Miracle-dz/UniFAR-FTUs huggingface dataset:
Maternal support during the first year of infancy.

BACKGROUND Mental health problems among children and adolescents are becoming more visible and some research indicates that they are increasing. Several studies suggest that social support counteracts the increasing risk of ill-health in families with children. However, there is a lack of studies which focus on the support that expectant mothers and parents might need. AIM The aim of the study was to describe mothers' experiences of pregnancy, labour and homecoming, support needs, and sources of support in their role as parents. METHODS One hundred and twenty-two mothers participated in the study by answering a questionnaire consisting of 37 questions. Data were analysed using descriptive statistics, chi-square tests and content analysis. FINDINGS Mothers of infants had a great need to talk about their experiences of labour soon afterwards and over the following months. Most of the mothers had generally received support from their partners. However, in some situations, other people in their networks, and maternity and child health services had been more supportive than partners. DISCUSSION The study highlights how important it is for expectant mothers and new mothers to be confirmed in their mothering role. Nurses in the maternity and child health services have an important task to support people in becoming and being parents, with regard to their emotional state. There is a need for more resources within these services for establishing parent groups, including groups for fathers. This could improve parents' physical, psychological and emotional health, and decrease their need for health and social services.
Comparison of Effects of Nitric Oxide Synthase (NOS) Inhibitors on Plasma Nitrite/Nitrate Levels and Tissue NOS Activity in Septic Organs

An excessive production of nitric oxide (NO) by NO synthase (NOS) is considered to contribute to circulatory disturbance, tissue damage, and refractory hypotention, which are often observed in septic disorders. It is anticipated that a selective inducible NOS (iNOS) inhibitor with excellent pharmacokinetics may be potentially effective as a novel and potent therapeutic intervention in sepsis. We examined whether or not a selective iNOS inhibitor shows iNOS selectivity at the tissue level, when administered systemically. The effects of four NOS inhibitors on plasma nitrite/nitrate (NOx) and tissue NOS levels were compared in major organs (lungs, liver, heart, kidneys, and brain) 6 hr after the injection of E. coli lipopolysaccharide (LPS) into male Wistar‐King rats. The rats treated with the three iNOS inhibitors (N‐(3‐(aminomethyl)benzyl)acetamidine (1400W), (1S, 5S, 6R, 7R)‐2‐aza‐7‐chloro‐3‐imino‐5‐methylbicyclo [4.1. 0] heptane hydrochloride (ONO‐1714), and aminoguanidine) administered 1 hr after LPS injection, showed dose‐dependent decreases in plasma NOx levels and NOS activity in the lungs. The non‐selective NOS inhibitor (NG‐methyl‐L‐arginine (L‐NMMA)) had an effect only at the maximum dose. The differences in in vitro iNOS selectivity among these drugs did not correlate with iNOS selectivity at the tissue level. The relationship between plasma NOx levels and NOS activity in the lungs showed a linear relationship with or without the NOS inhibitors. In conclusion, the iNOS selectivity of these drugs does not seem to differ at the tissue level. Plasma NOx levels may be a useful indicator of lung NOS activity.
Comparing the Usage Behavior and the Continuance Intention of Mobile Internet Services

While behavioral researches in IS literature have largely employed intention-based models to predict usage behavior, few research have tried to explore the difference between intention and behavior. This study attempts to fill in this gap by proposing a comprehensive theoretical framework and comparing antecedents' prediction of intention and usage behavior in the same framework. The theoretical framework incorporates rational factors such as cognitive, affective, judgmental components as well as an automatic factor like habit into the research model. Based on the same framework, usage behavior and continuance intention model are developed and compared in the context of mobile Internet services. Through comparison of two models, the comprehensive framework is proposed to be more suitable in predicting usage behavior than continuance intention. By identifying the different influences of determinants which drive usage behavior and continuance intention, the results of this study have thus helped advance IS theory and offered insights for mobile Internet services practitioners.
Is there sufficient evidence regarding signage-based stair use interventions? A sequential meta-analysis

