Behavioural impacts of following administration of Ficus carica leaves extract in animal model of acute and chronic unpredictable mild stressed exposed rats.

Stress is described as a noxious stimulus that affects the health of an individual and alters body homeostasis resulting in changes the individual behavioural and metabolic condition. Synthesis of drug from plants has main interest due the significant medicinal values. The recent investigation was designed to examine the pharmacological impacts of Ficus carica leaves extract on stress. In this experiment, the rodents were randomly distributed as (n=6) control rats were kept at standard condition, second group of rats were exposed with different stressors and Third group of rodents was exposed to stress and treated with extract of ficus carica leaves at the dose of 100 mg/kg. Acute behavioural alteration was observed after 7 days and prolonged impact was monitored after the 28 days. The current finding showed that administration of Ficus carica leaves extract produced anxiolytic behaviours and decreased depression like symptoms in CUMS treated rats. It also increased stimulatory, ambulatory, locomotor activity and enhanced spatial working memory and recognition memory in CUMS exposed rats. So, it can be concluded from recent study that leaves of Ficus carica can be utilized as secure drug for curing physiological stress with less side effect profile.

Bone marrow derived mesenchymal stem cells therapy for rheumatoid arthritis - a concise review of past ten years.

Rheumatoid arthritis is an autoimmune disorder characterized by swelling in synovial joints and erosion of bones. The disease is normally treated with conventional drugs which provide only temporary relief to the symptoms. Over the past few years, mesenchymal stromal cells have become the center of attention for treating this disease due to their immuno-modulatory and anti-inflammatory characteristics. Various studies on treatment of rheumatoid arthritis by using these cells have shown positive outcomes in terms of reduction in the level of pain as well as improvement of the function and structure of joints. Mesenchymal stromal cells can be derived from multiple sources, however, the ones derived from bone marrow are considered most beneficial for treating several disorders including rheumatoid arthritis on account of being safer and more effective. This review summarizes all the preclinical and clinical studies which were conducted over the last ten years for therapy of rheumatoid arthritis utilizing these cells. The literature was reviewed using the terms "mesenchymal stem/stromal cells and rheumatoid arthritis'' and "bone marrow derived mesenchymal stromal cells and therapy of rheumatoid arthritis''. Data was extracted to enable the readers to have access to the most relevant information regarding advancement in therapeutic potential of these stromal cells. Additionally, this review will also help in fulfilling any gap in current knowledge of readers about the outcome of using these cells in animal models, cell line and in patients suffering from rheumatoid arthritis and other autoimmune disorders as well.

Assessment of neuropharmacological consequences induced by dexamethasone administration in rats model of neurodegenerative diseases.

Stress is a well-known and frequently used term among present generation. It has been referred to the response of body to any challenge for a change. It is a natural process and our body is designed to cope with it. However, if stress becomes chronic, it can lead to mental health problems. Stress due to the prolonged administration of glucocorticoid is enabled to produce impressive alterations in rats model shoeing depressive like behavior. In this investigation; purpose was to study the impact of episodic treatment of dexamethasone with respect to behavioral changes in rats. It was hypothesized that repeated administration of dexamethasone could increase stress and thus, psychological stress leading to mood disorders and behavior deficits in rats. Rats were injected daily with DEX (10 mg/ml/kg, orally) and the different behavioral models of the animals were assessed. DEX-treated rats exhibited depressive behavior like greater time to start mobility in a novel environment and elevated anxiety-like behavior in elevated plus maze. However, time spent in light compartment was shorter with repeated administration of DEX. From results it is demonstrated that the administration of DXM for weeks induced stress and consequently, induced a depression-like behaviors in rats models.

Inhibition of drug induced Parkinsonism by chronic supplementation of quercetin in haloperidol-treated wistars.

