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Corona viruses (CoV) are known to cause extreme pandemics in the globe. The year 2020 will be a pandemic with the spread of the novel coronavirus (SARS-CoV-2) across the globe. Coronavirus 2019 (COVID-19) has been a part of our scary life for more than a quarter of a year in 2020. The Wuhan market and China have been the most commonly used terms in the world for at least a quarter of 2020. A zoonotic coronavirus has entered organisms to affect organisms for the third season in several centuries. CoV is a global pandemic prompted a drastic and rapid reconfiguration of society. CoV have extraordinary broad genomes of about 30 kilobases of RNA. There is no genetic relationship between the SARS-CoV, MERS and SARS-CoV-2. For health care strategies and for anticipating and preventing potential outbreaks, adequate description of the international spread of COVID-19 virus is imperative. The WHO has declared COVID-19 as endemic to pandemic in the first trimester of 2020. The biggest issues for diagnosis COVID-19 is not established apart from Real-time reverse transcriptase polymerase chain reaction (RT-PCR). In order to monitor the COVID-19 pandemic, testing of active SARS-CoV-2 infections is a fundamental public health method. The vast use of SARS-CoV-2 RT-PCR tests around the world has led to increased availability of test kits, which is also a major bottleneck. The technique RT-PCR was generally agreed in the present scenario to detect SARS-CoV-2 in the human body. This review discusses about the importance of molecular technique for diagnosing the pandemic disease of 2019. In conclusion, RT-PCR was found to be an apt technique for identification of SARS-CoV-2.

Diabetes is considered one of the most encyclopedic metabolic disorders owing to an alarming rise in the number of patients, which is increasing at an exponential rate. With the current therapeutics, which only aims to provide symptomatic and momentary relief, the scientists are shifting gears to explore alternative therapies which not only can target diabetes but can also help in limiting the progression of diabetic complications including diabetic neuropathy (DN).Parameters associated with the pathogenesis of diabetic neuropathy were evaluated. For general parameters, different doses ofThe leaves of

Extensive use of triclosan (2,4,4′‐trichloro‐2′‐hydroxydiphenyl ether) as an antimicrobial agent in household and personal care products has resulted in global exposure of the human population. Its presence in human tissues, including milk, and its oestrogen‐disrupting properties raise concerns for an involvement in breast cancer. Because metastatic tumour spread is the main cause of breast cancer mortality, we have investigated the effects of triclosan on cell migration and invasion using three human breast epithelial cell lines and using concentrations comparable with those in human tissues. Long‐term exposure to 10−7 M of triclosan resulted in increased migration and invasion as measured by xCELLigence technology for all three cell lines, for the immortalized but nontransformed MCF‐10F breast epithelial cells (after 28 weeks), the oestrogen‐responsive MCF‐7 breast cancer cells (after 17 weeks) and the oestrogen‐unresponsive MDA‐MB‐231 breast cancer cells (after 20 weeks). The effects were therefore not limited to cancerous cells or to oestrogen‐responsive cells. This was paralleled in the MCF‐10F and MCF‐7 (but not MDA‐MB‐231) cells by a reduction in levels of E‐cadherin mRNA as measured by reverse transcription–polymerase chain reaction (RT‐PCR) and of E‐cadherin protein as measured by western immunoblotting, suggesting a mechanism involving epithelial‐to‐mesenchymal transition. This adds triclosan to the increasing list of ingredients of personal care products that can not only enter human breast tissue and increase cell proliferation but also influence cell motility. If mixtures of components in household and personal care products contribute to increasing cell migration and invasion, then reduction in exposure could offer a strategy for reducing breast cancer spread., Long‐term (>15 weeks) exposure to 10−7 M of triclosan resulted in increased migration and invasion of three human breast epithelial cell lines as measured using xCELLigence technology. Effects were not limited to cancerous cells or to oestrogen‐responsive cells. In two cell lines, reduced levels of E‐cadherin (mRNA and protein) were observed, suggesting a mechanism involving epithelial‐to‐mesenchymal transition. Triclosan is therefore another ingredient of personal care products that is entering the human breast and increasing cell motility, which is a prerequisite for metastasis.

