Miracle-dz/UniFAR-FTUs huggingface dataset:
Energy Consumption-Economic Growth nexus in Sub-Saharan Countries: what can we learn from a meta-analysis? (1996-2016)

The relationship between energy consumption and economic growth remains one of the most debated topics in the economics literature. Studies in this field have been carried out in developed countries since the end of the 70s, but they not have led to consensus about the relationship other than finding four causality directions: unidirectional in two directions, bidirectional, or neutral. This lack of consensus remains one of the most relevant findings on energy issues. During the 2010s, the scope of the studies on this relationship broadened since, for example, energy demand in Sub-Saharan Africa has outpaced that in the North and the IEA has forecasted the greatest increase in energy consumption to come from this area. The relationship between energy consumption and economic growth began to be studied in Sub-Saharan Africa in the late 90s, using the same method as for developed countries and with the same lack of consensus on the direction of causality. This paper attempts to clarify this situation through a meta-analysis of fifty articles published since 1996 to 2016. This meta-analysis involves five analytical categories: type of publication, geographical area studied, econometrics method used, energy consumption indicators, and control variables. Each of these dimensions includes many disaggregated variables. Logistic regressions are run on the variables presented above for each of the four causality hypotheses. In research that studies single countries, the likelihood of finding for a given causality hypothesis is very sensitive to the econometric method implemented. Findings on a panel of countries are then presented; their methods assert the neutrality hypothesis
Pulmonary Surfactant Protein-A (SP-A) Restores the Surface Properties of Surfactant after Oxidation by a Mechanism That Requires the Cys6 Interchain Disulfide Bond and the Phospholipid Binding Domain*

Reactive oxygen species produced by activated leuko-cytes in the alveolar epithelial lining fluid have been implicated in the inactivation of pulmonary surfactant and the impairment of lung function. Oxidation of bovine lipid extract surfactant (BLES), a therapeutic surfactant, with hypochlorous acid (H-BLES) or the Fenton reaction (F-BLES) led to temporary increases in conjugated dienes and formation of malondialdehyde and 4-hydroxy-2-nonenal. Electrospray ionization mass spectrometry revealed the appearance of lipid hydroperoxides, peroxides, lysophospholipids, and free fatty acids. Captive bubble tensiometer studies of H-BLES demonstrated prolonged adsorption times, film instability at low surface tensions during film compression, and reduced respreadability during film expansion. F-BLES exhibited prolonged adsorption times, a marked effect on increasing compressibility during compression, and a lesser effect on reducing respreadability on expansion. Addition of native bovine or rat surfactant-associated protein A (SP-A) reversed the effects of oxidation on surfactant biophysical properties. Studies using mutant recombinant rat SP-As indicated that an intact carbohydrate recognition domain and disulfide-dependent oligomeric assembly are critical for these effects, but the collagen-like region is not required. We conclude that SP-A can reverse the detrimental effects of surfactant oxidation on the biophysical properties of surfactant, by a mechanism that is dependent on interchain disulfide bond formation and the C-terminal domains of the protein.
Organization of human interferon gamma-heparin complexes from solution properties and hydrodynamics.

Heparan sulfate (HS) recognizes a variety of proteins, one of which is the pleiotropic cytokine IFN-gamma, and as such modulates many biological processes. IFN-gamma is a homodimer with a well-defined core and two flexible C-termini that constitute HS binding domains. We show here using molecular modeling that an extended IFN-gamma structure overlaps a HS fragment of 16 disaccharides (16 nm). Since a 21-24-disaccharide HS fragment was experimentally defined as the minimum size that interacts with IFN-gamma [Lortat-Jacob, H. , Turnbull, J. E. , and Grimaud, J. A. (1995) Biochem. J. 310 (Part 2), 497-505], this raises the question of the complexe organization. We combine analytical ultracentrifugation, size exclusion chromatography, and hydrodynamic bead modeling to characterize the complexes formed in solution with heparin oligosaccharides. For oligosaccharides of 14 and 20 nm, two types of complexes are formed with one IFN-gamma and one or two heparin molecules. Complexes consisting of two IFN-gamma and one or two heparin molecules are present for a fragment of 25 nm and aggregates for a fragment of 35 nm. The complexes are rather compact and can be formed without major conformational changes of the partners. The complex pattern of interaction is related to the size of the partners and their multiple binding possibilities. These various possibilities suggest networks of interactions at the crowded surface of the cells. Hydrodynamic methods used here proved to be very efficient tools for describing protein-HS complexes that, due to the intrinsic heterogeneity and flexibility of the partners, are otherwise very difficult to analyze.
Nuclear fractal dimension in oral squamous cell carcinoma: a novel method for the evaluation of grading, staging, and survival.

