Highly elastic, fatigue-resistant, antibacterial, conductive, and nanocellulose-enhanced hydrogels with selenium nanoparticles loading as strain sensors.

The fabrication of highly elastic, fatigue-resistant and conductive hydrogels with antibacterial properties is highly desirable in the field of wearable devices. However, it remains challenging to simultaneously realize the above properties within one hydrogel without compromising excellent sensing ability. Herein, we fabricated a highly elastic, fatigue-resistant, conductive, antibacterial and cellulose nanocrystal (CNC) enhanced hydrogel as a sensitive strain sensor by the synergistic effect of biosynthesized selenium nanoparticles (BioSeNPs), MXene and nanocellulose. The structure and potential mechanism to generate biologically synthesized SeNPs (BioSeNPs) were systematically investigated, and the role of protease A (PrA) in enhancing the adsorption between proteins and SeNPs was demonstrated. Additionally, owing to the incorporation of BioSeNPs, CNC and MXene, the synthesized hydrogels showed high elasticity, excellent fatigue resistance and antibacterial properties. More importantly, the sensitivity of hydrogels determined by the gauge factor was as high as 6.24 when a high strain was applied (400-700 %). This study provides a new horizon to synthesize high-performance antibacterial and conductive hydrogels for soft electronics applications.

Bioactive triterpenoid compounds of Poria cocos (Schw.) Wolf in the treatment of diabetic ulcers via regulating the PI3K-AKT signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Diabetic ulcers represent a chronic condition characterized by prolonged hyperglycemia and delayed wound healing, accompanied by endocrine disorders, inflammatory responses, and microvascular damage in the epidermal tissue, demanding effective clinical treatment approaches. For thousands of years, ancient Chinese ethnopharmacological studies have documented the use of Poria cocos (Schw.) Wolf in treating diabetic ulcers. Recent research has substantiated the diverse pharmacological effects of Poria cocos (Schw.) Wolf, including its potential to alleviate hyperglycemia and exhibit anti-inflammatory, antioxidant, and immune regulatory properties, which could effectively mitigate diabetic ulcer symptoms. Furthermore, being a natural medicine, Poria cocos (Schw.) Wolf has demonstrated promising therapeutic effects and safety in the management of diabetic ulcers, holding significant clinical value. Despite its potential clinical efficacy and applications in diabetic ulcer treatment, the primary active components and underlying pharmacological mechanisms of Poria cocos (Schw.) Wolf remains unclear. Further investigations are imperative to establish a solid foundation for drug development in this domain. AIM OF THE STUDY AND MATERIALS AND METHODS: In this study, we aimed to identify the active compounds and potential targets of Poria cocos (Schw.) Wolf using UHPLC-Q-TOF-MS and TCMSP databases. Additionally, we attempt to identify targets related to diabetic ulcers. Following enrichment analysis, a network of protein-protein interactions was constructed to identify hub genes based on the common elements between the two datasets. To gain insights into the binding activities of the hub genes and active ingredients, molecular docking analysis was employed. Furthermore, to further validate the therapeutic effect of Poria cocos (Schw.) Wolf, we exerted in vitro experiments using human umbilical vein vascular endothelial cells and human myeloid leukemia monocytes (THP-1). The active ingredient of Poria cocos (Schw.) Wolf was applied in these experiments. Our investigations included various assays, such as CCK-8, scratch test, immunofluorescence, western blotting, RT-PCR, and flow cytometry, to explore the potential of Poria cocos (Schw.) Wolf triterpenoid extract (PTE) in treating diabetic ulcers. RESULTS: The findings here highlighted PTE as the primary active ingredient in Poria cocos (Schw.) Wolf. Utilizing network pharmacology, we identified 74 potential targets associated with diabetic ulcer treatment for Poria cocos (Schw.) Wolf, with five hub genes (JUN, MAPK1, STAT3, AKT1, and CTNNB1). Enrichment analysis revealed the involvement of multiple pathways in the therapeutic process, with the PI3K-AKT signaling pathway showing significant enrichment. Through molecular docking, we discovered that relevant targets within this pathway exhibited strong binding with the active components of Poria cocos (Schw.) Wolf. In vitro experiments unveiled that PTE (10 mg/L) facilitated the migration of human umbilical vein vascular endothelial cells (P < 0.05). PTE also increased the expression of CD31 and VEGF mRNA (P < 0.05) while activating the expressions of p-PI3K and p-AKT (P < 0.05). Moreover, PTE demonstrated its potential by reducing the expression of IL-1ß, IL-6, TNF-α, and NF-κB mRNA in THP-1 (P < 0.05) and fostering M2 macrophage polarization. These results signify the potential therapeutic effects of PTE in treating diabetic ulcers, with its beneficial actions mediated through the PI3K-AKT signaling pathway. CONCLUSIONS: PTE is the main active ingredient in Poria cocos (Schw.) Wolf that exerts therapeutic effects. Through PI3K-AKT signaling pathway activation and inflammatory response reduction, PTE promotes angiogenesis, thereby healing diabetic ulcers.