Saussurea lappa Clarke (Compositae) is well known as a medicinal plant. Its roots are traditionally used in alleviating pain and swelling. In the current research, we have evaluated the antinociceptive activity of essential oil obtained from the roots of S. lappa. In addition, the development and evaluation of a pharmaceutical-grade cream was also conducted in this study. Extraction of essential oil from the roots of the plant was performed by a steam distillation method using the Clevenger apparatus. The antinociceptive activity was assessed in Sprague Dawley rats using tail flick, hot plate, and analgesic-meter, where diclofenac was used as a standard reference analgesic agent. S. lappa showed analgesic activity in all test systems in a dose- and time-dependent manner. In addition, the formulated cream obtained from the essential oil showed very promising pharmaceutical and pharmacological properties. The analgesic activity of S. lappa may be due to its interaction with opioid receptors and involvement of peripheral analgesia. The ability of S. lappa to show both slow- and fast-onset analgesic effects suggests it could be used as a drug candidate for pain management. The current findings thus warrant further research in the development of this novel analgesic agent.

Purpose DNA damage is a continuous process occurring within the cells caused by intrinsic and extrinsic factors, but it gets repaired regularly. If the DNA repair process is faulty, the incidences of damages/mutations can accumulate in cells resulting in cell transformation. It is hypothesized that the negative variations in DNA repair pathways in even at one point viz. genetic, translational or posttranslational stage may fairly be crucial for the beginning and development of carcinogenesis. Therefore, we investigated the potential of tobacco specific nitrosamines (TSNs) related carcinogens to interact with the enzymes involved in DNA repair mechanisms in the current study. Methods The derivatives of cigarettes' smoke like NNK and NNAL are very well known and recognized carcinogens. Therefore, almost 120 enzymes playing crucial role in the DNA repair process have been analysed for their reactivity with NNK and NNAL. Results The molecular docking study helped to screen out, 07 possible DNA repair enzyme targets for NNK, and 12for NNAL. Present study revealed the loss of activity of DNA repair enzymes in the presence of NNK and NNAL, and this accumulation may induce the tendency of DNA damage which can lead the transformation of exposed normal cells in to cancerous cells. This study also demonstrated the protective potential of nanoparticles like SWCNTs/MWCNTs against TSN's induced toxicity; here SWCNT against NNK (-17.16 Kcal/Mol) and MWCNT against NNK -17.01 Kcal/Mol were showing maximum binding affinities than the known biomolecular target of NNK 1UGH (Uracil-DNA glycosylase,-7.82Kcal/Mol). Conclusion CNTs can be applied as chemo-preventive agents against environmental and tobacco induced carcinogens owing to their scavenging potential and warrants for in vivo and in vitro experimental validation of the results obtained from the present study. .

Perception of hub genes engaged in metastatic gastric cancer (mGC) promotes novel ways to diagnose and treat the illness. The goal of this investigation is to recognize the hub genes and reveal its molecular mechanism. In order to explore the potential facts for gastric cancer, the expression profiles of two different datasets were used (GSE161533 and GSE54129). The genes were confirmed to be part of the PPI network for gastric cancer pathogenesis and prognosis. In Cytoscape, the CytoHubba module was used to discover the hub genes. Responsible hub genes were identified. Data from Kaplan–Meier plotter confirmed the predictive value of these distinct genes in various stages of gastric malignancy. Upregulated and downregulated genes were identified to utilize for further analysis. Positive regulation by a host of viral process, positive regulation of granulocyte differentiation, negative regulation of histone H3–K9 methylation were found in DEGs analysis. In addition, five KEGG pathways were identified as an essential enhancer that include nucleotide excision repair; base excision repair; DNA replication; homologous recombination; and complement and coagulation cascades. POLE, BUB1B, POLD4, C3, BLM, CCT7, PRPF31, APEX1, PSMA7, and CDC45 were chosen as hub genes after combining the PPI results. Our study recommends that BUB1B, CCT7, APEX1, PSMA7, and CDC45 might be potential biomarkers for gastric cancer. These biomarkers are upregulated genes. Therefore, suppression of these genes will increase the survival rate in gastric cancer patients.

