Analysis of the epidemiological burden of acne vulgaris in China based on the data of global burden of disease 2019.

Acne vulgaris is a chronic, inflammatory skin disease, which has brought an increasing disease burden to patients and society. But there is no systematic study on the disease burden and social development of acne vulgaris in China. This study aimed to analyze the epidemiological burden and trend of acne vulgaris in China from 1990 to 2019 based on the data in the global burden of disease 2019 (GBD 2019). The number of incidences/illnesses, age-standardized incidence/prevalence rates, disability-adjusted life years (DALYs), and DALY rate of acne vulgaris in China from 1990 to 2019 were obtained from the GBD 2019 to evaluate the epidemiological trends and age-period-cohort trends. The associations between disease burden and social development degrees were analyzed using a sociodemographic index. In 2019, the age-standardized prevalence and incidence of acne vulgaris in China were both at low levels in the world. From 1990 to 2019, the prevalent cases and incident cases of acne vulgaris in China rose firstly and then fell (peaked in 2005 and 2003, respectively), and the age-standardized prevalence/incidence/DALY rates showed growth trends continuously. The prevalence of acne vulgaris peaked in the 15-19 age group while the incidence peak age was 10-14 years old and there was an obvious gender difference, females were higher than males. With the increase of sociodemographic index (SDI) value, the morbidity of acne vulgaris showed a linear growth trend (P < 0.05). From 1990 to 2019, the disease burden of acne vulgaris is increasing in China, which is correlated with social and medical development. Active research on the epidemiological data of acne vulgaris and its relationship with the level of social development is important for both the diagnosis and treatment of acne vulgaris and for the development of health policies.

Increased Level of Serum Wingless-Type Mouse Mammary Tumor Virus Integration Site Family Member 5a in Patients with Cutaneous Lichen Planus.

PURPOSE: Cutaneous lichen planus (CLP) is an autoinflammatory skin disorder, and it is associated with metabolic syndrome. Wingless-type mouse mammary tumor virus integration site family member 5a (Wnt5a) is a potential factor in metabolic complications and it was shown to be upregulated in CLP lesions. Whether Wnt5a is altered in the circulation of patients with CLP is unclear. This study aimed to measure serum Wnt5a level in patients with CLP and to assess its relationship with body mass index (BMI). METHODS: We included 46 adult patients with CLP and 38 healthy adults as control. Serum Wnt5a was measured using enzyme-linked immunosorbent assay. RESULTS: The mean serum Wnt5a was significantly higher in patients than controls (all P-value <0.001). The mean serum Wnt5a levels in obese (BMI between 30 and 40) patients were significantly higher than lean (BMI between 20 and 25) patients (P-value <0.001). Compared to lean patients with CLP, the concentration of serum Wnt5a levels was increased gradually with BMI score (all P-value <0.05). CONCLUSION: Serum Wnt5a might be a potential biomarker for CLP and it was associated with BMI. An increase in serum Wnt5a may contribute to the development of metabolic comorbidity in CLP patients.

Lentivirus­mediated CD44s expression increases human basal cell carcinoma cell resistance against vismodegib.

High drug resistance, which is usually mediated by drug resistance­associated genes, is a characteristic of human tumours. CD44s, an ATP­binding cassette multidrug resistance transporter, is expressed in a variety of human cancers. In the present study, the effect of CD44s expression was investigated on BCC resistance against vismodegib. Lentiviral vectors were constructed to allow efficient CD44s expression. Cell clones expressing the CD44s construct were selected and expanded and then identified using qRT­PCR and western blotting. A lentiviral vector containing a blank sequence was used as a control. Cellular growth capacity and cell sensitivity to vismodegib were detected by MTT and Transwell assays, respectively. BCC cell growth was evaluated in vivo with a transplanted BCC nude mouse model. The cell clones expressing CD44s at high levels were identified by qRT­PCR and western blotting, and the difference in the cell proliferation rate between these cells and LV­CON BCC cells was assessed by growth curve analysis. The in vitro study revealed that treatment with vismodegib decreased BCC cell growth and migration; however, these effects were reversed by LV­CD44s overexpression. The in vivo study revealed that BCC tumour growth was significantly increased in nude mice transplanted with cells stably infected with CD44s compared with nude mice transplanted with cells infected with a control vector. Our investigation demonstrated that lentivirus­mediated CD44s expression may reverse the effects of vismodegib treatment on BCC.

Successful treatment of verruca plana with NB-UVB: A case report.