Objective The proliferation of studies using motivational signs to promote stair use continues unabated, with their oft-cited potential for increasing population-level physical activity participation. This study examined all stair use promotional signage studies since 1980, calculating pre-estimates and post-estimates of stair use. The aim of this project was to conduct a sequential meta-analysis to pool intervention effects, in order to determine when the evidence base was sufficient for population-wide dissemination. Design Using comparable data from 50 stair-promoting studies (57 unique estimates) we pooled data to assess the effect sizes of such interventions. Results At baseline, median stair usage across interventions was 8.1%, with an absolute median increase of 2.2% in stair use following signage-based interventions. The overall pooled OR indicated that participants were 52% more likely to use stairs after exposure to promotional signs (adjusted OR 1.52, 95% CI 1.37 to 1.70). Incremental (sequential) meta-analyses using z-score methods identified that sufficient evidence for stair use interventions has existed since 2006, with recent studies providing no further evidence on the effect sizes of such interventions. Conclusions This analysis has important policy and practice implications. Researchers continue to publish stair use interventions without connection to policymakers' needs, and few stair use interventions are implemented at a population level. Researchers should move away from repeating short-term, small-scale, stair sign interventions, to investigating their scalability, adoption and fidelity. Only such research translation efforts will provide sufficient evidence of external validity to inform their scaling up to influence population physical activity.
Ubc9 and Protein Inhibitor of Activated STAT 1 Activate Chicken Ovalbumin Upstream Promoter-Transcription Factor I-mediated Human CYP11B2 Gene Transcription*

Aldosterone synthase (CYP11B2) is involved in the final steps of aldosterone biosynthesis and expressed exclusively in the adrenal zona glomerulosa cells. Using an electrophoretic mobility shift assay, we demonstrate that COUP-TFI binds to the –129/–114 element (Ad5) of human CYP11B2 promoter. Transient transfection in H295R adrenal cells demonstrated that COUP-TFI enhanced CYP11B2 reporter activity. However, the reporter construct with mutated Ad5 sequences showed reduced basal and COUP-TFI-enhanced activity, suggesting that binding of COUP-TFI to Ad5 is important for CYP11B2 transactivation. To elucidate molecular mechanisms of COUP-TFI-mediated activity, we subsequently screened for COUP-TFI-interacting proteins from a human adrenal cDNA library using a yeast two-hybrid system and identified Ubc9 and PIAS1, which have small ubiquitin-related modifier-1 (SUMO-1) conjugase and ligase activities, respectively. The coimmunoprecipitation assays confirmed that COUP-TFI forms a complex with Ubc9 and PIAS1 in mammalian cells. Immunohistochemistry showed that Ubc9 and PIAS1 are markedly expressed in rat adrenal glomerulosa cells. Coexpression of Ubc9 and PIAS1 synergistically enhanced the COUP-TFI-mediated CYP11B2 reporter activity, indicating that both proteins function as coactivators of COUP-TFI. However, sumoylation-defective mutants, Ubc9 (C93S) and PIAS1 (C351S), continued to function as coactivators of COUP-TFI, indicating that sumoylation activity are separable from coactivator ability. In addition, chromatin immunoprecipitation assays demonstrated that ectopically expressed COUP-TFI, Ubc9, and PIAS1 were recruited to an endogenous CYP11B2 promoter. Moreover, reduction of Ubc9 or PIAS1 protein levels by small interfering RNA inhibited the CYP11B2 transactivation by COUP-TFI. Our data support a physiological role of Ubc9 and PIAS1 as transcriptional coactivators in COUP-TFI-mediated CYP11B2 transcription.
Minocycline Exerts Multiple Inhibitory Effects on Vascular Endothelial Growth Factor–Induced Smooth Muscle Cell Migration: The Role of ERK1/2, PI3K, and Matrix Metalloproteinases

