Miracle-dz/UniFAR-FTUs huggingface dataset:
Neuropsychological assessment of cognitive disorders in patients with fibromyalgia, rheumatoid arthritis, and systemic lupus erythematosus.

INTRODUCTION This study assesses the possible existence of cognitive disorder associated with chronic diseases [fibromyalgia (FM), rheumatoid arthritis (RA) and lupus (SLE)], and the influence of the variables age, educational level and psychiatric symptoms on those disorders. MATERIALS AND METHODS The patients were referred by the Rheumatology Outpatient Clinic of the Hospital Universitário de Brasília (HUB), with ages ranging from 30 to 80 years, and were divided into the following three groups: FM, 13 patients; RA, 13 patients; and SLE, 11 patients. Their performance in the neuropsychological tests of memory, language, executive functions and neuropsychiatric inventory was assessed considering their type of chronic disease, educational level and age. In addition, the cutoff points of cognitive normality of population samples were compared with the patients' performances. RESULTS The cognitive disorders were shown to be associated with the three diseases studied, but with significant differences between them. CONCLUSION The variables studied (low educational level and advanced age) were associated with various degrees of impairment in the different cognitive functions in the three pathological groups. However, FM and SLE groups showed significantly higher means of the neuropsychiatric symptoms of anxiety, irritability and hallucinations than the RA group in the neuropsychiatric inventory.
Mapping of three translocation breakpoints associated with orofacial clefting within 6p24 and identification of new transcripts within the region

Orofacial clefting (OFC) is a common congenital malformation. Here we report the refinement of three translocation breakpoints of patients exhibiting OFC within the 6p24 region, and the isolation and characterisation of novel genes, one of which is directly disrupted by the translocation breakpoint of a patient. The gene has been characterized and orthologues identified in bovine, murine and pufferfish.
Variable interstellar radiation fields in simulated dwarf galaxies: supernovae versus photoelectric heating

We present high-resolution hydrodynamical simulations of isolated dwarf galaxies including self-gravity, non-equilibrium cooling and chemistry, interstellar radiation fields (ISRF) and shielding, star formation, and stellar feedback. This includes spatially and temporally varying photoelectric (PE) heating, photoionization, resolved supernova (SN) blast waves and metal enrichment. A new flexible method to sample the stellar initial mass function allows us to follow the contribution to the ISRF, the metal output and the SN delay times of individual massive stars. We find that SNe play the dominant role in regulating the global star formation rate, shaping the multiphase interstellar medium (ISM) and driving galactic outflows. Outflow rates (with mass-loading factors of a few) and hot gas fractions of the ISM increase with the number of SNe exploding in low-density environments where radiative energy losses are low. While PE heating alone can suppress star formation as efficiently as SNe alone can do, it is unable to drive outflows and reproduce the multiphase ISM that emerges naturally whenever SNe are included. We discuss the potential origins for the discrepancy between our results and another recent study that claimed that PE heating dominates over SNe. In the absence of SNe and photoionization (mechanisms to disperse dense clouds), the impact of PE heating is highly overestimated owing to the (unrealistic) proximity of dense gas to the radiation sources. This leads to a substantial boost of the infrared continuum emission from the UV-irradiated dust and a far-infrared line-to-continuum ratio too low compared to observations.
Continuous Template Collection and Updating for Electrogram Morphology Discrimination in Implantable Cardioverter Defibrillators

Introduction: Electrogram morphology analysis improves discrimination of supraventricular tachycardias (SVTs) from ventricular tachycardias (VTs) in implantable cardioverter defibrillators (ICDs), but electrogram morphology may change with lead maturation, drugs, or disease progression. We report the clinical performance of an automatic algorithm that creates and updates templates from non‐paced, slow rhythm and continuously checks the quality of the template used for arrhythmia discrimination.
Early CT Findings in Unknown-Onset and Wake-Up Strokes

