Miracle-dz/UniFAR-FTUs huggingface dataset:
Molecular characterization of clinical multiresistant isolates of Acinetobacter sp. from hospitals in Porto Alegre, State of Rio Grande do Sul, Brazil.

INTRODUCTION Hospitals around the world have presented multiresistant Acinetobacter sp. outbreaks. The spread of these isolates that harbor an increasing variety of resistance genes makes the treatment of these infections and their control within the hospital environment more difficult. This study aimed to evaluate the occurrence and dissemination of Acinetobacter sp. multiresistant isolates and to identify acquired resistance genes. METHODS We analyzed 274 clinical isolates of Acinetobacter sp. from five hospitals in Porto Alegre, RS, Brazil. We evaluated the susceptibility to antimicrobial, acquired resistance genes from Ambler's classes B and D, and performed molecular typing of the isolates using enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR) technique. RESULTS A high (68%) percentage of multiresistant isolates of Acinetobacter sp. was observed, and 69% were resistant to carbapenems. We identified 84% of isolates belonging to species A. baumannii because they presented the gene blaOXA-51. The gene blaOXA-23 was detected in 62% of the isolates, and among these, 98% were resistant to carbapenems. Using the ERIC-PCR technique, we identified clones of Acinetobacter sp. spread among the four hospitals analyzed during the sampling period. CONCLUSIONS The data indicate the dissemination of Acinetobacter sp. isolates among hospitals and their permanence in the hospital after one year.
Induction of arthritis by single monoclonal IgG anti‐collagen type II antibodies and enhancement of arthritis in mice lacking inhibitory FcγRIIB

IgG anti‐collagen type II (CII) antibodies (Ab) can induce arthritis in healthy mice. Here we have investigated if single monoclonal IgG anti‐CII Ab can induce arthritis in CIA‐susceptible DBA/1 mice and if there is an IgG subclass dependency. The involvement of Fc receptors for IgG (FcγR) in anti‐CII Ab‐mediated arthritis was also investigated by comparing the clinical outcome in DBA/1 mice to those in FcγR‐deficient mice. We demonstrate for the first time that single mAb to naive DBA/1 mice can induce persistent arthritis. Histology of the inflamed joints revealed massivecellular infiltrate and cartilage and bone destruction. All IgG subclasses tested (IgG1, IgG2a and IgG2b) were arthritogenic, with the IgG1 and IgG2b isotypes as the dominating arthritogenic Ab. Pathogenicity was dependent on engagement of activating FcγR, as FcRγ‐deficient mice were completely resistant to Ab‐mediated arthritis. The arthritis induced with the IgG1 and IgG2b Ab was also inhibited by FcγRIII disruption, whereas arthritis mediated by the IgG2a Ab was not substantially affected. The arthritic response of the IgG1 and IgG2b isotypes, but not of the IgG2a Ab, was further enhanced in mice lacking the inhibitory FcγRIIB. These results demonstrate that single IgG anti‐CII mAb can induce erosive arthritis and that IgG anti‐CII Ab mediate arthritis by engagement of FcγR.
The effect of brexpiprazole (OPC-34712) and aripiprazole in adult patients with acute schizophrenia: results from a randomized, exploratory study

The aim of this study was to explore the effects of brexpiprazole and aripiprazole on efficacy, cognitive functioning, and safety in patients with acute schizophrenia. Patients who would benefit from hospitalization/continued hospitalization for acute relapse of schizophrenia were enrolled and randomized (2 : 1) to target doses of open-label brexpiprazole 3 mg/day or aripiprazole 15 mg/day for 6 weeks. Outcomes included change from baseline to week 6 in the Positive and Negative Syndrome Scale total score, Barratt Impulsiveness Scale 11-item score, and Cogstate computerized cognitive test battery scores. Patients treated with brexpiprazole (n=64) or aripiprazole (n=33) showed reductions in symptoms of schizophrenia as assessed by Positive and Negative Syndrome Scale total score (−22.9 and −19.4, respectively). A modest reduction in impulsivity was observed with brexpiprazole, but not aripiprazole (mean change in the Barratt Impulsiveness Scale 11-item total score: −2.7 and 0.1, respectively). No change in Cogstate scores was observed for either treatment. Brexpiprazole was well tolerated and the incidence of akathisia was lower in patients treated with brexpiprazole (9.4%) than aripiprazole (21.2%). Clinically relevant improvements in psychopathology were observed in patients with acute schizophrenia treated with brexpiprazole or aripiprazole. Brexpiprazole was well tolerated, with a lower incidence of akathisia than aripiprazole.
Interactions Between Commensal Bacteria and Gut Sensorimotor Function in Health and Disease

