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Parkinson's disease is one of the vital neurodegenerative ailments attributed to a rise in Alpha-synuclein proteins leading to the advancement of motor and cognitive deterioration. Interestingly, in PD lncRNAs, miRNAs and siRNAs are also key regulators of SNCA and alpha-synuclein aggregation. This review will focus on the roles of these three types of small RNAs in trebling the development of PD through regulating SNCA expression or alpha-synuclein protein mediating the RNA from acting. Parkinson's disease is deï¬ned by the build-up of alpha-synuclein protein resulting predominantly from the elevated expression level of the SNCA gene. Non-coding RNAs have gained broad appeal as fundamental modulators of gene expression and protein aggregation dynamics, with significant implications on the aetiology of PD. LncRNAs modulate SNCA transcription and edit epigenetic modifications, while miRNA target mRNA is involved in the stability and translation of count alpha-synuclein. Considering all these data, siRNAs can achieve the precise gene silencing effect that directly induces the downregulation of SNCA mRNA. This review also summarizes some recent reports about the interaction between these ncRNAs with the SNCA gene and alpha-synuclein protein, each through its independent in addition to synergistic mechanisms. This review highlights the possibility of therapeutic interventions to perturb SNCA expression to prevent alpha-synuclein aggregation via targeting ncRNAs that might be spun off novel drug development for PD.
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BACKGROUND: COVID-19 has presented significant obstacles to healthcare. Stem cell therapy, particularly mesenchymal stem cells (MSCs), has emerged as a potential treatment modality due to its immunomodulatory and regenerative properties. This umbrella review aims to synthesize current evidence from systematic reviews on the safety and efficacy of stem cell therapy in COVID-19 treatment. METHODS: A thorough literature search was performed across Embase, PubMed, Cochrane and Web of Science from December 2019 to February 2024. Systematic reviews focusing on the use of stem cell therapy for COVID-19 were included. Evidence was synthesized by meta-analysis using R software (V 4.3) for each outcome. The certainty of evidence was assessed using the GRADE approach. RESULTS: A total of 24 systematic reviews were included. Stem cell therapy was associated with reduced mortality (RR 0.72, 95% CI: 0.60-0.86); shorter hospital stays (MD -4.00 days, 95% CI: -4.68 to -3.32), and decreased need for invasive ventilation (RR 0.521, 95% CI: 0.320 to 0.847). Symptom remission rates improved (RR 1.151, 95% CI: 0.998 to 1.330), and a reduction in CRP levels was noted (SMD -1.198, 95% CI: -2.591 to 0.195), albeit with high heterogeneity. For adverse events, no significant differences were found between stem cell therapy and standard care (RR 0.87, 95% CI: 0.607 to 1.265). The certainty of evidence ranged from low to moderate. CONCLUSION: Stem cell therapy demonstrates a potential benefit in treating COVID-19, particularly in reducing mortality and hospital stay duration. Despite these promising findings, the evidence is varied, and future large-scale randomized trials are essential to confirm the efficacy and optimize the therapeutic protocols for stem cell therapy in the management of the disease. The safety profile is encouraging, with no significant increase in adverse events, suggesting a viable avenue for treatment expansion.
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[This corrects the article DOI: 10.1155/2021/2347506.].
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Breast cancer is one of the most common causes of cancer-related mortality globally, and its aggressive phenotype results in poor treatment outcomes. Growth Arrest-Specific 5 long non-coding RNA has attracted considerable attention due to its pivotal function in apoptosis regulation and tumor aggressiveness in breast cancer. Gas5 enhances apoptosis by regulating apoptotic proteins, such as caspases and BCL2 family proteins, and the sensitivity of BCCs to chemotherapeutic agents. At the same time, low levels of GAS5 increased invasion, metastasis, and overall tumor aggressiveness. GAS5 also regulates EMT markers, critical for cancer metastasis, and influences tumor cell proliferation by regulating various signaling components. As a result, GAS5 can be restored to suppress tumor development as a possible therapeutic strategy, which might present promising prospects for a patient's treatment. Its activity levels might also be a crucial indicator and diagnostic parameter for prediction. This review highlights the significant role of GAS5 in modulating apoptosis and tumor aggressiveness in breast cancer, emphasizing its potential as a therapeutic target for breast cancer treatment and management.
