Raf-1 Activation Prevents Caspase 9 Processing Downstream of Apoptosome Formation

In many cell types, growth factor removal induces the release of cytochrome-c from mitochondria that leads to activation of caspase-9 in the apoptosome complex. Here, we show that sustained stimulation of the Raf-1/MAPK1,3 pathway prevents caspase-9 activation induced by serum depletion in CCL39/ΔRaf-1:ER fibroblasts. The protective effect mediated by Raf-1 is sensitive to MEK inhibition that is sufficient to induce caspase-9 cleavage in exponentially growing cells. Raf-1 activation does not inhibit the release of cytochrome-c from mitochondria while preventing caspase-9 activation. Gel filtration chromatography analysis of apoptosome formation in cells shows that Raf-1/MAPK1,3 activation does not interfere with APAF-1 oligomerization and recruitment of caspase 9. Raf-1-mediated caspase-9 inhibition is sensitive to emetine, indicating that the protective mechanism requires protein synthesis. However, the Raf/MAPK1,3 pathway does not regulate XIAP. Taken together, these results indicate that the Raf-1/MAPK1,3 pathway controls an apoptosis regulator that prevents caspase-9 activation in the apoptosome complex

Changes in plant metabolism and accumulation of fungal metabolites in response to Esca proper and apoplexy expression in the whole grapevine

Trunk diseases have become among the most important grapevine diseases worldwide. They are caused by fungal pathogens that attack the permanent woody structure of the vines and cause various symptoms in woody and annual organs. This study examined modifications of plant responses in green stem, cordon and trunk of grapevines expressing Esca proper (E) or apoplexy (A) event, which are the most frequent grapevine trunk disease symptoms observed in Europe. Transcript expression of a set of plant defense- and stress-related genes was monitored by quantitative RT-PCR while plant phytoalexins and fungal metabolites were quantified by HPLC-MS in order to characterize the interaction between the grapevine and trunk disease agents. Expression of genes encoding enzymes of the phenylpropanoid pathway and trans-resveratrol content were altered in the three organs of diseased plants, especially in the young tissues of A plants. PR proteins and the antioxidant system were severely modulated in A plants, which indicates a drastic stress effect. In the meantime, fungal polyketides 6-MSA, (R)-mellein and (3R,4R)-4-hydroxymellein, were accumulated in A plants that suggests their potential effect on plant metabolism during the appearance of foliar symptoms

Multi-Zone Shell Model for Turbulent Wall Bounded Flows

We suggested a \emph{Multi-Zone Shell} (MZS) model for wall-bounded flows accounting for the space inhomogeneity in a "piecewise approximation", in which cross-section area of the flow, $S$, is subdivided into "$j$-zones". The area of the first zone, responsible for the core of the flow, $S_1\simeq S/2$, and areas of the next $j$-zones, $S_j$, decrease towards the wall like $S_j\propto 2^{-j}$. In each $j$-zone the statistics of turbulence is assumed to be space homogeneous and is described by the set of "shell velocities" $u_{nj}(t)$ for turbulent fluctuations of the scale $\propto 2^{-n}$. The MZS-model includes a new set of complex variables, $V_j(t)$, $j=1,2,... \infty$, describing the amplitudes of the near wall coherent structures of the scale $s_j\sim 2^{-j}$ and responsible for the mean velocity profile. Suggested MZS-equations of motion for $u_{nj}(t)$ and $V_j(t)$ preserve the actual conservations laws (energy, mechanical and angular momenta), respect the existing symmetries (including Galilean and scale invariance) and account for the type of the non-linearity in the Navier-Stokes equation, dimensional reasoning, etc. The MZS-model qualitatively describes important characteristics of the wall bounded turbulence, e.g., evolution of the mean velocity profile with increasing Reynolds number, \RE, from the laminar profile towards the universal logarithmic profile near the flat-plane boundary layer as \RE\to \infty.Comment: 27 pages, 17 figs, included, PRE, submitte

Maladie de Krabbe : a propos d’un cas

Introduction Le diagnostic d’une maladie lysosomiale est utile surtout dans les familles à risque en vue d’effectuer un conseil génétique. Nous rapportons l’observation d’un enfant vu pour la première fois à 13 mois, pour une perte progressive des acquisitions psychomotrices. Dans ses antécédents on notait une consanguinité parentale de premier degré. L’imagerie par résonance magnétique cérébrale révélait des hypersignaux diffus bilatéraux et symétriques periventriculaires, des noyaux lenticulaires et des noyaux dentelés du cervelet sur les séquences T2 et Flair associés à des hyposignaux T2 des thalamus. Le dosage de la Bêta galatocérébrosidase chez l’enfant et les deux parents a permis de faire le diagnostic de maladie deKrabbe.Conclusion Une maladie métabolique doit être recherchée de parti pris chez tout enfant présentant une régression progressive des acquisitions psycho-motrices mais l’insuffisance du plateau technique en Afrique limite considérablement les possibilités diagnostiques

