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The vertebral endplate forms a structural boundary between intervertebral disc and the trabecular bone of the vertebral body. As a mechanical interface between the stiff bone and resilient disc, the endplate is the weakest portion of the vertebral-disc complex and is predisposed to mechanical failure. However, the literature concerning the bone mineral density (BMD) distribution within the spinal endplate is comparatively sparse. The objective of this study is to investigate the three-dimensional (3D) distribution of computed tomography (CT) attenuation across the lumbosacral endplate measured in Hounsfield Units (HU). A total of 308 endplates from 28 cadaveric fresh-frozen lumbosacral spines were used in this study. Each spine was CT-scanned and the resulting DICOM data was used to obtain HU values of the bone endplate. Each individual endplate surface was subdivided into five clinically-relevant topographic zones. Attenuation was analyzed by spinal levels, sites (superior or inferior endplate) and endplate region. The highest HU values were found at the S1 endplate. Comparisons between the superior and inferior endplates showed the HU values in inferior endplates were significantly higher than those in the superior endplates within the same vertebra and the HU values in endplates cranial to the disc were significantly higher than those in the endplates caudal to the disc within the same disc. Attenuation in the peripheral region was significantly higher than in the central region by 32.5%. Regional comparison within the peripheral region showed the HU values in the posterior region were significantly higher than those in the anterior region and the HU values in the left region were significantly higher than those in the right region. This study provided detailed data on the regional HU distribution across the lumbosacral endplate, which can be useful to understand causes of some endplate lesions, such as fracture, and also to design interbody instrumentation. [ABSTRACT FROM AUTHOR]

Aim Adhesion after pelvic surgery causes infertility, ectopic pregnancy, and ileus or abdominal pain. The materials currently available for clinical use are insufficient. The purpose of this study was to develop an anti-adhesive material that overcomes the limitations of conventional anti-adhesive agents. Methods The adhesion prevention effects of three methods - a two-layered sheet composed of gelatin film and gelatin sponge, Seprafilm and INTERCEED - were evaluated in 37 dogs. Anti-adhesive effects were investigated macroscopically and microscopically in a cauterized uterus adhesion model. Cell growth on the materials in vitro using human peritoneal mesothelial cells, fibroblasts and uterine smooth muscle cells were also evaluated. Results The two-layered gelatin sheet had significantly superior anti-adhesive effects compared to the conventional materials (Seprafilm and INTERCEED). A single-cell layer of mature mesothelium formed three weeks after surgery in the gelatin group. Peritoneum regeneration in the Seprafilm and INTERCEED groups was delayed and incomplete in the early phase. Little inflammation around the materials occurred and cell growth was significantly proliferated with the gelatin sheet. Conclusion The anti-adhesive effects of a two-layered gelatin sheet were superior to conventional agents in a cauterized canine uterus model, demonstrating early regeneration of the peritoneum, little inflammation and material endurance. The newly developed two-layered gelatin sheet is a useful option as an anti-adhesive agent for deeply injured and hemorrhagic sites. [ABSTRACT FROM AUTHOR]

Postoperative intra-abdominal or intrathoracic adhesions sometimes cause significant morbidity. We have designed three types of alginate-based treatments using strongly cross-linked (SL), weakly cross-linked (WL), and non-cross-linked (NL) alginate with calcium gluconate. In rat experiments, we compared the antiadhesive effects of the three types of alginate-based treatments, fibrin glue treatment (a standard treatment), and no treatment against adhesions caused by polyglycolic acid (PGA) mesh (PGA-induced adhesions). The antiadhesive materials were set on the PGA sheet fixed on the parietal peritoneum of the abdomen. Fifty-six days later, the adhesions were evaluated macroscopically by the adhesion scores and microscopically by hematoxylin-eosin staining and immunostaining. We also tested the fibroblast growth on the surface of the antiadhesive materials in vitro. The antiadhesive effects of WL and NL were superior to the no treatment and fibrin glue treatment. A microscopic evaluation confirmed that the PGA sheet was covered by a peritoneal layer constructed of well-differentiated mesothelial cells, and the inflammation was most improved in the NL and WL. The fibroblast growth was inhibited most on the surfaces of the NL and WL. These results suggest that either the WL or NL treatments are suitable for preventing PGA-induced adhesions compared to SL or the conventional treatment. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a global pandemic. The prevalence/severity of COVID-19 is higher among patients with cardiovascular risk factors. Despite the expression of angiotensin-converting enzyme 2 (ACE2), a receptor for SARS-CoV-2 infection, in cardiomyocytes, there has been no conclusive evidence of direct viral infection although the presence of viral genome within COVID-19 patients' hearts has been reported. Here, we overexpressed SARS-CoV-2 genes in A549 lung epithelial cells. We then isolated extracellular vesicles (EVs) and detected the presence of viral RNA within these EVs. We observed that human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) are receptive to these EVs, and viral genes were detectable in the cardiomyocytes. Accordingly, the uptake of viral RNA-harboring EVs led to an upregulation of inflammation-related genes in hiPSC-CMs. Thus, our findings indicate that SARS-CoV-2 RNA containing EVs represents an indirect route of viral RNA entry into cardiomyocytes. [ABSTRACT FROM AUTHOR]