The Potential Use of Nanofilters to Supply Potable Water in Persian Gulf and Oman Sea Watershed Basin

In a world worried about water resources with the shadow of drought and famine looming all around, the quality of water is as important as its quantity. The source of all concerns is the constant reduction of per capita quality water for different uses. Iran With an average annual precipitation of 250 mm compared to the 800 mm world average, Iran is considered a water scarce country and the disparity in the rainfall distribution, the limitations of renewable resources and the population concentration in the margins of desert and water scarce areas have intensified the problem. The shortage of per capita renewable freshwater and its poor quality in large areas of the country, which have saline, brackish or hard water resources, and the profusion of natural and artificial pollutant have caused the deterioration of water quality. Among methods of treatment and use of these waters one can refer to the application of membrane technologies, which have come into focus in recent years due to their great advantages. This process is quite efficient in eliminating multi-capacity ions; and due to the possibilities of production at different capacities, application as treatment process in points of use, and the need for less energy in comparison to Reverse Osmosis processes, it can revolutionize the water and wastewater sector in years to come. The article studied the different capacities of water resources in the Persian Gulf and Oman Sea watershed basins, and processes the possibility of using nanofiltration process to treat brackish and non-conventional waters in these basins

Nephroprotective effect of Gallic acid against mercuric chloride (HgCl2) induced damage in rats

Introduction: Mercury has hematotoxic, hepatotoxic, neurotoxic, nephrotoxic and genotoxic effects. Tissue damage induced by mercuric chloride (HgCl2) is associated with the promotion of oxidative stress. In this study, Gallic acid (GA), as potent antioxidant compound, was examined against mercuric chloride (HgCl2)-induced kidney injury in Wistar rats. Methods and Results: In this experimental study, animals were divided into five groups (n=7). Groups 1 and 2 respectively received normal saline (2 ml/kg, orally.) and HgCl2 (0.4 mg/kg, orally) for 28 consecutive days. Group 3 only received GA (200 mg/kg, orally) for 28 consecutive days. Groups 4 and 5 received orally GA at doses of 50 and 200 mg/kg, respectively, one hour after administration of HgCl2 for 28 consecutive days. Then On the 29th day, the rats were sacrificed, and blood samples were collected to determine biochemical parameters such as serum creatinine (Cr) and blood urea nitrogen (BUN) levels. For oxidative stress evaluation, malondialdehyde (MDA) and reduced glutathione (GSH) levels and also catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity were evaluated in left kidney tissue. The right kidney was used for histological examination. The results obtained from our study showed a significant increase in the levels of MDA, Cr and BUN, and decrease of GSH, CAT and SOD after ingestion of HgCl2 (p<0.05). Pre-treatment with GA showed diminished in the levels of MDA, Cr and BUN and enhanced of GSH, CAT, GPx and SOD activity (p<0.05). Additionally the nephroprotective effect of the GA was established by the histological evaluation of the kidneys. Conclusions: Our results indicate that GA has protective effect against HgCl2-induced renal damage probably by scavenging free radicals, reducing the oxidative stress, and increasing the antioxidant defense mechanism

HMGA2 regulation by miRNAs in cancer:Affecting cancer hallmarks and therapy response

High mobility group A 2 (HMGA2) is a protein that modulates the structure of chromatin in the nucleus. Importantly, aberrant expression of HMGA2 occurs during carcinogenesis, and this protein is an upstream mediator of cancer hallmarks including evasion of apoptosis, proliferation, invasion, metastasis, and therapy resistance. HMGA2 targets critical signaling pathways such as Wnt/β-catenin and mTOR in cancer cells. Therefore, suppression of HMGA2 function notably decreases cancer progression and improves outcome in patients. As HMGA2 is mainly oncogenic, targeting expression by non-coding RNAs (ncRNAs) is crucial to take into consideration since it affects HMGA2 function. MicroRNAs (miRNAs) belong to ncRNAs and are master regulators of vital cell processes, which affect all aspects of cancer hallmarks. Long ncRNAs (lncRNAs) and circular RNAs (circRNAs), other members of ncRNAs, are upstream mediators of miRNAs. The current review intends to discuss the importance of the miRNA/HMGA2 axis in modulation of various types of cancer, and mentions lncRNAs and circRNAs, which regulate this axis as upstream mediators. Finally, we discuss the effect of miRNAs and HMGA2 interactions on the response of cancer cells to therapy. Regarding the critical role of HMGA2 in regulation of critical signaling pathways in cancer cells, and considering the confirmed interaction between HMGA2 and one of the master regulators of cancer, miRNAs, targeting miRNA/HMGA2 axis in cancer therapy is promising and this could be the subject of future clinical trial experiments.</p

Atorvastatin’s Therapeutic Potential in Atherosclerosis: Inhibiting TGF-β-Induced Proteoglycan Glycosaminoglycan Chain Elongation through ROS-ERK1/2-Smad2L Signaling Pathway Modulation in Vascular Smooth Muscle Cells