Associations between maternal psychological distress and mother-infant bonding: a systematic review and meta-analysis

Purpose: Maternal psychological distress and mother-infant bonding problems each predict poorer offspring outcomes. They are also related to each other, yet the extensive literature reporting their association has not been meta-analysed. Methods: We searched MEDLINE, PsycINFO, CINAHL, Embase, ProQuest DTG, and OATD for English-language peer-reviewed and grey literature reporting an association between mother-infant bonding, and multiple indicators of maternal psychological distress. Results: We included 133 studies representing 118 samples; 99 samples (110,968 mothers) were eligible for meta-analysis. Results showed concurrent associations across a range of timepoints during the first year postpartum, between bonding problems and depression (r = .27 [95% CI 0.20, 0.35] to r = .47 [95% CI 0.41, 0.53]), anxiety (r = .27 [95% CI 0.24, 0.31] to r = .39 [95% CI 0.15, 0.59]), and stress (r = .46 [95% CI 0.40, 0.52]). Associations between antenatal distress and subsequent postpartum bonding problems were mostly weaker and with wider confidence intervals: depression (r = .20 [95% CI 0.14, 0.50] to r = .25 [95% CI 0.64, 0.85]), anxiety (r = .16 [95% CI 0.10, 0.22]), and stress (r = .15 [95% CI − 0.67, 0.80]). Pre-conception depression and anxiety were associated with postpartum bonding problems (r = − 0.17 [95% CI − 0.22, − 0.11]). Conclusion: Maternal psychological distress is associated with postpartum mother-infant bonding problems. Co-occurrence of psychological distress and bonding problems is common, but should not be assumed. There may be benefit in augmenting existing perinatal screening programs with well-validated mother-infant bonding measures

A novel model of liver cancer stem cells developed from induced pluripotent stem cells

Background Liver cancer is the second most common cause of cancer-related death. Every type of tumours including liver cancer contains cancer stem cells (CSCs). To date, the molecular mechanism regulating the development of liver CSCs remains unknown. Methods In this study, we tried to generate a new model of liver CSCs by converting mouse induced pluripotent stem cells (miPSCs) with hepatocellular carcinoma (HCC) cell line Huh7 cells conditioned medium (CM). miPSCs treated with CM were injected into the liver of BALB/c nude mice. The developed tumours were then excised and analysed. Results The primary cultured cells from the malignant tumour possessed self-renewal capacity, differentiation potential and tumorigenicity in vivo, which were found rich in liver cancer-associated markers as well as CSC markers. Conclusions We established a model of liver CSCs converting from miPS and showed different stages of stemness during conversion process. Our CSC model will be important to assess the molecular mechanisms necessary to develop liver CSCs and could help in defeating liver cancer

A study of cytokeratin 20 immunostaining in the urothelium of neuropathic bladder of patients with spinal cord injury

BACKGROUND: Normal urothelium is characterised by terminally differentiated superficial cells, which express cytokeratin 20 in the cytoplasm. In contrast, cultured human stratified urothelium, which does not undergo complete terminal differentiation of its superficial cells, does not express cytokeratin 20. If spinal cord injury (SCI) affects urothelial differentiation or induces squamous or other metaplastic change undetected by histological analysis, the superficial urothelial cells of the neuropathic bladder might be expected to show absence of immunostaining for cytokeratin 20. PATIENTS AND METHODS: We studied immunostaining for cytokeratin 20 in bladder biopsies taken from 63 consecutive SCI patients. Immunostaining was performed on paraffin-embedded tissue using a mouse monoclonal antibody (clone: Ks20.8). RESULTS: Of 63 biopsies, the epithelium was scarce in two. Eight biopsies showed squamous metaplasia and immunostaining for cytokeratin 20 was absent in all the eight biopsies. Of the remaining 53 cases, in which the umbrella cell layer of the urothelium was intact, immunostaining for cytokeratin 20 was seen only in ten biopsies. CONCLUSION: Superficial cells in the transitional epithelium showed immunostaining for cytokeratin 20 in 10 of 53 bladder biopsies taken from SCI patients. The reasons for this could be either that there is an underlying metaplasia or that changes in the neuropathic bladder affect urothelial differentiation. Taken with evidence from other systems, such as loss of cytokeratin 20 expression from static organ cultures of urothelial tissue, this might suggest that other factors, such as impairment of voluntary voiding in SCI patients, could affect expression of markers such as cytokeratin 20

