Surface-structured bacterial cellulose loaded with hUSCs accelerate skin wound healing by promoting angiogenesis in rats.

Promotion of wound healing is one of the most important fields in clinical medical research. This study aimed to evaluate the potential use of a new surface-structured bacterial cellulose(S-BC) biomaterial with human urine-derived stem cells (hUSCs) for wound healing. In vitro, EA.hy926 were inoculated on structured/non-structured bacterial cellulose, and the growth of EA.hy926 on bacterial cellulose in medium with/without conditioned medium of the hUSCs were observed to explore the effect of bacterial cellulose's surface structure and hUSCs-CM on vascular endothelial cell growth. In vivo, we covered wound surface with various BC materials and/or injected the hUSCs into the wound site on group BC, group S-BC, group hUSCs, group BC + hUSCs, group S-BC + hUSCs to evaluate the effect of S-BC and hUSCs on wound healing in rat full-thickness skin defect model. In vitro study, surface structure of S-BC could promote the growth and survival of EA.hy926, and the hUSCs-CM could further promote the proliferation of EA.hy926 on S-BC. In vivo study, wound healing rate of the group BC, group S-BC, group hUSCs was significantly accelerated, accompanied by faster re-epithelialization, collagen production and neovascularization than control group. It is note worthy that the effect of S-BC on wound healing was better than BC, the effect of S-BC + hUSCs on wound healing was better than BC + hUSCs. Moreover, the effect of S-BC combined with hUSCs on wound is better than treated with S-BC or hUSCs alone. All the findings suggest that the combination of S-BC and hUSCs could facilitate skin wound healing by promoting angiogenesis. This combination of the role of stem cells and biomaterial surface structures may provide a new way to address clinical wound healing problems.

Ratios of biochemical markers in peritoneal fluid to those in venous blood for the diagnosis of ruptured tubal pregnancy: A prospective study.

OBJECTIVES: Ectopic pregnancies are among the leading causes of maternal morbidity and mortality in both developed and emerging nations, but tests for early, accurate, and convenient detection are lacking. STUDY DESIGN: Between January 2013 and February 2015, 504 women with tubal pregnancy were prospectively recruited, and their clinical characteristics were recorded. Samples of peritoneal fluid were collected by culdocentesis, and venous blood was drawn from the antecubital vein. In samples from each source, levels of the following biochemical markers were measured: cancer antigen 125 (CA125), human chorionic gonadotropin (hCG), progesterone, vascular endothelial growth factor, and creatine kinase. RESULTS: The ratios of biochemical markers in the peritoneal fluid and in the blood (Rp/v) were calculated. The median of Rp/v-CA125 and Rp/v-hCG were significantly lower in the ruptured ectopic pregnancy group than in the unruptured group. The optimal cutoff value to detect ectopic pregnancy rupture was 401.5U/mL as the upper limit for peritoneal CA125, with a sensitivity of 93.5% and specificity of 74.2%. The optimal cutoff value was 18.7 as the upper limit in the peritoneal fluid/blood ratio (Rp/v) of CA125, with a sensitivity of 77.5% and specificity of 68.4%. CONCLUSIONS: In countries with poor access to laparoscopy, culdocentesis is useful. In this study, culdocentesis provided additional information for management of abdominal pain when laparoscopy is not available. The authors propose Rp/v cutoff values that can be used conveniently and quickly to diagnose ruptured ectopic pregnancies and bleeding, enabling rapid and appropriate therapeutic responses.

RelB/NF-κB links cell cycle transition and apoptosis to endometrioid adenocarcinoma tumorigenesis.

Dysfunction of nuclear factor-κB (NF-κB) signaling has been causally associated with numerous human malignancies. Although the NF-κB family of genes has been implicated in endometrial carcinogenesis, information regarding the involvement of central regulators of NF-κB signaling in human endometrial cancer (EC) is limited. Here, we investigated the specific roles of canonical and noncanonical NF-κB signaling in endometrial tumorigenesis. We found that NF-κB RelB protein, but not RelA, displayed high expression in EC samples and cell lines, with predominant elevation in endometrioid adenocarcinoma (EEC). Moreover, tumor cell-intrinsic RelB was responsible for the abundant levels of c-Myc, cyclin D1, Bcl-2 and Bcl-xL, which are key regulators of cell cycle transition, apoptosis and proliferation in EEC. In contrast, p27 expression was enhanced by RelB depletion. Thus, increased RelB in human EC is associated with enhanced EEC cell growth, leading to endometrial cell tumorigenicity. Our results reveal that regulatory RelB in noncanonical NF-κB signaling may serve as a therapeutic target to block EC initiation.