Many common respiratory illnesses like bronchitis, asthma, and chronic obstructive pulmonary disease (COPD) lead to bronchial inflammation and, subsequently, a blockage. However, there are many difficulties in measuring the severity of the blockage. A numeric metric to determine the degree of the blockage severity is necessary. To tackle this demand, we aimed to develop a novel human respiratory model and design a deep-learning program that can constantly monitor and report bronchial blockage by recording breath sounds in a non-intrusive way.
In this study, the effects of vitamin C, ginger, or curcumin supplements on C-reactive protein levels in healthy participants are determined in an eight-week open-label trial.
Anticholinergics are used in treating asthma, a chronic inflammation of the airways. These drugs block human M1 and M2 muscarinic acetylcholine receptors, inhibiting bronchoconstriction. However, studies have reported complications of anticholinergic usage, such as exacerbated eosinophil production and worsened urinary retention. Modification of known anticholinergics using bioisosteric replacements to increase efficacy could potentially minimize these complications. The present study focuses on identifying viable analogs of anticholinergics to improve binding energy to the receptors compared to current treatment options. Glycopyrrolate (G), ipratropium (IB), and tiotropium bromide (TB) were chosen as parent drugs of interest, due to the presence of common functional groups within the molecules, specifically esters and alcohols. Docking score analysis via AutoDock Vina was used to evaluate the binding energy between drug analogs and the muscarinic acetylcholine receptors. The final results suggest that G-A3, IB-A3, and TB-A1 are the most viable analogs, as binding energy was improved when compared to the parent drug. G-A4, IB-A4, IB-A5, TB-A3, and TB-A4 are also potential candidates, although there were slight regressions in binding energy to both muscarinic receptors for these analogs. By researching the effects of bioisosteric replacements of current anticholinergics, it is evident that there is a potential to provide asthmatics with more effective treatment options.
Neuroinflammation and oxidative stress are both known to play a role in the occurrence and severity of seizures. This study tested effects of oxidative stress from seizures by evaluating the longevity, egg-laying, and electroshock resilience of C. elegans. Results revealed that oxidative stress and neuroinflammation diminish longevity and reproductivity while also increasing recovery time after seizures in C. elegans. This research can help lead to future studies and may also lead to finding new therapeutics for epilepsy.
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.
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.
Nonalcoholic fatty liver disease (NAFLD) is one of the most prevalent chronic liver diseases worldwide, but there are few studied warning signs for early detection of the disease. Here, researchers study alterations that occur in a mouse model of NAFLD, which indicate the onset of NAFLD sooner. Earlier detection of diseases can lead to better prevention and treatment.
The authors found that treatment with AS20 suppressed phorbol 12-myristate 13-acetate (PMA) and 5-flurouracil (5-FU) induction of COX2 expression. We also observed AS20 treated cells showed DNA fragmentation in HeLa cells.
Cellular senescence plays a key role in aging cells and is attributed to a number of disease and pathology. These authors find that genetic editing of both RPS6KB1 and PPARGC1A revitalizes a human skin fibroblast cell line.
