Signaling emotion and reason in cooperation

We explore the signal value of emotion and reason in human cooperation. Across four experiments utilizing dyadic prisoner dilemma games, we establish three central results. First, individuals infer prosocial feelings and motivations from signals of emotion. As a result, individuals believe that a reliance on emotion signals that one will cooperate more so than a reliance on reason. Second, these beliefs are generally accurate—those who act based on emotion are more likely to cooperate than those who act based on reason. Third, individuals’ behavioral responses towards signals of emotion and reason depends on their own decision mode: those who rely on emotion tend to conditionally cooperate (that is, cooperate only when they believe that their partner has cooperated), whereas those who rely on reason tend to defect regardless of their partner’s signal. These findings shed light on how different decision processes, and lay theories about decision processes, facilitate and impede cooperation

Pengembangan Modul Intervensi Untuk Meningkatkan Resiliensi Pada Individu Yang Mengalami Perubahan Fisik Menjadi Penyandang Disabilitas

Penelitian ini bertujuan untuk menindaklanjuti temuan sebelumnya dengan mengembangkan modul intervensi secara terperinci, yang selanjutnya dapat digunakan sebagai panduan dalam membantu meningkatkan resiliensi individu yang mengalami Perubahan kondisi fisik menjadi penyandang disabilitas. Penulis menyusun serta merinci rancangan implementasi awal yang direkomendasikan oleh penelitian sebelumnya kedalam langkah-langkah yang lebih sistematis dan operasional hingga memperoleh hasil akhir berupa modul. Metode yang digunakan berbasis tahapan riset aksi, meskipun proses yang dilakukan hanya sampai pada langkah ketiga, yaitu Perumusan solusi dari persoalan yang diangkat. Partisipan terdiri dari delapan individu yang mengalami Perubahan kondisi menjadi penyandang disabilitas. Selain partisipan, empat orang psikolog juga dilibatkan dalam penelitian ini sebagai penelaah modul. Hasil penelitian ini berupa sebuah paket modul intervensi untuk peningkatan resiliensi melalui penguatan faktor protektif serta pengembangan strategi koping dan adaptasi pada individu yang mengalami Perubahan kondisi fisik menjadi penyandang disabilitas. Paket modul tersebut terdiri dari 5 sub-modul yang telah disusun sedemikian rupa untuk memudahkan pelaksanaannya, terdiri dari modul: (1) memperkuat dukungan keluarga terhadap penyandang disabilitas; (2) pendampingan awal penyandang disabilitas; (3) intervensi lanjut 1 (penguatan faktor protektif internal); (4) intervensi lanjut 2 (pengembangan strategi koping); dan (5) intervensi lanjut 3 (langkah adaptasi positif)

Risk factors for oral mucositis in paediatric oncology patients receiving alkylant chemotherapy

BACKGROUND: We describe the risk indicators for oral mucositis (OM) in paediatric oncology patients hospitalised in the Institut Gustave Roussy (Villejuif-Paris) and treated with alkylant chemotherapy with autologous peripheral blood progenitor cells. METHODS: The sample was selected using PIGAS software. Three groups of subjects received different chemotherapy regimens: A. Melphalan, B. Busulfan and C. other alkylant protocols. The degree of mucositis was recorded by CTC version 2.0 (Common Toxicity Criteria). Descriptive statistics were performed. The association between mucositis and risk indicator variables was tested using a χ(2 )test. The association between case status and covariates was tested using unconditional logistic regression analysis. RESULTS: Of the 337 children enrolled, 241 showed mucositis (group 1) and 96 did not show mucositis (group 2) during alkylant chemotherapy. There was a higher prevalence of male patients in both groups. The three different chemotherapy regimen groups are correlated with the appearance of oral mucositis (χ(2 )= 22.42, p < 0.01). Weight loss was higher in group 1 (χ(2 )= 6.31, p = 0.01). The duration of aplasia was lower in the Busulfan protocol (7.5 days) than in the Melphalan group (9.3 days) or the other regimens (8.6 days). The use of Bufulfan(® )was directly associated with case status (presence of oral mucositis): odds ratio [OR] = 2.1 and confidence interval [95%CI] = 1.3–3.0. Also, occurrences of germinal tumours and secondary bacterial infections were directly linked with case status: [OR] = 1.4 and 1.8, confidence interval [95%CI] = 1.2 – 1.7 and 1.1 – 2.5, respectively. CONCLUSION: The presence of OM was associated with the three different chemotherapy regimens considered; in particularly patients treated with Busulfan had the highest prevalence

