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Enrofloxacin (ENFX) has a broad-spectrum antibiotic activity, which is widely used in aquaculture. The effect of different ENFX exposure ways on the gut microbiota of tilapia is unclear. This study was conducted to investigate the effects of ENFX exposure on the gut microbiota of tilapia fish (Oreochromis niloticus). Three methods of ENFX exposure were selected: injection (IEG), oral administration (OEG) and soaking (SEG). After 48 h of exposure period, the intestine of tilapia was collected for high-throughput sequencing. PCoA analysis revealed a distinct clustering of control group, and which was located rather far away from ENFX exposure groups. The dominant phyla in the gut microbiota of tilapia fish were Proteobacteria , Actinobacteriota , Fusobacteria and Firmicutes. Compared to the control group, phylum Fusobacteriota was increased in SEG and IEG while decreased in OEG. ENFX treatment led to a decline in Corynebacterium , Clostridium sensu stricto_3 and Bacillus in treated fish compared with control fish, accompanied by an increase in Akkermansia , Ralstonia and Romboutsia. IEG had the least effect on gut microbiota of tilapia because it retained more microbes among treatment groups. Alpha- diversity decreased the most in SEG, but retained more probiotics such as Cetobacterium and Akkermansia. We assessed the effect of enrofloxacin on tilapia by changes in intestinal flora. The result indicated that either exposure method significantly reduced the diversity of tilapia gut microbiota. It may provide basic data for the scientific use of ENFX in aquaculture. [Display omitted] • Exposure of ENFX markly reduced the diversity of intestinal microflora in tilapia. • Injection groups had the least effect on gut microbiota of tilapia. • The soaking group retained more probiotic. [ABSTRACT FROM AUTHOR]

Type 1 diabetes mellitus (T1DM) patients have osteopenia and impaired fracture healing due to decreased osteoblast activity. Further, no adequate treatments are currently available that can restore impaired healing in T1DM; hence a significant need exists to investigate new therapeutics for treatment of orthopedic complications. Sclerostin (SOST), a WNT antagonist, negatively regulates bone formation, and SostAb is a potent bone anabolic agent. To determine whether SOST antibody (SostAb) treatment improves fracture healing in streptozotocin (STZ) induced T1DM mice, we administered SostAb twice weekly for up to 21 days post-fracture, and examined bone quality and callus outcomes at 21 days and 42 days post-fracture (11 and 14 weeks of age, respectively). Here we show that SostAb treatment improves bone parameters; these improvements persist after cessation of antibody treatment. Markers of osteoblast differentiation such as Runx2, collagen I, osteocalcin, and DMP1 were reduced, while an abundant number of SP7/osterix-positive early osteoblasts were observed on the bone surface of STZ calluses. These results suggest that STZ calluses have poor osteogenesis resulting from failure of osteoblasts to fully differentiate and produce mineralized matrix, which produces a less mineralized callus. SostAb treatment enhanced fracture healing in both normal and STZ groups, and in STZ + SostAb mice, also reversed the lower mineralization seen in S TZ calluses. Micro-CT analysis of calluses revealed improved bone parameters with SostAb treatment, and the mineralized bone was comparable to Controls . Additionally, we found sclerostin levels to be elevated in STZ mice and β-catenin activity to be reduced. Consistent with its function as a WNT antagonist, SostAb treatment enhanced β-catenin activity, but also increased the levels of SOST in the callus and in circulation. Our results indicate that SostAb treatment rescues the impaired osteogenesis seen in the STZ induced T1DM fracture model by facilitating osteoblast differentiation and mineralization of bone. [ABSTRACT FROM AUTHOR]

Abstract: Short durations of extremely small magnitude, high-frequency, mechanical stimuli can promote anabolic activity in the adult skeleton. Here, it is determined if such signals can influence trabecular and cortical formative and resorptive activity in the growing skeleton, if the newly formed bone is of high quality, and if the insertion of rest periods during the loading phase would enhance the efficacy of the mechanical regimen. Eight-week-old female BALB/cByJ mice were divided into four groups, baseline control (n = 8), age-matched control (n = 10), whole-body vibration (WBV) at 45 Hz (0.3 g) for 15 min day−1 (n = 10), and WBV that were interrupted every second by 10 of rest (WBV-R, n = 10). In vivo strain gaging of two additional mice indicated that the mechanical signal induced strain oscillations of approximately 10 microstrain on the periosteal surface of the proximal tibia. After 3 weeks of WBV, applied for 15 min each day, osteoclastic activity in the trabecular metaphysis and epiphysis of the tibia was 33% and 31% lower (P <0.05) than in age-matched controls. Bone formation rates (BFR·BS−1) on the endocortical surface of the metaphysis were 30% greater (P <0.05) in WBV than in age-matched control mice but trabecular and middiaphyseal BFR were not significantly altered. The insertion of rest periods (WBV-R) failed to potentiate the cellular effects. Three weeks of either WBV or WBV-R did not negatively influence body mass, bone length, or chemical bone matrix properties of the tibia. These data indicate that in the growing skeleton, short daily periods of extremely small, high-frequency mechanical signals can inhibit trabecular bone resorption, site specifically attenuate the declining levels of bone formation, and maintain a high level of matrix quality. If WBV prove to be efficacious in the growing human skeleton, they may be able to provide the basis for a non-pharmacological and safe means to increase peak bone mass and, ultimately, reduce the incidence of osteoporosis or stress fractures later in life. [Copyright &y& Elsevier]

