6%, 54.5% and 54.5%, respectively. No additional surgery was performed, and no recurrences were found. Bleeding occurred in only one case and there was no perforation after the operation.

Overall, ESD is safe and effective in the treatment of MECPL emerging at the AS after curative surgical resection of CRC. Especially for patients with anastomotic recurrence close to anal margin, this method can avoid the risks of reoperation and improve the rate of anal preservation.

Overall, ESD is safe and effective in the treatment of MECPL emerging at the AS after curative surgical resection of CRC. Especially for patients with anastomotic recurrence close to anal margin, this method can avoid the risks of reoperation and improve the rate of anal preservation.

Parenchymal hematoma (PH) is the most feared complication of reperfusion therapy after stroke. The opacification of the superficial middle cerebral vein (SMCV) on computed tomography perfusion (CTP) has been associated with poor functional outcomes after stroke, while its association with PH has not been verified for acute stroke patients undergoing thrombectomy.

Consecutive patients with acute anterior large artery occlusion (LAO) who received thrombectomy were retrospectively enrolled between May 2018 and May 2019. Absent filing of the SMCV (SMCV-) on CTP-derived CT angiography was defined as no contrast filling of the SMCV across the whole venous phase in the ischemic hemisphere, while SMCV+ was defined as the presence of contrast filling of the SMCV at any time point of the venous phase.

A total of 52 patients were enrolled in the study, and 15 patients (28.8%) developed a PH within 48 hours after thrombectomy. SMCV- was not associated with PH in both the univariate and multivariate logistic regressed.

Myocardial injury is a major cause of myocardial remodeling. Macrophages are important in cardiac repair as a result of their interactions with fibroblasts. As regulatory macrophages, M2b macrophages modulate inflammatory immune responses without participating in wound healing and could have enhanced protective effects on myocardial remodeling. Therefore, we tested the hypothesis that M2b macrophages could improve cardiac function and ameliorate myocardial fibrosis after the myocardial ischemia/reperfusion injury (MI/RI).

, MI/RI models were established with Sprague-Dawley (SD) rats and either M2b macrophages (MT group) or the same volume of vehicle (CK group) was injected into the ischemic zone. Two weeks after the operation, cardiac function and diameters were determined by echocardiography examination. Level of myocardial fibrosis was measured by Sirius red staining and the expression of fibrosis-related factors.

, cardiac fibroblasts (CFs) were co-cultured with M2b macrophages or cultured with M2b mf the protective mechanism.

Our study demonstrated that the administration of M2b macrophages could attenuate myocardial remodeling after MI/RI. The regulation of the activation of PDGFRs in CFs is an important part of the protective mechanism.

Human papilloma virus (HPV) infection is an important risk factor for vaginal intraepithelial neoplasia (VAIN). Recent studies have suggested that the microbiome may play a potential role in cervicovaginal diseases. This study aimed to explore the characteristics of the types and viral load of HPV in VAIN, as well as the association between vaginal microbiota and VAIN.

A total of 176 women, either with VAIN, or without VAIN but with HPV infection were enrolled in the study. Among them, 109 HPV positive cases were qualified for viral load assay. The vaginal microbiota of 122 HPV positive women, who were matched by severity of cervical lesions and menopause status, was determined by 16S ribosomal RNA (16S rRNA) sequencing.

The top 5 types of HPV-associated vaginal lesions were HPV16 (24.2%), HPV52 (24.2%), HPV53 (16.1%), HPV58 (14.5%) and HPV66 (14.5%). The viral load of HPV types 16, 52, and 58 appeared higher in separate vaginal lesions than in histopathologically normal cases (P=0.026, 0.002, and 0.013, respectively). The vaginal microbiota of HPV-positive patients with VAIN did not exhibit a large change in diversity. Vaginal microbiota of VAIN was characterized by an increased abundance of

and

, as well as decreased abundance of

,

and

. A higher level of

and some specific

. might be associated with an elevated risk of VAIN2/3.

A higher level of viral load of HPV16, 52, and 58 may indicate VAIN. The composition of vaginal microbiota changes during the progression of VAIN and specific bacteria such as

,

and

, may help to promote its development.

A higher level of viral load of HPV16, 52, and 58 may indicate VAIN. The composition of vaginal microbiota changes during the progression of VAIN and specific bacteria such as Atopobium, Gardnerella, Allobaculum, Enterococcus and Clostridium, may help to promote its development.

Rupture of intracranial aneurysm (IA) is the leading cause of subarachnoid hemorrhage. However, there are few pharmacological therapies available for the prevention of IA rupture. Therefore, exploring the molecular mechanisms which underlie IA rupture and identifying the potential molecular targets for preventing the rupture of IA is of vital importance.

We used the Gene Expression Omnibus (GEO) datasets GSE13353, GSE15629, and GSE54083 in our study. The 3 datasets were merged and normalized. Differentially expressed gene (DEG) screening and weighted correlation network analysis (WGCNA) were conducted. The co-expression patterns between ruptured IA samples and unruptured IA samples were compared. Then, the DEGs were mapped into the whole co-expression network of ruptured IA samples, and a DEG co-expression network was generated. Molecular Complex Detection (MCODE) (http//baderlab.org/Software/MCODE) was used to identify key genes based on the DEG co-expression network. Finally, key genes were validated used by another GEO dataset and might serve as potential targets for pharmacological therapies and diagnostic markers in predicting IA rupture. find more Further studies are needed to elucidate the detailed molecular mechanisms and biological functions of these key genes which underlie the rupture of IA.

Using a weighted gene co-expression network approach, we identified 8 and 6 modules for ruptured IA and unruptured IA, respectively. After that, we identified the hub genes for each module and key genes based on the DEG co-expression network. All these key genes were validated by another GEO dataset and might serve as potential targets for pharmacological therapies and diagnostic markers in predicting IA rupture. Further studies are needed to elucidate the detailed molecular mechanisms and biological functions of these key genes which underlie the rupture of IA.