Transcription factor TFCP2L1 patterns cells in the mouse kidney collecting ducts

Although most nephron segments contain one type of epithelial cell, the collecting ducts consists of at least two: intercalated (IC) and principal (PC) cells, which regulate acid-base and salt-water homeostasis, respectively. In adult kidneys, these cells are organized in rosettes suggesting functional interactions. Genetic studies in mouse revealed that transcription factor Tfcp2l1 coordinates IC and PC development. Tfcp2l1 induces the expression of IC specific genes, including specific H(+)-ATPase subunits and Jag1. Jag1 in turn, initiates Notch signaling in PCs but inhibits Notch signaling in ICs. Tfcp2l1 inactivation deletes ICs, whereas Jag1 inactivation results in the forfeiture of discrete IC and PC identities. Thus, Tfcp2l1 is a critical regulator of IC-PC patterning, acting cell-autonomously in ICs, and non-cell-autonomously in PCs. As a result, Tfcp2l1 regulates the diversification of cell types which is the central characteristic of 'salt and pepper' epithelia and distinguishes the collecting duct from all other nephron segments

Localization of a gene for nonsyndromic renal hypodysplasia to chromosome 1p32-33.

Nonsyndromic defects in the urinary tract are the most common cause of end-stage renal failure in children and account for a significant proportion of adult nephropathy. The genetic basis of these disorders is not fully understood. We studied seven multiplex kindreds ascertained via an index case with a nonsyndromic solitary kidney or renal hypodysplasia. Systematic ultrasonographic screening revealed that many family members harbor malformations, such as solitary kidneys, hypodysplasia, or ureteric abnormalities (in a total of 29 affected individuals). A genomewide scan identified significant linkage to a 6.9-Mb segment on chromosome 1p32-33 under an autosomal dominant model with reduced penetrance (peak LOD score 3.5 at D1S2652 in the largest kindred). Altogether, three of the seven families showed positive LOD scores at this interval, demonstrating heterogeneity of the trait (peak HLOD 3.9, with 45% of families linked). The chromosome 1p32-33 interval contains 52 transcription units, and at least 23 of these are expressed at stage E12.5 in the murine ureteric bud and/or metanephric mesenchyme. These data show that autosomal dominant nonsyndromic renal hypodysplasia and associated urinary tract malformations are genetically heterogeneous and identify a locus for this common cause of human kidney failure

A Grhl2-dependent gene network controls trophoblast branching morphogenesis

Healthy placental development is essential for reproductive success; failure of the feto-maternal interface results in pre-eclampsia and intrauterine growth retardation. We found that grainyhead-like 2 (GRHL2), a CP2-type transcription factor, is highly expressed in chorionic trophoblast cells, including basal chorionic trophoblast (BCT) cells located at the chorioallantoic interface in murine placentas. Placentas from Grhl2-deficient mouse embryos displayed defects in BCT cell polarity and basement membrane integrity at the chorioallantoic interface, as well as a severe disruption of labyrinth branching morphogenesis. Selective Grhl2 inactivation only in epiblast-derived cells rescued all placental defects but phenocopied intraembryonic defects observed in global Grhl2 deficiency, implying the importance of Grhl2 activity in trophectoderm-derived cells. ChIP-seq identified 5282 GRHL2 binding sites in placental tissue. By integrating these data with placental gene expression profiles, we identified direct and indirect Grhl2 targets and found a marked enrichment of GRHL2 binding adjacent to genes downregulated in Grhl2(-/-) placentas, which encoded known regulators of placental development and epithelial morphogenesis. These genes included that encoding the serine protease inhibitor Kunitz type 1 (Spint1), which regulates BCT cell integrity and labyrinth formation. In human placenta, we found that human orthologs of murine GRHL2 and its targets displayed co-regulation and were expressed in trophoblast cells in a similar domain as in mouse placenta. Our data indicate that a conserved Grhl2-coordinated gene network controls trophoblast branching morphogenesis, thereby facilitating development of the site of feto-maternal exchange. This might have implications for syndromes related to placental dysfunction

