Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980-2015 : a systematic analysis for the Global Burden of Disease Study 2015

Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14 294 geography-year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61.7 years (95% uncertainty interval 61.4-61.9) in 1980 to 71.8 years (71.5-72.2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11.3 years (3.7-17.4), to 62.6 years (56.5-70.2). Total deaths increased by 4.1% (2.6-5.6) from 2005 to 2015, rising to 55.8 million (54.9 million to 56.6 million) in 2015, but age-standardised death rates fell by 17.0% (15.8-18.1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14.1% (12.6-16.0) to 39.8 million (39.2 million to 40.5 million) in 2015, whereas age-standardised rates decreased by 13.1% (11.9-14.3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42.1%, 39.1-44.6), malaria (43.1%, 34.7-51.8), neonatal preterm birth complications (29.8%, 24.8-34.9), and maternal disorders (29.1%, 19.3-37.1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146 000 deaths, 118 000-183 000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393 000 deaths, 228 000-532 000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost [YLLs]) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Copyright (C) The Author(s). Published by Elsevier Ltd.Peer reviewe

Investigation of the protective effect of boric acid and omega-3 fatty acid in model of acute myocardial infarction changes in myocardial rats

41st FEBS Congress on Molecular and Systems Biology for a Better Life -- SEP 03-08, 2016 -- Kusadasi, TURKEYWOS: 000383616901564…FEB

Possible protective effects of betaine on liver and kidney tissues of long term therapeutic doses of paracetamol (acetaminophen) administered on pregnant rat's newborn puppies

41st FEBS Congress on Molecular and Systems Biology for a Better Life -- SEP 03-08, 2016 -- Kusadasi, TURKEYWOS: 000383616901798…FEB

Protective effect of betaine against skeleton muscle apoptosis in rats induced by chronic alcohol and statin consumption

AIM: The aim of the present study was to investigate the effect of apoptosis on rat skeletal muscle caused by chronic alcohol and statin consumption with modified liquid diet and to elucidate protective effects of betaine supplementation.METHODS: TNF-alpha (tumor necrosis factor), NF-kappa B (Nuclear Factor kappa B), cytochrome c and caspase-3 levels with or without betaine treatment in alcohol and/or statin-induced skeleton muscle apoptosis rats as well as in controls were measured in serum and tissue. Histologic examinations of the muscle tissues were also performed.RESULTS: In our study, betaine treated treatment groups we found that calpain and caspase activities and cytokine c release were decreased caused by alcohol, statin and more importantly alcohol+statin group and TNF and NF-kappa B levels were also close to the levels of control group. Similarly, significant improvements have been observed in our morphological and histological examination results also supporting our biochemical data.CONCLUSION: We found that combined consumption of ethanol and statin is capable of triggering apoptotic cell death in rat muscles more than the consumption of only alcohol or only statin. Betaine was able to reduced this muscle cell death induced by alcohol and/or statin consumption

