Miracle-dz/UniFAR-FTUs huggingface dataset:
Food Insecurity and Common Mental Disorders among Ethiopian Youth: Structural Equation Modeling

Background Although the consequences of food insecurity on physical health and nutritional status of youth living have been reported, its effect on their mental health remains less investigated in developing countries. The aim of this study was to examine the pathways through which food insecurity is associated with poor mental health status among youth living in Ethiopia. Methods We used data from Jimma Longitudinal Family Survey of Youth (JLFSY) collected in 2009/10. A total of 1,521 youth were included in the analysis. We measured food insecurity using a 5-items scale and common mental disorders using the 20-item Self-Reporting Questionnaire (SRQ-20). Structural and generalized equation modeling using maximum likelihood estimation method was used to analyze the data. Results The prevalence of common mental disorders was 30.8% (95% CI: 28.6, 33.2). Food insecurity was independently associated with common mental disorders (β = 0.323, P<0.05). Most (91.8%) of the effect of food insecurity on common mental disorders was direct and only 8.2% of their relationship was partially mediated by physical health. In addition, poor self-rated health (β = 0.285, P<0.05), high socioeconomic status (β = -0.076, P<0.05), parental education (β = 0.183, P<0.05), living in urban area (β = 0.139, P<0.05), and female-headed household (β = 0.192, P<0.05) were associated with common mental disorders. Conclusions Food insecurity is directly associated with common mental disorders among youth in Ethiopia. Interventions that aim to improve mental health status of youth should consider strategies to improve access to sufficient, safe and nutritious food.
Sinking, swimming and sailing: experiences of job satisfaction and emotional exhaustion in child welfare employees

The authors conducted a mixed-method study after a previous study of child welfare employees revealed a subgroup exhibiting surprisingly high levels of both emotional exhaustion (EE) and job satisfaction (JS). This subgroup included direct service workers, supervisors and managers. As these findings appeared to conflict with previous studies, we re-reviewed the literature and undertook the current study to account for the co-existence of EE and JS. We explored and compared this subgroup with two others: workers who found their work satisfying without experiencing high levels of EE and those whose high levels of EE were associated with low JS. Using a survey that included several standardized measures with 226 employees and semi-structured interviews with a criteria-based subsample of 25, we explored the role that personality, career expectations, coping styles, stage of life, education, gender and social networks play in outcomes for individual employees. Analyses of quantitative and qualitative data yielded a profile for each subgroup, offering insights into the subjective experiences of workers within individual, social and organizational contexts. These findings have implications for recruitment, training and support of child welfare workers.
An empirical examination of job stress and management of emotionally-based behavior: Frontline social service personnel perspective

Frontline service personnel (FSP) play an invaluable role in the marketing mix by directly influencing the customer’s perception of both the service organization as well as the service quality during the face-to-face delivery service encounter (Ashforth & Humphrey 1993). The purpose of this dissertation is to examine how sources of job stress for FSP such as perceived customer demands, role ambiguity, role conflict, role overload, and emotional labor and various mediators such as job autonomy, emotional intelligence, and emotion-focused coping directly and indirectly influence job stress and outcome variables such as attitudes, behaviors, physical consequences, emotional exhaustion, job performance, and intentions. Research from frontline social service personnel’s (FSSP) perspective was collected in three phases: 1) eight personal in-depth interviews to determine the fit of the constructs in the model in a social service environment, 2) a cognitive response survey gathered from 86 FSSP to identify appropriate line items, and 3) a survey questionnaire gathered from 533 members of the National Association of Social Workers-Florida.
Dapagliflozin suppresses glucagon signaling in rodent models of diabetes