Alcohol, microbiome, life style influence alcohol and non-alcoholic organ damage

This paper is based upon the "8th Charles Lieber's Satellite Symposium" organized by Manuela G. Neuman at the Research Society on Alcoholism Annual Meeting, on June 25, 2016 at New Orleans, Louisiana, USA. The integrative symposium investigated different aspects of alcohol-induced liver disease (ALD) as well as non alcohol -induced liver disease (NAFLD) and possible repair. We revealed the basic aspects of alcohol metabolism that may be responsible for the development of liver disease as well as the factors that determine the amount, frequency and which type of alcohol misuse leads to liver and gastrointestinal diseases. We aimed to (1) describe the immuno-pathology of ALD, (2) examine the role of genetics in the development of alcoholic hepatitis (ASH) and NAFLD, (3) propose diagnostic markers of ASH and non-alcoholic steatohepatitis (NASH), (4) examine age and ethnic differences as well as analyze the validity of some models, (5) develop common research tools and biomarkers to study alcohol-induced effects, 6) examine the role of alcohol in oral health and colon and gastrointestinal cancer and (7) focus on factors that aggravate the severity of organ-damage. The present review includes pre-clinical, translational and clinical research that characterizes ALD and NAFLD. Strong clinical and experimental evidence lead to recognition of the key toxic role of alcohol in the pathogenesis of ALD with simple fatty infiltrations and chronic alcoholic hepatitis with hepatic fibrosis or cirrhosis. These latter stages may also be associated with a number of cellular and histological changes, including the presence of Mallory's hyaline, megamitochondria, or perivenular.and perisinusoidal fibrosis. Genetic polymorphisms of ethanol metabolizing enzymes and cytochrome p450 (CYP) 2E1 activation may change the severity of ASH and NASH. Other risk factors such as its co-morbidities with chronic viral hepatitis in the presence or absence of human deficiency virus were discussed. Dysregulation of metabolism, as a result of ethanol exposure, in the intestine leads to colon carcinogenesis. The hepatotoxic effects of ethanol undermine the contribution of malnutrition to the liver injury. Dietary interventions such as micro and macronutrients, as well as changes to the microbiota have been suggested. The clinical aspects of NASH, as part of the metabolic syndrome in the aging population, have been presented. The symposium addressed mechanisms and biomarkers of alcohol induced damage to different organs, as well as the role of the microbiome in this dialog. The microbiota regulates and acts as a key element in harmonizing immune responses at intestinal mucosal surfaces. It is known that microbiota is an inducer of proinflammatory T helper 17 cells and regulatory T cells in the intestine. The signals at the sites of inflammation mediate recruitment and differentiation in order to remove inflammatory inducers and promote tissue homeostasis restoration. The change in the intestinal microbiota also influences the change in obesity and regresses the liver steatosis. Evidence on the positive role of moderate alcohol consumption on heart and metabolic diseases as well on reducing steatosis have been looked up. Moreover nutrition as a therapeutic intervention in alcoholic liver disease has been discussed. In addition to the original data, we searched the literature (2008-2016) for the latest publication on the described subjects. In order to obtain the updated data we used the usual engines (Pub Med and Google Scholar). The intention of the eighth symposia was to advance the international profile of the biological research on alcoholism. We also wish to further our mission of leading the forum to progress the science and practice of translational research in alcoholism. (C) 2017 Elsevier Inc. All rights reserved.Peer reviewe

A Case of Left Atrial Metastasis From Hepatocellular Carcinoma: Life-Saving Palliative Resection Using Cardiopulmonary Bypass

Hepatocellular carcinoma (HCC) with metastasis to the heart is uncommon. We report a rare case of left atrial metastasis of HCC which was resected palliatively as a live-saving procedure with the use of cardiopulmonary bypass. Despite chemoembolization, which was undertaken 11 times, cardiac metastasis occurred. Moreover, the right and left atria and left ventricle were involved simultaneously. The severe dyspnea improved dramatically after surgery. Following this, the patient underwent systemic chemotherapy and lived a life without recurrence of symptoms associated with mitral valve obstruction