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Soft surfaces, including textiles are found throughout healthcare settings. Pathogens can survive for long periods of time on textiles, and can be transferred to and from the skin. Antimicrobial fabrics are used as an engineering control to prevent infection. Efficacy testing standards have limitations, including single microorganism challenges, multiple fabric plies tested, and lengthy contact times. We developed a novel method that better models in-use conditions through testing standardized mixtures of pathogens and normal skin microorganisms, artificial soils, and a 15-min contact time. Reproducible growth of all microorganisms from frozen stocks was achieved using this method. A novel rechargeable, monitorable N-halamine cotton cellulose fabric, containing 5885 ± 98 ppm of active chlorine, was evaluated with the new method using PBS, artificial sweat, and artificial sweat plus 5% serum as soil. Pathogens tested included Acinetobacter baumannii , Candida albicans , Escherichia coli , vancomycin-resistant Enterococcus faecalis , methicillin-resistant Staphylococcus aureus, methicillin-susceptible Staphylococcus aureus , and Pseudomonas aeruginosa. Each was tested singly and in the presence of a representative normal skin flora mixture, including: Acinetobacter lwoffii , Corynebacterium striatum , Micrococcus luteus , and Staphylococcus epidermidis. When tested singly, all microorganisms were reduced by 3.00 log 10 or greater, regardless of artificial soil. In mixture, 4.00 log 10 or greater reductions were achieved for all microorganisms. These results suggest that the novel testing method can be used to provide more comprehensive and realistic efficacy information for antimicrobial textiles intended for use in healthcare. Furthermore, the N-halamine fabric demonstrated efficacy against multiple pathogens, singly and in mixtures, regardless of the presence of artificial soils. • Simulated in-use conditions provide a more complete test of antimicrobial textiles. • Standardized mixtures of normal and pathogenic microorganisms were tested. • The impact of soils (artificial sweat and 5% serum) were tested. • N-halamine fabric performance was not impacted by microorganisms or soils. • The novel method is reproducible and can be adapted for specific in-use conditions. [ABSTRACT FROM AUTHOR]

• Fluvoxamine treatment reversed the effects of CUMS on the hippocampal mTOR signaling. • Fluvoxamine treatment restored the effects of CUMS on mTOR in the prefrontal cortex. • Blockade of the mTOR system prevented the antidepressant effects of fluvoxamine in mice. Recent studies have suggested that activation of the mammalian target of rapamycin (mTOR) signaling may be related to antidepressant actions. Although thought as a selective serotonin reuptake inhibitor (SSRI), the antidepressant mechanisms of fluvoxamine remain elusive. Therefore, this study aims to evaluate whether mTOR underlies the antidepressant-like effects of fluvoxamine. Male C57BL/6 J mice were subjected to 8 weeks of chronic unpredictable mild stress (CUMS) with fluvoxamine administered during the last 2 weeks. Western blotting analyses were then used to assess the expression of the mTOR signaling cascade in the hippocampus and prefrontal cortex (PFC) among all groups. The selective inhibitor of mTOR, rapamycin, was further used. It was found that fluvoxamine treatment fully reversed the effects of CUMS on the mTOR signaling in the hippocampus and PFC, and the usage of rapamycin significantly prevented the antidepressant-like effects of fluvoxamine in the CUMS model of depression. Taken together, the mTOR system is involved in the antidepressant mechanisms of fluvoxamine. [ABSTRACT FROM AUTHOR]

• AQACs with different alkyl chain length were synthesized via an external acid-free reaction. • Longer alkyl chains led to lower antifungal activity against free-floating fungal cells in water. • AQACs with longer alkyl chains showed much more potent fungicidal activity against fungal cells in biofilms. • All the AQACs was cytocompatible in their fungicidal concentrations. Fungal biofilm formation is an emerging problem in a wide range of health-related applications. This study aims to design and synthesize amphiphilic quaternary ammonium chitosans (AQACs) that could bind onto fungal biofilms to kill adherent fungal cells, and establish their structural/fungicidal activity relationships. AQACs with different hydrophobic alkyl chain length (C 4 , C 8 , and C 12) were synthesized by quaternization of 3-bromopropionic acid with the corresponding tertiary amines, followed by reacting with chitosan using the EDC/NHS chemistry. The new AQACs were soluble in water, yet formed self-aggregates in the solution with different sizes. In antifungal tests against free-floating Candida albicans , shorter alkyl chains (C 4) in the AQACs resulted in the most potent fungicidal effect. However, in the treatment of Candida biofilms formed on solid surfaces, AQACs with longer alkyl chains (C 8 and C 12) were much more effective than their shorter chain counterpart (C 4). The effects of alkyl chain self-aggregation on the opposite trend in fungicidal and anti-biofilm activities were discussed. All the AQACs showed excellent cytocompatibility with mammalian cells. [ABSTRACT FROM AUTHOR]

• Wheat germ agglutinin conjugated liposomes with surface grafted cyclodextrins were engineered. • High encapsulation of hydrophobic and hydrophilic drugs demonstrated its efficacy as a dual drug nanocarrier. • The nanocarriers showed fast attachment to oral cells and controlled co- drug release in saliva. • Synergistic therapeutic activity was observed in bacteria-infected oral cells. Topical management of oral infection requires combined use of multiple classes of drugs and frequent dosing due to low drug retention rates. The sustained, co-delivery of drugs with different solubilities to cells using nanoparticle drug delivery systems remains a challenge. Here, we developed wheat germ agglutinin (WGA) conjugated liposomes with surface grafted cyclodextrin (WGA-liposome-CD) as bioadhesive dual-drug nanocarriers. We effectively encapsulated two physiochemically different drugs (ciprofloxacin and betamethasone) and demonstrated sustained co-drug release in saliva over a 24 h period in vitro. As proof of therapeutic utility in oral cells, we infected oral keratinocytes with Aggregatibacter actinomycetemcomitans , a bacterial pathogen responsible for chronic periodontal disease. Drug release, resulting from nanocarrier cell binding, produced a significant increase in oral cell survival and synergistically reduced inflammation. These results suggest that WGA-liposome-CD nanocarriers are novel cyto-adhesive candidates for delivering multiple drugs with sustained therapeutic activity for localized drug delivery to oral cells. [ABSTRACT FROM AUTHOR]

Formation of fungal biofilms on health care-related materials causes serious clinical consequences. This study reports a novel fungal repelling strategy to control fungal biofilm formation on denture biomaterials through layer-by-layer self-assembly (LBL). Amphiphilic quaternary ammonium chitosans (CS612) were synthesized and used as the antimicrobial positive layer, and sodium alginate (SA) was chosen as the negative layer to construct LBL multilayers on poly (methyl methacrylate) (PMMA)-based denture materials. The presence of LBL multilayers on denture disc was confirmed and characterized by surface zeta potential, water contact angle, AFM, and FT-IR analyses. The multilayer coatings, especially CS612 as the outmost layer, effectively prevented the fungal initial adhesion and biofilm formation. The Candida cells avoided the multilayer coatings and suspended in broth solution instead of forming biofilms, suggesting that the LBL multilayers had fungal repelling effects. The LBL multilayers were biocompatible toward mammalian cells. In stability tests, after immersion in PBS for 4 weeks under constant shaking and repeated brushing with a denture brush for up to 3000 times, the biofilm-controlling effects of the LBL multilayers were not affected, pointing to a novel long-term strategy in controlling fungal biofilms on denture and other related biomaterials. Unlabelled Image • Denture surface was modified by layer-by-layer (LBL) self-assembly of quaternary ammonium chitosan (CS612) and sodium alginate (SA). • The multilayer coatings repelled fungal cells and prevented biofilm formation. • The LBL multilayer was cytocompatible with mammalian fibroblast cells and stable upon PBS immersing and brushing. [ABSTRACT FROM AUTHOR]

