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Low expression of Frataxin might contribute to diabetic peripheral neuropathy in a mouse model.

Biochem Biophys Res Commun

December 2024

Yancheng Clinical College, Xuzhou Medical University, Yancheng, 224000, PR China. Electronic address:

Diabetes is one of the most prevalent metabolic disorders, and its incidence has been experiencing a steady annual rise in recent years. Diabetic peripheral neuropathy (DPN) represents the most frequent adverse complication, exerting a profound impact on the quality of life for those suffering from diabetes. The etiology of DPN is complex, including impaired mitochondrial function.

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Description: Gastric cancer (GC) is a leading cause of preventable cancer and mortality in certain US populations. The most impactful way to reduce GC mortality is via primary prevention, namely Helicobacter pylori eradication, and secondary prevention, namely endoscopic screening and surveillance of precancerous conditions, such as gastric intestinal metaplasia (GIM). An emerging body of evidence supports the possible impact of these strategies on GC incidence and mortality in identifiable high-risk populations in the United States.

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Preventive vaccination is a crucial strategy for controlling and preventing infectious diseases, offering both effectiveness and cost-efficiency. However, despite the widespread success of vaccination programs, there are still certain population groups who struggle to mount adequate responses to immunization. These at-risk groups include but are not restricted to the elderly, overweight individuals, individuals with chronic infections and cancer patients.

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The advent of chimeric antigen receptor (CAR) T-cells has revolutionized the treatment landscape for hematologic malignancies, and emerging evidence suggests their potential in autoimmune diseases (AIDs). This article examines the early successes and future implications of B-cell-targeting CAR T-cell therapy in AIDs. Initial applications, particularly in refractory systemic lupus erythematosus (SLE), have demonstrated significant and durable clinical remissions, with accompanying evaluation of the immune system suggesting a so-called "reset" of innate inflammation and adaptive autoimmunity.

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Models for viral populations with high replication error rates (such as RNA viruses) rely on the quasispecies concept, in which mutational pressure beyond the so-called "error threshold" leads to a loss of essential genetic information and population collapse, an effect known as the "error catastrophe." We explain how crossing this threshold, as a result of increasing mutation rates, can be understood as a second-order phase transition, even in the presence of lethal mutations. In particular, we show that, in fitness landscapes with a single peak, this collapse is equivalent to a ferroparamagnetic transition, where the back-mutation rate plays the role of the external magnetic field.

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