Significance Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower blood glucose in humans with diabetes. These drugs inhibit the reabsorption of glucose in the kidney, resulting in its urine excretion. It was reported that SGLT2 inhibitors increase the secretion of glucagon and increase endogenous glucose production by the liver. These effects would elevate blood glucose, counteracting the effect of urinary glucose loss. Here we show in a rodent model of type 1 diabetes that the SGLT2 inhibitor dapagliflozin inhibited the secretion of glucagon from the pancreas. In two rodent models of severe type 2 diabetes, livers from animals treated with dapagliflozin showed decreased glucagon signaling and had reduced expression of the glucagon receptor. Our results suggest dapagliflozin lowers blood glucose concentrations in diabetic animals in part through inhibiting hepatic glucagon signaling. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a class of antidiabetic drug used for the treatment of diabetes. These drugs are thought to lower blood glucose by blocking reabsorption of glucose by SGLT2 in the proximal convoluted tubules of the kidney. To investigate the effect of inhibiting SGLT2 on pancreatic hormones, we treated perfused pancreata from rats with chemically induced diabetes with dapagliflozin and measured the response of glucagon secretion by alpha cells in response to elevated glucose. In these type 1 diabetic rats, glucose stimulated glucagon secretion by alpha cells; this was prevented by dapagliflozin. Two models of type 2 diabetes, severely diabetic Zucker rats and db/db mice fed dapagliflozin, showed significant improvement of blood glucose levels and glucose disposal, with reduced evidence of glucagon signaling in the liver, as exemplified by reduced phosphorylation of hepatic cAMP-responsive element binding protein, reduced expression of phosphoenolpyruvate carboxykinase 2, increased hepatic glycogen, and reduced hepatic glucose production. Plasma glucagon levels did not change significantly. However, dapagliflozin treatment reduced the expression of the liver glucagon receptor. Dapagliflozin in rodents appears to lower blood glucose levels in part by suppressing hepatic glucagon signaling through down-regulation of the hepatic glucagon receptor.
Negative Checkpoint Regulatory Molecule 2B4 (CD244) Upregulation Is Associated with Invariant Natural Killer T Cell Alterations and Human Immunodeficiency Virus Disease Progression

The CD1d-restricted invariant natural killer T (iNKT) cells are implicated in innate immune responses against human immunodeficiency virus (HIV). However, the determinants of cellular dysfunction across the iNKT cells subsets are seldom defined in HIV disease. Herein, we provide evidence for the involvement of the negative checkpoint regulator (NCR) 2B4 in iNKT cell alteration in a well-defined cohort of HIV-seropositive anti-retroviral therapy (ART) naïve, ART-treated, and elite controllers (ECs). We report on exaggerated 2B4 expression on iNKT cells of HIV-infected treatment-naïve individuals. In sharp contrast to CD4−iNKT cells, 2B4 expression was significantly higher on CD4+ iNKT cell subset. Notably, an increased level of 2B4 on iNKT cells was strongly correlated with parameters associated with HIV disease progression. Further, iNKT cells from ART-naïve individuals were defective in their ability to produce intracellular IFN-γ. Together, our results suggest that the levels of 2B4 expression and the downstream co-inhibitory signaling events may contribute to impaired iNKT cell responses.
Quantitative methods in syntax/semantics research: A response to Sprouse and Almeida (2013)

Sprouse and Almeida (S&A) present quantitative results that suggest that intuitive judgments utilised in syntax research are generally correct in two-condition comparisons: the sentence type that is presented as “good/grammatical” is usually rated better than the sentence type that is presented as “bad/ungrammatical” in controlled experiments. Although these evaluations of intuitive relative judgments are valuable, they do not justify the use of nonquantitative linguistic methods. We argue that objectivity is a universal value in science that should be adopted by linguistics. In addition, the reliability measures that S&A report are not sufficient for developing sophisticated linguistic theories. Furthermore, quantitative methods yield two additional benefits: consistency of judgments across many pairs of judgments; and an understanding of the relative effect sizes across sets of judgments. We illustrate these points with an experiment that demonstrates five clear levels of acceptability. Finally, we observe that S&A's experiments—where only two authors evaluated 10 years' worth of journal articles and one standard textbook within a few months—further emphasise one of our critical original points: conducting behavioural experiments is in many respects easy and fast with the advent of online research tools like Amazon's Mechanical Turk. Given the current ease of performing quantitative experiments (using a platform like Mechanical Turk) and the clear limitations of not doing so, linguistic hypotheses should be evaluated quantitatively whenever it is feasible.
In ̄ uence of the ® nite ionospheric conductivity on dispersive , nonradiative ® eld line resonances

