26 research outputs found

    Carbohydrate‐Based Polymer Brushes Prevent Viral Adsorption on Electrostatically Heterogeneous Interfaces

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    Chemical heterogeneity on biomaterial surfaces can transform its interfacial properties, rendering nanoscale heterogeneity profoundly consequential during bioadhesion. To examine the role played by chemical heterogeneity in the adsorption of viruses on synthetic surfaces, a range of novel coatings is developed wherein a tunable mixture of electrostatic tethers for viral binding, and carbohydrate brushes, bearing pendant α‐mannose, ÎČ‐galactose, or ÎČ‐glucose groups, is incorporated. The effects of binding site density, brush composition, and brush architecture on viral adsorption, with the goal of formulating design specifications for virus‐resistant coatings are experimentally evaluated. It is concluded that virus‐coating interactions are shaped by the interplay between brush architecture and binding site density, after quantifying the adsorption of adenoviruses, influenza, and fibrinogen on a library of carbohydrate brushes co‐immobilized with different ratios of binding sites. These insights will be of utility in guiding the design of polymer coatings in realistic settings where they will be populated with defects.A tunable coating comprising nonfouling carbohydrate brushes and electrostatic binding sites for viruses is employed to study the relationship between surface design parameters and viral adsorption. Ultimately, brush architecture determines whether the binding sites are exposed to, or shielded from viruses. These insights will guide the design of polymer coatings that can resist viral binding despite being populated with defects.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147118/1/marc201800530-sup-0001-SuppMat.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147118/2/marc201800530_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147118/3/marc201800530.pd

    Surgical periodontal therapy with and without initial scaling and root planing in the management of chronic periodontitis: a randomized clinical trial

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    Aim To compare the outcomes of surgical periodontal therapy with and without initial scaling and root planing. Methods Twenty‐four patients with severe chronic periodontitis were enrolled in this pilot, randomized controlled clinical trial. Patients were equally allocated into two treatment groups: Control group was treated with scaling and root planing, re‐evaluation, followed by Modified Widman Flap surgery and test group received similar surgery without scaling and root planing. Clinical attachment level, probing depth and bleeding on probing were recorded. Standardized radiographs were analysed for linear bone change from baseline to 6 months. Wound fluid inflammatory biomarkers were also assessed. Results Both groups exhibited statistically significant improvement in clinical attachment level and probing depth at 3 and 6 months compared to baseline. A statistically significant difference in probing depth reduction was found between the two groups at 3 and 6 months in favour of the control group. No statistically significant differences in biomarkers were detected between the groups. Conclusions Combined scaling and root planing and surgery yielded greater probing depth reduction as compared to periodontal surgery without initial scaling and root planing.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/107504/1/jcpe12259.pd

    Effects of triclosan on host response and microbial biomarkers during experimental gingivitis

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    AimThis exploratory randomized, controlled clinical trial sought to evaluate anti‐inflammatory and ‐microbial effects of triclosan during experimental gingivitis as assessed by host response biomarkers and biofilm microbial pathogens.Materials and MethodsThirty participants were randomized to triclosan or control dentifrice groups who ceased homecare for 21 days in an experimental gingivitis (EG) protocol. Plaque and gingival indices and saliva, plaque, and gingival crevicular fluid (GCF) were assessed/collected at days 0, 14, 21 and 35. Levels and proportions of 40 bacterial species from plaque samples were determined using checkerboard DNA‐DNA hybridization. Ten biomarkers associated with inflammation, matrix degradation, and host protection were measured from GCF and saliva and analysed using a multiplex array. Participants were stratified as “high” or “low” responders based on gingival index and GCF biomarkers and bacterial biofilm were combined to generate receiver operating characteristic curves and predict gingivitis susceptibility.ResultsNo differences in mean PI and GI values were observed between groups and non‐significant trends of reduction of host response biomarkers with triclosan treatment. Triclosan significantly reduced levels of A. actinomycetemcomitans and P. gingivalis during induction of gingivitis.ConclusionsTriclosan reduced microbial levels during gingivitis development (ClinicalTrials.gov NCT01799226).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134115/1/jcpe12519.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134115/2/jcpe12519_am.pd

