The science behind wet wipes for infant skin: Ingredient review, safety, and efficacy.

In the diapered area, the continuous exposure to excess moisture and irritants from urine and feces weakens the stratum corneum, making the skin more susceptible to irritation. The use of wet wipes for infants (baby wipes) is a common practice to clean skin after urine or a bowel movement, and this practice even extends to cleaning the hands and face, resulting in repeated daily use. Therefore, ensuring that baby wipes contain ingredients that are safe and mild on skin is important to help minimize skin irritation and discomfort. While disposable baby wipes have been shown to be effective and gentle at cleaning infant skin, even the skin of premature infants, there is growing public concern regarding their safety and tolerability. Not all products are made the same, as differences exist in manufacturing processes, ingredients, materials, safety, and quality testing. Therefore, it is important that healthcare professionals have accessible evidenced-based information on the safety and tolerability of common ingredients found in baby wipes to optimally educate their patients and families. Herein, we provide a review on best practices for ingredient selection, safety, and efficacy of baby wipes.

Neonatal Opioid Withdrawal Syndrome: A Developmental Care Approach.

Tens of thousands of infants are impacted yearly by prenatal opioid exposure. The term neonatal opioid withdrawal syndrome (NOWS) is now replacing the more familiar term neonatal abstinence syndrome (NAS). Ongoing debate continues related to standard regimens for treatment of this oftentimes perplexing condition. Historically, treatment has focused on pharmacologic interventions. However, there is limited research that points to nonpharmacologic methods of treatment as viable options, whether alone or in addition to pharmacologic interventions. This article, utilizing a review of pertinent literature, outlines the physical aspects of NOWS, including its pathophysiology and the resulting physical clinical signs. In addition, we present an overview of how age-appropriate, nonpharmacologic interventions, centered on developmental care, may be a valuable approach to organize and prioritize routine care for these infants, their families, and the health care team facing the challenges of NOWS. Finally, the need for further research to better define evidence-based standards of care for these infants and their families is discussed.

Manipulation of valve composition to elucidate the role of collagen in aortic valve calcification.

BACKGROUND: Extracellular matrix (ECM) disarray is found in calcific aortic valvular disease (CAVD), yet much remains to be learned about the role of individual ECM components in valvular interstitial cell (VIC) function and dysfunction. Previous clinical analyses have shown that calcification is associated with decreased collagen content, while previous in vitro work has suggested that the presence of collagen attenuates the responsiveness of VICs to pro-calcific stimuli. The current study uses whole leaflet cultures to examine the contributions of endogenous collagen in regulating the phenotype and calcification of VICs. METHODS: A "top-down" approach was used to characterize changes in VIC phenotype in response to collagen alterations in the native 3D environment. Collagen-deficient leaflets were created via enzymatic treatment and cultured statically for six days in vitro. After culture, leaflets were harvested for analysis of DNA, proliferation, apoptosis, ECM composition, calcification, and gene/protein expression. RESULTS: In general, disruption of collagen was associated with increased expression of disease markers by VICs in whole organ leaflet culture. Compared to intact control leaflets, collagen-deficient leaflets demonstrated increased VIC proliferation and apoptosis, increased expression of disease-related markers such as alpha-smooth muscle actin, alkaline phosphatase, and osteocalcin, and an increase in calcification as evidenced by positive von Kossa staining. CONCLUSIONS: These results indicate that disruption of the endogenous collagen structure in aortic valves is sufficient to stimulate pathological consequences in valve leaflet cultures, thereby highlighting the importance of collagen and the valve extracellular matrix in general in maintaining homeostasis of the valve phenotype.

A purified feverfew extract protects from oxidative damage by inducing DNA repair in skin cells via a PI3-kinase-dependent Nrf2/ARE pathway.

BACKGROUND: Environmental factors such as solar ultraviolet (UV) radiation and other external aggressors provide an oxidative challenge that is detrimental to skin health. The levels of endogenous antioxidants decrease with age, thus resulting in less protection and a greater potential for skin damage. The NF-E2-related factor-2 (Nrf2) - antioxidant response element (ARE) pathway is a primary defense mechanism against oxidative stress, and induces the expression of antioxidant, detoxification and repair genes. Activation of ARE-Nrf2 can help restore oxidative homeostasis of the skin and play a role in inflammatory response and DNA repair mechanisms. OBJECTIVE: To evaluate the role of a purified parthenolide-depleted Feverfew (PD-Feverfew) extract on the ARE-Nrf2 pathway and DNA repair in skin cells. METHODS: These studies were undertaken in primary human keratinocytes or KB cells using Luciferase Promoter assay, siRNA transfection studies, Western blot analyses, Immunofluorescence microscopy, comet assay and quantitative real-time PCR. RESULTS: PD-Feverfew was found to induce Nrf2 nuclear translocation and to increase ARE activity in a dose dependent manner. Furthermore, knockdown of Nrf2 resulted in suppression of PD-Feverfew-induced ARE activity. PD-Feverfew was also found to induce phosphorylation of Akt, a kinase downstream of PI3K. Inhibition of PI3K via pre-treatment with the selective pharmacological inhibitor, LY294002, abolished PD-Feverfew-induced Nrf2/ARE activation. PD-Feverfew also reduced UV-induced DNA damage in a PI3K and Nrf2-dependent manner. CONCLUSIONS: Therefore, by increasing endogenous defense mechanisms and aid in DNA repair of damaged skin cells via activation of a PI3K-dependent Nrf2/ARE pathway, PD-Feverfew may help protect the skin from numerous environmental aggressors.

