Exploring ncRNAs in epilepsy: From oxidative stress regulation to therapy.

Epilepsy is a prevalent neurological illness which is linked with high worldwide burdens. Oxidative stress (OS) is recognized to be among the contributors that trigger the advancement of epilepsy, affecting neuronal excitability and synaptic transmission. Various types of non-coding RNAs (ncRNAs) are known to serve vital functions in many disease mechanisms, including epilepsy. The current review sought to understand better the mechanisms through which these ncRNAs regulate epilepsy's OS-related pathways. We investigated the functions of microRNAs in controlling gene expression at the post-translatory stage and their involvement in OS and neuroinflammation. We also looked at the different regulatory roles of long ncRNAs, including molecular scaffolding, enhancer, and transcriptional activator, during OS. Circular RNAs and their capability to act as miRNA decoys and their consequential impact on epilepsy development were also explored. Our review aimed to improve the current understanding of novel therapies for epilepsy based on the role of ncRNAs in OS pathways. We also demonstrated the roles of ncRNAs in epilepsy treatment and diagnosis, explaining that these molecules play vital roles that could be used in therapy as biomarkers.

Oxidative Coupling and Self-Assembly of Polyphenols for the Development of Novel Biomaterials.

In recent years, the development of biomaterials from green organic sources with nontoxicity and hyposensitivity has been explored for a wide array of biotherapeutic applications. Polyphenolic compounds have unique structural features, and self-assembly by oxidative coupling allows molecular species to rearrange into complex biomaterial that can be used for multiple applications. Self-assembled polyphenolic structures, such as hollow spheres, can be designed to respond to various chemical and physical stimuli that can release therapeutic drugs smartly. The self-assembled metallic-phenol network (MPN) has been used for modulating interfacial properties and designing biomaterials, and there are several advantages and challenges associated with such biomaterials. This review comprehensively summarizes current challenges and prospects of self-assembled polyphenolic hollow spheres and MPN coatings and self-assembly for biomedical applications.

Non-coding RNA mediated regulation of PI3K/Akt pathway in hepatocellular carcinoma: Therapeutic perspectives.

Hepatocellular carcinoma (HCC) is among the primary reasons for fatalities caused by cancer globally, highlighting the need for comprehensive knowledge of its molecular aetiology to develop successful treatment approaches. The PI3K/Akt system is essential in the course of HCC, rendering it an intriguing candidate for treatment. Non-coding RNAs (ncRNAs), such as long ncRNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs), are important mediators of the PI3K/Akt network in HCC. The article delves into the complex regulatory functions of ncRNAs in influencing the PI3K/Akt system in HCC. The study explores how lncRNAs, miRNAs, and circRNAs impact the expression as well as the function of the PI3K/Akt network, either supporting or preventing HCC growth. Additionally, treatment strategies focusing on ncRNAs in HCC are examined, such as antisense oligonucleotide-based methods, RNA interference, and small molecule inhibitor technologies. Emphasizing the necessity of ensuring safety and effectiveness in clinical settings, limitations, and future approaches in using ncRNAs as therapies for HCC are underlined. The present study offers useful insights into the complex regulation system of ncRNAs and the PI3K/Akt cascade in HCC, suggesting possible opportunities for developing innovative treatment approaches to address this lethal tumor.

Circular RNAs in the KRAS pathway: Emerging players in cancer progression.

Circular RNAs (circRNAs) have been recognized as key components in the intricate regulatory network of the KRAS pathway across various cancers. The KRAS pathway, a central signalling cascade crucial in tumorigenesis, has gained substantial emphasis as a possible therapeutic target. CircRNAs, a subgroup of non-coding RNAs known for their closed circular arrangement, play diverse roles in gene regulation, contributing to the intricate landscape of cancer biology. This review consolidates existing knowledge on circRNAs within the framework of the KRAS pathway, emphasizing their multifaceted functions in cancer progression. Notable circRNAs, such as Circ_GLG1 and circITGA7, have been identified as pivotal regulators in colorectal cancer (CRC), influencing KRAS expression and the Ras signaling pathway. Aside from their significance in gene regulation, circRNAs contribute to immune evasion, apoptosis, and drug tolerance within KRAS-driven cancers, adding complexity to the intricate interplay. While our comprehension of circRNAs in the KRAS pathway is evolving, challenges such as the diverse landscape of KRAS mutant tumors and the necessity for synergistic combination therapies persist. Integrating cutting-edge technologies, including deep learning-based prediction methods, holds the potential for unveiling disease-associated circRNAs and identifying novel therapeutic targets. Sustained research efforts are crucial to comprehensively unravel the molecular mechanisms governing the intricate interplay between circRNAs and the KRAS pathway, offering insights that could potentially revolutionize cancer diagnostics and treatment strategies.

MALAT1: A key regulator in lung cancer pathogenesis and therapeutic targeting.