Haloperidol is a neuroleptic medication that is used to treat a wide range of neuropsychiatric conditions. It has been shown to produce medicinal effects against hyperactivity, agitation and mania, as well as schizophrenia. Long-term usage of haloperidol raises the risk of acquiring a neurological condition like Parkinson's disease. Haloperidol causes drug-induced Parkinsonism (DIP) by blocking central dopamine receptors and causing extrapyramidal symptoms during long-term treatment. Quercetin has been shown to reduce the loss of striatal neurons, which may enhance motor capabilities and protect against agents that cause the production of reactive oxygen species (ROS). As a result, present study intended to evaluate the efficacy of quercetin on haloperidol-related motor abnormalities. To develop behavioral impairments, rats (n=24) randomly divided to control and haloperidol group for four weeks. The animals were split into four groups after four weeks: Control, quercetin, haloperidol and haloperidol + quercetin. Animals were administered haloperidol i.p injections of 5mg/kg and quercetin (100mg/kg) orally for 21 days. The treatment of haloperidol-treated rats with quercetin was successful in reversing the haloperidol alterations. It decreased animal food intake and alleviated anxiogenic behavior. The chronic treatment of quercetin further reduced the movement abnormalities in animal model of drug induced pseudo-Parkinson.

Quercetin impact against psychological disturbances induced by fat rich diet.

Obesity is a metabolic disease which promotes by consuming fat rich diet. The consequences may include leptin resistant and initiation of metabolic syndromes. Beside the fact, obesity has psychological impacts it act as a signal of depression by stimulating endogenous stress stimulation. Quercetin is a natural polyphenol, considered as nutraceutical agent which produce antioxidant effects. It is reported to promote energy expenditure and protective mechanism against obesity. This presented work was designed to observe the effects of quercetin on high fat diet treated obese animals with impaired psychological behavior. The study comprised on 36 animals, divided in to different groups as follow: I Normal Diet and II. High fat diet. After the induction of obesity both groups divided in to further three subgroups as control, Quercetin and sertraline. Food intake and body weight along with behavioral analysis for four weeks were done for the assessment of anti-obesity and antidepressant effects of quercetin. The results showed the effective treatment of quercetin in obese animals, it significantly reduced the food intake and body weight of animals. The behavioral test showed the increased locomotor activity in the activity box and improved psychological behavior in quercetin-treated rats in the open field and light-dark box. It is concluded from the present study that quercetin exhibits the ameliorative effects against obesity and associated neuroendocrine alterations.

Krebs cycle: activators, inhibitors and their roles in the modulation of carcinogenesis.

A fundamental metabolic feature of cancerous tissues is high glucose consumption. The rate of glucose consumption in a cancer cell can be 10-15 times higher than in normal cells. Isolation and cultivation of tumor cells in vitro highlight properties that are associated with intensive glucose utilization, the presence of minimal oxidative metabolism, an increase in lactate concentrations in the culture medium and a reduced rate of oxygen consumption. Although glycolysis is suggested as a general feature of malignant cells and recently identified as a possible contributing factor to tumor progression, several studies highlight distinct metabolic characteristics in some tumors, including a relative decrease in avidity compared to glucose and/or a glutamine dependency of lactate and even proliferative tumor cells. The aim of this review is to determine the particularities in the energy metabolism of cancer cells, focusing on the main nutritional substrates, such as glucose and glutamine, evaluating lactate dehydrogenase as a potential marker of malignancy and estimating activators and inhibitors in cancer treatment.

N-Acetyl Cysteine, Selenium, and Ascorbic Acid Rescue Diabetic Cardiac Hypertrophy via Mitochondrial-Associated Redox Regulators.

