392 research outputs found

    Comparison of body temperature measurements obtained with otic digital thermometer and mercury axillary and rectal thermometers in children under the age of five

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    Indexación: Web of Science; ScieloIntroducción: En los últimos años han aparecido nuevos métodos para medir la temperatura en niños, como el termómetro digital ótico. Siendo este un método más rápido para medir la temperatura y por lo tanto ideal para el servicio de urgencias, es necesario conocer su confiabilidad. Objetivo: Comparar los valores de temperatura corporal que entrega el termómetro ótico digital con los termómetros de mercurio axilar y rectal. Pacientes y Método: Se efectuó la medición de la temperatura en 50 pacientes menores de 5 años elegidos al azar, que consultaron en el Servicio de Urgencia del Hospital de Niños y Cunas de Viña del Mar. Se les midió la temperatura con un termómetro digital ótico al lado izquierdo y derecho, y las temperaturas axilar derecha y rectal con termómetros de mercurio. EL análisis de los resultados se efectuó en el grupo estudiado, separado en dos grupos, menores y mayores de 6 meses. Resultados: Los resultados entre ambos subgrupos fueron los mismos. La temperatura media rectal obtenida fue 0,414°C más alta que la media ótica derecha (p < 0,001) y 0,438°C más alta que la temperatura media ótica izquierda (p < 0,001). Conclusión: El termómetro ótico digital entrega una temperatura significativamente más baja que la que entregan los termómetros de mercurio axilar y rectal.Background: In recent years, otic thermometers to measure body temperature in children have become increasingly popular as they reflect changes in body temperature sooner than other thermometers. The have become valuable assets in hospital emergency rooms; however, their accuracy and reliability need further studies. Objective: To compare corporal temperature readings between an otic thermometer and mercury axillary and rectal thermometers. Patients and Method: 50 patients under the age of 5, who were treated at the emergency room of our hospital, were randomly chosen to participate in this study. Temperature was measured on their right and left ears using an otic thermometer, and their rectal and right axillary temperature was taken using mercury thermometers. Patients were separated into 2 subgroups for comparison, children under and over 6 months old. Results: The results between the 2 subgroups were very similar. The average temperature obtained by rectal thermometers was 0.414°C higher than the average right-ear temperature (p < 0.001) and 0.438°c higher than the average left-ear temperature (p < 0.001). Conclusion: The otic thermometer's reading is significantly lower than the one obtained using mercury rectal and axillary thermometers.http://ref.scielo.org/72p3g

    Bcl-2 functionally interacts with inositol 1,4,5-trisphosphate receptors to regulate calcium release from the ER in response to inositol 1,4,5-trisphosphate

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    Inositol 1,4,5-trisphosphate (InsP3) receptors (InsP3Rs) are channels responsible for calcium release from the endoplasmic reticulum (ER). We show that the anti-apoptotic protein Bcl-2 (either wild type or selectively localized to the ER) significantly inhibited InsP3-mediated calcium release and elevation of cytosolic calcium in WEHI7.2 T cells. This inhibition was due to an effect of Bcl-2 at the level of InsP3Rs because responses to both anti-CD3 antibody and a cell-permeant InsP3 ester were decreased. Bcl-2 inhibited the extent of calcium release from the ER of permeabilized WEHI7.2 cells, even at saturating concentrations of InsP3, without decreasing luminal calcium concentration. Furthermore, Bcl-2 reduced the open probability of purified InsP3Rs reconstituted into lipid bilayers. Bcl-2 and InsP3Rs were detected together in macromolecular complexes by coimmunoprecipitation and blue native gel electrophoresis. We suggest that this functional interaction of Bcl-2 with InsP3Rs inhibits InsP3R activation and thereby regulates InsP3-induced calcium release from the ER

    INHIBITING CSF1R ALLEVIATES CEREBROVASCULAR WHITE MATTER DISEASE AND COGNITIVE IMPAIRMENT

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    White matter abnormalities, related to poor cerebral perfusion, are a core feature of small vessel cerebrovascular disease, and critical determinants of vascular cognitive impairment and dementia. Despite this importance there is a lack of treatment options. Proliferation of microglia producing an expanded, reactive population and associated neuroinflammatory alterations have been implicated in the onset and progression of cerebrovascular white matter disease, in patients and in animal models, suggesting that targeting microglial proliferation may exert protection. Colony-stimulating factor-1 receptor (CSF1R) is a key regulator of microglial proliferation. We found that the expression of CSF1R/Csf1r and other markers indicative of increased microglial abundance are significantly elevated in damaged white matter in human cerebrovascular disease and in a clinically relevant mouse model of chronic cerebral hypoperfusion and vascular cognitive impairment. Using the mouse model, we investigated long-term pharmacological CSF1R inhibition, via GW2580, and demonstrated that the expansion of microglial numbers in chronic hypoperfused white matter is prevented. Transcriptomic analysis of hypoperfused white matter tissue showed enrichment of microglial and inflammatory gene sets, including phagocytic genes that were the predominant expression modules modified by CSF1R inhibition. Further, CSF1R inhibition attenuated hypoperfusion-induced white matter pathology and rescued spatial learning impairments and to a lesser extent cognitive flexibility. Overall, this work suggests that inhibition of CSF1R and microglial proliferation mediates protection against chronic cerebrovascular white matter pathology and cognitive deficits. Our study nominates CSF1R as a target for the treatment of vascular cognitive disorders with broader implications for treatment of other chronic white matter diseases.<br/