Background: Approximately one quarter of the acute ischemic stroke patients notice the event at awakening. Such patients with stroke at awakening are usually excluded from thrombolysis, since the time of stroke onset cannot be definitely identified. We compared the hyperacute CT findings of awakening stroke patients with those of stroke patients with known onset to assess whether the time of stroke onset is shortly before awakening. Methods: Subjects were cardioembolic stroke patients who were consecutively admitted to our department within 3 h after the recognition of stroke during the period between January 2000 and March 2003. The patients were classified into three groups: group A with stroke of known onset, group B with stroke at awakening, and group C with stroke of unknown onset due to lack of a witness. The clinical and CT findings in each group were compared. Results: A total of 81 patients fulfilled the study criteria. There were 46 patients in group A, 17 patients in group B, and 18 patients in group C. There was no significant difference in CT findings between groups A and B. In group C, however, definite hypodense areas were more commonly found than in group A (56 vs. 0%; p < 0.001) or in group B (56 vs. 11%; p = 0.012). Conclusion: Based on our CT findings, stroke at awakening seems to be developing shortly before in a large subset of patients, making them potential candidates for acute stroke therapies.
Phytochemical composition , antioxidant and antibacterial potential of underutilized parts of some fruits

The study was aimed to evaluate phytochemical composition, antioxidant and antibacterial properties from powder of various underutilized fruits. Antibacterial activities from extracts of the underutilized parts of various fruit samples against Gram+ve (Staphylococcus aureus) and Gram-ve (Escherichia coli) bacteria were determined by using ELISA reader and expressed as relative inhibition (%), antioxidant profiles by β-carotene and linoleic acid and ferric thiocyanate reducing ability. The phytochemical screening was done by standard methods and their composition revealed total phenols ranging from 119.5 (stone apple) to 139.0 (acacia, mg GAE/g). Mango waste (156 mg QE/g) contained the maximum amount of flavonoids while stone apple waste (13 mg QE/g) showed the least. Maximum and minimum amount of proanthocyanidins were shown by grape waste (468 mg CE/g) and mosambi waste respectively. Grape and acacia waste powder showed the highest reducing power while least amount of reducing power was observed in apple waste sample. The waste powders from stone apple and orange exhibited potent antibacterial activity against microorganisms tested. Study revealed strong antioxidant profiles in acacia fruits and antibacterial activity in stone apple and orange.
Depth map estimation using modified Census transform and semi-global matching

Generating a dense disparity image is one of the essential prerequisite for many applications such as rendering virtual views, 3D scene reconstruction, and advanced driver assistance systems (ADAS). In this paper, a depth estimation technique is proposed which is based on non-parametric Census transform and semi-global optimization. Simulation results indicate that the proposed method fulfills the aims of the algorithm by enhancing the quality of the estimated depth maps and reducing the computational complexity.
Hypertensive vascular disease as a consequence of increased arterial pressure; quantitative study in rats with hydralazine-treated renal hypertension.

Debate concerning the association between arterial hypertension and hypertensive vascular disease began 8o years ago in England with the formulation of contrasting concepts by Gull and Sutton1 and by Mahomed.2 It has continued since, largely at the clinico-pathologic level, and has not been resolved by some 25 years study of experimental hypertension. However, the experiments of Wilson and Byrom,$ Byrom and Dodson,4 and of Ledingham and Floyer5 would seem to prove that relative normotension or hypotension, such as occurs also in the "endocrine kidney,"' protects the renal vascular bed of the rat from nephrosclerotic lesions. Since nephrosclerosis develops in kidneys exposed to high arterial pressure, it would seem to follow that hypertension is the primary cause of the vascular lesions. Unfortunately, the nature of these experiments is such that the differences observed are qualitative only. There have been relatively few attempts, and these in small series,7 to establish a quantitative association between the severity of hypertensive vascular disease and the concurrent level of arterial pressure. Nevertheless, many who are not fully convinced of this association believe that other factors, such as the presence8 or absence" of intact kidney tissue, partly or wholly determine the occurrence of hypertensive vascular disease, especially of that which is acute, fulminant, and severely destructive.
Monitoring Population Levels of Alcohol Consumption in Pregnant Women: A Case for Using Biomarkers

A challenge to biochemically monitoring alcohol consumption in pregnancy is the prohibitive costs of collecting thousands of blood samples. This pilot study looks at the feasibility of using residual samples to monitor chronic and acute alcohol consumption in pregnancy. Residual anomalies screening samples (n = 150, 2006/7) were tested for carbohydrate-deficient transferrin (CDT, chronic marker) and ethyl glucuronide (EtG, acute marker). Valid readings were obtained for CDT but not EtG. These results pave the way for a larger representative study, to provide, for the first time, a national biochemical baseline estimate of chronic alcohol consumption in the pregnant population.
Sulfated polyanions inhibit invasion of erythrocytes by plasmodial merozoites and cytoadherence of endothelial cells to parasitized erythrocytes

