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It is crucial to identify an efficient system for the sensing of formaldehyde (FD). The feasibility of utilising a B3S monolayer (B3SML) detector of FD was evaluated by analysing the adsorption, optical properties, gas-sensing behaviour, and electronic properties of FD and other gas molecules on the B3SML under density functional theory (DFT). The pristine B3SML was found to have satisfactory sensing toward FD molecules. The analysis of the adsorption mechanisms, geometric systems, adsorption energy, electronic and optical properties, charge transfer, and electron density differences revealed that the B3SML could potentially serve as an FD detector. It can be said that the B3SML is a promising sensor for detecting FD molecules. The present study contributes to the existing knowledge of gas-surface interactions and helps develop 2D sensor structures to detect FD gas molecules. [ABSTRACT FROM AUTHOR]

A substantial amount of scholarly inquiry has focused on the advancement of innovative methodologies for drug administration. In this research, both graphyne (GY) and BN-analog GY (BNY) nanosheets are presented. The study focuses on the carbon allotrope GY. Density Functional Theory (DFT) calculations were used to assess how GY, BNY, and the anticancer drug ciclopirox (CPX) interact with one another. It was observed that the inherent capability of pristine GY to augment CPX adsorption is intensified by the involvement of nitrogen (N) and boron (B) atoms. Furthermore, examination using Ultraviolet–Visible (UV-Vis) analysis exhibited a shift towards less energetic states, corresponding to longer wavelengths. Moreover, the interaction between CPX and BNY displayed chemical reactivity, rendering it conducive for forming bonds at the adsorption site. Additionally, a thorough investigation via the Atoms-In-Molecules (AIM) analysis furnished a more profound comprehension of the associations between the drug and the nanosheet. Notably robust connections between CPX and BNY were detected. As a consequence, the potential of BNY to function as a viable transporter for CPX in the realm of drug delivery was substantiated. [ABSTRACT FROM AUTHOR]

Background: Neurological disorders (NLDs) are widely acknowledged as a significant public health concern worldwide. Stroke, Alzheimer's disease (AD), and traumatic brain injury (TBI) are three of these disorders that have sparked major study attention. Neurological dysfunction, protein buildup, oxidation and neuronal injury, and aberrant mitochondria are all prevalent neuropathological hallmarks of these disorders. The signaling cascade of nuclear factor erythroid 2 related factor 2 (Nrf2) shares all of them as a common target. Several studies have found that overexpression of Nrf2 is a promising treatment method in NLDs. Effective treatment of these disorders continues to be a universal concern regardless of various medicines. In order to treat a variety of neurological problems, organic remedies may provide an alternative treatment. It has been demonstrated that polyphenols like quercetin (Que) offer considerable capabilities for treating NLDs. One of Que's greatest key targets, Nrf2, has the capacity to control the production of a number of cytoprotective enzymes that exhibit neuroprotective, detoxifying, and antioxidative effects. Additionally, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus. Objective: In this review, we have focused on Que's medicinal prospects as a neuroprotective drug. Methods: PubMed, Scopus, Science Direct, and Google Scholar were used to search articles for this study. Results: The findings of this research demonstrate that (1) Que protected the blood‐brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction. (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex. (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1‐4, antioxidant activity, and Nrf2 levels in the brain. Conclusion: We discuss recent research on Que‐mediated Nrf2 expression in the management of several NLDs in this paper. [ABSTRACT FROM AUTHOR]