Fractal dimension (FD) in tissue specimens from patients with oral squamous cell carcinoma (OSCC) was evaluated. FD values in different stages of OSCC, and the correlations with clinicopathological variables and patient survival were investigated. Histological sections from OSCC and control non-neoplastic mucosa specimens were stained with hematoxylin-eosin for pathological analysis and with Feulgen for nuclear evaluation. FD in OSCC groups vs. controls revealed statistically significant differences (P < 0.001). In addition, a progressive increase of FD from stage I and II lesions and stage III and IV lesions was observed, with statistically significant differences (P = 0.003). Moreover, different degrees of tumor differentiation showed a significant difference in the average nuclear FD values (P = 0.001). A relationship between FD and patients' survival was also detected with lower FD values associated to longer survival time and higher FD values with shorter survival time (P = 0.034). These data showed that FD significantly increased during OSCC progression. Thus, FD could represent a novel prognostic tool for OSCC, as FD values significantly correlated with patient survival. Fractal geometry could give insights into tumor morphology and could become an useful tool for analyzing irregular tumor growth patterns.
Development of the Spatial Representation System in the Rat

The Space in Your Head Space, and events associated with places and spaces, are represented in the brain by a circuitry made of place cells, head direction cells, grid cells, and border cells. These cell types form a collective dynamic representation of our position as we move through the environment. How this representation is formed has remained a mystery. Is it acquired, or are we born with the ability to represent external space (see the Perspective by Palmer and Lynch)? Langston et al. (p. 1576) and Wills et al. (p. 1573) investigated the early development of spatial activity in the hippocampal formation and the entorhinal cortex of rat pups when they first began to explore their environment. Rudiments of place cells, head direction cells, and grid cells already existed when the pups made their first movements out of the nest. A neural representation of external space at this early time points to strong innate components for perception of space. These findings provide experimental support for Kant's 200-year-old concept of space as an a priori faculty of the mind. Space and direction are already represented in specific neurons when rat pups navigate a location for the first time. In the adult brain, space and orientation are represented by an elaborate hippocampal-parahippocampal circuit consisting of head-direction cells, place cells, and grid cells. We report that a rudimentary map of space is already present when 2½-week-old rat pups explore an open environment outside the nest for the first time. Head-direction cells in the pre- and parasubiculum have adultlike properties from the beginning. Place and grid cells are also present but evolve more gradually. Grid cells show the slowest development. The gradual refinement of the spatial representation is accompanied by an increase in network synchrony among entorhinal stellate cells. The presence of adultlike directional signals at the onset of navigation raises the possibility that such signals are instrumental in setting up networks for place and grid representation.
A 0.13 CMOS integrated circuit for electrical impedance spectroscopy from 1 kHz to 10 GHz

The design of an electrical impedance spectroscopy acquisition and processing system using a 0.13 μm CMOS technology with a 1kHz to 10 GHz functional frequency range is presented. The system is based on a quadrature modulator in a lock-in architecture. The design of each one of the modules of the system is explained, and post-layout simulations are used to validate the main features of the design such as frequency response, gain, noise, linearity, and error characterization.
EFFECT OF SIMVASTATIN ON GLIOMA CELL PROLIFERATION, MIGRATION, AND APOPTOSIS