Thermally activated delayed fluorescence (TADF)-based materials are attracting widespread attention for different applications owing to their ability of harvesting both singlet and triplet excitons without noble metals in their structures. As compared to the conventional fluorescence and room-temperature phosphorescence pathways, TADF originates from the reverse intersystem crossing process from the excited triplet state (T 1 ) to the singlet state (S 1 ). Therefore, TADF emitters enabling activated and long lifetime T 1 excitons are potential candidates for generating long-lived afterglow emission, an effect that can still be observed for a while by the naked eye after the removal of the excitation light source. Recently, TADF-based organic afterglow materials featuring high photoluminescence quantum yields and long lifetimes above 100 ms under ambient conditions, have emerged for advanced information security, high-contrast biological imaging, optoelectronic devices, and intelligent sensors, whereas the related systematic review is still lacking. Herein, the recent progress in TADF-based organic afterglow materials is summarized and an overview of the photophysical mechanism, design strategies, and the performances for relevant applications is given. In addition, the challenge and perspective of this area are given at the end of the review., (© 2024 Wiley‐VCH GmbH.)

Injury to the peripheral nervous system disconnects targets to the central nervous system, disrupts signal transmission, and results in functional disability. Although surgical and therapeutic treatments improve nerve regeneration, it is generally hard to achieve fully functional recovery after severe peripheral nerve injury. A better understanding of pathological changes after peripheral nerve injury helps the development of promising treatments for nerve regeneration. Single-cell analyses of the peripheral nervous system under physiological and injury conditions define the diversity of cells in peripheral nerves and reveal cell-specific injury responses. Herein, we review recent findings on the single-cell transcriptome status in the dorsal root ganglia and peripheral nerves following peripheral nerve injury, identify the cell heterogeneity of peripheral nerves, and delineate changes in injured peripheral nerves, especially molecular changes in neurons, glial cells, and immune cells. Cell-cell interactions in peripheral nerves are also characterized based on ligand-receptor pairs from coordinated gene expressions. The understanding of cellular changes following peripheral nerve injury at a single-cell resolution offers a comprehensive and insightful view for the peripheral nerve repair process, provides an important basis for the exploration of the key regulators of neuronal growth and microenvironment reconstruction, and benefits the development of novel therapeutic drugs for the treatment of peripheral nerve injury., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Zhao, Jiang, Yu, Zhu, Sun and Yi.)

Spinal cord injury (SCI) is one of the most severe injuries, characterized by multiple positive feedback regulatory signaling networks formed by oxidative stress and inflammation in the injury microenvironment, leading to neuronal cell damage and even death. Here, astragaloside IV (AS), known for its regulatory role in ferroptosis, was encapsulated in the cavity of apoferritin (HFn) after an in situ biomineralization process involving MnO 2 , resulting in the synthesis of HFn@MnO 2 /AS nanoparticles. These nanoparticles were then dispersed in chitosan/polyvinyl alcohol/glutaraldehyde/sodium β-glycerophosphate (CGPG) hydrogels to form CGPG-HFn@MnO 2 /AS injectable thermosensitive hydrogels that can scavenge reactive oxygen species (ROS) in the microenvironment. Our findings indicated that the prepared CGPG-HFn@MnO 2 /AS hydrogel exhibited remarkable efficacy in scavenging ROS in vitro, effectively ameliorating the oxidative stress microenvironment post-SCI. Furthermore, it inhibited oxidative stress-induced ferroptosis in vitro and in vivo by regulating SIRT1 signaling, thereby promoting neuronal cell migration and repair. Hence, the developed hydrogel combining MnO 2 and AS exhibited multifaceted abilities to modulate the pathological microenvironment, providing a promising therapeutic strategy for central nervous system (CNS) diseases.

Osteoarthritis (OA) is a low-grade, nonspecific inflammatory disease that affects the entire joint. This condition is characterized by synovitis, cartilage erosion, subchondral bone defects, and subpatellar fat pad damage. There is mounting evidence demonstrating the significance of crosstalk between synovitis and cartilage destruction in the development of OA. To comprehensively explore the phenotypic alterations of synovitis and cartilage destruction, it is important to elucidate the crosstalk mechanisms between chondrocytes and synovial cells. Furthermore, the updated iteration of single-cell sequencing technology reveals the interaction between chondrocyte and synovial cells. In the present review, the histological and pathological alterations between cartilage and synovium during OA progression are described, and the mode of interaction and molecular mechanisms between synovial cells and chondrocytes in OA, both of which affect the OA process mainly by altering the inflammatory environment and cellular state, are elucidated. Finally, the current OA therapeutic approaches are summarized and emerging therapeutic targets are reviewed in an attempt to provide potential insights into OA treatment., Competing Interests: The authors declare that they have no competing interests., (Copyright: © 2024 Chen et al.)

Background: Zhuang-Gu-Fang (ZGF) has been proved to treat osteoporosis in ovariectomized rats by increasing osteogenic related factors Leptin, Ghrelin and Peptide YY(PYY). However, the mechanism of ZGF in the treatment of diabetic osteoporosis (DOP) remains unclear. The aim of this study was to explore the therapeutic effect of ZGF on DOP and its potential molecular mechanism., Methods: Using GK rats as models, the pharmacodynamic effects of ZGF on bone loss were evaluated by hematoxylin-eosin (H&E) staining and micro-computed.tomography (micro-CT). The expression levels of CD31 and endomucin (Emcn) were detected by immunofluorescence to assess the role of ZGF in angiogenic osteogenic coupling. Finally, real-time quantitative PCR (RT-PCR) and Western Blot (WB)were used to detect the expression levels of osteogenic and angiogenesis-related genes and proteins Notch1, Noggin and vascular endothelial growth factor (VEGF)., Results: Administration of ZGF demonstrated a significant mitigation of bone loss attributable to elevated glucose levels. H&E staining and micro-CT showed that ZGF notably improved the integrity of the trabecular and cortical bone microarchitecture. Moreover, ZGF was found to augment the density of type H vessels within the bone tissue, alongside elevating the expression levels of Osterix, a transcription factor pivotal for bone formation. Furthermore, our findings suggest that ZGF facilitates the activation of the Notch1/Noggin/VEGF pathway, indicating a potential mechanism through which ZGF exerts its osteoprotective effects., Conclusion: Our results suggest that ZGF potentially facilitates the formation of type H vessels through the Notch1/Noggin/VEGF pathway. This action not only enhances angiogenic-osteogenic coupling but also contributes to the improvement of bone structure and density. Consequently, ZGF emerges as a promising therapeutic agent for the prevention and management of DOP, offering a novel approach by leveraging angiogenesis-dependent osteogenesis., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2024 The Authors.)

Most cancers have a downregulation of Fidgetin (FIGN), which has been linked to tumor growth. However, there aren't many papers that mention FIGN's connection to hepatocellular carcinoma (HCC). Here, FIGN expression in HCC tissues was markedly reduced as compared to nearby normal liver tissues. According to univariate and multivariate Cox regression, it served as an independent predictor of survival outcomes. Patients with high levels of FIGN expression had a worse outcome. FIGN was shown to be engaged in immune-related pathways and to have a positive correlation with immunological score and immune cells according to KEGG pathway analysis. In HCC patients, FIGN was substantially linked with immunological checkpoints and the hot tumor state. Additionally, immunotherapy and chemotherapy showed a significant therapeutic response in HCC patients with low FIGN expression. This research revealed that FIGN expression was tightly related to hepatoma immunity and might be employed as a biomarker to predict patient prognosis and guide medication.