Commensal bacteria inhabiting the human intestine (i.e., intestinal microflora) participate in the development and maintenance of gut sensory and motor functions, including the promotion of intestinal propulsive activity. On the other hand, intestinal motility represents one of the major control systems of gut microflora, through the sweeping of excessive bacteria from the lumen. There is emerging evidence indicating that changes in this bidirectional interplay contribute to the pathogenesis of gut diseases, such as small intestinal bacterial overgrowth and intestinal pseudo-obstruction. Recent interest has also been directed to the potential role of intestinal microflora in the pathogenesis of the irritable bowel syndrome. Although the status of intestinal microflora in the irritable bowel syndrome remains unsettled, small intestinal bacterial overgrowth (as detected with breath testing) and increased fermentation of foods with gas production, provide indirect evidence that microflora may contribute to symptom generation in irritable bowel syndrome. The potential benefit of antibiotic and probiotic therapy is currently under investigation and opens new perspectives in irritable bowel syndrome treatment.
Smart device paradigm, Standardization for online labs

This paper introduce the smart device paradigm and it usage to streamline the development of the next generation of online labs where more intelligence is placed at the server side and little or no assumption is made about the client. The requirements, the standards and protocols for implementation are presented. Finally a possible evolution toward Massive Open Online Labs (MOOLs) is discussed.
Accuracy of outpatient service data for activity-based funding in New South Wales, Australia

Background: Despite increasing research on activity-based funding (ABF), there is no empirical evidence on the accuracy of outpatient service data for payment. Objective: This study aimed to identify data entry errors affecting ABF in two drug and alcohol outpatient clinic services in Australia. Methods: An audit was carried out on healthcare workers’ (doctors, nurses, psychologists, social workers, counsellors, and aboriginal health education officers) data entry errors in an outpatient electronic documentation system. Results: Of the 6919 data entries in the electronic documentation system, 7.5% (518) had errors, 68.7% of the errors were related to a wrong primary activity, 14.5% were due to a wrong activity category, 14.5% were as a result of a wrong combination of primary activity and modality of care, 1.9% were due to inaccurate information on a client’s presence during service delivery and 0.4% were related to a wrong modality of care. Conclusion: Data entry errors may affect the amount of funding received by a healthcare organisation, which in turn may affect the quality of treatment provided to clients due to the possibility of underfunding the organisation. To reduce errors or achieve an error-free environment, there is a need to improve the naming convention of data elements, their descriptions and alignment with the national standard classification of outpatient services. It is also important to support healthcare workers in their data entry by embedding safeguards in the electronic documentation system such as flags for inaccurate data elements.
Functional, global and cognitive decline correlates to accumulation of Alzheimer's pathology in MCI and AD.

BACKGROUND Cognitive, global and functional instruments have been extensively investigated for correlations with neuropathological changes such as neurofibrillary tangles (NFTs), plaques, and synapse loss in the brain. OBJECTIVE Our objective is to correlate the functional, global and cognitive decline assessed clinically with the neuropathological changes observed in a large prospectively characterized cohort of mild cognitive impairment (MCI) and Alzheimer's disease (AD). METHODS We examined 150 subjects (16 MCI and 134 AD) that were prospectively assessed and longitudinally followed to autopsy. MCI subjects clinically met Petersen criteria for single or multi-domain amnestic MCI. AD subjects clinically met NINCDS-ADRDA criteria for probable or possible AD. All subjects received the Functional Assessment Staging (FAST), the Global Deterioration Scale (GDS), and the Mini Mental State Examination (MMSE) ante-mortem. Plaque and tangle counts were gathered for hippocampus, entorhinal cortex, frontal, temporal and parietal cortices. Braak staging was performed as well. RESULTS The GDS, FAST and MMSE correlated with plaque counts in all regions. The GDS, FAST and MMSE correlated with tangle counts in in all regions. The three instruments also correlated with the Braak score. The MMSE and GDS correlate better than the FAST in most regions. CONCLUSIONS Accumulation of neuropathology appears to correlate with functional, global, and cognitive decline as people progress from MCI through AD.
Trophoblast CD274 (B7-H1) Is Differentially Expressed Across Gestation: Influence of Oxygen Concentration1