OBJECTIVEIn this study, we investigated the effects of simvastatin on proliferation, migration, and apoptosis in human U251 and U87 glioma cells and the underlying molecular mechanism. METHODSWe used colony formation assay to test the cell proliferation, in vitro scratch assay to examine the cell migration, and caspase-3 activity assay, annexin V staining, and cytochrome C release to evaluate the cell apoptosis. Lipid raft fractions were isolated from glioma cells. Total cholesterol content assay was used to test the change of cholesterol level in lipid raft fractions. Immunocytochemistry staining was performed to detect the changes of lipid rafts in cell membranes. Western blotting analysis was performed to examine the signal transduction both in cells and in lipid raft fractions. RESULTSSimvastatin inhibited proliferation and migration of U251 and U87 cells dose dependently. Simvastatin induced an increase of caspase-3 activity and annexin V staining, and down-regulated the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Simvastatin also decreased cholesterol content in lipid raft fractions, suppressed caveolin-1 expression in the lipid rafts, and induced Fas translocation into lipid rafts, suggesting that simvastatin may inhibit the prosurvival PI3K/Akt pathway and trigger caspase-3–dependent apoptotic cell death through the modulation of lipid rafts. CONCLUSIONThese results suggest that modulation of lipid rafts, Fas translocation, and PI3K/Akt/caspase-3 pathway are involved in the antitumor effect of simvastatin and may have a potential role in cancer prevention and treatment.
Toll‐like receptor 4 knockout mice are protected from endothelial overactivation in the absence of Kupffer cells after total hepatic ischemia/reperfusion

Kupffer cells (KCs) have been shown to be critical mediators of ischemia/reperfusion (I/R) injury in the murine liver. Using liposomal clodronate (LC), we found that KCs were protective in models of total hepatic ischemia with bowel congestion. We investigated the role of toll‐like receptor 4 (TLR4) in the damage that occurs after I/R in KC‐depleted livers. We injected 8‐week‐old C57BL/10J mice and C57BL/10ScN [toll‐like receptor 4 knockout (TLR4KO)] mice with LC 48 hours before 35 minutes of warm hepatic ischemia with bowel congestion, which was followed by either 6 or 24 hours of reperfusion. The KC‐depleted animals had increased mortality as well as a 10‐fold increase in their aminotransferase levels that correlated with increases in centrilobular necrosis. These changes were absent in the TLR4KO animals. Lipopolysaccharide was bound extensively to endothelial cells after I/R, and this binding was diminished in the TLR4KO animals. In conjunction with this, there was an up‐regulation of endothelial cell adhesion molecules in the LC‐treated animals that was absent in the TLR4KO animals. Finally, there was a dramatic increase in the proinflammatory cytokine levels of the LC‐treated animals, and the TLR4KO animals were protected against this increase. In conclusion, TLR4 promotes endothelial overactivation after I/R in the absence of KCs. Liver Transpl 17:1089–1098, 2011. © 2011 AASLD.
Salud pública y situación hospitalaria en Cartagena

Analisis de los servicios de salud publica en Cartagena durante 1998 y 2004, donde presenta estadisticas, indicadores, cobertura, mortalidad infantil, finanzas publicas, presupuesto del estado para la salud, y la comparacion con otras ciudades del pais.
Possible epistatic role of ADH7 in the protection against alcoholism

In recent studies of the role of the alcohol dehydrogenase genes (ADH) in alcoholism the ADH1B Arg47His polymorphism appears to affect risk via a protective effect associated with the ADH1B*47His. Here we present evidence for an additional effect from outside the Class I ADH genes, presumably from functional variation at the ADH7 gene. The protective effect is restricted to one of two haplotypes identical at ADH1B but differing at an intronic SNP at ADH7 suggesting epistasis or strong linkage disequilibrium (LD). © 2003 Wiley‐Liss, Inc.
Metabolic syndrome and cardiovascular risk assessment tools’ estimations of 10-year cardiovascular risk: a population-based study

