Psychometric Evaluation of the Arabic Version of the Spiritual Well-Being Scale on a Sample of Jordanian Arab Christians

This paper assesses the psychometric properties of the Arabic version of the Spiritual Well-Being Scale (SWBS) in an Arab Christian sample by analyzing its internal structure. A convenience sample of 340 Arab Christians was recruited from the adult community population of northern Jordan. Data were collected through a self-completion, anonymous questionnaire distributed through church and community groups. Principal Components factor analysis, non-parametric bivariate statistics, and Cronbach's alpha were used to assess the psychometric properties of the total scale and its subscales. The findings broadly supported the factor structure of the SWBS in other Arab samples in that the scale consists of three factors, representing positive existential well-being, affiliation, and alienation subscales. In conclusion, these preliminary findings suggest that the Arabic version of the SWBS can be used as an instrument to measure levels of spiritual well-being in Arab Christian populations. </jats:p

Regulated functional alternative splicing in Drosophila

Alternative splicing expands the coding capacity of metazoan genes, and it was largely genetic studies in the fruit-fly Drosophila melanogaster that established the principle that regulated alternative splicing results in tissue- and stage-specific protein isoforms with different functions in development. Alternative splicing is particularly prominent in germ cells, muscle and the central nervous system where it modulates the expression of various proteins including cell-surface molecules and transcription factors. Studies in flies have given us numerous insights into alternative splicing in terms of upstream regulation, the exquisite diversity of their forms and the key differential cellular functions of alternatively spliced gene products. The current inundation of transcriptome sequencing data from Drosophila provides an unprecedented opportunity to gain a comprehensive view of alternative splicing

Variants in STXBP3 are Associated with Very Early Onset Inflammatory Bowel Disease, Bilateral Sensorineural Hearing Loss and Immune Dysregulation

Background and aims: Very early onset inflammatory bowel disease [VEOIBD] is characterized by intestinal inflammation affecting infants and children less than 6 years of age. To date, over 60 monogenic aetiologies of VEOIBD have been identified, many characterized by highly penetrant recessive or dominant variants in underlying immune and/or epithelial pathways. We sought to identify the genetic cause of VEOIBD in a subset of patients with a unique clinical presentation. Methods: Whole exome sequencing was performed on five families with ten patients who presented with a similar constellation of symptoms including medically refractory infantile-onset IBD, bilateral sensorineural hearing loss and, in the majority, recurrent infections. Genetic aetiologies of VEOIBD were assessed and Sanger sequencing was performed to confirm novel genetic findings. Western analysis on peripheral blood mononuclear cells and functional studies with epithelial cell lines were employed. Results: In each of the ten patients, we identified damaging heterozygous or biallelic variants in the Syntaxin-Binding Protein 3 gene [STXBP3], a protein known to regulate intracellular vesicular trafficking in the syntaxin-binding protein family of molecules, but not associated to date with either VEOIBD or sensorineural hearing loss. These mutations interfere with either intron splicing or protein stability and lead to reduced STXBP3 protein expression. Knock-down of STXBP3 in CaCo2 cells resulted in defects in cell polarity. Conclusion: Overall, we describe a novel genetic syndrome and identify a critical role for STXBP3 in VEOIBD, sensorineural hearing loss and immune dysregulation.info:eu-repo/semantics/publishedVersio

Para que servem os inventários de fauna?

Inventários de fauna acessam diretamente a diversidade de uma localidade, em um determinado espaço e tempo. Os dados primários gerados pelos inventários compõem uma das ferramentas mais importantes na tomada de decisões a respeito do manejo de áreas naturais. Entretanto, vários problemas têm sido observados em diversos níveis relacionados aos inventários de fauna no Brasil e vão desde a formação de recursos humanos até a ausência de padronização, de desenho experimental e de seleção de métodos inadequados. São apresentados estudos de caso com mamíferos, répteis, anfíbios e peixes, nos quais são discutidos problemas como variabilidade temporal e métodos para detecção de fauna terrestre, sugerindo que tanto os inventários quanto os programas de monitoramento devam se estender por prazos maiores e que os inventários devem incluir diferentes metodologias para que os seus objetivos sejam plenamente alcançados.Inventories of fauna directly access the diversity of a locality in a certain period of time. The primary data generated by these inventories comprise one of the most important steps in decisions making regarding the management of natural areas. However, several problems have been observed at different levels related to inventories of fauna in Brazil, and range from the training of humans to the lack of standardization of experimental design and selection of inappropriate methods. We present case studies of mammals, reptiles, amphibians and fishes, where they discussed issues such temporal variability and methods for detection of terrestrial fauna, suggesting that both inventories and monitoring programs should be extended for longer terms and that inventories should include different methodologies to ensure that their goals are fully achieved

