Magnetic nanocomposite based on chitosan-gelatin hydrogel embedded with copper oxide nanoparticles: A novel and promising catalyst for the synthesis of polyhydroquinoline derivatives.

Nanocatalysts are vital in several domains, such as chemical processes, energy generation, energy preservation, and environmental pollution mitigation. An experimental study was conducted at room temperature to evaluate the catalytic activity of the new gelatin-chitosan hydrogel/CuO/Fe3O4 nanocomposite in the asymmetric Hantzsch reaction. All components of the nanocomposite exhibit a synergistic effect as a Lewis acid, promote the reaction. Dimedone, ammonium acetate, ethyl acetoacetate, and other substituted aldehydes were used to synthesize diverse polyhydroquinoline derivatives. The nanocomposite exhibited exceptional efficacy (over 90 %) and durability (retaining 80 % of its original capacity after 5 cycles) as a catalyst in the one-pot asymmetric synthesis of polyhydroquinoline derivatives. Also, turnover numbers (TON) and turnover frequency (TOF) have been checked for catalyst (TON and TOF = 50,261 and 100,524 h-1) and products. The experiment demonstrated several benefits, such as exceptional product efficacy, rapid reaction time, functioning at ambient temperature without specific requirements, and effortless separation by the use of an external magnet after the reaction is finished. The results suggest the development of a magnetic nanocatalyst with exceptional performance. The composition of the Ge-CS hydrogel/CuO/Fe3O4 nanocomposite was thoroughly analyzed using several methods including FT-IR, XRD, FE-SEM, EDX, VSM, BET, and TGA. These analyses yielded useful information into the composition and characteristics of the nanocomposite, hence further enhancing the knowledge of its possible uses.

Discovering the strength of immunometabolism in cancer therapy: Employing metabolic pathways to enhance immune responses.

Immunometabolism, which studies cellular metabolism and immune cell function, is a possible cancer treatment. Metabolic pathways regulate immune cell activation, differentiation, and effector functions, crucial to tumor identification and elimination. Immune evasion and tumor growth can result from tumor microenvironment metabolic dysregulation. These metabolic pathways can boost antitumor immunity. This overview discusses immune cell metabolism, including glycolysis, oxidative phosphorylation, amino acid, and lipid metabolism. Amino acid and lipid metabolic manipulations may improve immune cell activity and antitumor immunity. Combination therapy using immunometabolism-based strategies may enhance therapeutic efficacy. The complexity of the metabolic network, biomarker development, challenges, and future approaches are all covered, along with a summary of case studies demonstrating the effectiveness of immunometabolism-based therapy. Metabolomics, stable isotope tracing, single-cell analysis, and computational modeling are also reviewed for immunometabolism research. Personalized and combination treatments are considered. This review adds to immunometabolism expertise and sheds light on metabolic treatments' ability to boost cancer treatment immunological response. Also, in this review, we discussed the immune response in cancer treatment and altering metabolic pathways to increase the immune response against malignancies.

COX 2-inhibitors; a thorough and updated survey into combinational therapies in cancers.

Cyclooxygenase (COX) enzymes are pivotal in inflammation and cancer development. COX-2, in particular, has been implicated in tumor growth, angiogenesis, and immune evasion. Recently, COX-2 inhibitors have arisen as potential therapeutic agents in cancer treatment. In addition, combining COX inhibitors with other treatment modalities has demonstrated the potential to improve therapeutic efficacy. This review aims to investigate the effects of COX inhibition, both alone and in combination with other methods, on signaling pathways and carcinogenesis in various cancers. In this study, a literature search of all major academic databases was conducted (PubMed, Scholar google), including the leading research on the mechanisms of COX-2, COX-2 inhibitors, monotherapy with COX-2 inhibitors, and combining COX-2-inhibitors with chemotherapeutic agents in tumors. The study encompasses preclinical and clinical evidence, highlighting the positive findings and the potential implications for clinical practice. According to preclinical studies, multiple signaling pathways implicated in tumor cell proliferation, survival, invasion, and metastasis can be suppressed by inhibiting COX. In addition, combining COX inhibitors with chemotherapy drugs, targeted therapies, immunotherapies, and miRNA-based approaches has enhanced anti-tumor activity. These results suggest that combination therapy has the potential to overcome resistance mechanisms and improve treatment outcomes. However, caution must be exercised when selecting and administering combination regimens. Not all combinations of COX-2 inhibitors with other drugs result in synergistic effects; some may even have unfavorable interactions. Therefore, personalized approaches that consider the specific characteristics of the cancer and the medications involved are crucial for optimizing therapeutic strategies. In conclusion, as monotherapy or combined with other methods, COX inhibition bears promise in modulating signaling pathways and inhibiting carcinogenesis in various cancers. Additional studies and well-designed clinical trials are required to completely elucidate the efficacy of COX inhibition and combination therapy in enhancing cancer treatment outcomes. This narrative review study provides a detailed summary of COX-2 monotherapy and combination targeted therapy in cancer treatment.

