The combined manifestations of dramatically sore throat, congested and edematous mucosa, no-swelling tonsil are specific in acute Omicron pharyngitis.

Objective: To identify specific clinical signs of Omicron pharyngitis infection.

Methods: A clinical cross-sectional retrospective study was designed to analyze the primary symptoms of pharyngitis in outpatients seeking treatment for sore throat. Pharyngeal congestion, mucosal edema, were measured using a visual analogue assessment score (0-10) while the presence of ulcers, no-tonsil-swelling, no-tonsil-exudate.

Induction of MUC5AC mucin expression by histamine through the activation of its core promoter region.

Conclusion: This study provides evidence that histamine induced MUC5AC mRNA expression through the activation of the core region of its promoter. It may also help in approaching new therapeutic strategies in airway mucins hypersecretory diseases.

Objective: Mucin hypersecretion characterizes several respiratory diseases.

BRCA1 and ERCC1 mRNA levels are associated with lymph node metastasis in Chinese patients with colorectal cancer.

Background: Although both excision repair cross-complementing group 1 (ERCC1) and breast cancer susceptibility gene 1 (BRCA1) can be effective biomarkers for chemosensitivity in primary malignant tumors, their applicability to metastases is poorly understood. Here, ERCC1 and BRCA1, which are linked to lymph node metastasis (LNM) in colorectal cancer (CRC), were evaluated in primary CRC samples from Chinese patients with LNM (LNM CRC) or without LNM (non-LNM CRC). mRNA levels of ERCC1 and BRCA1 in CRC samples, and their relationships to primary CRC and LNM, were also examined.

Unglycosylation at Asn-633 made extracellular domain of E-cadherin folded incorrectly and arrested in endoplasmic reticulum, then sequentially degraded by ERAD.

The human E-cadherin is a single transmembrane domain protein involved in Ca(2+)-dependent cell-cell adhesion. In a previous study, we demonstrated that all of four potential N-glycosylation sites in E-cadherin are occupied by N-glycans in human breast carcinoma cells in vivo and the elimination of N-glycan at Asn-633 dramatically affected E-cadherin expression and made it degraded. In this study we investigated the molecular mechanism of E-cadherin, which lacks N-glycosylation at Asn-633 (M4), degradation and the role of the N-glycan at Asn-633 in E-cadherin folding.

N-glycosylation affects the adhesive function of E-Cadherin through modifying the composition of adherens junctions (AJs) in human breast carcinoma cell line MDA-MB-435.

E-cadherin mediates calcium-dependent cell-cell adhesion between epithelial cells. The ectodomain of human E-cadherin contains four potential N-glycosylation sites at Asn residues 554, 566, 618, and 633. In this study, the role of N-glycosylation in E-cadherin-mediated cell-cell adhesion was investigated by site-directed mutagenesis.

MAGI-2 Inhibits cell migration and proliferation via PTEN in human hepatocarcinoma cells.

MAGI-2, a multidomain scaffolding protein, contains nine potential protein-protein interaction modules, including a GuK domain, two WW domains and six PDZ domains. In this study, we examined eight human hepatocarcinoma cell lines (HHCCs) and found that MAGI-2 was expressed only in 7721 cells. After 7721, 7404 and 97H cells were transfected with myc-MAGI-2 plasmid, their migration and proliferation was significantly inhibited, which was associated with downregulation of p-FAK and p-Akt.

Phosphatidylinositol 3-kinase/protein kinase B pathway stabilizes DNA methyltransferase I protein and maintains DNA methylation.

DNA methylation, which affects gene expression and chromatin stability, is catalyzed by DNA methyltransferases (DNMTs) of which DNMT1 possesses most abundant activity. PI3K/PKB pathway is an important pathway involved in cell proliferation, viability, and metabolism and often disrupted in cancer. Here we investigated the impact of PKB on DNMT1 and DNA methylation.

Comparative glycoproteomics based on lectins affinity capture of N-linked glycoproteins from human Chang liver cells and MHCC97-H cells.

We present here an effective technique for the large-scale separation and identification of N-linked glycoproteins from Chang liver cells, the human normal liver cells. To enrich N-linked glycoproteins from the whole cells, a procedure containing the lysis of human liver cells, the solubilization of total proteins, lectin affinity chromatography including Concanavalin A and wheat germ agglutinin was established. Furthermore, captured N-linked glycoproteins were separated by 2-DE, and identified by MS and database searching.

Study of the PTEN gene expression and FAK phosphorylation in human hepatocarcinoma tissues and cell lines.

The tumor suppressor PTEN gene maps to chromosome 10q23.3 and encodes a dual specificity phosphatase. Mutations of this gene had been found in a variety of human tumors.

[The effects of PTEN gene on migration and FAK phosphorylation of SMMC-7721 human hepatocarcinoma cell line].

PTEN is a major tumor suppressor gene that encodes a dual-specificity phosphatase with high sequence similarity to the cytoskeletal protein tensin. PTEN may be involved in the formation and disassembly of focal adhesion and affect cell migration. In the present study, PTEN expression plasmid was constructed and transfected into the hepatoma cell line SMMC-7721 to analyze the alterations of cell motility and FAK tyrosine phosphorylation.