Verruca plana is a kind of benign proliferative skin disease that generally occurs in exposed parts, but the treatment of warts poses a therapeutic challenge for physicians, as there is no method, among numerous approaches, that has been proven effective for completely curing this disease. We report a case of verruca plana cured by narrow-band ultraviolet B (NB-UVB), which provides a new treatment of verruca plana.

A unified mitochondria mechanistic target of rapamycin acyl-coenzyme A dehydrogenase 10 signal relay modulation for metformin growth inhibition in human immortalized keratinocytes cells.

Metformin exhibits antiproliferative and proapoptotic effects in a variety of diseases, characterized by malignant and nonmalignant hyperplastic cells; however, the underlying molecular mechanism of metformin in psoriasis has not been elucidated. In the current study, we found that after metformin treatment the proliferation of human immortalized keratinocytes (HaCaT) was significantly inhibited, while cell apoptosis was increased in a dose-dependent manner, accompanied with enhanced protein expression of acyl-coenzyme A dehydrogenase 10 (ACAD10). Furthermore, mechanism analysis revealed that ACAD10 expression is induced by downregulated activities of mechanistic target of rapamycin 1 (mTORC1) signaling rather than AMP-activated protein kinase signaling. The inactivation of mTORC1 by rapamycin pretreatment or rotenone-induced mitochondrial complex inhibition showed a similar effect because of the metformin treatment on the proliferation and apoptosis of HaCaT keratinocytes. Overexpression of mTORC1 almost reversed the antiproliferation and proapoptosis effects induced by metformin. This study showed that the metformin treatment inhibited HaCaT cells proliferation and promoted apoptosis by affecting the mitochondrial-mTORC1 signaling and elevated the ACAD10 expression. Hence, metformin can be used as a potential therapeutic agent for psoriasis.

MicroRNA-485-5p represses melanoma cell invasion and proliferation by suppressing Frizzled7.

MicroRNAs (miRNAs) have emerged as critical regulators for malignant melanoma development. miR-485-5p has been suggested as a tumor-suppressive miRNA in many types of human malignancies. However, the role of miR-485-5p in melanoma remains unknown. In this study, we aimed to explore the potential role and underlying mechanism of miR-485-5p in the regulation of melanoma development. Here, we showed that miR-485-5p was significantly decreased in melanoma tissues and cell lines compared with their corresponding controls. Transwell invasion assay showed that miR-485-5p overexpression markedly inhibited melanoma cell invasion. WST-1 and cell cycle assays exhibited that miR-485-5p overexpression significantly suppressed melanoma cell proliferation. By contrast, miR-485-5p suppression promoted the invasion and proliferation of melanoma cells. Using bioinformatics analysis, we observed that miR-485-5p potentially targets the 3'-untranslated region (3'-UTR) of Frizzled7 (FZD7). Dual-luciferase assay confirmed the direct binding between miR-485-5p and FZD7 3'-UTR. Meanwhile, real-time quantitative polymerase chain reaction and Western blot analysis showed that miR-485-5p overexpression suppressed FZD7 expression, whereas miR-485-5p suppression resulted in the opposite effect. Moreover, miR-485-5p expression was observed to be inversely correlated with FZD7 mRNA expression in melanoma tissues. Further experiments showed that miR-485-5p regulated Wnt signaling. The restoration of FZD7 expression markedly reversed the antitumor effects induced by miR-485-5p overexpression in melanoma cells. Taken together, our study suggests that miR-485-5p represses melanoma cell invasion and proliferation by suppressing FZD7, indicating a new tumor-suppressive role for miR-485-5p in melanoma. The miR-485-5p/FZD7 axis may provide novel insights into understanding the molecular pathogenesis of melanoma and may be a promising therapeutic target for melanoma.

Meta-Analysis of the Association between Vitiligo and Human Leukocyte Antigen-A.

Objective. The objective of this study was to systematically evaluate the association between vitiligo and human leukocyte antigen- (HLA-) A. Methods. PubMed, Embase, Web of Science, Chinese National Knowledge Infrastructure, and reference lists were searched for relevant original articles. Results. Nineteen case-control studies comprising 3042 patients and 5614 controls were included, in which 33 HLA-A alleles were reported. Overall, three alleles (HLA-A⁎02, A⁎33, and Aw⁎31) were significantly associated with increased risk of vitiligo, two (HLA-A⁎09 and Aw⁎19) were associated with decreased risk, and the remaining 28 were unassociated. Twelve alleles, seven alleles, and 19 alleles were common to three ethnicities, both types of vitiligo, and both typing methods, respectively. In the subgroup analysis by ethnicity and typing methods, the association of six alleles and five alleles was inconsistent in three populations and both typing methods, respectively. In the subgroup analysis by clinical type, the association of all seven alleles was consistent in both types of vitiligo. Conclusion. The meta-analysis suggests that HLA-A⁎02, A⁎33, and Aw⁎31 are associated with increased risk of vitiligo, while HLA-A⁎09 and Aw⁎19 are associated with decreased risk of vitiligo. The association of some alleles varies in terms of ethnicity and typing methods.