Introduction: Menstrual blood-derived stem cells (MenSCs) are vital in treating many degenerative and traumatic disorders. However, the underlying molecular mechanisms remain obscure in MenSCs-treating spinal cord injury (SCI) rats., Methods: MenSCs were adopted into the injured sites of rat spinal cords at day 7 post surgery and the tissues were harvested for total RNA sequencing analysis at day 21 after surgery to investigate the expression patterns of RNAs. The differentially expressed genes (DEGs) were analyzed with volcano and heatmap plot. DEGs were sequentially analyzed by weighted gene co-expression network, functional enrichment, and competitive endogenous RNAs (ceRNA) network analysis. Next, expression of selected miRNAs, lncRNAs, circRNAs and mRNAs were validated by quantitative real-time polymerase chain reaction (qRT-PCR). Bioinformatics packages and extra databases were enrolled to scoop the genes functions and their interaction relationships., Results: A total of 89 lncRNAs, 65 circRNAs, 120 miRNAs and 422 mRNAs were significantly upregulated and 65 lncRNAs, 72 circRNAs, 74 miRNAs, and 190 mRNAs were significantly downregulated in the MenSCs treated rats compared to SCI ones. Current investigation revealed that MenSCs treatment improve the recovery of the injured rats and the most significantly involved pathways in SCI regeneration were cell adhesion molecules, nature killer cell mediated cytotoxicity, primary immunodeficiency, chemokine signaling pathway, T cell receptor signaling pathway and B cell receptor signaling pathway. Moreover, the lncRNA-miRNA-mRNA and circRNA-miRNA-mRNA ceRNA network of SCI was constructed. Finally, the protein-protein interaction (PPI) network was constructed using the top 100 DE mRNAs. The constructed PPI network included 47 nodes and 70 edges., Discussion: In summary, the above results revealed the expression profile and potential functions of differentially expressed (DE) RNAs in the injured spinal cords of rats in the MenSCs-treated and SCI groups, and this study may provide new clues to understand the mechanisms of MenSCs in treating SCI., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Qi, Jiang, He, Li, Wu, Chen, Liao, Yu, Liu, Sun, Wu, Dong and Wang.)

Background: Osteosarcoma is a malignant tumor originating from the skeletal system. There is no effective treatment other than surgery and chemotherapy, which seriously endangers the health of children and adolescents. NEK6 is a novel discovered Serine/Threonine protein kinase that can regulate cell cycle and activate several oncogenic pathways., Methods: NEK6 expression in pan-cancer including sarcoma was evaluated using analysis tools of TIMER, UALCNA and GEPIA with TCGA database, and its association with overall survival in patients with sarcoma was also analyzed. TargetScan, tarbase, microT-CDS and Starbase online software were used to predict NEK6-targeted miRNAs, including miR-26a-5p. Tumor tissues from patients with osteosarcoma were collected for NEK6 and miRNA detection using RT-qPCR. NEK6 down-regulated by siRNAs or miR-26a-5p in osteosarcoma cells was detected by RT-qPCR, Western blot and Immunofluorescence staining assays. Effects of NEK6 knockdown on proliferation, migration, invasion and apoptosis of osteosarcoma cells were detected by CCK-8, wound healing, transwell and flow cytometry, respectively. The expressions of STAT3, metastasis and apoptosis-related genes were detected by Western blot., Results: High expression of NEK6 and low expression of miR-26a-5p were lowly expressed in osteosarcoma and they were negative correlation. NEK6 has been confirmed as a direct target for miR-26a-5p. In addition, NEK6 down-regulated by siRNAs or miR-26a-5p led to inhibition of cell proliferation, migration and invasion while promoting cell apoptosis. The levels of phosphorylated STAT3 and metastasis genes (MMP-2, MMP-9) were inhibited, while apoptotic gene Bax was promoted and Bcl2 was inhibited by miR-26a-5p upregulation., Conclusion: NEK6 can promote osteosarcoma progression via activating STAT3 signaling pathway, which is inhibited by miR-26a-5p, suggesting that NEK6 is a potential oncogene and miR-26a-5p is a suppressor of osteosarcoma. The strategy of inhibiting of NEK6 by miR-26a-5p may be an effective approach for osteosarcoma therapy., Competing Interests: The authors declare that they have no conflicts of interest in this work., (© 2023 Zhu et al.)

Herpesviral hematopoietic necrosis disease causes by cyprinid herpesvirus 2 (CyHV-2) infection is a high mortality disease that leads to great economic damage to gibel carp, Carassius auratus gibelio aquaculture. In this study, an attenuated strain of CyHV-2 G-RP7 was achieved by subculture on RyuF-2 cells derived from the fin of Ryukin-variety goldfish and GiCF cells derived from fin of gibel carp. As the attenuated vaccine candidate, there are no clinical symptoms of gibel carp that immersion or intraperitoneal injection with G-RP7 strain. The protection rates of G-PR7 to gibel carp by immersion and intraperitoneal injection were 92% and 100%, respectively. In the test for virulence reversion, the candidate was propagated through gibel carp six times by intraperitoneal injection with kidney and spleen homogenate of the inoculated fish. During in vivo passages in gibel carp, no abnormality and mortality of the inoculated fish were observed, and the virus DNA copies maintain a low level from the first passage to the sixth passage. The dynamic of virus DNA in each tissue of G-RP7 vaccination fish increased within 1, 3, and 5 days post-immunization, and subsequently decreased and stabilized within 7 and 14 days. In addition, the increase of anti-virus antibody titer was detected both immersion and injection immunization fish 21 days after vaccination by ELISA. These results demonstrated that G-RP7 can be a promising live attenuated vaccine candidate against the disease., Competing Interests: Declaration of competing interest None., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Vibrio parahaemolyticus, a causative agent of seafood-associated gastroenteritis, undergoes opaque-translucent (OP-TR) colony switching associated with capsular polysaccharide (CPS) production. Here, we showed that V. parahaemolyticus was also able to naturally and reversibly switch between wrinkly and smooth phenotypes. More than 1,000 genes were significantly differentially expressed during colony morphology switching, including the major virulence gene loci and key biofilm-related genes. The genes responsible for type III secretion system 1 (T3SS1), type VI secretion systems (T6SS1 and T6SS2), and flagellar synthesis were downregulated in the wrinkly spreader phenotype, whereas genes located on the pathogenicity island Vp-PAI and those responsible for chitin-regulated pili (ChiRP) and Syp exopolysaccharide synthesis were upregulated. In addition, we showed that the wrinkly spreader grew faster, had greater motility and biofilm capacities, and produced more c-di-GMP than the smooth type. A dozen genes potentially associated with c-di-GMP metabolism were shown to be significantly differentially expressed, which may account for the differences in c-di-GMP levels between the two phenotypes. Most importantly, dozens of putative regulators were significantly differentially expressed, and hundreds of noncoding RNAs were detected during colony morphology switching, indicating that phenotype switching is strictly regulated by a complex molecular regulatory network in V. parahaemolyticus. Taken together, the presented work highlighted the gene expression profiles related to wrinkly-smooth switching, showing that the significantly differentially expressed genes were involved in various biological behaviors, including virulence factor production, biofilm formation, metabolism, adaptation, and colonization. IMPORTANCE We showed that Vibrio parahaemolyticus was able to naturally and reversibly switch between wrinkly and smooth phenotypes and disclosed the gene expression profiles related to wrinkly-smooth switching, showing that the significantly differentially expressed genes between the two colony morphology phenotypes were involved in various biological behaviors, including virulence factor production, biofilm formation, metabolism, adaptation, and colonization.