Untargeted metabolomics yields insight into extramammary Paget's disease mechanisms.

Background: Extramammary Paget's disease (EMPD) is a rare cutaneous malignancy, commonly affecting the external genitalia and perianal area of the elderly with unclear pathogenesis. Metabolomics provides a novel perspective for uncovering the metabolic mechanisms of a verity of cancers. Materials and methods: Here, we explored the metabolome of EMPD using an untargeted strategy. In order to further investigate the potential relationship between metabolites and gene expression, we re-analyzed the gene expression microarray data (GSE117285) using differential expression analysis and functional enrichment analyses. Results: Results showed that a total of 896 metabolites were identified and 87 metabolites including 37 upregulated and 50 downregulated significantly in EMPD were sought out. In the following feature selection analyses, four metabolites, namely, cyclopentyl fentanyl-d5, LPI 17:0, guanosine-3',5'-cyclic monophosphate, kynurenine (KYN, high in EMPD) were identified by both random forest and support vector machine analyses. We then identified 1,079 dysfunctional genes: 646 upregulated and 433 downregulated in EMPD. Specifically, the tryptophan-degrading enzyme including indoleamine-2,3-dioxygenase-1 (IDO1) and tryptophan 2,3-dioxygenase (TDO2) were also increased. Generally, cancers exhibit a high expression of IDO1 and TDO2 to catabolize tryptophan, generating abundant KYN. Moreover, we also noticed the abnormal activation of sustaining proliferative signaling in EMPD. Conclusion: In conclusion, this study was the first to reveal the metabolome profile of EMPD. Our results demonstrate that IDO1/TDO2-initialized KYN metabolic pathway may play a vital role in the development and progression of EMPD, which may serve as a potential therapeutic target for treating EMPD.

A deep learning fusion network trained with clinical and high-frequency ultrasound images in the multi-classification of skin diseases in comparison with dermatologists: a prospective and multicenter study.