Pregabalinin gastrik ülser oluşumu ve antioksidan parametreler üzerine etkileri

Pregabalin, a drug used in epilepsy, anxiety, neuropathic pain is reported to have analgesic effects in inflammatory pain. We aimed to investigate whether pregabalin have gastric side effects and to compare with a non steroidal antiinflammatory drug (NSAID) in rats. The effects of pregabalin on antioxidant levels, which are suggested to protect against gastric mucosal damage were also studied. Pregabalin 30, 50, 100 mg/kg, indomethacin 5 mg/kg (reference-NSAID), saline (control group) were administered orally for 10 days. At the end of 10 day treatment, rats were sacrificed, gastric tissues were removed out, mucus secretion was determined spectrophotometrically, ulcer index was scored from score 0:(no-petechia) to score 3:(petechia>5mm). Also, to evaluate the antioxidant effects of pregabalin, malondialdehyde (MDA) levels, catalase and superoxide dismutase (SOD) activities in gastric tissue were studied. Pregabalin 50 mg/kg and 100 mg/kg similar to indomethacin significantly reduced mucus secretion and increased ulcer index compared to control while pregabalin 30 mg/kg did not. Pregabalin 30 mg/kg and 100 mg/kg decreased SOD and catalase levels. Pregabalin 100 mg/kg dose increased MDA levels. 50 mg/kg and 100 mg/kg pregabalin showed gastric side effects as reduced mucus secretion and ulcer formation similar to indomethacin and 30 mg/kg pregabalin may be reasonable dose without showing gastric side effects. Pregabalin 50 mg/kg seems to have enhancing effects on antioxidant levels.Pregabalin epilepsi, ankisiyete ve nöropatik ağrıda kullanılan analjezik etkiye sahip antiinflamatuvar bir ajandır. Biz çalışmamızda pregabalinin sıçanlarda mide üzerine yan etkilerinin olup olmadığını ve bir non-steridal antiinflamatuvar bir ajan ile etkisini karşılaştırmayı amaçladık. Pregabalinin gastrik mukozal hasara karşı koruyucu olduğu düşünülen antioksidan seviyeleri üzerine olan etkilerini de araştırdık. Pregabalin 30, 50, 100 mg/kg, indometasin 5 mg/kg (referans-NSAID), salin (kontrol grubu) 10 gün boyunca oral olarak uygulandı. 10 günlük tedavinin sonunda, sıçanlar sakrifiye edildi, mide dokuları çıkarıldı, mukus salgılanması spektrofotometrik olarak belirlendi, ülser indeksi 0'dan (no-peteşi) skor 3'e (peteşi> 5mm) kadar skorlandı. Ayrıca pregabalinin mide dokusundaki antioksidan etkilerini değerlendirmek üzere malondialdehid (MDA), katalaz ve süperoksit dismutaz (SOD) aktiviteleri çalışıldı. Pregabalin 50 mg/kg ve 100 mg/kg dozları kontrol grubu ile karşılaştırıldığında indometazine benzer şekilde anlamlı olarak mukus salgılanmasını azalttı ve ülser indeksini artırdı. Pregabalin 30 mg/kg dozunda bu etki görülmedi. Pregabalin 30 mg/kg ve 100 mg/kg SOD ve katalaz seviyelerini düşürüyorken pregabalin 100 mg/kg dozunda MDA seviyeleri artmıştır. 50 mg/kg and 100 mg/kg pregabalin mukus salgılanmasını ve ülser oluşumu indometazin 30 mg/kg dozuna benzer şekilde azaltarak gastrik yan etkiler göstermiştir. Pregabalin 30 mg/kg dozu ise gastrik yan etkilerin ortaya çıkmadığı uygun doz olabilir. Pregabalin 50 mg/kg dozunun ise antioksidan seviyelerini artırıcı etkiye sahip olduğu görülmüştür

Dose-dependent effects of vitamin 1,25(OH)2D3 on oxidative stress and apoptosis

The purpose of this study is to examine the dose-dependent effects of vitamin 1,25(OH)2D3 on apoptosis and oxidative stress. In this study, 50 male Balb/c mice were used as control and experiment groups. The mice were divided into 5 groups each consisting of 10 mice. Calcitriol was intraperitoneally administered as low dose, medium dose, medium-high dose and high dose Vitamin D groups (at 0.5, 1, 5 and 10 µg/kg, respectively), for three times a week during 14 days. At the end of the study, annexin V was measured by enzyme-linked immunosorbent assay method, and total antioxidant capacity and total oxidant status values were measured by colorimetric method in serum. Hematoxylin eosin staining was performed in liver tissues and periodic acid schiff staining was performed in kidney tissues. While comparing the results of medium-high dose (5 µg/kg) and high dose (10 µg/kg) Vitamin D administration to that of the control group, it was observed that serum antioxidant status and annexin V levels decreased and glomerular mesenchial matrix ratio increased in kidney (p<0.05). In addition to these findings, in the group receiving high dose Vitamin D (10 µg/kg), it was observed that the damage to the liver increased together with the the oxidative stress index values (p<0.05). As a result, this study was the first in the literature to report that use of high-dose Vitamin D (10 µg/kg) results in oxidant effect, rather than being an antioxidant, and causes severe histopathological toxicity in the liver and kidney