Metabolic disorders often lead to cardiac complications. Metabolic deregulations during diabetic conditions are linked to mitochondrial dysfunctions, which are the key contributing factors in cardiac hypertrophy. However, the underlying mechanisms involved in diabetes-induced cardiac hypertrophy are poorly understood. In the current study, we initially established a diabetic rat model by alloxan-administration, which was validated by peripheral glucose measurement. Diabetic rats displayed myocardial stiffness and fibrosis, changes in heart weight/body weight, heart weight/tibia length ratios, and enhanced size of myocytes, which altogether demonstrated the establishment of diabetic cardiac hypertrophy (DCH). Furthermore, we examined the expression of genes associated with mitochondrial signaling impairment. Our data show that the expression of PGC-1α, cytochrome c, MFN-2, and Drp-1 was deregulated. Mitochondrial-signaling impairment was further validated by redox-system dysregulation, which showed a significant increase in ROS and thiobarbituric acid reactive substances, both in serum and heart tissue, whereas the superoxide dismutase, catalase, and glutathione levels were decreased. Additionally, the expression levels of pro-apoptotic gene PUMA and stress marker GATA-4 genes were elevated, whereas ARC, PPARα, and Bcl-2 expression levels were decreased in the heart tissues of diabetic rats. Importantly, these alloxan-induced impairments were rescued by N-acetyl cysteine, ascorbic acid, and selenium treatment. This was demonstrated by the amelioration of myocardial stiffness, fibrosis, mitochondrial gene expression, lipid profile, restoration of myocyte size, reduced oxidative stress, and the activation of enzymes associated with antioxidant activities. Altogether, these data indicate that the improvement of mitochondrial dysfunction by protective agents such as N-acetyl cysteine, selenium, and ascorbic acid could rescue diabetes-associated cardiac complications, including DCH.

Health benefits of xylitol.

Many diseases, including caries, chronic inflammatory diseases, diabetes, and obesity, are associated with uncontrolled sugar consumption. Artificial sweeteners are commonly used in food and pharmaceutical industries as sugar substitutes for the prevention of several dental and body diseases; they also have a favorable impact on body weight as they may help to restrict simple sugar consumption. Xylitol is a sugar alcohol that is commonly used as a sweetener. It can be found naturally or artificially prepared mainly from plant materials chemically or by fermentation of hemicelluloses from agricultural biomass by yeast or bacteria strains. This polyol has a significant antiplaque effect on teeth surface and can reduce the gingival inflammation; it is being used as a preventive agent for dental caries due to decreasing the growth levels of pathogenic Streptococcus mutans and Streptococcus sangui at the very early stages. Xylitol can bind with calcium ion leading to consequent remineralization of teeth enamel; it is also able to prevent osteoporosis. This polyol can treat respiratory tract and middle ear diseases due to its antibacterial and anti-inflammatory potential and prevent some diseases which cannot be cured through antibiotics or surgery. Xylitol can reduce constipation, diabetes, obesity, and other body syndromes or illnesses; it has also revealed its stimulating effect on digestion and immune system. However, it can produce some side effects such as irritable bowel syndrome, diarrhea, nephrolithiasis, etc., when consumed in excessive amounts. Different vehicles are used for delivering the xylitol into the human body, but chewing gums occupy a leading position. The present review is devoted to comprehensive analyses of the positive and negative effects of this polyol on human health.Key Points• The health benefits of xylitol are not limited to oral hygiene.• Xylitol efficiently stimulates the immune system, digestion, lipid and bone metabolism.• Xylitol helps in glycemic and obesity control; reduces ear and respiratory infections.• Xylitol treats diseases that cannot be cured through antibiotics or by surgery.

Identification of most damaging nsSNPs in human CCR6 gene: In silico analyses.