Background: Clinical appearance and high-frequency ultrasound (HFUS) are indispensable for diagnosing skin diseases by providing internal and external information. However, their complex combination brings challenges for primary care physicians and dermatologists. Thus, we developed a deep multimodal fusion network (DMFN) model combining analysis of clinical close-up and HFUS images for binary and multiclass classification in skin diseases. Methods: Between Jan 10, 2017, and Dec 31, 2020, the DMFN model was trained and validated using 1269 close-ups and 11,852 HFUS images from 1351 skin lesions. The monomodal convolutional neural network (CNN) model was trained and validated with the same close-up images for comparison. Subsequently, we did a prospective and multicenter study in China. Both CNN models were tested prospectively on 422 cases from 4 hospitals and compared with the results from human raters (general practitioners, general dermatologists, and dermatologists specialized in HFUS). The performance of binary classification (benign vs. malignant) and multiclass classification (the specific diagnoses of 17 types of skin diseases) measured by the area under the receiver operating characteristic curve (AUC) were evaluated. This study is registered with www.chictr.org.cn (ChiCTR2300074765). Findings: The performance of the DMFN model (AUC, 0.876) was superior to that of the monomodal CNN model (AUC, 0.697) in the binary classification (P = 0.0063), which was also better than that of the general practitioner (AUC, 0.651, P = 0.0025) and general dermatologists (AUC, 0.838; P = 0.0038). By integrating close-up and HFUS images, the DMFN model attained an almost identical performance in comparison to dermatologists (AUC, 0.876 vs. AUC, 0.891; P = 0.0080). For the multiclass classification, the DMFN model (AUC, 0.707) exhibited superior prediction performance compared with general dermatologists (AUC, 0.514; P = 0.0043) and dermatologists specialized in HFUS (AUC, 0.640; P = 0.0083), respectively. Compared to dermatologists specialized in HFUS, the DMFN model showed better or comparable performance in diagnosing 9 of the 17 skin diseases. Interpretation: The DMFN model combining analysis of clinical close-up and HFUS images exhibited satisfactory performance in the binary and multiclass classification compared with the dermatologists. It may be a valuable tool for general dermatologists and primary care providers. Funding: This work was supported in part by the National Natural Science Foundation of China and the Clinical research project of Shanghai Skin Disease Hospital.

Anoikis patterns via machine learning strategy and experimental verification exhibit distinct prognostic and immune landscapes in melanoma.

BACKGROUND: Anoikis is a cell death programmed to eliminate dysfunctional or damaged cells induced by detachment from the extracellular matrix. Utilizing an anoikis-based risk stratification is anticipated to understand melanoma's prognostic and immune landscapes comprehensively. METHODS: Differential expression genes (DEGs) were analyzed between melanoma and normal skin tissues in The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression data sets. Next, least absolute shrinkage and selection operator, support vector machine-recursive feature elimination algorithm, and univariate and multivariate Cox analyses on the 308 DEGs were performed to build the prognostic signature in the TCGA-melanoma data set. Finally, the signature was validated in GSE65904 and GSE22155 data sets. NOTCH3, PIK3R2, and SOD2 were validated in our clinical samples by immunohistochemistry. RESULTS: The prognostic model for melanoma patients was developed utilizing ten hub anoikis-related genes. The overall survival (OS) of patients in the high-risk subgroup, which was classified by the optimal cutoff value, was remarkably shorter in the TCGA-melanoma, GSE65904, and GSE22155 data sets. Low-risk patients exhibited low immune cell infiltration and high expression of immunophenoscores and immune checkpoints. They also demonstrated increased sensitivity to various drugs, including dasatinib and dabrafenib. NOTCH3, PIK3R2, and SOD2 were notably associated with OS by univariate Cox analysis in the GSE65904 data set. The clinical melanoma samples showed remarkably higher protein expressions of NOTCH3 (P = 0.003) and PIK3R2 (P = 0.009) than the para-melanoma samples, while the SOD2 protein expression remained unchanged. CONCLUSIONS: In this study, we successfully established a prognostic anoikis-connected signature using machine learning. This model may aid in evaluating patient prognosis, clinical characteristics, and immune treatment modalities for melanoma.

Multiple gene-drug prediction tool reveals Rosiglitazone based treatment pathway for non-segmental vitiligo.