Abstract Background: This cross-sectional study determines the association between 10-year cardiovascular disease (CVD) risk, estimated using four CVD risk assessment tools, and metabolic syndrome (MetS) in northern Iranian general population. Methods: We used the data of 2371 participants aged 40–74 without any history of diabetes mellitus from a cohort study conducted among 6140 subjects aged 10–90 years in northern Iran. Three definitions of MetS were used. The four CVD risk assessment tools used to estimate the 10-year CVD risk included pooled cohort equations of ACC/AHA, Systematic Coronary Risk Evaluation (SCORE) equations (for low-risk and high-risk European countries), and Framingham general cardiovascular risk profile for use in primary care. Logistic regression was used to determine the association between various definitions of MetS and 10-year CVD risk of ≥5%, ≥ 7.5%, and ≥10%, based on the related risk assessment tools. Results: In men, univariate logistic regression analysis showed the strongest association between 10-year risk of ≥0.1 estimated by Framingham risk profile and the three definitions of MetS. In women, the 10-year risks by Framingham risk profile and SCORE equations for high-risk European countries had stronger associations with various definitions of MetS than others. No significant associations were detected between estimated risks of four risk assessment tools and various definitions of MetS in multivariate logistic regression analyses. Conclusion: No independent associations were observed between estimations of 10-year CVD risk using four risk assessment tools and various definitions of MetS.
Anti‐inflammatory effects of activated protein C on human dendritic cells

Activated protein C (APC) has an anticoagulant action and plays an important role in blood coagulation homeostasis. In addition to its anticoagulant action, APC is known to have cytoprotective effects, such as anti‐apoptotic action and endothelial barrier protection, on vascular endothelial cells and monocytes. However, the effects of APC on DCs have not been clarified. To investigate the effects of APC on human DCs, monocytes were isolated from peripheral blood and DC differentiation induced with LPS. APC significantly inhibited the production of inflammatory cytokines TNF‐α and IL‐6 during differentiation of immature DCs to mature DCs, but did not inhibit the production of IL‐12 and anti‐inflammatory cytokine IL‐10. Interestingly, treatment with 5 μg/mL, but not 25 μg/mL, of APC significantly enhanced production of IL‐10. In addition, protein C, which is the zymogen of APC, did not affect production of these cytokines. On the other hand, flow cytometric analysis of DC's surface molecules indicated that APC does not significantly affect expression of CD83, a marker of mDC differentiation, and the co‐stimulatory molecules CD40, CD80 and CD86. These results suggest that APC has anti‐inflammatory effects on human DCs and may be effective against some inflammatory diseases in which the pathogenesis involves TNF‐α and/or IL‐6 production.
Synergistic activity of 5-trifluoromethylthioribose and inhibitors of methionine synthesis against Klebsiella pneumoniae

5-Methylthioribose (MTR) is an intermediate in the methionine recycling pathway of organisms containing the enzyme MTR kinase. Analogs of MTR have been proposed as a new class of antimicrobial agents because of their ability to perturb the growth of MTR kinase-containing pathogens through inhibition of methionine salvage or by conversion to toxic products. One such analog, 5-trifluoromethylthioribose (TFMTR), has demonstrated potent inhibitory effects on the growth of Klebsiella pneumoniae (A. G. Gianotti, P. A. Tower, J. H. Sheley, P. A. Conte, C. Spiro, J. H. Fitchen, and M. K. Riscoe, J. Biol. Chem. 265:831-837, 1990). Although the mode of action of TFMTR has yet to be determined, it is believed that the drug is converted to the toxic products trifluoromethionine or carbonothioic difluoride via MTR kinase and the methionine recycling pathway. On the basis of this assumption, we theorized that blocking de novo methionine synthesis would increase dependence on the methionine salvage pathway and lead to an increased rate of synthesis of toxic metabolites from TFMTR. In this report, we show that three separate inhibitors of de novo methionine synthesis (1,2,4-triazole, azaserine, and propargylglycine) act synergistically with TFMTR in inhibiting the growth of K. pneumoniae.
Rodent models in bone-related research: the relevance of calvarial defects in the assessment of bone regeneration strategies