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. This study aimed to investigate the potential protective effect of the lungs in sepsis by modulating inflammatory and oxidative stress markers. Twenty-four adult male Swiss-albino mice, aged 8-12 weeks and weighing 20-30 g, were divided into four equal groups (n=6): sham (laparotomy only), CLP (laparotomy plus cecal ligation and puncture), vehicle (DMSO administered one hour before CLP), and Ticagrelor (50 mg/kg IP administered one hour before CLP). Tissue levels of pro-inflammatory and oxidative stress markers in the lung were assessed using ELISA. F2 isoprostane levels were significantly higher in the sepsis group (p<0.05) compared to the sham group, while Ticagrelor significantly decreased the inflammatory and oxidative stress markers compared to the sepsis group. All mice in the sepsis group had considerable (p=0.05) lung tissue damage, but Ticagrelor considerably decreased lung tissue injury (p=0.05). Furthermore, Ticagrelor was found to reduce tissue cytokine levels of the lung (IL-1, TNF a, IL-6, F2 isoprostane, GPR 17, MIF) in male mice during CLP-induced polymicrobial sepsis by modulation of pro-inflammatory and oxidative stress cascade signaling pathways. [ABSTRACT FROM AUTHOR]

Renal ischemia reperfusion injury promotes tissue damage through inducing uncontrolled inflammation, oxidative stress and excessive renal tubular epithelial cell death. Renal ischemia reperfusion injury is one of the main causes of acute kidney injury, it occurs in various clinical situations such as partial nephrectomy, renal transplantation, cardiopulmonary resuscitation, sepsis and shock. Nuclear factor Erythroid 2-related factor 2 pathways are essential in protecting the kidney against renal ischemia reperfusion injury. U-50488H is a highly selective Kappa-opioid receptor agonist. It has anti-inflammatory effect. The present study aims to study the nephro-protective potential effect of U-50488H in renal ischemia reperfusion injury in rats' model via modulation of Nrf2 pathway. At the end of the experiment, in Control group, as compared with Sham group, the renal tissue levels of Nrf2, HO-1, P-Akt, NF-kB, IL-1β, F2-isoprostane, NGAL and levels of blood Urea and serum Creatinine were significantly (p<0.05) increased, in addition, Control group causes a significant histopathological tissue damage (p<0.05). Pretreatment with U-50488H exert protective role in the kidney against injury by a significant (p<0.05) more increase in the tissue level of Nrf2, HO-1, P-Akt and decrease in the tissue levels of IL-1β, NF-kB, F2-isoprostane, NGAL and levels of blood Urea and serum Creatinine. Furthermore, U-50488H a significantly (p<0.05) reverse the severity score of renal tissue damage. From the overall results, we conclude that U-50488H a significantly decrease renal ischemia reperfusion injury in adult male rats model through Nrf2 pathway via it is pleiotropic effects as anti-oxidant, anti-inflammatory and anti-apoptotic. [ABSTRACT FROM AUTHOR]