A possible protective role of betain and omega-3 supplementation in traumatic brain injury

WOS: 000471139700013PubMed ID: 31182701INTRODUCTION: Due to irreversible damage following head trauma, many overlapping pathophysiological events occur including excitotoxicity, acidotoxicity, ionic imbalance, edema, oxidative stress inflammation and apoptosis. MATERIAL AND METHODS: In this this study, after the rats were separated in to groups theserats were fed throughout fourteen days with betaine, omega-3 or betaine+omega-3 combination in physiological limits prior to the trauma. After a closed head trauma, the damaged brain tissues were collected for biochemically and histologically analyses. This examination involved analyses of levels of caspase-3 and cytochrome C and neuron-specific enolase (NSE) levels in brain tissue. RESULTS: These analyses showed that traumatic brain injury (TBI) caused an increase in the levels of caspase-3, cytochrome C and neuron-specific enolase (NED) in the brain tissues examined. DISCUSSION: In this study, apoptotic and/or necrotic cell death via mitochondrial cytochrome C caspase pathway in traumatized cells and neuron-specific enolase (NED) increase indicative of neuronal damage confirmed the research hypothesis. CONCLUSION: Level of the biomarkers induced by brain injury in the groups fed with betaine, omega-3 and betaine+omega-3 combination before the traumatic damage approximated to that of control group values, suggesting that these products may have a neuroprotective role

Evaluation of the neuroprotective role of boric acid in preventing traumatic brain injury-mediated oxidative stress

AIM: To investigate the possible neuroprotective effect of boric acid (BA) by examining the changes in catalase (CAT) activity and levels of CAT and malondialdehyde (MDA) in brain tissues from rats with closed head trauma. MATERIAL and METHODS: The study consisted of three groups: control, traumatic brain injury (TBI) and TBI + BA. Animals in the control and TBI groups received saline, while animals in the TBI + BA group received BA through daily oral gavage, for 14 days prior to TBI was performed using the modified Marmarou impact acceleration model. After 24 hours, animals were euthanized, and brain tissue obtained to measure the levels of MDA and to assess the activity of CAT. RESULTS: MDA levels and CAT activity were significantly higher in the TBI group versus the control group. However, they were significantly lower in the TBI + BA group compared to TBI alone. Similarly, edema and necrotic neurons were observed in the TBI group, but not in the control or TBI + BA groups. CONCLUSION: Based on biochemical and histopathological evidence, we determined that TBI induced lipid peroxidation and oxidative stress were inhibited by pre-treatment with BA.Turkish Neurosurgical Societ

Anomalous Rheological Behavior of Dendritic Nanoparticle/Linear Polymer Nanocomposites

We investigated the effects of soft dendritic polyethylene (dPE) nanoparticles on the rheological properties of a linear polystyrene (PS) matrix. The viscosity of PS–dPE nanocomposites is found to exhibit nonmonotonic dependence on the dPE concentration. In particular, with the addition of 1% dPE nanoparticles, we already observe more than 1 order of magnitude reduction in viscosity. The minimum viscosity was observed at 5% nanoparticles. At dPE concentrations higher than 5%, nanocomposite viscosity increases by addition of nanoparticles, yet it remains below the viscosity of PS. Addition of nanoparticles not only influences the terminal relaxation times of the nanocomposites but also affects their whole relaxation spectra. The viscosity of PS–dPE nanocomposites at high temperature is found to reversibly evolve with time, which proves the existence of supramolecular interactions between the PS matrix and the nanoparticles. Atomic force microscopy confirms that dPE nanoparticles are well distributed in the PS matrix, though each component of the nanocomposite exhibits its own glass transition. While the origin of viscosity reduction remains unknown, it cannot be attributed to confinement, free volume effect, change of entanglement density, surface slippage, shear banding, or particle induced shear thinning