    Mobilizing governments and society to combat obesity: Reflections on how data from the WHO European Childhood Obesity Surveillance Initiative are helping to drive policy progress

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    To meet the need for regular and reliable data on the prevalence of overweight andobesity among children in Europe, the World Health Organization (WHO) EuropeanChildhood Obesity Surveillance Initiative (COSI) was established in 2007. Theresulting robust surveillance system has improved understanding of the public healthchallenge of childhood overweight and obesity in the WHO European Region. For the past decade, data from COSI have helped to inform and drive policy action onnutrition and physical activity in the region. This paper describes illustrative examplesof how COSI data have fed into national and international policy, but the real scopeof COSI's impact is likely to be much broader. In some countries, there are signs thatpolicy responses to COSI data have helped halt the rise in childhood obesity. As thecountries of the WHO European Region commit to pursuing United Action for BetterHealth in Europe in WHO's new European Programme of Work, COSI provides anexcellent example of such united action in practice. Further collaborative action willbe key to tackling this major public health challenge which affects children through-out the regionThe authors gratefully acknowledge support through a grant from the Russian government in the context of the WHO European Office for the Prevention and Control of NCDs. The Ministries of Health of Austria, Croatia, Greece, Italy, Malta, Norway, and the Russian Federation provided financial support for the meetings at which the protocol, data collection procedures, and analyses were discussed. Data collection in the countries featured in this paper was made possible through funding from: Bulgaria: Ministry of Health, National Center of Public Health and Analyses, WHO Regional Office for Europe; Croatia: Ministry of Health, Croatian Institute of Public Health, and WHO Regional Office for Europe; Georgia: WHO; Ireland: Health Service Executive; Italy: Ministry of Health and Italian National Institute of Health; Latvia: Centre for Disease Prevention and Control, Ministry of Health, Latvia; Malta: Ministry of Health; North Macedonia: funded by the Government of North Macedonia through National Annual Program of Public Health and implemented by the Institute of Public Health and Centers of Public Health. WHO country office provides support for training and data management; Portugal: Ministry of Health Institutions, the National Institute of Health, Directorate General of Health, Regional Health Directorates and the kind technical support from the Center for Studies and Research on Social Dynamics and Health (CEIDSS); Turkey: Turkish Ministry of Health and World Bank.info:eu-repo/semantics/publishedVersio

    Microglia regulate myelin growth and integrity in the central nervous system

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    Myelin is required for the function of neuronal axons in the central nervous system, but the mechanisms that support myelin health are unclear. Although macrophages in the central nervous system have been implicated in myelin health(1), it is unknown which macrophage populations are involved and which aspects they influence. Here we show that resident microglia are crucial for the maintenance of myelin health in adulthood in both mice and humans. We demonstrate that microglia are dispensable for developmental myelin ensheathment. However, they are required for subsequent regulation of myelin growth and associated cognitive function, and for preservation of myelin integrity by preventing its degeneration. We show that loss of myelin health due to the absence of microglia is associated with the appearance of a myelinating oligodendrocyte state with altered lipid metabolism. Moreover, this mechanism is regulated through disruption of the TGFβ1–TGFβR1 axis. Our findings highlight microglia as promising therapeutic targets for conditions in which myelin growth and integrity are dysregulated, such as in ageing and neurodegenerative disease(2,3)

    Methodology and implementation of the WHO European Childhood Obesity Surveillance Initiative (COSI)