Lumbar facet osteoarthritis (FJOA) is a major cause of severe lower back pain and disability worldwide. However, the mechanism underlying cartilage degeneration in FJOA remains unclear. The purpose of this study was to investigate the regulation and mechanism of P2Y12 on chondrocyte apoptosis in FJOA. The experimental rats were randomly divided into non-operation (n = 20) and operation groups (n = 20). In the operation group, Sodium iodoacetate (MIA, Sigma, 200 mg/mL) was injected into the right L4/5 facet process using a blunt nanoneedle 26 (WPI, Sarasota, FL, USA) under the control of an injection pump. The final injection volume was 5µL and the injection rate was 2µL/min. The facet joint was removed four weeks after surgery. After the operation, samples were stored at -80 °C until further use, whereby the right facet joints in each group were tested. Hematoxylin and eosin (HE) and iron-red solid green staining were used to observe the degeneration of articular chondrocytes in rats. Immunohistochemistry and western blotting were used to observe the expressions of P2Y12, Matrix metalloproteinase 13 (MMP13), Collagen II (COL2), and other cartilage degeneration and apoptosis-related genes. Co-localization of P2Y12-cleaved caspase-3 in the apoptosis model was detected by dual-standard immunofluorescence staining. Apoptosis was also detected by flow cytometry and TUNEL assay.P2Y12 is highly expressed in OA cartilage tissue, and inhibits IL-1β -induced chondrocyte apoptosis through PI3K/AKT signaling pathway, thus playing a certain protective role on cartilage., (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

The aquaculture industry is vital in providing a valuable protein food source for humans, but generates a huge amount of solid and dissolved wastes that pose great risks to the environment and aquaculture sustainability. Suspended solids (in short SS), one of the aquaculture wastes, are very difficult to be treated due to their high organic contents. The bioconversion from wastewater, food effluents, and activated sludge into poly-β-hydroxybutyrate (PHB) is a sustainable alternative to generate an additional income and could be highly attractive to the agricultural and environmental management firms. However, little is known about its potential application in aquaculture wastes. In the present study, we first determined that 7.2% of SS was PHB. Then, the production of PHB was increased two-fold by the optimal fermentation conditions of wheat bran and microbial cocktails at a C/N ratio of 12. Also, the PHB-enriched SS showed a higher total ammonia nitrogen removal rate. Importantly, we further demonstrated that the PHB-enriched SS as a feed could promote fish growth and up-regulate the expression of the immune-related genes. Our study developed an eco-friendly and simple approach to transforming problematic SS wastes into PHB-enriched high-quality food for omnivorous fish, which will increase the usage efficiency of SS and provide a cheaper diet for aquatic animals., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Qiao, Li, Li, Zhang, Shen, Zhao, Zhang, Qi, Chen, Sun, Cang, Liu, Wangkahart and Wang.)

Bcl2-associated athanogene3 (BAG3) protein, mainly induced by stressful stimuli, has been confirmed to participate in apoptosis and autophagy. In recent studies, BAG3 has gradually become a key molecule in tumors. However, the role of BAG3 in the progression of lumbar facet joint osteoarthritis (FJOA) and whether it can regulate chondrocyte apoptosis and autophagy are still unknown. In both human and FJOA rat models, we observed an upregulation of BAG3 and apoptosis and autophagy-related proteins compared with healthy tissues. Then, we established the chondrocytes injury model in vitro by using IL-1β to stimulate human SW1353 cells. Western blot analysis data showed significant expression of BAG3, apoptosis, and autophagy-related proteins in SW1353 cells. Finally, by knocking down and overexpressing BAG3, we discovered possible anti-apoptotic and autophagy-promoted effects of BAG3 in FJOA through various experimental methods. This study demonstrated that BAG3 actively participates in regulating chondrocyte apoptosis and autophagy in FJOA and may be a highly interesting target for pharmacological interventions., (© 2022. The Author(s) under exclusive licence to University of Navarra.)

Tumor necrosis factor receptor-associated factor 6 (TRAF6), a regulator of NF-κB signaling, has been discovered recently to be probably related to osteoarthritis, while the function of TRAF6 in lumbar facet joint osteoarthritis(FJOA)still remains unknown. The aim of this study was to probe the specific function of TRAF6 in chondrocytes and its connection with the pathophysiology of FJOA. We found upregulation of TRAF6 in FJOA cartilage by western blot analysis. In vitro, we stimulated immortalized human chondrocytes by LPS to establish the cells apoptosis model. Western blot analysis demonstrated that levels of TRAF6 and cleaved caspase-3/8 in the chondrocyte injury model increased significantly. Knockdown of TRAF6 suppressed the expression of matrix metallopeptidase-13 (MMP-13) and interleukin-6 (IL-6) induced by LPS, and alleviated cell apoptosis. Meanwhile, western blot and immunofluorescent staining demonstrated that IκBα degradation and p65 nuclear transportation were also inhibited, revealing that knockdown of TRAF6 suppressed activation of the NF-κB pathway in LPS-induced chondrocytes apoptosis model. Collectively, our findings suggest that TRAF6 plays a crucial role in FJOA development by regulating NF-κB signaling pathway. Knockdown of TRAF6 may supply a potential therapeutic strategy for FJOA.

This study reports a simple and practical method to introduce antimicrobial and biofilm-controlling functions into hydroxyl- or amino-containing polymers such as cellulose using compounds derived from widely used reactive dyes. Two dichloro- s -triazine-based dyes, reactive blue 4 and sodium 4-(4,6-dichloro-1,3,5-triazinylamino)-benzenesulfonate (a colorless reactive "dye"), were covalently attached to cellulose at room temperature by replacing one chloride on the dyes with the hydroxyl groups on cellulose followed by hydrolysis under alkaline conditions to transform the remaining chloride into hydroxyl groups. The chemical reactions were confirmed by FT-IR studies, energy-dispersive X-ray spectroscopy, water contact angle measurement, and zeta potential analysis. The resulting cellulose provided powerful antimicrobial activities against Staphylococcus epidermidis ( S. epidermidis , ATCC 35984, Gram-positive bacteria), Escherichia coli ( E. coli , ATCC 15597, Gram-negative bacteria), and Candida albicans ( C. albicans , ATCC 10231, yeast) and effectively prevented the formation of bacterial or fungal biofilms. The minimum inhibition concentrations of the hydrolyzed dyes were similar to that of phenol. In the zone of inhibition studies using phenolic compounds as positive controls, the hydrolyzed dyes and their model compound cyanuric acid demonstrated antimicrobial functions, suggesting that the antimicrobial activities were associated with the phenol-like hydroxyl groups on the triazine rings. Antimicrobial mechanism investigation indicated that the phenol-like structures on the dyed cellulose caused microbial lysis and leakage of intracellular components. The antimicrobial functions were durable upon repeated washing, and the dyed cellulose showed outstanding biocompatibility toward mammalian cells.