The CLEC-2 receptor protein belongs to the C-type lectin superfamily of transmembrane receptors that have one or more C-type lectin-like domains. CLEC-2 is a physiological binding receptor of podoplanin (PDPN), which is expressed on specific tumour cell types and involved in tumour cell-induced platelet aggregation and tumour metastasis. CLEC-2 and podoplanin-expressing tumour cells interact to increase angiogenesis, tumour development, and metastasis. CLEC-2 is a hemi-immunoreceptor tyrosine-based activation motif (hemi-ITAM) receptor located on platelets and a subset of dendritic cells that are expressed constitutively. This molecule is secreted by activated platelets around tumours and has been shown to inhibit platelet aggregation and tumour metastasis in colon carcinoma by binding to the surface of tumour cells. Pharmacokinetic studies were carried using a DrugLiTo, and molecular docking was performed using AutoDock Tools 1.5.6 (ADT). Twenty-nine bioactive compounds were included in the study, and four of them, namely, piperine, dihydrocurcumin, bisdemethoxycurcumin, and demothoxycurcumin, showed potential antagonist properties against the target. The resultant best bioactive was compared with commercially available standard drugs. Further, validation of respective compounds with an intensive molecular dynamics simulation was performed using Schrödinger software. To the best of our knowledge, this is the first report on major bioactive found on clove as natural antagonists for CLEC-2 computationally. To further validate the bioactive and delimit the screening process of potential drugs against CLEC-2, in vitro and in vivo studies are needed to prove their efficacy.

The study investigated the effects of Zingiber officinale root and Vernonia amygdalina leaf on the brain redox status of Wistar rats. Twenty-four (24) rats weighing 160 ± 20 g were randomly assigned into four (4) groups, each with six (6) rats. Animals in Group 1 (control) were orally administered distilled water (1 mL), while the test groups were orally administered 5 mg/mL of either Z. officinale, V. amygdalina infusion, or a combination of both, respectively, for 7 days. The rats were sacrificed at the end of treatments and blood and tissue were harvested and prepared for biochemical assays. Results showed that administration of V. amygdalina and Z. officinale, as well as their coadministration, reduced the levels of malondialdehyde (MDA), nitric oxide (NO), acetylcholinesterase (AChE), and myeloperoxidase (MPO) in rat brain tissue compared with the control group. Conversely, coadministration of V. amygdalina and Z. officinale increased the levels of reduced glutathione (GSH) in rat brain tissue compared with the control group. However, the administration of the infusions singly, as well as the combination of both infusions, did not have any effect on the rat brain levels of glutathione peroxidase (GPx) and catalase (CAT) antioxidant enzymes compared to the control. Taken together, the findings indicate that the V. amygdalina and Z. officinale tea infusions have favorable antioxidant properties in the rat brain. The findings are confirmatory and contribute to deepening our understanding of the health-promoting effects of V. amygdalina and Z. officinale tea infusions.

The effects of nitric oxide modulators (NO-modulators) and antioxidants on acute (RSx1) restraint stress induced endocrine, cellular and oxidative/nitrosative stress markers was studied in Wistar rats. The results of our study revealed that exposure to RS(x1) enhanced malondialdehyde (MDA), heat shock protein (HSP-70), corticosterone, nuclear factor kappa B (NF-κB) levels and suppressed glutathione (GSH), superoxide dismutase (SOD) and total nitrites and nitrates (NOx) levels. NO precursor and NO synthase inhibitors were found to differentially modulate stress mechanisms, by altering NF-κB, HSP-70 and corticosterone levels. l-Ascorbic acid significantly suppressed acute stress induced elevation of NF-κB and HSP-70 levels depicting protective effects, as also evidenced by reversal of elevated plasma corticosterone levels. Therefore, modulation of oxidative and nitrosative pathways, offers an approach in modulating stress induced changes associated with various disorders.

