Psoriasis is a heritable autoimmune disorder characterized by abnormal red and itchy skin patches. The authors study the family of a man with psoriasis. They explore whether the man's children, who do not show any symptoms of psoriasis, demonstrate gene expression consistent with the disease.
Alzheimer's disease (AD) involves the reduction of cholinergic activity due to a decrease in neuronal levels of nAChR α7. In this work, Sanyal and Cuellar-Ortiz explore the role of the nAChR α7 in learning and memory retention, using Drosophila melanogaster as a model organism. The performance of mutant flies (PΔEY6) was analyzed in locomotive and olfactory-memory retention tests in comparison to wild type (WT) flies and an Alzheimer's disease model Arc-42 (Aβ-42). Their results suggest that the lack of the D. melanogaster-nAChR causes learning, memory, and locomotion impairments, similar to those observed in Alzheimer's models Arc-42.
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.
Pandemics involve the high transmission of a disease that impacts global and local health and economic patterns. Epidemiological models help propose pandemic control strategies based on non-pharmaceutical interventions such as social distancing, curfews, and lockdowns, reducing the economic impact of these restrictions. In this research, we utilized an epidemiological Susceptible, Exposed, Infected, Recovered, Deceased (SEIRD) model – a compartmental model for virtually simulating a pandemic day by day.
Bennett and Joykutty test whether growth hormone directly or indirectly affected the rate at which cartilage renewed itself. Growth hormone could exert a direct effect on cartilage or chondrocytes by modifying the expression of different genes, whereas an indirect effect would come from growth hormone stimulating insulin-like growth factor. The results from this research support the hypothesis that growth hormone increases proliferation rate using the direct pathway. This research can be used in the medical sciences for people who suffer from joint damage and other cartilage-related diseases, since the results demonstrated conditions that lead to increased proliferation of chondrocytes. These combined results could be applied in a clinical setting with the goal of allowing patient cartilage to renew itself at a faster pace, therefore keeping those patients out of pain from these chondrocyte-related diseases.
The emergence of antibiotic-resistant pathogenic bacteria is a major concern for human health, rendering some antibiotics ineffective in treating diseases. The authors of this study tested the hypothesis that exposing rumen bacteria to tetracycline will gradually lead to the development of tetracycline-resistant bacteria, some of which will develop multidrug resistance.
Human cytomegalovirus (HCMV) causes serious infections in immunocompromised patients and therapies to inhibit latent HCMV are not developed. Using CRISPR/Cas9, the authors were able to delete an important promoter region in HCMV.
Here, the authors investigated the role of nonpharmacological interventions in preventing or delaying cognitive impairment in individuals with and without dementia. By using a retrospective case-control study of 22 participants across two senior centers in San Diego, they found no significant differences in self-reported activities. However, they found that their results reflected activity rather than the activity itself, suggesting the need for an alternative type of study.
Levy & Levy tackle the optimization of the coronary artery bypass graft, a life-saving surgical technique that treats artery blockage due to coronary heart disease. The authors develop a novel auto-suturing method that saves time, allows for an increased number of sutures, and improves graft quality over hand suturing. The authors also show that increasing the number of sutures from four to five with their new method significantly improves graft quality. These promising findings may help improve outcomes for patients undergoing surgery to treat coronary heart disease.
Naturally occurring neuroactive alkaloids are often studied for their potential to treat Neurological diseases. This team of students study Rivastigmine, a potent cholinesterase inhibitor that is a synthetic analog of physostigmine, which comes from the Calabar bean plant Physostigma venenosum. By comparing the effects of optimized synthetic analogs to the naturally occurring alkaloid, they determine the most favorable analog for inhibition of acetylcholinesterase (AChE), the enzyme that breaks down the neurotransmitter acetylcholine (ACh) to terminate neuronal transmission and signaling between synapses.