[In situ semiconductor laser fenestration of type A aortic dissection during thoracic endovascular aortic repair].

Objective: To investigate the feasibility, efficacy and safety of semiconductor laser in situ fenestration of type A aortic dissection during thoracic endovascular aortic repair. Methods: The clinical data of 68 patients with type A aortic dissection treated by semiconductor laser in situ fenestration from June 2016 to January 2020 in Department of Vascular Surgery, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiaotong University were analyzed retrospectively. Of the patients, 45 were male, 23 were female, the mean age was (52±14) years. The technical success rate and complication rates were assessed. Results: The technical success rate of 68 patients was 92.6% (63/68), only 5 patients failed due to the complex aortic arch type, 3 patients underwent chimney stent implantation, 2 patients underwent artificial vessel bypass. During the perioperative period, 1 patient died due to severe pulmonary infection, 4 patients developed neurological symptoms such as cerebral infarction after surgery, and the remaining patients had no related complications. Postoperative CTA follow-up indicated that the primary intercalation rupture was completely closed, and the main and branch stents were patency, 8 (8.8%) type Ⅰ leakage were occurred. Conclusion: It showed that in situ semiconductor laser fenestration is a feasible, effective and safe method to treat type A aortic dissection.

Circular RNA hsa_circ_0000285 acts as an oncogene in laryngocarcinoma by inducing Wnt/ß-catenin signaling pathway.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Circular RNA hsa_circ_0000285 acts as an oncogene in laryngocarcinoma by inducing Wnt/ß-catenin signaling pathway, by J.-B. Qin, W. Chang, G.-H. Yuan, L. Huang, Z.-F. Qiu, published in Eur Rev Med Pharmacol Sci 2019; 23 (24): 10803-10809-DOI: 10.26355/eurrev_201912_19783-PMID: 31858548" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19783.

Circular RNA hsa_circ_0000285 acts as an oncogene in laryngocarcinoma by inducing Wnt/ß-catenin signaling pathway.

OBJECTIVE: Laryngocarcinoma is one of the most ordinary head and neck cancers worldwide. Recent studies have revealed that circular RNAs (circRNAs) act as an important role in malignant tumors and participate in tumorigenesis. The purpose of our work is to uncover how hsa_circ_0000285 functions in laryngocarcinoma. PATIENTS AND METHODS: In this research, the Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was performed to monitor hsa_circ_0000285 expression in laryngocarcinoma samples. Besides, function assays were performed in laryngocarcinoma cells transfected with hsa_circ_0000285 shRNA or lentivirus. Furthermore, the RT-qPCR and Western blot assay were conducted to explore the target-signaling pathway of hsa_circ_0000285. RESULTS: Hsa_circ_0000285 expression was found to be upregulated in laryngocarcinoma samples compared with adjacent tissues. The function assays showed that the inhibition of the cell proliferation was induced via knockdown of hsa_circ_0000285 in laryngocarcinoma in vitro, while the promotion of cell apoptosis was induced via the knockdown of hsa_circ_0000285 in laryngocarcinoma in vitro. On the other hand, the overexpression of hsa_circ_0000285 had the opposite function. In addition, the Wnt/ß-catenin signaling pathway was repressed via knockdown of hsa_circ_0000285 in laryngocarcinoma, while the Wnt/ß-catenin signaling pathway was promoted via overexpression of hsa_circ_0000285 in laryngocarcinoma. CONCLUSIONS: In our study, hsa_circ_0000285 was first identified as a novel oncogene and could induce the Wnt/ß-catenin signaling pathway in laryngocarcinoma.

[KLF3 regulates the movement, migration and invasion of breast cancer cells through STAT3].