Progress in pathogenesis and therapy of acute myeloid leukemia (AML) is presently accelerating. The Janus kinase 2 gene (JAK2) mutations are rare in de novo AML. The gene codes for the tyrosine kinase that has a significant role in the signal transduction in hematopoietic cells. The aim of this study was to induce V617F mutation in the JAK2 gene in the AML patients diagnosed in the Saudi population. In this case-control study, 100 AML patients and 100 healthy controls were recruited. Genotyping was performed with polymerase chain reaction followed with restriction fragment length polymorphism analysis. The mean age of the AML patients and healthy controls was found to be almost similar (p=0.60). In this study, 15% of VF mutation was documented in the AML cases and none of the mutations were documented either in FF mutation in AML cases or VF and FF mutations in the healthy control subjects. VF mutations [VF vs VV; OR-18.79; (95%CIs: 2.442–144.6) and p=0.0001; F vs V; OR-87.76; (95% CIs: 11.76–654.7) and p

One and one only most unforgettable pandemic is coronavirus 2019 (COVID 19) which is the most memorable pandemic of the twenty-first century. The diagnosis of COVID19 is based on purely clinical symptoms and real time reverse transcription polymerase chain reaction (RT-PCR) test. The role of COVID19 during this pandemic was horrible in diagnosing the disease with RT-PCR as this disease was documented to be a symptomatic disease. Serum ferratin and D-dimer tests plays a major role in identifying the infections in the human body specifically, patients diagnosed with COVID19. Serum ferritin levels are important for an immune response mediator that rises in severe COVID-19 instances, and elevated ferritin levels may trigger a cytokine storm by exerting direct immunosuppressive and pro-inflammatory effects. d-dimer is used to identify the clots in the blood. COVID-19 patients were found to be clotting of blood and d-dimer is recommended. The blood of the COVID-19 patients were found to clotted than the patients were prescribed the anticoagulant Injections are prescribed. d-dimer can be used as a biomarker in the COVID-19 patients by measuring the d-dimer levels and analyse the mortality and severity. Pulmonary complication risk can also be identified. d-dimer is a mandatory and an essential test in the COVID-19. Numerous COVID-19 vaccines have been shown to have great efficacy levels through clinical trials. COVID-19 vaccines are not 100% effective, although the condition is mild or moderate and can be controlled if COVID-19 is affected. In this review, I have only included serum ferritin and d-dimer; however, C-reactive protein, vitamin D levels, and prolactin were also attributed to COVID-19. This review concludes the importance of RT-PCR, serum ferratin, and d-dimer testing in identifying COVID-19 infection in humans.

We investigated the protective and in vivo antioxidant effects of p-coumaric acid on carbon tetrachloride-induced hepatotoxicity in Sprague-Dawley rats. The rats were orally pre-treated with p-coumaric acid (at 50 and 100 mg/kg body weight) for 15 days before the subcutaneous injection of carbon tetrachloride (1.5 mL/kg). Silymarin served as a positive control for hepatoprotection. Blood and tissue samples were obtained and used to assess the effects of p-coumaric acid using quantitative and qualitative histological evaluation, glutathione levels, protein determination, and liver enzymes. p-Coumaric acid treatment did not demonstrate any toxicological abnormalities in mice. p-Coumaric acid and silymarin reduced the extent of carbon tetrachloride-induced liver damage and preserved normal hepatic enzymes (P < 0.05). p-Coumaric acid pre-treatment led to a diminution in increased malondialdehyde and decreased glutathione following carbon tetrachloride administration (P < 0.05). Furthermore, p-coumaric acid restored changes in superoxide dismutase and caspase-3 gene expression as a result of carbon tetrachloride exposure. In conclusion, p-coumaric acid helps restore toxicant-induced liver injury in rats via avoidance of lipid peroxidation, inhibition of cell death and preservation of antioxidant mechanism.

Objective: This study aims to investigate the genetic association of acute myeloid leukemia and glutathione S-transferase (GST) gene polymorphisms in a Saudi population. Method: 100 AML cases and 100 healthy controls were recruited from the Riyadh regional hospital. In the GST gene, GSTM1 and GSTT1 variants were genotyped by multiplex PCR, and GSTP1 variants were genotyped by PCR-RFLP analysis. Statistical analysis between AML cases and controls included anthropometric measurements and evaluation of the genotypic and allelic frequencies. Result: The null genotypes of GSTM1 and GSTT1 showed no association with AML [OR 0.56 (0.26–1.19); p = 0.31 and OR 0.65 (0.37–1.16); p = 0.14]. Similarly, the GSTP1 genotype and allele frequencies did not indicate any association with AML [GG + AG vs. AA: OR 0.75 (0.43–1.31) and p = 0.32; GG vs. AA: OR 1.73 (0.55–5.44) and p = 0.34; G vs. A: OR 0.95 (0.61–1.46) and p = 0.82]. Further, a haplotype analysis between AML cases and controls did not show any positive association (p