Abstract Modulation of the maternal immune system by the placenta is a mechanism by which the fetus ensures its own survival in a genetically foreign environment. The immunoinhibitor CD274 (also called B7-H1 or PD-L1) is highly expressed in the placenta, positioned to interact with maternal leukocytes. Further, immunoblot analysis of first- and second-trimester placental lysates showed that CD274 expression is low in the first trimester but dramatically rises around the onset of the second trimester. As this coincides with the expected onset of maternal blood flow to the placenta and a corresponding rise in local oxygen tension, we explored the possibility that oxygen regulates CD274 expression in trophoblast cells by culturing term trophoblast cells under oxygen concentrations similar to those found in vivo. Indeed, CD274 protein levels paralleled the in vivo situation: expression increased with rising oxygen concentrations. Furthermore, downregulation of CD274 mRNA by low oxygen was rapid, occurring within 4–12 h. We conclude that oxygen is a potential mediator of CD274 expression in vivo such that it is induced coincidentally on exposure of fetal tissues to maternal blood. Further, the regulation of this immunomodulator by oxygen may implicate its alteration during and involvement in the pathogenesis of complications of pregnancy such as preeclampsia.
Distinct pharmacological regulation of evoked dopamine efflux in the amygdala and striatum of the rat in vivo

The pharmacological regulation of evoked extracellular dopamine was compared in the basolateral amygdaloid nucleus (BAN) and caudate‐putamen (CP) of the urethane‐anesthetized rat. The effects of drugs, which alter dopamine uptake, release or degradation, were examined. Dopamine efflux was elicited by electrical stimulation of ascending dopamine fibers and was monitored by fast‐scan cyclic voltammetry at Nafioncoated, carbon‐fiber microelectrodes. Dopamine uptake inhibitors, nomifensine (25 mg/kg) and cocaine (20 mg/kg), and the dopamine receptor antagonist, haloperidol (0.5 mg/kg), robustly increased evoked extracellular dopamine in the CP. In sharp contrast, these drugs were much less effective in the BAN. The relative potencies of the uptake inhibitors varied between the two regions. Nomifensine was more potent than cocaine in the CP, whereas cocaine was more potent that nomifensine in the BAN. The monoamine oxidase inhibitor, pargyline (75 mg/kg), and the catechol‐O‐methyltransferase (COMT) inhibitor, Ro 40‐7592 (40 mg/kg), had small or negligible effects in either region. No electrochemical evidence was found for the formation of 3‐methoxytyramine, the dopamine metabolite formed by the action of COMT on released dopamine, on the time scale of the measurements in control or after pharmacological manipulation of the degradative enzymes for dopamine. The conclusions reached are: (1) potent mechanisms for uptake and autoreceptor inhibition of release, which exist in the CP to tightly control the concentration of extracellular dopamine, are considerably weaker in the BAN; (2) the extracellular clearance of evoked dopamine in the BAN and CP is the result of cellular uptake and not degradation; and (3) these results support the view that the pharmacological regulation of extracellular dopamine is regionally distinct in the brain. © 1995 Wiley‐Liss, Inc.
Genotypic Characterization of Ureaplasma Serovars from Clinical Isolates by Pulsed-Field Gel Electrophoresis

ABSTRACT Genetic relationships within ureaplasma serovars were investigated by pulsed-field gel electrophoresis (PFGE). One hundred thirteen Ureaplasma parvum isolates and 78 Ureaplasma urealyticum isolates were different from their ATCC serovar type strains and different within the same serovars. The organisms were geographically widespread. No unique patterns were associated with invasive disease.
CD40 Engagement Enhances Antigen-Presenting Langerhans Cell Priming of IFN-γ-Producing CD4+ and CD8+ T Cells Independently of IL-121