Sulfated proteoglycans have been shown to be involved in the binding of sporozoites of malaria parasites to hepatocytes. In this study, we have evaluated the effect of sulfated glycosaminoglycans on the invasion of erythrocytes by Plasmodium falciparum merozoites and cytoadherence of parasitized erythrocytes (PRBC) to endothelial cells. Invasion of erythrocytes by HB3EC-6 (an HB3 line selected for high binding to endothelial cells) was inhibited by dextran sulfate 500K, dextran sulfate 5K, sulfatides, fucoidan, and heparin but not by chondroitin sulfate A. With the exception of sulfatides, the invasion-inhibitory effect was not mediated by killing of parasites. Cytoadherence of HB3EC-6 to human microvascular endothelial cells (HMEC-1) and inhibited by these sulfated glycoconjugates. The highly sulfated dextran sulfate 500K had the highest inhibitory effect on both invasion and cytoadherence, whereas the positively charged protamine sulfate promoted cytoadherence. Because preincubation of PRBC with sulfated glycosaminoglycans and treatment of target cells with heparinase had no significant inhibition on cytoadherence, it is unlikely that sulfated glycoconjugates are used directly by endothelial cells as cytoadhesion receptors. In an vivo experiment, we found that the administration of dextran sulfate 500K to CBA/Ca mice infected with Plasmodium berghei ANKA reduced parasitemia and delayed the death associated with anemia. These observations suggest that sulfated polyanions inhibit the invasion of erythrocytes by merozoites and cytoadherence of PRBC to endothelial cells by increasing negative repulsive charge and sterically interfering with the ligand-receptor interaction after binding to target cells.
Endogenous α2‐antiplasmin does not enhance glomerular fibrin deposition or injury in glomerulonephritis

Summary. Background: Fibrin deposition is an important mechanism of glomerular injury in crescentic glomerulonephritis (GN), a severe form of immune renal injury. Both coagulation and fibrinolysis (via the plasminogen–plasmin system) are important in net glomerular fibrin accumulation in GN. α2‐Antiplasmin (α2‐AP) is the major circulating inhibitor of plasmin and is expressed in the renal tubulointerstitium. Objective: To determine whether endogenous α2‐AP contributes to glomerular fibrin accumulation in GN. Methods: Crescentic autologous phase antiglomerular basement membrane GN was induced in mice with intact and deficient endogenous α2‐AP (α2‐AP+/+ and α2‐AP−/− mice). Results: In mice with crescentic GN, α2‐AP was detected in the tubulointerstitium and in segmental deposits within some glomeruli. α2‐AP+/+ mice developed crescentic GN (38 ± 9% glomeruli affected) with glomerular fibrin deposition and renal impairment (serum creatinine 30 ± 1 µmol L−1, normal without GN 11 ± 1 µmol L−1). Genetic deficiency of α2‐AP did not result in attenuated glomerular fibrin deposition, crescent formation (39 ± 8% glomeruli affected), glomerular leukocyte infiltration or renal impairment (serum creatinine 33 ± 7 µmol L−1). α2‐AP was unmeasurable in kidneys from α2‐AP−/− mice, which did not develop compensatory changes in plasminogen, tissue type plasminogen activator (tPA), urokinase type PA (uPA) or plasminogen activator inhibitor‐1 proteins, or changes in tPA or uPA activity. α2‐AP−/− mice did have enhanced total renal fibrinolytic capacity as assessed by in situ fibrin overlay (α2‐AP+/+ 0.19 ± 0.01, α2‐AP−/− 0.36 ± 0.03 lyzed area/total area). Conclusions: α2‐AP is not important to net glomerular fibrin deposition, crescent formation or renal impairment in crescentic GN.
Characterization of CTX-M and SHV extended-spectrum beta-lactamases and associated resistance genes in Escherichia coli strains of food samples in Tunisia.

OBJECTIVES To assess the occurrence of extended-spectrum beta-lactamases (ESBLs) in Escherichia coli isolates of faecal samples of animals (n = 40) and food samples (n = 38) obtained in Tunisia in 2006, and to characterize the type of ESBLs, their genetic environments and the associated resistance genes. METHODS Samples were inoculated in supplemented media (2 mg/L cefotaxime) for isolation of broad-spectrum cephalosporin-resistant E. coli isolates (one isolate/sample). ESBLs and their genetic environments as well as integrons and their gene cassette composition were characterized by PCR and sequencing. RESULTS ESBL-producing E. coli isolates were detected in 10 of the 38 food samples analysed (26%) and in none of the tested animal faecal samples. Genes found were as follows (number of isolates): bla(CTX-M-1) (5), bla(CTX-M-1) + bla(TEM-1b) (1), bla(CTX-M-14) + bla(TEM-1b) (2), bla(CTX-M-8) (1) and bla(SHV-5) (1). All ESBL-positive isolates showed unrelated PFGE patterns. ISEcp1 and IS903 were detected surrounding bla(CTX-M-14), and ISEcp1/IS26 and orf477 surrounding some of the bla(CTX-M-1) genes. Four of the ESBL-positive strains harboured class 1 integrons including different gene cassette combinations. CONCLUSIONS ESBLs, mainly of the CTX-M class, are detected in E. coli of food origin in Tunisia, being the first time that this mechanism has been detected in food E. coli strains in Africa.
Do ultrasound renal resistance indices reflect systemic rather than renal vascular damage in chronic kidney disease?

BACKGROUND In patients suffering from chronic kidney disease (CKD), ultrasound renal resistance indices predict progression of kidney disease and death. Although ultrasound resistance indices were initially considered to directly reflect intrarenal vascular resistance, they are complex composite parameters that are influenced by various vascular factors. We hypothesized that renal resistance indices reflect systemic vascular disease rather than local renal damage in patients with CKD. METHODS In 140 patients suffering from CKD not receiving renal replacement therapy, intrarenal resistance indices were measured in interlobar arteries. For assessment of systemic atherosclerotic disease, common carotid intima-media thickness (IMT) and ankle-brachial blood pressure index were determined. Categories of risk for coronary heart diseases were defined by Framingham risk scoring. RESULTS Increased renal resistance indices were associated with high Framingham risk scores and with the presence of atherosclerotic disease. In addition, ultrasound renal resistance indices progressively increased with the stage of renal function impairment, and patients suffering from diabetic nephropathy had higher resistance indices than patients suffering from other renal diseases. In a multivariate linear regression analysis, IMT, Framingham risk score, renal function, presence of diabetic nephropathy and pulse pressure independently predicted resistance indices. However, when additionally adjusting for age, IMT and Framingham risk score were no longer independent predictors of resistance indices. CONCLUSIONS In patients suffering from CKD, intrarenal resistance indices are independently associated with cardiovascular risk score and systemic vascular disease as well as with aetiology and stage of CKD. This may explain their strong association with both impaired renal outcome and death.
Medical injury compensation. A time for testing new approaches.

Despite an improved climate for professional liability insurance, medical injury compensation remains a subject of serious concern. The current tort system has been assailed as too slow, too costly, too complicated, and inconsistent in awards. Some critics assert that it induces overutilization through "defensive" medicine while limiting access by influencing physicians to forgo high-risk procedures or to shift to specialties with less liability exposure. Many medical practitioners also contend that it often stigmatizes physicians unfairly. Legislative reform in the 1970s and 1980s produced changes in the tort system in response to perceived crises arising from the increasing cost and diminishing availability of professional liability insurance. Because of limited understanding about the nature and dimensions of the problems at which they were directed, it was highly conjectural whether those remedies would effect anything close to a cure. Today's situation differs significantly. We now have a significant body of research, and such
Low-power sensor node with addressable wake-up on-demand capability

The ambition to equip more and more consumer products with sensor intelligence and communication capability entails two major demands for wireless sensor nodes. First, they have to operate for several years. Second, they must be permanently accessible for communication requests. These two demands are in contrast to each other. Regarding a transceiver in permanent receiving mode, the power consumption of a few milliwatts implicates a lifetime in the order of days for a common battery. Addressing the challenge to solve these conflicts, we present a new wake-up receiver approach in this paper. Our solution consumes 5.6 μW of power while listening for a communication request. Furthermore, it possesses a 16-bit address coding for specific WSN wake-up. And moreover, an improved impedance matching with a high sensitivity improves the wake-up distance significantly to 40 m at +10 dBm output power. This approach empowers wireless sensor nodes for the first time to be usable for a wide range of applications.
Chronic activation of cannabinoid receptors in vitro does not compromise mouse islet function.