Vitiligo is a skin disease characterized by selective loss of melanocytes, which seriously affects the appearance and causes great psychological stress to patients. In this study, we performed a comprehensive analysis of two vitiligo microarray datasets from the GEO database using bioinformatics tools to identify 297 up-regulated mRNAs and 186 down-regulated mRNAs, revealing important roles for pathways related to melanin synthesis, tyrosine metabolism, and inflammatory factors, such as "PPAR signaling pathway", "tyrosine metabolism", "nonalcoholic fatty liver disease (NAFLD) pathway", "melanogenesis", and "IL-17 signaling pathway". Combining the Search Tool for Interacting Chemicals (STITCH) database 5.0 and the drug-gene interaction database 3.0 (DGIdb), we identified that the PPAR-γ agonist rosiglitazone may promote melanin synthesis via EDNRB. Next, we investigated the mechanism of rosiglitazone and PPAR-γ pathway in promoting melanin production. Consistent with the results of bioinformatics analysis, the expression levels of PPAR-γ, EDNRB, and TYR were significantly reduced in human non-segmental vitiligo skin along with the reduction of MITF, a key gene for epidermal melanogenesis. Meanwhile, rosiglitazone increased melanin synthesis capacity in melanocytes and zebrafish by activating PPAR-γ and upregulating TYR, TYRP-1, and TYRP-2. Conversely, treatment of melanocytes with the PPAR-γ antagonist GW resulted in inhibition of melanin synthesis and expression of melanin-related factors. At the same time, simultaneous treatment of rosiglitazone with GW reversed the inhibitory effect of GW on melanin synthesis. In this study, we identified that rosiglitazone, an important insulin sensitizer, promotes melanin synthesis in melanocytes by increasing PPAR-γ activity and upregulating the expression levels of EDNRB and TYR. These findings may provide new ideas for exploring the pathogenesis and potential therapeutic targets of non-segmental vitiligo.

Mechanisms of resveratrol against diabetic wound by network pharmacology and experimental validation.

BACKGROUND: Resveratrol (RSV) that possesses anti-oxidative, anti-inflammatory, and pro-angiogenic effects is an effective drug for diabetic wound (DW), while its pharmacological mechanism remains to be elucidated. In this study, we apply network pharmacology and experimental validation approach to reveal the potential mechanism of RSV against DW. METHODS: We obtained potential targets for RSV and DW from the publicly available database. Using interaction networks and conducting GO and KEGG pathway enrichment analyses, we constructed target-pathway networks to explore the relationship between RSV and DW. To validate the pharmacological mechanism of RSV, we induced the DW model. RESULTS: Ninety overlapped targets between RSV and DW were obtained, and the hub genes of the PPI network included TNF, IL-6, CASP3, MAPK3, VEGFA, IL-1ß, AKT1, and JUN. Based on target-pathway networks, the AGE-RAGE signalling pathway was involved in the RSV treatment of DW. Furthermore, in vivo experiments revealed that RSV significantly promoted wound healing in diabetic mice and attenuated the expression of pro-inflammatory cytokines in wound tissue. Meanwhile, RSV could inhibit the AGE-RAGE signalling pathway and thus reduce the activation of NF-κB. CONCLUSION: This study initially revealed the biological mechanism of RSV for treating DW through multi-target and multi-pathway. AGE-RAGE, FoxO, MAPK, PI3K-AKT and other signalling pathways may be the main pathways of RSV in treating DW. RSV reduces the inflammatory response by inhibiting the AGE-RAGE signalling pathway, which in turn promotes DW healing.

Whole genome methylation sequencing reveals epigenetic landscape and abnormal expression of FABP5 in extramammary Paget's disease.

BACKGROUND: Extramammary Paget's disease (EMPD) is a rare cutaneous malignant tumor with a high recurrence rate after surgery. However, the genetic and epigenetic alterations underlying its pathogenesis remain unknown. DNA methylation is an important epigenetic modification involved in many biological processes. METHODS: In this study, enzymatic methyl-sequencing (EM-seq) technique was used to investigate the landscape of genome-wide DNA methylation from three pairs of tumor tissues and adjacent tissues of patients with EMPD. Additionally, we conducted histopathological examinations to assess the expression of fatty acid-binding protein 5 (FABP5) in another three paired samples from EMPD patients. RESULTS: The cluster analysis showed the good quality of the samples. A differential methylation region (DMR) heat map was used to quantitatively characterize genome-wide methylation differences between tumors and controls. Global DNA methylation level is lower in EMPD tissue compared to matched controls, indicating that DNA methylation discriminates between tumor and normal skin. And the top hypomethylation gene on the promoter region in tumor tissues was FABP5 on chromosome 8 with 38.44% decreased median methylation. We next identified the expression of FABP5 in paired tumors and adjacent tissues in three additional patients with EMPD. Immunofluorescence results showed FABP5 highly expressed in tumor tissues and co-located with CK7, CK20 and EMA. GO and KEGG enrichment analysis showed DMR genes on promoter are mainly enriched in the calcium ion transport, GTPase mediated signal transduction, Rap1 signaling pathway and GnRH signaling pathway. CONCLUSION: Taken together, our findings provide the first description of the whole genome methylation map of EMPD and identify FABP5 as a pathogenic target of EMPD.

