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This article investigates differences in gene expression in the brains of patients with and without Parkinson's disease. The authors identify a crucial transcriptional regulator may be a relevant target for future therapeutic treatment for Parkinson's disease.

Treatments inhibiting Notch signaling pathways have been explored by researchers as a new approach for the treatment of glioblastoma tumors, which is a fast-growing and aggressive brain tumor. Recently, retinoic acid (RA) therapy, which inhibits Notch signaling, has shown a promising effect on inhibiting glioblastoma progression. RA, which is a metabolite of vitamin A, is very important in embryonic cellular development, which includes the regulation of multiple developmental processes, such as brain neurogenesis. However, high doses of RA treatment caused many side effects such as headaches, nausea, redness around the injection site, or allergic reactions. Therefore, we hypothesized that a combination treatment of RA and siRNA targeting NOTCH1 (siNOTCH1), the essential gene that activates Notch signaling, would effectively inhibit brain cancer cell proliferation. The aim of the study was to determine whether inhibiting NOTCH1 would inhibit the growth of brain cancer cells by cell viability assay. We found that the combination treatment of siNOTCH1 and RA in low concentration effectively decreased the NOTCH1 expression level compared to the individual treatments. However, the combination treatment condition significantly decreased the number of live brain cancer cells only at a low concentration of RA. We anticipate that this novel combination treatment can provide a solution to the side effects of chemotherapy.

Human intelligence is correlated with variation in the protein neuroplastin-65, which is encoded by the NPTN gene. The authors examine the evolution of this gene across different animal species.

Major Depressive Disorder (MDD), and Post-Traumatic Stress Disorder (PTSD) are two of the fastest growing comorbid diseases in the world. Using publicly available datasets from the National Institute for Biotechnology Information (NCBI), Ravi and Lee conducted a differential gene expression analysis using 184 blood samples from either control individuals or individuals with comorbid MDD and PTSD. As a result, the authors identified 253 highly differentially-expressed genes, with enrichment for proteins in the gene ontology group 'Ribosomal Pathway'. These genes may be used as blood-based biomarkers for susceptibility to MDD or PTSD, and to tailor treatments within a personalized medicine regime.

The goal of this project was to assess the relationships among low myopia, behavioral and demographic factors, and a single-nucleotide polymorphism (SNP) in the TGFβ1 gene.

In the United States, there are currently 17.8 million affected by atopic dermatitis (AD), commonly known as eczema. It is characterized by itching and skin inflammation. AD patients are at higher risk for infections, depression, cancer, and suicide. Genetics, environment, and stress are some of the causes of the disease. With the rise of personalized medicine and the acceptance of gene-editing technologies, AD-related variations need to be identified for treatment. Genome-wide association studies (GWAS) have associated the Filaggrin (FLG) gene with AD but have not identified specific problematic single nucleotide polymorphisms (SNPs). This research aimed to refine known SNPs of FLG for gene editing technologies to establish a causal link between specific SNPs and the diseases and to target the polymorphisms. The research utilized R and its Bioconductor packages to refine data from the National Center for Biotechnology Information's (NCBI's) Variation Viewer. The algorithm filtered the dataset by coding regions and conserved domains. The algorithm also removed synonymous variations and treated non-synonymous, frameshift, and nonsense separately. The non-synonymous variations were refined and ordered by the BLOSUM62 substitution matrix. Overall, the analysis removed 96.65% of data, which was redundant or not the focus of the research and ordered the remaining relevant data by impact. The code for the project can also be repurposed as a tool for other diseases. The research can help solve GWAS's imprecise identification challenge. This research is the first step in providing the refined databases required for gene-editing treatment.

Engineered bacteria that degrade oil are currently being considered as a safe option for the treatment of oil spills. For this approach to be successful, the bacteria must effectively express oil-degrading genes they uptake as part of an external genoming vehicle called a "plasmid". Using a computational approach, the authors investigate plasmid-bacterium compatibility to find pairs that ensure high levels of gene expression.

With disruption of DNA repair pathways pertinent to the timeline of cancer, thorough evaluation of mutations relevant to DNA repair proteins is crucial within cancer research. One such mutation includes S815L PMS2 - a mutation that results in significant decrease of DNA repair function by PMS2 protein. While mutation of PMS2 is associated with significantly increased colorectal and endometrial cancer risk, much work is left to do to establish the functional effects of the S815L PMS2 mutation in ovarian cancer progression. In this article, researchers contribute to this essential area of research by uncovering the tumor-progressive effects of the S815L PMS2 mutation in the context of ovarian cancer cell lines.

Numerous organisms, including the marine bacterium Aliivibrio fischeri, produce light. This bioluminescence is involved in many important symbioses and may one day be an important source of light for humans. In this study, the authors investigated ways to increase bioluminescence production from the model organism E. coli.

Major depressive disorder (MDD) is a prevalent mood disorder. The direct causes and biological mechanisms of depression still elude understanding, though genetic factors have been implicated. This study looked to identify the mechanism behind the aberrant response to the dexamethasone suppression test (DST) displayed by MDD patients, in which they display a lack of cortisol suppression. Analysis revealed several pro-inflammatory genes that were significant and differentially expressed between affected and non-affected groups in response to the DST. Looking at ways to decrease the inflammatory response could have implications for treatment and may explain why some people treated for depression still display symptoms or may lead researchers to different classes of drugs for treatment.