Widely used tetracycline antibiotics affect many cellular functions relevant to human vascular disease including cell proliferation, migration, and matrix remodeling. We examined whether minocycline inhibited human aortic smooth muscle cell (HASMC) migration induced by vascular endothelial growth factor (VEGF). After the establishment of an optimal dose, minocycline treated HASMC were exposed to VEGF. HASMC migration, matrix metalloproteinase (MMP)-2 and MMP-9 activities, mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K) phosphorylation were determined by smooth muscle cell (SMC) invasion assay, real-time polymerase chain reaction, zymograms, and Western blot analysis, respectively. We demonstrated that VEGF and platelet-derived growth factor (PDGF)-induced SMC migration in a dose-dependent manner. MMP-9, but not MMP-2, mRNA was increased during VEGF stimulation. MMP-9 activity was increased from 1.5- to 2.5-fold in a dose-dependent manner (P<0.05). Both ERK1/2 and PI3K/AKt pathways were activated during VEGF-induced HASMCs migration. We then demonstrated that minocycline can inhibit VEGF-induced HASMC migration (P<0.05). The effects may be through the inhibition of MMP-9 mRNA transcription, protein activities and downregulation of ERK1/2 and PI3K/Akt pathway phosphorylation. Our results indicated that minocycline exerts multiple effects on VEGF-induced SMC migration, including inhibition of MMP-9 mRNA transcription and protein activities and downregulating ERK1/2 and PI3K signal pathways, suggesting minocycline may be a potentially therapeutic approach to inhibit disease process induced angiogenesis.
Population Pharmacokinetics of Mycophenolic Acid and Metabolites in Patients With Glomerulonephritis

Mycophenolic acid (MPA) is an inosine monophosphate dehydrogenase inhibitor used for glomerulonephritis treatment. The objective of the current study was to develop a population pharmacokinetic model for MPA and metabolites in glomerulonephritis to enable appropriate design of MPA regimens in these patients with alterations in kidney structure and function. Thirty-nine patients with glomerulonephritis and receiving mycophenolate mofetil were recruited to participate in a 24-hour pharmacokinetic study. Blood was collected at times 0, 0.5, 1.0, 1.5, 2, 3, 4, 6, 8, 12, and 24 hours and urine was collected over the intervals of 0 to 6, 6 to 12, and 12 to 24 hours. Plasma and urine samples were assayed for MPA and MPA glucuronide (MPAG) by high-performance liquid chromatography and for acyl-MPA glucuronide (AcMPAG) by liquid chromatography/mass spectrometry. Population pharmacokinetic analysis and covariate model building were evaluated using Non-linear Mixed Effect Modeling software (NONMEM, Version 6.2.0; ICON Development Solutions, Ellicott City, MD). The final model for MPA and its metabolites consisted of nine discrete compartments; 1) depot gastrointestinal; 2) central MPA; 3) peripheral MPA; 4) gallbladder; 5) MPA urine; 6) MPAG central; 7) MPAG urine; 8) AcMPAG central; and 9) AcMPAG urine compartment. The MPA population mean estimates for apparent nonrenal clearance (ClNR/F) and apparent central volume of distribution were 14.3 L/hr and 21.1 L, respectively. The mean population estimate for apparent renal clearance (ClR/F) was dependent on estimated creatinine clearances (eClcr); 0.0975 L/hr for eClcr 80 mL/min or less and 0.157 L/hr for eClcr greater than 80 mL/min. Covariate analyses identified: eClcr on CLNR,MPA/F (P < 0.001), eClcr (with a cutoff value at 80 mL/min) on CLR,MPA/F (P < 0.025), serum albumin on CLNR,MPA/F (P < 0.01), eClcr on CLR,MPAG/F (P < 0.001), and eClcr on CLR,AcMPAG/F (P < 0.001). Evaluation of the final model by visual predictive check showed that most of the observed values were within the 95th percent prediction interval generated from 100 simulations of the final model. The current population pharmacokinetic model demonstrated eClcr and serum albumin influenced the renal and nonrenal components of Cl/F, suggesting patients with glomerulonephritis would have highly altered MPA exposures.
Identification of Phytophthora citrophthora with Cloned DNA Probes