TLR-4 receptor plays an important role in the pathogenesis of many inflammatory diseases like diabetes mellitus. The present study was designed to examine TLR-4 gene expression in Type 2 diabetes. Gene expression of TLR-4 the mean± SD of ΔCt (normalization Ct values) of each study group: The mean ±SD Ct value of TLR-4 cDNA amplification was (22.28± 0.36) Normo Albuminuria group, Microalbuminuria group was 20.28± 0.41). The Ct values of Macro Albuminuria group 21.51± 0.31). There was a significant difference in the mean Ct values between different groups, (p=0.0001). The mean Ct values of control (Normo Albuminuria) group were higher than the Macro and this in turn was higher than that of Micro groups the mean± SD of ΔCt (normalization Ct values) of each study group, for the Micro Albuminuria (3.04±2.5). For Macro Albuminuria group the mA significant difference was noticed between the study groups (p=0.001). Results of 2-ΔCt revealed significantly higher results for the Micro Albuminuria group from the other two groups (p=0.0001). 2-ΔCt for micro Albuminuria group (0.121). In the Macro Albuminuria group and Normo Albuminuria group a 2-ΔCt were (0.051), (0.029) respectively. There is a significantly increased expression of TLR-4 gene in macro and Micro Albuminuria groups as compared to Normoalbuminuria group. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) with all advances in nursing measures and therapeutic strategies, such as kidney transplantation and dialysis, mortality rate of patients with AKI is very high in past 30 years. Despite the pathophysiology of IRI is not totally understood, several critical mechanisms cause reversal of kidney damage have been demonstrated. In ischemic kidney and successive of generation of reactive oxygen species (ROS), reoxygenation at reperfusion phase activate a cascade of destroying cellular responses causing to cell death, inflammation, and acute kidney failure. Valsartan is an Angotensin2 receptor blocker which is used as antihypertensive drug. It demonstrates organ protective effects in hypertension, attenuated renal injury possibly through its anti-inflammatory and antioxidant effects and it offer kidney protection as evidence by significant reduction in kidney injury score. Objective: To study the potential Nephroprotective effect of Valsartan in RIRI Materials & methods: After one week of acclimatization, the rat was randomly classified into four groups (6 rat in each) as follows: 1-IRI (control) group: rats subjected to the renal ischemia for 30 min by clamping renal artery and reperfusion for 2 hour. 2-sham group: rats underwent the same anesthetic and surgical procedure except clamping of bilateral renal artery. 3-control vehicle group: rats received 10 % dimethyl sulfoxide by I.P route and underwent renal ischemia for 30 min by clamping of renal artery and then 2hour reperfusion. 4-Valsartan treated group: rats pretreated with Valsartan 10 mg/kg I.P, 30 min before clamping of renal artery and then underwent renal ischemia for 30 min and then reperfusion for 2 hour. At the end of reperfusion time renal tissue and blood samples were collected. Blood samples used for measurement of IL1β, NF-KB p65, TLR4, NGAL and urea and creatinine for measurement of renal function. Renal tissue used for determination of histopathological changes. Results: Renal IRI causes significant (p=0.05) increase in tissue level of IL-1β, NGAL, TLR-4 and NF-KB p65 and serum urea, creatinine, pretreatment with Valsartan cause significant (p =0.05) decrease in tissue level of IL-1β, NF-KB p65, TLR-4, NGAL and serum urea, creatinine, also cause significant reversal of tissue damage when compared with IRI group. Conclusion: Pretreatment with Valsartan significantly decreases renal ischemia reperfusion injury in the rat via their pleiotropic effects as anti-oxidant, anti-inflammatory and anti-apoptotic activity. [ABSTRACT FROM AUTHOR]

Cancer is a multifaceted and complex disorder characterized by uncontrolled rates of cell proliferation and its ability to spread and attack other organs. Emerging data indicated several pathways and molecular targets are engaged in cancer progression. Among them, the Wnt signaling pathway was shown to have a crucial role in cancer onset and progression. Dishevelled (DVL) acts in a branch point of canonical and non-canonical Wnt pathway. DVL not only acts in the cytoplasm to inactivate the destruction complex of β-catenin but is also transported into the nucleus to affect the transcription of target genes. Available data revealed that the expression levels of DVL increased in cell and clinical specimens of various cancers, proposing that it may have an oncogenic role. DVL promoted cell invasion, migration, cell cycle, survival, proliferation, 3D-spheroid formation, stemness, and epithelial mesenchymal transition (EMT) and it suppressed cell apoptosis. The higher levels of DVL is associated with the clinicopathological characteristic of cancer-affected patients, including lymph node metastasis, tumor grade, histological type, and age. In addition, the higher levels of DVL could be a promising diagnostic and prognostic biomarker in cancer as well as it could be a mediator in cancer chemoresistance to Methotrexate, paclitaxel, and 5-fluorouracil. This study aimed to investigate the underlying molecular mechanism of DVL in cancer pathogenesis as well as to explore its importance in cancer diagnosis and prognosis as well as its role as a mediator in cancer chemotherapy., Competing Interests: Declaration of Competing Interest The authors declare they have no conflict of interest., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Cancer is a complex genetic anomaly involving coding and non-coding transcript structural and expressive irregularities. A class of tiny non-coding RNAs known as microRNAs (miRNAs) regulates gene expression at the post-transcriptional level by binding only to messenger RNAs (mRNAs). Due to their capacity to target numerous genes, miRNAs have the potential to play a significant role in the development of tumors by controlling several biological processes, including angiogenesis, drug resistance, metastasis, apoptosis, proliferation, and drug resistance. According to several recent studies, miRNA-214 has been linked to the emergence and spread of tumors. The human genome's q24.3 arm contains the DNM3 gene, which is about 6 kb away and includes the microRNA-214. Its primary purpose was the induction of apoptosis in cancerous cells. The multifaceted and complex functions of miR-214 as a modulator in neoplastic conditions have been outlined in the current review., Competing Interests: Declaration of Competing Interest The authors declare they have no conflict of interests., (Copyright © 2023. Published by Elsevier GmbH.)