WITHDRAWN: Application of Nanoparticles in the Management of Polycystic Ovary Syndrome

The article has been withdrawn at the request of the Corresponding author.Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php. BENTHAM SCIENCE DISCLAIMER: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

STAT3 signaling in pancreatic ductal adenocarcinoma: a candidate therapeutic target.

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a poor prognosis which is lethal in over 90% of cases despite the standard therapies. Mainly activated by Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3) is a key transcription factor, capable of exerting the expression of multitude of genes involved in survival. Moreover, STAT3 activity is regulated by the interleukin 28 receptor α (IL28RA) and glutathione s-transferase mu-3 (GSTM3), up-regulation of both contributes to the invasiveness of pancreatic cancer cells. In this regard, STAT3 overactivity has an important pathogenic role in the development of PDAC as it is associated with enhanced cell proliferation, survival, angiogenesis, and metastasis. STAT3-associated expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 3 and 9 are implicated in the angiogenic and metastatic behavior of the PDAC. Multitude of evidence underline the protective role of STAT3 inhibition against PDAC both in cell cultures and in tumor grafts. However, specific inhibition of STAT3 was not feasible until recently, when a selective potent chemical STAT3 inhibitor, termed N4, were developed and it turned out to be highly effective against PDAC in vitro, as well as in vivo. This review aims to discuss the most recent advances in our understanding of STAT3 role in the pathogenesis of PDAC and its therapeutic applications.

Harnessing function of EMT in hepatocellular carcinoma: From biological view to nanotechnological standpoint.

Management of cancer metastasis has been associated with remarkable reduction in progression of cancer cells and improving survival rate of patients. Since 90% of mortality are due to cancer metastasis, its suppression can improve ability in cancer fighting. The EMT has been an underlying cause in increasing cancer migration and it is followed by mesenchymal transformation of epithelial cells. HCC is the predominant kind of liver tumor threatening life of many people around the world with poor prognosis. Increasing patient prognosis can be obtained via inhibiting tumor metastasis. HCC metastasis modulation by EMT and HCC therapy by nanoparticles are discussed here. First of all, EMT happens during progression and advanced stages of HCC and therefore, its inhibition can reduce tumor malignancy. Moreover, anti-cancer compounds including all-trans retinoic acid and plumbaging, among others, have been considered as inhibitors of EMT. The EMT association with chemoresistance has been evaluated. Moreover, ZEB1/2, TGF-ß, Snail and Twist are EMT modulators in HCC and enhancing cancer invasion. Therefore, EMT mechanism and related molecular mechanisms in HCC are evaluated. The treatment of HCC has not been only emphasized on targeting molecular pathways with pharmacological compounds and since drugs have low bioavailability, their targeted delivery by nanoparticles promotes HCC elimination. Moreover, nanoparticle-mediated phototherapy impairs tumorigenesis in HCC by triggering cell death. Metastasis of HCC and even EMT mechanism can be suppressed by cargo-loaded nanoparticles.

The Role of Ferroptosis in the Pathogenesis of Osteoarthritis.

Osteoarthritis (OA) is the most common type of arthritis. Its high prevalence, especially in the elderly, and its negative impact on physical function make it a leading cause of disability in the elderly. Joint pain as well joint stiffness are the common classic signs of OA. Chondrocyte death together with loss of articular cartilage integrity are the main pathologic changes in OA. Non-steroidal anti-inflammatory drugs (NSAIDs) and glucocorticoids are commonly used for the management of OA; still, their effectiveness is limited, and no therapeutic strategy is able to fully stop OA progression. Ferroptosis is a kind of cell death, distinct from apoptosis and necroptosis, caused by iron-dependent peroxidation of membrane phospholipids that terminates cell life by disintegrating all plasma membranes. It has been suggested that ferroptosis has a critical role in decreased viability of chondrocytes in OA, and here, we review recent findings regarding the pathologic pathways that lead to chondrocyte ferroptosis, and discuss the possible therapeutic utility of ferroptosis inhibition in OA.

Implications of biomimetic nanocarriers in targeted drug delivery.

Nanomaterials and nanostructures have shown fascinating performances in various biomedicine fields, from cosmetic to cancer diagnosis and therapy. Engineered nanomaterials can encapsulate both lipophilic and hydrophilic substances/drugs to eliminate their limitations in the free forms, such as low bioavailability, multiple drug administration, off-target effects, and various side effects. Moreover, it is possible to deliver the loaded cargo to the desired site of action using engineered nanomaterials. One approach that has made nanocarriers more sophisticated is the "biomimetic" concept. In this scenario, biomolecules (e.g., natural proteins, peptides, phospholipids, cell membranes) are used as building blocks to construct nanocarriers and/or modify agents. For instance, it has been reported that specific cells tend to migrate to a particular site during specific circumstances (e.g., inflammation, tumor formation). Employing the cell membrane of these cells as a coating for nanocarriers confers practical targeting approaches. Accordingly, we introduce the biomimetic concept in the current study, review the recent studies, challenge the issues, and provide practical solutions.

