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Peripherally inserted central catheters (PICCs) can provide nutritional and medical support for very low birth weight or critically ill newborns. The aim of this study was to retrospectively analyze the use of PICCs in our clinic for critically ill newborns to evaluate the relationship between catheter related factors and the occurrence of complications. Retrospective analysis was conducted for all newborns consecutively admitted at the Neonatal Intensive Care Unit (NICU), Chongqing Health Center for Women and Children, who underwent PICC insertion between May 2011 and March 2018. Data collected included total puncture success rate, one puncture success rate, infection rate, complication rate, unplanned catheter withdrawal rate, device days, and catheter indwelling time. Five-hundred eighty-eight infants (304 males and 284 females) aged 3.4 ± 3.9 days, mean gestational age of 30.9 ± 2.7 weeks and a mean body mass of 1.38 ± 0.47 kg at insertion were included. Total puncture success rate was 99.65%, one puncture success rate was 77.77%. The mean catheter retention was 13.6 ± 6.7 days: more than 30 days in 15 (2.61%) cases, 20 to 30 days in 60 (10.43%) cases, 10 to 19 days in 372 (64.70%) cases, and 62 days in 1 case. Complications occurred in 63 (10.71%) cases: with PICC insertion within 24 hours after birth in 29 (15.43%), within 48 hours in 13 (6.63%), and after 48 hours in 21 (10.99%) cases. Catheter tip culture was positive in 3 cases and there was 1 case of catheter-related bloodstream infection. Nursing measures of the maintenance of body temperature and the evaluation of blood vessels were important conditions for improving the success rate of one puncture in critically ill neonates. PICC catheterization as early as 48 hours will not increase the difficulty of PICC puncture. Nor did it increase the incidence of PICC complications.

Ascorbic acid, β-glycerophosphate, and dexamethasone have been used in osteogenesis differentiation medium for in vitro cell culture, nothing is known for delivering these three bioactive compounds in vivo. In this study, we synthesized a novel bioactive scaffold by combining these three compounds with a lysine diisocyanate-based polyurethane. These bioactive compounds were released from the scaffold during the degradation process. The cell culture showed that the sponge-like structure in the scaffold was critical in providing a large surface area to support cell growth and all degradation products of the polymer were non-toxic. This bioactive scaffold enhanced the bone regeneration as evidenced by increasing the expression of three bone-related genes including collagen type I, Runx-2 and osteocalcin in rabbit bone marrow stem cells (BMSCs) in vitro and in vivo. The osteogenesis differentiation of BMSCs cultured in this bioactive scaffold was similar to that in osteogenesis differentiation medium and more extensive in this bioactive scaffold compared to the scaffold without these three bioactive compounds. These results indicated that the scaffold containing three bioactive compounds was a good osteogenesis differentiation promoter to enhance the osteogenesis differentiation and new bone formation in vivo.

Background: miR-124-3p has been reported to be involved in the pathogenesis of many diseases by modulating a variety of signaling pathways. In this study, we aimed to understand the impact of miR-124-3p expression level on the fracture healing in the patients of metaphyseal fracture of distal tibia, who received minimal invasive percutaneous plate osteosynthesis. Methods: We firstly collected 195 patients of metaphyseal fracture of distal tibia, and the genotype of rs531564 was determined: GG (n=124) and GC+CC (n=71). We collected information of the participants including age, gender, total in-hospital time, smoking and alcohol consumption. Subsequently, we searched the miRNA database online to identify the possible binding sequence of miR-124-3p located within the 3’-UTR of the target gene. We did correlation analysis and luciferase to understand the regulatory relationship between miR-124-3p and BMP6. Meanwhile, we also conducted real time PCR and western blotting analysis to study the mRNA and protein expression level of BMP6 in different genotype groups. We then treated the cells with scramble control, miR-124-3p mimics, BMP6 siRNA and miR-124-3p inhibitors to investigate the influence of miR-124-3p on the expression of BMP6, viability and apoptosis of cells. Results: Total in-hospital time was significantly longer in GC+CC group than GG group. MiR-124-3p was up-regulated in GG group than GC and CC groups. BMP6 was virtual target of miR-124-3p. There existed negative regulatory relationship betweenmiR-124-3p and BMP6. The mRNA and protein expression level of BMP6 decreased in GG group. MiR-124-3p decreased the expression of BMP6. MiR-124-3p negatively interfered with the viability of cells and BMP6 positively interfered with the viability of cells. MiR-124-3p reduced apoptosis and BMP6 promoted apoptosis. Conclusion: These data proved the expression of miR-124-3p was associated with the healing of metaphyseal fracture of distal tibia, and could be recognized as a biomarker to predict the healing of metaphyseal fracture of distal tibia.

Objective. Nucleus pulposus (NP) and annulus fibrosus (AF) are two main components of intervertebral disc (IVD). We aimed to figure out whether NP and AF also contain stem cells and whether these stem cells share common properties with chondrocytes and/or fibroblasts in their phenotypes or whether they are completely different types of cells with different characteristics. Design. The disk cells were isolated from AF and NP tissues of the same lumbar spine of the rabbits. The properties of these disk cells were characterized by their morphology, population doubling time (PDT), stem cell marker expression, and multidifferentiation potential using tissue culture techniques, immunocytochemistry, and RT-PCR. Results. Both disk cells formed colonies in culture and expressed stem cell markers, nucleostemin, Oct-4, SSEA-4, and Stro-1, at early passages. However, after 5 passages, AFSCs became elongated and NPSCs appeared senescent. Conclusion. This study indicated that IVD contains stem cells and the characteristics of AFSCs and NPSCs are intrinsically different. The findings of this study may provide basic scientific data for understanding the properties of IVD cells and the mechanisms of lower back pain.

