Differences in lower extremity kinematics during single-leg lateral drop landing of healthy individuals, injured but asymptomatic patients, and patients with chronic ankle instability- a cross-sectional observational study.

The lower-extremity kinematics associated with forward jump landing after an ankle injury is known to differ for patients with Chronic Ankle Instability (CAI), copers (injured but asymptomatic patients), and healthy individuals. However, the differences in the lower extremity kinematics of these groups associated with a Single-leg Lateral Drop Landing (SLDL) are unknown. The purpose of this study is to characterize the lower limb and foot kinematics during SLDL in CAI patients and to compare these characteristics with those of the copers and healthy individuals. This was a cross-sectional observational study. Nineteen participants, each, were selected from the CAI, Coper, and control groups. The lower-extremity kinematics during SLDL was measured using three-dimensional motion analysis over an interval progressing from 200 ms before landing to 200 ms after landing. Either one-way ANOVA or the Kruskal-Wallis test was used to compare the attributes of the respective groups, with each parameter measured every 10 ms. The maximum values and excursions of the parameters were established over time intervals progressing from 200 ms before landing to 200 ms after landing. Significant observations were subjected to post hoc analysis. Compared to the Coper group, the CAI group exhibited significantly smaller hip adduction angles at 160 ms, ankle dorsiflexion angles in the 110-150 ms interval, and maximum ankle dorsiflexion angles after landing. Compared to the control group, the CAI group exhibited significantly smaller excursions of MH inversion/eversion after landing. Our findings confirm the necessity of focusing on the kinematics of hip adduction/abduction and plantar/dorsiflexion during SLDL in evaluating patients with ankle injuries.

Association between Smoking during Pregnancy and Short Root Anomaly in Offspring.

Short root anomaly (SRA) is a dental anomaly with short dental roots and its pathogenesis is poorly understood. This study investigated the association between maternal smoking during pregnancy and SRA in offspring. A survey was conducted on 558 children aged 8-16 years from two public schools in Ulaanbaatar, Mongolia. SRA was diagnosed using cases with a root-crown ratio of maxillary central incisors of ≤1.0. A questionnaire survey was conducted to assess maternal lifestyle habits. Multiple logistic regression was used to analyse the association between maternal smoking during pregnancy and SRA in offspring after adjusting for possible confounders. The prevalence of SRA in these children was 14.2%. Children whose mothers smoked from pregnancy to date were found to be 4.95 times (95% confidence interval [CI]: 1.65-14.79) more likely to have SRA than those whose mothers never smoked, after adjusting for possible confounders. Additionally, children whose mothers had been exposed to passive smoking during pregnancy were found to be 1.86 times (95% CI: 1.02-3.40) more likely to have SRA than those whose mothers had not been exposed to passive smoke. Our population-based study suggests that maternal and passive smoking exposure during pregnancy can affect tooth root formation in children.

Protective Effects of Sacran, a Natural Polysaccharide, Against Adverse Effects on the Skin Induced by Tobacco Smoke.

Recent increases in air pollution have raised concerns about its adverse effects on human health. Sacran is a natural polysaccharide isolated from a cyanobacterium. We previously reported that sacran improves skin conditions because of its effects as an artificial barrier against external stimuli, which suggested that sacran might protect the skin against air pollutants. The goal of this study was to characterize the potential of sacran to protect human skin against damage from air pollutants and to compare sacran with hyaluronic acid (HA). Sacran that was topically applied on the skin stayed on the surface or in the stratum corneum. Sacran-treated filters had a shielding effect against benzo[a]pyrene (BaP) and aldehyde compounds contained in tobacco smoke. Sacran suppressed the upregulation of cytochrome P4501A1 messenger ribonucleic acid (mRNA), which is a xenobiotic-metabolizing enzyme induced by BaP, and other responses against tobacco smoke in HaCaT keratinocytes. Furthermore, topical application of a serum containing 0.04% sacran on the skin reduced levels of carbonylated proteins in corneocytes of tobacco smokers. Sacran showed superior effects in every characteristic measured, compared with HA. We conclude that sacran ameliorates the oxidative stress initiated by tobacco smoke by shielding the skin surface and protects human skin.

Defensive Effects of a Unique Polysaccharide, Sacran, to Protect Keratinocytes against Extracellular Stimuli and Its Possible Mechanism of Action.

Sacran, a polysaccharide isolated from the alga Aphanothece sacrum (Suizenji-nori), has unique physical and physiological characteristics. In a previous study, we reported that sacran improves skin conditions in individuals who suffer from atopic dermatitis (AD), focusing on its trapping function against extrinsic stimuli compared with hyaluronic acid (HA). First, we examined the penetration of sacran through stratum corneum (SC) with an impaired barrier function using immature reconstructed human epidermal equivalents. Sacran penetrates the SC to living cell layers of the epidermis, which suggested that sacran would attenuate adverse influences in keratinocytes caused by extracellular factors such as irritants or proinflammatory cytokines such as interleukin 1α (IL-1α). Sacran markedly reduced the cell damage induced by a nonionic detergent, sodium lauryl sulfate (SLS). Moreover, sacran restored the elevation of intracellular reactive oxygen species (ROS) levels stimulated by SLS and by IL-1α. These effects of sacran were superior to those of HA. In order to investigate the restoration effects of sacran, the influence of sacran on the physical properties of lipid bilayers was evaluated by measuring the order parameter using the ESR spin-labeling method. Because sacran failed to cause changes in the order parameters of liposomes and HaCaT keratinocytes, these results indicate that sacran does not interact with lipid bilayers although it restored changes in the order parameter caused by SLS. The sum of these results demonstrates that sacran reduces the influence of extracellular stimuli by its trapping effects. We conclude that the improving action of sacran is based on its trapping effect.