Effects of photobiomodulation at various irradiances on normal and dihydrotestosterone-treated human hair dermal papilla cells in vitro.

Androgenetic alopecia (AGA) is the most common type of hair loss caused by dihydrotestosterone (DHT) binding to androgen receptors in dermal papilla cells (DPCs). Photobiomodulation (PBM) is a promising treatment for AGA but suffers from inconsistent outcomes and inconsistent effective light parameters. This study investigated the impact of red light at various irradiances on normal and DHT-treated DPCs. Our results suggested that red light at 8 mW/cm2 was most effective in promoting DPCs growth. Furthermore, a range of irradiances from 2 to 64 mW/cm2 modulated key signaling pathways, including Wnt, FGF, and TGF, in normal and DHT-treated DPCs. Interestingly, 8 mW/cm2 had a greater impact on these pathways in DHT-treated DPCs and altered the Shh pathway, suggesting that the effect of PBM varies with the cellular environment. This study highlights specific factors that influence PBM effectiveness and provides insight into the need for personalized PBM treatment approaches.

An epidemiological study on skin tumors of the elderly in a community in Shanghai, China.

The morbidity of skin tumors (ST) in China is a great concern as the population ages. No epidemiological survey on ST in elderly communities in China has been reported. A questionnaire survey was conducted among the residents over 60 years old in a community in Shanghai, China from May 1, 2011 to November 30, 2011. The prevalence of cutaneous tumors and associated factors were analyzed. Among 2038 valid cases, a total of 78 (3.8%, 95% CI 3.0-4.7) skin cancers (SC) were confirmed. According to the final multivariate regression analysis, age, gender and previous occupation were the significantly influential factors for SC. Actinic keratosis (AK) accounted for the largest proportion (63, 3.1%) in SC. The head and neck was the physiological site with the highest incidence of SC (64, 82.1%), and AK was the most common (55, 87.3%) in head and neck SC. The common concomitant diseases of SC were hypertension (26, 33.3%) and diabetes mellitus (9, 11.5%). Seborrheic keratosis (SK) was the most common benign skin tumor with a prevalence of 100%. Men and women developed SK in significantly different parts of the body (P < 0.0001). The incidence of ST in the elderly population in Shanghai community increased with age. ST preferred to occur in the head and neck, which might be attributed to excessive ultraviolet (UV) exposure in these areas. Therefore, early diagnosis and sun-protection education are essential interventions for ST in the elderly.

Comparative study of alginate and type I collagen as biomaterials for cartilage stem/progenitor cells to construct tissue-engineered cartilage in vivo.

With the help of biomaterials, cartilage stem/progenitor cells (CSPCs) derived from cartilage tissue present a promising choice for cartilage regeneration. In our previous study, we investigated whether CSPCs could be ideal seeding cells for cartilage tissue regeneration. Biomaterials are fabricated to accelerate tissue regeneration, providing a suitable environment for cell attachment, proliferation, and differentiation. Among the biomaterials used in cartilage regeneration medicine, alginate and collagen are classified as natural biomaterials and are characterized by high biocompatibility, bioactivity, and non-toxic degradation products. However, it is unclear which material would have a competitive advantage in CSPC-based cartilage regeneration in vivo. In the present study, we employed alginate and type Ⅰ collagen as substrates for CSPCs and chondrocytes, which was made control group, to explore a more suitable biomaterials for CSPCs to fabricate tissue-engineered cartilage, in vivo. Hematoxylin and eosin (HE) staining, Safranin O, immunohistochemical assay, and quantitative real-time polymerase chain reaction (qRT-PCR) were used to evaluate the tissue-engineered cartilage in vivo. Compared with the alginate group, collagen enhanced the expression of cartilage-specific genes, such as ACAN, SOX9, and COLII, more markedly. Furthermore, the marker genes of expression, dedifferentiation, and hypertrophy, COLI and COLX, were downregulated in the collagen group. The results demonstrated that collagen as a substrate was superior to alginate in increasing the accumulation of cartilage-like ECM for CSPCs in vivo. In summary, compared with alginate, collagen hydrogel is an effective biomaterial for CSPC-based cartilage regeneration.

