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Background: Acinetobacter baumannii is an opportunistic multidrugresistant, aerobic, glucose non-fermentative, and oxidative-negative coccobacilli bacteria. This life-threatening nosocomial infection is associated with immunocompromised patients. Objective: This review aims to investigate the multiple drug resistance mechanisms and new emerging diagnostics & treatments for Acinetobacter baumannii. Methods: All the articles that were most relevant to A. baumannii virulence and drug resistance mechanisms were founded by a literature search on PubMed. Google Patents were used to find discoveries related to diagnostics and treatment. Results: Efflux pumps, β-lactamases, aminoglycosides, outer membrane proteins, and alteration of the target sites were identified in the Acinetobacter baumannii pathogen as the most prevalent drug resistance mechanisms. Gene detection, peptide detection, and antigen-antibody-associated detection were the latest diagnostics. Novel antimicrobial peptides, sterilization techniques using blue light, and combination therapies are being developed to effectively treat A. baumannii infections. Conclusion: This review concludes that new drugs and formulations with high efficiency, low cytotoxicity, and no nephrotoxicity are in absolute need. In the near future, we can expect omics technology to play a significant role in discovering new drugs and potential targets.

Background: One of the major disturbing pathways within cancer is “The Kirsten rat sarcoma viral oncogene homolog (KRAS) pathway”, and it has recently been demonstrated to be the most crucial in therapies and diagnostics. KRAS pathway includes numerous genes. This multi-component signaling system promotes cell growth, division, survival, and death by transferring signals from outside the cell to its interior. KRAS regulates the activation of a variety of signaling molecules. The KRAS oncogene is a key player in advancing a wide range of malignancies, and the mutation rank of this gene is a key feature of several tumors. For some malignancies, the mutation type of the gene may offer information about prognostic, clinical, and predictive. KRAS belongs to the RAS oncogene family, which consists of a compilation of minor GTP-binding proteins that assimilate environmental inputs and trigger internal signaling pathways that control survival, cell differentiation, and proliferation. Objective: This review aims to examine the recent and fascinating breakthroughs in the identification of new therapies that target KRAS, including the ever-expanding experimental approaches for reducing KRAS activity and signaling as well as direct targeting of KRAS. Methods: A literature survey was performed. All the relevant articles and patents related to the KRAS pathway, the mutation in the KRAS gene, cancer treatment, and diagnostics were found on PubMed and Google Patents. Results: One of the most prevalent causes of cancer in humans is a mutation in the K-RAS protein. It is extremely difficult to decipher KRAS-mediated signaling. It allows transducing signals to go from the cell's outer surface to its nucleus, having an influence on a variety of crucial cellular functions including cell chemotaxis, division, dissemination, and cell death. Other involved signaling pathways are RAF, and the phosphatidylinositol 3 kinase also known as AKT. The EGFR pathway is incomplete without KRAS. The activation of PI3K significantly contributes to acquiring resistance to a mixture of MEK inhibitors and anti-EGFR in colorectal cancer cell lines which are mutated by KRAS. Conclusion: A series of recent patent studies towards cancer diagnostics and therapeutics reveals the paramount importance of mutated protein KRAS as an extensive driver in human tumors. For the prognosis, diagnosis, and treatment of colorectal cancer, KRAS plays a critical role. This review concludes the latest and vowing developments in the discovery of novel techniques for diagnosis and drugs that target KRAS, the advancements in experimental techniques for signaling and inhibiting KRAS function, and the direct targeting of KRAS for cancer therapeutics.

Abstract: Within a decade the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9 system), an advanced gene-editing technology became one of the celebrated approaches in modern disease therapeutics and was reported to have a potential role in the alteration of non-coding RNAs segment which are the pivotal causes behind the several mental disorder such as Schizophrenia. In general, Schizophrenia is referred as a neurodevelopmental disorder and symptomatically exhibited by social deficit, cognitive dysfunction, apathy, delusions, hallucinations, etc. At a genomics level large number of loci are susceptible for genetic alteration in schizophrenia and are mostly located in the genome’s non-coding region. With the growing variants and mutations in ncRNA genes (miRNA and lncRNA) strongly associated with schizophrenia, the need to develop a genetic tool to help with the treatment and study of schizophrenia increases. Recently the use of CRISPR/cas9 technology in the productive alteration of non-coding RNAs genes such as miRNA; miR-291, miR-141, and miR-21, lncRNA, lncRNA-21A, AK023948, and LncRNA Rian has been reported. The Cas9 protein and guide RNA (gRNA) together form the CRISPR/Cas9 system is known to be highly specific and efficient for manipulating the impact of gene mutations linked to genomic DNA like ncRNA besides other inheritable genetic diseases. Copy number variations are also found to be linked with schizophrenia. The generation of reciprocal CNVs of 15q13.3 and 16p11.2 in human-induced pluripotent stem cells (iPSCs) with the CRISPR/Cas 9 system has opened new possibilities. Still, there are some limitations and challenges yet to be defeated, like the blood-brain barrier poses an obstacle to treating mental disorders and ethical issues like genomic DNA manipulation of eggs and embryos. This review brings schizophrenia-associated ncRNAs and CRISPR gene-editing technology for the non-coding parts of the genomic DNA together and recent challenges.

Approximately 6.8 million people die annually because of problems related to the central nervous system (CNS), and out of them, approximately 1 million people are affected by neurodegenerative diseases that include Alzheimer’s disease, multiple sclerosis, epilepsy, and Parkinson’s disease. CNS problems are a primary concern because of the complexity of the brain. There are various drugs available to treat CNS disorders and overcome problems with toxicity, specificity, and delivery. Barriers like the blood–brain barrier (BBB) are a challenge, as they do not allow therapeutic drugs to cross and reach their target. Researchers have been searching for ways to allow drugs to pass through the BBB and reach the target sites. These problems highlight the need of nanotechnology to alter or manipulate various processes at the cellular level to achieve the desired attributes. Due to their nanosize, nanoparticles are able to pass through the BBB and are an effective alternative to drug administration and other approaches. Nanotechnology has the potential to improve treatment and diagnostic techniques for CNS disorders and facilitate effective drug transfer. With the aid of nanoengineering, drugs could be modified to perform functions like transference across the BBB, altering signaling pathways, targeting specific cells, effective gene transfer, and promoting regeneration and preservation of nerve cells. The involvement of a nanocarrier framework inside the delivery of several neurotherapeutic agents used in the treatment of neurological diseases is reviewed in this study.