Qualite de vie apres un accident vasculaire cerebral au Senegal: a propos de 50 cas

Introduction: L’accident vasculaire cérébral (AVC) constitue une cause majeure de mortalité et de handicap chez les survivants. La qualité de vie dépend de la nature du handicap et de sa perception par le patient, son entourage et la communauté.Objectif: Notre objectif était d’évaluer le handicap après un AVC et d’apprécier son retentissement sur la qualité de vie des patients victimes.Patients et Méthodes: Nous avons mené une étude prospective, longitudinale de février 2008 à mai 2009, à la clinique neurologique de FANN. Les patients étaient vus à la phase initiale de l’AVC et 6 mois après et soumis à un questionnaire comportant plusieurs items relatifs à la nature de l’accident vasculaire cérébral, le vécu psychoaffectif et socioprofessionnel, l’index de Barthel a été utilisé chez tous les malades.Résultats: Nous avons colligé 50 patients âgés de 15 à 82 ans, avec une sex-ratio de 1,27. L’accident était ischémique dans 70%, hémorragique dans 30% des cas. 66% des patients avaient un index de Barthel entre (60-100), 6% étaient entre (0-20). Le score était meilleur chez les jeunes (15ans-34ans) qui avait tous un index entre (60-100). Par ailleurs 50% des patients de la tranche supérieure à 75ans étaient dans l’intervalle (60-100). Les AVCH avaient des Meilleurs résultats avec 73,3% à un index entre (60-100). seul 12% ont été réinsérés, sur le plan professionnel. 54,05%, n’ont pas noté de changement dans leur vie conjugale. Sur le plan familial, 56% ne notaient aucun changement. Une grande partie de notre série 44% acceptaient bien leurs  déficits,. 70% ne faisaient plus d’activités de temps libre.Conclusion: La qualité de vie est un concept multidimensionnel qui incorpore outre la santé physique les aspects mentaux et sociaux de la maladie.Mots clés: AVC, qualité de vie, SénégalEnglish Title: Quality of life after stroke in Senegal: about 50 casesEnglish AbstractIntroduction: Stroke is a major cause of mortality and disability in survivors. The quality of life depends on the nature of disability and its perception by the patient, his or her environment and community. The aim of this study was to assess disability after stroke and its impact on quality of life of patients (victims).Patients And Methods: We conducted a prospective, longitudinal study from February 2008 to May 2009, at the Neurological Clinic of Fann. Patients were seen at the initial phase of stroke and 6 months later and answered a questionnary containing 13 items like nature of stroke disability psychological emotional and socioprofessional filds. The index of barthel was used at all the patient’s.Results: We collected, were like this 50 patients aged 15-82 years with a sex ratio of 1.27. The accident was ischemic in 70% of cases, hemorrhagic in 30% of cases. 66% had a Barthel index between (60-100), 6% were between (0-20). The score was significantly better in young series (15-34), which all have a Barthel index between (60-100), more over 50% of patients in the portion above 75 years were in the range (60 - 100). Hemorragic stroke had the best results with 73.3% a Barthel index between (60-100). On a professional level, only 12% patients were rehabilitated. 54.05% didn’t notice any change in their marital life. On the home front, 56% noted any change. A large part of our series 44% accepted although their deficits. 70% didn’t have any more free time activities.Keywords: quality of life, stroke, Senega

KIRA1 and ORESARA1 terminate flower receptivity by promoting cell death in the stigma of Arabidopsis

Flowers have a species-specific functional life span that determines the time window in which pollination, fertilization and seed set can occur. The stigma tissue plays a key role in flower receptivity by intercepting pollen and initiating pollen tube growth toward the ovary. In this article, we show that a developmentally controlled cell death programme terminates the functional life span of stigma cells in Arabidopsis. We identified the leaf senescence regulator ORESARA1 (also known as ANAC092) and the previously uncharacterized KIRA1 (also known as ANAC074) as partially redundant transcription factors that modulate stigma longevity by controlling the expression of programmed cell death-associated genes. KIRA1 expression is sufficient to induce cell death and terminate floral receptivity, whereas lack of both KIRA1 and ORESARA1 substantially increases stigma life span. Surprisingly, the extension of stigma longevity is accompanied by only a moderate extension of flower receptivity, suggesting that additional processes participate in the control of the flower's receptive life span