Abstract. Interleukin-1β (IL-1β) has a significant role in osteoarthritis (OA). The purinergic receptor, P2X4, has previously been implicated in IL-1β secretion. The NLRP1 inflammasome mediates the production of IL-1β in inflammatory disorders. However, it is unknown whether P2X4 modulates NLRP1-mediated IL-1β release. In the present study, the correlation between the P2X4 receptor and NLRP1 was investigated in OA fibroblast-like synoviocytes (OAFLS). The expression of P2X4 and NLRP1 was detected in the OAFLS. The OAFLS were stimulated with P2X4 and the levels of IL-1β and matrix metalloproteinases (MMPs) were measured. To determine whether P2X4 is involved in NLRP1-triggered IL-1β production, NLRP1 small interfering RNA (siRNA) was used. In the OAFLS, a markedly higher expression of P2X4 and NLRP1 was revealed compared with that in the normal FLS. OAFLS stimulated by P2X4 resulted in concentration-dependent increases in the production of IL-1β, MMP-3 and MMP-9. Furthermore, P2X4-mediated IL-1β production was attenuated by the NLRP1 siRNA. The results of the present study indicate that P2X4 induced IL-1β, MMP-3 and MMP-9 production in the OAFLS. IL-1β induced by P2X4 is mediated via NLRP1. P2X4/NLRP1 may be important in the pathogenesis of OA and may represent a novel therapeutic target. IntroductionAs the most common form of arthritis, osteoarthritis (OA) is one of the most significant causes of disability in older adults (1), yet its exact etiology remains unknown (2). The diagnosis and evaluation of joint damage are predominantly based on clinical and radiological findings. With medical advances, molecular markers are likely to become promising indicators for evaluating local inflammation, joint alterations and cartilage damage (3).Fibroblast-like synoviocytes (FLS) have been accepted to be key in OA inflammation and joint destruction, primarily through their secretion of a wide range of proinflammatory mediators (4,5). In response to the proinflammatory cytokines, including interleukin-1β (IL-1β), the OAFLS produce chemokines that promote inflammation, neovascularization and cartilage degradation via activation of matrix-degrading enzymes, including matrix metalloproteinases (MMPs) (5). IL-1β is a multifunctional cytokine that contributes to the pathogenesis of OA (6). Investigations into the IL-1β signaling pathway led to the identification of novel potential drugs for the treatment of OA (7). However, current treatment with these drugs remains unsatisfactory, and further research is required to achieve the desired therapeutic goals (7).The inflammasome is a multi-protein complex that mediates the activation of caspase-1, which in turn produces the proinflammatory cytokines, . The human NLRP1 inflammasome was the first caspase-1-activating protein complex to be identified (9). Recent studies have indicated that NLRP3 is involved in the genetic predisposition and pathogenesis of crystal arthritis, including gouty and rheumatoid arthritis (10,11). Recently, a study has revealed that the expression of the P2X4...

Spinal cord injury [SCI] leads to complex cellular and molecular interactions which affects various organ systems. The present study focused on determining the protection offered by Vitamin C against spinal injury-induced kidney damage in wistar rats. The experimental protocol was performed with three groups; Sham, SCI and Vitamin C [20 mg/kg/bw] followed by SCI. The kidney tissue was investigated for oxidative stress parameters [reactive oxygen species, protein carbonyl, sulphydryl content, thiobarbituric acid reactive species [TBARS], and myeloperoxidase activity] and antioxidant status [glutathione, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase activity]. Further, inflammation studies were performed by analyzing expression of NF-κB, cycloxygenase-2, iNOS through western blot analysis and inflammatory cytokines by TNF-α and IL-1β levels. The present study shows clear evidence that Vitamin C treatment abrogated spinal injury-induced oxidative stress and inflammatory responses and enhanced the antioxidant status. Thus, the protection offered by Vitamin C against spinal cord injury-induced kidney damage is attributed to its anti-oxidant and anti-inflammatory effects.

The objective of this study is to elucidate the primary action of methylmercury chloride (MMC) intoxication on peripheral nervous system. We chronologically observed the pathological changes of sciatic nerve, dorsal root ganglion (DRG) neurons, ventral and dorsal roots in rats given 4 mg/kg/day of MMC on consecutive days and killed on days 11, 15, 18 and 21. On day 11, an initial axonal degeneration of type B neuron occurred, predominantly in the distal portions of sciatic nerve. The DRG type A neuron was infiltrated by MRF-1-positive macrophages on day 11. Electron microscopy also demonstrated degenerated mitochondria in type A neuron. On day 21, most of type A neurons seemed to have disappeared. However, type B neurons were well preserved. Immunoblotting with monoclonal antibodies, P0 and neurofilament, demonstrated that both of proteins significantly decreases from day 15. In conclusion, these results indicate that the primary action on type A neuron is the neuron body that consequently results in an anterograde degeneration of nerve fibers, while the type B neuron degeneration occurs in a dying-back process in this subacute model. These findings suggest that the mechanisms involved in the degeneration induced by MMC vary and may depend on certain intrinsic factors peculiar to these neurons.