Two different DNA fragments, one of 2.9 kilobases and the other of 5.1 kilobases, were cloned from Phytophthora citrophthora and showed no homology with DNA from plants and other related fungi. These DNA probes hybridized with DNA from 12 different P. citrophthora isolates obtained from a variety of hosts but did not hybridize with DNA from 6 P. citrophthora isolates obtained from cacao. Southern blot analysis revealed that the probes contained repetitive DNA, and restriction fragment length polymorphisms were identified among several P. citrophthora isolates. Of the isolates tested, two major groups were observed whose genetic similarity correlated with geographical distribution. One of the DNA probes was used to detect P. citrophthora growing from infected citrus roots incubated on semiselective medium. P. citrophthora was not detected by a hybridization assay of total DNA extracted directly from infected roots.
Inhibition of cellular responses to insulin in a rat liver cell line. A role for PKC in insulin resistance

The initial response of liver cells to insulin is mediated through exocytosis of Cl− channel‐containing vesicles and a subsequent opening of plasma membrane Cl− channels. Intracellular accumulation of fatty acids leads to profound defects in metabolism, and is closely associated with insulin resistance. It is not known whether the activity of Cl− channels is altered in insulin resistance and by which mechanisms. We studied the effects of fatty acid accumulation on Cl− channel opening in a model liver cell line. Overnight treatment with amiodarone increased the fat content by ∼2‐fold, and the rates of gluconeogenesis by ∼5‐fold. The ability of insulin to suppress gluconeogenesis was markedly reduced indicating that amiodarone treatment induces insulin resistance. Western blot analysis showed that these cells express the same number of insulin receptors as control cells. However, insulin failed to activate exocytosis and Cl− channel opening. These inhibitory effects were mimicked in control cells by exposures to arachidonic acid (15 μm). Further studies demonstrated that fatty acids stimulate the PKC activity, and inhibition of PKC partially restored exocytosis and Cl− channel opening in insulin‐resistant cells. Accordingly, activation of PKC with PMA in control cells potently inhibited the insulin responses. These results suggest that stimulation of PKC activity in insulin resistance contributes to the inhibition of cellular responses to insulin in liver cells.
Epithelial membrane protein 2 (EMP2) deficiency alters placental angiogenesis, mimicking features of human placental insufficiency

Epithelial membrane protein‐2 (EMP2) is a tetraspan protein predicted to regulate placental development. Highly expressed in secretory endometrium and trophectoderm cells, previous studies suggest that it may regulate implantation by orchestrating the surface expression of integrins and other membrane proteins. In order to test the role of EMP2 in pregnancy, mice lacking EMP2 (Emp2−/−) were generated. Emp2−/− females are fertile but have reduced litter sizes when carrying Emp2−/− but not Emp2+/− fetuses. Placentas of Emp2−/− fetuses exhibit dysregulation in pathways related to neoangiogenesis, coagulation, and oxidative stress, and have increased fibrin deposition and altered vasculature. Given that these findings often occur due to placental insufficiency resulting in an oxygen‐poor environment, the expression of hypoxia‐inducible factor‐1 alpha (HIF‐1α) was examined. Placentas from Emp2−/− fetuses had increased total HIF‐1α expression in large part through an increase in uterine NK (uNK) cells, demonstrating a unique interplay between uNK cells and trophoblasts modulated through EMP2. To determine if these results translated to human pregnancy, placentas from normal, term deliveries or those complicated by placental insufficiency resulting in intrauterine growth restriction (IUGR) were stained for EMP2. EMP2 was significantly reduced in both villous and extravillous trophoblast populations in IUGR placentas. Experiments in vitro using human trophoblast cells lines indicate that EMP2 modulates angiogenesis by altering HIF‐1α expression. Our results reveal a novel role for EMP2 in regulating trophoblast function and vascular development in mice and humans, and suggest that it may be a new biomarker for placental insufficiency. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
An empirical study of the classification of eating disorders.

