting as a micromanager of hippocampal neurogenesis. They further clarify the signals and the pathways involved in the hippocampal response to fluoxetine, which may help refine therapeutic strategies to alleviate depressive disorders

The Role of Purported Mucoprotectants in Dealing with Irritable Bowel Syndrome, Functional Diarrhea, and Other Chronic Diarrheal Disorders in Adults

Chronic diarrhea is a frequent presenting symptom, both in primary care medicine and in specialized gastroenterology units. It is estimated that more than 5% of the global population suffers from chronic diarrhea. and that about 40% of these subjects are older than 60 years. The clinician is frequently faced with the need to decide which is the best therapeutic approach for these patients. While the origin of chronic diarrhea is diverse, impairment of intestinal barrier function, dysbiosis. and mucosal micro-inflammation are being increasingly recognized as underlying phenomena characterizing a variety of chronic diarrheal diseases. In addition to current pharmacological therapies, there is growing interest in alternative products such as mucoprotectants, which form a mucoadhesive film over the epithelium to reduce and protect against the development of altered intestinal permeability, dysbiosis, and mucosal micro-inflammation. This manuscript focuses on chronic diarrhea in adults, and we will review recent evidence on the ability of these natural compounds to improve symptoms associated with chronic diarrhea and to exert protective effects for the intestinal barrier

A Crucial Role of Activin A-Mediated Growth Hormone Suppression in Mouse and Human Heart Failure

Infusion of bone marrow-derived mononuclear cells (BMMNC) has been reported to ameliorate cardiac dysfunction after acute myocardial infarction. In this study, we investigated whether infusion of BMMNC is also effective for non-ischemic heart failure model mice and the underlying mechanisms. Intravenous infusion of BMMNC showed transient cardioprotective effects on animal models with dilated cardiomyopathy (DCM) without their engraftment in heart, suggesting that BMMNC infusion improves cardiac function via humoral factors rather than their differentiation into cardiomyocytes. Using conditioned media from sorted BMMNC, we found that the cardioprotective effects were mediated by growth hormone (GH) secreted from myeloid (Gr-1(+)) cells and the effects was partially mediated by signal transducer and activator of transcription 3 in cardiomyocytes. On the other hand, the GH expression in Gr-1(+) cells was significantly downregulated in DCM mice compared with that in healthy control, suggesting that the environmental cue in heart failure might suppress the Gr-1(+) cells function. Activin A was upregulated in the serum of DCM models and induced downregulation of GH levels in Gr-1(+) cells and serum. Furthermore, humoral factors upregulated in heart failure including angiotensin II upregulated activin A in peripheral blood mononuclear cells (PBMNC) via activation of NFκB. Similarly, serum activin A levels were also significantly higher in DCM patients with heart failure than in healthy subjects and the GH levels in conditioned medium from PBMNC of DCM patients were lower than that in healthy subjects. Inhibition of activin A increased serum GH levels and improved cardiac function of DCM model mice. These results suggest that activin A causes heart failure by suppressing GH activity and that inhibition of activin A might become a novel strategy for the treatment of heart failure