In vivo research with animal models has been a preferred experimental system in bone-related biomedical research since, by approximation, it allows relevant data gathering regarding physiological and pathological conditions that could be of use to establish more effective clinical interventions. Animal models, and more specifically rodent models, have been extensively used and have contributed greatly to the development and establishment of a wide range of translational approaches aiming to regenerate the bone tissue. In this regard, the calvarial defect model has found great application in basic and applied research, nonetheless the controversial rationalization for the use of critical size defects – defects that are unable to report spontaneous healing – or subcritical size defects in the proposed applications. Accordingly, this work aims to review the advantages and limitations of the use of rodent models in biomedical bone-related research, emphasizing the problematic issues of the use of calvarial critical and subcritical size defects. Additionally, surgical protocols for the establishment of both defects in rat calvarial bone, as well as the description and exemplification of the most frequently used techniques to access the bone tissue repair, are portrayed.
Induction of experimental autoimmune encephalomyelitis in Dark Agouti rats without adjuvant

Experimental autoimmune encephalomyelitis (EAE) is a well‐recognized model for multiple sclerosis (MS) in humans. However, adjuvants used with encephalitogens to induce EAE produce non‐specific effects interfering with the mechanisms involved in the autoimmune response to the central nervous system (CNS) tissue. It is therefore important to establish a more suitable model of EAE for analysis of autoimmune phenomena resembling those operative in MS. Here we report that EAE can be induced regularly in Dark Agouti (DA) strain of rats with spinal cord tissue without any adjuvant, as judged by both clinical and histological parameters. The incidence and severity of EAE depended on the origin of the encephalitogen, the rat versus guinea pig spinal cord homogenate being more efficient. Furthermore, EAE could be reinduced in animals which had recovered from disease that had been induced actively with encephalitogen alone, suggesting the role of adjuvant‐generated non‐specific mechanisms in resistance to reinduction of EAE. Thus, EAE induced in DA rats with encephalitogen alone provides a reproducible model for defining pathogenically relevant events in CNS autoimmunity devoid of the potentially misleading effects of adjuvants.
The economic contribution of children in peasant agriculture and the effect of education: evidence from the Philippines.

In the context of a commodity demand-labor supply framework, the interaction between education and child labor supply in peasant agriculture is explored with particular with particular attention to how child labor supply is related to farm-household characteristics; how adult and child labor supply and the cost of schooling are related in the agricultural household; and how the cost of schooling affects labor supply decisions for children. The analysis is conducted to better understand the behavioral model of consumption-leisure choice. Empirical evidence is drawn from a subset of 34 tenants and 60 landholders from 1978-79 Philippine farm-household survey data. The study found that increasing wage rates of adults and children increases labor supply and decreases demand for leisure. Labor supply of adults and children is upward-sloping and elastic, with the supply of child labor being more elastic. Given the complementarity between adult and child labor in farm operations, children make positive economic contributions to farm households in peasant agriculture. Education may therefore have only a limited impact in reducing fertility in rural households. It is instead recommended to develop policy aimed at reducing the demand for labor in agriculture operations or to provide income-generating opportunities for peasant households with interventions in the organization of peasant farming. This approach would bolster the degree of mass education and lead to eventual decreases in desired family size.
Spanish food patterns

Abstract Data from household food budgetary surveys and regional, population-based, crosssectional studies show a declining trend in energy intake in the last decades, also applicable to protein, fat and carbohydrate intakes in absolute terms. The pattern suggests a lower fat content in the diet. Protein intake is 200% of the recommended level. Spanish food patterns underwent dramatic changes between the 1960s and the 1980s, including an important increase in fat intake, up to 44% energy intake from fat in the 1980s. The trend changed in the 1990s, and current fat supply provides an average of 37% of energy intake. Main sources of fat in the Spanish diet are added fats for cooking (49% of total fat intake), especially olive oil; meat and meat products (25%); and a lower percentage provided by milk and dairy products. Most saturated fatty acids are supplied by meats (30%) and dairy products (27%). Rapid urbanisation processes and the growing proportion of females in the active workforce have led to important changes in food patterns in the last decades. On the one hand, some changes had a positive impact, such as increasing variety in the diet and access to food; on the other hand, some changes moved the Spanish diet away from the traditional Mediterranean food pattern. Current food patterns evidence high consumption of animal products: meat, fish, milk and dairy products. It seems advisable to increase consumption of plant foods, particularly whole-grain cereals, potatoes and pulses. Intake of fruit and vegetables shows a shift towards a greater consumption of processed foods rather than fresh products, and overall a greater consumption would be recommended.