ISRN Dermatology最新文献

Background. Cutaneous alterations are common in neonates. The majority of lesions are physiological, transient, or self-limited and require no therapy. Although much has been reported on the various disorders peculiar to the skin of infant, very little is known about variations and activity of the skin in neonates. Objective. To study the various pattern of skin lesions in newborn and to estimate the prevalence of physiological and pathological skin lesions in newborn. Methods. A total of 1000 newborns were examined in a hospital-based, cross-sectional prospective study in the period of November 2007 to May 2009. Results. The physiological skin changes observed in order of frequency were sebaceous gland hyperplasia (89.4%), Epstein pearls (89.1%), Mongolian spot (84.7%), knuckle pigmentation (57.9%), linea nigra (44.5%), hypertrichosis (35.3%), miniature puberty (13.3%), acrocyanosis (30.9%), physiological scaling (10.8%), and vernix caseosa (7.7%). Of the transient noninfective conditions, erythema toxicum neonatorum was seen in 23.2% newborns and miliaria crystallina in 3% newborns. The birthmarks in descending order of frequency were salmon patch (20.7%), congenital melanocytic nevi (1.9%), and café-au-lait macule (1.3%). Cutaneous signs of spinal dysraphism were sacral dimple (12.8%), meningomyelocele (0.5%), acrochordons (0.1%), and dermoid cyst (0.1%). Conclusion. The physiological and transient skin lesions are common in newborns particularly sebaceous gland hyperplasia, Epstein pearls, Mongolian spots, and erythema toxicum neonatorum. It is important to differentiate them from other more serious skin conditions to avoid unnecessary therapeutic interventions.

Objective. This study was conducted to assess the knowledge, beliefs, and psychosocial effect of acne vulgaris among acne patients attending referral dermatology clinic in Al-Khobar city. Material and Methods. A cross-sectional study was conducted on all Saudi acne patients (males and females) attending referral dermatology clinic in Al-Khobar Governmental Hospital. The data were collected by using a structured self-administered questionnaire. Results. Like other studies conducted before, we found that 58.33% of our sample have poor knowledge about factors that affect acne vulgaris with a significant correlation with both age and gender (P = 0.012 and P = 0.031, resp.). There was significant association of reporting affected social activities with age and educational level (P = 0.023 and P = 0.013, resp.). Variation between both genders regarding reporting feeling stressed due to acne was significant (P = 0.001). The majority of our sample sought medical advice after one year. The most commonly used treatment for acne vulgaris before seeking medical help was peeling products. The majority of our patients thought that acne needs no treatment by physicians. Doctors' treatment is considered guaranteed and safe by the vast majority of our patients. Conclusion. This study showed that knowledge about acne is still insufficient among acne patients.

Uncontrolled blood sugar is a major cause of vascular complications and delayed wound healing in diabetes mellitus. During wound healing process, normally, apoptosis is responsible for events such as removal of inflammatory cells and evolution of granulation tissue into scar which occur during the late phase of wound healing. Early apoptosis can lead to abnormal wound healing by removing granulation tissue including fibroblast, endothelial cell, and small vessels. To determine the role of apoptosis in association with hyperglycemia in diabetic wound healing, apoptosis-related intracellular marker such as expression of Bcl-2 protein by immunohistochemistry and normal histology has been studied. Histological findings show higher level of apoptosis and diminished granulation tissue formation in diabetic rats wounds along with minimal expression of Bcl-2 in diabetic rats wounds when compared with nondiabetic rats wounds. It can be concluded from this study that elevated blood sugar level may be associated with increased apoptosis and the least expression of Bcl-2 protein which might cause deregulation of the wound healing processes in streptozotocin-induced diabetic rats.

Recent genome-wide association studies (GWAS) have identified multiple genetic risk factors for psoriasis, but data on their association with age of onset have been marginally explored. The goal of this study was to evaluate known risk alleles of psoriasis for association with age of psoriasis onset in three well-defined case-only cohorts totaling 1,498 psoriasis patients. We selected 39 genetic variants from psoriasis GWAS and tested these variants for association with age of psoriasis onset in a meta-analysis. We found that rs10484554 and rs12191877 near HLA-C and rs17716942 near IFIH1 were associated with age of psoriasis onset with false discovery rate < 0.05. The association between rs17716942 and age of onset was not replicated in a fourth independent cohort of 489 patients (P = 0.94). The imputed HLA-C∗06:02 allele demonstrated a much stronger association with age of psoriasis onset than rs10484554 and rs12191877. We conclude that despite the discovery of numerous psoriasis risk alleles, HLA-C∗06:02 still plays the most important role in determining the age of onset of psoriasis. Larger studies are needed to evaluate the contribution of other risk alleles, including IFIH1, to age of psoriasis onset.

Photoaging of the skin depends primarily on the degree of ultraviolet radiation (UVR) and on an amount of melanin in the skin (skin phototype). In addition to direct or indirect DNA damage, UVR activates cell surface receptors of keratinocytes and fibroblasts in the skin, which leads to a breakdown of collagen in the extracellular matrix and a shutdown of new collagen synthesis. It is hypothesized that dermal collagen breakdown is followed by imperfect repair that yields a deficit in the structural integrity of the skin, formation of a solar scar, and ultimately clinically visible skin atrophy and wrinkles. Many studies confirmed that acute exposure of human skin to UVR leads to oxidation of cellular biomolecules that could be prevented by prior antioxidant treatment and to depletion of endogenous antioxidants. Skin has a network of all major endogenous enzymatic and nonenzymatic protective antioxidants, but their role in protecting cells against oxidative damage generated by UV radiation has not been elucidated. It seems that skin's antioxidative defence is also influenced by vitamins and nutritive factors and that combination of different antioxidants simultaneously provides synergistic effect.

