Publications

Postacute sequelae of COVID-19 (PASC), also referred to as “Long COVID”, sometimes follows COVID-19, a disease caused by SARS-CoV-2. Although SARS-CoV-2 is well known to promote a prothrombotic state, less is known about the thrombosis risk in PASC. Our objective was to evaluate platelet function and thrombotic potential in patients following recovery from SARS-CoV-2, but with clear symptoms of patients with PASC.

• Link: https://journals.sagepub.com/doi/10.1177/1358863X231224383

Hepatocellular carcinoma (HCC) has the highest mortality rate among malignant tumors worldwide. This study aimed to analyze the biological characteristics of serum proteins in hepatitis B (HBV)-related liver diseases, identify diagnostic biomarkers for HBV-infected HCC, and provide a scientific basis for its prevention and treatment.

• Link: https://www.sciencedirect.com/science/article/abs/pii/S0009898123005296?via%3Dihub

Hepatocellular carcinoma (HCC) has the highest mortality rate among malignant tumors worldwide. This study aimed to analyze the biological characteristics of serum proteins in hepatitis B (HBV)-related liver diseases, identify diagnostic biomarkers for HBV-infected HCC, and provide a scientific basis for its prevention and treatment.

• Link: https://www.sciencedirect.com/science/article/abs/pii/S0009898123005296?via%3Dihub

Nonalcoholic steatohepatitis (NASH) is a metabolism-associated fatty liver disease with accumulated mitochondrial stress, and targeting mitochondrial function is a potential therapy. The mitochondrial genome-encoded bioactive peptide MOTS-c plays broad physiological roles, but its effectiveness and direct targets in NASH treatment are still unclear. Here, we show that long-term preventive and short-term therapeutic effects of MOTS-c treatments alleviate NASH-diet-induced liver steatosis, cellular apoptosis, inflammation, and fibrosis. Mitochondrial oxidative capacity and metabolites profiling analysis show that MOTS-c significantly reverses NASH-induced mitochondrial metabolic deficiency.

• Link: https://www.cell.com/cell-reports/fulltext/S2211-1247(23)01599-1?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124723015991%3Fshowall%3Dtrue

ARL6IP1 is implicated in hereditary spastic paraplegia (HSP), but the specific pathogenic mechanism leading to neurodegeneration has not been elucidated. Here, we clarified the molecular mechanism of ARL6IP1 in HSP using in vitro and in vivo models. The Arl6ip1 knockout (KO) mouse model was generated to represent the clinically involved frameshift mutations and mimicked the HSP phenotypes. Notably, in vivo brain histopathological analysis revealed demyelination of the axon and neuroinflammation in the white matter, including the corticospinal tract.

• Link: https://pubmed.ncbi.nlm.nih.gov/37934410/

R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is a standard first-line treatment for diffuse large B-cell lymphoma (DLBCL). However, 20%–40% of patients survive less than 5 years. Novel prognostic biomarkers remain in demand.

• Link: https://acsjournals.onlinelibrary.wiley.com/doi/10.1002/cncr.35158

Over 200,000 individuals in the United States alone live with Down Syndrome (DS), the most common genetic disorder associated with intellectual disability. DS has a constellation of features across the body, including dysregulation of the immune system. Individuals with DS have both a higher frequency of autoimmunity and more severe infections than the general population, highlighting the importance of understanding the immune system in this population. Individuals with DS present with dysregulation of both the innate and adaptive immune systems.

• Link: https://onlinelibrary.wiley.com/doi/10.1111/imr.13296

The role of lncRNAs in the pathogenesis of cancer, including colorectal cancer (CRC), has repeatedly been demonstrated. However, very few lncRNAs have been well annotated functionally. Our study identified a novel lncRNA upregulated in CRC, NONHSAT136151, which was correlated with clinical progression. In functional assays, NONHSAT136151 significantly enhanced CRC cell proliferation, migration and invasion. Mechanistically, NONHSAT136151 interacted with RNA-binding protein (RBP) QKI (Quaking) to interfere with QKI binding to target mRNAs and regulate their expression.

• Link: https://onlinelibrary.wiley.com/doi/10.1111/jcmm.18068

We have previously isolated a highly mutated (83% homologous to predicted heavy chain germline) antibody (Ab) termed C group 76-Q13-6F5 (6F5) that targets a conformational epitope on gp41. 6F5, though non-neutralizing, has the capacity to mediate Ab dependent cell cytotoxicity (ADCC). When the variable chain (predicted to be VH1-02 derived) was mutated to germline (termed C group 76 ancestor, or 76Canc), surprisingly this Ab still exhibited significant ADCC activity.

• Link: https://academic.oup.com/ofid/article/10/Supplement_2/ofad500.346/7448046

Studying the potential etiology and pathogenesis of tuberculosis-associated chronic obstructive pulmonary disease (TOPD) from an autoimmunity perspective may provide insights into peripheral blood autoantibodies and immune cells, as well as their interactions.

• Link: https://www.dovepress.com/characteristics-of-serum-autoantibody-repertoire-and-immune-subgroup-v-peer-reviewed-fulltext-article-COPD