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Brothers in arms: Libyan revolutionaries bond like family.

ABSTRACT: What motivates ordinary civilians to sacrifice their lives for revolutionary causes? We surveyed 179 Libyan revolutionaries during the 2011 conflict in Libya. These civilians-turned-fighters rejected Gaddafi's jamahiriyya (state of the masses) and formed highly cohesive fighting units typical of intense conflicts. Fighters reported high levels of "identity fusion"--visceral, family-like bonds between fighters and their battalions. Fusion of revolutionaries with their local battalions and their own families were extremely high, especially relative to Libyans who favored the revolution but did not join battalions. Additionally, frontline combatants were as strongly bonded to their battalion as they were to their own families, but battalion members who provided logistical support were more fused with their families than battalions. Together, these findings help illuminate the social bonds that seem to motivate combatants to risk their lives for the group during wartime.

SUBMITTER: Whitehouse H

PROVIDER: S-EPMC4273349 | biostudies-other | 2014 Dec

REPOSITORIES: biostudies-other

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Tooth agenesis and orofacial clefting: genetic brothers in arms?

Project description:Tooth agenesis and orofacial clefts represent the most common developmental anomalies and their co-occurrence is often reported in patients as well in animal models. The aim of the present systematic review is to thoroughly investigate the current literature (PubMed, EMBASE) to identify the genes and genomic loci contributing to syndromic or non-syndromic co-occurrence of tooth agenesis and orofacial clefts, to gain insight into the molecular mechanisms underlying their dual involvement in the development of teeth and facial primordia. Altogether, 84 articles including phenotype and genotype description provided 9 genomic loci and 26 gene candidates underlying the co-occurrence of the two congenital defects: MSX1, PAX9, IRF6, TP63, KMT2D, KDM6A, SATB2, TBX22, TGFα, TGFβ3, TGFβR1, TGFβR2, FGF8, FGFR1, KISS1R, WNT3, WNT5A, CDH1, CHD7, AXIN2, TWIST1, BCOR, OFD1, PTCH1, PITX2, and PVRL1. The molecular pathways, cellular functions, tissue-specific expression and disease association were investigated using publicly accessible databases (EntrezGene, UniProt, OMIM). The Gene Ontology terms of the biological processes mediated by the candidate genes were used to cluster them using the GOTermMapper (Lewis-Sigler Institute, Princeton University), speculating on six super-clusters: (a) anatomical development, (b) cell division, growth and motility, (c) cell metabolism and catabolism, (d) cell transport, (e) cell structure organization and (f) organ/system-specific processes. This review aims to increase the knowledge on the mechanisms underlying the co-occurrence of tooth agenesis and orofacial clefts, to pave the way for improving targeted (prenatal) molecular diagnosis and finally to reflect on therapeutic or ultimately preventive strategies for these disabling conditions in the future.

| S-EPMC5065589 | biostudies-literature

Brothers in Arms: Structure, Assembly and Function of Arenaviridae Nucleoprotein.

Project description:Arenaviridae is a family of viruses harbouring important emerging pathogens belonging to the Bunyavirales order. Like in other segmented negative strand RNA viruses, the nucleoprotein (NP) is a major actor of the viral life cycle being both (i) the necessary co-factor of the polymerase present in the L protein, and (ii) the last line of defence of the viral genome (vRNA) by physically hiding its presence in the cytoplasm. The NP is also one of the major players interfering with the immune system. Several structural studies of NP have shown that it features two domains: a globular RNA binding domain (NP-core) in its N-terminal and an exonuclease domain (ExoN) in its C-terminal. Further studies have observed that significant conformational changes are necessary for RNA encapsidation. In this review we revisited the most recent structural and functional data available on Arenaviridae NP, compared to other Bunyavirales nucleoproteins and explored the structural and functional implications. We review the variety of structural motif extensions involved in NP-NP binding mode. We also evaluate the major functional implications of NP interactome and the role of ExoN, thus making the NP a target of choice for future vaccine and antiviral therapy.

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Brothers in arms: emerging roles of RNA epigenetics in DNA damage repair.

Project description:N6-methyladenosine (m6A) is a widespread posttranscriptional RNA modification that occurs in tRNA, rRNA, snRNA, viral RNAs, and more recently is shown to occur in mRNA in a dynamic, reversible manner. At the epicenter of RNA epigenetics, m6A influences essentially all stages of RNA metabolism. As a result, m6A modulates cell differentiation and pluripotency, cell cycle and tumorigenesis, and several types of stress responses, etc. A recent report by Shi and colleagues uncovers a novel pathway in which m6A RNA, its associated enzymes, and DNA polymerase ? constitute an early-response system that confers cellular resistance to ultraviolet irradiation, separate from the canonical nucleotide excision repair (NER) pathway that normally repairs UV-induced DNA damage.

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ARMS

Project description:ARMS Raw sequence reads

| PRJNA1062720 | ENA

Comparing treatment fidelity between study arms of a randomized controlled clinical trial for stroke family caregivers.