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    Establishment of the WHO European Childhood Obesity Surveillance Initiative (COSI)has resulted in a surveillance system which provides regular, reliable, timely, andaccurate data on children's weight status—through standardized measurement ofbodyweight and height—in the WHO European Region. Additional data on dietaryintake, physical activity, sedentary behavior, family background, and schoolenvironments are collected in several countries. In total, 45 countries in the EuropeanRegion have participated in COSI. The first five data collection rounds, between 2007and 2021, yielded measured anthropometric data on over 1.3 million children. In COSI,data are collected according to a common protocol, using standardized instrumentsand procedures. The systematic collection and analysis of these data enables inter-country comparisons and reveals differences in the prevalence of childhood thinness,overweight, normal weight, and obesity between and within populations. Furthermore,it facilitates investigation of the relationship between overweight, obesity, and poten-tial risk or protective factors and improves the understanding of the development ofoverweight and obesity in European primary-school children in order to supportappropriate and effective policy responses.The authors gratefully acknowledge support through a grant from the Russian Government in the context of the WHO European Office for the Prevention and Control of NCDs. The ministries of health of Austria, Croatia, Greece, Italy, Malta, Norway, and the Russian Federation provided financial support for the meetings at which the protocol, data collection procedures, and analyses were discussed. Data collection in countries was made possible through funding from the following: Albania: WHO through the Joint Programme on Children, Food Security and Nutrition “Reducing Malnutrition in Children,” funded by the Millennium Development Goals Achievement Fund, and the Institute of Public Health. Austria: Federal Ministry of Labor, Social Affairs, Health and Consumer Protection of Austria. Bulgaria: Ministry of Health, National Center of Public Health and Analyses, and WHO Regional Office for Europe. Bosnia and Herzegovina: WHO country office support for training and data management. Croatia: Ministry of Health, Croatian Institute of Public Health, and WHO Regional Office for Europe. Czechia: Ministry of Health of the Czech Republic, grant number 17-31670A and MZCR—RVO EU 00023761. Denmark: Danish Ministry of Health. Estonia: Ministry of Social Affairs, Ministry of Education and Research (IUT 42-2), WHO Country Office, and National Institute for Health Development. Finland: Finnish Institute for Health and Welfare. France: Santé publique France (the French Agency for Public Health). Georgia: WHO. Greece: International Hellenic University and Hellenic Medical Association for Obesity. Hungary: WHO Country Office for Hungary. Ireland: Health Service Executive. Italy: Ministry of Health. Kazakhstan: Ministry of Health of the Republic of Kazakhstan, WHO, and UNICEF. Kyrgyzstan: World Health Organization. Latvia: Ministry of Health and Centre for Disease Prevention and Control. Lithuania: Science Foundation of Lithuanian University of Health Sciences and Lithuanian Science Council and WHO. Malta: Ministry of Health. Montenegro: WHO and Institute of Public Health of Montenegro. North Macedonia: Government of North Macedonia through National Annual Program of Public Health and implemented by the Institute of Public Health and Centers of Public Health; WHO country office provides support for training and data management. Norway: the Norwegian Ministry of Health and Care Services, the Norwegian Directorate of Health, and the Norwegian Institute of Public Health. Poland: National Health Programme, Ministry of Health. Portugal: Ministry of Health Institutions, the National Institute of Health, Directorate General of Health, Regional Health Directorates, and the kind technical support from the Center for Studies and Research on Social Dynamics and Health (CEIDSS). Romania: Ministry of Health. Russian Federation: WHO. San Marino: Health Ministry, Educational Ministry, and Social Security Institute and Health Authority. Serbia: WHO and the WHO Country Office (2015-540940 and 2018/873491-0). Slovakia: Biennial Collaborative Agreement between WHO Regional Office for Europe and Ministry of Health SR. Slovenia: Ministry of Education, Science and Sport of the Republic of Slovenia within the SLOfit surveillance system. Spain: Spanish Agency for Food Safety and Nutrition. Sweden: Public Health Agency of Sweden. Tajikistan: WHO Country Office in Tajikistan and Ministry of Health and Social Protection. Turkmenistan: WHO Country Office in Turkmenistan and Ministry of Health. Turkey: Turkish Ministry of Health and World Bank.info:eu-repo/semantics/publishedVersio

    K70Q Adds High-Level Tenofovir Resistance to “Q151M Complex” HIV Reverse Transcriptase through the Enhanced Discrimination Mechanism

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    HIV-1 carrying the “Q151M complex” reverse transcriptase (RT) mutations (A62V/V75I/F77L/F116Y/Q151M, or Q151Mc) is resistant to many FDA-approved nucleoside RT inhibitors (NRTIs), but has been considered susceptible to tenofovir disoproxil fumarate (TFV-DF or TDF). We have isolated from a TFV-DF-treated HIV patient a Q151Mc-containing clinical isolate with high phenotypic resistance to TFV-DF. Analysis of the genotypic and phenotypic testing over the course of this patient's therapy lead us to hypothesize that TFV-DF resistance emerged upon appearance of the previously unreported K70Q mutation in the Q151Mc background. Virological analysis showed that HIV with only K70Q was not significantly resistant to TFV-DF. However, addition of K70Q to the Q151Mc background significantly enhanced resistance to several approved NRTIs, and also resulted in high-level (10-fold) resistance to TFV-DF. Biochemical experiments established that the increased resistance to tenofovir is not the result of enhanced excision, as K70Q/Q151Mc RT exhibited diminished, rather than enhanced ATP-based primer unblocking activity. Pre-steady state kinetic analysis of the recombinant enzymes demonstrated that addition of the K70Q mutation selectively decreases the binding of tenofovir-diphosphate (TFV-DP), resulting in reduced incorporation of TFV into the nascent DNA chain. Molecular dynamics simulations suggest that changes in the hydrogen bonding pattern in the polymerase active site of K70Q/Q151Mc RT may contribute to the observed changes in binding and incorporation of TFV-DP. The novel pattern of TFV-resistance may help adjust therapeutic strategies for NRTI-experienced patients with multi-drug resistant (MDR) mutations
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