Empowering high-dimensional optical fiber communications with integrated photonic processors.

Mode-division multiplexing (MDM) in optical fibers enables multichannel capabilities for various applications, including data transmission, quantum networks, imaging, and sensing. However, high-dimensional optical fiber systems, usually necessity bulk-optics approaches for launching different orthogonal fiber modes into the optical fiber, and multiple-input multiple-output digital electronic signal processing at the receiver to undo the arbitrary mode scrambling introduced by coupling and transmission in a multi-mode fiber. Here we show that a high-dimensional optical fiber communication system can be implemented by a reconfigurable integrated photonic processor, featuring kernels of multichannel mode multiplexing transmitter and all-optical descrambling receiver. Effective mode management can be achieved through the configuration of the integrated optical mesh. Inter-chip MDM optical communications involving six spatial- and polarization modes was realized, despite the presence of unknown mode mixing and polarization rotation in the circular-core optical fiber. The proposed photonic integration approach holds promising prospects for future space-division multiplexing applications.

Clinical effects of 3D printing-assisted posterolateral incision in the treatment of ankle fractures involving the posterior malleolus.

Objective: To explore the clinical outcomes of a 3D printing-assisted posterolateral approach for the treatment of ankle fractures involving the posterior malleolus. Methods: A total of 51 patients with ankle fractures involving the posterior malleolus admitted to our hospital from January 2018 to December 2019 were selected. The patients were divided into 3D printing group (28 cases) and control group (23 cases). 3D printing was performed for ankle fractures, followed by printing of a solid model and simulation of the operation on the 3D model. The operation was then performed according to the preoperative plan, including open reduction and internal fixation via the posterolateral approach with the patient in the prone position. Routine x-ray and CT examinations of the ankle joint were performed, and ankle function was evaluated using the American Foot and Ankle Surgery Association (AOFAS) ankle-hindfoot score. Results: All patients underwent x-ray and CT examinations. All fractures healed clinically, without loss of reduction or failure of internal fixation. Good clinical effects were achieved in both groups of patients. The operation time, intraoperative blood loss and intraoperative fluoroscopy frequency in the 3D printing group were significantly less than those in the control group (p < 0.05). There was no significant difference between the two groups in the anatomical reduction rate of fractures or the incidence of surgical complications (p > 0.05). Conclusion: The 3D printing-assisted posterolateral approach is effective in the treatment of ankle fractures involving the posterior malleolus. The approach can be well planned before the operation, is simple to perform, yields good fracture reduction and fixation, and has good prospects for clinical application.

Preparation and properties of composite manganese/fluorine coatings on metallic titanium.

Titanium is widely used in implants because of its good mechanical properties and biocompatibility. However, titanium has no biological activity and is prone to causing implant failure after implantation. In this study, we prepared a manganese- and fluorine-doped titanium dioxide coating on a titanium surface by microarc oxidation technology. The surface characteristics of the coating were evaluated by field emission scanning electron microscopy, X-ray diffraction, X-ray photoelectron spectroscopy, and atomic force microscopy and profiler, and the corrosion resistance and wear resistance of the coating were also evaluated. The bioactivity of the coating on bone marrow mesenchymal stem cells was evaluated by in vitro cell experiments, and the antibacterial properties of the coating were evaluated by in vitro bacterial experiments. The results confirmed that the manganese- and fluorine-doped titanium dioxide coating was successfully prepared on the titanium surface, and manganese and fluorine were successfully introduced into the coating. The doping of manganese and fluorine did not change the surface morphology of the coating, and the coating had good corrosion resistance and wear resistance. The results of the in vitro cell experiment showed that the titanium dioxide coating with manganese and fluoride could promote the proliferation, differentiation and mineralization of bone marrow mesenchymal stem cells. The results of the bacterial experiment in vitro showed that the coating material could inhibit the propagation of Staphylococcus aureus and had a good antibacterial effect. Conclusion: it is feasible to prepare a manganese- and fluorine-doped titanium dioxide coating on titanium surfaces by microarc oxidation. The coating not only has good surface characteristics but also has good bone-promoting and antibacterial properties and has potential for clinical application.

Pravastatin ameliorated osteoarthritis susceptibility in male offspring rats induced by prenatal ethanol exposure.