Amentoflavone protects against psoriasis-like skin lesion through suppression of NF-κB-mediated inflammation and keratinocyte proliferation.

Psoriasis is a one of the most common chronic skin diseases, which affects 0.6-4.8% of the general population. Amentoflavone (AMF) belongs to the biflavonoid class of flavonoids, possessing various biological effects, such as anti-inflammatory, antioxidant, and anti-apoptotic effects. In the present study, we aimed to investigate the effect of AMF on psoriasis in imiquimod (IMQ) psoriasis-like lesions in mice and keratinocyte proliferation in HaCaT cells. We showed that AMF reduced skinfold thickening, and improved erythema and scaling scores and histological lesions in IMQ-treated mice. AMF exerted potent anti-inflammatory effect via influencing a variety of proinflammatory cytokines, including tumor necrosis factor α, interleukin (IL)-17A, IL-22, and IL-23 in local skin lesions and the whole body. In M5 (a cocktail of cytokines)-treated HaCaT cells, AMF significantly inhibited cell proliferation, promoted apoptosis, and inhibited the increase of expression of cyclin D1, cyclin E, IL-17A, and IL-22. In addition, AMF inhibited the upregulation of p65 NF-κB under psoriatic condition. Moreover, overexpression of p65 NF-κB significantly suppressed the effect of AMF on keratinocyte proliferation, apoptosis, and expression of cyclin D1, cyclin E, IL-17A, and IL-22. These results demonstrated that suppression of NF-κB was involved in AMF-resulted anti-proliferative, apoptosis-promoting, anti-inflammatory effects in keratinocytes. The data demonstrate that AMF may serve as potential therapeutic option for patients with psoriasis.

MiR-135 post-transcriptionally regulates FOXO1 expression and promotes cell proliferation in human malignant melanoma cells.

Malignant melanoma is the deadliest form of all skin cancers. Recently, microRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression by targeted repression of transcription and translation and play essential roles during cancer development. Our study showed that miR-135a is upregulated in malignant melanoma tissues and cell lines by using Real-time PCR assay. Enforced expression of miR-135a in malignant melanoma cells promotes cell proliferation, tumorigenicity, and cell cycle progression, whereas inhibition of miR-135a reverses the function. Additionally, we demonstrated FOXO1 is a direct target of miR-135a and transcriptionally down-regulated by miR-135a. Ectopic expression of miR-135a led to downregulation of the FOXO1 protein, resulting in upregulation of Cyclin D1, and downregulation of P21(Cip1) and P27(Kip1) through AKT pathway. Our findings suggested that miR-135a represents a potential onco-miRNA and plays an important role in malignant melanoma progression by suppressing FOXO1 expression.

Complement activation contributes to the anti-methicillin-resistant Staphylococcus aureus effect of natural anti-keratin antibody.

Methicillin-resistant Staphylococcus aureus (MRSA) remains a major public health problem worldwide because of its strong resistance to a variety of antibiotics. Natural immunoglobulin (Ig) M antibodies have been reported to protect against microbial infections. In the present study, the function of a monoclonal natural anti-keratin antibody IgM (named 3B4) in MRSA infection was evaluated. The binding of 3B4 to MRSA was studied using immunofluorescence assay and flow cytometry (FCM). The binding of 3B4 to mannose-binding lectin (MBL) and complement activation were detected by ELISA. For the in vivo study, transgenic mice for the VH gene from 3B4 (TgVH 3B4) were used. After infection, the bacterial burden was examined in the kidney, spleen and enterocelia. Inflammatory cytokine levels and the neutrophil ratio in peritoneal lavage fluid (PLF) were assessed by ELISA and FCM, respectively. Additionally, the total serum hemolytic activity (CH50) in the early stage of infection was detected by ELISA. The results showed that 3B4 bound directly to MRSA and MBL, and the interaction between 3B4 and MRSA/MBL led to the activation of the classic and the MBL pathway in vitro. After 48 h of MRSA infection, the bacterial load in the kidney, spleen and enterocelia was significantly decreased in TgVH 3B4 mice (P < 0.05) compared with wild-type mice. Levels of IL-6, TNF-α, and IFN-γ were increased after MRSA infection. The levels of IL-6 and TNF-α in TgVH 3B4 mice were decreased by 49.1% and 59.4% compared to wild-type mice. Additionally, the neutrophil ratio in the PLF of TgVH 3B4 mice was decreased by 65.9%. The CH50 value was significantly higher in TgVH 3B4 mice than in wild-type mice, indicating that 3B4 promoted the activation of the complement system in MRSA infected mice. The results reveal an important role of 3B4 in the anti-MRSA immune response, and the complement activation contributes to this effect.