Glabellar wrinkle correction by autologous fat transplantation and evidence of human adipose tissue regeneration in a nude mouse model.

BACKGROUND: Fat grafts are increasingly applied in augmenting soft tissue defects and correcting static wrinkles, but the outcome is always unpredictable because of high absorption rate. Perilipin1 (Plin1) and perilipin2 (Plin2), two perilipin family proteins on lipid droplets in adipocytes, are reported to be used as biomarkers to evaluate adipocyte regeneration in vivo. AIMS: The aim of this study was to assess the efficacy of glabellar wrinkle correction with autologous fat grafting and to observe human adipose regeneration in a nude mouse model. PATIENTS/METHODS: Ten patients with 16 moderate or severe glabellar wrinkles underwent wrinkle correction by subcutaneously injecting autologous lipoaspirates obtained from the abdomen. The injection dose was 0.05 ml per 5 mm. The aspirated adipose tissue (0.05 ml) was also injected under the scalps of nude mice. Fat grafts were explanted at 3, 7, 15, 30, and 120 days after transplantation and the dynamic cellular changes were evaluated by HE staining and immunostaining of Plin1 and Plin2. RESULTS: Among the sixteen wrinkle lines, thirteen were obviously improved 4 months after procedure. Eight of the ten patients were satisfied with their wrinkle correction effects. The fat grafts demonstrated a continuous changing process from degeneration to regeneration in the mouse model without significant absorption and necrosis. It was Plin1, not Plin2 that was expressed in mature adipocytes. After transplantation, Plin1 expression was lost in dead fat cells while Plin2 expression was activated in newly regenerated adipocytes. After 120 days, all the surviving adipocytes were negative for Plin2 but positive for Plin1 again. CONCLUSIONS: Micro-volume fat transplantation was an easy and safe method to improve glabellum wrinkle lines, and the regenerative process of human adipose tissue could be verified in the mouse model.

Identification of key candidate genes involved in melanoma metastasis.