Single nucleotide polymorphisms in CCR6 (C-C chemokine receptor type 6) gene have been found to be the possible cause of many diseases like rheumatoid arthritis, psoriasis, lupus nephritis and systemic sclerosis and other autoimmune diseases. Therefore, identification of structurally and functionally important polymorphisms in CCR6 is important in order to study its potential malfunctioning and discovering therapeutic targets. Several bioinformatics tools were used to identify most damaging nsSNPs that might be vital for CCR6 structure and function. The in silico tools included PROVEAN, SIFT, SNP&GO and PolyPhen2 followed by I-Mutant MutPred and ConSurf. Phyre2 and I-TASSER were used for protein 3-D Modelling while gene-gene interaction was predicted by STRING and GeneMANIA. Our study suggested that three nsSNPs rs1376162684, rs751102128 and rs1185426631 are the most damaging in CCR6 gene while 7 missense SNPs rs1438637216, rs139697820, rs768420505, rs1282264186, rs1394647982, rs769360638 and rs1263402382 are found to revert into stop codons. Prediction of post-transcriptional modifications highlighted the significance of rs1376162684 because it effected potential phosphorylation site. Gene-gene interactions showed relation of CCR6 with other genes depicting its importance in several pathways and co-expressions. In future, studying diseases related to CCR6 should include investigation of these 10 nsSNPs. Being the first of its type, this study also proposes future perspectives that will help in precision medicines. For such purposes, CCR6 proteins from patients of autoimmune diseases should be explored. Animal models can also be of significance find out the effects of CCR6 in diseases.

T cell activation Rho GTPase activating protein (TAGAP) is upregulated in clinical and experimental arthritis.

Genome-wide association studies have identified various susceptibility variants and loci associated with incidence of rheumatoid arthritis (RA) in different populations. One of these is T cell activation Rho GTPase activating protein (TAGAP). The present study sought to measure the expression of TAGAP in RA patients, CD4+ T cells subsets from healthy humans and in mice with collagen-induced arthritis. Peripheral blood mononuclear cells (PBMC) from RA patients and tissues of arthritic mice at different stages of the disease were used for the evaluation of TAGAP mRNA expression. Increased TAGAP expression was observed in RA patients compared to healthy controls, and there were differences in the expression level of TAGAP in the tissues of mice with experimental arthritis. Gene expression in CD4+ T cells from healthy humans was greatest 4 h after activation and protein expression was greatest after 24 h. The expression of TAGAP was not correlated with CD4+ lymphocyte subsets which were enriched for functionally defined subsets (Th17, Treg, Th1), further indicating its utility as an indicator of lymphocyte activation. These findings indicate that increased TAGAP expression is a distinguishing feature of inflammatory disease and further highlight the role of TAGAP in RA susceptibility.

In silico and in vitro evaluation of two novel oximes (K378 and K727) in comparison to K-27 and pralidoxime against paraoxon-ethyl intoxication.

Organophosphate (OP) poisoning is a major global health issue; while compounds from this group have been used intensively over the last century, an effective antidote is still lacking. Oxime-type acetylcholinesterase (AChE) reactivators are used to reactivate the OP inhibited AChE. Pralidoxime is the only US Food and Drug Administration approved oxime for therapeutic use but its efficacy has been disappointing. Two novel oximes (K378 and K727) were investigated in silico and in vitro and compared with an experimental oxime (kamiloxime; K-27) and pralidoxime. In silico the molecular interactions between AChE and oximes were examined and binding energies were assessed. LogP (predicted log of the octanol/water partition coefficient) was estimated. In vitro the intrinsic ability of the oximes to inhibit AChE (IC50) and their reactivation potency (R50) when used in paraoxon inhibited human RBC-AChE was determined. Molecular docking revealed that K378 and K727 bind to the peripheral site(s) with high binding energies in contrast to the central binding of K-27 and pralidoxime. LogP values indicating that the novel compounds are significantly less hydrophilic than K-27 or pralidoxime. IC50 of K378 and K727 were comparable (0.9 and 1 µM, respectively) but orders of magnitude lower than comparators. R50 values revealed their inability to reactivate paraoxon inhibited AChE. It is concluded that the novel oximes K378 and K727 are unlikely to be clinically useful. The in silico and in vitro studies described allow avoidance of unnecessary in vivo animal work and contribute to the reduction of laboratory animal use.