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Apoptose , Biomarcadores Tumorais , Neoplasias da Mama , RNA Longo não Codificante , Humanos , RNA Longo não Codificante/genética , Neoplasias da Mama/genética , Neoplasias da Mama/patologia , Neoplasias da Mama/terapia , Feminino , Biomarcadores Tumorais/genética , Biomarcadores Tumorais/metabolismo , Apoptose/genética , Regulação Neoplásica da Expressão GênicaRESUMO
Long non-coding RNAs (lncRNAs) are a diverse class of RNA molecules that do not code for proteins but play critical roles in gene regulation. One such role involves the modulation of cell cycle progression and proliferation through interactions with cyclin-dependent kinases (CDKs), key regulators of cell division. Dysregulation of CDK activity is a hallmark of cancer, contributing to uncontrolled cell growth and tumor formation. These lncRNA-CDK interactions are part of a complex network of molecular mechanisms underlying cancer pathogenesis, involving various signaling pathways and regulatory circuits. Understanding the interplay between lncRNAs, CDKs, and cancer biology holds promise for developing novel therapeutic strategies targeting these molecular targets for more effective cancer treatment. Furthermore, targeting CDKs, key cell cycle progression and proliferation regulators, offers another avenue for disrupting cancer pathways and overcoming drug resistance. This can open new possibilities for individualized treatment plans and focused therapeutic interventions.
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Quinases Ciclina-Dependentes , Progressão da Doença , Neoplasias , RNA Longo não Codificante , Humanos , Neoplasias/genética , Neoplasias/patologia , Neoplasias/enzimologia , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Quinases Ciclina-Dependentes/genética , Quinases Ciclina-Dependentes/metabolismo , Regulação Neoplásica da Expressão Gênica , Animais , Transdução de Sinais/genética , Proliferação de Células/genética , Ciclo Celular/genética , Ciclo Celular/fisiologiaRESUMO
Lumpy skin disease (LSD) caused by LSD virus is a WOAH notifiable, high-impact, transboundary poxviral disease of bovines. The first official report of LSDV in India is from Odisha state during August 2019. Since then, cases have been reported from many states including Tamil Nadu, a Southern state of India. The present study deals with isolation and molecular characterization of LSDV from Tamil Nadu during the period August 2020 to July 2022. LSDV was isolated in embryonated chicken eggs (ECE) and BHK 21 cells and was characterized based on P32, RPO30, and GPCR genes. The phylogenetic analysis revealed that Tamil Nadu isolates from India are closely related to other Indian strains, Kenyan strains and strains from neighboring countries such as Bangladesh, Nepal, and Myanmar confirming the common exotic source for the transboundary spread across borders. The presence of unique signature of amino acid (aa) at specific positions (A11, T12, T34, S99, and P199) in the GPCR sequence confirmed the identity of LSDV. A twelve nucleotide (nt94-105) insertion and corresponding aa (TILS) at 30-33 position was found in GPCR sequence and characteristic amino acid proline at 98 position (P98) in the RPO30 gene sequence of our isolates was similar to strains from Bangladesh, Nepal, and Myanmar. Further, dissimilarity of our isolates from Neethling like vaccine strains confirms the circulation of virulent filed strains responsible for the outbreaks.
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Vírus da Doença Nodular Cutânea , Animais , Bovinos , Vírus da Doença Nodular Cutânea/genética , Índia/epidemiologia , Filogenia , Quênia , Surtos de Doenças , Aminoácidos/genéticaRESUMO
The human gut microbiota (GM), which consists of a complex and diverse ecosystem of bacteria, plays a vital role in overall wellness. However, the delicate balance of this intricate system is being compromised by the widespread presence of environmental toxins. The intricate connection between contaminants in the environment and human well-being has garnered significant attention in recent times. Although many environmental pollutants and their toxicity have been identified and studied in laboratory settings and animal models, there is insufficient data concerning their relevance to human physiology. Consequently, research on the toxicity of environmental toxins in GM has gained prominence in recent years. Various factors, such as air pollution, chemicals, heavy metals, and pesticides, have a detrimental impact on the composition and functioning of the GM. This comprehensive review aims to comprehend the toxic effects of numerous environmental pollutants, including antibiotics, endocrine-disrupting chemicals, heavy metals, and pesticides, on GM by examining recent research findings. The current analysis concludes that different types of environmental toxins can lead to GM dysbiosis and have various potential adverse effects on the well-being of animals. We investigate the alterations to the GM composition induced by contaminants and their impact on overall well-being, providing a fresh perspective on research related to pollutant exposure.