The role of endoplasmic reticulum stress in endometriosis.

Endometriosis is a chronic gynecologic disorder characterized by abnormal growth of endometrium-like tissues in the ectopic regions of the pelvic peritoneum. The pathophysiology of endometriosis is not completely understood; however, excessive endometrial cell proliferation together with resistance to apoptosis facilitates the migration, implantation, and survival of endometrial cells in the distant sites. Endoplasmic reticulum (ER) stress response (also called unfolded protein response) is a cellular defense mechanism triggered by ER stress. When severe enough, the so-called response initiates cell suicide, i.e., apoptosis. Therefore, therapeutic induction of ER stress in endometriotic cells could promote apoptosis and contribute to the management of disease. In this review, we discuss the pathogenic role of ER stress in endometriosis and the most recent findings regarding the induction of ER stress in connection with endometriosis.

Adsorption of Thiotepa anticancer drugs on the BC3 nanotube as a promising nanocarriers for drug delivery.

By applying periodic DFT computations, the possible employment of BC3 nanotube (BC3NT) as a drug delivery system (DDS) for Thiotepa (TPA) anticancer medicine has been examined. Quantum mechanics computations by the B3LYP-6-31 +G(d,p) method with dispersion correction including to be used for calculation the details of electronic, geometric, and energetic features of the interactions between TPA drug and BC3NT. The appropriate orientation for the TPA interacting with BC3NT has been assessed and adsorption energies (ΔEad) have been computed. The band distance of S and B atom in complex C2 is about 1.89 Å, also the value of ΔEad of - 29.83 kcal/mol in most stable compounds. By applying frontier molecular orbital analysis, it has been assessed that during stimulation, TPA medicine performs as HOMO and delivers the charge towards the LUMO, i.e., BC3NT. In the aqueous phase, the λmax of BC3NT-AP complex is blue-shifted by 36 nm. Drug delivery to the specific cells after protonation has been studied, due to the point that cancer cells have lower pH than others. The value of computed solvation energy (ΔEsolvation) shows the solubility BC3NT@TPA system in the water phase. The effects of the present investigation verified the ability of BC3NT as a drug delivery agent for TPA in the treatment of cancer.

Non-coding RNAs, another side of immune regulation during triple-negative breast cancer.

Triple-negative breast cancer (TNBC) is considered about 12-24 % of all breast cancer cases. Patients experience poor overall survival, high recurrence rate, and distant metastasis compared to other breast cancer subtypes. Numerous studies have highlighted the crucial roles of non-coding RNAs (ncRNAs) in carcinogenesis and proliferation, migration, and metastasis of tumor cells in TNBC. Recent research has demonstrated that long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) play a role in the regulation of the immune system by affecting the tumor microenvironment, the epithelial-mesenchymal transition, the regulation of dendritic cells and myeloid-derived stem cells, and T and B cell activation and differentiation. Immune-related miRNAs and lncRNAs, which have been established as predictive markers for various cancers, are strongly linked to immune cell infiltration and could be a viable therapeutic target for TNBC. In the current review, we discuss the recent updates of ncRNAs, including miRNAs and lncRNAs in TNBC, including their biogenesis, target genes, and biological function of their targets, which are mostly involved in the immune response.

SRF/MRTF-A and liver cirrhosis: Pathologic associations.

Liver cirrhosis results from prolonged and extensive liver fibrosis in which fibrotic tissues replace functional hepatic cells. Chronic liver disease due to various viral, chemical, or metabolic factors initiates hepatic fibrogenesis. Cirrhosis is associated with multiple clinical complications and a poor patient prognosis; therefore, developing novel antifibrotic therapies to prevent cirrhosis is of high priority. Mounting evidence points to the key role of serum response factor (SRF) and myocardin-related transcription factor (MRTF)-A in the pathogenesis of liver fibrosis. SRF is a transcription factor and MRTF-A is a co-activator of SRF and normally resides in the cytoplasm. Upon the induction of fibrotic pathways, MRTF-A translocates into the nucleus and forms the active SRF/MRTF-A complex, leading to the expression of a multitude of fibrotic proteins and components of extracellular matrix. Silencing or inhibiting MRTF-A impedes hepatic stellate cell transdifferentiation into myofibroblasts and slows down the deposition of extracellular matrix in the liver, making it a potential therapeutic target. Here, we review the recent findings regarding the role of the SRF/MRTF-A complex in liver fibrosis and its therapeutic potential for the management of cirrhosis.