Cardiovascular disorders are among the critical side effects of cancer therapy. Damage to the function and normal structure of the heart can cause serious threats to patients that are being treated for cancer. Cardiovascular complications may be induced by various types of chemotherapy drugs and also radiation therapy. The severity of cardiovascular toxicity depends on several factors, such as types of drugs, tumor location for radiotherapy, the presence of cardiac disease history, the dose of drugs or ionizing radiation, etc. Radiotherapy and chemotherapy can cause heart diseases through various mechanisms, such as oxidative stress, inflammation, cell death, fibrosis, endothelial to mesenchymal transition (EndMT), etc. Chronic inflammation following damage to a huge number of cells can trigger more accumulation of inflammatory cells and chronic release of reactive oxygen species (ROS) and nitric oxide (NO). Oxidative stress can induce more cell death and cardiac remodeling through damage to vessels and valvular and disruption of the normal structure of the extracellular matrix. These changes may lead to cardiomyopathy, myocarditis, pericarditis, and vascular disorders that may lead to heart attack and death. This review provides basic information on cellular and molecular mechanisms of different types of cardiovascular disorders following cancer therapy by radiation or chemotherapy. We also recommend some adjuvants and targets to reduce the risk of heart toxicity by radiation/chemotherapy., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

In the current body of research, a very quick and effectual procedure for the synthesis of pyrido[2,3- d :6,5- d ']dipyrimidines has been developed. This method is accomplished through the one-pot multi-component reaction of 2-thiobarbituric acid, NH 4 OAc and aldehydes utilizing Ni-TMEDA@βSiO 2 @αSiO 2 @Fe 3 O 4 as a novel mesoporous nanomagnetic catalyst at room temperature. This protocol is one of the few reports of the preparation of these derivatives without the use of conventional heating as well as energies such as microwave and ultrasound radiation. The characterization of the prepared catalyst was well accomplished by different techniques such as FT-IR, ICP-OES, SEM, TEM, BET, XRD, VSM, TGA, EDX and Elemental mapping. This organometallic catalyst was reusable for seven times with negligible decrement in its catalytic performance. In addition, all of the products were produced with high TON and TOF values, which demonstrates that our catalyst has a very high level of activity in the preparation of pyrido[2,3- d :6,5- d ']dipyrimidines., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Signal transducers and activators of transcription 3 (STAT 3) have been proposed to be responsible for breast cancer development. Moreover, evidence depicted that upregulation of STAT3 is responsible for angiogenesis, metastasis, and chemo-resistance of breast cancer. Tamoxifen (TAM) resistance is a major concern in breast cancer management which is mediated by numerous signaling pathways such as STAT3. Therefore, STAT3 targeting inhibitors would be beneficial in breast cancer treatment. The information on the topic in this review was gathered from scientific databases such as PubMed, Scopus, Google Scholar, and ScienceDirect. The present review highlights STAT3 signaling axis discoveries and TAM targeting STAT3 in breast cancer. Based on the results of this study, we found that following prolonged TAM treatment, STAT3 showed overexpression and resulted in drug resistance. Moreover, it was concluded that STAT3 plays an important role in breast cancer stem cells, which correlated with TAM resistance., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)