Volume 102 Issue 1, January 2022

During the COVID-19 pandemics, sensitive and reliable assays for SARS-CoV-2 detection are essential for screening the population, identifying asymptomatic individuals, making diagnoses, monitoring treatment responses, and determining viral clearance. This review summarizes the principles, advantages, disadvantages, and specific applications of currently available assays for detection of the viral nucleotide, genome or proteins, as well as host antibody responses, and provide overall guidelines for selection of optimal assays for specific usage.

The prevalence and contribution of viruses to heart failure phenotypes are increasingly recognized, while still underappreciated and underreported. We designed a tissue microarray with cardiac muscle tissue from 78 heart failure patients and probed for common cardiotropic viruses via in situ hybridization. Viral RNA was detected in 46.4% of patients, higher than anticipated for these heart failure conditions that include those not previously associated with a viral trigger or an exacerbating role.

A proposed regulatory model of FABP4 in Hcy-induced macrophage inflammation in atherosclerosis of ApoE^−/− mice. FABP4 activates the JAK2/STAT2 pathway via Rap1a in Hcy-induced macrophage inflammatory response and atherosclerosis in ApoE^−/− mice, which is attributed to Rap1a-dependent promotion of the c-Src phosphorylation at Tyr416 and membrane translocation. SOCS1 has a negative regulatory role in FABP4-dependent activation of the JAK2/STAT2 pathway and Rap1a in macrophage inflammatory response induced by Hcy.

This study determined that circN4BP2L2 acts as an oncogene that promotes tumor growth and metastasis of colorectal cancer (CRC) by regulating the miR-340-5p/CXCR4 axis. The authors reveal a novel mechanism for the ceRNA regulatory network in CRC progression and identify a potential therapeutic target for CRC treatment.

The expression and functional levels of TRPC3, a nonselective cation channel, and NCX1, a Na⁺/Ca2⁺ exchanger, are increased in the bladders of rats with partial bladder outlet obstruction-induced detrusor overactivity. The synergistic effects of TRPC3 and NCX1 significantly increase the concentration of Ca²⁺_i in smooth muscle cells, which induces bladder hyperactivity in this animal model of overactive bladder. TRPC3 and NCX1 may be new therapeutic targets for detrusor overactivity.

Mother-to-child transmission is the major cause of chronic hepatitis B virus (HBV) infection. This study shows that an unconventional protein secretion pathway that depends on autophagy may be hijacked by HBV to complete the process of intracellular transport. In HBV-infected trophoblasts, AnxA2-S100A10-mediated exocytosis may result in HBV intrauterine transmission.

This report provides new evidence supporting the role of ATP synthase inhibitory factor subunit 1 (IF1), an endogenous ATP synthase inhibitory protein, in regulating β-cell function. Investigations on genetic mouse models and an β-cell line indicate that IF1 negatively regulates cellular respiration and mitochondrial homeostasis, thus controlling insulin storage and release from islets.

Ameloblastoma (AB) is the most common benign odontogenic tumor. In this study, we investigated the expression and distribution of acetylated α-tubulin and αTAT1 in AB specimens. We analyzed tubulin acetylation caused by αTAT1 activation in a human AB cell line, AM-1. Results of the histopathological and in vitro studies clarified that TAK1 was phosphorylated by TGF-β stimulation, then, induced tubulin acetylation via αTAT1 activation, which subsequently activated the migration and invasion of AB cells.

In this study, the authors demonstrated that bioactive glass promotes granulation formation, collagen deposition and angiogenesis to accelerate wound healing. Bioactive glass down-regulaties the connexin 43/reactive oxygen species signaling pathway to inhibit endothelial cell pyroptosis in vitro and in vivo.

Aggrecan degradation by ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) is essential to cartilage destruction in osteoarthritis, but its expression profile and regulation are unclear. The authors show overexpression of ADAMTS4 in osteoarthritis synovium and synergistic upregulation by interleukin-1α, tumor necrosis factor-α, and transforming growth factor-β in osteoarthritis synovial fibroblasts. These findings suggest that concurrent therapy with an anti-TNF-α drug and inhibitor(s) may be useful for prevention against aggrecan degradation in OA.