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the intermolecular binding free energy of the complex was increased, regardless of whether HB was formed.

The findings of this study suggest that the hydrophobic nature of the amino acids inside or outside the disulfide bonds on the TCR may be associated with the intermolecular interaction and binding between the TCR and polypeptide. The residues located outside the TCR α or β single-chain disulfide bond and forming the pi-stack force showed a beneficial effect on the intermolecular interaction and binding of the complex. In addition, the part of the residues on the TCR α or β single chain that produced bond types of interaction with the polypeptide after being replaced by Ala or Gly, the intermolecular binding free energy of the complex was increased, regardless of whether HB was formed.

Roxithromycin (RXM), a macrolide antibiotic, exhibits anti-asthmatic effects, but its specific mechanism of action remains elusive. We evaluated the effects of RXM on airway inflammation, the expression of calprotectin, and the activity of the receptor of advanced glycation end products (RAGE) to determine whether RXM alleviates inflammation by regulating RAGE activation, and thereby calprotectin expression, in neutrophilic asthma.

Male Brown Norway rats were sensitized with ovalbumin (OVA) and Freund's complete adjuvant (FCA) mixture, followed by OVA challenge to induce neutrophilic asthma. RXM (30 mg/kg) or FPS-ZM1 (RAGE inhibitor, 1.5 mg/kg) was administered 30 min prior to each challenge. The infiltration of airway inflammatory cells and cytokines, as well as the expression of calprotectin and RAGE, was assessed.

The expression of airway inflammatory cells and cytokines was found to be significantly elevated in OVA + FCA-induced rats. Increased expression of both calprotectin and RAGE was also detecession of calprotectin and RAGE in a neutrophilic asthma model. Our findings provide novel insights into the mechanisms underlying the effect of RXM pretreatment on neutrophilic asthma. Furthermore, FPS-ZM1 may be useful as an intervention specific to the neutrophilic asthma phenotype.

Approximately 30-70% percent of patients with non-small cell lung cancer (NSCLC) still relapse after receiving complete resection and even suffer distant metastasis. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have gradually replaced chemotherapy to become the first-line postoperative NSCLC treatment because they can effectively inhibit the postoperative recurrence of lung cancer. However, the clinical efficacy of neoadjuvant EGFR-TKIs in

mutant NSCLC patients is still unclear. The purpose of this study was to evaluate their clinical efficacy and to further explore factors affecting recurrence in such patients.

-mutated patients receiving neoadjuvant EGFR-TKI treatment in our hospital from July 2016 to September 2020 were retrospectively included. These patients underwent radical tumor resection after treatment. The primary endpoint was the objective response rate (ORR). The secondary endpoints were the major pathological response (MPR), disease-free survival (DFS), and over Neoadjuvant EGFR-TKIs had good effects on

-mutant NSCLC patients at different stages, especially those with MPR. Patients with high-risk subtypes (solid or micropapillary) should be closely followed up after surgery because of the high risk of recurrence.

Neoadjuvant EGFR-TKIs had good effects on EGFR-mutant NSCLC patients at different stages, especially those with MPR. AZD9291 in vitro Patients with high-risk subtypes (solid or micropapillary) should be closely followed up after surgery because of the high risk of recurrence.

Extracellular matrix proliferation is an issue which leads to lung tissue damage in diabetes mellitus. Glucagon-like peptide-1 (GLP-1) analogues can improve the proliferation of extracellular matrix in diabetic pulmonary disease. In this study, we investigated the effect of GLP-1 on pulmonary fibrosis through the AMPK/microRNA-27a (miR-27a) pathway.

Human embryonic lung fibroblast (MRC-5) cells were cultured with a high-glucose medium, and were treated with miR-27a inhibitor, GLP-1 analogues, and AMPK inhibitor. Cell Counting Kit-8 (CCK-8) detected the proliferation of MRC-5 cells. The fibrosis-related genes were analyzed, including Col-IV, fibronectin, NF-κB p65, α-SMA, and TGF-β1. Bioinformatics and dual-luciferase reporter assays were used to identify the targets for miR-27a.

Compared with the control group, the expression of miR-27a in the hyperglycemic group was significantly up-regulated (P<0.01) and the expression of peroxisome proliferator-activated receptor γ (PPARγ) significantly down-regulon in MRC-5 cells.

MiR-27a plays an important regulatory role in diabetic pulmonary fibrosis. GLP-1 could down-regulate the expression level of miR-27a by activating AMPK. Furthermore, the target gene PPARγ was up-regulated, consequently improving extracellular matrix proliferation in MRC-5 cells.

Artificial intelligence technology is widely used in the medical industry. Our retrospective study evaluated the effectiveness of an AI-CDSS in improving the incidence of hospital-related VTE and the impact of anticoagulant drug use.

This study collected relevant data on adult patients over 18 years of age who are not discharged 24 hours, from January to July 2019 and from January to July 2020, the VTE high-risk department of Ruijin Hospital. Before and after using AI-CDSS, the incidence of hospital-related VTE and using anticoagulants were analyzed.

Between January to July 2019 and January to July 2020, 3,565 and 4,423 adult patients over 18 years old were hospitalized in our hospital and were designed as a control group and intervention group, respectively (7,988 in total). Both groups had similar baseline characteristics. There were 4,716 (59.03%) male patients, the mean age was 60.43±13.09 years, and the mean stay was 7.56±7.76 days. More than half of the patients (4,605, 57.58%) came from the respised VTE risk, take effective preventive measures, and improve clinicians' compliance with the American College of Chest Physicians (ACCP) guidelines.

Implementing AI-CDSS can help clinicians identify hospitalized patients at increased VTE risk, take effective preventive measures, and improve clinicians' compliance with the American College of Chest Physicians (ACCP) guidelines.