In vivo study on osteogenic efficiency of nHA/ gel porous scaffold with nacre water-soluble matrix.

BACKGROUND/PURPOSE: Nano-hydroxyapatite (nHA)/ gel porous scaffolds loaded with WSM carriers are promising bone replacement materials that can improve osseointegration ability. This investigation aimed to evaluate the osteoinductive activity by implanting the composition of nano-hydroxyapatite (nHA)/ Gel porous scaffolds as a carrier of WSM via an animal model. MATERIALS AND METHODS: WSM was extracted and nHA was added to the matrix to construct porous composite scaffolds. The dose-effect curve of WSM concentration and alkaline phosphatase (ALP) activity was made by culturing rat osteoblasts and examining the absorbance. Three different materials were implanted into critical size defects (CSD) in the skulls of rats, which were further divided into four groups: WSM nHA /Gel group, n-WSM nHA /Gel group, HA powder group, and control group. RESULTS: WSM (150 µg/mL-250µg/mL) effectively improved the activity of ALP in rat osteoblasts. All rats in each group had normal healing. WSM-loaded nHA /Gel group showed better performance on newly-formed bone tissue of rat skull and back at 4th week and 8th week, respectively. At the 4th week, the network of woven bone formed in the WSM-loaded nHA/Gel scaffold material. At 8th week, the reticular trabecular bone in the WSM-loaded scaffold material became dense lamellar bone, and the defect was mature lamellar bone. In the subcutaneous implantation experiment, WSM-loaded nHA/Gel scaffold material showed a better performance of heterotopic ossification than the pure nHA/Gel scaffold material. CONCLUSION: WSM promotes osteoblast differentiation and bone mineralization. The results confirm that the nHA/ Gel Porous Scaffold with Nacre Water-Soluble Matrix has a significant bone promoting effect and can be used as a choice for tissue engineering to repair bone defects.

Clinical benefits of therapeutic drug monitoring of vancomycin therapy in patients with postoperative intracerebral hemorrhage: a retrospective cohort study.

OBJECTIVE: The objective of this study was to investigate the clinical efficacy and safety of conducting therapeutic drug monitoring (TDM) of vancomycin in patients with postoperative intracerebral haemorrhage. METHODS: We conducted a retrospective analysis of 435 patients who experienced postoperative cerebral haemorrhage and were treated with vancomycin in the Department of Neurosurgery of Inner Mongolia Autonomous Region People's Hospital from January 2017 to December 2021. Patients were then matched using the propensity score matching method in a ratio of 1:1. Ninety-two pairs of cases were successfully matched, and the data before and after performing vancomycin TDM were analysed. RESULTS: After PSM, the baseline data of the two groups were balanced. There were no significant differences in the 14-day mortality and length of hospital stay (p>0.05) between the two groups. Compared with the non-TDM group, the TDM group had a higher proportion of patients with normal white blood cells (83.7% vs 56.5%, p=0.000), neutrophil count (57.6% vs 25.0%, p=0.000) and attaining desirable reductions of 80% in procalcitonin (65.2% vs 10.9%, p=0.000) and C-reactive protein (78.3% vs 41.3%, p=0.000) levels. At US$15.82 per additional TDM, TDM significantly promoted patient outcomes, as seen in improvements in the proportion of patients attaining desirable levels of white blood cells, neutrophil count, procalcitonin and C-reactive protein. CONCLUSIONS: Vancomycin TDM is a safe and effective approach for the treatment of patients with postoperative intracerebral haemorrhage. The empirical use of TDM of vancomycin significantly improved normal values of white blood cells and neutrophil count, achieved desirable reductions of 80% in procalcitonin and C-reactive protein, and reduced nephrotoxicity in patients with postoperative intracerebral haemorrhage.

Modulation of ovine SBD-1 expression by Saccharomyces cerevisiae in ovine ruminal epithelial cells.

BACKGROUND: The ovine rumen is involved in host defense responses and acts as the immune interface with the environment. The ruminal mucosal epithelium plays an important role in innate immunity and secretes antimicrobial innate immune molecules that have bactericidal activity against a variety of pathogens. Defensins are cationic peptides that are produced by the mucosal epithelia and have broad-spectrum antimicrobial activity. Sheep ß-defensin-1 (SBD-1) is one of the most important antibacterial peptides in the rumen. The expression of SBD-1 is regulated by the probiotic, Saccharomyces cerevisiae (S.c); however, the regulatory mechanism has not yet been elucidated. In the current study, the effects of S.c on the expression and secretion of SBD-1 in ovine ruminal epithelial cells were investigated using quantitative real-time PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA). In addition, specific inhibitors were used to block the nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB), p38, JNK, and ERK1/2 signalling pathways separately or simultaneously, to determine the regulatory mechanism(s) governing S.c-induced SBD-1 upregulation. RESULTS: Incubation with S.c induced release of SBD-1 by ovine ruminal epithelial cells, with SBD-1 expression peaking after 12 h of incubation. The highest SBD-1 expression levels were achieved after treatment with 5.2 × 107 CFU∙mL- 1 S.c. Treatment with S.c resulted in significantly increased NF-κB, p38, JNK, ERK1/2, TLR2, and MyD88 mRNA expression. Whereas inhibition of mitogen-activated protein kinases (MAPKs) and NF-κB gene expression led to a decrease in SBD-1 expression. CONCLUSIONS: S.c was induced SBD-1 expression and the S.c-induced up-regulation of SBD-1 expression may be related to TLR2 and MyD88 in ovine ruminal epithelial cells. This is likely simultaneously regulated by the MAPKs and NF-κB pathways with the p38 axis of the MAPKs pathway acting as the primary regulator. Thus, the pathways regulating S.c-induced SBD-1 expression may be related to TLR2-MyD88-NF-κB/MAPKs, with the TLR2-MyD88-p38 component of the TLR2-MyD88-MAPKs signalling acting as the main pathway.