10 research outputs found
Global impact of COVID-19 on food safety and environmental sustainability: Pathways to face the pandemic crisis
No full textThe COVID-19 pandemic poses ongoing challenges to the sustainability of various socioeconomic sectors, including agriculture, the food supply chain, the food business, and environmental sustainability. This study employs data obtained from the World Health Organization (WHO), and Food and Agriculture Organization (FAO), as well as scientific and technical research publications, to evaluate the impacts of COVID-19 on agriculture and food security. This article seeks to highlight the profound influence of the COVID-19 pandemic on agriculture, the supply and demand of food, and the overall safety of food. The article also explores the several pathways by which COVID-19 can be transmitted in these areas and the various technologies employed for its detection. The ongoing and post-pandemic ramifications are substantial since they could decrease agricultural output due to limitations on migration, a downturn in international trade, less buying capacity, and disturbances in food production and processing. Therefore, based on this thorough investigation, recommendations are issued for mitigating and controlling the pandemic's effects
A computational approach for the unsteady flow of maxwell fluid with Caputo fractional derivatives
No full textA computational approach for the unsteady flow of maxwell fluid with Caputo fractional derivatives
No full textIn this paper, the velocity field and the time dependent shear stress of Maxwell fluid with Caputo fractional derivatives in an infinite long circular cylinder of radius R is discussed. The motion in the fluid is produced by the circular cylinder. The fluid is initially at rest and at time t=0+, cylinder begins to oscillate with the velocity fsinωt, due to time dependent shear stress acting on the cylinder tangentially. The hybrid technique used in this paper for the solution of the problem has less computational efforts and time cost as compared to other commonly used methods. The obtained solutions are in transformed domain, which are expressed in terms of modified Bessel functions I0(·) and I1(·). The inverse Laplace transformation has been calculated numerically by using MATLAB package. The semi analytical solutions for Maxwell fluid with fractional derivatives are reduced to the similar solutions for Newtonian and ordinary Maxwell fluids as limiting cases. In the end, numerical simulations have been performed to analyze the behavior of fractional parameter α, kinematic viscosity ν, relaxation time λ, radius of the circular cylinder R and dynamic viscosity μ on our obtained solutions of velocity field and shear stress. Keywords: Shear stress, Maxwell fluid, Laplace transformation, Velocity field, Modified Bessel functio
Production of biodiesel and water conservation through conversion of free fatty acids from a domestic wastewater drain
No full textWastewater discharge from restaurants, hotels, household kitchens, confectionaries, meat, fruits, and vegetable processing units contain free fatty acids (FFAs) from fats, oils, and greases (FOG). These FFAs are one of the major causes of sewer overflows and blockages that cause health and environmental issues. This study has investigated the use of sewer wastewater as a source of lipids for the production of alkyl esters (Biodiesel) and provides a characterization of the resulting processed water. Amberlyst A21 basic resin in a column reactor was used to recover the FFAs by adsorption from an oily layer collected from the domestic wastewater drain (Chakri drain, Rawalpindi, Pakistan) having a 33.0 ± 2.08% oily fraction with 59.7 ± 1.1% FFAs. The recovered ethanol washed FFAs from the Amberlyst A21 surface were then turned into Fatty Acid Ethyl Esters (FAEEs) in the presence of an acidic resin catalyst Amberlyst 15. The esterification reaction was studied at temperatures 50, 60, and 70°C, molar ratios of 1:2 to 1:3, acidic resin weight % of 2 to 6, and reaction time of 2 to 8 hr, respectively. A maximum FFAs conversion into esters of 91.38 ± 1.13% was noted at an esterification temperature of 70°C, molar ratio of 1:3, acidic resin weight of 6%, and a reaction time of 8 h. The fractional distillation of the esterified reaction product at 100°C improved the ester content in the reaction mixture up to 96.6 ± 0.18%, with a distilled biodiesel yield of 95.52 ± 0.21%. The collected top oily layer from sewer drain wastewater was found to have a density 947.31 kg/m3, kinematic viscosity 32.69 mm2/sec, flash point 283°C, and LHV and HHV of 26 and 28 MJ/kg, respectively, while for the produced biodiesel the density was 886 kg/m3, kinematic viscosity 4.3 mm2/sec, flash point 137°C, and LHV and HHV of 39 and 41 MJ/kg was noted, respectively. Only oily layer free wastewater after passing through PAC was found to meet Pakistan NEQS, with COD <150 mg/L, pH 6–8, Alkalinity <1000 mg/L, and Ammonia-nitrogen <40 mg/L. For every 1000 gallons of domestic sewer drain wastewater treated per 8 h work shift or 3 work shifts in a day with FFAs recovered and their conversion into biodiesel, a net profit of 54.89 and 93.32 million Pakistani rupees can be gained in the first year and then in successive years, respectively. Thus, this research provides a way to produce renewable energy fuel, biodiesel from the waste lipids (FFAs) of wastewater drains to meet the energy requirements and a solution for the conservation of water bodies.</p