Background: Spinal cord injuries (SCIs), along with subsequent secondary injuries, often result in irreversible damage to both sensory and motor functions. However, a thorough view of the underlying pathological mechanisms of SCIs, especially in a temporal-spatial manner, is still lacking., Methods: To obtain a comprehensive, real-time view of multiple subsets of the cellular mechanisms involved in SCIs, we applied RNA-sequencing technology to characterize the temporal changes in gene expression around the lesion site of contusion SCI in rats. First, we identified the differentially expressed genes (DEGs) in contrast to sham controls at 1, 4, and 7 days post SCI. Through bioinformatics analysis, including Pathway analysis, Gene-act-net, and Pathway-act-net, we screened and verified potential key pathways and genes associated with either the acute or subacute stages of SCI pathology., Results: The top three overrepresented pathways were associated with cytokine-cytokine receptor interaction, TNF signaling pathway, and cell cycle at day 1; lysosome, cytokine-cytokine receptor interaction, phagosome at day 4; and phagosome, lysosome, cytokine-cytokine receptor interaction at day 7 post injury. Further, we identified uniquely enriched genes at each time point, such as Ccr1 and Nos2 at day 1; as well as Mgst2, and Pla2g3 at 4 and 7 days post-injury., Conclusions: Our pathway analysis suggested a transition from inflammatory responses to multiple forms of cell death processes from the acute to subacute stages of SCI. Further, our results revealed a continuous transformation from a more inflammatory to an apoptotic/self-repairing transcriptome following the time-course of SCIs. Our research provides novel insights into the molecular mechanisms of SCI pathophysiology and identifies potential targets for therapeutic intervention after SCI., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/atm-20-6519). The authors have no conflicts of interest to declare., (2020 Annals of Translational Medicine. All rights reserved.)

The pathophysiological changes in cartilage are a crucial feature of lumbar facet joint (LFJ) degeneration and arthritis. However, the molecular mechanism of human LFJ degeneration remains largely defined. This study aimed to examine the changes in chondrocytes at different stages of degenerative LFJ using hematoxylin and eosin and Safranin O staining. The significant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot). In vitro, chondrocytes scraped from the LFJs during surgery were stimulated by interleukin (IL)-1β to establish the injury model. The association of C/EBPβ and RUNX2 with active caspase-3 on chondrocytes was analyzed. The high expression level of C/EBPβ, RUNX2, and MMP13 was consistent with that of caspase-3, which reached a peak after 36 h of stimulation. Immunofluorescence suggested that C/EBPβ, RUNX2, and MMP13 co-labeled with active caspase-3. Moreover, immunoprecipitation data prompted that C/EBPβ was able to interact with RUNX2. The knockdown of C/EBPβ significantly decreased the expression levels of MMP13 and active caspase-3 (2.48 and 2.89 times as detected by Western blot analysis) and inhibited chondrocyte apoptosis, which was further demonstrated using flow cytometry. Taken together, the findings of this study uncovered that C/EBPβ could interact with RUNX2 to induce chondrocyte apoptosis in human LFJ degeneration by regulating the expression of MMP13.

Background: Osteoarthritis (OA) is a prevalent degenerative joint disease, which was characterized by inflammation and cartilage degradation. Accumulating evidence has demonstrated that Tanshinone I has an anti-inflammatory effect in various diseases. However, the efficacy of Tanshinone I as an anti-inflammatory agent in OA remains unclear. This study aimed to explore the role of Tanshinone I on OA both in vitro and in vivo., Methods: CHON-001 cells were treated with IL-1β (10 ng/mL) for 72 hrs to induce OA model in vitro. Meanwhile, CHON-001 cells were pre-treated with 20 μM Tanshinone I for 24 hrs and then stimulated with IL-1β (10 ng/mL) for 72 hrs. CCK-8, immunofluorescence and flow cytometry assays were used to detect the viability, proliferation and apoptosis in CHON-001 cells, respectively. Western blotting assay was used to detect the levels of collagen II, aggrecan, MMP-13, cleaved caspase 1, Gasdermin D, SOX11 and p-NF-κB in CHON-001 cells. In addition, the mouse model of OA was built by anterior cruciate ligament transection (ACLT) in the right knee. Meanwhile, the mice were administrated with 10 or 30 mg/kg Tanshinone I for 8 weeks. Safranin-O/Fast Green staining was used to assess cartilage destruction in a mouse model of OA., Results: In this study, IL-1β significantly induced apoptosis, extracellular matrix degradation and inflammatory response in CHON-001 cells. Tanshinone I significantly inhibited IL-1β-induced apoptosis in CHON-001 cells. In addition, the IL-1β-induced collagen II, aggrecan degradation, SOX11 downregulation, and MMP-13 and p-NF-κB upregulation in CHON-001 cells were notably reversed by Tanshinone I treatment. Moreover, Tanshinone I alleviated cartilage destruction and synovitis and reduced OARSI scores and subchondral bone thickness in a mouse model of OA., Conclusion: Our findings showed that Tanshinone I could alleviate the progression of OA in vitro and in vivo. These results demonstrated that Tanshinone I might be regarded as a promising therapeutic agent for the treatment of OA., Competing Interests: The authors report no conflicts of interest in this work., (© 2019 Wang et al.)

Dexamethasone (DEX) induces significant cytotoxicity to human osteoblasts. cPWWP2A is recently-indentified novel circular RNA (circRNA), acting as an endogenous sponge of microRNA-579 (miR-579). The present study tested the expression and potential functions of the cPWWP2A-miR-579 axis in DEX-treated osteoblasts. We show that cPWWP2A is downregulated in the necrotic femoral head tissues of DEX-taking human patients as well as in DEX-treated human osteoblasts. In OB-6 osteoblastic cells and primary human osteoblasts ectopic overexpression of cPWWP2A potently inhibited DEX-induced miR-579 accumulation, cell death, apoptosis and programmed necrosis. Silencing miR-579, by targeted siRNAs, also attenuated DEX-induced cytotoxicity in human osteoblasts. Significantly, mimicking DEX-induced actions, cPWWP2A silencing or forced miR-579 overexpression induced significant cytotoxicity in human osteoblasts. Further analyses demonstrated that miR-579's targets, including SIRT1 and PDK1 (phosphoinositide-dependent protein kinase 1), were downregulated in DEX-treated osteoblasts. Their levels were decreased as well in the necrotic femoral head tissues of DEX-taking human patients. Taken together we show that dysregulation of the cPWWP2A-miR-579 axis is involved in DEX-induced cytotoxicity in human osteoblasts., (Copyright © 2019 Elsevier Inc. All rights reserved.)

In order to prepare multifunctional fibrous membranes with hydrophobicity, antibacterial properties and UV resistance, we used silica and titanium dioxide for preparing SiO 2 @TiO 2 nanoparticles (SiO 2 @TiO 2 NPs) to create roughness on the fibrous membranes surfaces. The introduction of TiO 2 was used for improving UV resistance. N-Halamine precursor and silane precursor were introduced to modify SiO 2 @TiO 2 NPs to synthesize SiO 2 @TiO 2 -based core@shell composite nanoparticles. The hydrophobic antibacterial fibrous membranes were prepared by a dip-pad process of electrospun biodegradable polyhydroxybutyrate/poly-ε-caprolactone (PHB/PCL) with the synthesized SiO 2 @TiO 2 -based core@shell composite nanoparticles. TEM, SEM and FT-IR were used to characterize the synthesized SiO 2 @TiO 2 -based core@shell composite nanoparticles and the hydrophobic antibacterial fibrous membranes. The fibrous membranes not only showed excellent hydrophobicity with an average water contact angle of 144° ± 1°, but also appreciable air permeability. The chlorinated fibrous membranes could inactivate all S. aureus and E. coli O157:H7 after 5 min and 60 min of contact, respectively. In addition, the chlorinated fibrous membranes exhibited outstanding cell compatibility with 102.1% of cell viability. Therefore, the prepared hydrophobic antibacterial degradable fibrous membranes may have great potential application for packaging materials., Competing Interests: There are no conflicts to declare., (This journal is © The Royal Society of Chemistry.)