The delivery of CD40 signaling to APCs during T cell priming enhances many T cell-mediated immune responses. Although CD40 signaling up-regulates APC production of IL-12, the impact of this increased production on T cell priming is unclear. In this study an IL-12-independent T cell-mediated immune response, contact hypersensitivity (CHS), was used to further investigate the effect of CD40 ligation on the phenotypic development of Ag-specific CD4+ and CD8+ T cells. Normally, sensitization for CHS responses induces hapten-specific CD4+ T cells producing type 2 cytokines and CD8+ T cells producing IFN-γ. Treatment of mice with agonist anti-CD40 mAb during sensitization with the hapten 2,4-dinitrofluorobenzene resulted in CHS responses of increased magnitude and duration. These augmented responses in anti-CD40 Ab-treated mice correlated with increased numbers of hapten-specific CD4+ and CD8+ T cells producing IFN-γ in the skin draining lymph nodes. Identical results were observed using IL-12−/− mice, indicating that CD40 ligation promotes CHS responses and development of IFN-γ-producing CD4+ and CD8+ T cells in the absence of IL-12. Engagement of CD40 on hapten-presenting Langerhans cells (hpLC) up-regulated the expression of both class I and class II MHC and promoted hpLC migration into the T cell priming site. These results indicate that hpLC stimulated by CD40 ligation use a mechanism distinct from increased IL-12 production to promote Ag-specific T cell development to IFN-γ-producing cells.
Economic Complexity and Inequality : Does Productive Structure Affect Regional Wage Differentials in Brazil?

Brazil is an upper middle income economy, with a GDP per capita of close to 12,000 (constant) dollars in 2014. Nonetheless, Brazil has a significant amount of people living under poverty. 7.6% of the population was poor in 2014 (Poverty headcount ratio at $3.10 a day, 2011 PPP), making Brazil one of the most unequal countries in the world. Concomitantly, Brazil's different regions and states are highly heterogeneous with respect to income levels, inequality, and prevalence of poverty. Moreover, in the last past decades, the dispersion of inequality between states has increased. This paper shows that Brazilian states are also heterogenous in terms of economic complexity; and analyzes how economic complexity affects income inequality. To test the relationship between economic complexity and income inequality we employ panel data analysis for the 27 Brazilian states over the period 2002-2014. Our main proposition is that economic complexity affects regional wage differentials in a nonlinear way. Our findings confirm this proposition and point to an inverted U-shaped relationship, whereby higher economic complexity is initially associated with higher, and subsequently lower, inequality levels.
Identifying the Topology of Undirected Networks From Diffused Non-Stationary Graph Signals

We address the problem of inferring an undirected graph from nodal observations, which are modeled as non-stationary graph signals generated by local diffusion dynamics that depend on the structure of the unknown network. Using the so-called graph-shift operator (GSO), which is a matrix representation of the graph, we first identify the eigenvectors of the shift matrix from observations of the diffused signals, and then estimate the eigenvalues by imposing desirable properties on the graph to be recovered. Different from the stationary setting where the eigenvectors can be obtained directly from the covariance matrix of the measurements, here we need to estimate first the unknown diffusion (graph) filter – a polynomial in the GSO that preserves the sought eigenbasis. To carry out this initial system identification step, we exploit different sources of information on the arbitrarily-correlated input signal driving the diffusion on the graph. We first explore the setting where the observations, the input information, and the unknown graph filter are linearly related. We then address the case where the relation is given by a system of matrix quadratic equations, which arises in pragmatic scenarios where only the second-order statistics of the inputs are available. While such a quadratic filter identification problem boils down to a non-convex fourth-order polynomial minimization, we discuss identifiability conditions, propose algorithms to approximate the solution, and analyze their performance. Numerical tests illustrate the effectiveness of the proposed topology inference algorithms in recovering brain, social, financial, and urban transportation networks using synthetic and real-world signals.
Hormonal Influences on Growth and Somatotropic Actions of Autonomous Mammotropes.∗

