Type 1 Diabetes (T1D) is an autoimmune disease that results from the destruction of insulin-producing beta cells in the Islets of Langerhans of the pancreas. This destruction is caused by T cells and leads to insulin deficiency (Chen et al.). Insulin regulates blood glucose levels by facilitating the uptake of blood sugar into cells, which the cells can then use for energy. Without insulin, sugar builds up in the bloodstream, leading to hyperglycemia (CDC). Two HLA genes involved in antigen presentation, DR3 and DR4-DQ8, as well as around 60 non-HLA genes, are associated with the development of T1D (DiMeglio et al.); HLA genes code for surface proteins that are used to identify body cells and foreign cells (Nordquist and Radia). Also, viral infections, including enterovirus infections, might be linked to the development of T1D (DiMeglio et al.).

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Spider silks demonstrate extraordinary mechanical performance. They rely on an intricate hierarchical structure that gives rise to unique properties. Of the many types of spider silks that are produced, dragline spider silk has attracted the most research attention due its extremely high strength. Since data on dragline spider silk is readily available, much can be understood about the nature of spider silk by analyzing the structure of dragline spider silk. Moreover, the study of spider silk can inspire the design of new materials. Here, we review the structure of dragline silk, present a particular material model to explain their behavior, and discuss the potential outlook in the area.

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The liver is no doubt one of the most vital organs of the human body. With ranged roles in digestion, energy, and protein synthesis, liver cells house a network of metabolic pathways that are crucial for survival. From the citric acid cycle, urea cycle, glycogenolysis, gluconeogenesis, lipogenesis, and ketone body synthesis, reaching out to GABA and myelin formation in the brain, we see a chemical interconnectedness which makes the liver the most metabolically active organ in the body. However, that same nature of metabolism – the reliance of one pathway to another – is perhaps what also makes our body so vulnerable to the smallest anomaly in the system. One such case revolves around an enzyme named pyruvate carboxylase.

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Viruses existed long before humans, and we have coevolved alongside them for thousands of years. While at first they represented a serious threat to the survival of our species, in the modern age we are now able to use them as tools. To exemplify this, we discuss existing uses of viruses in medicine, such as in live vaccines or the production of CAR-T cells for cancer therapies. Finally, we present an innovation surrounding the use of modified HIV to target CD4+ T cell related cancers. In the future, technological developments will allow scientists to modify additional strains of viruses in a safe and effective way. Rather than existing as disease-causing detriments, they can be used to serve a beneficial purpose to humanity.

KDM5B, a histone lysine demethylase “eraser” protein, is a transcriptional repressor of active promoter regions on histone three lysine K4. KDM5B is crucial to regulating gene expression and development. Previously, all mutations in KDM5B were described in cancer. High-performance sequencing revealed missense, frameshift, and nonsense mutations in KDM5B that can be linked to developmental disorders like autism spectrum disorder (ASD). This review summarizes KDM5B’s role in ASD and other developmental disorders.

There are many genes that have been identified to cause Autism Spectrum Disorder (ASD for short), as well as all the other disorders related to it One such gene is the chromatin remodeler CHD8 and methyltransferase KMT2A, the former of which is known to cause intellectual disability (ID) and the latter to cause Wiedemann-Steiner syndrome. Is there any mechanistical link between the two genes, and does this mean that CHD8 also causes Wiedemann-Steiner syndrome? It appears that there is, and that it also points at a larger pattern for other similarly linked genes, and could help with identifying other genes that cause known disorders - for instance, perhaps useful in finding new genes that may also cause ASD.

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