Although thought as a selective serotonin reuptake inhibitor (SSRI), the antidepressant mechanisms of paroxetine remain unknown. Previous studies have shown the role of the mammalian target of rapamycin (mTOR) signaling in depression. In this study, we investigated whether the antidepressant effects of paroxetine require mTOR signaling. We first examined whether chronic paroxetine administration restores the effects of CUMS and CSDS on the mTOR signaling cascade in the hippocampus and prefrontal cortex. Then, the pharmacologcial inhibitors of mTOR signaling (LY294002, U0126 and rapamycin) were used to assay if the paroxetine-induced reversing effects in the CUMS and CSDS models were prevented by mTOR system blockade. Furthermore, gene knockdown of mTOR by mTOR-shRNA was also used to test whether mTOR is necessary for the antidepressant effects of paroxetine. It was found that paroxetine treatment fully reversed the effects of CUMS and CSDS on the mTOR signaling in the hippocampus, but not the prefrontal cortex. Pharmacological inhibition of the mTOR signaling significantly blocked the antidepressant effects of paroxetine in the CUMS and CSDS models. Moreover, gene silencing of hippocampal mTOR by mTOR-shRNA also abolished the antidepressant effects of paroxetine. Taken together, hippocampal mTOR signaling is necessary for the antidepressant effects of paroxetine., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Vimentin, among the family of the intermediate filament, plays as the organizer of some critical proteins involved in migration, attachment, and cell signaling. In this study, the role of vimentin in chronic constriction injury (CCI) was investigated. Western blot revealed increased protein level of vimentin following CCI, peaking at 7 days. Double immunofluorescent staining showed that vimentin was mostly co-localized with astrocytes, not with neurons or microglia. In vitro, sensory neuronal injury stimulated astrocytes to produce more pro-inflammation cytokines, p-ERK (phosphorylated extracellular signal-regulated protein kinase), and vimentin. However, vimentin knockdown by siRNA (small interfering RNA) reversed the upregulation of p-ERK and vimentin expression and reduced the release of pro-inflammatory cytokines. Overall, stimulated astrocytes might release pro-inflammatory cytokines to promote the development of neuropathic pain via vimentin/ERK signaling.

Bacterial colonization and biofilm formation on dental resin composites cause secondary caries that shortens the service life of dental restorative materials. In this study, commercial barium borosilicate based glass powders, fillers widely used in dental composites, were covalently immobilized with silver sulfadiazine to provide antimicrobial effects. The chemical reactions were followed by FT-IR study, elemental analysis, and energy dispersive spectroscopy (EDS), and the reaction pathway was confirmed by model compound studies. The resulting glass powders demonstrated potent antimicrobial effects against Streptococcus mutans (S. mutans). BisGMA (2,2-bis[4-(2-hydroxy-3-methacrylyloxypropoxy)phenyl] propane)-based dental resins containing 2% to 10% of the new silver sulfadiazine glass powders exhibited powerful and durable antimicrobial efficacy against S. mutans. The mechanical properties of the antimicrobial resins were not negatively affected by the silver sulfadiazine glass powders, making them attractive candidates as antimicrobial fillers for dental composites and other related biomedical applications., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Annexin A2 (ANXA2), is a member of the annexin family of proteins that exhibit Ca 2+ -dependent binding to phospholipids. One attractive biological function of ANXA2 is participating in DNA synthesis and cell proliferation. Previous studies have shown that ANXA2 play a role in the development of the central nervous system. However, the biological function of ANXA2 after spinal cord injury (SCI) is still with limited acquaintance. In the present study, we performed a SCI model in adult rats and investigated the dynamic changes of ANXA2 expression in the spinal cord. Western blot analysis indicated a striking expression upregulation of ANXA2 after SCI. Immunohistochemistry further confirmed that ANXA2 immunoactivity was expressed at low levels in normal condition and increased at 5day after SCI. Double immunofluorescence staining prompted that ANXA2 immunoreactivity was found in astrocytes and neurons. Interestingly, ANXA2 expression was increased predominantly in astrocytes. We also examined the expression profiles of proliferating cell nuclear antigen (PCNA), Cyclin D1 and active caspase-3 in the injured spinal cords by western blot. Co-expression of ANXA2/PCNA, ANXA2/Cyclin D1 was detected in glial fibrillary acidic protein. Importantly, double immunofluorescence staining revealed that cell proliferation evaluated by PCNA appeared in many ANXA2-expressing cells and rare caspase-3 was observed in ANXA2-expressing cells after SCI. In addition, ANXA2 knockdown in astrocytes resulted in the increase of PCNA expression after LPS stimulation, showing that ANXA2 inhibited astrocyte proliferation after inflammation. Our data suggested that ANXA2 might play important roles in CNS pathophysiology after SCI., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

This study aims to compare two kinds of modified poly(lactic acid)(PLA)materials:PLA-chitosan(PLA-CTS)and PLA-poly(glycolic acid)(PLA-PGA).PLA-CTS and PLA-PGA scaffolds were prepared and observed under electron microscope.The scaffold porosity was calculated and the pH of the degradation solution was measured.Then rat olfactory ensheathing cells(OECs)were cultivated,and mixed cultured respectively with two scaffolds as two groups.The proliferation,adhesion rate and growth condition of the OECs were observed and compared between the two groups.Results showed that both the prepared PLA-CTS and PLA-PGA scaffolds were threedimensional porous structure and the porosity of PLA-CTS was 91%,while that of PLA-PGA was 87%.The pH of degradation solution decreased gradually,of which PLA-PGA fell faster than PLA-CTS.After added to the two scaffolds,most OECs could grow well,and there were no significant differences between the two groups on MTT test and nuclei number determined by fluorescent microscope.However,the cell adhesion rate of PLA-CTS group was significantly higher than that of PLA-PGA.It can be concluded that compared with PLA-PGA,PLA-CTS might be a better choice as OECs scaffold.

Fungal biofilm formation on healthcare materials is a significant clinical concern, often leading to medical-device-related infections, which are difficult to treat. A novel fungal repellent strategy is developed to control fungal biofilm formation. Methylacrylic acid (MAA) is grated onto poly methyl methacrylate (PMMA)-based biomaterials via plasma-initiated grafting polymerization. A cationic polymer, trimethylchitosan (TMC), is synthesized by reacting chitosan with methyl iodide. Sodium alginate (SA) is used as an anionic polymer. TMC/SA multilayers are coated onto the MAA-grafted PMMA via layer-by-layer self-assembly. The TMC/SA multilayer coatings significantly reduce fungal initial adhesion, and effectively prevent fungal biofilm formation. It is concluded that the anti-adhesive property of the surface is due to its hydrophilicity, and that the biofilm-inhibiting action is attributed to the antifungal activity of TMC as well as the chelating function of TMC and SA, which may have acted as fungal repellents. Phosphate buffered saline (PBS)-immersion tests show that the biofilm-modulating effect of the multilayer coatings is stable for more than 4 weeks. Furthermore, the presence of TMC/SA multilayer coatings improves the biocompatibility of the original PMMA, offering a simple, yet effective, strategy for controlling fungal biofilm formation., (© 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Previous studies have found inconsistent results from testing methods used to measure heterotrophic plate count (HPC) bacteria in dental unit waterline (DUWL) samples. This study used 63 samples to compare the results obtained from an in-office chairside method and 2 currently used commercial laboratory HPC methods (Standard Methods 9215C and 9215E). The results suggest that the Standard Method 9215E is not suitable for application to DUWL quality monitoring, due to the detection of limited numbers of heterotrophic organisms at the required 35°C incubation temperature. The results also confirm that while the in-office chairside method is useful for DUWL quality monitoring, the Standard Method 9215C provided the most accurate results.

Hypoxia and other adverse conditions are usually encountered by rapidly growing cells. The RNA-binding motif protein 3 (RBM3) is induced by low temperature and hypoxia. However, its expression and function in spinal cord injury are still unclear. To investigate the certain expression and biological function in the central nervous system, we performed an acute spinal cord contusion injury (SCI) model in adult rats. Western blot analysis indicated a striking expression upregulation of RBM3 after spinal cord injury (SCI). Double immunofluorescence staining prompted that RBM3 immunoreactivity was found in astrocytes and neurons. Interestingly, RBM3 expression was increased predominantly in astrocytes. Furthermore, colocalization of RBM3 with proliferating cell nuclear antigen (PCNA) was detected in astrocytes. To further understand whether RBM3 plays a role in astrocyte proliferation, we applied lipopolysaccharide (LPS) to induce astrocyte proliferation in vitro. Western blot analysis demonstrated that RBM3 expression was positively correlated with PCNA expression following LPS stimulation. Immunofluorescence analysis showed that the expression of RBM3 was also changed following the stimulation of astrocytes with LPS, which was parallel with the data in vivo. Additionally, knocking RBM3 down with small interfering RNA (siRNA) demonstrated that RBM3 might play a significant role in the proliferation of astrocytes treated by hypoxia in vitro. These results suggest that RBM3 may be involved in the proliferation of astrocytes after SCI. To summarize, we firstly uncover the temporal and spatial expression changes of RBM3 in spinal cord injury. Our data suggest that RBM3 might be implicated in central nervous system pathophysiology after SCI.

Background: More and more attention has been focused on the inflammation or degeneration caused by biochemical factors in radiculopathy during lumbar facet joint degeneration. This study was designed to examine the expression and relationship of MMP-1/TIMP-1 and interleukin-1β (IL-1β), and to analyze the possible mechanism in degenerative lumbar facet joint disease., Methods: Lumbar facet joint cartilage and synovial tissues in 36 cases of posterior lumbar surgery were harvested to investigate IL-1β and MMP-1/TIMP-1 by immunohistochemistry and Western blot analysis. Double labeling immunofluorescence and real-time PCR, respectively, were used to assess the relationship between IL-1β and MMP-1., Results: IL-1β and MMP-1 were low in the lumbar disc herniation (LDH) group, and increased markedly in the lumbar spinal canal stenosis (LSCS) group (P < 0.05). However, there is no significant difference of TIMP-1 between LDH group and LSCS group (P > 0.05). Double staining results indicated that IL-1β overlapped with MMP-1 in the LSCS group. Moreover, real-time PCR results showed that MMP-1 mRNA in chondrocytes in vitro was affected in a dose- and time-dependent manner in response to IL-1β stimulation., Conclusions: Overexpression of MMP-1, induced by IL-1β, plays an important role in the inflammatory process of lumbar facet joint degeneration.

Minichromosome maintenance protein 7 (MCM7), a member of the minichromosome maintenance protein family, is essential for eukaryotic DNA replication initiation and the early stage of the elongation process. MCM7 participates in the cell cycle control of genome duplication. While it is ubiquitously expressed in all tissues, the biological function of MCM7 in the central nervous system is still with limited acquaintance. In the present study, we performed a spinal cord injury (SCI) model in adult rats. Western blotting indicated a marked alteration of MCM7 after SCI. Immunohistochemistry analysis revealed a wide distribution of MCM7 in the spinal cord. Double immunofluorescence staining showed that MCM7 immunoreactivity was increased predominantly in neurons, astrocytes, and microglia after SCI. We also examined the expression profiles of active caspase-3, proliferating cell nuclear antigen (PCNA), and Ki67, whose changes were correlated with the expression profiles of MCM7. Moreover, colocalization of MCM7/active caspase-3 was detected in neuronal nuclei (NeuN), and colocalization of MCM7/PCNA was detected in NeuN, glial fibrillary acidic protein, and CD11b, respectively. Our results suggest that MCM7 might be implicated in the apoptosis of neuron and proliferation of astrocytes and microglia after SCI.

In this study, a berberine-loaded electrospun poly-(epsilon-caprolactone) nanofibrous membrane (B-NFM) was formulated. The B-NFM was composed of uniform nanofibers with the average diameter of 190 +/- 53 nm. Whole blood assay revealed that the B-NFM had higher absorption capacity than gauze wound dressing (GWD) and non-drug-loaded nanofibrous membrane (NFM). Hemostatic studies showed that the B-NFM was more efficient at promoting blood clotting than GWD and NFM. B-NFM was also demonstrated to possess broad-spectrum antimicrobial activity. Biocompatibility studies indicated that B-NFM had good compatibility with skin fibroblast cells. These results suggested that the B-NFM can promote in vitro hemostasis to minimize wound bleeding, absorb biofluid to provide a favorable environment, inhibit on-site microbial agents to prevent wound infection, and support skin cell growth to facilitate wound healing. These data highly suggest a potential clinical use of B-NFM as wound dressing material.

Myelin and lymphocyte protein (MAL) was identified as a tetraspan proteolipid that is highly expressed by oligodendrocytes and Schwann cells as a component of compact myelin. It has also been reported to be a tumour suppressor and induces apoptosis through the Fas pathway. However, its expression and function in spinal cord injury are still unclear, especially in gray matter. In this study, we performed a spinal cord contusion injury (SCI) model in adult rats and detected the dynamic changes of MAL expression in spinal cord. Western blot and immunohistochemistry analysis revealed that MAL was present in gray and white matter of normal spinal cord. It gradually increased, got a peak at 1 day, and then declined to basal levels after spinal cord injury. Double immunofluorescence staining showed that MAL immunoreactivity was found in neurons and oligodendrocytes. Interestingly, MAL expression was increased predominantly in neurons rather than oligodendrocytes. We also examined the expression profiles of active caspase-3, whose changes were correlated with the expression profiles of MAL. Moreover, co-localization of MAL with active caspase-3 was detected. In conclusion, this is the first description of MAL expression changes in gray matter after spinal cord injury. Our results prompted that MAL might participate in CNS pathophysiology after SCI.