Objective: To observe the effect of KLF3 on the expression of STAT3 in breast cancer cells, and to explore the potential mechanism of KLF3 affecting the movement, migration and invasion of breast cancer cells. Methods: Firstly, the expression of STAT3 was detected by Western blot, real-time fluorescent quantitative PCR, luciferase reporter system and chromatin immunoprecipitation in breast cancer cells. Secondly, the STAT3 promoter mutant was constructed. The plasmid further confirmed the effect of KLF3 on the activity of STAT3 promoter; the cell scratching test and Transwell method were used to detect the ability of cell movement, migration and invasion. Finally, animal experiments were conducted to verify the effect of knockdown of KLF3 on tumor metastasis in animals. Results: In breast cancer cells, knockdown of KLF3 promoted STAT3 protein expression. The mRNA level of STAT3 was increased by (3.58±0.65) fold after knockdown of KLF3 in MDA-MB-231 cells, while the mRNA level of STAT3 was increased by (2.28±0.19) fold after KLF3 knockdown in MCF-7 cells (P<0.001). KLF3 boundto the promoter region of STAT3. The transcriptional activity of STAT3 increased by (2.47±0.87) fold after knockdown of KLF3 in MDA-MB-231 cells, while the transcriptional activity of STAT3 increased by (2.63±0.65) fold after KLF3 knockdown in MCF-7 cells, P<0.01. KLF3 knockdown inhibitedthe movement,migrate and invade of breast cancer cells. Based on this, silence STAT3 partially reversed the function of KLF3. Knockdown of KLF3 promotedtumor metastasis in mice. Conclusions: KLF3 knockdown can promote the transcriptional activity of STAT3, which promotes the protein expression of the latter. KLF3 can affect the movement, migration and invasion of breast cancer cells through STAT3. KLF3 may be a potential target for the treatment of metastatic breast cancer.

[The effect of extending proximal landing zone in thoracic endovascular aortic repair on the prognosis of Stanford type B aortic dissection].

With the continuous development of endovascular surgery, thoracic endovascular aortic repair (TEVAR) has gradually replaced traditional open surgery and has become the preferred treatment strategy for Stanford type B aortic dissection. However, the disadvantage of the short proximal landing zone greatly limited the indication of TEVAR surgery and affected the prognosis. In recent years, many strategies such as hybrid surgery, in vitro fenestrated and branched aortic endo-graft, chimney technique, in-situ fenestration technique, etc., have been developed, which greatly broadens the TEVAR indication and improved the prognosis.

Transplantation of RADA16-BDNF peptide scaffold with human umbilical cord mesenchymal stem cells forced with CXCR4 and activated astrocytes for repair of traumatic brain injury.

Due to the poor self-regeneration of brain tissue, stem cell transplantation therapy is purported to enable the replacement of lost neurons after traumatic brain injury (TBI). The main challenge of brain regeneration is whether the transplanted cells can survive and carry out neuronal functions in the lesion area. The brain is a complex neuronal network consisting of various types of cells that significantly influence on each other, and the survival of the implanted stem cells in brain is critically influenced by the surrounding cells. Although stem cell-based therapy is developing rapidly, most previous studies just focus on apply single type of stem cells as cell source. Here, we found that co-culturing human umbilical cord mesenchymal stem cells (hUC-MSCs) directly with the activated astrocytes benefited to the proliferation and neuron differentiation of hUC-MSCs in vitro. In this study, hUC-MSCs and the activated astrocytes were seeded in RADA16-BDNF peptide scaffold (R-B-SPH scaffold), a specifical self-assembling peptide hydrogel, in which the environment promoted the differentiation of typical neuron-like cells with neurites extending in three-dimensional directions. Moreover, the results showed co-culture of hUC-MSCs and activated astrocytes promoted more BDNF secretion which may benefit to both neural differentiation of ectogenic hUC-MSCs and endogenic neurogenesis. In order to promote migration of the transplanted hUC-MSCs to the host brain, the hUC-MSCs were forced with CXC chemokine receptor 4 (CXCR4). We found that the moderate-sized lesion cavity, but not the large cavity caused by TBI was repaired via the transplantation of hUC-MSCsCXCR4 and activated astrocytes embedded in R-B-SPH scaffolds. The functional neural repair for TBI demonstrated in this study is mainly due to the transplantation system of double cells, hUC-MSCs and activated astrocytes. We believe that this novel cell transplantation system offers a promising treatment option for cell replacement therapy for TBI. STATEMENT OF SIGNIFICANCE: In this reach, we specifically linked RGIDKRHWNSQ, a functional peptide derived from BDNF, to the C-terminal of RADARADARADARADA (RADA16) to structure a functional self-assembling peptide hydrogel scaffold, RADA16-BDNF (R-B-SPH scaffold) for the better transplantation of the double cell unit. Also, the novel scaffold was used as cell-carrier for transplantation double cell unit (hUC-MSCs/astrocyte) for treating traumatic brain injury. The results of this study showing that R-B-SPH scaffold was pliancy and flexibility to fit the brain lesion cavity and promotes the outgrowth of axons and dendrites of the neurons derived from hUC-MSCs in vitro and in vivo, indicating the 3D R-B-SPH scaffold provided a suitable microenvironment for hUC-MSC survival, proliferation and differentiation. Also, our results showing the double-cells transplantation system (hUC-MSCs/astrocyte) may be a novel cell-based therapeutic strategy for neuroregeneration after TBI with potential value for clinical application.

