An attenuated strain of cyprinid herpesvirus 2 as a vaccine candidate against herpesviral hematopoietic necrosis disease in gibel carp, Carassius auratus gibelio.

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.

Upregulation of P2Y12 inhibits chondrocyte apoptosis in lumbar osteoarthritis through the PI3K/AKT signaling pathway.

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-1ß -induced chondrocyte apoptosis through PI3K/AKT signaling pathway, thus playing a certain protective role on cartilage.

Knockdown of TRAF6 inhibits chondrocytes apoptosis and inflammation by suppressing the NF-κB pathway in lumbar facet joint osteoarthritis.

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.

Network analysis of population flow among major cities and its influence on COVID-19 transmission in China.

Large-scale and diffuse population flow amplifies the localized COVID-19 outbreak into a widespread pandemic. Network analysis provides a new methodology to uncover the topology and evolution of the population flow and understand its influence on the early dynamics of COVID-19 transmission. In this paper, we simulated 42 transmission scenarios to show the distribution of the COVID-19 outbreak across China. We predicted some original (Guangzhou, Shanghai, Shenzhen) had higher total aggregate population outflows than Wuhan, indicating larger spread scopes and faster growth rates of COVID-19 outbreak. We built an importation risk model to identify some major cities (Dongguan and Foshan) with the highest total importation risk values and the highest standard deviations, indicating the core transmission chains (Dongguan-Shenzhen, Foshan-Guangzhou). We built the population flow networks to analyze their Spatio-temporal characteristics and identify the influential sub-groups and spreaders. By removing different influential spreaders, we identified Guangzhou can most influence the network's topological characteristics, and some major cities' degree centrality was significantly decreased. Our findings quantified the effectiveness of travel restrictions on delaying the epidemic growth and limiting the spread scope of COVID-19 in China, which helped better derive the geographical COVID-19 transmission related to population flow networks' structural features.

Triad1 regulates the expression and distribution of EHD1 contributing to the neurite outgrowth of neurons after spinal cord injury.

Traumatic spinal cord injury is a common and severe complication after an accident. As we all know that neurite outgrowth of neurons is difficult after a spinal cord injury. Endosome system is associated with cargoes transportation and contributes in promoting the neuronal capability for neurite outgrowth. EH domain-containing protein 1 (EHD1) transports proteins through the endosome system, especially in the recycling endosomes and regulating the neurite outgrowth. In mammalian cells, the involvement of the ubiquitin-proteasome system in endosomal sorting has been well established. Two RING fingers and a DRIL (double RING finger-linked) 1 (Triad1) plays an important role in membrane trafficking and its mutant results in the wrong accumulation of receptors in endosomes and plasma membrane. In this current study, we reasonably integrated the results of the above research and investigated the regulating function of Triad1 to EHD1 following the spinal cord injury. We characterized the upregulated expression and distribution of Triad1 and EHD1 in the neurons after SCI and declared the interaction between Triad1 with EHD1 both in vitro and in vivo. Triad1 regulated the interaction between itself and the full-length or EH domain of EHD1, which influenced the neurite outgrowth of PC12 cells. Our data delineate a novel interaction between Triad1 and EHD1 that may contribute to the regulation of neurite outgrowth for neurons after the spinal cord injury.

Dysregulation of cPWWP2A-miR-579 axis mediates dexamethasone-induced cytotoxicity in human osteoblasts.

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.

Up-regulation of TRAF2 inhibits chondrocytes apoptosis in lumbar facet joint osteoarthritis.

Tumor necrosis factor receptor-associated factor 2 (TRAF2) has been demonstrated that it plays a significant role in cell death receptor signal transduction. The purpose of this study was to investigate the expression of TRAF2 and its possible role in FJOA. We observed an up-regulation of TRAF2 in FJOA by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) compared to normal tissues. In vitro, we used TNF-α to stimulate Human SW1353 chondrosarcoma cells to establish the chondrocytes injury model. Western blot analysis revealed significant expression of TRAF2 and cleaved caspase-3/8 in SW1353 cells. Co-localization of TRAF2/cleaved caspase-3/8 was detected in the cells injury model by double-labeling immunofluorescent staining. We demonstrated a possible anti-apoptotic effect of TRAF2 in chondrocyte apoptosis in FJOA by knockdown of its expression with siRNA. Moreover, TRAF2 knockdown was demonstrated to enhance TNF-α-induced apoptosis by flow cytometry assay. In conclusion, our results show that the up-regulation of TRAF2 may play an important role in the inhibition of chondrocyte apoptosis of FJOA.

E3 Ubiquitin Ligase c-cbl Inhibits Microglia Activation After Chronic Constriction Injury.