Design and development of a peptide-based adiponectin receptor agonist for cancer treatment

<p>Abstract</p> <p>Background</p> <p>Adiponectin, a fat tissue-derived adipokine, exhibits beneficial effects against insulin resistance, cardiovascular disease, inflammatory conditions, and cancer. Circulating adiponectin levels are decreased in obese individuals, and this feature correlates with increased risk of developing several metabolic, immunological and neoplastic diseases. Thus, pharmacological replacement of adiponectin might prove clinically beneficial, especially for the obese patient population. At present, adiponectin-based therapeutics are not available, partly due to yet unclear structure/function relationships of the cytokine and difficulties in converting the full size adiponectin protein into a viable drug.</p> <p>Results</p> <p>We aimed to generate adiponectin-based short peptide that can mimic adiponectin action and be suitable for preclinical and clinical development as a cancer therapeutic. Using a panel of 66 overlapping 10 amino acid-long peptides covering the entire adiponectin globular domain (residues 105-254), we identified the 149-166 region as the adiponectin active site. Three-dimensional modeling of the active site and functional screening of additional 330 peptide analogs covering this region resulted in the development of a lead peptidomimetic, ADP 355 (H-DAsn-Ile-Pro-Nva-Leu-Tyr-DSer-Phe-Ala-DSer-NH₂). In several adiponectin receptor-positive cancer cell lines, ADP 355 restricted proliferation in a dose-dependent manner at 100 nM-10 μM concentrations (exceeding the effects of 50 ng/mL globular adiponectin). Furthermore, ADP 355 modulated several key signaling pathways (AMPK, Akt, STAT3, ERK1/2) in an adiponectin-like manner. siRNA knockdown experiments suggested that ADP 355 effects can be transmitted through both adiponectin receptors, with a greater contribution of AdipoR1. <it>In vivo</it>, intraperitoneal administration of 1 mg/kg/day ADP 355 for 28 days suppressed the growth of orthotopic human breast cancer xenografts by ~31%. The peptide displayed excellent stability (at least 30 min) in mouse blood or serum and did not induce gross toxic effects at 5-50 mg/kg bolus doses in normal CBA/J mice.</p> <p>Conclusions</p> <p>ADP 355 is a first-in-class adiponectin receptor agonist. Its biological activity, superior stability in biological fluids as well as acceptable toxicity profile indicate that the peptidomimetic represents a true lead compound for pharmaceutical development to replace low adiponectin levels in cancer and other malignancies.</p

Asymptotic behavior of solutions to the σk\sigma_k-Yamabe equation near isolated singularities

$\sigma_k$-Yamabe equations are conformally invariant equations generalizing the classical Yamabe equation. In an earlier work YanYan Li proved that an admissible solution with an isolated singularity at $0\in \mathbb R^n$ to the $\sigma_k$-Yamabe equation is asymptotically radially symmetric. In this work we prove that an admissible solution with an isolated singularity at $0\in \mathbb R^n$ to the $\sigma_k$-Yamabe equation is asymptotic to a radial solution to the same equation on $\mathbb R^n \setminus \{0\}$. These results generalize earlier pioneering work in this direction on the classical Yamabe equation by Caffarelli, Gidas, and Spruck. In extending the work of Caffarelli et al, we formulate and prove a general asymptotic approximation result for solutions to certain ODEs which include the case for scalar curvature and $\sigma_k$ curvature cases. An alternative proof is also provided using analysis of the linearized operators at the radial solutions, along the lines of approach in a work by Korevaar, Mazzeo, Pacard, and Schoen.Comment: 55 page

Human malarial disease: a consequence of inflammatory cytokine release

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease