Miracle-dz/UniFAR-FTUs huggingface dataset:
[Geostatistical analysis of leprosy cases in the State of São Paulo, 1991-2002].

OBJECTIVE To analyze the spatial pattern of leprosy case occurrences in order to identify areas with a probability of disease transmission risks. METHODS This was an ecological study in which the analysis units were municipalities in the State of São Paulo that were georeferenced at their centroids. The data source was the electronic database of notified leprosy cases at the Epidemiological Surveillance Center of the State of São Paulo, from 1991 to 2001. Geostatistical techniques were used for detecting areas with a probability of leprosy risk, and for quantifying the spatial dependency of cases. RESULTS The spatial dependence detected extended outwards to 0.55 degrees from the georeferenced coordinates, which corresponded to approximately 60 km. The main areas identified as presenting a probability of risk were the northeastern, northern and northwestern regions of the State. CONCLUSIONS Verification of areas with the probability of leprosy risk using spatial dependence analysis may be a useful tool for assessing health conditions and planning budget allocations.
THE ROLE OF BIOMARKERS IN THE EARLY DETECTION OF ANTHRACYCLINE-INDUCED CARDIOTOXICITY IN CHILDREN: A Review of the Literature

Anthracycline-induced cardiotoxicity can cause serious health problems for an increasing number of children surviving childhood malignancies. Early detection of cardiac failure is critically important for the prevention and management of anthracycline-induced cardiotoxicity. The aim of this research was to determine the role of biomarkers in the early detection of anthracycline-induced cardiotoxicity in children. A literature review is presented of studies regarding the use of the biomarkers B-type natriuretic peptide (BNP), N-terminal pro-BNP (NT-pro-BNP), cardiac troponin T (cTnT), and cardiac troponin I (cTnI) in relation with anthracycline-induced cardiotoxicity in children. Six of 14 studies in children showed a significant relation between elevated biomarkers BNP, NT-pro-BNP, and cTnT and cardiac dysfunction. Six studies, although small, suggest that BNP, NT-pro-BNP, and cTnT might be useful markers in the early detection of anthracycline-induced cardiotoxicity.
Tumour necrosis factor and interleukin‐6 production induced by components associated with merozoite proteins of Plasmodium falciparum

P. falciparum merozoite antigens, merozoite surface protein‐l (MSP‐1) and rhoptry associated protein‐1 (RAP‐1), were shown to be liberated into the supernatant of in vitro parasite cultures and to be included in the endotoxin‐like exoantigen complex, previously designated Ag7. Material affinity purified from culture supernatants, using immobilized monoclonal antibodies specific for RAP‐1 or MSP‐1, stimulated normal human mononuclear cells to produce TNF and IL‐6 in vitro. However, stimulation of TNF was absent, and that of IL‐6 was reduced, when the antigens were purified from detergent extracts of infected erythro‐cytes. These results indicate that the RAP‐1 and MSP‐1 proteins themselves do not stimulate the production of TNF. Instead, other components associating with these exoantigens may be responsible for the TNF production. Mouse antisera blocking TNF production stimulated by P. yoelii exoantigens also blocked TNF production stimulated by material affinity purified from P. falciparum culture supernatants using RAP‐1 specific monoclonal antibody, indicating the conserved structure of the TNF inducing component.
Cromolyn sodium prophylaxis inhibits pulmonary proinflammatory cytokines in infants at high risk for bronchopulmonary dysplasia.

An imbalance of proinflammatory cytokines such as TNF-alpha, IL-1 beta, and the neutrophil chemotactic factor IL-8 and inhibitors (e.g., soluble TNF receptors and IL-1ra) in the lung during the first week of life may contribute to prolonged pulmonary inflammation and fibrosis in bronchopulmonary dysplasia (BPD). Disodium cromoglycate (DSCG) has anti-inflammatory effects in asthma, a disease with many similarities with BPD. In a prospective, randomized, blinded study, we examined whether early DSCG therapy inhibits proinflammatory cytokines in infants at risk for BPD. Twenty-six infants who were identified as high risk (> or = 75% probability) for oxygen-dependency at 28 d by a 12-h predictive score and survived 48 h were randomized to nebulized DSCG 20 mg (n = 13) or 2 cc NS (control, n = 13) every 6 h from Day 3 to Day 28. Lung lavage was collected on Day 3 (pre-study) and Day 7 and analyzed for cell count and differential and TNF-alpha, sTNFR1, sTNFR2, IL-1 beta, IL-1ra, and IL-8 concentrations. The groups' pre-study lavage cytokine concentrations were similar, but TNF-alpha and IL-8 concentrations were 3.6- and 4.9-fold lower in the DSCG group on Day 7 compared with levels in the control group. Soluble TNF receptors were unaffected by DSCG. There was a trend towards lower IL-1 beta levels in DSCG-treated infants on Day 7, but IL-1ra levels were unaffected by DSCG therapy. Three control subjects, but no DSCG-treated infants, died during the study period (p = 0.07). There were no significant differences between survivors of the two groups for oxygen-dependency at 28 d (100% control subjects; 85% DSCG). These results suggest that nebulized DSCG may exert an anti-inflammatory effect in the lungs of infants < or = 1,000 g at risk for BPD.
Responses of Clonal Eucalypt Plantations to N, P and K Fertilizer Application in Different Edaphoclimatic Conditions

Eucalypt plantations in Brazil have the highest mean productivity when compared to other producing countries, and fertilizer application is one of the main factors responsible for these productivities. Our aim was to identify appropriate rates of N, P and K in eucalypt plantations and their interactions with edaphoclimatic factors. Four trials with four rates and three nutrients (N, P and K) were set up. Each nutrient was studied separately, and the trees received sufficient rates of all of the other nutrients through fertilization, to avoid limitations not related to the desired nutrient. We assessed solid wood volume (SV), productivity gains (PG), leaf nutrient content and leaf area index (LAI) to determine the responses to fertilization. PG, regarding N, rates ranged from 104% to 127% at 60 months after planting. P fertilizer application led to gains in productivity in soils with levels of P-resin up to 5 mg·kg−1, but decreased with stand age. K fertilizer application responses increased within age in three sites. In Paulistania, responses to K application were close to zero. N and K responses were climate related. Leaf nutrient content and LAI were not able to predict the highest yields obtained.
TNF activates calcium–nuclear factor of activated T cells (NFAT)c1 signaling pathways in human macrophages

Acute activation of cells by tumor necrosis factor (TNF) has been well characterized, but little is known about later phases of TNF responses that are relevant for cells exposed to TNF for several days during inflammation. We found that prolonged exposure of human macrophages to TNF resulted in a wave of delayed but sustained activation of c-Jun and nuclear factor κB (NF-κB) proteins and of calcium oscillations that became apparent 1–3 d after TNF stimulation. These signaling events culminated in the induction and activation of the calcium-dependent transcription factor, nuclear factor of activated T cells (NFAT)c1, which mediated a gene expression program leading to cell fusion and osteoclast differentiation. TNF-induced NFATc1 activity primed macrophages for enhanced osteoclastogenesis in response to RANKL. High NFATc1 expression was apparent in synovial macrophages in a subset of patients with TNF-driven inflammatory arthritis. Thus, long-term exposure to TNF activates calcium-dependent signaling and an NFATc1-mediated gene activation program important for cell fusion and osteoclastogenesis. These findings identify a signaling pathway activated by TNF that is important for myeloid cell differentiation and suggest a role for TNF-induced calcium and NFAT signaling in chronic inflammation and associated bone resorption.
Cortical Evoked Potential and Extracellular K+ and H+ at Critical Levels of Brain Ischemia

As shown previously, the electrical function of the brain is critically dependent on cerebral blood flow in the sense that reduction beyond an ischemic threshold of approximately 15 ml/100 gm per minute (approximately 35% of control) in the baboon leads to complete failure of the somatosensory evoked response. This study tests the hypothesis that electrical failure in ischemia may be directly associated with a massive release of intracellular K+ or with a critical degree of extracellular acidosis. By microelectrode techniques, measurements of blood flow, extracellular activity of K+ and H+ as well as evoked potential were made in the baboon neocortex. Reductions in blood flow were obtained by occlusion of the middle cerebral artery and depression beyond the ischemic threshold of electrical function achieved by a reduction of systemic blood pressure which, in the ischemic zones, changed local cerebral blood flow proportionally. Abolition of evoked response could not be explained by depolarization by release of intracellular K+, nor was it critically dependent on cortical pH. However, the massive release of intracellular K+ was by itself critically dependent on cortical blood flow and occurred at 18 > 6 > 2 ml/100 gm per minute (median with 5% confidence limits). Thus a dual threshold in ischemia for neuronal functions is described, the threshold for release of K+ being clearly lower than the threshold for complete electrical failure. Further, the findings support the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive. That neurons can survive for some time in this state of lethargy is evidenced by the observations that an increase in rCBF, if sufficient, can restore evoked potential and normalize extracellular K+ activity as well as pH. Abolition of evoked response could not be explained by depolarization by release of intracellular K+, nor was it critically dependent on cortical pH. However, the massive release of intracellular K+ was by itself critically dependent on cortical blood flow and occurred at 18 > 6 > 2 ml/100 gm per minute (median with 5% confidence limits). Thus a dual threshold in ischemia for neuronal functions is described, the threshold for release of K+ being clearly lower than the threshold for complete electrical failure. Further, the findings support the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive. That neurons can survive for some time in this state of lethargy is evidenced by the observations that an increase in rCBF, if sufficient, can restore evoked potential and normalize extracellular K+ activity as well as pH.
Impaired mitochondrial fat oxidation induces adaptive remodeling of muscle metabolism

Significance Many theories regarding the causes of insulin resistance in skeletal muscle center on the ability of muscle to oxidize fat, with evidence supporting either decreased or increased fatty acid oxidation (FAO) as causal to insulin resistance. Inhibition of fatty acid transport into mitochondria specifically in mouse muscle results in a rather remarkable phenotype. Despite an accumulation of lipids in muscle, insulin sensitivity is maintained. The muscle responds to decreased FAO by adapting muscle metabolism to use other fuel sources, and by an increased reliance upon peroxisomal fat oxidation. There is also an increase in mitochondrial biogenesis. At the whole-body level, the mice seem to enter an energy conservation mode with reduced activity, energy expenditure, and resistance to diet-induced obesity. The correlations between intramyocellular lipid (IMCL), decreased fatty acid oxidation (FAO), and insulin resistance have led to the hypothesis that impaired FAO causes accumulation of lipotoxic intermediates that inhibit muscle insulin signaling. Using a skeletal muscle-specific carnitine palmitoyltransferase-1 KO model, we show that prolonged and severe mitochondrial FAO inhibition results in increased carbohydrate utilization, along with reduced physical activity; increased circulating nonesterified fatty acids; and increased IMCLs, diacylglycerols, and ceramides. Perhaps more importantly, inhibition of mitochondrial FAO also initiates a local, adaptive response in muscle that invokes mitochondrial biogenesis, compensatory peroxisomal fat oxidation, and amino acid catabolism. Loss of its major fuel source (lipid) induces an energy deprivation response in muscle coordinated by signaling through AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) to maintain energy supply for locomotion and survival. At the whole-body level, these adaptations result in resistance to obesity.
Are all medial frontal negativities created equal ? Toward a richer empirical basis for theories of action monitoring

14 Ullsperger M, von Cramon DY (2001) Subprocesses of performance monitoring: a dissociation of error processing and response competition revealed by event-related fMRI and ERPs. Neuroimage 14:1387-401. Van 't Ent D, Apkarian P (1999) Motoric response inhibition in finger movement and saccadic eye movement: a comparative study. Clin Neurophysiol 110:1058-72. Van 't Ent D (2002) Perceptual and motor contributions to performance and ERP components after incorrect motor activation in a flanker reaction task. Clin Neurophysiol 113:270-83. Van Veen V, Carter CS (2002) The timing of action-monitoring processes in the anterior cingulate cortex. J Cogn Neurosci 14:593-602. Vidal F, Hasbroucq T, Grapperon J, Bonnet M (2000) Is the 'error negativity' specific to errors? Biol Psychol 51:109-28. West R, Alain C (1999) Event-related neural activity associated with the Stroop task. Brain Res Cogn Brain Res 8:15764. Yordanova J, Falkenstein M, Hohnsbein J, Kolev V (this issue) Parallel Systems of Error Processing in the Brain.
Differential diagnosis of malignant lymphoma and nonlymphoid tumors using monoclonal anti‐leucocyte antibody

Pathologic samples from 34 cases of human solid malignancies were tested for reactivity with monoclonal anti‐human leucocyte antibody, designated 2D1. This antibody detects a human leucocyte antigen (HLe‐I) that is expressed strongly on B and T lymphoid cells and weakly on early hemopoietic cells, but is not found on normal mesenchymal and epithelial tissues. This study demonstrates the use of this reagent in cryostat sections of tumor samples using indirect immunofluorescence in combination with other lymphoid markers such as anti‐T cell serum, anti‐Ia‐like serum (detecting p28, 33 “B cell associated” membrane antigen) and antisera to different immunoglobulin isotypes. Tumor cells from all 12 cases of epithelial malignancies and sarcomas were HLe‐I− although adjacent (normal) lymphoid cells showed strong positive staining. In contrast, 20 cases of lymphoma (B‐ as well as T‐cell types) were HLe‐I+. Two other malignancies involving the lymphoid system were HLe‐I− and failed to express any of the other lymphoid markers tested.
Potentiation of Kinin Analogues by Ramiprilat Is Exclusively Related to Their Degradation

Abstract—The potentiation of kinin actions represents a cardioprotective property of ACE inhibitors. Although a clear contribution to this effect is related to the inhibition of bradykinin (BK) breakdown, the high efficacy of potentiation and the ability of ACE inhibitors to provoke a B2-receptor-mediated response even after receptor desensitization has also triggered hypotheses concerning additional mechanisms of kinin potentiation. The application of kinin analogues with enhanced metabolic stability for the demonstration of degradation-independent mechanisms of potentiation, however, has yielded inconsistent results. Therefore, the relation between the susceptibility of B2-agonists to ACE and the potentiation of their actions by ACE inhibitors was investigated with the use of minimally modified kinin derivatives that varied in their degree of ACE resistance. The B2-agonists BK, d-Arg-[Hyp3]-BK, [Hyp,3 Tyr(Me)8]-BK, [&Dgr;Phe5]-BK, [D-NMF7]-BK, and [Phe8&psgr;(CH2-NH)Arg9]-BK were tested for degradation by purified rabbit ACE and for their potency in contracting the endothelium-denuded rabbit jugular vein in the absence and presence of ramiprilat. Purified ACE degraded d-Arg-[Hyp3]-BK and [Hyp,3 Tyr(Me)8]-BK at 81% and 71% of BK degradation activity, respectively, whereas other peptides were highly ([&Dgr;Phe5]-BK) or completely ([D-NMF7]-BK, [Phe8&psgr;(CH2-NH)Arg9]-BK) resistant. The EC50 of BK-induced venoconstriction (1.15±0.2 nmol/L) was reduced by a factor of 5.7 in the presence of ramiprilat. Likewise, d-Arg-[Hyp3]-BK and [Hyp,3 Tyr(Me)8]-BK were both significantly potentiated by a factor of 4.4, whereas the activities of the other agonists were not affected. Ramiprilat exerted no influence on the maximum contraction induced by any of the agonists. It is concluded that the potentiation of kinin analogues during ACE inhibition correlates quantitatively with the susceptibility of each substance to degradation by ACE. As such, no evidence of degradation-independent potentiating actions of ACE inhibitors could be obtained.
Gene Expression Programming: A New Adaptive Algorithm for Solving Problems

Gene expression programming, a genotype/phenotype genetic algorithm (linear and ramified), is presented here for the first time as a new technique for the creation of computer programs. Gene expression programming uses character linear chromosomes composed of genes structurally organized in a head and a tail. The chromosomes function as a genome and are subjected to modification by means of mutation, transposition, root transposition, gene transposition, gene recombination, and oneand two-point recombination. The chromosomes encode expression trees which are the object of selection. The creation of these separate entities (genome and expression tree) with distinct functions allows the algorithm to perform with high efficiency that greatly surpasses existing adaptive techniques. The suite of problems chosen to illustrate the power and versatility of gene expression programming includes symbolic regression, sequence induction with and without constant creation, block stacking, cellular automata rules for the density-classification problem, and two problems of boolean concept learning: the 11-multiplexer and the GP rule problem.
Use of Collagen Membranes for Guided Bone Regeneration: A Review

&NA; There has been an increase in the use of the resorbable membranes that do not require a second stage surgery for removal in guided bone regeneration. The purpose of this review is to discuss the immune response of the host to the collagen, the use of resorbable membranes derived from Type I collagen of bovine Achilles tendon around dental implants, and its potential significance in the future of dental implantology. (Implant Dent 1900;9:63‐66)
An insulator element 3′ to the CFTR gene binds CTCF and reveals an active chromatin hub in primary cells

Regulation of expression of the CFTR gene is poorly understood. Elements within the basal promoter of the gene do not fully explain CFTR expression patterns, suggesting that cis-regulatory elements are located elsewhere, either within the locus or in adjacent chromatin. We previously mapped DNase I hypersensitive sites (DHS) in 400 kb spanning the CFTR locus including a cluster of sites close to the 3′-end of the gene. Here we focus on a DHS at +6.8 kb from the CFTR translation end-point to evaluate its potential role in regulating expression of the gene. This DHS, which encompasses a consensus CTCF-binding site, was evident in primary human epididymis cells that express abundant CFTR mRNA. We show by DNase I footprinting and electophoretic mobility shift assays that the cis-regulatory element within this DHS binds CTCF in vitro. We further demonstrate that the element functions as an enhancer blocker in a well-established in vivo assay, and by using chromatin immunoprecipitation that it recruits CTCF in vivo. Moreover, we reveal that in primary epididymis cells, the +6.8 kb DHS interacts closely with the CFTR promoter, suggesting that the CFTR locus exists in a looped conformation, characteristic of an active chromatin hub.
Effector‐based attention systems

Visual processing is known to be enhanced at the end point of eye movements. Feedback within the oculomotor system has been shown to drive these alterations in visual processing. However, we do not simply view the world; we also reach out and interact using our hands. Consequently, it is not surprising that visual processing has also been shown to be altered in near‐hand space. A growing body of work documents a myriad of alterations in near‐hand visual processing, with little consensus on the neural underpinnings of the effect of the hand. Since movement of the eyes and hands is governed by parallel frontoparietal networks and since within the oculomotor system feedback from these motor control regions has been shown to drive enhanced visual processing at saccade end points, it is plausible that a similar feedback mechanism is at play in near‐hand improvements in visual processing. Here, we compare and contrast oculomotor‐driven and hand‐driven changes in visual processing and provide support for the hypothesis that feedback within the reaching and grasping systems enhances visual processing near the hand in a novel way.
Effect of an angiotensin II type 1 receptor blocker on caveolin-1 expression in prostate cancer cells

Introduction Caveolin-1, the major structural protein of caveolae, interacts directly with the AT1 receptor. The biological functions of caveolin-1 in cancer are compound, multifaceted, and depend on cell type, tumour grade and cancer stage. The AT1-R-caveolin complex in caveolae may coordinate angiotensin II (Ang II) induced signalling. The aim of this study was to determine the effect of the angiotensin II receptor type 1 blocker candesartan on caveolin expression in human metastatic prostate adenocarcinoma cells PC-3. Material and methods WST-1 and BrdU assays were used as indicators of cell viability and proliferation after angiotensin II and/or candesartan stimulation. Real-time RT–PCR and western blot were used to study the effect of Ang II and/or candesartan on the expression of Cav-1 and AT1-R in PC-3 cells Results We found that the expression of caveolin-1 mRNA in the PC-3 cells treated with CV was significantly decreased in comparison with the control (2.9 ±0.17, 4.7 ±0.6, p < 0.05), whereas a higher caveolin-1 mRNA expression was observed in those after Ang II treatment (6.0 ±0.43, 4.7 ±0.6, p < 0.05). Protein analysis indicate that the expression of caveolin-1 protein in the PC-3 cells treated with candesartan was significantly decreased when compared with the control (0.69 ±0.05, 1.6 ±0.12, p < 0.05), whereas higher caveolin-1 protein expression was observed after Ang II treatment (2.5 ±0.20, 1.6 ±0.12, p < 0.05). Conclusions These results provide new information on the action of candesartan and may improve the knowledge about AT1 receptor inhibitors, which can be potentially useful in prostate cancer therapy.
Trends and treatment outcomes

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