To present a meta-analysis of high-quality published reports comparing laparoscopic rectal resection (LRR) and open rectal resection (ORR) for rectal cancer. Studies that compared LRR and ORR and were published within the last 5 years were identified. All eligible randomized controlled trials (RCTs) and non-randomized comparative trials (NRCTs) were evaluated based on the Jadad score, the Cochrane risk of bias assessment tool and modified Methodological Indices for Nonrandomized Studies (MINORS). The mean differences (MD) and odds ratios (OR) were used to compare the operative time, blood loss, mortality, complications, harvested lymph nodes, hospital stay, distal resection margin, and circumferential resection margin. The risk ratio (RR) method was used to examine recurrence and survival. Fourteen studies were identified and included 7 RCTs and 7 NRCTs and 4353 patients (2251 LRR, 2102 ORR). Although the operation time of the LRR group was obviously longer than that of the conventional surgery group (MD = 25.64, 95%CI = [5.17,46.10], P = 0.01), LRR was associated with fewer overall complications (OR = 0.67, 95%CI = [0.52,0.87], P = 0.002), less blood loss (MD = -66.49, 95%CI = [-88.31, -44.66], P < 0.00001), shorter postoperative hospital stays (OR = -1.26,95%CI = [-2.45, -0.07],P = 0.004) and shorter bowel function recovery times (MD = -0.93, 95%CI = [-1.27,-0.58], P < 0.00001). Moreover, the difference in the DRM was statistically clear (MD = 0.14, 95%CI = [0.02,0.27], P = 0.03). However, no significant differences between the LRR and ORR groups were observed in terms of the number of lymph nodes harvested, mortality, positive CRM, local and distal recurrence, or overall and disease-free survival. This study indicates that there are no significant differences between LRR and ORR in terms of survival and pathological outcomes with the exception of the DRM. Moreover, this study suggests that LRR can be performed safely and elicits faster recovery times compared with conventional surgery.

Inflammatory Bowel Disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract with an unknown etiology. Although dysbiosis is implicated in its pathogenesis, deep sequencing and oral microbiota study in Chinese IBD patients is absent. To explore the role of oral / intestinal microbiota in patients with IBD and the potential associations therein. Clinical data, fecal and saliva samples were harvested from 80 patients with IBD (Crohn's disease, CD, n = 69; Ulcerative colitis, UC, n = 11) and 24 normal controls. Microbiomics (16S rRNA sequencing and 16S rRNA full-length sequencing) were used to detect and analyze the difference between IBD patients and normal control. Compared with normal controls, a higher abundance of the intestinal Shigella spp. (Shigella flexneri and Shigella sonnei, which were positively relate to the severity of IBD), lower abundance of intestinal probiotics (Prevotella, Faecalibacterium and Roseburia), and higher abundance of oral Neisseria were present in IBD patients with microbiome. The higher inflammation-related markers, impaired hepatic and renal function, and dyslipidaemia were present in patients with IBD. A higher intake of red meat and increased abundance of Clostridium in the gut were found in CD patients, while the elevated abundance of Ruminococcus in the gut was showed in UC ones. The bacterial composition of saliva and fecal samples was completely different, yet there was some correlation in the distribution of dominant probiotics. Enteric dysbacteriosis and the infections of pathogenic bacteria (Shigella) may associate with the occurrence or development of IBD.

G protein-coupled receptor kinase 2 (GRK2) is one of the cytosolic enzymes, and GRK2 translocation induces prostaglandin E2 receptor 4 (EP4) over-desensitization and reduces the level of cyclic adenosine monophosphate (cAMP) to regulate macrophage polarization. However, the role of GRK2 in the pathophysiology of ulcerative colitis (UC) remains unclear. In this study, we investigated the role of GRK2 in macrophage polarization in UC, using biopsies from patients, a GRK2 heterozygous mouse model with dextran sulfate sodium (DSS)-induced colitis, and THP-1 cells. The results showed that a high level of prostaglandin E2 (PGE2) stimulated the receptor EP4 and enhanced the transmembrane activity of GRK2 in colonic lamina propria mononuclear cells (LPMCs), resulting in a down-regulation of membrane EP4 expression. Then, the suppression of cAMP–cyclic AMP responsive element-binding (CREB) signal inhibited M2 polarization in UC. Paroxetine is acknowledged as one of the selective serotonin reuptake inhibitors (SSRI), which is also considered as a potent GRK2 inhibitor with a high selectivity for GRK2. We found that paroxetine could alleviate symptoms of DSS-induced colitis in mice by regulating GPCR signaling to affect macrophage polarization. Taken together, the current results show that GRK2 may act as a novel therapeutic target in UC by regulating macrophage polarization, and paroxetine as a GRK2 inhibitor may have therapeutic effect on mice with DSS-induced colitis.