Summary and Conclusions 1. The role of gonadal, adrenal, and hypophyseal hormones on growth and somatotropic actions of a transplantable, functional mammotropic pituitary tumor (MtT) was studied in rats. 2. Although this tumor is autonomous (in that it grows in normal rats of both sexes) it is highly responsive to estrogen, the rate of tumor growth and body growth of the host being roughly proportional to the quantity of estrogen administered. Hormones of mammotropes stimulate body growth and growth of many organs. Somatotropic and mammotropic effects are marked in hypophysectomized rats bearing mammotropic tumors; thus they are independent of other pituitary factors.
Anthropometric Determinants of a Clustering of Lipid-Related Metabolic Risk Factors in Overweight and Non-Overweight Adolescents – Influence of Cardiorespiratory Fitness

Background/Aims: To explore in adolescents the associations between simple anthropometric variables with a continuously distributed summary score for lipid-related metabolic risk in both overweight and non-overweight adolescents, and to test whether these associations are modified by the level of cardiorespiratory fitness. Methods: Cardiorespiratory fitness, BMI, skinfold thicknesses, body circumferences, and a continuously distributed clustering of lipid- related metabolic risk (calculated from LDL and HDL choles- terol, triglycerides, and glucose) were measured in 524 adolescents (265 males, 259 females, 15.3 ± 1.4 years) from the cross-sectional multicentric AVENA study. Participants were classified as overweight (including obesity) or non-overweight. Results: Most anthropometric parameters were univariately related to the continuous lipid-related metabolic risk. However, after multicollinear analysis and generalized linear modelling, suprailiac skinfold thickness in males (p < 0.001, explained variance 12.2%) and waist-to-height ratio in females (p < 0.001, explained variance 10.0%) were the best determinants of the continuous metabolic risk score, after adjustment for age, sexual maturation, and economic status. These associations were slightly weakened in overweight males (p = 0.034) and females (p = 0.087), and did not interact with cardiorespiratory fitness. Conclusion: Our data emphasize the usefulness of suprailiac skinfold thickness in males and waist-to-height ratio in females as simple anthropometric measurements associated to an overall lipid-related metabolic risk, mainly in non-overweight adolescents and regardless their cardiorespiratory status.
A Chronic Obstructive Pulmonary Disease Susceptibility Gene, FAM13A, Regulates Protein Stability of β-Catenin.

RATIONALE A genetic locus within the FAM13A gene has been consistently associated with chronic obstructive pulmonary disease (COPD) in genome-wide association studies. However, the mechanisms by which FAM13A contributes to COPD susceptibility are unknown. OBJECTIVES To determine the biologic function of FAM13A in human COPD and murine COPD models and discover the molecular mechanism by which FAM13A influences COPD susceptibility. METHODS Fam13a null mice (Fam13a(-/-)) were generated and exposed to cigarette smoke. The lung inflammatory response and airspace size were assessed in Fam13a(-/-) and Fam13a(+/+) littermate control mice. Cellular localization of FAM13A protein and mRNA levels of FAM13A in COPD lungs were assessed using immunofluorescence, Western blotting, and reverse transcriptase-polymerase chain reaction, respectively. Immunoprecipitation followed by mass spectrometry identified cellular proteins that interact with FAM13A to reveal insights on FAM13A's function. MEASUREMENTS AND MAIN RESULTS In murine and human lungs, FAM13A is expressed in airway and alveolar type II epithelial cells and macrophages. Fam13a null mice (Fam13a(-/-)) were resistant to chronic cigarette smoke-induced emphysema compared with Fam13a(+/+) mice. In vitro, FAM13A interacts with protein phosphatase 2A and recruits protein phosphatase 2A with glycogen synthase kinase 3β and β-catenin, inducing β-catenin degradation. Fam13a(-/-) mice were also resistant to elastase-induced emphysema, and this resistance was reversed by coadministration of a β-catenin inhibitor, suggesting that FAM13A could increase the susceptibility of mice to emphysema development by inhibiting β-catenin signaling. Moreover, human COPD lungs had decreased protein levels of β-catenin and increased protein levels of FAM13A. CONCLUSIONS We show that FAM13A may influence COPD susceptibility by promoting β-catenin degradation.