The in ̄uence of the ®nite ionospheric conductivity on the structure of dispersive, nonradiative ®eld line resonances (FLRs) is investigated for the ®rst four odd harmonics. The results are based on a linear, magnetically incompressible, reduced, twōuid MHD model. The model includes eects of ®nite electron inertia (at low altitude) and ®nite electron pressure (at high altitude). The ionosphere is treated as a highintegrated conducting substrate. The results show that even very low ionospheric conductivity (RP  2 mho) is not sucient to prevent the formation of a largeamplitude, small-scale, nonradiative FLR for the third and higher harmonics when the background transverse plasma inhomogeneity is strong enough. At the same time, the fundamental FLR is strongly aected by a state of low conductivity, and when RP  2 mho, this resonance forms only small-amplitude, relatively broad electromagnetic disturbance. The dierence in conductivities of northern and southern ionospheres does not produce signi®cant asymmetry in the distribution of electric and magnetic ®elds along the resonant ®eld line. The transverse gradient of the background AlfveÂ n speed plays an important role in structure of the FLR when the ionospheric conductivity is ®nite. In cases where the transverse inhomogeneity of the plasma is not strong enough, the low ionospheric conductivity can prevent even higher-harmonic FLRs from contracting to small scales where dispersive eects are important. The application of these results to the formation and temporal evolution of small-scale, active auroral arc forms is discussed.
Impairment of Catecholamine Systems during Induction of Long-Term Potentiation at Hippocampal CA1 Synapses in HPC-1/Syntaxin 1A Knock-out Mice

The membrane protein HPC-1/syntaxin 1A is believed to play a key role in synaptic vesicle exocytosis, and it was recently suggested to be required for synaptic plasticity. Despite evidence for the function of HPC-1/syntaxin 1A in synaptic plasticity, the underlying cellular mechanism is unclear. We found that although fast synaptic transmission and long-term depression were unaffected, HPC-1/syntaxin 1A knock-out (STX1A−/−) mice showed impaired long-term potentiation (LTP) in response to theta-burst stimulation in CA1 hippocampal slices. The impairment in LTP was rescued by the application of forskolin, an adenylyl cyclase activator, or more robust stimulation, suggesting that cAMP/protein kinase A signaling was suppressed in these mice. In addition, catecholamine release from the hippocampus was significantly reduced in STX1A−/− mice. Because HPC-1/syntaxin 1A regulates exocytosis of dense-core synaptic vesicles, which contain neuromodulatory transmitters such as noradrenaline, dopamine and 5-HT, we examined the effect of neuromodulatory transmitters on LTP induction. Noradrenaline and dopamine enhanced LTP induction in STX1A−/− mice, whereas catecholamine depletion reduced LTP induction in wild-type mice. Theses results suggest that HPC-1/syntaxin 1A regulates catecholaminergic systems via exocytosis of dense-core synaptic vesicles, and that deletion of HPC-1/syntaxin 1A causes impairment of LTP induction.
Effect of Probe-Site Mismatches on Detection of Virulent Newcastle Disease Viruses Using a Fusion-Gene Real-Time Reverse Transcription Polymerase Chain Reaction Test

Virulent forms of Newcastle disease virus (NDV) are a major concern for poultry producers around the world and the rapid diagnosis of an outbreak is crucial to any control program. A validated real-time reverse transcription-PCR test (fusion test) directed at the fusion-cleavage site of NDV was developed to differentiate virulent Newcastle disease virus strains from those of low virulence, however one virulent isolate, Dove/Italy/2736/2000, escaped detection during the initial evaluation of the test. The objectives of this study were to determine how this isolate differed from other detectable isolates, to identify other isolates that may fail detection, and to characterize the effect of specific probe-site mutations on the fusion test at a range of annealing temperatures. Using a virulent NDV isolate (Game fowl/US(CA)/2002) as a backbone that has 100% identity to the fusion-test probe, specific changes were made to the fusion-test probe-site to reflect the unique mismatches found in Dove/Italy/2736/2000 and other selected regions of the probe. Mutated clones with mismatches unique to Dove/Italy/2736/2000 at positions 6, 13, and 14 were not detected until annealing temperatures were lowered to 50°C. Those detected at 58°C contained 1–2 mismatches (position 1 and 6, 13 and 14, or 14 only) although increased cycle threshold values compared to the parent clone indicated decreased sensitivity. Data from this study predicts that the fusion test may fail to detect some viruses among lineage 4b and potential solutions to identify this subset of viruses include lowering the annealing temperature or modifying the probe.
Do depression symptoms predict early hypertension incidence in young adults in the CARDIA study? Coronary Artery Risk Development in Young Adults.