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Poluentes Ambientais , Microbioma Gastrointestinal , Metais Pesados , Praguicidas , Animais , Humanos , Microbioma Gastrointestinal/fisiologia , Ecossistema , Poluentes Ambientais/toxicidade , Metais Pesados/toxicidade , Praguicidas/toxicidadeRESUMO
Herbal products in dentistry have grown significantly. In the current scenario, herbal products are believed to be an effective adjunct to other medications. The present study aims to evaluate Eucalyptus oil and miswak (Salvadora persica) toothpaste for its efficacy in observable reduction in plaque and gingival bleeding. Sixty participants with gingivitis were enrolled in the present study. The study included an interim period (washout) comparing miswak and Eucalyptus toothpaste. Plaque scores were measured at designated time intervals. Both herbal toothpastes significantly decreased plaque index. Nevertheless, with relation to miswak (P = 0.002), Eucalyptus oil-based toothpaste exhibited reduction in bleeding scores. When participants were asked to return to their routine toothpaste, no changes were observed. Results from the study showed that the toothpaste containing Eucalyptus showed a significant decrease in gingival bleeding. More investigations should be looked on the medicinal applications of Eucalyptus toothpaste on commonly seen periodontal parameters.
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Background: A pooled estimate of stunting prevalence in refugee and internally displaced under-five children can help quantify the problem and focus on the nutritional needs of these marginalized groups. We aimed to assess the pooled prevalence of stunting in refugees and internally displaced under-five children from different parts of the globe. Methods: In this systematic review and meta-analysis, seven databases (Cochrane, EBSCOHost, EMBASE, ProQuest, PubMed, Scopus, and Web of Science) along with "preprint servers" were searched systematically from the earliest available date to 14 February 2023. Refugee and internally displaced (IDP) under-five children were included, and study quality was assessed using "National Heart, Lung, and Blood Institute (NHLBI)" tools. Results: A total of 776 abstracts (PubMed = 208, Scopus = 192, Cochrane = 1, Web of Science = 27, Embase = 8, EBSCOHost = 123, ProQuest = 5, Google Scholar = 209, and Preprints = 3) were retrieved, duplicates removed, and screened, among which 30 studies were found eligible for qualitative and quantitative synthesis. The pooled prevalence of stunting was 26% [95% confidence interval (CI): 21-31]. Heterogeneity was high (I2 = 99%, p < 0.01). A subgroup analysis of the type of study subjects revealed a pooled stunting prevalence of 37% (95% CI: 23-53) in internally displaced populations and 22% (95% CI: 18-28) among refugee children. Based on geographical distribution, the stunting was 32% (95% CI: 24-40) in the African region, 34% (95% CI: 24-46) in the South-East Asian region, and 14% (95% CI: 11-19) in Eastern Mediterranean region. Conclusion: The stunting rate is more in the internally displaced population than the refugee population and more in the South-East Asian and African regions. Our recommendation is to conduct further research to evaluate the determinants of undernutrition among under-five children of refugees and internally displaced populations from different regions so that international organizations and responsible stakeholders of that region can take effective remedial actions. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=387156, PROSPERO [CRD42023387156].
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Desnutrição , Refugiados , Criança , Humanos , Prevalência , Bibliometria , Transtornos do Crescimento/epidemiologiaRESUMO
Long non-coding RNAs (lncRNAs) have emerged as pivotal regulators of gene expression, contributing significantly to a diverse range of cellular processes, including apoptosis. One such lncRNA is NEAT1, which is elevated in several types of cancer and aid in cancer growth. However, recent studies have also demonstrated that the knockdown of NEAT1 can inhibit cancer cells proliferation, movement, and infiltration while enhancing apoptosis. This article explores the function of lncRNA NEAT1 knockdown in regulating apoptosis across multiple cancer types. We explore the existing understanding of NEAT1's involvement in the progression of malignant conditions, including its structure and functions. Additionally, we investigate the molecular mechanisms by which NEAT1 modulates the cell cycle, cellular proliferation, apoptosis, movement, and infiltration in diverse cancer types, including acute myeloid leukemia, breast cancer, cervical cancer, colorectal cancer, esophageal squamous cell carcinoma, glioma, non-small cell lung cancer, ovarian cancer, prostate cancer, and retinoblastoma. Furthermore, we review the recent studies investigating the therapeutic potential of NEAT1 knockdown in cancer treatment. Targeting the lncRNA NEAT1 presents a promising therapeutic approach for treating cancer. It has shown the ability to suppress cancer cell proliferation, migration, and invasion while promoting apoptosis in various cancer types.
