Recent advances in metal nanoparticles to treat periodontitis.

The gradual deterioration of the supporting periodontal tissues caused by periodontitis, a chronic multifactorial inflammatory disease, is thought to be triggered by the colonization of dysbiotic plaque biofilms in a vulnerable host. One of the most prevalent dental conditions in the world, periodontitis is now the leading factor in adult tooth loss. When periodontitis does develop, it is treated by scraping the mineralized deposits and dental biofilm off the tooth surfaces. Numerous studies have shown that non-surgical treatment significantly improves clinical and microbiological indices in individuals with periodontitis. Although periodontal parameters have significantly improved, certain bacterial reservoirs often persist on root surfaces even after standard periodontal therapy. Periodontitis has been treated with local or systemic antibiotics as well as scaling and root planning. Since there aren't many brand-new antibiotics on the market, several researchers are currently concentrating on creating alternate methods of combating periodontal germs. There is a delay in a study on the subject of nanoparticle (NP) toxicity, which is especially concerned with mechanisms of action, while the area of nanomedicine develops. The most promising of them are metal NPs since they have potent antibacterial action. Metal NPs may be employed as efficient growth inhibitors in a variety of bacteria, making them useful for the treatment of periodontitis. In this way, the new metal NPs contributed significantly to the development of efficient anti-inflammatory and antibacterial platforms for the treatment of periodontitis. The current therapeutic effects of several metallic NPs on periodontitis are summarized in this study. This data might be used to develop NP-based therapeutic alternatives for the treatment of periodontal infections.

Molecular mechanisms of long non-coding RNAs in differentiation of T Helper17 cells.

T helper (Th) 17 cells are one of the most important T cell subsets in a number of autoimmune and chronic inflammatory diseases. During infections, Th17 cells appear to play an important role in the clearance of extracellular pathogens. Th17 cells, on the other hand, are engaged in inflammation and have been linked to the pathophysiology of a number of autoimmune illnesses and human inflammatory disorders. A diverse group of RNA molecules known as lncRNAs serve critical functions in gene expression regulation. They may interact with a wide range of molecules, including DNA, RNA, and proteins, and have a complex structure. LncRNAs, which have restricted or no protein-coding activity, are implicated in a number of illnesses due to their regulatory impact on a variety of biological processes such as cell proliferation, apoptosis, and differentiation. Several lncRNAs have been associated with Th7 cell development in the context of immune cell differentiation. In this article, we cover new studies on the involvement of lncRNAs in Th17 cell differentiation in a variety of disorders, including auto-immune diseases, malignancies, asthma, heart disease, and infections.

Translational research of new developments in targeted therapy of colorectal cancer.

A severe global health concern is the rising incidence and mortality rate of colorectal cancer (CRC). Chemotherapy, which is typically used to treat CRC, is known to have limited specificity and can have noticeable side effects. A paradigm shift in cancer treatment has been brought about by the development of targeted therapies, which has led to the appearance of pharmacological agents with improved efficacy and decreased toxicity. Epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), human epidermal growth factor receptor 2 (HER2), and BRAF are among the molecular targets covered in this review that are used in targeted therapy for CRC. The current discussion also covers advancements in targeted therapeutic approaches, such as antibody-drug conjugates, immune checkpoint inhibitors, and chimeric antigen receptor (CAR) T-cell therapy. A review of the clinical trials and application of these particular therapies in treating CRC is also done. Despite the improvements in targeted therapy for CRC, problems such as drug resistance and patient selection remain to be solved. Despite this, targeted therapies have offered fresh possibilities for identifying and treating CRC, paving the way for the development of personalized medicine and extending the life expectancy and general well-being of CRC patients.

Long non-coding RNAs: controversial roles in drug resistance of solid tumors mediated by autophagy.

Current genome-wide studies have indicated that a great number of long non-coding RNAs (lncRNAs) are transcribed from the human genome and appeared as crucial regulators in a variety of cellular processes. Many studies have displayed a significant function of lncRNAs in the regulation of autophagy. Autophagy is a macromolecular procedure in cells in which intracellular substrates and damaged organelles are broken down and recycled to relieve cell stress resulting from nutritional deprivation, irradiation, hypoxia, and cytotoxic agents. Autophagy can be a double-edged sword and play either a protective or a damaging role in cells depending on its activation status and other cellular situations, and its dysregulation is related to tumorigenesis in various solid tumors. Autophagy induced by various therapies has been shown as a unique mechanism of resistance to anti-cancer drugs. Growing evidence is showing the important role of lncRNAs in modulating drug resistance via the regulation of autophagy in a variety of cancers. The role of lncRNAs in drug resistance of cancers is controversial; they may promote or suppress drug resistance via either activation or inhibition of autophagy. Mechanisms by which lncRNAs regulate autophagy to affect drug resistance are different, mainly mediated by the negative regulation of micro RNAs. In this review, we summarize recent studies that investigated the role of lncRNAs/autophagy axis in drug resistance of different types of solid tumors.