    Bacterial and Salivary Biomarkers Predict the Gingival Inflammatory Profile

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/141936/1/jper0632-sup-0001.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141936/2/jper0632-sup-0002.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/141936/3/jper0079.pd

    Adenovirus Encoding Human Platelet-Derived Growth Factor-B Delivered to Alveolar Bone Defects Exhibits Safety and Biodistribution Profiles Favorable for Clinical Use

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    Abstract Platelet-derived growth factor (PDGF) gene therapy offers promise for tissue engineering of tooth-supporting alveolar bone defects. To date, limited information exists regarding the safety profile and systemic biodistribution of PDGF gene therapy vectors when delivered locally to periodontal osseous defects. The aim of this preclinical study was to determine the safety profile of adenovirus encoding the PDGF-B gene (AdPDGF-B) delivered in a collagen matrix to periodontal lesions. Standardized alveolar bone defects were created in rats, followed by delivery of matrix alone or containing AdPDGF-B at 5.5-108 or 5.5-109 plaque-forming units/ml. The regenerative response was confirmed histologically. Gross clinical observations, hematology, and blood chemistries were monitored to evaluate systemic involvement. Bioluminescence and quantitative polymerase chain reaction were used to assess vector biodistribution. No significant histopathological changes were noted during the investigation. Minor alterations in specific hematological and blood chemistries were seen; however, most parameters were within the normal range for all groups. Bioluminescence analysis revealed vector distribution at the axillary lymph nodes during the first 2 weeks with subsequent return to baseline levels. AdPDGF-B was well contained within the localized osseous defect area without viremia or distant organ involvement. These results indicate that AdPDGF-B delivered in a collagen matrix exhibits acceptable safety profiles for possible use in human clinical studies.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78106/1/hum.2008.114.pd

    Porphyromonas gingivalis oral infection exacerbates the development and severity of collagen-induced arthritis

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    Abstract Introduction Clinical studies suggest a direct influence of periodontal disease (PD) on serum inflammatory markers and disease assessment of patients with established rheumatoid arthritis (RA). However, the influence of PD on arthritis development remains unclear. This investigation was undertaken to determine the contribution of chronic PD to immune activation and development of joint inflammation using the collagen-induced arthritis (CIA) model. Methods DBA1/J mice orally infected with Porphyromonas gingivalis were administered with collagen II (CII) emulsified in complete Freund’s adjuvant (CFA) or incomplete Freund’s adjuvant (IFA) to induce arthritis. Arthritis development was assessed by visual scoring of paw swelling, caliper measurement of the paws, mRNA expression, paw micro-computed tomography (micro-CT) analysis, histology, and tartrate resistant acid phosphatase for osteoclast detection (TRAP)-positive immunohistochemistry. Serum and reactivated splenocytes were evaluated for cytokine expression. Results Mice induced for PD and/or arthritis developed periodontal disease, shown by decreased alveolar bone and alteration of mRNA expression in gingival tissues and submandibular lymph nodes compared to vehicle. P. gingivalis oral infection increased paw swelling and osteoclast numbers in mice immunized with CFA/CII. Arthritis incidence and severity were increased by P. gingivalis in mice that received IFA/CII immunizations. Increased synovitis, bone erosions, and osteoclast numbers in the paws were observed following IFA/CII immunizations in mice infected with P gingivalis. Furthermore, cytokine analysis showed a trend toward increased serum Th17/Th1 ratios when P. gingivalis infection was present in mice receiving either CFA/CII or IFA/CII immunizations. Significant cytokine increases induced by P. gingivalis oral infection were mostly associated to Th17-related cytokines of reactivated splenic cells, including IL-1ÎČ, IL-6, and IL-22 in the CFA/CII group and IL-1ÎČ, tumor necrosis factor-α, transforming growth factor-ÎČ, IL-6 and IL-23 in the IFA/CII group. Conclusions Chronic P. gingivalis oral infection prior to arthritis induction increases the immune system activation favoring Th17 cell responses, and ultimately accelerating arthritis development. These results suggest that chronic oral infection may influence RA development mainly through activation of Th17-related pathways.http://deepblue.lib.umich.edu/bitstream/2027.42/112639/1/13075_2013_Article_4062.pd