A homozygous MED11 C-terminal variant causes a lethal neurodegenerative disease
No full textThe mediator (MED) multisubunit-complex modulates the activity of the transcriptional machinery, and genetic defects in different MED subunits (17, 20, 27) have been implicated in neurologic diseases. In this study, we identified a recurrent homozygous variant in MED11 (c.325C>T; p.Arg109Ter) in 7 affected individuals from 5 unrelated families
Bi-allelic genetic variants in the translational GTPases GTPBP1 and GTPBP2 cause a distinct identical neurodevelopmental syndrome
No full textThe homologous genes GTPBP1 and GTPBP2 encode GTP-binding proteins 1 and 2, which are involved in ribosomal homeostasis. Pathogenic variants in GTPBP2 were recently shown to be an ultra -rare cause of neurodegenerative or neurodevelopmental disorders (NDDs). Until now, no human phenotype has been linked to GTPBP1. Here, we describe individuals carrying bi-allelic GTPBP1 variants that display an identical phenotype with GTPBP2 and characterize the overall spectrum of GTP-binding protein (1/2) -related disorders. In this study, 20 individuals from 16 families with distinct NDDs and syndromic facial features were investigated by whole-exome (WES) or whole-genome (WGS) sequencing. To assess the functional impact of the identified genetic variants, semi -quantitative PCR, western blot, and ribosome profiling assays were performed in fibroblasts from affected individuals. We also investigated the effect of reducing expression of CG2017, an ortholog of human GTPBP1/2, in the fruit fly Drosophila melanogaster. Individuals with bi-allelic GTPBP1 or GTPBP2 variants presented with microcephaly, profound neurodevelopmental impairment, pathognomonic craniofacial features, and ectodermal defects. Abnormal vision and/or hearing, progressive spasticity, choreoathetoid movements, refractory epilepsy, and brain atrophy were part of the core phenotype of this syndrome. Cell line studies identified a loss -of -function (LoF) impact of the disease -associated variants but no significant abnormalities on ribosome profiling. Reduced expression of CG2017 isoforms was associated with locomotor impairment in Drosophila. In conclusion, bi-allelic GTPBP1 and GTPBP2 LoF variants cause an identical, distinct neurodevelopmental syndrome. Mutant CG2017 knockout flies display motor impairment, highlighting the conserved role for GTPbinding proteins in CNS development across species
Biallelic MED27 variants lead to variable ponto-cerebello-lental degeneration with movement disorders
No full textMED27 is a subunit of the Mediator multiprotein complex, which is involved in transcriptional regulation. Biallelic MED27 variants have recently been suggested to be responsible for an autosomal recessive neurodevelopmental disorder with spasticity, cataracts, and cerebellar hypoplasia. We further delineate the clinical phenotype of MED27-related disease by characterizing the clinical and radiological features of 57 affected individuals from 30 unrelated families with biallelic MED27 variants. Utilizing exome sequencing and extensive international genetic data sharing, 39 unpublished affected individuals from 18 independent families with biallelic missense variants in MED27 have been identified (29 females, mean age at last follow-up 17±12.4 years, range 0.1-45). Follow-up and hitherto unreported clinical features were obtained from the published 12 families. Brain MRI scans from 34 cases were reviewed. MED27-related disease manifests as a broad phenotypic continuum ranging from developmental and epileptic-dyskinestic encephalopathy to variable neurodevelopmental disorder with movement abnormalities. It is characterised by mild to profound global developmental delay/intellectual disability (100%), bilateral cataracts (89%), infantile hypotonia (74%), microcephaly (62%), gait ataxia (63%), dystonia (61%), variably combined with epilepsy (50%), limb spasticity (51%), facial dysmorphism (38%), and death before reaching adulthood (16%). Brain MRI revealed cerebellar atrophy (100%), white matter volume loss (76.4%), pontine hypoplasia (47.2%), and basal ganglia atrophy with signal alterations (44.4%). Previously unreported 39 affected individuals had seven homozygous pathogenic missense MED27 variants, five of which were recurrent. An emerging genotype-phenotype correlation was observed. This study provides a comprehensive clinical-radiological description of MED27-related disease, establishes genotype-phenotype and clinical-radiological correlations, and suggests a differential diagnosis with syndromes of cerebello-lental neurodegeneration and other subtypes of "neuro-MEDopathies".</p