Central obesity and risks of pre- and postmenopausal breast cancer: a dose-response meta-analysis of prospective studies.

Epidemiologic evidence has shown inconsistent findings regarding the relationships between abdominal fatness, as measured by waist circumferences (WC) or waist-to-hip ratio (WHR), and risks of pre- and postmenopausal breast cancer (BC). A dose-response meta-analysis of prospective studies was conducted to address these issues. Potentially eligible studies were identified by searching PubMed and EMBASE databases, and by carefully reviewing the bibliographies of retrieved publications and related reviews. The summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated using a random-effects model. When the most fully adjusted RRs were combined, both WC (14 studies, RR per 10-cm increase = 1.06, 95% CI: 1.04-1.09, I2 = 29.9%) and WHR (15 studies, RR per 0.1-unit increase = 1.07, 95% CI: 1.01-1.14, I2 = 52.9%) were significantly positively associated with postmenopausal BC, but neither WC (eight studies, RR per 10-cm increase = 1.05, 95% CI: 0.99-1.10, I2 = 0%) nor WHR (11 studies, RR per 0.1-unit increase = 1.07, 95% CI: 0.95-1.21, I2 = 59.7%) were associated with premenopausal BC. The WHR-postmenopausal BC association lost statistical significance after correcting publication bias (RR per 0.1-unit increase = 1.06, 95% CI: 0.99-1.13). When considering BMI-adjusted RRs, WC was associated with both pre- (five studies, RR per 10-cm increase = 1.09, 95% CI: 1.02-1.16, I2 = 0%) and postmenopausal BC (seven studies, RR per 10-cm increase = 1.05, 95% CI: 1.02-1.08, I2 = 6.3%), whereas WHR was not associated with either pre- (seven studies, RR per 0.1-unit increase = 1.12, 95% CI: 0.94-1.34, I2 = 70.9%) or postmenopausal BC (eight studies, RR per 0.1-unit increase = 1.05, 95% CI: 0.98-1.13, I2 = 57.3%). Among non-current (former or never) users of hormone replacement therapy, the summary RR per 10-cm increase of postmenopausal BC associated with WC was 1.08 (95% CI: 1.03-1.05, I2 = 69.2%, seven studies; BMI-adjusted RR = 1.05, 95% CI: 1.02-1.09, I2 = 22.8%, four studies). This meta-analysis indicates that central obesity measured by WC, but not by WHR, is associated with modestly increased risks of both pre- and postmenopausal BC independent of general obesity.