Progression pattern of rheumatoid arthritis: A study of 500 Pakistani patients.

To estimate the most prevalent age of patients and disease status and progression in terms of severity at different age groups in the Pakistani Rheumatoid Arthritis (RA) patients. A total of five hundred (500) RA patients were enrolled during October, 2009 to October, 2013. A screening questionnaire was filled for each patient satisfying America College of Rheumatology (ACR) criteria under the supervision of certified rheumatologists. Epidemiological and demographic variables were statistically analyzed for correlation with progression of the disease using SPSS ver 17.0.1 software. In general, rheumatoid arthritis preferentially affects women with female to male ratio of about 3:1; however, patients with above 60 years of age have equal female to male ratio. The most prevalent age is 45-60 years. The disease severity increases with increase in the age and reaches to its peak in above 60 years of age (p=0.001). The pattern of progression of RA in the Pakistani patients is almost consistent with other relevant studies conducted on European and European derived populations.

Rheumatoid arthritis: What have we learned about the causing factors?

Rheumatoid Arthritis (RA) is a common inflammatory autoimmune disease characterized by the synovitis of both small and large joints, which may lead to the destruction of cartilage and bones causing significant disabilities due to erosion of bones surfaces, if left untreated. It is a multifactorial and heterogeneous disease having contribution of both genetic (50-60%) and environmental factors. The unawareness of general public might be a contributing factor in the high prevalence rate of RA world-wide. This review article focuses on the causing factors (genetics and environmental) involved in this devastating disease. We also gave brief overview of the treatment options and animal models of RA. The literature was reviewed using mesh terms in PubMed search ''etiology of RA, genetics of RA, environmental factors in RA, Genome Wide Association Studies (GWAS) in RA''. The data was thoroughly reviewed and comprehensive information was extracted to help the readers in improving understanding towards the mechanisms, which trigger the outcomes of RA. The more we increase awareness about RA, the better we manage this disease and hence can improve life style and socio-economic status.

Hepatoprotective efficacy of quinoa seed extract against CCl4- induced acute liver toxicity in rat model.

The current research explored the possible protective effect of chenopodium quinoa extract against CCl4 acute liver toxicity in Sprague Dawley rats. Thirty rats were divided into five groups with six rats in each group. CCl4 (Carbon tetrachloride) was administered at a dose rate of 2 mL/kg b.w. intra-peritoneally once a week for 3 weeks. The plant extract was given through oral gavage for a period of 21 days. Group I served as a normal group which was given with basal diet. Group II was referred to as a positive control group and received CCl4 2 mL/kg body weight (i.p.). Group III was the standard treatment group and received 2 mL/kg CCl4 (i.p.) and 16 mg/kg body weight (p.o.) silymarin. Group IV was the plant treatment group, which received 2 mL/kg CCl4 (i.p.) and 600 mg/kg body weight of quinoa seed extract (p.o.). Group V was the combined treatment group, which received 2 mL/kg CCl4 (i.p.) accompanied with a combination of silymarin (p.o.) 16 mg/kg body weight and quinoa seed extract (p.o.) 600 mg/kg body weight. The liver biomarkers were assessed along with histopathological analysis to observe the changes in the liver. The outcome suggested that the treatment, which was given with the combination of silymarin and quinoa seed extract, significantly enhanced the antioxidant levels, reduced the oxidative stress, and restored the liver function as evidenced by biochemical parameters histopathological studies. The hepatoprotective potential may be due to the antioxidant and anti-inflammatory properties of quinoa seed extract.

Ayurvedic and Chinese Herbs against Coronaviruses.