BACKGROUND Hypertension has been linked to several psychological factors, including depression, but the relation between hypertension incidence and depressive symptoms has not been adequately examined. OBJECTIVE To determine if depressive symptoms independently predict hypertension incidence. DESIGN AND SETTING A prospective, multicenter, epidemiological cohort of young adults (aged 23-35 years at study entry) from the general community without hypertension followed up for 5 years. SUBJECTS A sample of 3343 adults from 4 urban areas stratified for race (black and white) from the CARDIA (Coronary Artery Risk Development in Young Adults) study. MAIN OUTCOME MEASURE Hypertension incidence, which was defined as blood pressure higher than 160/95 mm Hg (assessed on a single occasion) or the use of prescribed antihypertensive medication. RESULTS Participants with high scores (> or = 16) on the Center for Epidemiological Studies Depression (CES-D) Scale were at significant risk for hypertension incidence compared with those with low CES-D scores (< or =7; odds ratio, 2.10; 95% confidence interval, 1.22-3.61) after adjustment for other hypertension risk factors (eg, age, resting systolic blood pressure at the 5-year examination, physical activity, daily alcohol use, parental history of hypertension, education, presence of diabetes mellitus or heart disease, sex, and race) in fixed logistic models. Those with intermediate depressive symptoms (CES-D scores 8-15) were also at significant risk (adjusted odds ratio, 1.78; 95% confidence interval, 1.06-2.98). These associations were significant in blacks alone but were not found in whites, who had a lower hypertension incidence (29 [2%] of 1806) than blacks (89 [6%] of 1537). CONCLUSIONS Depressive symptoms were predictive of later hypertension incidence in young adults, and young blacks with depressive symptoms were at high risk of developing hypertension.
Autosomal Dominant Distal Renal Tubular Acidosis Is Associated in Three Families with Heterozygosity for the R589H Mutation in the AE1 (Band 3) Cl−/HCO3 −Exchanger*

Distal renal tubular acidosis (dRTA) is characterized by defective urinary acidification by the distal nephron. Cl−/HCO3 − exchange mediated by the AE1 anion exchanger in the basolateral membrane of type A intercalated cells is thought to be an essential component of lumenal H+ secretion by collecting duct intercalated cells. We evaluated the AE1 gene as a possible candidate gene for familial dRTA. We found in three unrelated families with autosomal dominant dRTA that all clinically affected individuals were heterozygous for a single missense mutation encoding the mutant AE1 polypeptide R589H. Patient red cells showed ∼20% reduction in sulfate influx of normal 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid sensitivity and pH dependence. Recombinant kidney AE1 R589H expressed in Xenopus oocytes showed 20–50% reduction in Cl−/Cl− and Cl−/HCO3 − exchange, but did not display a dominant negative phenotype for anion transport when coexpressed with wild-type AE1. One apparently unaffected individual for whom acid-loading data were unavailable also was heterozygous for the mutation. Thus, in contrast to previously described heterozygous loss-of-function mutations in AE1 associated with red cell abnormalities and apparently normal renal acidification, the heterozygous hypomorphic AE1 mutation R589H is associated with dominant dRTA and normal red cells.
Carbamylated erythropoietin is neuroprotective in an experimental model of traumatic brain injury