We have demonstrated previously that mouse and human islets express ECS (endocannabinoid system) elements, and that short-term activation of islet cannabinoid CB1r and CB2r (cannabinoid type 1 and 2 receptors respectively) stimulates insulin secretion in vitro. There is evidence that the ECS is overactive in Type 2 diabetes, impairing glucose homoeostasis, but little is known about whether it is implicated in islet dysfunction. Therefore the aim of the present study was to investigate the effect of chronic exposure of isolated mouse islets to cannabinoid receptor agonists on islet gene expression and function. Quantitative RT-PCR (reverse transcription-PCR) indicated that mRNAs encoding synthesis [NAPE-PLD (N-acyl-phosphatidyl ethanolamide-hydrolysing phospholipase D)] and degradation [FAAH (fatty acid amide hydrolase)] of the endocannabinoid AEA (anandamide) were the most abundant ECS elements in mouse islets, with much lower levels of CB1r, CB2r, DAGL (diacylglycerol lipase) and MAGL (monoacylglycerol lipase) mRNAs. Maintenance of islets for up to 7 days in the presence of the CB1r agonist ACEA [N-(2-chloroethyl)-5Z,8Z,11Z,14Z-eiscosatetraenamide] or the CB2r agonist JWH015 [(2-methyl-1propyl-1H-indol3-yl)-1-napthalenylmethanone] did not compromise islet viability, as assessed by islet morphology and caspase activities, but there were some changes in mRNAs encoding ECS components. Neither glucose-stimulated insulin secretion nor acute insulin secretory responses to ACEA or JWH015 at 16 mM glucose were substantially modified by a 48 h or 7 day pre-exposure to these cannabinoid receptor agonists, but the stimulation of secretion at 3 mM glucose by 100 nM ACEA was significantly reduced after prolonged treatment with ACEA. Despite JWH015-induced reductions in islet glucagon content at 48 h and 7 days, there were no reductions in arginine-induced glucagon secretion from islets pre-exposed to JWH015 or ACEA. These data indicate that treatment of islets with agonists of CB1r and CB2r for up to 7 days does not have any major impact on islet function, suggesting that the impairments in glucose homoeostasis observed following overactivation of the ECS should be sought in relation to insulin resistance rather than β-cell dysfunction.
NEUROPEPTIDES AND ADRENOCORTICAL PROLIFERATION IN VITRO

Vasoactive intestinal peptide (VIP) and Neuropeptide Y (NPY) are localised in the capsule and zona glomerulosa region of the adrenal cortex, where they play an important role in regulating steroidogenesis and adrenal blood flow. This study investigates the effect of these neuropeptides on adrenocortical cellular proliferation and steroidogenesis in vitro. Capsular/glomerulosa and innerzone/medulla preparations were either stimulated acutely with NPY or VIP (both 10–6 M) for up to 2 hours or for 24 hours, four and eight days in vitro in eagles MEM (3.4 mM K+). DNA synthesis was determined using immunocytochemistry through the incorporation of the thymidine analogue 5-bromo-2′-deoxyridine (BrdU, 20 mg/mL). Phosphorylation of mitogen activated protein kinase ERK1/2 was assessed by western blotting. Both VIP (10–6 M) and NPY (10–6 M) treatment caused an increase in DNA synthesis after four days in culture. Acute NPY treatment caused an increase in ERK1 and 2 phosphorylation (p < 0.01) in the capsular/zona glomerulosa. Vasoactive intestinal peptide treatment caused a significant increase in ERK1/2 phosphorylation (p < 0.05) only in innerzones/medulla preparations. Both responses were maximal between 10 and 30 min of incubation and decrease thereafter. These data provide further evidence for the role of the mitogen activated protein kinases ERK1 and 2 in the proliferative events in the adrenal gland and demonstrate stimulation of cell division by the adrenal neuropeptides VIP and NPY in vitro.