Global age-sex-specific all-cause mortality and life expectancy estimates for 204 countries and territories and 660 subnational locations, 1950–2023: a demographic analysis for the Global Burden of Disease Study 2023
No full textComprehensive, comparable, and timely estimates of demographic metrics—including life expectancy and age-specific mortality—are essential for evaluating, understanding, and addressing trends in population health. The COVID-19 pandemic highlighted the importance of timely and all-cause mortality estimates for being able to respond to changing trends in health outcomes, showing a strong need for demographic analysis tools that can produce all-cause mortality estimates more rapidly with more readily available all-age vital registration (VR) data. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) is an ongoing research effort that quantifies human health by estimating a range of epidemiological quantities of interest across time, age, sex, location, cause, and risk. This study—part of the latest GBD release, GBD 2023—aims to provide new and updated estimates of all-cause mortality and life expectancy for 1950 to 2023 using a novel statistical model that accounts for complex correlation structures in demographic data across age and time. We used 24 025 data sources from VR, sample registration, surveys, censuses, and other sources to estimate all-cause mortality for males, females, and all sexes combined across 25 age groups in 204 countries and territories as well as 660 subnational units in 20 countries and territories, for the years 1950–2023. For the first time, we used complete birth history data for ages 5–14 years, age-specific sibling history data for ages 15–49 years, and age-specific mortality data from Health and Demographic Surveillance Systems. We developed a single statistical model that incorporates both parametric and non-parametric methods, referred to as OneMod, to produce estimates of all-cause mortality for each age-sex-location group. OneMod includes two main steps: a detailed regression analysis with a generalised linear modelling tool that accounts for age-specific covariate effects such as the Socio-demographic Index (SDI) and a population attributable fraction (PAF) for all risk factors combined; and a non-parametric analysis of residuals using a multivariate kernel regression model that smooths across age and time to adaptably follow trends in the data without overfitting. We calibrated asymptotic uncertainty estimates using Pearson residuals to produce 95% uncertainty intervals (UIs) and corresponding 1000 draws. Life expectancy was calculated from age-specific mortality rates with standard demographic methods. For each measure, 95% UIs were calculated with the 25th and 975th ordered values from a 1000-draw posterior distribution. In 2023, 60·1 million (95% UI 59·0–61·1) deaths occurred globally, of which 4·67 million (4·59–4·75) were in children younger than 5 years. Due to considerable population growth and ageing since 1950, the number of annual deaths globally increased by 35·2% (32·2–38·4) over the 1950–2023 study period, during which the global age-standardised all-cause mortality rate declined by 66·6% (65·8–67·3). Trends in age-specific mortality rates between 2011 and 2023 varied by age group and location, with the largest decline in under-5 mortality occurring in east Asia (67·7% decrease); the largest increases in mortality for those aged 5–14 years, 25–29 years, and 30–39 years occurring in high-income North America (11·5%, 31·7%, and 49·9%, respectively); and the largest increases in mortality for those aged 15–19 years and 20–24 years occurring in Eastern Europe (53·9% and 40·1%, respectively). We also identified higher than previously estimated mortality rates in sub-Saharan Africa for all sexes combined aged 5–14 years (87·3% higher in GBD 2023 than GBD 2021 on average across countries and territories over the 1950–2021 period) and for females aged 15–29 years (61·2% higher), as well as lower than previously estimated mortality rates in sub-Saharan Africa for all sexes combined aged 50 years and older (13·2% lower), reflecting advances in our modelling approach. Global life expectancy followed three distinct trends over the study period. First, between 1950 and 2019, there were considerable improvements, from 51·2 (50·6–51·7) years for females and 47·9 (47·4–48·4) years for males in 1950 to 76·3 (76·2–76·4) years for females and 71·4 (71·3–71·5) years for males in 2019. Second, this period was followed by a decrease in life expectancy during the COVID-19 pandemic, to 74·7 (74·6–74·8) years for females and 69·3 (69·2–69·4) years for males in 2021. Finally, the world experienced a period of post-pandemic recovery in 2022 and 2023, wherein life expectancy generally returned to pre-pandemic (2019) levels in 2023 (76·3 [76·0–76·6] years for females and 71·5 [71·2–71·8] years for males). 