Antimicrobial Peptide-Polymer Conjugates for Dentistry.

Bacterial adhesion and growth at the composite/adhesive/tooth interface remain the primary cause of dental composite restoration failure. Early colonizers, including , play a critical role in the formation of dental caries by creating an environment that reduces the adhesive's integrity. Subsequently, other bacterial species, biofilm formation, and lactic acid from demineralize the adjoining tooth.

Peptide Mediated Antimicrobial Dental Adhesive System.

The most common cause for dental composite failures is secondary caries due to invasive bacterial colonization of the adhesive/dentin (a/d) interface. Innate material weakness often lead to an insufficient seal between the adhesive and dentin. Consequently, bacterial by-products invade the porous a/d interface leading to material degradation and dental caries.

Biosilver nanoparticle interface offers improved cell viability.

Silver nanoparticles (AgNP) are promising candidates for fighting drug-resistant infections because of their intrinsic antimicrobial effect. The design of high-yield antimicrobial molecules may inadvertently cause variation in host cells' biological responses. While many factors affect AgNPs' efficacy, their surface is exposed to the biological environment and thus plays a critical role in both the preservation of antimicrobial efficacy against pathogens and the modulation of host cells cytotoxicity.

New Generation of Tunable Bioactive Shape Memory Mats Integrated with Genetically Engineered Proteins.

Aligned poly(l-lactide)/poly(methyl methacrylate) binary blend fibers and mats loaded with a chimeric green fluorescence protein having a bioactive peptide with hydroxyapatite binding and mineralization property are prepared by pressurized gyration. The effect of processing parameters on the product morphologies, and the shape memory properties of these samples are investigated. Integration of hydroxyapatite nanoparticles into the fiber assembly is self-directed using the hydroxyapatite-binding property of the peptide genetically engineered to green fluorescence protein.

Controlling the Biomimetic Implant Interface: Modulating Antimicrobial Activity by Spacer Design.

Surgical site infection is a common cause of post-operative morbidity, often leading to implant loosening, ultimately requiring revision surgery, increased costs and worse surgical outcomes. Since implant failure starts at the implant surface, creating and controlling the bio-material interface will play a critical role in reducing infection while improving host cell-to-implant interaction. Here, we engineered a biomimetic interface based upon a chimeric peptide that incorporates a titanium binding peptide (TiBP) with an antimicrobial peptide (AMP) into a single molecule to direct binding to the implant surface and deliver an antimicrobial activity against and , two bacteria which are linked with clinical implant infections.

Mechanisms of Cigarette Smoke Effects on Human Airway Smooth Muscle.

Cigarette smoke contributes to or exacerbates airway diseases such as asthma and COPD, where airway hyperresponsiveness and airway smooth muscle (ASM) proliferation are key features. While factors such as inflammation contribute to asthma in part by enhancing agonist-induced intracellular Ca(2+) ([Ca(2+)]i) responses of ASM, the mechanisms by which cigarette smoke affect ASM are still under investigation. In the present study, we tested the hypothesis that cigarette smoke enhances the expression and function of Ca(2+) regulatory proteins leading to increased store operated Ca(2+) entry (SOCE) and cell proliferation.

Coupling Infusion and Gyration for the Nanoscale Assembly of Functional Polymer Nanofibers Integrated with Genetically Engineered Proteins.

Nanofibers featuring functional nanoassemblies show great promise as enabling constituents for a diverse range of applications in areas such as tissue engineering, sensing, optoelectronics, and nanophotonics due to their controlled organization and architecture. An infusion gyration method is reported that enables the production of nanofibers with inherent biological functions by simply adjusting the flow rate of a polymer solution. Sufficient polymer chain entanglement is obtained at Berry number > 1.

Cigarette smoke enhances proliferation and extracellular matrix deposition by human fetal airway smooth muscle.

Cigarette smoke is a common environmental insult associated with increased risk of developing airway diseases such as wheezing and asthma in neonates and children. In adults, asthma involves airway remodeling characterized by increased airway smooth muscle (ASM) cell proliferation and increased extracellular matrix (ECM) deposition, as well as airway hyperreactivity. The effects of cigarette smoke on remodeling and contractility in the developing airway are not well-elucidated.

Brain-derived neurotrophic factor in cigarette smoke-induced airway hyperreactivity.

Enhanced airway smooth muscle (ASM) contractility contributes to increased resistance to airflow in diseases such as bronchitis and asthma that occur in passive smokers exposed to secondhand smoke. Little information exists on the cellular mechanisms underlying such airway hyperreactivity. Sputum samples of patients with chronic sinusitis, bronchitis, and asthma show increased concentrations of growth factors called neurotrophins, including brain-derived growth factor (BDNF), but their physiological significance remains unknown.

Caveolin-1 knockout mice exhibit airway hyperreactivity.

Caveolae are flask-shaped plasma membrane invaginations expressing the scaffolding caveolin proteins. Although caveolins have been found in endothelium and epithelium (where they regulate nitric oxide synthase activity), their role in smooth muscle is still under investigation. We and others have previously shown that caveolae of human airway smooth muscle (ASM), which express caveolin-1, contain Ca(2+) and force regulatory proteins and are involved in mediating the effects of inflammatory cytokines such as TNF-α on intracellular Ca(2+) concentration responses to agonist.

Caveolin-1 in cytokine-induced enhancement of intracellular Ca(2+) in human airway smooth muscle.

Diseases such as asthma are characterized by airway hyperresponsiveness. Enhanced airway smooth muscle (ASM) intracellular Ca(2+) ([Ca(2+)](i)) response to agonist stimulation leading to increased airway constriction has been suggested to contribute to airway hyperresponsiveness. Caveolae are flask-shaped plasma membrane invaginations that express the scaffolding protein caveolin and contain multiple proteins important in [Ca(2+)](i) signaling (e.

Caveolin-1 and force regulation in porcine airway smooth muscle.

Caveolae are specialized membrane microdomains expressing the scaffolding protein caveolin-1. We recently demonstrated the presence of caveolae in human airway smooth muscle (ASM) and the contribution of caveolin-1 to intracellular calcium ([Ca(2+)](i)) regulation. In the present study, we tested the hypothesis that caveolin-1 regulates ASM contractility.