Osteoarthritis (OA) is a disease associated with a disorder of cholesterol metabolism. Our previous studies showed that prenatal ethanol exposure (PEE) caused cholesterol accumulation in articular cartilage and increased the susceptibility to OA in offspring. However, we did not determine whether pravastatin, a cholesterol-lowering agent, could rescue PEE-induced susceptibility to OA. Here, fetal rats were divided into a PEE group and a control group during pregnancy. At postnatal week (PW) 8, sixteen male offspring rats from both groups were injected papain through the articular cavity. Eight of them from each group were treated with pravastatin (20 mg/kg·d) by gavage for four weeks simultaneously. We found that pravastatin ameliorated papain-induced high expression of inflammatory factors [interleukin (IL)-1, IL-6], matrix degradation enzymes [matrix metalloproteinase (MMP)-3, MMP-13], and apoptosis factors (caspase-3 and caspase-8) in the cartilage of the PEE group. Also, pravastatin significantly reduced the content of TCH in the blood and cartilage of the PEE offspring and improved cholesterol efflux pathway. Our in vitro findings further confirmed that pravastatin partially reversed cholesterol-induced inflammation and apoptosis of chondrocytes. In conclusion, pravastatin effectively reduced inflammation and matrix degradation, and thus ameliorate OA susceptibility in articular cartilage by relieving cholesterol accumulation in chondrocyte.

Prenatal nicotine exposure increases osteoarthritis susceptibility in male elderly offspring rats via low-function programming of the TGFß signaling pathway.

Epidemiological investigations indicate that effects related to prenatal adverse environments on the organs of the offspring could continue to adulthood. This study intends to confirm that prenatal nicotine exposure (PNE) increases the susceptibility of osteoarthritis (OA) in the male offspring, and to explore the potential intrauterine programming mechanism. During pregnancy, rats were divided into a PNE group and a control group. After birth, rats were given a high-fat diet for 6 months and long-distance running for 6 weeks. The rats were euthanized at 18 months after birth (PM18) and on gestational day 20 (GD20), respectively. Knee joints were collected for histochemistry, immunohistochemistry, and quantitative polymerase chain reaction (qPCR) assays. Histological analyses and the Mankin's score showed increased cartilage destruction and accelerated OA progression in adult offspring from the PNE group. Immunohistochemistry results showed decreased expression of transforming growth factor beta (TGFß) signaling pathway. Furthermore, the expression of apoptosis factors (caspase-3 and caspase-8), inflammatory factors [interleukin (IL)-1, IL-6] and matrix degradation enzymes [matrix metalloproteinase (MMP)-3, MMP-13] were also significantly increased. Traced back to the intrauterine period, it was found that the number of chondrocytes and the contents of Col2A1 and aggrecan in the matrix in the PNE group were decreased. And, the expression of the TGFß signaling pathway was inhibited. These results suggested that PNE enhanced the susceptibility of OA in male elderly offspring rats by down-regulating TGFß signaling, which increased articular cartilage local inflammation, matrix degradation, and cell apoptosis. This study confirmed the developmental origin of OA, and clarified the congenital and the living environment impact on the occurrence and development of OA. Our findings provide a theoretical and experimental basis for OA early prevention.

Prenatal caffeine exprosure increases adult female offspring rat's susceptibility to osteoarthritis via low-functional programming of cartilage IGF-1 with histone acetylation.

Our previous in vivo studies showed that prenatal caffeine exposure (PCE) could restrain the development of chondrogenesis, which may delay fetal articular cartilage development and increase susceptibility to osteoarthritis in adults. So, the goal of the current study is to clarify theincreasing susceptibility to adult osteoarthritis in caffeine-exposed female offspring and its'mechanism. Pregnant rats were treated with 120 mg/kg·d caffeine or equal volumes of saline from gestational day (GD) 9 to 20. knee joints were collected from GD20 female fetuses and 18-week old female offspring which was treated with strenuous running for 6 weeks (55 min/day at 20 m/min) load to induce osteoarthritis. Knee joints from GD20 fetuses and adult offspring were collected for histochemistry and immunohistochemistry. Next, chondrocytes were isolated from 1-day-old newborn rats and in vitro studies were conducted where the cells in primary culture were exposed to 1, 10, and 100 µM caffeine and 250, 500, and 1,250 nM corticosterone. Insulin-like growth factor 1 (IGF-1) signal pathway genes' expression levels in fetal chondrocytes were studied, and IGF-1 histone acetylation was detected in vitro. Immunohistochemical results showed low expression levels of IGF-1 signaling genes (IGF-1, IRS-1, AKT, and COL2A1) both in fetal and adult cartilage with PCE. For adult offspring, histological results and Mankin score revealed increased cartilage destruction and accelerated osteoarthritis progression in PCE group with strenuous running exercise. Analysis in vitro revealed that caffeine and corticosterone impeded the expression of IGF-1 signaling pathway aggrecan and COL2A1 genes, but only corticosterone decreased H3K9 and H3K27 acetylation in the IGF-1 promoter region. In concluson, PCE low functional programmed cartilage IGF-1 by histone acetylation modification via overexposure to corticosterone and delayed articular cartilage development from fetus to adults. Then, the delayed cartilage development increased susceptibility to osteoarthritis in offsprings.

