A flow cytometry-based Hoechst 33342 efflux assay was applied to assess the proportion of the side population (SP) within total CRC cells.

Elevated levels of SNTB1 were identified in CRC tissues and cell lines. The elevation of SNTB1 was positively correlated with the degree of malignancy and poor prognosis in CRC. We further revealed that, by modulating the β-catenin signaling pathway, silencing SNTB1 expression suppressed tumor growth and cancer stemness

, as well as tumorigenesis

.

These findings suggest that SNTB1 plays a crucial role in colorectal tumorigenesis and progression by modulating β-catenin signaling and the stemness maintenance of cancer cells.

These findings suggest that SNTB1 plays a crucial role in colorectal tumorigenesis and progression by modulating β-catenin signaling and the stemness maintenance of cancer cells.

The cannabinoid receptor 2 (CNR2) plays a critical role in relieving asthma, with the mechanism still unclear. We aimed to investigate the mechanism of the CNR2 agonist (β-caryophyllene, β-Car) in regulating the balance of regulatory T cells (Treg) and T helper cell 17 (Th17) and thus its role in asthma.

The study group of 50 pathogen-free female BALB/c mice were randomly divided at 6-8 weeks old into five groups of Control, Asthma, Asthma + β-Car (10 mg/kg), Asthma + β-Car + SR144528 (specific CNR2 antagonist, 3 mg/kg), and Asthma + β-Car + CMD178 (inhibitor of Treg cell, 10 mg/kg). ELISA was conducted to evaluate the main inflammatory cytokines [interleukin (IL)-6, IL-8, and tumor necrosis factor-α], and those secreted by Treg (transforming growth factor-β and IL-10), and Th17 (IL-17A and IL-22). Markers of Treg and Th17 cells were assessed by flow cytometry.

, the CD4

T cells were sorted and directed to differentiate to Treg and Th17 cells. The expression levels of CNR2, STAT5 and JNK1/2 were investigated by western blot and immunofluorescence assay.

β-Car relieved neutrophilic asthma severity in mice by elevating the marker genes’ expression of Treg and inhibiting those of Th17, causing an increased proportion of Treg to Th17. β-Car also promoted the directed differentiation of CD4

T cells into Treg, but not Th17. Activation of the CNR2 regulated the Treg/Th17 balance and relieved neutrophilic asthma possibly through promotion of phosphorylation of STAT5 and JNK1/2.

The effect of the selective CNR2 agonist activating STAT5 and JNK1/2 signaling was to change the Treg/Th17 balance and reduce the inflammatory reaction, thus ameliorating neutrophilic asthma in a mouse model.

The effect of the selective CNR2 agonist activating STAT5 and JNK1/2 signaling was to change the Treg/Th17 balance and reduce the inflammatory reaction, thus ameliorating neutrophilic asthma in a mouse model.

Alectinib and crizotinib have been approved as first-line therapies for advanced non-small cell lung cancer (NSCLC) with anaplastic lymphoma kinase (ALK) gene fusion. However, the therapeutic efficacy and side effects are still largely unknown of patients who switched to next-generation ALK tyrosine kinase inhibitors (ALK-TKIs), such as alectinib, after experiencing no disease progression with initial crizotinib treatment.

This prospective real-world study enrolled patients who were treated with alectinib after experiencing no disease progression with initial crizotinib treatment. The patients’ baseline characteristics, objective response rate (ORR) of crizotinib and alectinib, size change of target tumor lesions, treatment regimen and adverse events (AEs) were collected and analyzed.

The study included 53 patients, the majority of whom (96.2%) had non-squamous NSCLC. The median age was 51 (range, 31-80) years old. The ORR of first-line crizotinib was 54.7%. The ORR of sequential alectinib was 73.6%, and 90.5% of patients showed further tumor shrinkage after the alectinib treatment. The median progression-free survival was not reached, and 90.5% of patients were still enrolled in the study at the last follow-up. Among them, 34.0% of patients switched to alectinib treatment due to the toxicity. Crizotinib was associated with a higher frequency of AEs of grades 3 and 4 than alectinib (15.1%

0%). Neither group had any AEs resulting in death.

Switching to alectinib might be an option for patients who do not experience disease progression with initial crizotinib therapy, and may promote better treatment compliance.

Switching to alectinib might be an option for patients who do not experience disease progression with initial crizotinib therapy, and may promote better treatment compliance.

The aim of this study was to compare the short and long-term outcomes of robotic assisted proctectomy (RP) and laparoscopic assisted proctectomy (LP) for rectal cancer below the peritoneal reflection using propensity score matching (PSM) analysis.

We evaluated the medical records of 200 patients who underwent proctectomy for rectal cancer below the peritoneal reflection through a robotic (n=81) or laparoscopic (n=119) approach between Jan 2015 and Dec 2017. The data were prospectively collected, and the patients were matched at a ratio of 11 according to age, sex, body mass index (BMI), previous abdominal surgeries, comorbidities, American Society of Anesthesiologist score (≤2/>2), and pathologic stage.

After matching, each group included 74 patients. Compared to the LP group, the RP group showed shorter postoperative hospital stays (PHS) [7 (±2)

. 9 (±2.3) d, P=0.003], shorter time to liquid diet [3 (±2)

. selleck 5 (±3) d, P<0.001], and shorter time to removal of catheter [6 (±2)

. 7 (±2.3) d, p=0ection.

Myocardial infarction (MI) is the single most critical event in coronary disease. Platelets are involved in the processes of acute MI (AMI). They lack nuclear DNA but retain megakaryocyte mRNAs, hence, their transcriptome could provide information preceding coronary events. However, their mechanisms are not clear. In this study, we obtained a gene expression atlas of platelets from patients after their very first AMI, and our purpose was to clarify the mechanisms of platelet involvement in the occurrence of AMI through bioinformatics analyses and animal models of AMI

.

We obtained a gene expression atlas of platelets from patients after their very first AMI from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were retrieved using R language. Weighted gene co-expression network analysis (WGCNA) was implemented in order to construct a gene co-expression correlation network among DEGs. Animal models of AMI

were constructed to confirm the results of the bioinformatics analysis.

Gene integration analysis yielded 2,852 DEGs (P<0.