A series of the title curcuminoids with structural variance in the heteroatom of the cycloalkanone and the p-substituents of the phenyl rings were tested for their activities against Leishmania major and Toxoplasma gondii parasites. The majority of them showed high activities against both parasite forms with EC50 values in the sub-micromolar concentration range. Bis(p-pentafluorothio)-substituted 3,5-di[(E)-benzylidene]piperidin-4-one 1b was not just noticeable antiparasitic, but also exhibited a considerable selectivity for L. major promastigotes over normal Vero cells. While derivatives differing only in the p-phenyl substituents being CF3 or SF5 showed similar antiparasitic activities, the cyclic ketone hub was more decisive both for the anti-parasitic activities and the selectivities for the parasites vs. normal cells. QSAR calculations confirmed the observed structure-activity relations and suggested structural variations for a further improvement of the antiparasitic activity. Docking studies based on DFT calculations revealed L. major pteridine reductase 1 as a likely molecular target protein of the title compounds.

Introduction: Cardiovascular disease (CVD) is a common term used to refer to disorders affecting the blood vessels or the heart that have led to the majority of deaths worldwide. Aim: The aim of the present study was to explore nurse's perception of their role and their experiences in relation to engaging with cardiovascular disease prevention in the primary care setting. Methods: In the selection of clinical nurses who were interested in primary care to participate, qualitative describing design and impracticable sampling were used. The data collection methods include semi-structured and one-on-one interviews. The results were analyzed by the methodology for qualitative content analysis. Results: In this study, 10 nurses were participated and their role in CVD prevention plays a part in health education, diagnosis and consultation, reassurance, monitoring of vital signs, and collecting blood samples. The challenges include cultural obstacles and vocabulary, negative attitudes, contradictory regulations, a lack of equipment, a shortage of nursing staff and the lack of knowledge and information. Electronic information, patient education, nurse training, and communication workshops are the facilitators for nurses that prevent heart disease. Conclusion: Cardiovascular disease is lethal, but adequate preventive programs can accommodate it. In addition, nurses play an important role in preventing CVD in primary healthcare and should therefore concentrate efforts on the enhancement of their capacity. The aim of future research should be to understand how patients interpret and incorporate data on the prevention of CVD provided by nurses.

Extensive use of triclosan (2,4,40-trichloro-20-hydroxydiphenyl ether) as an antimicrobial agent in household and personal care products has resulted in global exposure of the human population. Its presence in human tissues, including milk, and its oestrogen-disrupting properties raise concerns for an involvement in breast cancer. Because metastatic tumour spread is the main cause of breast cancer mortality, we have investigated the effects of triclosan on cell migration and invasion using three human breast epithelial cell lines and using concentrations comparable with those in\ud human tissues. Long-term exposure to 10−7 M of triclosan resulted in increased migration and invasion as measured by xCELLigence technology for all three cell\ud lines, for the immortalized but nontransformed MCF-10F breast epithelial cells (after 28 weeks), the oestrogen-responsive MCF-7 breast cancer cells (after 17 weeks) and\ud the oestrogen-unresponsive MDA-MB-231 breast cancer cells (after 20 weeks). The effects were therefore not limited to cancerous cells or to oestrogen-responsive cells. This was paralleled in the MCF-10F and MCF-7 (but not MDA-MB-231) cells by a reduction in levels of E-cadherin mRNA as measured by reverse transcription–polymerase chain reaction (RT-PCR) and of E-cadherin protein as measured by western immunoblotting, suggesting a mechanism involving epithelialto-mesenchymal transition. This adds triclosan to the increasing list of ingredients of personal care products that can not only enter human breast tissue and increase cell proliferation but also influence cell motility. If mixtures of components in household and personal care products contribute to increasing cell migration and invasion, then reduction in exposure could offer a strategy for reducing breast cancer spread.

We describe here the draft genome sequence of AY1MRC, a Mycobacterium tuberculosis strain belonging to lineage 1 (Indo-Oceanic) and the East African Indian spoligotype, isolated from a patient with tuberculosis in Jazan, Saudi Arabia.