Coronavirus disease 2019 (COVID-19) is a viral disease that infects the lower airways, causing severe acute respiratory syndrome (SARS) and fatal pneumonia. The ripple effect of the COVID-19 outbreak has created serious problems in the healthcare systems of many countries and had far-reaching consequences for the global economy. Thus, effective control measures should be implemented for this coronavirus infection in the future. The ongoing episode of the SARS-CoV-2 sickness, COVID-19, in China, and the subsequent irregular spread of contamination to different nations, has alarmed the clinical and academic community primarily due to the deadly nature of this disease. Being a newly identified virus in the viral classification and having the highest mutation rate, rapid therapeutics are not readily available for treating this ailment, leading to the widespread of the disease and causing social issues for affected individuals. Evidence of Ayurveda and traditional Chinese medicine (TCM) has been found in ancient civilizations, such as those of the Hindus, Babylonians, Hebrews, and Arabs. Although TCM and Ayurvedic herbs do not promise to be very effective treatments for this pandemic, they can reduce infectivity and virulence by enhancing immunity and showing effectiveness in rehabilitation after COVID-19 disease. Thus, they could be used as sources of inhibitor molecules for certain phenomena, such as viral replication, attachment to the host, 3CL protease inhibition, 3a ion channel inhibitors, and reverse transcription inhibition. Medicinal plants from TCM and Ayurveda and their biologically active phytoconstituents can effectively modulate the targets and pathways relevant to inflammation and immune responses in human bodies. The present review analyzes the role of certain TCM and Ayurvedic medicinal plants in healing COVID-19 infection. Medicinal plants such as Glycyrrhiza glabra (licorice), Curcuma longa (turmeric), and Zingiber officinale (ginger) are regarded as the main antiviral herbs. Their extracts and individual bioactive compounds could be used as potential substances for developing remedies to prevent or cure the coronavirus disease. Generally, antiviral phytochemicals obtained from natural sources are considered potent candidates for fighting COVID-19 infection and rehabilitation after it.

In silico analysis of missense SNPs in TNFR1a and their possible therapeutic or pathogenic role in immune diseases.

Tumor necrosis factor alpha (TNFa) is an inflammatory cytokine that is involved in the pathogenesis of various inflammatory disorders including rheumatoid arthritis. TNF-alpha receptor I (TNFR1a) is one of the receptors TNFa binds with for its activation. Any variation in this receptor might affect the role of TNFa in successive events. Amino acid residue substitutions might happen in TNFR1a through non-synonymous single nucleotide polymorphisms (nsSNPs) which may alter the functioning of TNFa, hence, identifying any such substitutions is of paramount significance. In this study, six nsSNPs at five different evolutionary conserved regions are predicted to be detrimental to the structure and/or function of TNFR1a by using numerous computational tools. Their 3D models are also proposed in this study. Besides, they were found to reduce the stability and affect the molecular mechanisms of this protein. Two contrasting possibilities might happen because of these substitutions. One, they might reduce the production of TNFa which is overexpressed in inflammatory diseases, hence can play therapeutic role in such diseases. Second, they might possibly hinder the apoptosis to occur which can effectuate the uncontrolled division of cells, hence can be pathogenic in diseases like cancer. Further investigations on these nsSNPs using animal models and at cellular level will open doors to understand the underlying mechanisms behind various diseases.

The role of sugar-rich diet and salivary proteins in dental plaque formation and oral health.

BACKGROUND: Dental plaque is a complex colorless film of bacteria that develops on the surfaces of teeth. Different mechanisms of microbial adhesion to tooth surfaces exist. Both non-specific and specific types of adherence have been anticipated. HIGHLIGHT: The present review evaluated the effect of sugar-rich diet and salivary proteins on oral hygiene and dental plaque development. CONCLUSION: The oral microbiota is essential for maintaining and reestablishing a healthy oral cavity. Different types of sugars have different effects on the inhibition and formation of dental plaque. The peptides, proteins, and amino acids secreted by parotid glands in the oral cavity facilitate neutralizing the acidity in dental plaque and preventing dental caries. A properly balanced diet is crucial for both a healthy oral cavity and the oral microbiome.