Objective:The well-documented neuroprotective effects of recombinant human erythropoietin (rhEPO) are commonly associated with untoward erythrocyte-stimulating effects (polycythemia), with subsequent risk of thromboembolic complications. A carbamylated-rhEPO (CEPO) derivative, which is neuroprotective but lacks hematopoietic activity, has been recently developed. In this study, we evaluated the neuroprotective capability of CEPO in an in vitro model of cerebral trauma in which rhEPO was previously shown to reduce posttraumatic cell death. Design:Prospective, controlled experiment. Setting:Animal, basic science laboratory. Subjects:Wistar rats, 8 days old. Interventions:Organotypic hippocampal slices, obtained from rat brains, were subjected to a well-characterized model of mechanical injury followed by addition of 10 IU/mL rhEPO, 10–100 IU/mL CEPO, or vehicle (injured control) to the incubation medium at different times to assess the temporal window of therapeutic neuroprotection. Measurements and Main Results:Posttraumatic cell death was quantified at 12, 24, or 48 hrs after injury by measuring propidium iodide fluorescence in the selectively vulnerable CA1 hippocampal area. Posttraumatic injury, observed in injured, vehicle-treated hippocampal slices, was significantly attenuated by addition of either 10 IU/mL rhEPO or 10 IU/mL CEPO. The neuroprotective efficacy of 10 IU/mL rhEPO or CEPO remained intact even when administration was delayed 1 hr after trauma. Qualitative microscopy in semithin sections showed that both rhEPO and CEPO exerted a marked pyramidal neuron-sparing effect. Conclusion:Our study shows that 10 IU/mL CEPO exerts neuroprotective effects comparable with those of rhEPO in an in vitro model of mechanical cerebral trauma. Because CEPO lacks hematopoietic effects and seems to possess a prolonged therapeutic time window, this erythropoietin derivative may represent an exciting new pharmacologic tool in treating patients with mechanical injury to the brain.
NGF promotes cell cycle progression by regulating D-type cyclins via PI3K/Akt and MAPK/Erk activation in human corneal epithelial cells

Purpose Nerve growth factor (NGF) plays an important role in promoting the healing of corneal wounds. However, the molecular mechanism by which NGF functions is unknown. We investigated the possible effects of NGF on phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and mitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (Erk) pathways and cell growth in human corneal epithelial cells (HCECs). Methods We examined the effect of NGF on cell cycle and proliferation in HCECs by flow cytometry and cell proliferation assay, respectively. The levels of D-type cyclins in NGF-treated HCECs were determined by western blot. The tyrosine kinase A (TrkA), PI3K/Akt and MAPK/Erk pathways were then checked in cells stimulated with NGF for different time periods or cells undergoing a dose-dependent treatment. Furthermore, HCECs were treated with pathway inhibitors, LY294002 or PD98059, to confirm NGF-induced activations. Results We found that NGF had a positive effect on the growth of HCECs, and D-type cyclins, and it was correlated with the percentage of the G1 to S progression. We also observed a time-dependent and dose-dependent effect of NGF on the PI3K/Akt and MAPK/Erk pathways. Furthermore, NGF affected cell cycle progression of HCECs by regulating cyclin D through Akt and Erk activation upon treatment with the pathway inhibitors, LY294002 for Akt or PD98059 for Erk pathways. Conclusions NGF stimulation could promote cell proliferation and cell cycle progression of HCECs by activation of cyclin D via the PI3K/Akt and MAPK/Erk signaling pathways.
Electrosprayed Metal Oxide Semiconductor Films for Sensitive and Selective Detection of Hydrogen Sulfide

Semiconductor metal oxide films of copper-doped tin oxide (Cu-SnO2), tungsten oxide (WO3) and indium oxide (In2O3) were deposited on a platinum coated alumina substrate employing the electrostatic spray deposition technique (ESD). The morphology studied with scanning electron microscopy (SEM) and atomic force microscopy (AFM) shows porous homogeneous films comprising uniformly distributed aggregates of nano particles. The X-ray diffraction technique (XRD) proves the formation of crystalline phases with no impurities. Besides, the Raman cartographies provided information about the structural homogeneity. Some of the films are highly sensitive to low concentrations of H2S (10 ppm) at low operating temperatures (100 and 200 °C) and the best response in terms of Rair/Rgas is given by Cu-SnO2 films (2500) followed by WO3 (1200) and In2O3 (75). Moreover, all the films exhibit no cross-sensitivity to other reducing (SO2) or oxidizing (NO2) gases.