Objective: According to the response-to-retention hypothesis, the inception of atherosclerosis is attributed to thedeposition and retention of lipoprotein in the arterial intima, facilitated by altered proteoglycans with hyperelongatedglycosaminoglycan (GAG) chains. Recent studies have elucidated a signaling pathway whereby transforming growthfactor-β (TGF-β) promotes the expression of genes linked to proteoglycan GAG chain elongation (CHSY1 and CHST11)via reactive oxygen species (ROS) and the downstream phosphorylation of ERK1/2 and Smad2L. Atorvastatin is knownto exhibit pleiotropic effects, including antioxidant and anti-inflammatory. The purpose of the present research wasto ascertain the influence of atorvastatin on TGF-β-stimulated expression of CHST11 and CHSY1 and associatedsignaling pathways using an in vitro model.Materials and Methods: In this experimental study, vascular smooth muscle cells (VSMCs) were pre-incubatedwith atorvastatin (0.1-10 μM) prior to being stimulated with TGF-β (2 ng/ml). The experiment aimed to evaluate thephosphorylation levels of Smad2C, Smad2L, ERK1/2, the NOX p47phox subunit, ROS production, and the mRNAexpression of CHST11 and CHSY1.Results: Our research results indicated that atorvastatin inhibited TGF-β-stimulated CHSY1 and CHST11 mRNAexpression. Further experiments showed that atorvastatin diminished TGF-β-stimulated ROS production and weakenedTGF-β-stimulated phosphorylation of p47phox, ERK1/2, and Smad2L; however, we observed no effect on the TGF-β-Smad2C pathway.Conclusion: These data suggest that atorvastatin demonstrates anti-atherogenic properties through the modulationof the ROS-ERK1/2-Smad2L signaling pathway. This provides valuable insight into the potential mechanisms by whichatorvastatin exerts its pleiotropic effects against atherosclerosis

Effects of exosomes of mesenchymal stem cells on cholesterol-induced hepatic fibrogenesis

Objective(s): Free cholesterol in the diet can cause liver fibrosis by accumulating in Hepatic stellate cells (HSCs). The rate of mortality of this disease is high worldwide and there is no definite remedy for it, but might be treated by anti-fibrotic therapies. MSCs-derived exosomes are known as the new mechanism of cell-to-cell communication, showing that exosomes can be used as a new treatment. In this study, we investigated the ability of exosomes of WJ-MSCs as a new remedy to reduce cholesterol-induced liver fibrosis in the LX2 cell line.Materials and Methods: MSCs were isolated from Wharton’s jelly of the umbilical cord and the exosomes were extracted. The LX2 cell line was cultured in DMEM medium with 10% FBS, then cells were treated with 75 and 100 μM concentrations of cholesterol for 24 hr. The mRNA expression of TGF-β, αSMA, and collagen1α genes, and the level of Smad3 protein were measured to assess liver fibrosis. Results: Cholesterol increased the expression of TGF-β, αand -SMA, and collagen1α genes by increasing the phosphorylation of the Smad3 protein. Treatment with Exosomes significantly reduced the expression of TGF-β, α-SMA, and collagen1α genes (fibrosis genes). Treatment with exosomes prevented the activation of HSCs by inhibiting the phosphorylation of the Smad3 protein. Conclusion: The exosomes of WJ-MSCs can inhibit the TGFβ/Smad3 signaling pathway preventing further activation of HSCs and progression of liver fibrosis. So, the exosomes of WJ-MSCs s could be introduced as a treatment for liver failure

Machine Learning-Based Assessment of Watershed Morphometry in Makran

This study proposes an artificial intelligence approach to assess watershed morphometry in the Makran subduction zones of South Iran and Pakistan. The approach integrates machine learning algorithms, including artificial neural networks (ANN), support vector regression (SVR), and multivariate linear regression (MLR), on a single platform. The study area was analyzed by extracting watersheds from a Digital Elevation Model (DEM) and calculating eight morphometric indices. The morphometric parameters were normalized using fuzzy membership functions to improve accuracy. The performance of the machine learning algorithms is evaluated by mean squared error (MSE), mean absolute error (MAE), and correlation coefficient (R2) between the output of the method and the actual dataset. The ANN model demonstrated high accuracy with an R2 value of 0.974, MSE of 4.14 × 10−6, and MAE of 0.0015. The results of the machine learning algorithms were compared to the tectonic characteristics of the area, indicating the potential for utilizing the ANN algorithm in similar investigations. This approach offers a novel way to assess watershed morphometry using ML techniques, which may have advantages over other approaches

Global, regional, and national burden of colorectal cancer and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Funding: F Carvalho and E Fernandes acknowledge support from Fundação para a Ciência e a Tecnologia, I.P. (FCT), in the scope of the project UIDP/04378/2020 and UIDB/04378/2020 of the Research Unit on Applied Molecular Biosciences UCIBIO and the project LA/P/0140/2020 of the Associate Laboratory Institute for Health and Bioeconomy i4HB; FCT/MCTES through the project UIDB/50006/2020. J Conde acknowledges the European Research Council Starting Grant (ERC-StG-2019-848325). V M Costa acknowledges the grant SFRH/BHD/110001/2015, received by Portuguese national funds through Fundação para a Ciência e Tecnologia (FCT), IP, under the Norma Transitória DL57/2016/CP1334/CT0006.proofepub_ahead_of_prin