Dermal absorption of components of personal care products (PCPs) may contribute to breast cancer development. Cyclic volatile methylsiloxanes (cVMS) are used widely in the formulation of PCPs, and their presence has been recently detected in human blood. The objectives of this study were to investigate any genotoxic effects after short- (1 week) or longer-term (30 weeks) exposure to hexamethylcyclotrisiloxane (D3), octamethylcyclotetrasiloxane (D4) or decamethylcyclopentasiloxane (D5) in MCF-10 A and MCF-10F immortalized non-transformed human breast epithelial cells. Genotoxic effects were assessed by an ability of cells to grow in suspension culture, from DNA damage measured by comet assays, and from a reduction in levels of DNA repair proteins measured by RT-PCR and western immunoblotting. Dose-dependent anchorage-independent growth in methocel culture was observed after exposure to D3 (10-13 M-10-5 M) and D4/D5 (10-9 M-10-5 M). DNA damage was measured by the comet assay after 1-h exposure to D3 (10-6 M-10-5 M) and D4 (10-5 M). BRCA1 mRNA and BRCA1 protein levels were reduced after 30-week exposure to 10-5 M D4 and D5 in both cell lines. Reduced levels of mRNAs for other DNA repair proteins (BRCA2, ATM, ATR, CHK1 and CHK2) were also observed after exposure to 10-5 M D5 in both cell lines, and some reductions after exposure to D3 and D4. If cVMS can not only enable anchorage-independent growth of non-transformed breast epithelial cells and damage DNA, but also compromise DNA repair systems, then there is the potential for them to impact on breast carcinogenesis. Further risk assessment now requires information concerning the extent to which cVMS may be present in human breast tissues. Copyright © 2016 John Wiley & Sons, Ltd.

The role of niacin's metabolite, nicotinamide adenine dinucleotide (NAD), in DNA repair via base-excision repair pathway is well documented. We evaluated if niacin deficiency results in genetic instability in normal human fetal lung fibroblasts (MRC-5), and further, does it leads to enhanced accumulation of cigarette smoke-induced genetic damage? MRC-5 cells were grown discretely in niacin-proficient/deficient media, and exposed to nicotine-derived nitrosamine ketone (NNK, a cigarette smoke carcinogen). Niacin deficiency abated the NAD polymerization, augmented the spontaneous induction of micronuclei (MN) and chromosomal aberrations (CA) and raised the expression of 10 genes and suppressed 12 genes involved in different biological functions. NNK exposure resulted in genetic damage as measured by the induction of MN and CA in cells grown in niacin-proficient medium, but the damage became practically marked when niacin-deficient cells were exposed to NNK. NNK exposure raised the expression of 16 genes and suppressed the expression of 56 genes in cells grown in niacin-proficient medium. NNK exposure to niacin-deficient cells raised the expression of eight genes including genes crucial in promoting cancer such as FGFR3 and DUSP1 and suppressed the expression of 33 genes, including genes crucial in preventing the onset and progression of cancer like RASSF2, JUP, and IL24, in comparison with the cells grown in niacin-proficient medium. Overall, niacin deficiency interferes with the DNA damage repair process induced by chemical carcinogens like NNK, and niacin-deficient population are at the higher risk of genetic instability caused by cigarette smoke carcinogen NNK.

The main objective of this research is Risks Evaluation of Sahand New Town 1226 housing Project by means of Project Management Body of Knowledge (PMBOK) model in Iran. PMBOK presents a set of standards and guidelines for project management. After reviewing the literatures, 22 risk items have been identified. 19 risks were finalized under 5 factors of Administrative, environmental, economic and political and organizational using exploratory analysis. Technique for Order of Preference by Similarity to Ideal Solution (TOPSIS) method under four criteria cost, time, quality and safety was used to select 2 work packages as the most important work packages. Consequently, the activities of the selected work packages were obtained via opinion’s experts. Then, the risks were categorized into direct risks and indirect risks using semi-structural interview with experts. Results showed that financial risk was known as most important indirect threat and risk of delay in supply and mistakes in construction were the most important direct threat. Finally, the impact of risks on time and cost of the project were obtained as the follow: the project with 90% probability would finish with 29.39 months delay. Similarly, with 90% probability will have 4003.837IRR increase in cost.