Role of TGFß Signaling in Maternal Ethanol-Induced Fetal Articular Cartilage Dysplasia and Adult Onset of Osteoarthritis in Male Rats.

Based on our previous findings that prenatal ethanol exposure in offspring increased susceptibility to adult osteoarthritis, this study aimed to further investigate the direct toxicity of ethanol on fetal articular cartilage development. Rat bone marrow-derived stroma cells were capsulated in alginate beads, incubated in a chondrogenic differentiation medium, and cultured for 4 weeks with ethanol treatment at concentrations of 0, 4, 20, and 100 mM. Pregnant rats were treated with ethanol (4 g/kg/day) from gestational days (GDs) 9 to 20. At GD20 and postnatal weeks 2, 6, and 12, 8 male offspring were sacrificed, and 8 male offspring rats of 8-weeks old in each group were treated with or without intraarticular injection of papain for 4 weeks to verify the susceptibility of adult osteoarthritis. Ethanol treatment resulted in poor differentiation of bone marrow-derived stroma cells to chondrocytes and suppressed the expression of the transforming growth factor-ß (TGFß)-smad2/3-Sox9 signaling pathway. In animal experiments, the shape of articular cartilage in the ethanol treatment group was more disordered than that of the control group, the matrix was not deep, and the cartilage was thin, which showed poor cartilage development. The TGFß signaling pathway in the ethanol treatment group was persistently low at all time points. After intraarticular injection of papain, histological analyses, and the Mankin score revealed increased cartilage destruction in the ethanol treatment group. Ethanol caused articular cartilage dysplasia that was programmed in adulthood via a low-functional TGFß signaling pathway, and the tolerance of this articular cartilage to external stimuli was significantly decreased.

Potential role of andrographolide in the proliferation of osteoblasts mediated by the ERK signaling pathway.

The aim of the present study was to explore the effects of andrographolide (AG) and the ERK signaling pathway on the proliferation of osteoblasts (OBs) in vitro. The calvarial OBs from Sprague Dawley (SD) rats were collected and treated at different concentrations of AG and U0126. The concentrations of AG were measured by colorimetry. Based on different treatment methods, the cells were separated into four groups: control group, U0126 group, AG group, and AG+U0126 group. The cells were cultured for 24h, 48h and 72h. An inverted phase contrast microscope was used to observe the morphologies of treated OBs. The MTT assay was performed to plot OB proliferation curves, and to measure the changes in alkaline phosphatase and hydroxyproline contents after U0126 treatments. The expressions of proliferating cell nuclear antigen (PCNA), Ki67, core binding factor alpha-1 (Cbfa1), type I collagen (Col I), osterix (OSX), p38, extracellular signal regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) were measured by fluorescent quantitative polymerase chain reaction (PCR) and Western blotting. In different cell groups, the in vitro proliferation rates of OBs reached the highest at an AG concentration of 20µmol/L, and the amounts of alkaline phosphatase, hydroxyproline, PCNA, Ki67, Cbfa1, Col I, OSX, and ERK were significantly higher than at other concentrations (all P<0.05). U0126 intervention significantly decreased the expressions of these factors (all P<0.05). At the meantime, p38 and JNK were not affected by AG and were only inhibited by U0126. In conclusion, ERK played an important role in mediating the functions of AG in the proliferation of OBs, indicating that the ERK signaling pathway may be the main pathway through which AG exerts its effects.

The effects of levofloxacin on rabbit fibroblast-like synoviocytes in vitro.

It is widely accepted that tendon and cartilage are adversely affected with the toxic effects of quinolones. However, the effects of quinolones on synovium have not been deciphered completely. In this study, our main objective was to investigate the effects of levofloxacin, a typical quinolone antibiotic drug, on fibroblast-like synoviocytes (FLSs) in vitro. FLSs of rabbits were treated with levofloxacin at different concentrations (0, 14, 28, 56, 112 and 224 µM). The possible cytotoxic effects of levofloxacin on FLS were determined. Levofloxacin significantly reduced the cell viabilities, gene expression of hyaluronan synthase-2 (HAS-2), and the level of hyaluronan in FLSs. Moreover, levofloxacin-induced concentration-dependent increases of apoptosis and active caspase-3 were determined in this study. Ultrastructural damages of FLSs were observed by electron microscopy. The mRNA expression levels of matrix metalloproteinase (MMP)-3 and MMP-13 were increased in FLSs treated with levofloxacin. In addition, levofloxacin played a role in suppressing the expression of interleukin (IL)-1 and IL-6. Our data suggest that the cytotoxic effects of levofloxacin on FLS were shown to be able to affect cell viability and HA synthesis capacity. The potential mechanisms of the cytotoxic effects may be attributed to the apoptosis and increased expression of MMPs.