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Apoptose , Neoplasias , RNA Longo não Codificante , Humanos , Carcinoma Pulmonar de Células não Pequenas/genética , Linhagem Celular Tumoral , Proliferação de Células , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , Animais , Neoplasias/metabolismoRESUMO
Lung cancer is the leading cause of cancer-related deaths worldwide. Molecular profiling has contributed to a new classification of lung cancer, driving advancements in research and therapy. The ataxia telangiectasia and rad3/checkpoint kinase 1 (ATR/CHK1) pathway plays a crucial role in maintaining genomic stability, and its activation has been linked to the development of lung cancer, drug resistance and poor prognosis. Clinical and preclinical studies have demonstrated promising results in targeting this pathway. ATR and CHK1 are proteins that collaborate to repair DNA damage caused by radiation or chemotherapy. ATR/CHK1 inhibitors are currently under investigation in preclinical and clinical trials. This article explores the ATR/CHK1 pathway and its potential for treating lung cancer.
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Neoplasias Pulmonares , Humanos , Neoplasias Pulmonares/metabolismo , Proteínas Mutadas de Ataxia Telangiectasia/genética , Proteínas Mutadas de Ataxia Telangiectasia/metabolismo , Dano ao DNA , Inibidores de Proteínas Quinases/farmacologia , Inibidores de Proteínas Quinases/uso terapêutico , Proteínas de Ciclo CelularRESUMO
Breast cancer is a complex and diverse condition that disrupts multiple signaling pathways essential for cell proliferation, survival, and differentiation. Recently, the significant involvement of long-chain non-coding RNAs (lncRNAs) in controlling key signaling pathways associated with breast cancer development has been discovered. This review aims to explore the interaction between lncRNAs and various pathways, including the AKT/PI3K/mTOR, Wnt/ß-catenin, Notch, DNA damage response, TGF-ß, Hedgehog, and NF-κB signaling pathways, to gain a comprehensive understanding of their roles in breast cancer. The AKT/PI3K/mTOR pathway regulates cell growth, survival, and metabolic function. Recent data suggests that specific lncRNAs can influence the functioning of this pathway, acting as either oncogenes or tumor suppressors. Dysregulation of this pathway is commonly observed in breast cancer cases. Moreover, breast cancer development has been associated with other pathways such as Wnt/ß-catenin, Notch, TGF-ß, Hedgehog, and NF-κB. Emerging studies have identified lncRNAs that modulate breast cancer's growth, progression, and metastasis by interacting with these pathways. To advance the development of innovative diagnostic tools and targeted treatment options, it is crucial to comprehend the intricate relationship between lncRNAs and vital signaling pathways in breast cancer. By fully harnessing the therapeutic potential of lncRNAs, there is a possibility of developing more effective and personalized therapy choices for breast cancer patients. Further investigation is necessary to comprehensively understand the role of lncRNAs within breast cancer signaling pathways and fully exploit their therapeutic potential.
