Titanium net (meshes) with excellent mechanical properties can promote bone compatibility and has been used as a repairing material for bone defects in clinical settings. In the present study, using spiral computed tomography (CT) and histomorphological techniques, we investigated the effect of a novel kind of titanium web with a three-dimensional (3D) porous structure on bone formation in rabbit skull (os parietal) defect. The images from the spiral CT scan demonstrate that the titanium web is completely fused with the surrounding bone tissue, even at the first month after implantation. The histomorphological findings show that different cells and tissues, including osseous tissue, connective tissue, and adipose cells, can easily grow into the 3D scaffold meshes of the titanium web, even in the center of the web and combine together as a whole body, suggesting that the titanium web possesses a very good biocompatibility, which is beneficial to the growth of bone tissue and promotes healing of the defected rabbit skull.

Ionic liquids (ILs) have elicited attention due to their unique properties. ILs may pose environmental risks to aquatic ecosystems once released into water during generation and application. Therefore, the toxic and antimicrobial properties of ILs should be analysed. This study aims to evaluate the cytotoxicity of 1-octyl-3-methylimidazolium chloride ([C8mim] [Cl]) on Escherichia coli DH5α by MTT (3-[4,5-dimethylthiazol-2yl]-2,5 diphenyl tetrazolium bromide) assay, and to determine the effect of [C8mim] [Cl] on the replication and membrane permeability of E. coli DH5α. The results showed that [C8mim] [Cl] decreased cell viability and inhibited bacterial cell replication. [C8mim] [Cl] increased protein and nucleic acid contents in the extracellular fluid, damaged the cell membrane, and increased membrane permeability. The increase of cell membrane permeability induced by [C8mim] [Cl] could be the cause of decreased cell viability and replication.

ABSTRACT. We investigated the expression and distribution of N-cadherin during the development of a rat heart. Immunohistochemistry (IHC) was performed to detect the expression and distribution of N-cadherin in the myocardial tissues of rats at embryonic day 18 (E18d), postnatal day 5 (P5d), postnatal day 19 (P19d), postnatal day 40 (P40d), and postnatal year 1 (P1y). Reverse transcription polymerase chain reaction was used to determine mRNA expression levels of N-cadherin in the myocardial tissues at E18d, P5d, P19d, P40d, and P1y. The IHC results showed that at E18d N-cadherin was dispersedly distributed both on the cell surface and in the cytoplasm of the myocardial cells, and gradually became concentrated at the end-to-end intercalated discs of the cardiomyocytes from birth through immaturity. In the young, middle-aged, and old rats, N-cadherin was typically distributed at the (2015) intercalated discs at the end of the myocardial cells. No significant differences in the mRNA expression levels of N-cadherin were detected in the myocardial tissue of rats at E18d, P5d, P19d, P40d, and P1y. During the development of the rat heart, observable changes in the distribution of N-cadherin occurred in the myocardial tissues, but there were no detectable changes in the expression of N-cadherin, indicating that N-cadherin is indispensable to maintaining the physical structure and function of the heart.

A chimeric plasmin‑resistant vascular endothelial growth factor (VEGF)165/VEGF183 (132-158) protein, named as VEGF183 (according to the nomenclature of VEGF), designed by a previous study, was demonstrated to have an enhanced affinity for the extracellular matrix (ECM) amongst other bioactivities. However, it is now accepted that mutant VEGFs frequently demonstrate different angiogenic activities and produce different vascular patterning from the parental molecule. The present study hypothesized that VEGF183, due to its enhanced binding affinity to the ECM, would exhibit a different angiogenic activity and produce a different vascular patterning compared to those of VEGF165. Murine breast cancer EMT‑6 cells were manipulated to stably overexpress VEGF165 or VEGF183. These cells were then inoculated intradermally into BALB/c mice in order to monitor the formation of vascular patterning in skin proximal to tumors. In vivo angiogenesis experiments revealed that overexpression of VEGF183 in murine breast cancer cells resulted in irregular, disorganized and dense vascular patterning as well as induced a significant inhibition of tumor growth compared with that of VEGF165. In addition, allograft tumor immunochemical assays of VEGF183‑overexpressing tumors demonstrated significantly lower vascular densities than those of VEGF165‑overexpressing tumors; however, VEGF183 tumors had a significantly enlarged vascular caliber. Conversely, cell wound healing experiments revealed that VEGF183‑overexpressing EMT‑6 cells had significantly decreased migration rates compared with those of VEGF165‑overexpressing EMT‑6 cells. In conclusion, the results of the present study supported the hypothesis that the altered ECM affinity of VEGF induced structural alterations to vasculature. In addition, these results provided a novel insight into VEGF design and indirect evidence for the function of exon 8 in VEGF. [Corrected]

The aim of the present study was to examine the expression of N-cadherin in the myocardial tissues of isoproterenol-induced myocardial hypertrophy in rats. In addition, the present study provided morphological data to investigate the signal transduction mechanisms of myocardial hypertrophy and reverse myocardial hypertrophy. A myocardial hypertrophy model was established by subcutaneously injecting isoprenaline into healthy adult Sprague-Dawley rats. The myocardial tissue was collected, embedded in conventional paraffin, sectioned and stained with hematoxylin and the pathological changes were observed. The expression and distribution of N-cadherin were detected by immunohistochemistry (IHC) and the changes in mRNA expression of N-cadherin in the myocardial tissues of rats were detected by reverse transcription polymerase chain reaction. Image analysis software was used to quantitatively analyze the expression of N-cadherin. The IHC and immunofluorescence results showed that there was no statistically significant difference between the experimental and control groups in the positive expression of N-cadherin. Furthermore, mRNA expression of N-cadherin, in the myocardial tissues of rats, was consistent with the IHC and immunofluorescence results. Thus, N-cadherin may have a significant function in the occurrence and development of myocardial hypertrophy.