Tryptophan inhibits biofilm formation by Pseudomonas aeruginosa.

Biofilm formation by Pseudomonas aeruginosa has been implicated in the pathology of chronic wounds. Both the d and l isoforms of tryptophan inhibited P. aeruginosa biofilm formation on tissue culture plates, with an equimolar ratio of d and l isoforms producing the greatest inhibitory effect. Addition of d-/l-tryptophan to existing biofilms inhibited further biofilm growth and caused partial biofilm disassembly. Tryptophan significantly increased swimming motility, which may be responsible in part for diminished biofilm formation by P. aeruginosa.

Regulation of valvular interstitial cell phenotype and function by hyaluronic acid in 2-D and 3-D culture environments.

Disruption of the extracellular matrix (ECM) is frequently found in calcific aortic valve disease (CAVD), yet the role of ECM components in valvular interstitial cell (VIC) function and dysfunction remains poorly understood. This study examines the contributions of exogenous and endogenous hyaluronic acid (HA), in both two-dimensional (2-D) and 3-D environments, in regulating the phenotype and calcification of VICs. VIC calcification was first assessed in a 2-D setting in which the cells were exposed to different molecular weights of exogenous HA presented in either an immobilized or soluble form. Delivery of HA suppressed nodule formation in a molecular weight-dependent manner, while blocking VIC recognition of HA via an antibody to CD44 abolished these nodule-suppressive effects and stimulated other hallmarks of valvular dysfunction. These 2-D results were then validated in a more physiologically-relevant setting, using an approach that allowed the characterization of VIC phenotype in response to HA alterations in the native 3-D environment. In this approach, leaflet organ cultures were analyzed following treatment with anti-CD44 or with hyaluronidase to specifically remove HA. Disruption of VIC-HA interactions upregulated markers of VIC disease and induced leaflet mineralization. Similarly, HA-deficient leaflets exhibited numerous hallmarks of CAVD, including increased VIC proliferation, apoptosis, increased expression of disease-related markers, and mineralization. These findings suggest that VIC-HA interactions are crucial in maintaining a healthy VIC phenotype. Identification ECM components that can regulate VIC phenotype and function has significant implications for understanding native valve disease, investigating possible treatments, and designing new biomaterials for valve tissue engineering.

Regulation of valvular interstitial cell calcification by components of the extracellular matrix.

Understanding the interactions between extracellular matrix (ECM) components and valvular interstitial cells (VICs) is relevant to both treating heart valve disease and designing heart valve tissue engineering scaffolds, yet the VIC-ECM relationship has not been well characterized. Thus, the aim of this study was to characterize VIC-ECM interactions, paying specific attention to whether ECM composition affected the in vitro calcification of VICs. Our results show that the number and size of calcific nodules formed in VIC cultures, as well as the expression of the mineralization markers alkaline phosphatase (ALP) and CBFa1, were highly dependent upon the composition of the culture surface. VICs cultured on certain ECM components, that is, collagen and fibronectin, were resistant to calcification, even upon treatment with mineralization-inducing growth factors. Meanwhile, cultures of VICs on fibrin, laminin, and heparin coatings had a high number of calcified nodules, although only VICs on fibrin expressed significantly elevated levels of ALP and CBFa1. Nodule composition analysis revealed the presence of multiple types of mineralization. Although apoptotic and necrotic cells were more concentrated in nodules, these nodules did contain a strong majority population of viable cells. Characterizing this ECM-dependence of VIC calcification will help us to identify appropriate biomaterial environments for heart valve tissue engineering as well as elucidate mechanisms of valvular disease.

Template synthesis of arrays of nano fuel cells.

A method for the construction of an array of fuel cells wherein each cell is 200 nm in diameter is presented. Electrodeposition of Pt-Cu nanowires inside the cylindrical pores of an Anodisc filter membrane and the subsequent dealloying of the Cu by soaking the filter in fuming nitric acid for several hours are used to construct an array of porous platinum electrodes. About 10(9) electrically isolated cylindrical porous electrodes, each 200 nm in diameter, are formed in this manner. Utilizing two arrays of porous electrodes with a polymer electrolyte membrane or an electrolyte support matrix sandwiched between, an array of nano fuel cells is produced. This method of producing an array of coplanar fuel cells allows for the series connection of fuel cells outside the array and eliminates the need for fuel and air manifolds, greatly reducing the overall system complexity. Initial prototypes utilizing an aqueous solution of NaBH(4) as a fuel have produced power densities of ca. 1 mW/cm(2) based on an estimate of the area of the current collectors in contact with the nano-fuel-cell array and have demonstrated the ability to wire bundles of fuel cells either in parallel or in series.