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The editors of Laboratory Investigation are proud to present a Web Focus that showcases research by authors from institutions across China. We selected recent papers to highlight the significant contributions of Chinese scientists and to introduce the journal to an even wider audience.
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.
Most current biomedical datasets are rectangular in shape and have few missing data, but the sample sizes are very large. Rigorous analyses of these huge datasets demand considerably more efficient and more accurate machine-learning algorithms to classify outcomes. This paper aims to determine the performance and efficiency of classifying multi-category outcomes of such rectangular data.
In this paper, the authors describe the development and validation of a novel image signature-based radiomics model. A total of 655 glioma patients were enrolled to build this model which is shown to be an effective tool to achieve multilayer preoperative diagnosis and prognostic stratification of gliomas.
This study reveals that the long non-coding RNA H19 is highly expressed in exosomes derived from adipose mesenchymal stem cells and accelerates the proliferation, migration and invasion of human skin fibroblasts by upregulation of SOX9 and activation of the Wnt/β-catenin pathway The authors show that H19 affects SOX9 expression via the microRNA miR-19b to promote wound healing in injured skin.
The correlation between SMAD4 mutations and clinico-molecular features in a Chinese non-small cell lung cancer (NSCLC) cohort was studied using next-generation sequencing. Integrated bioinformatics analyses based on public databases were conducted to further investigate the prognostic value of SMAD4. Results showed that SMAD4 alteration was associated with poor survival and resistance to platinum-based chemotherapy, suggesting that SMAD4 alteration might be a predictive marker in NSCLC.
This study investigated the effect of valproic acid (VPA) on epithelial–mesenchymal transition (EMT). In vitro, VPA prevents EMT in a time- and concentration-dependent manner. In vivo, pretreatment with VPA attenuates pulmonary fibrosis development through EMT inhibition in mice, which was associated with Smad2/3 deactivation but without Akt signal involvement.
Immune cells are involved in skeletal muscle regeneration, but the mechanisms are unclear. In this paper, the authors show that programmed death-1 (PD-1), a key immunosuppressive receptor that is involved in adaptive immune responses, can promote contused skeletal muscle regeneration by regulating Treg cell generation and macrophage polarization.
The therapeutic effects of CP-25 on experimental Sjögren’s syndrome has been shown to be associated with the inhibition of the JAK1-STAT1/2-CXCL13 signaling pathway in HSGEC, which impedes the migration of B cells into the salivary gland. The study provides an experimental foundation for CP-25 as a potential drug in the treatment of human autoimmune disorder, Sjögren’s syndrome.
This study shows that exercise increases adropin levels and inhibits NLRP3 inflammasome activation in mice with diet-induced nonalcoholic steatohepatitis (NASH). Furthermore, adropin suppresses palmitic acid-induced NLRP3 inflammasome activation in hepatocytes and Kupffer cells. These results indicate that exercise may inhibit NLRP3 inflammasome activation via adropin induction, resulting in NASH improvement.
The findings of the present study demonstrate that inflammasome NLRP3 deficiency did not attenuate, but enhanced hepatocellular steatosis, injury and death, inflammation, and fibrosis, as well as insulin resistance in both liver and adipose tissues. This effect is probably due to an enhanced inflammatory response with elevated monocyte chemotactic protein-1 and M1 microphages.
Prostacyclin synthase (PTGIS) levels are decreased by elevated miR-140-3p.1 expression in chronic alcoholic liver disease. Inducing PTGIS expression alleviates chronic alcohol-induced liver injury by promoting macrophage M2 polarization and inhibiting the M1 phenotype through the JAK/STAT pathway. Interestingly, inducing PTGIS expression also increases IL-6 expression, which has not yet been explained.
This manuscript describes a methodology to quantify the abnormalities in digital cytology images. This automatic AI-system incorporates deep learning structures, mathematical algorithms, and image processing methods to locate and segment abnormal and suspicious cells. Characterized as more informative, objective, and reproducible, it has the potential to assist clinical practice.
Resistance to chemotherapy is frequently driven by aberrantly activated kinases. RSK2 was identified as a potential regulator of methotrexate resistance in gestational trophoblastic neoplastic cells. RSK2 activation promotes methotrexate resistance via upregulation of SOX8 and attenuation of reactive oxygen species. RSK2 inhibitors might therefore be useful to treat methotrexate-resistant gestational trophoblastic neoplasia.
PLODs play important roles in cancer progression. In silico analysis of PLOD expression in ovarian cancer was performed. PLOD-enriched pathways and related genes were validated by immunohistochemistry in OvCa tissue blocks and in vivo xenograft murine models. PLODs are generally overexpressed in OvCa and each PLOD may be functionally non-redundant.
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.
An increase in podocyte apoptosis is positively correlated with the cytoplasmic distribution of YAP in focal segmental glomerulosclerosis (FSGS). YAP inhibition by verteporfin induces nuclear exclusion of YAP, thus increasing the podocyte apoptosis and accelerating disease progression. Therefore, this study suggests that YAP activation and nuclear distribution in podocytes is an endogenous anti-apoptotic mechanism during the progression of FSGS.