We demonstrated that glyphosate possesses tumor promoting potential in mouse skin carcinogenesis and SOD 1, calcyclin (S100A6), and calgranulin B (S100A9) have been associated with this potential, although the mechanism is unclear. We aimed to clarify whether imbalance in between [Ca(2+)] i levels and oxidative stress is associated with glyphosate-induced proliferation in human keratinocytes HaCaT cells. The [Ca(2+)] i levels, ROS generation, and expressions of G1/S cyclins, IP3R1, S100A6, S100A9, and SOD 1, and apoptosis-related proteins were investigated upon glyphosate exposure in HaCaT cells. Glyphosate (0.1 mM) significantly induced proliferation, decreases [Ca(2+)] i , and increases ROS generation in HaCaT cells, whereas antioxidant N-acetyl-L-cysteine (NAC) pretreatment reverts these effects which directly indicated that glyphosate induced cell proliferation by lowering [Ca(2+)] i levels via ROS generation. Glyphosate also enhanced the expression of G1/S cyclins associated with a sharp decrease in G0/G1 and a corresponding increase in S-phases. Additionally, glyphosate also triggers S100A6/S100A9 expression and decreases IP3R1 and SOD 1 expressions in HaCaT cells. Notably, Ca(2+) suppression also prevented apoptotic related events including Bax/Bcl-2 ratio and caspases activation. This study highlights that glyphosate promotes proliferation in HaCaT cells probably by disrupting the balance in between [Ca(2+)] i levels and oxidative stress which in turn facilitated the downregulation of mitochondrial apoptotic signaling pathways.

Curcuma longa L. or turmeric of the family Zingiberaceae is widely used in Thai traditional medicines for the treatment of rash, itching, tinea, and ringworm. Previous studies on turmeric oil reported effective antifungal activity against dermatophytes, a group of fungi that causes skin diseases. In this study, turmeric creams containing 6 and 10% w/w turmeric oil were prepared and tested against clinical strains of dermatophytes using broth dilution technique. Minimum fungicidal concentrations of 6 and 10% w/w turmeric creams were found to be 312  μ g/mL. Ar-turmerone, a major compound separated from turmeric oil, promoted more effective antidermatophytic activity with the MICs of 1.56-6.25  μ g/mL, compared to 3.90-7.81  μ g/mL of standard ketoconazole. The results indicated that 6% w/w turmeric oil in the cream was suitable to be formulated as antidermatophytic preparation. Further research should be done on long-term chemical and antifungal stabilities of the preparation.

From an engineering standpoint, both the skin and subcutaneous tissue act as interconnected load-transmitting structures. They are subject to a variety of intrinsic and environmental influences. Changes in the cutaneous viscoelasticity represent an important aspect in a series of skin conditions. The aim of this work was to explore the methodology of biomechanical measurements in order to better appreciate the evolution and severity of some connective tissue diseases. The Cutometer MPA 580 (C+K electronic) was used in the steep and progressive suction procedures. Adapting measurement modalities was explored in order to mitigate any variability in data collection. The repeat steep suction procedure conveniently reveals the creep phenomenon. By contrast, the progressive suction procedure highlights the hysteresis phenomenon. These viscoelastic characteristics are presently described using the 2 and 4 mm probes on normal skin and in scleroderma, acromegaly, corticosteroid-induced dermatoporosis, and Ehlers-Danlos syndrome. The apposition of an additional outer contention on the skin altered differently the manifestations of the creep extension and hysteresis among the tested skin conditions. Any change in the mechanical test procedure affects the data. In clinical and experimental settings, it is mandatory to adhere to a strict and controlled protocol.

Chromolaena odorata (L.) King and Robinson (Siam weed) extract has been used to stop bleeding and in wound healing in many tropical countries. However, its detailed mechanisms have not been elucidated. In this study, we examined the molecular mechanisms by which Siam weed extract (SWE) affected hemostatic and wound healing activities. SWE promoted Balb/c 3T3 fibroblast cell migration and proliferation. Subsequently, we found that heme oxygenase-1 (HO-1), the accelerating wound healing enzyme, was increased at the transcriptional and translational levels by SWE treatments. The HO-1 promoter analyzed with luciferase assay was also increased by treatment of SWE in a dose-dependent manner. This induction may be mediated by several kinase pathways including MEK, p38MAPK, AKT, and JNK. Quantitative real-time PCR using undifferentiated promonocytic cell lines revealed that thromboxane synthase (TXS), a potent vasoconstrictor and platelet aggregator, was increased and MMP-9, an anti platelet aggregator, was decreased in the presence of SWE. Our studies presented that SWE accelerated hemostatic and wound healing activities by altering the expression of genes, including HO-1, TXS, and MMP-9.

Endothelin-1 (ET-1) is a potent endogenous vasoconstrictor, which mediates vascular wall cells proliferation, fibrosis, and inflammation through two types of ET-1 receptors (ET-A and ET-B). In our retrospective study the serum levels of ET-1 in 18 systemic sclerosis (SSc) patients with and without digital ulcers (DUs) were assessed to observe possible correlation between the levels of ET-1, the evolution of SSc, and the therapy with an ET-1 antagonist (bosentan). In all our patients, the levels of ET-1 were found higher than normal range and correlate with the severity of the disease. Furthermore we also observed that in patients without DUs the levels of ET-1 were higher and did not correlate with new DUs development. In conclusion, the levels of ET-1 in our studied patients do not correlate with the possible development of DUs. The reduction of ET-1 levels in DUs patients in therapy with bosentan confirms the efficacy of this molecule both for treatment and prevention of digital ulcers. The inhibition of ET-A receptor by its antagonist may activate the opposite ET-B receptors, with well-known function ET-1 degradation and reducing of ET-1 serum level as confirmed in our pilot study.