Topical treatment with sacran, a sulfated polysaccharide from Aphanothece sacrum, improves corneocyte-derived parameters.

Sacran, a polysaccharide isolated from Aphanothece sacrum (Suizenji-nori) alga, has unique characteristics in terms of its physiological properties and effects on the skin, and has recently become a focus of attention as a novel biomaterial. In a previous study, we reported the unique physical characteristics of sacran, which forms a gel-like film containing water in the presence of polyols. This film resists penetration by water and chemicals. We expected this unique physical characteristic to act as an artificial barrier upon the application of sacran to the skin. In the present study, we tested the efficacy of sacran application in healthy individuals who reported previous symptoms of dry or inflamed skin, to evaluate the potential benefits of sacran for skin care in patients with mild atopic dermatitis. Compared with placebo, sacran-containing serum did not significantly alter either the water content of the skin surface or transepidermal water loss. However, subjects using the serum showed improvements in corneocyte parameters including size, percentage of thick abrasion, ratio of SH to SS groups, ratio of interleukin (IL)-1 receptor antagonist to IL-1α, and carbonylated protein level. These results indicate that the sulfated polysaccharide sacran is an effective agent for improving or maintaining the skin conditions.

Sodium Lauryl Sulfate Stimulates the Generation of Reactive Oxygen Species through Interactions with Cell Membranes.

Sodium lauryl sulfate (SLS), a representative anionic surfactant, is well-known to induce rough skin following single or multiple topical applications. The mechanism by which SLS induces rough skin is thought to result from the disruption of skin moisture function consisting of NMF and epidermal lipids. However, a recent study demonstrated that topically applied SLS easily penetrates into the living cell layers of the epidermis, which suggests that physiological alterations of keratinocytes might cause the SLS-induced rough skin. This study was conducted to clarify the effects of SLS on keratinocytes to demonstrate the contribution of SLS to the induction of rough skin. In addition, the potentials of other widely used anionic surfactants to induce rough skin were evaluated. HaCaT keratinocytes treated with SLS had increased levels of intracellular ROS and IL-1α secretion. Application of SLS on the surface of a reconstructed epidermal equivalent also showed the increased generation of ROS. Further, SLS-treated cells showed an increase of intracellular calpain activity associated with the increase of intracellular Ca2+ concentration. The increase of intracellular ROS was abolished by the addition of BAPTA-AM, a specific chelator of Ca2+. In addition, IL-1α also stimulated ROS generation by HaCaT keratinocytes. An ESR spin-labeling study demonstrated that SLS increased the fluidity of membranes of liposomes and cells. Together, those results indicate that SLS initially interacts with cell membranes, which results in the elevation of intracellular Ca2+ influx. Ca2+ stimulates the secretion of IL-1α due to the activation of calpain, and also increases ROS generation. IL-1α also stimulates ROS generation by HaCaT keratinocytes. We conclude from these results that the elevation of intracellular ROS levels is one of the causes of SLS-induced rough skin. Finally, among the other anionic surfactants tested, sodium lauryl phosphate has less potential to induce rough skin because of its lower generation of ROS.

Carbonylated proteins exposed to UVA and to blue light generate reactive oxygen species through a type I photosensitizing reaction.

BACKGROUND: Carbonylated proteins (CPs) are generated by the reaction of basic amino acid residues in proteins with aldehyde compounds produced during lipid peroxidation. CPs in the stratum corneum (SC) impact skin conditions such as skin moisture functions including water content and transepidermal water loss (TEWL). In addition, CPs can be frequently seen in the SC from sun-exposed sites compared with sun-protected sites. OBJECTIVE: The aim of this study was to reveal whether CPs could be a generation source of reactive oxygen species (ROS) in the SC following exposure to ultraviolet (UV) radiation and to identify the type of ROS and its generation mechanism. METHODS: ROS generation was detected using a methyl cypridina luciferin analog (MCLA) chemiluminescence system and an ESR spin-trapping method. CPs in porcine SC, in a keratin film and in bovine serum albumin (BSA) were prepared by reaction with acrolein. Levels of protein carbonylation were quantified by detecting aldehyde residues. RESULTS: CP levels in the SC were increased in a UVA energy-dependent manner. That result suggested that a source of ROS generation existed in the SC initiated and produced the carbonylation of SC proteins. Carbonylated BSA and carbonylated porcine SC sheets exhibited fluorescence spectra at an excitation wavelength of 430nm and an emission wavelength of 520nm. Irradiation of the SC with UVA increased protein carbonylation and the amount of autofluorescence in the SC. ROS generation in the SC caused by UVA and by short-wavelength visible light (blue light, 400-470nm) was detected by the MCLA chemiluminescence system. Artificially carbonylated porcine SCs and keratin films had increases of chemiluminescence intensity after exposure to both light sources as well. The addition of superoxide dismutase to the MCLA system completely abolished the incremental chemiluminescence intensity after both UVA and blue light exposure of the SC. In addition, acrolein-treated BSA gave ESR signals like hydroxyl radicals (OH) converted from superoxide anion radicals (O2-) during irradiation with a xenon arc lamp containing UVA and visible light. From the sum of these results, we consider that CPs are produced from O2- initially generated from exposure to UVA and blue light. CONCLUSION: CPs are excited by absorbing sunlight, particularly UVA and blue light, and result in the generation of O2- through a CPs progress new protein carbonylation in stratum corneum through ROS generation. photosensitizing reaction. Further, the results suggest that the O2- produces CPs in the SC through lipid peroxidation in the sebum, and finally affects skin conditions including color and moisture functions.