OBJECTIVE The nosology for eating disorders, despite having been extensively revised over time, may not capture the natural clustering of eating-related pathology as it occurs in general population samples. METHOD Detailed information about anorectic and bulimic behaviors was assessed through personal interviews of 2,163 Caucasian female twins from a population-based registry. Latent class analysis was applied to nine eating disorder symptoms to develop an empirically based typology. Demographic, comorbidity, personality, and co-twin diagnosis data were used to validate the resultant classes. RESULTS A six-class solution provided the best fit. One class displayed distorted eating attitudes without low body weight. Two classes demonstrated low weight without the psychological features of eating disorders. Three classes broadly resembled the DSM-IV classifications of anorexia nervosa, bulimia nervosa, and binge-eating disorder. For all classes, and especially for the three that reflected current diagnoses of eating disorders, monozygotic twins resembled one another much more in terms of class membership than did dizygotic twins. CONCLUSIONS The authors found within a community sample, and through an empirical method, classes of eating-related pathology that broadly resembled the current classifications of anorexia nervosa, bulimia nervosa, and binge-eating disorder. Additional classes were marked by either the psychological features of eating disorders or low body weight. Individuals in the three eating-disorder classes had similar personality profiles but displayed differences in symptom expression and co-twin risk for anorexia nervosa, bulimia nervosa, and obesity.
The C‐terminus of complement regulator Factor H mediates target recognition: evidence for a compact conformation of the native protein

The complement inhibitor Factor H has three distinct binding sites for C3b and for heparin, but in solution uses specifically the most C‐terminal domain, i.e. short consensus repeats (SCR) 20 for ligand interaction. Two novel monoclonal antibodies (mABs C14 and C18) that bind to the most C‐terminal domain SCR 20 completely blocked interaction of Factor H with the ligands C3b, C3d, heparin and binding to endothelial cells. In contrast, several mAbs that bind to the N‐terminus and to the middle regions of the molecule showed no or minor inhibitory effects when assayed by enzyme‐linked immunosorbent assay (ELISA) and ligand interaction assays. This paradox between a single functional binding site identified for native Factor H versus multiple interaction sites reported for deletion constructs is explained by a compact conformation of the fluid phase protein with one accessible binding site. On zymosan particles mAbs C14 and C18 blocked alternative pathway activation completely. Thus demonstrating that native Factor H makes the first and initial contact with the C terminus, which is followed by N terminally mediated complement regulation. These results are explained by a conformational hypothetical model: the native Factor H protein has a compact structure and only one binding site accessible. Upon the first contact the protein unfolds and exposes the additional binding sites. This model does explain how Factor H mediates recognition functions during complement control and the clustering of disease associated mutations in patients with haemolytic uraemic syndrome that have been reported in the C‐terminal recognition domain of Factor H.
The prepuce: specialized mucosa of the penis and its loss to circumcision.

OBJECTIVE To assess the type and amount of tissue missing from the adult circumcised penis. MATERIALS AND METHODS The gross and histological features of the prepuces of 22 adults obtained at autopsy were assessed, primarily focusing on the inner or mucosal surface of the prepuce. RESULTS Skin and mucosa sufficient to cover the penile shaft was frequently missing from the circumcised penis. Missing tissue included a band of ridged mucosa located at the junction of true penile skin with smooth preputial mucosa. This ridged band contains more Meissner's corpuscles than does the smooth mucosa and exhibits features of specialized sensory mucosa. CONCLUSION The amount of tissue loss estimated in the present study is more than most parents envisage from pre-operative counselling. Circumcision also ablates junctional mucosa that appears to be an important component of the overall sensory mechanism of the human penis.
Performance verification of low-frequency learning adaptive controllers

While adaptive control has been used in numerous applications, the ability to obtain a predictable transient and steady state closed-loop performance is still a challenging problem from the verification and validation standpoint. To that end, we considered a recently developed robust adaptive control methodology called, low-frequency learning adaptive control, and utilize a set theoretic analysis to show that the transitory performance of this approach can be expressed, analyzed, and optimized via a convex optimization problem based on linear matrix inequalities. This key feature of the analysis framework allows one to tune the adaptive control design parameters rigorously so that the tracking error components of the closed-loop nonlinear system evolve in a priori specified region of the state space. Numerical examples are provided to demonstrate the efficacy of the proposed verification and validation architecture.