    Porphyromonas gingivalis oral infection exacerbates the development and severity of collagen-induced arthritis

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    Abstract Introduction: Clinical studies suggest a direct influence of periodontal disease (PD) on serum inflammatory markers and disease assessment of patients with established rheumatoid arthritis (RA). However, the influence of PD on arthritis development remains unclear. This investigation was undertaken to determine the contribution of chronic PD to immune activation and development of joint inflammation using the collagen-induced arthritis (CIA) model. Methods: DBA1/J mice orally infected with Porphyromonas gingivalis were administered with collagen II (CII) emulsified in complete Freund’s adjuvant (CFA) or incomplete Freund’s adjuvant (IFA) to induce arthritis. Arthritis development was assessed by visual scoring of paw swelling, caliper measurement of the paws, mRNA expression, paw micro-computed tomography (micro-CT) analysis, histology, and tartrate resistant acid phosphatase for osteoclast detection (TRAP)-positive immunohistochemistry. Serum and reactivated splenocytes were evaluated for cytokine expression. Results: Mice induced for PD and/or arthritis developed periodontal disease, shown by decreased alveolar bone and alteration of mRNA expression in gingival tissues and submandibular lymph nodes compared to vehicle. P. gingivalis oral infection increased paw swelling and osteoclast numbers in mice immunized with CFA/CII. Arthritis incidence and severity were increased by P. gingivalis in mice that received IFA/CII immunizations. Increased synovitis, bone erosions, and osteoclast numbers in the paws were observed following IFA/CII immunizations in mice infected with P gingivalis. Furthermore, cytokine analysis showed a trend toward increased serum Th17/Th1 ratios when P. gingivalis infection was present in mice receiving either CFA/CII or IFA/CII immunizations. Significant cytokine increases induced by P. gingivalis oral infection were mostly associated to Th17-related cytokines of reactivated splenic cells, including IL-1ÎČ, IL-6, and IL-22 in the CFA/CII group and IL-1ÎČ, tumor necrosis factor-α, transforming growth factor-ÎČ, IL-6 and IL-23 in the IFA/CII group. Conclusions: Chronic P. gingivalis oral infection prior to arthritis induction increases the immune system activation favoring Th17 cell responses, and ultimately accelerating arthritis development. These results suggest that chronic oral infection may influence RA development mainly through activation of Th17-related pathways

    Fiber Optical Cable and Connector System (FOCCoS) for PFS/Subaru

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    FOCCoS, Fiber Optical Cable and Connector System, has the main function of capturing the direct light from the focal plane of Subaru Telescope using optical fibers, each one with a microlens in its tip, and conducting this light through a route containing connectors to a set of four spectrographs. The optical fiber cable is divided in 3 different segments called Cable A, Cable B and Cable C. Multi-fibers connectors assure precise connection among all optical fibers of the segments, providing flexibility for instrument changes. To assure strong and accurate connection, these sets are arranged inside two types of assemblies: the Tower Connector, for connection between Cable C and Cable B; and the Gang Connector, for connection between Cable B and Cable A. Throughput tests were made to evaluate the efficiency of the connections. A lifetime test connection is in progress. Cable C is installed inside the PFI, Prime Focus Instrument, where each fiber tip with a microlens is bonded to the end of the shaft of a 2-stage piezo-electric rotatory motor positioner; this assembly allows each fiber to be placed anywhere within its patrol region, which is 9.5mm diameter.. Each positioner uses a fiber arm to support the ferrule, the microlens, and the optical fiber. 2400 of these assemblies are arranged on a motor bench plate in a hexagonal-closed-packed disposition.Comment: 11 pages, 20 figure
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