Lung cancer remains a formidable global health burden, necessitating a comprehensive understanding of the underlying molecular mechanisms driving its progression. Recently, lncRNAs have become necessary controllers of various biological functions, including cancer development. MALAT1 has garnered significant attention due to its multifaceted role in lung cancer progression. Lung cancer, among other malignancies, upregulates MALAT1. Its overexpression has been associated with aggressive tumor behavior and poor patient prognosis. MALAT1 promotes cellular proliferation, epithelial-mesenchymal transition (EMT), and angiogenesis in lung cancer, collectively facilitating tumor growth and metastasis. Additionally, MALAT1 enhances cancer cell invasion by interacting with numerous signaling pathways. Furthermore, MALAT1 has been implicated in mediating drug resistance in lung cancer, contributing to the limited efficacy of conventional therapies. Recent advancements in molecular biology and high-throughput sequencing technologies have offered fresh perspectives into the regulatory networks of MALAT1 in lung cancer. It exerts its oncogenic effects by acting as a ceRNA to sponge microRNAs, thereby relieving their inhibitory effects on target genes. Moreover, MALAT1 also influences chromatin remodeling and post-translational modifications to modulate gene expression, further expanding its regulatory capabilities. This review sheds light on the multifaceted roles of MALAT1 in lung cancer progression, underscoring its potential as an innovative therapeutic target and diagnostic biomarker. Targeting MALAT1 alone or combined with existing therapies holds promise to mitigate lung cancer progression and improve patient outcomes.

From LncRNA to metastasis: The MALAT1-EMT axis in cancer progression.

Cancer is a complex disease that causes abnormal genetic changes and unchecked cellular growth. It also causes a disruption in the normal regulatory processes that leads to the creation of malignant tissue. The complex interplay of genetic, environmental, and epigenetic variables influences its etiology. Long non-coding RNAs (LncRNAs) have emerged as pivotal contributors within the intricate landscape of cancer biology, orchestrating an array of multifaceted cellular processes that substantiate the processes of carcinogenesis and metastasis. Metastasis is a crucial driver of cancer mortality. Among these, MALAT1 (Metastasis-Associated Lung Adenocarcinoma Transcript 1) has drawn a lot of interest for its function in encouraging metastasis via controlling the Epithelial-Mesenchymal Transition (EMT) procedure. MALAT1 exerts a pivotal influence on the process of EMT, thereby promoting metastasis to distant organs. The mechanistic underpinning of this phenomenon involves the orchestration of an intricate regulatory network encompassing transcription factors, signalling cascades, and genes intricately associated with the EMT process by MALAT1. Its crucial function in transforming tumor cells into an aggressive phenotype is highlighted by its capacity to influence the expression of essential EMT effectors such as N-cadherin, E-cadherin, and Snail. An understanding of the MALAT1-EMT axis provides potential therapeutic approaches for cancer intervention. Targeting MALAT1 or its downstream EMT effectors may reduce the spread of metastatic disease and improve the effectiveness of already available therapies. Understanding the MALAT1-EMT axis holds significant clinical implications. Therefore, directing attention towards MALAT1 or its downstream mediators could present innovative therapeutic strategies for mitigating metastasis and improving patient prognosis. This study highlights the importance of MALAT1 in cancer biology and its potential for cutting back on metastatic disease with novel treatment strategies.

Exploring the role of lncrna neat1 knockdown in regulating apoptosis across multiple cancer types: A review.

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.

Gut Microbiota Disruption in COVID-19 or Post-COVID Illness Association with severity biomarkers: A Possible Role of Pre / Pro-biotics in manipulating microflora.

Coronavirus disease (COVID-19), a coronavirus-induced illness attributed to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) transmission, is thought to have first emerged on November 17, 2019. According to World Health Organization (WHO). COVID-19 has been linked to 379,223,560 documented occurrences and 5,693,245 fatalities globally as of 1st Feb 2022. Influenza A virus that has also been discovered diarrhea and gastrointestinal discomfort was found in the infected person, highlighting the need of monitoring them for gastro intestinal tract (GIT) symptoms regardless of whether the sickness is respiration related. The majority of the microbiome in the intestines is Firmicutes and Bacteroidetes, while Bacteroidetes, Proteobacteria, and Firmicutes are found in the lungs. Although most people overcome SARS-CoV-2 infections, many people continue to have symptoms months after the original sickness, called Long-COVID or Post COVID. The term "post-COVID-19 symptoms" refers to those that occur with or after COVID-19 and last for more than 12 weeks (long-COVID-19). The possible understanding of biological components such as inflammatory, immunological, metabolic activity biomarkers in peripheral blood is needed to evaluate the study. Therefore, this article aims to review the informative data that supports the idea underlying the disruption mechanisms of the microbiome of the gastrointestinal tract in the acute COVID-19 or post-COVID-mediated elevation of severity biomarkers.

A study of abnormal cannabidiols system-mediated cardiovascular protection in disrupted gut/brain axis associated depression.