194 (95·1%) of 204 countries and territories experienced at least partial post-pandemic recovery in age-standardised mortality rates by 2023, with 61·8% (126 of 204) recovering to or falling below pre-pandemic levels. There were several mortality trajectories during and following the pandemic across countries and territories. Long-term mortality trends also varied considerably between age groups and locations, demonstrating the diverse landscape of health outcomes globally. This analysis identified several key differences in mortality trends from previous estimates, including higher rates of adolescent mortality, higher rates of young adult mortality in females, and lower rates of mortality in older age groups in much of sub-Saharan Africa. The findings also highlight stark differences across countries and territories in the timing and scale of changes in all-cause mortality trends during and following the COVID-19 pandemic (2020–23). Our estimates of evolving trends in mortality and life expectancy across locations, ages, sexes, and SDI levels in recent years as well as over the entire 1950–2023 study period provide crucial information for governments, policy makers, and the public to ensure that health-care systems, economies, and societies are prepared to address the world's health needs, particularly in populations with higher rates of mortality than previously known. The estimates from this study provide a robust framework for GBD and a valuable foundation for policy development, implementation, and evaluation around the world. Gates Foundation
Biallelic MED27 variants lead to variable ponto-cerebello-lental degeneration with movement disorders
No full textMED27 is a subunit of the Mediator multiprotein complex, which is involved in transcriptional regulation. Biallelic MED27 variants have recently been suggested to be responsible for an autosomal recessive neurodevelopmental disorder with spasticity, cataracts and cerebellar hypoplasia. We further delineate the clinical phenotype of MED27-related disease by characterizing the clinical and radiological features of 57 affected individuals from 30 unrelated families with biallelic MED27 variants. Using exome sequencing and extensive international genetic data sharing, 39 unpublished affected individuals from 18 independent families with biallelic missense variants in MED27 have been identified (29 females, mean age at last follow-up 17 ± 12.4 years, range 0.1-45). Follow-up and hitherto unreported clinical features were obtained from the published 12 families. Brain MRI scans from 34 cases were reviewed. MED27-related disease manifests as a broad phenotypic continuum ranging from developmental and epileptic-dyskinetic encephalopathy to variable neurodevelopmental disorder with movement abnormalities. It is characterized by mild to profound global developmental delay/intellectual disability (100%), bilateral cataracts (89%), infantile hypotonia (74%), microcephaly (62%), gait ataxia (63%), dystonia (61%), variably combined with epilepsy (50%), limb spasticity (51%), facial dysmorphism (38%) and death before reaching adulthood (16%). Brain MRI revealed cerebellar atrophy (100%), white matter volume loss (76.4%), pontine hypoplasia (47.2%) and basal ganglia atrophy with signal alterations (44.4%). Previously unreported 39 affected individuals had seven homozygous pathogenic missense MED27 variants, five of which were recurrent. An emerging genotype-phenotype correlation was observed. This study provides a comprehensive clinical-radiological description of MED27-related disease, establishes genotype-phenotype and clinical-radiological correlations and suggests a differential diagnosis with syndromes of cerebello-lental neurodegeneration and other subtypes of 'neuro-MEDopathies'
Biallelic variants in PCDHGC4 cause a novel neurodevelopmental syndrome with progressive microcephaly, seizures, and joint anomalies.
No full textPURPOSE: We aimed to define a novel autosomal recessive neurodevelopmental disorder, characterize its clinical features, and identify the underlying genetic cause for this condition. METHODS: We performed a detailed clinical characterization of 19 individuals from nine unrelated, consanguineous families with a neurodevelopmental disorder. We used genome/exome sequencing approaches, linkage and cosegregation analyses to identify disease-causing variants, and we performed three-dimensional molecular in silico analysis to predict causality of variants where applicable. RESULTS: In all affected individuals who presented with a neurodevelopmental syndrome with progressive microcephaly, seizures, and intellectual disability we identified biallelic disease-causing variants in Protocadherin-gamma-C4 (PCDHGC4). Five variants were predicted to induce premature protein truncation leading to a loss of PCDHGC4 function. The three detected missense variants were located in extracellular cadherin (EC) domains EC5 and EC6 of PCDHGC4, and in silico analysis of the affected residues showed that two of these substitutions were predicted to influence the Ca2+-binding affinity, which is essential for multimerization of the protein, whereas the third missense variant directly influenced the cis-dimerization interface of PCDHGC4. CONCLUSION: We show that biallelic variants in PCDHGC4 are causing a novel autosomal recessive neurodevelopmental disorder and link PCDHGC4 as a member of the clustered PCDH family to a Mendelian disorder in humans
