Thymosin alpha 1: A comprehensive review of the literature

Thymosin alpha 1 is a peptide naturally occurring in the thymus that has long been recognized for modifying, enhancing, and restoring immune function. Thymosin alpha 1 has been utilized in the treatment of immunocompromised states and malignancies, as an enhancer of vaccine response, and as a means of curbing morbidity and mortality in sepsis and numerous infections. Studies have postulated that thymosin alpha 1 could help improve the outcome in severely ill corona virus disease 2019 patients by repairing damage caused by overactivation of lymphocytic immunity and how thymosin alpha 1 could prevent the excessive activation of T cells. In this review, we discuss key literature on the background knowledge and current clinical uses of thymosin alpha 1. Considering the known biochemical properties including antibacterial and antiviral properties, time-honored applications, and the new promising findings regarding the use of thymosin, we believe that thymosin alpha 1 deserves further investigation into its antiviral properties and possible repurposing as a treatment against severe acute respiratory syndrome coronavirus-2.     

Sleep,self-management,neurocognitive function,and glycemia in emerging adults with Type 1 diabetes mellitus: A research protocol

Type 1 Diabetes (T1D) affects 1.6 million Americans, and only 14% of emerging adults ages 18–25 years achieve targets for glycemic control (A1C < 7.0%). Sleep deficiency, including habitual short sleep duration (<6.5 hr total sleep time and high within-person variability in total sleep time), is associated with poorer glycemic control. Emerging adults with T1D have a more pronounced sleep extension on weekends compared with matched controls, consistent with sleep deficiency; however, associations among sleep variability and glycemic control have not been explored in this population. Sleep deficiency may affect the complex higher-order neurocognitive functioning needed for successful diabetes self-management (DSM). We report the protocol for an ongoing study designed to characterize sleep and the associations among sleep deficiency, neurocognitive function, DSM, diabetes quality of life, and glycemia among a sample of 40 emerging adults with T1D. We monitor sleep via wrist-worn actigraphy and glucose via continuous glucose monitoring concurrently over 14 days. We are collecting data on self-report and objective sleep, a 10-min psychomotor vigilance test on a PVT-192 device, a 3-min Trail Making Test on paper, and questionnaires, including twice-daily Pittsburgh sleep diaries using Research Electronic Data Capture (REDCap)^TM. Results from this study will be used to support the development and testing of the efficacy of a tailored sleep self-management intervention that may improve total sleep time, sleep variability, neurocognitive function, DSM, glycemic control, and glucose variability among emerging adults with T1D.     

Triggering receptor expressed on myeloid cells 2 knockdown exacerbates aging-related neuroinflammation and cognitive deficiency in senescence-accelerated mouse prone 8 mice

As a major characteristic of aging process, neuroinflammation is involved in the pathogenesis of several aging-related diseases including Alzheimer's disease (AD). Triggering receptor expressed on myeloid cells 2 (TREM2) is a newly identified risk gene for AD, which regulates inflammatory process in peripheral tissues via modulating the release of inflammatory cytokines. However, the role of TREM2 in aging-related neuroinflammation, cognitive deficiency, and AD-like neuropathology is unclear so far. Here, we detected the protein levels of TREM2 in brain of 3-, 7-, and 11-month-old senescence-accelerated mouse prone 8 (SAMP8) mice and observed that TREM2 levels were increased during aging process. We then knocked down TREM2 expression in brain of SAMP8 mice by nonviral RNA interference and found a significant increase in proinflammatory cytokines including tumor necrosis factor-α and interleukin (IL)-6, which was accompanied by a reduction in IL-10. Meanwhile, more obvious neuronal and synaptic losses and cognitive impairment were observed. These findings indicate that TREM2 may play a protective role against aging-related neuroinflammation and cognitive impairment.     

Hemophagocytic lymphohistiocytosis and primary immune deficiency disorders

Hemophagocytic lymphohistiocytosis (HLH) is characterized by uncontrolled immune activation and is traditionally associated with inherited gene defects or acquired causes. In addition to abnormalities in cytotoxic granules and lysosomes, various primary immune deficiency disorders (PID) have been identified among patients suffering from HLH. Our purpose was twofold: to better characterize and detail the association between PID and HLH.