An N-halamine precursor, 5,5-dimethylhydantoin (DMH), was covalently linked to the surface of polyurethane (PU) with 1,6-hexamethylene diisocyanate (HDI) as the coupling agent. The reaction pathways were investigated using propyl isocyanate (PI) as a model compound. The results suggested that the imide and amide groups of DMH have very similar reactivities toward the isocyanate groups on PU surfaces activated with HDI. After bleach treatment the covalently bound DMH moieties were transformed into N-halamines. The new N-halamine-based PU provided potent antimicrobial effects against Staphylococcus aureus (Gram-positive bacterium), Escherichia coli (Gram-negative bacterium), methicillin-resistant Staphylococcus aureus (MRSA, drug-resistant Gram-positive bacterium), vancomycin-resistant Enterococcus faecium (VRE, drug-resistant Gram-positive bacterium), and Candida albicans (fungus), and successfully prevented bacterial and fungal biofilm formation. The antimicrobial and biofilm controlling effects were stable for longer than 6 months under normal storage in open air. Furthermore, if the functions were lost due to prolonged use they could be recharged by another chlorination treatment. The recharging could be repeated as needed to achieve long-term protection against microbial contamination and biofilm formation., (Copyright © 2011 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.)

The present research was aimed to explore the biocompatibility of IKVAV self-assembling peptide nanofiber scaffold with olfactory ensheathing cells (OECs) of rats. The OECs were seeded onto the surface of coverslips covered with IKVAV self-assembling peptide nanofiber scaffold hydrogel (2D culture system), and implanted within IKVAV self-assembling peptide nanofiber scaffold hydrogel (3D culture system), respectively. The adhesion, viability of OECs were observed with inverted microscope. Then the characteristics for survival and adhesion of cells by image processing were observed, and statistical analysis on the number of S-100 positive cell, the area of the cell bodies and the perimeter of the cell and MTT method were carried out. It was found that the OECs could survive and migrate in IKVAV self-assembling peptide nanofiber scaffold. The result of the cell MTT exam, of the shape and quantity of cells had no significant difference compared to those of the OECs cultured with poly-L-lysine (PLL). It has been proved that IKVAV self-assembling peptide nanofiber scaffold has good biocompatibility with rat OECs.

This study examined bacterial growth and type on biofilm-controlling dental unit waterline (DUWL) tubing (T) and control manufacturer's tubing (C) in a laboratory DUWL model using ultrapure source water that was cycled through the lines. Sections of tubing lines were detached and examined for biofilm growth using SEM imaging at six sampling periods. Bacteria from inside surfaces of T and C, source unit, and reservoir were cultured and enumerated. At six months, organisms were molecularly identified from the alignment matches obtained from the top three BLAST searches for the 16S region. There was a 1-3 log increase in organism growth in a clean, nonsterile reservoir within an hour. Biofilm was established on the inside surfaces of C within three weeks, but not on T. Proteobacteria, and Sphingomonas spp. were identified in the source reservoir and C line, and a variation of the genera was found in T line.

Objective: A study was conducted to test the biofilm-controlling functions of N-halamine tubing over an eight-month period., Methods: A laboratory system, simulating a teaching dental clinic, was used to test rechargeable N-halamine tubing (T) compared to an untreated control (C) using the unit manufacturer's tubing. For the long-term study, a recharged tubing (RC) treated with bleach was used to compare with the test (T) and the control (C) tubing. Source tap water was cycled through the lines at 1.4 mL/minute, five minutes on and 25 minutes off, eight hours/day, five days/week. Every three weeks, samples of effluent, recovered adherent bacteria from inside tubing surfaces, and SEM images were examined for bacterial and biofilm growth. After sampling, a recharging solution of chlorine bleach (1 : 10 dilution) was run through T and RC lines, left overnight, and rinsed out the next morning. One-way ANOVAs and Spearman correlations were performed to detect significant differences for T, RC, and C, and determine significance with time period and source water, respectively., Results: Mean log CFU/mL for C effluent > T (p = 0.028), and C tubing > T (p = 0.035). Spearman correlations were significant between effluent and source water level for T (rho = 0.817), and T tubing (0.750); between RC tubing and source water level (rho = 0.836), and time (rho = 0.745); and between C and time (rho = 0.873). SEM imaging confirmed the presence of biofilm inside RC and C, but not inside T., Conclusion: N-halamine tubing completely inhibited biofilm formation without negatively affecting the physical properties of the effluent water. Further research on N-halamine tubing using a pure water source is recommended, as T effluent bacterial levels reflected the source tap water quality and proliferation of planktonic bacteria with no biofilm activity.

N-chloro-2,2,6,6-tetramethyl-4-piperidinol laurate (Cl-TMPL) was prepared by reacting 2,2,6,6-tetramethyl-4-piperidinol hydrochloride (TMP·HCl) with lauroyl chloride, followed by chlorination with sodium dichloroisocyanurate. The chemical structure of Cl-TMPL was characterized with FT-IR, NMR, DSC, and TGA analyses. The antimicrobial performance of Cl-TMPL against Gram-positive and Gram-negative bacteria was compared with 1-chloro-3-dodecyl-5,5-dimethylhydantoin (Cl-DDMH), a amide N-halamine, and chloro-2,4-diamino-6-dodecyl-1,3,5-triazine (Cl-DADT), a melamine (imino) N-halamine. The three classes of N-halamines were used as additives for polyurethane (PU). Visible light transparency data indicated that up to 6% of Cl-DDMH or Cl-DADT could be compatibly mixed with PU, but Cl-TMPL had low compatibility with PU at higher than 2% of Cl-TMPL. With the same additive content, Cl-DDMH and Cl-DADT provided more powerful antimicrobial and biofilm-controlling effects than Cl-TMPL. In stability studies, however, PU samples with Cl-TMPL released the lowest amount of active chlorine into the immersing solution, suggesting the highest stability of the antimicrobial and biofilm-controlling efficacy.

Chitosan, a natural cationic polymer, strongly binds anionic antibiotics (e.g., rifampin) through the formation of ionic complexes. The new system shows sustained rifampin release, leading to potent antimicrobial and biofilm-controlling functions against gram-positive bacteria including Staphylococcus epidermidis and Staphylococcus aureus, which are responsible for a wide range of medical device-related infections, for longer than 30 days. Moreover, the released drugs can be recharged to further extend antimicrobial durations. Drug release mechanisms and potential applications of the new system are also discussed., (Copyright 2008 Wiley Periodicals, Inc.)

In this study, the surfaces of polypropylene tubing were hydroxylated with potassium persulfate. The resultant tubing surfaces were grafted with methacrylamide (MAA) using ceric(IV) ammonium nitrate as an initiator. Upon chlorination treatment with diluted chlorine bleach, some of the amide groups in the grafted MAA side chains were transformed into stable acyclic N-halamines. The reactions were confirmed with attenuated total reflectance infrared, X-ray photoelectron spectra, and iodimetric titration. The resultant tubing was challenged with Pseudomonas aeruginosa (P. aeruginosa) in a continuous flowing model. Bacteria culturing and scanning electron microscope studies showed that the chlorinated MAA-grafted tubing could provide potent and rechargeable biofilm-controlling functions against the test microorganisms., ((c) 2007 Wiley Periodicals, Inc.)

An N-halamine-based polymeric additive, poly[(6-morpholino-s-triazine-2,4-diyl)-N-chloro-[2,2,6,6-tetramethyl-4-piperidyl)imino]-hexamethylene[(2,2,6,6-4-piperidyl) imino]] (APA-1), was prepared in this study. The chemical structure of APA-1 was confirmed by iodometric titration, (1)H NMR, and (13)C NMR analysis. APA-1 was incorporated into polyurethane through solvent casting. The resultant materials demonstrated potent antimicrobial functions against Staphylococcus epidermidis. Zone of inhibition studies showed that APA-1 inactivated the bacteria through contact, without leaching out of the polyurethane samples. In vitro studies illustrated that APA-1-containing polyurethane could prevent the colonization and biofilm formation of S. epidermidis for at least 28 days.