The biggest challenge in the present-day healthcare scenario is the rapid emergence and spread of antimicrobial resistance due to the rampant use of antibiotics in daily therapeutics. Such drug resistance is associated with the enhancement of microbial virulence and the acquisition of the ability to evade the host’s immune response under the shelter of a biofilm. Quorum sensing (QS) is the mechanism by which the microbial colonies in a biofilm modulate and intercept communication without direct interaction. Hence, the eradication of biofilms through hindering this communication will lead to the successful management of drug resistance and may be a novel target for antimicrobial chemotherapy. Chitosan shows microbicidal activities by acting electrostatically with its positively charged amino groups, which interact with anionic moieties on microbial species, causing enhanced membrane permeability and eventual cell death. Therefore, nanoparticles (NPs) prepared with chitosan possess a positive surface charge and mucoadhesive properties that can adhere to microbial mucus membranes and release their drug load in a constant release manner. As the success in therapeutics depends on the targeted delivery of drugs, chitosan nanomaterial, which displays low toxicity, can be safely used for eradicating a biofilm through attenuating the quorum sensing (QS). Since the anti-biofilm potential of chitosan and its nano-derivatives are reported for various microorganisms, these can be used as attractive tools for combating chronic infections and for the preparation of functionalized nanomaterials for different medical devices, such as orthodontic appliances. This mini-review focuses on the mechanism of the downregulation of quorum sensing using functionalized chitosan nanomaterials and the future prospects of its applications.

Background: The introduction of Monoclonal Antibodies (mAbs) and small-molecule Tyrosine Kinase Inhibitors (TKIs) that target the Epidermal Growth Factor Receptor (EGFR), marks a huge step forward in the Pancreatic Cancer (PC) therapy. However, anti-EGFR therapy is found to be successful only in a fraction of patients. Although anti-EGFR agents have shown considerable clinical promise, a serious adverse event associated with anti- EGFR therapy has been challenging. At this juncture, there is still more to be done in the search for effective predictive markers with therapeutic applicability. Methods: A focused literature search was conducted to summarize the existing evidence on anti-EGFR agents in pancreatic cancer therapy. Results: This review discusses various anti-EGFR agents currently in use for PC therapy and potential adverse effects associated with it. Existing evidence on EGFR TKIs demonstrated better tolerant effects and outcomes with multiple toxic regimens. Anti-EGFR therapy in combination with chemotherapy is necessary to achieve the best clinical outcomes. Conclusion: Future prospective studies on the identification of additional biological agents and novel anti-EGFR agents are warranted.

Exosomes being non-ionized micro-vesicles with a size range of 30–100 nm possess the ability to bring about intracellular communication and intercellular transport of various types of cellular components like miRNA, mRNA, DNA, and proteins. This is achieved through the targeted transmission of various inclusions to nearby or distant tissues. This is associated with the effective communication of information to bring about changes in physiological properties and functional attributes. The extracellular vesicles (EVs), produced by fungi, parasites, and bacteria, are responsible to bring about modulation/alteration of the immune responses exerted by the host body. The lipids, nucleic acids, proteins, and glycans of EVs derived from the pathogens act as the ligands of different families of pattern recognition receptors of the host body. The bacterial membrane vesicles (BMVs) are responsible for the transfer of small RNA species, along with other types of noncoding RNA thereby playing a key role in the regulation of the host immune system. Apart from immunomodulation, the BMVs are also responsible for bacterial colonization in the host tissue, biofilm formation, and survival therein showing antibiotic resistance, leading to pathogenesis and virulence. This mini-review would focus on the role of exosomes in the development of biofilm and consequent immunological responses within the host body along with an analysis of the mechanism associated with the development of resistance.

Introduction: Diabetic nephropathy (DN) is a progressive renal disease characterized by persistent albuminuria that leads to end-stage renal disease in both type 1 diabetes (T1DM) and type 2 diabetes (T2DM) patients. The renin-angiotensin-aldosterone system (RAAS) plays a major role in the onset and progression of DN. Objectives: The present meta-analysis is intended to synthesize evidence on the association between ACE gene insertion and deletion (ACE I/D) polymorphism and the risk of DN. Methods: PubMed, Scopus, Google Scholar and Embase were searched to retrieve relevant publications. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to evaluate the association between ACE I/D polymorphism and DN risk. The Cochrane Q test and I2 statistic were used to detect heterogeneity. To assess between-study heterogeneity, subgroup analysis and sensitivity analysis were performed. Funnel plots and Egger’s test were used to estimate publication bias. Results: Around 45 articles (47 studies) with 6124 patients of DN and 2492 T2DM patients (controls) were ultimately considered for meta-analysis. Overall, the ACE I/D polymorphism was associated with DN under three different genetic models (allelic model: OR = 1.34; 95% CI: 1.20- 1.49; P<0.001; dominant model: OR= 1.54; 95% CI: 1.31- 1.81; P<0.001; and recessive model: OR= 1.39; 95% CI: 1.19- 1.63; P<0.001). Significant heterogeneity (I2 > 50%) was present in the analysis for all ethnic groups. Further, there is no evidence for publication bias in this meta-analysis. Conclusion: The current meta-analysis provided confirmation that the ACE I/D polymorphism is correlated with an increased risk of DN in patients with T2DM and the D allele of ACE I/D was a susceptible factor.

Introduction: Sickle cell anemia (SCA) exhibits a host of complications that contribute to increased morbidity and mortality at the youngest ages. Objectives: The aim of this investigation is to look into the association between ACE I/D polymorphism and renal function in Indian patients with SCA. Patients and Methods: About 190 SCA patients confirmed by hemoglobin (Hb) electrophoresis were selected for this study. The severity of the disease was determined using anemia, clinical complications, total white blood cells count, and scores of blood transfusion. To define different renal function phases, estimated glomerular filtration rate (eGFR) was computed in adults and children using the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) and Schwartz equations respectively. The ACE I/D polymorphism was conducted using polymerase chain reaction (PCR) and separation through agarose electrophoresis. Results: The risk of impaired renal function was not statistically distinct between ACE I/D genotypes and alleles. Further, the genotypes of ACE I/D and the risk of disease severity was not found to be associated with each other. Conclusion: This investigation found that ACE I/D is an insignificant genetic modifier of renal function or severity of disease in patients with SCA.