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Neoplasias da Mama , RNA Longo não Codificante , Humanos , Feminino , Animais , Neoplasias da Mama/genética , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , beta Catenina/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , NF-kappa B/metabolismo , Ouriços/genética , Ouriços/metabolismo , Transdução de Sinais , Serina-Treonina Quinases TOR/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Regulação Neoplásica da Expressão Gênica/genéticaRESUMO
Lung cancer (LC) continues to pose a significant global medical burden, necessitating a comprehensive understanding of its molecular foundations to establish effective treatment strategies. The mitogen-activated protein kinase (MAPK) signaling system has been scientifically associated with LC growth; however, the intricate regulatory mechanisms governing this system remain unknown. Long non-coding RNAs (lncRNAs) are emerging as crucial regulators of diverse cellular activities, including cancer growth. LncRNAs have been implicated in LC, which can function as oncogenes or tumor suppressors, and their dysregulation has been linked to cancer cell death, metastasis, spread, and proliferation. Due to their involvement in critical pathophysiological processes, lncRNAs are gaining attention as potential candidates for anti-cancer treatments. This article aims to elucidate the regulatory role of lncRNAs in MAPK signaling in LC. We provide a comprehensive review of the key components of the MAPK pathway and their relevance in LC, focusing on aberrant signaling processes associated with disease progression. By examining recent research and experimental findings, this article examines the molecular mechanisms through which lncRNAs influence MAPK signaling in lung cancer, ultimately contributing to tumor development.
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Neoplasias Pulmonares , Sistema de Sinalização das MAP Quinases , RNA Longo não Codificante , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/genética , RNA Longo não Codificante/metabolismo , Humanos , Epigênese GenéticaRESUMO
Among 17 Panax species identified across the world, Panax ginseng (Korean ginseng), Panax quinquefolius (American ginseng), and Panax notoginseng (Chinese ginseng) are highly recognized for the presence of bioactive compound, ginsenosides and their pharmacological effects. P. ginseng is widely used for synthesis of different types of nanoparticles compared to P. quinquefolius and P. notoginseng. The use of nano-ginseng could increase the oral bioavailability, membrane permeability, and thus provide effective delivery of ginsenosides to the target sites through transport system. In this review, we explore the synthesis of ginseng nanoparticles using plant extracts from various organs, microbes, and polymers, as well as their biomedical applications. Furthermore, we highlight transporters involved in transport of ginsenoside nanoparticles to the target sites. Size, zeta potential, temperature, and pH are also discussed as the critical parameters affecting the quality of ginseng nanoparticles synthesis.
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Ginsenosídeos , Panax , Humanos , Ginsenosídeos/farmacologia , Panax/química , Extratos Vegetais/químicaRESUMO
We are experiencing a revolution in regenerative medicine. Recent developments in organoid technology have provided unique opportunities for studying human biology and diseases. Indeed, organoid models have revolutionized the in vitro culture tools for biomedical research by creating robust three-dimensional (3D) architecture to recapitulate the primary tissues' cellular heterogeneity, structure, and functions. Such organoid technology enables researchers to re-create human organs and diseases model in a culture dish. It thus holds excellent promises for many translational applications such as regenerative medicine, drug discovery, and precision medicine. This review summarizes the current knowledge on the progression and promotion of organoid models, particularly with the heart disease approach. We discuss the usefulness of clinical applications of cardiac organoids and ultimately highlight the currently advanced therapeutic strategies in vitro model of organoids aimed at personalizing heart disease treatment.
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Pesquisa Biomédica , Cardiopatias , Humanos , Medicina Regenerativa/métodos , Organoides , Coração , Cardiopatias/terapiaRESUMO
Algae are effective predecessors of nutrient foods and preventive drugs, gaining global attraction in recent years. It exhibits potent antiviral, antibacterial, antifungal, anti-inflammatory, antioxidant, anti-glycemic, and cholesterol-lowering properties due to their richness in highly valuable secondary metabolites. Nevertheless, algae produce valuable bioproducts, its application in dentistry is in its primitive stage. This review focuses on the emergence and emerging role of micro/macroalgae as a natural source of therapeutic, preventive, and biocompatible agents in dentistry. Several studies unveiled that Cyanobacteria, Spirulina, and Chlorella species offer high oral antibacterial and antifungal properties compared to gold standard agents. The characteristic of algae to scavenge superoxide and hydroxyl free radicals, fabricate them as an anti-oxidative and anti-cancer agent. Either alone or by synergism with pinnacle therapies they are found to produce promising curative actions against periodontitis by embattling proinflammatory cytokines. Technologies extend the functions of microalgae as a detoxifying agent, potent drug delivery system, and adjunct regenerative material in chronic periodontitis. Its application as thickening, binding, anticariogenic agent in toothpaste, antibacterial agent in mouthwash, and biocompatible agent in dental impression materials remains very primitive. Low-cost and eco-friendly technologies are needed for the production of oral hygiene products using algal biomass.