Both E. coli and S. aureus growed well on pure GO coating, but were significantly inhibited on GO-Cu coating. Therefore, the prepared GO-Cu and GO-Cu-GO coatings have great development potential in antibacterial coatings such as implant surface coating applications. [Display omitted] • The synthesis of GO-Cu coatings was prepared sing a spin-coating and chemical in-situ formation method. • Both E. coli and S. aureus were significantly inhibited on GO-Cu coating. • Cu-GO has good biocompatibility in the form of coating materials. Recently, graphene oxide (GO)-based materials have shown great potential as coatings for implant surfaces owing to their biocompatibility, surface functionalisation, and antibacterial activity. However, there is some disagreement regarding the antibacterial effect of GO, particularly when GO is used in the form of coatings. In this study, for the first time, we demonstrate the synthesis of copper-decorated GO (GO-Cu) coatings using a spin coating and chemical in-situ method. The growth of Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) on GO-Cu and pure GO coatings was compared via systematic antibacterial study. The results showed that both E. coli and S. aureus grew well on the pure GO coating, but their growth was significantly inhibited on the GO-Cu coating. In addition, bone mesenchymal stem cell (BMSC) adhesion, viability, and proliferation tests indicated that the two GO-based coatings did not show obvious toxicity compared with the SiO 2 control. The combined antibacterial performance and good biocompatibility of the GO-Cu coatings indicates their significant potential for application in biomedical implants. [ABSTRACT FROM AUTHOR]

Loss of Sostdc1, a growth factor paralogous to Sost, causes the formation of ectopic incisors, fused molars, abnormal hair follicles, and resistance to kidney disease. Sostdc1 is expressed in the periosteum, a source of osteoblasts, fibroblasts and mesenchymal progenitor cells, which are critically important for fracture repair. Here, we investigated the role of Sostdc1 in bone metabolism and fracture repair. Mice lacking Sostdc1 ( Sostdc1 − / − ) had a low bone mass phenotype associated with loss of trabecular bone in both lumbar vertebrae and in the appendicular skeleton. In contrast, Sostdc1 − / − cortical bone measurements revealed larger bones with higher BMD, suggesting that Sostdc1 exerts differential effects on cortical and trabecular bone. Mid-diaphyseal femoral fractures induced in Sostdc1 − / − mice showed that the periosteal population normally positive for Sostdc1 rapidly expands during periosteal thickening and these cells migrate into the fracture callus at 3 days post fracture. Quantitative analysis of mesenchymal stem cell (MSC) and osteoblast populations determined that MSCs express Sostdc1 , and that Sostdc1 − / − 5 day calluses harbor > 2-fold more MSCs than fractured wildtype controls. Histologically a fraction of Sostdc1 -positive cells also expressed nestin and α-smooth muscle actin, suggesting that Sostdc1 marks a population of osteochondral progenitor cells that actively participate in callus formation and bone repair. Elevated numbers of MSCs in D5 calluses resulted in a larger, more vascularized cartilage callus at day 7, and a more rapid turnover of cartilage with significantly more remodeled bone and a thicker cortical shell at 21 days post fracture. These data support accelerated or enhanced bone formation/remodeling of the callus in Sostdc1 − / − mice, suggesting that Sostdc1 may promote and maintain mesenchymal stem cell quiescence in the periosteum. [ABSTRACT FROM AUTHOR]

Abstract: The hollow Fe3O4/poly (lactic-co-glycolic acid) (PLGA) composite microspheres have been successfully prepared via emulsion–solvent evaporation method. The composite microspheres exhibited superparamagnetism, good magnetic response and narrow size distribution. The composite microspheres could assemble into linear aligned arrays under an ultra-low magnetic field. Once the ultra-low magnetic field was removed, the linear assemblies could be easily re-dispersed in aqueous solution to recover to the assembly units, namely the Fe3O4/PLGA composite microspheres. Such reversibly transformational morphologies between the linear assemblies and the assembly units would contribute to giving full play to the functions of the material. [Copyright &y& Elsevier]

Heterotopic ossification (HO), the formation of ectopic bone in soft tissues, has been extensively studied in its two primary forms: post-traumatic HO (tHO) typically found in patients who have experienced musculoskeletal or neurogenic injury and in fibrodysplasia ossificans progressiva (FOP), where it is genetically driven. Given that in both diseases HO arises via endochondral ossification, the molecular mechanisms behind both diseases have been postulated to be manifestations of similar pathways including those activated by BMP/TGFβ superfamily ligands. A significant step towards understanding the molecular mechanism by which HO arises in FOP was the discovery that FOP causing ACVR1 variants trigger HO in response to activin A, a ligand that does not activate signaling from wild type ACVR1, and that is not inherently osteogenic in wild type settings. The physiological significance of this finding was demonstrated by showing that activin A neutralizing antibodies stop HO in two different genetically accurate mouse models of FOP. In order to explore the role of activin A in tHO, we performed single cell RNA sequencing and compared the expression of activin A as well as other BMP pathway genes in tHO and FOP HO. We show that activin A is expressed in response to injury in both settings, but by different types of cells. Given that wild type ACVR1 does not transduce signal when engaged by activin A, we hypothesized that inhibition of activin A will not block tHO. Nonetheless, as activin A was expressed in tHO lesions, we tested its inhibition and compared it with inhibition of BMPs. We show here that anti-activin A does not block tHO, whereas agents such as antibodies that neutralize ACVR1 or ALK3-Fc (which blocks osteogenic BMPs) are beneficial, though not completely curative. These results demonstrate that inhibition of activin A should not be considered as a therapeutic strategy for ameliorating tHO. [ABSTRACT FROM AUTHOR]