24 Y-chromosomal STR haplotypic polymorphisms for Chinese Uygur ethnic group and its phylogenic analysis with other Chinese groups.

The Uygur ethnic minority is the largest ethnic group in the Xinjiang Uygur Autonomous Region of China, and is a precious resource for the study of ethnogeny and forensic biology. Previous studies have focused on the genetic background of the Uygur group, however, the patrilineal descent of the group is still unclear. In this study, we investigated the genetic diversity of 24 Y-STR loci in the Uygur group and analyzed the population differentiations as well as the genetic relationships between the Uygur group and other previously reported populations using 17 Y-filer loci. According to haplotypic analysis of the 24 Y-STR loci in 109 Uygur individuals, 104 different haplotypes were obtained, 99 of which were unique. The haplotypic diversity and discrimination capacity of these 24 Y-STR loci in Uygur group were 0.9992 and 0.9541, respectively. An additional 7 loci (DYS388, DYS444, DYS447, DYS449, DYS522, and DYS527a,b) showed high genetic diversity and improved the overall discrimination capacity of the 24 Y-STR system. Pairwise Fst and neighbor-joining analysis showed that the Uygur group was genetically close to the Han populations from different regions.

Hepatotoxicity due to etanercept abated after dose reduction in a patient with pustular psoriasis and without compromised efficacy / Hepatotoxicidad por supresión del etanercept tras reducción de dosis en un paciente con psoriasis pustular y sin eficacia comprometida

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Hyper IgE syndrome.

Hyper IgE syndrome (HIES) is a rare disorder characterized by eczema, recurrent infections of the skin and lungs, typically with Staphylococcus aureus, Candida albicans and certain viruses, and elevated levels of serum IgE. Other clinical manifestations include characteristic facies (prominent forehead, broad nasal bridge and facial asymmetry), chronic eczematous dermatitis, retained primary dentition, recurrent pathological fractures, hyper-extensibility and scoliosis. The central nervous system (CNS) involvement in HIES has been rarely reported. Here we presented a case of HIES with rare associations of epilepsy in a young patient to raise awareness for this disorder.

Two novel frameshift mutations of the DSRAD gene in Chinese pedigrees with dyschromatosis symmetrica hereditaria.

BACKGROUND: Dyschromatosis symmetrica hereditaria (DSH) is an autosomal dominant disorder characterized by a mixture of hyperpigmented and hypopigmented macules localized on the back of the extremities and caused by the mutations in the DSRAD gene. METHODS: Two Chinese pedigrees of typical DSH were subjected to mutation detection in DSRAD. Direct sequencing of all PCR products of the whole coding regions of DSRAD was performed to identify the mutation. RESULTS: The c.1615delG (p.V539fs) mutation was found in the affected members but not in the healthy individuals in family 1 and the c.ins1372-9 CCACAGAT (p.D458fs) mutation was found in patients but not in the healthy members of family 2. CONCLUSION: Our study found two novel frameshift mutations in the DSRAD gene. We add new variants to the knowledge of DSRAD mutations in DSH.

[Effect of curcumin on IL-17-induced nitric oxide production and expression of iNOS in human keratinocytes].

AIM: To investigate the effect of curcumin on IL-17-induced NO production, mRNA and protein expression of iNOS in human keratinocyte cell lines(HaCaT cells). METHODS: HaCaT cells were stimulated with IL-17 and incubated with three doses of curcumin for 24h in vitro. After collections of supernatant, total RNA and protein, NO levels in supernatant were detected and fluorescence quantitative PCR and Western blot were performed to determine the effect of curcumin on NO levels and iNOS. RESULTS: IL-17 increased NO levels, and expression of iNOS in HaCaT cells(P<0.01). Curcumin decreased IL-17 induced NO production and the iNOS expression at mRNA (P<0.01) and protein (P<0.01) levels significantly. CONCLUSION: Curcumin down-regulates IL-17-induced NO secretions and iNOS expression in HaCaT cells, thus provides a theoretical basis for the treatment of inflammatory diseases of skin related to keratinocytes.