E3 ubiquitin ligase c-Caritas B cell lymphoma (c-cbl) is associated with negative regulation of receptor tyrosine kinases, signal transduction of antigens and cytokine receptors, and immune response. However, the expression and function of c-cbl in the regulation of neuropathic pain after chronic constriction injury (CCI) are unknown. In rat CCI model, c-cbl inhibited the activation of spinal cord microglia and the release of pro-inflammatory factors including tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1ß) and interleukin 6 (IL-6), which alleviated mechanical and heat pain through down-regulating extracellular signal-regulated kinase (ERK) pathway. Additionally, exogenous TNF-α inhibited c-cbl protein level vice versa. In the primary microglia transfected with c-cbl siRNA, when treated with TNF-α or TNF-α inhibitor, the corresponding secretion of IL-1ß and IL-6 did not change. In summary, CCI down-regulated c-cbl expression and induced the activation of microglia, then activated microglia released inflammatory factors via ERK signaling to cause pain. Our data might supply a novel molecular target for the therapy of CCI-induced neuropathic pain.

Demonstration of biofilm removal from type 304 stainless steel using pulsed-waveform electropolishing.

This article describes an electrochemical method to remove bacterial biofilm from a stainless steel (SS) surface using a potential pulse/reverse pulse technique. This technique employs a periodic waveform that consists of anodic and cathodic pulses. The pulses can effectively strip a thin layer of metal off the SS surface, along with the adherent biofilm, in a saline solution. Not only can the pulses effectively remove biofilm from the SS surface, but they also regenerate the original mirror-like shiny surface. The importance of this electrochemical biofilm removal method is its wide applicability for any types of biofilms. That is, instead of directly removing the biofilm, it removes a very thin layer of the metal under the biofilm. Thus, the removal process is independent to the nature of the biofilms. Furthermore, this electrochemical biofilm removal method is rapid (less than 30 s of potential pulse time) and does not require hazardous chemicals.

Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing.

Facet joint osteoarthritis is common lumbar osteoarthritis characterized by facet joint cartilage degeneration. However, the molecular basis of facet joint osteoarthritis remains largely undetermined. In the current study, we collected facet joint tissue samples from 10 control patients and 48 patients with facet joint osteoarthritis (20 patients with moderate degeneration and 28 with severe degeneration). The control patients underwent internal fixation of the lumbar spine due to vertebral fracture. RNA deep sequencing was performed, and Bioinformatic tools were applied. Among top 30 enriched signaling pathways, we focused on two inflammation-related signaling pathways, Wnt and NF-κB signaling pathways. Subsequently, using the quantitative RT-PCR analysis, we confirmed that in Wnt signaling pathway, the mRNA levels of Dickkopf WNT Signaling Pathway Inhibitor 2 (DKK2), Sex-determining Region Y-box 17 (SOX17), MYC, Cyclin D1, Calcium/Calmodulin Dependent Protein Kinase II Alpha (CAMK2A), and Wnt Family Member 11 and 5 were increased in facet joint osteoarthritis, while the mRNA levels of WNT Inhibitory Factor 1, Casein Kinase 1 Alpha 1, Transcription Factor 7/Lymphoid Enhancer Binding Factor 1 (TCF7/LEF1), and VANGL Planar Cell Polarity Protein 2 were decreased. In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.

Effects of Nerve Growth Factor and Basic Fibroblast Growth Factor Promote Human Dental Pulp Stem Cells to Neural Differentiation.

Dental pulp stem cells (DPSCs) were the most widely used seed cells in the field of neural regeneration and bone tissue engineering, due to their easily isolation, lack of ethical controversy, low immunogenicity and low rates of transplantation rejection. The purpose of this study was to investigate the role of basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) on neural differentiation of DPSCs in vitro. DPSCs were cultured in neural differentiation medium containing NGF and bFGF alone or combination for 7 days. Then neural genes and protein markers were analyzed using western blot and RT-PCR. Our study revealed that bFGF and NGF increased neural differentiation of DPSCs synergistically, compared with bFGF and NGF alone. The levels of Nestin, MAP-2, ßIII-tubulin and GFAP were the most highest in the DPSCs + bFGF + NGF group. Our results suggested that bFGF and NGF signifiantly up-regulated the levels of Sirt1. After treatment with Sirt1 inhibitor, western blot, RT-PCR and immunofluorescence staining showed that neural genes and protein markers had markedly decreased. Additionally, the ERK and AKT signaling pathway played a key role in the neural differentiation of DPSCs stimulated with bFGF + NGF. These results suggested that manipulation of the ERK and AKT signaling pathway may be associated with the differentiation of bFGF and NGF treated DPSCs. Our date provided theoretical basis for DPSCs to treat neurological diseases and repair neuronal damage.

The Expression of IGFBP6 after Spinal Cord Injury: Implications for Neuronal Apoptosis.

IGFBP6, a member of the insulin-like growth factor-binding proteins family that contains six high affinity IGFBPs, modulates insulin-like growth factor (IGF) activity and also showed an independent effect of IGF, such as growth inhibition and apoptosis. However, the role of IGFBP6 in spinal cord injury (SCI) remains largely elusive. In this study, we have performed an acute SCI model in adult rats and investigated the dynamic changes of IGFBP6 expression in the spinal cord. Our results showed that IGFBP6 was upregulated significantly after SCI, which was paralleled with the levels of apoptotic proteins p53 and active caspase-3. Immunofluorescent labeling showed that IGFBP6 was co-localizated with active caspase-3 and p53 in neurons. To further investigate the function of IGFBP6, an apoptosis model was established in primary neuronal cells. When IGFBP6 was knocked down by specific short interfering RNA (siRNA), the protein levels of active caspase-3 and Bax as well as the number of apoptotic primary neurons were significantly decreased in our study. Taken together, our findings suggest that the change of IGFBP6 protein expression plays a key role in neuronal apoptosis after SCI.

Controlling bacterial fouling with polyurethane/N-halamine semi-interpenetrating polymer networks.

N -halamine-based interpenetrating polymer networks were developed as a simple and effective strategy in the preparation of antimicrobial polymers. An N-halamine monomer, N-chloro-2, 2, 6, 6-tetramethyl-4-piperidyl methacrylate, was incorporated into polyurethane in the presence of a cross-linker and an initiator. Post-polymerization of the monomers led to the formation of polyurethane/N-halamine semi-interpenetrating polymer networks. The presence of N-halamines in the semi-interpenetrating polymer networks was confirmed by attenuated total reflectance infrared, water contact angle, and energy-dispersive X-ray spectroscopy analysis. The N-halamine contents in the semi-interpenetrating polymer networks could be readily controlled by changing reaction conditions. The distribution of active chlorines within the semi-interpenetrating polymer networks was characterized with energy-dispersive X-ray spectroscopy. Contact mode antimicrobial tests, zone of inhibition studies, and scanning electron microscopy observations showed that the semi-interpenetrating polymer networks had potent antimicrobial and antifouling effects against both Gram-positive and Gram-negative bacteria. Release tests demonstrated the outstanding stability of the N-halamine structures in the new semi-interpenetrating polymer networks.

Chitosan scaffolds induce human dental pulp stem cells to neural differentiation: potential roles for spinal cord injury therapy.

Cell-based transplantation strategies hold great potential for spinal cord injury (SCI) repair. Chitosan scaffolds have therapeutic benefits for spinal cord regeneration. Human dental pulp stem cells (DPSCs) are abundant available stem cells with low immunological incompatibility and can be considered for cell replacement therapy. The purpose of this study is to investigate the role of chitosan scaffolds in the neural differentiation of DPSCs in vitro and to assess the supportive effects of chitosan scaffolds in an animal model of SCI. DPSCs were incubated with chitosan scaffolds. Cell viability and the secretion of neurotrophic factors were analyzed. DPSCs incubated with chitosan scaffolds were treated with neural differentiation medium for 14 days and then neural genes and protein markers were analyzed by Western blot and reverse transcription plus the polymerase chain reaction. Our study revealed a higher cell viability and neural differentiation in the DPSC/chitosan-scaffold group. Compared with the control group, the levels of BDNF, GDNF, b-NGF, and NT-3 were significantly increased in the DPSC/chitosan-scaffold group. The Wnt/ß-catenin signaling pathway played a key role in the neural differentiation of DPSCs combined with chitosan scaffolds. Transplantation of DPSCs together with chitosan scaffolds into an SCI rat model resulted in the marked recovery of hind limb locomotor functions. Thus, chitosan scaffolds were non-cytotoxic and provided a conducive and favorable microenvironment for the survival and neural differentiation of DPSCs. Transplantation of DPSCs might therefore be a suitable candidate for treating SCI and other neuronal degenerative diseases.

Upregulation of PSMB4 is Associated with the Necroptosis after Spinal Cord Injury.

Spinal cord injury (SCI) is one of the most common and severe complications in spine injury. It is difficult to prevent cell necroptosis and promote the survival of residual neurons after SCI. Proteasome beta-4 subunit (PSMB4) is the first proteasomal subunit with oncogenic properties promoting cancer cell survival and tumor growth in vivo, and our previous study showed that PSMB4 is significantly associated with neuronal apoptosis in neuroinflammation. However, PSMB4 function in the necroptosis after SCI is unkown. RIP3, a key regulatory factor of necroptosis, correlates with the induction of necroptosis in various types of cells and signaling pathway. Upregulation of the RIP3 expression may play a role as a novel molecular mechanism in secondary neural tissue damage following SCI. In this study, we established an acute spinal cord contusion injury model in adult rats to investigate the potential role of PSMB4 during the pathological process of SCI. We found PSMB4 expression was significantly up-regulated 3 days after injury by western blot and immunohistochemical staining. Double immunofluorescent staining indicated obvious changes of PSMB4 expression occurred in neurons. Significant up-regulation of PSMB4 expression was observed in Rip3 positive neurons at 3 days after SCI, which indicated that PSMB4 might play a vital role in the regulation of Rip3. Overexpress and knockdown PSMB4 could intervene the RIP3 and Mixed lineage kinase domain-like protein (MLKL) pathway in Tumor necrosis factor-α (TNF-α) induced necroptosis cell model. Based on our experimental data, we boldly conclude that PSMB4 is associated with RIP3 involved necroptosis after SCI.

[Experimental Comparison Research between Two Kinds of Modified Poly(lactic acid)Material In Vitro].

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.

Expression of Peroxiredoxin 1 After Traumatic Spinal Cord Injury in Rats.

Reactive astrogliosis and microgliosis after spinal cord injury (SCI) contribute to glial scar formation that impedes axonal regeneration. The mechanisms underlying reactive astrocyte and microglia proliferation upon injury remain partially understood. Peroxiredoxin 1 (PRDX1) is an antioxidant participating in cell proliferation, differentiation, and apoptosis. However, PRDX1 functions in SCI-induced astrocyte and microglia proliferation are unknown. In this study, we established an acute spinal cord contusion injury model in adult rats to investigate the potential role of PRDX1 during the pathological process of SCI. We found the palpable expression increase of PRDX1 after SCI by western blot and immunohistochemistry staining. Double immunofluorescence staining showed that PRDX1 expression mainly increased in astrocytes and microglia. In addition, PRDX1/proliferating cell nuclear antigen (PCNA) colocalized in astrocytes and microglia. Furthermore, PCNA expression also elevated after SCI, as well as was positively correlated with PRDX1 expression. In vitro, PRDX1 expression in primary rat spinal cord astrocytes and microglia changed in a concentration- and time-dependent manner according to LPS treatment. In addition, PRDX1 knockdown in astrocytes and microglia resulted in the decrease of PCNA expression after LPS stimulation, showing that PRDX1 promoted astrocyte and microglia proliferation after inflammation. Our results suggested that PRDX1 might play a crucial role in astrocyte and microglia proliferation after SCI.

Fluorinated and Un-fluorinated N-halamines as Antimicrobial and Biofilm-controlling Additives for Polymers.

The objective of this study was to evaluate the effects of fluorination on the antimicrobial and biofilm-controlling activities of N-halamine-based additives for polymers. A fluorinated N-halamine, 1-chloro-3-1H,1H,2H,2H-perflurooctyl-5,5-dimetylhydantoin (Cl-FODMH), and its un-fluorinated counterpart, 1-chloro-3-octyl-5,5-dimethylhydantoin (Cl-ODMH), were synthesized and characterized with FT-IR, 1H-NMR, and DSC studies. Polyurethane (PU) films containing Cl-ODMH and Cl-FODMH as antimicrobial additives were fabricated through solvent casting. With the same additive contents (1wt%-5 wt%), PU films with Cl-FODMH showed higher contact angle values. AFM, SEM and DSC results revealed that while Cl-ODMH distributed evenly within PU, Cl-FODMH aggregated and formed macro-domains in PU. Antimicrobial studies showed that PU films with Cl-ODMH had higher antimicrobial and biofilm-controlling potency against Gram-positive and Gram-negative bacteria than PU samples with Cl-FODMH. These results demonstrated the importance of distribution of additives in polymers on antimicrobial performances, shedding lights on future antimicrobial material design strategies.

Acyclic N-halamine-immobilized polyurethane: Preparation and antimicrobial and biofilm-controlling functions.

Hydroxyl groups were introduced onto polyurethane surfaces through 1,6-hexamethylene diisocyanate activation, followed by diethanolamine hydroxylation. Polymethacrylamide was covalently attached to the hydroxylated polyurethane through surface grafting polymerization of methacrylamide using cerium (IV) ammonium nitrate as an initiator. After bleach treatment, the amide groups of the covalently bound polymethacrylamide chains were transformed into N-halamines. The new N-halamine-immobilized polyurethane provided a total sacrifice of 107-108 colony forming units per milliliter of Staphylococcus aureus (Gram-positive bacteria), Escherichia coli (Gram-negative bacteria), and Candida albicans (fungi) within 10 min and successfully prevented bacterial and fungal biofilm formation. The antimicrobial and biofilm-controlling effects were both durable and rechargeable, pointing to great potentials of the new acyclic N-halamine-immobilized polyurethane for a broad range of related applications.

Evaluation of 3 dental unit waterline contamination testing methods.

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.