The global burden of adolescent and young adult cancer in 2019 : a systematic analysis for the Global Burden of Disease Study 2019

Background In estimating the global burden of cancer, adolescents and young adults with cancer are often overlooked, despite being a distinct subgroup with unique epidemiology, clinical care needs, and societal impact. Comprehensive estimates of the global cancer burden in adolescents and young adults (aged 15-39 years) are lacking. To address this gap, we analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, with a focus on the outcome of disability-adjusted life-years (DALYs), to inform global cancer control measures in adolescents and young adults. Methods Using the GBD 2019 methodology, international mortality data were collected from vital registration systems, verbal autopsies, and population-based cancer registry inputs modelled with mortality-to-incidence ratios (MIRs). Incidence was computed with mortality estimates and corresponding MIRs. Prevalence estimates were calculated using modelled survival and multiplied by disability weights to obtain years lived with disability (YLDs). Years of life lost (YLLs) were calculated as age-specific cancer deaths multiplied by the standard life expectancy at the age of death. The main outcome was DALYs (the sum of YLLs and YLDs). Estimates were presented globally and by Socio-demographic Index (SDI) quintiles (countries ranked and divided into five equal SDI groups), and all estimates were presented with corresponding 95% uncertainty intervals (UIs). For this analysis, we used the age range of 15-39 years to define adolescents and young adults. Findings There were 1.19 million (95% UI 1.11-1.28) incident cancer cases and 396 000 (370 000-425 000) deaths due to cancer among people aged 15-39 years worldwide in 2019. The highest age-standardised incidence rates occurred in high SDI (59.6 [54.5-65.7] per 100 000 person-years) and high-middle SDI countries (53.2 [48.8-57.9] per 100 000 person-years), while the highest age-standardised mortality rates were in low-middle SDI (14.2 [12.9-15.6] per 100 000 person-years) and middle SDI (13.6 [12.6-14.8] per 100 000 person-years) countries. In 2019, adolescent and young adult cancers contributed 23.5 million (21.9-25.2) DALYs to the global burden of disease, of which 2.7% (1.9-3.6) came from YLDs and 97.3% (96.4-98.1) from YLLs. Cancer was the fourth leading cause of death and tenth leading cause of DALYs in adolescents and young adults globally. Interpretation Adolescent and young adult cancers contributed substantially to the overall adolescent and young adult disease burden globally in 2019. These results provide new insights into the distribution and magnitude of the adolescent and young adult cancer burden around the world. With notable differences observed across SDI settings, these estimates can inform global and country-level cancer control efforts. Copyright (C) 2021 The Author(s). Published by Elsevier Ltd.Peer reviewe

The global burden of cancer attributable to risk factors, 2010-19 : a systematic analysis for the Global Burden of Disease Study 2019

Background Understanding the magnitude of cancer burden attributable to potentially modifiable risk factors is crucial for development of effective prevention and mitigation strategies. We analysed results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 to inform cancer control planning efforts globally. Methods The GBD 2019 comparative risk assessment framework was used to estimate cancer burden attributable to behavioural, environmental and occupational, and metabolic risk factors. A total of 82 risk-outcome pairs were included on the basis of the World Cancer Research Fund criteria. Estimated cancer deaths and disability-adjusted life-years (DALYs) in 2019 and change in these measures between 2010 and 2019 are presented. Findings Globally, in 2019, the risk factors included in this analysis accounted for 4.45 million (95% uncertainty interval 4.01-4.94) deaths and 105 million (95.0-116) DALYs for both sexes combined, representing 44.4% (41.3-48.4) of all cancer deaths and 42.0% (39.1-45.6) of all DALYs. There were 2.88 million (2.60-3.18) risk-attributable cancer deaths in males (50.6% [47.8-54.1] of all male cancer deaths) and 1.58 million (1.36-1.84) risk-attributable cancer deaths in females (36.3% [32.5-41.3] of all female cancer deaths). The leading risk factors at the most detailed level globally for risk-attributable cancer deaths and DALYs in 2019 for both sexes combined were smoking, followed by alcohol use and high BMI. Risk-attributable cancer burden varied by world region and Socio-demographic Index (SDI), with smoking, unsafe sex, and alcohol use being the three leading risk factors for risk-attributable cancer DALYs in low SDI locations in 2019, whereas DALYs in high SDI locations mirrored the top three global risk factor rankings. From 2010 to 2019, global risk-attributable cancer deaths increased by 20.4% (12.6-28.4) and DALYs by 16.8% (8.8-25.0), with the greatest percentage increase in metabolic risks (34.7% [27.9-42.8] and 33.3% [25.8-42.0]). Interpretation The leading risk factors contributing to global cancer burden in 2019 were behavioural, whereas metabolic risk factors saw the largest increases between 2010 and 2019. Reducing exposure to these modifiable risk factors would decrease cancer mortality and DALY rates worldwide, and policies should be tailored appropriately to local cancer risk factor burden. Copyright (C) 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license.Peer reviewe