Project description:ObjectiveTo compare treatment fidelity among treatment arms in the Telephone Assessment and Skill-Building Kit study for stroke caregivers (TASK II) with respect to: 1) protocol adherence; 2) intervention dosage and 3) nurse intervener perspectives.DesignA randomized controlled clinical trial design.SettingUrban, community, midwestern United States.SubjectsA total of 254 stroke caregivers (mean ±SD age, 54.4 ±11.8 years), 55 (22.0%) males and 199 (78.4%) females) randomized to the TASK II intervention (n=123) or an Information, Support, and Referral comparison group (n=131).InterventionsTASK II participants received the TASK II Resource Guide; Information, Support, and Referral participants received a standard caregiver brochure. At approximately 8 weeks after discharge, both groups received 8 weekly calls from a nurse, with a booster call 4 weeks later.MeasuresProtocol adherence was evaluated with the TASK II Checklist for Monitoring Adherence. Intervention dosage was measured by the number of minutes caregivers spent reading materials and talking with the nurse. Nurse intervener perspectives were obtained through focus groups.ResultsProtocol adherence was 80% for the TASK II and 92% for the Information, Support, and Referral. As expected, intervention dosage differed between TASK II and Information, Support, and Referral with respect to caregiver time spent reading materials (t=-6.49; P<.001) and talking with the nurse (t=-7.38; P<.001). Focus groups with nurses yielded further evidence for treatment fidelity and recommendations for future trials.ConclusionsThese findings substantiate treatment fidelity in both study arms of the TASK II stroke caregiver intervention trial (NIH R01NR010388; ClinicalTrials.govNCT01275495).

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Hermansky-Pudlak syndrome in two African-American brothers.

Project description:Hermansky-Pudlak syndrome (HPS) is an autosomal recessive disorder characterized by oculocutaneous albinism, a bleeding disorder, and, in some patients, granulomatous colitis and/or a fatal pulmonary fibrosis. There are eight different subtypes of HPS, each due to mutations in one of eight different genes, whose functions are thought to involve intracellular vesicle formation and trafficking. HPS has been identified in patients of nearly all ethnic groups, though it has primarily been associated with patients of Puerto Rican, Northern European, Japanese and Israeli descent. We report on the diagnosis of HPS type 1 in two African-American patients. Both brothers carried compound heterozygous mutations in HPS1: previously reported p.M325WfsX6 (c.972delC) and a novel silent mutation p.E169E (c.507G > A), which resulted in a splice defect. HPS may be under-diagnosed in African-American patients and other ethnic groups. A history of easy bruising or evidence of a bleeding disorder, combined with some degree of hypopigmentation, should prompt investigation into the diagnosis of HPS.

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Autosomal Recessive ACTG2-Related Visceral Myopathy in Brothers.

Project description:Pediatric intestinal pseudo-obstruction (PIPO) is a heterogeneous condition characterized by impaired gastrointestinal propulsion, a broad clinical spectrum, and variable severity. Several molecular bases underlying primary PIPO have been identified, of which autosomal dominant ACTG2-related visceral myopathy is the most common in both familial or sporadic primary PIPO cases. We present a family with autosomal recessive ACTG2-related disease in which both parents have mild gastrointestinal symptoms and sons have severe PIPO and bladder dysfunction.MethodsClinical genome sequencing was performed on the patients and the mother. Immunohistochemistry was performed on intestinal tissue from the patients to show expression levels of the ACTG2.ResultsGenome sequencing identified a 6.8 kb 2p13.1 loss that includes the ACTG2 gene and a maternally inherited missense variant p.Val10Met in the ACTG2 gene.DiscussionThis case demonstrates that monoallelic hypomorphic ACTG2 variants may underly mild primary gastrointestinal symptoms, while biallelic mild variants can cause severe diseases. The Deletions of the noncoding ACTG2 exon can be an under-recognized cause of mild gastrointestinal symptoms unidentifiable by exome sequencing, explaining some instances of interfamilial variability with an apparent autosomal dominant inheritance. Genome sequencing is recommended as a genetic work-up for primary or idiopathic PIPO because of genetic heterogeneity.

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Empty arms: the effect of the arms trade on mothers and children.

Project description: Not available

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Disulphide bond inhibitors in 2 cancer cell lines

Project description:To elucidate which ER cargo maturation processes may be oxygen dependent, we first reasoned that the transcriptional response may be tailored specifically to counteract the mechanism of the imposed stress. Therefore, we compared the transcriptional regulation of the ERome during anoxic conditions to ER stress caused by lack of glycosylation (tunicamycin) or chaperone inactivation by calcium depletion (thapsigargin)

2013-11-06 | GSE41666 | GEO

Christ-siemens-touraine syndrome: case report of 2 brothers.

Project description:Ectodermal dysplasia is a rare disorder. Christ-Siemens-Touraine syndrome (Hypohidrotic Ectodermal dysplasia (HED)) is a diffuse, non-progressive disease present at birth and involves at least two tissues of ectodermal origin. It is caused by mutation in gene ectodysplasin (EDA, EDA1) located at Xq12-13. Main clinical feature of HED is sparse or absent eccrine gland as well as hypotrichosis, nail, and teeth abnormality with characteristic faces. The absence or diminished activity of sweat gland results in patients having more chances of developing hyperthermia and with intolerance to warm environment. Most do well with simple measures such as wet clothes, air conditioning, wet bands etc. We present cases of two brothers, born of non-consanguineous marriage, who presented to us with complaints of heat intolerance and abnormal facial features.

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