Uncontrolled stress can lead to vascular injury, hypertension, arrhythmia, compromised immune system alteration in microbiota activity, and neurobehavioral changes, including depression. The gut microbiota has been recently developed, not only for major depressive disorders but also cardiovascular problems, as a therapeutic concern. Since then, >100 studies have studied the link between depression and cardiovascular disease (CVD), and have shown that depression is common (≈20%-35%) in patients with CVD, and seems to be indicative of negative heart effects in patients. Depressive symptoms patients have demonstrated an elevated platelet reactivity, reduced cardiac variability, and enhanced proinflammatory signals, which are all cardiovascular-related risk factors. The pathophysiology of depression-related CVD is nevertheless a challenge because of the heterogeneous depressive syndromes and the etiologies. The cardiovascular effects of tetrahydrocannabinol (THC) (the key psychotropic credential of cannabis) and endocannabinoids (THC endogenous equivalents which cause type 1 [CB1] and 2 [CB2] cannabinoids) have been extensively examined based on well-documented effects of marijuana smoke on blood pressure (BP) and heart rate (HR). Therefore, the aim of the review article is to establish the relationship of abnormal cannabidiols system-mediated cardiovascular protection in disrupted gut/brain axis associated depression to determine the translational potential of targeting abnormal cannabidiols receptors in clinical studies.

A molecular explanation of cardiovascular protection through abnormal cannabidiol: Involving the dysfunctional ß-adrenergic and ATP-sensitive K+ channel activity in cardiovascular compromised preterm infants.

Growing cannabis efficacy, usage frequency, legal supply, and declining awareness of danger recently led to expanded United States cannabis exposure. In turn, cannabis use among elderly people over 50 has more than tripled in a decade and has contributed toward a positive association of cannabis use with pathological conditions, which include type II diabetes, metabolic syndrome, neurovascular and cardiovascular disease. Remarkably, all these outcome results are mediated by the involvement of the ATP-sensitive K+ channel. Cardiovascular compromise is a common syndrome in preterm infants that leads to incidence and death and has been distinguished by poor systemic flow or hypotension. Conditions of cardiovascular compromise include vasodysregulation and myocardial malfunction through dysfunctional ß-adrenergic activity. To avoid organ hypoperfusion progressing to tissue hypoxia-ischemia, inotropic drugs are used. Many premature children, however, respond insufficiently to inotropic activity with adrenergic agonists. The clinical disturbance including myocardial dysfunction through the activation of the ATP-sensitive K+ channel is often involved and the comparative efficacy of the nonpsychotropic cannabinoid, abnormal cannabidiol (Abn-CBD) is not yet known. Therefore, our primary aim was to investigate the molecular exploration of the cannabinoid system specifically Abn-CBD in cardiovascular protection involving dysregulated KATP.

Parents' self-directed practices towards the use of antibiotics for upper respiratory tract infections in Makkah, Saudi Arabia.

BACKGROUND: Excessive and inappropriate antimicrobial use in the community is one risk factor that can result in the spread of antimicrobial resistance. Upper respiratory tract infections are most frequently reported among children and mainly of viral origin and do not require antibiotics. We have conducted Knowledge, Attitude and Perception (KAP) survey of parents to explore the parent's knowledge, attitude & perception of Saudi parents. METHODS: A knowledge attitude perception questioner was adopted from a previous study conducted in Greece by Panagakou et al. Raosoft online sample size calculator calculated the sample size by adding the total estimated Makkah population of 5,979,719 with a response rate of 30%, 5% margin of error and 99% confidence interval. Based on the described criteria five hundred & fifty-eight was the required sample size of the study. Incomplete questioners were excluded from the statistical analysis. SPSS version 21 was used to analyse data and to produce descriptive statistics. RESULTS: Most of the mothers (95%) responded among parents. 67% had no health insurance to cover medications costs. Most of them (74%) were related to medium income level. Seventy per cent of the parents believed physicians as a source of information for judicious antibiotics use. Interestingly, only 8% were agreed that most of the upper respiratory tract infections are caused by viral reasons. Majority of Saudi parents (53%) expect pediatricians to prescribe antimicrobials for their children for symptoms like a cough, nose discharge, sore throat and fever. Moreover, most the parents had the poor knowledge to differentiate commonly used OTC medications for URTI and antibiotics like Augmentin (Co-amoxiclav), Ceclor (cefaclor) and Erythrocin (Erythromycin). While comparing males and female's knowledge level, few males have identified Amoxil (Amoxicillin). Similarly, parents of age 20-30 years have good knowledge about the antibiotics. CONCLUSIONS: Majority of Saudi parents believe in pediatricians and use antibiotics on physician's advice. Most of them expect antibiotics from their physicians as a primary treatment for upper respiratory tract infections. There is need for more educational activities to parents by the pharmacists to prevent antibiotics overuse among children.