Оценка эндоскопической картины и микробного пейзажа бронхиального дерева при хронических неспецифических заболеваниях легких у детей

БРОНХОСКОПИЯДЕТИ, СЛУЖБЫ ОХРАНЫ ЗДОРОВЬЯЛЕГКИХ БОЛЕЗНИ ОБСТРУКТИВНЫ

Field Testing of Alternative Cookstove Performance in a Rural Setting of Western India

Nearly three billion people use solid fuels for cooking and heating, which leads to extremely high levels of household air pollution and is a major cause of morbidity and mortality. Many stove manufacturers have developed alternative cookstoves (ACSs) that are aimed at reducing emissions and fuel consumption. Here, we tested a traditional clay chulha cookstove (TCS) and five commercially available ACSs, including both natural draft (Greenway Smart Stove, Envirofit PCS-1) and forced draft stoves (BioLite HomeStove, Philips Woodstove HD4012, and Eco-Chulha XXL), in a test kitchen in a rural village of western India. Compared to the TCS, the ACSs produced significant reductions in particulate matter less than 2.5 µm (PM2.5) and CO concentrations (Envirofit: 22%/16%, Greenway: 24%/42%, BioLite: 40%/35%, Philips: 66%/55% and Eco-Chulha: 61%/42%), which persisted after normalization for fuel consumption or useful energy. PM2.5 and CO concentrations were lower for forced draft stoves than natural draft stoves. Furthermore, the Philips and Eco-Chulha units exhibited higher cooking efficiency than the TCS. Despite significant reductions in concentrations, all ACSs failed to achieve PM2.5 levels that are considered safe by the World Health Organization (ACSs: 277–714 μg/m3 or 11–28 fold higher than the WHO recommendation of 25 μg/m3)

Dmrt5, a novel neurogenic factor, reciprocally regulates Lhx2 to control the neuron-glia cell fate switch in the developing hippocampus

Regulation of the neuron-glia cell-fate switch is a critical step in the development of the CNS. Previously, we demonstrated that Lhx2 is a necessary and sufficient regulator of this process in the mouse hippocampal primordium, such that Lhx2 overexpression promotes neurogenesis and suppresses gliogenesis, whereas loss of Lhx2 has the opposite effect.Wetested a series of transcription factors for their ability to mimic Lhx2 overexpression and suppress baseline gliogenesis, and also to compensate for loss of Lhx2 and suppress the resulting enhanced level of gliogenesis in the hippocampus. Here, we demonstrate a novel function of Dmrt5/Dmrta2 as a neurogenic factor in the developing hippocampus. We show that Dmrt5, as well as known neurogenic factors Neurog2 and Pax6, can each not only mimic Lhx2 overexpression, but also can compensate for loss of Lhx2 to different extents. We further uncover a reciprocal regulatory relationship between Dmrt5 and Lhx2, such that each can compensate for loss of the other. Dmrt5 and Lhx2 also have opposing regulatory control on Pax6 and Neurog2, indicating a complex bidirectionally regulated network that controls the neuron-glia cell-fate switch. Finally, we confirm that Lhx2 binds a highly conserved putative enhancer of Dmrt5, suggesting an evolutionarily conserved regulatory relationship between these factors. Our findings uncover a complex network that involves Lhx2, Dmrt5, Neurog2, and Pax6, and that ensures the appropriate amount and timing of neurogenesis and gliogenesis in the developing hippocampus.Significance Statement Weidentify Dmrt5 as a novel regulator of the neuronglia cell-fate switch in the developing hippocampus.Wedemonstrate Dmrt5 to be neurogenic, and reciprocally regulated by Lhx2: loss of either factor promotes gliogenesis; overexpression of either factor suppresses gliogenesis and promotes neurogenesis; each can substitute for loss of the other. Furthermore, each factor has opposing effects on established neurogenic genes Neurog2 and Pax6. Dmrt5 is known to suppress their expression, and we show that Lhx2 is required to maintain it. Our study reveals a complex regulatory network with bidirectional control of a fundamental feature of CNS development, the control of the production of neurons versus astroglia in the developing hippocampus.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

HIV/AIDS-related mortality in Africa and Asia : evidence from INDEPTH health and demographic surveillance system sites

BACKGROUND: As the HIV/AIDS pandemic has evolved over recent decades, Africa has been the most affected region, even though a large proportion of HIV/AIDS deaths have not been documented at the individual level. Systematic application of verbal autopsy (VA) methods in defined populations provides an opportunity to assess the mortality burden of the pandemic from individual data. OBJECTIVE: To present standardised comparisons of HIV/AIDS-related mortality at sites across Africa and Asia, including closely related causes of death such as pulmonary tuberculosis (PTB) and pneumonia. DESIGN: Deaths related to HIV/AIDS were extracted from individual demographic and VA data from 22 INDEPTH sites across Africa and Asia. VA data were standardised to WHO 2012 standard causes of death assigned using the InterVA-4 model. Between-site comparisons of mortality rates were standardised using the INDEPTH 2013 standard population. RESULTS: The dataset covered a total of 10,773 deaths attributed to HIV/AIDS, observed over 12,204,043 person-years. HIV/AIDS-related mortality fractions and mortality rates varied widely across Africa and Asia, with highest burdens in eastern and southern Africa, and lowest burdens in Asia. There was evidence of rapidly declining rates at the sites with the heaviest burdens. HIV/AIDS mortality was also strongly related to PTB mortality. On a country basis, there were strong similarities between HIV/AIDS mortality rates at INDEPTH sites and those derived from modelled estimates. CONCLUSIONS: Measuring HIV/AIDS-related mortality continues to be a challenging issue, all the more so as anti-retroviral treatment programmes alleviate mortality risks. The congruence between these results and other estimates adds plausibility to both approaches. These data, covering some of the highest mortality observed during the pandemic, will be an important baseline for understanding the future decline of HIV/AIDS