NUB1 and FAT10 Proteins as Potential Novel Biomarkers in Cancer: A Translational Perspective.

Cancer increases the global disease burden substantially, but it remains a challenge to manage it. The search for novel biomarkers is essential for risk assessment, diagnosis, prognosis, prediction of treatment response, and cancer monitoring. This paper examined NEDD8 ultimate buster-1 (NUB1) and F-adjacent transcript 10 (FAT10) proteins as novel biomarkers in cancer. This literature review is based on the search of the electronic database, PubMed. NUB1 is an interferon-inducible protein that mediates apoptotic and anti-proliferative actions in cancer, while FAT10 is a ubiquitin-like modifier that promotes cancer. The upregulated expression of both NUB1 and FAT10 has been observed in various cancers. NUB1 protein binds to FAT10 non-covalently to promote FAT10 degradation. An overexpressed FAT10 stimulates nuclear factor-kappa ß, activates the inflammatory pathways, and induces the proliferation of cancer. The FAT10 protein interacts with the mitotic arrest deficient 2 protein, causing chromosomal instability and breast tumourigenesis. FAT10 binds to the proliferating cell nuclear antigen protein and inhibits the DNA damage repair response. In addition, FAT10 involves epithelial-mesenchymal transition, invasion, apoptosis, and multiplication in hepatocellular carcinoma. Our knowledge about them is still limited. There is a need to further develop NUB1 and FAT10 as novel biomarkers.

Characterization of Rheumatoid Arthritis Risk-Associated SNPs and Identification of Novel Therapeutic Sites Using an In-Silico Approach.

Single-nucleotide polymorphisms (SNPs) are reported to be associated with many diseases, including autoimmune diseases. In rheumatoid arthritis (RA), about 152 SNPs are reported to account for ~15% of its heritability. These SNPs may result in the alteration of gene expression and may also affect the stability of mRNA, resulting in diseased protein. Therefore, in order to predict the underlying mechanism of these SNPs and identify novel therapeutic sites for the treatment of RA, several bioinformatics tools were used. The damaging effect of 23 non-synonymous SNPs on proteins using different tools suggested four SNPs, including rs2476601 in PTPN22, rs5029941 and rs2230926 in TNFAIP3, and rs34536443 in TYK2, to be the most damaging. In total, 42 of 76 RA-associated intronic SNPs were predicted to create or abolish potential splice sites. Moreover, the analysis of 11 RA-associated UTR SNPs indicated that only one SNP, rs1128334, located in 3'UTR of ETS1, caused functional pattern changes in BRD-BOX. For the identification of novel therapeutics sites to treat RA, extensive gene-gene interaction network interactive pathways were established, with the identification of 13 potential target sites for the development of RA drugs, including three novel target genes. The anticipated effect of these findings on RA pathogenesis may be further validated in both in vivo and in vitro studies.

Zoonotic and reverse zoonotic events of SARS-CoV-2 and their impact on global health.

Coronaviruses (CoVs) are enveloped, positive sense, single-stranded RNA viruses. The viruses have adapted to infect a large number of animal species, ranging from bats to camels. At present, seven CoVs infect humans, of which Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is responsible for causing the Coronavirus Disease 2019 (COVID-19) in humans. Since its emergence in late 2019, SARS-CoV-2 has spread rapidly across the globe. Healthcare systems around the globe have been stretched beyond their limits posing new challenges to emergency healthcare services and critical care. The outbreak continues to jeopardize human health, social life and economy. All known human CoVs have zoonotic origins. Recent detection of SARS-CoV-2 in pet, zoo and certain farm animals has highlighted its potential for reverse zoonosis. This scenario is particularly alarming, since these animals could be potential reservoirs for secondary zoonotic infections. In this article, we highlight interspecies SARS-CoV-2 infections and focus on the reverse zoonotic potential of this virus. We also emphasize the importance of potential secondary zoonotic events and the One-Health and One-World approach to tackle such future pandemics.