Metastasis is the most lethal stage of cancer progression. The present study aimed to investigate the underlying molecular mechanisms of melanoma metastasis using bioinformatics. Using the microarray dataset GSE8401 from the Gene Expression Omnibus database, which included 52 biopsy specimens from patients with melanoma metastasis and 31 biopsy specimens from patients with primary melanoma, differentially expressed genes (DEGs) were identified, subsequent to data preprocessing with the affy package, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. A protein­protein interaction (PPI) network was constructed. Mutated genes were analyzed with 80 mutated cases with melanoma from The Cancer Genome Atlas. The overall survival of key candidate DEGs, which were within a filtering of degree >30 criteria in the PPI network and involved three or more KEGG signaling pathways, and genes with a high mutation frequency were delineated. The expression analysis of key candidate DEGs, mutant genes and their associated genes were performed on UALCAN. Of the 1,187 DEGs obtained, 505 were upregulated and 682 were downregulated. 'Extracellular exosome' processes, the 'amoebiasis' pathway, the 'ECM­receptor interaction' pathway and the 'focal adhesion' signaling pathway were significantly enriched and identified as important processes or signaling pathways. The overall survival analysis of phosphoinositide­3­kinase regulator subunit 3 (PIK3R3), centromere protein M (CENPM), aurora kinase A (AURKA), laminin subunit α 1 (LAMA1), proliferating cell nuclear antigen (PCNA), adenylate cyclase 1 (ADCY1), BUB1 mitotic checkpoint serine/threonine kinase (BUB1), NDC80 kinetochore complex component (NDC80) and protein kinase C α (PRKCA) in DEGs was statistically significant. Mutation gene analysis identified that BRCA1­associated protein 1 (BAP1) had a higher mutation frequency and survival analysis, and its associated genes in the BAP1­associated PPI network, including ASXL transcriptional regulator 1 (ASXL1), proteasome 26S subunit, non­ATPase 3 (PSMD3), proteasome 26S subunit, non ATPase 11 (PSMD11) and ubiquitin C (UBC), were statistically significantly associated with the overall survival of patients with melanoma. The expression levels of PRKCA, BUB1, BAP1 and ASXL1 were significantly different between primary melanoma and metastatic melanoma. Based on the present study, 'extracellular exosome' processes, 'amoebiasis' pathways, 'ECM­receptor interaction' pathways and 'focal adhesion' signaling pathways may be important in the formation of metastases from melanoma. The involved genes, including PIK3R3, CENPM, AURKA, LAMA1, PCNA, ADCY1, BUB1, NDC80 and PRKCA, and mutation associated genes, including BAP1, ASXL1, PSMD3, PSMD11 and UBC, may serve important roles in metastases of melanoma.

[Analysis of KIT mutations in five patients from two Han Chinese pedigrees affected with Piebaldism].

OBJECTIVE: To screen for KIT gene mutations in two Han Chinese pedigrees affected with Piebaldism. METHODS: Clinical data of the pedigrees was collected. Genomic DNA was extracted from blood samples collected from the pedigrees and 120 unrelated healthy controls. All coding exons of the KIT gene were subjected to PCR amplification and direct sequencing. RESULTS: Two missense mutations, c.1861G>A(p.Ala621Thr) and c.1872G>A(p.Met624Ile), were identified respectively in the two pedigrees. Neither mutation was found among healthy members from the respective pedigree and the 120 unrelated healthy controls. c.1872G>A is a novel mutation. CONCLUSION: Mutations of the KIT gene may affect the structure and function of the transmembrane receptor KIT, which lead to the disease.

Can red-light 5-aminolevulinic photodynamic therapy cure port wine stains on comb animal model?

OBJECTIVE: To study the curative effect of red-light 5-Aminolevulinic photodynamic therapy(ALA-PDT) to port wine stains(PWS) on comb animal model. METHODS: 160 male cocks were randomly divided into 16 groups. The ALA only group was given ALA only topical or systemic application. Light only groups were only given 630 nm red light irradiation with different light density. ALA-PDT groups were given red light after the application of topical or systemic ALA. PDL group was given PDL irradiation. The distribution of fluorescence in tissue after topical or systemic application of ALA was detected. The morphological changes, the pathological changes and the capillary reduction rate of the comb were observed after treatment for 0, 1, 3, 5, 7, 14 days. RESULTS: The PpIX fluorescence generated after topical and systemic application of ALA. In the topical ALA-PDT group at low light density 80 J/cm2, the morphology and the histopathology had no obvious change. While under 160 J/cm2 and 200 J/cm2 light density, severe erosion and thick scab appeared. The histopathology showed epidermal necrosis and loss. The immunohistochemistry showed that there was no significant change in the number of capillaries under different light density (P > 0.05). In the systemic ALA-PDT group under low light density 80 J/cm2, only partial erosion and thin scab was observed on the treatment side. With the increase of light density, thick charred crust and even scar was observed. The histopathology showed that there were different degrees of damage to dermal and epidermal tissues. And the immunohistochemistry showed the capillary reduced significantly in the treatment side (P < 0.01). In control group, the comb is ruddy and plump. CONCLUSION: These results suggest that either topical or systemic red-light ALA-PDT is not suitable treatment methods for PWS.

Characteristics of human papillomaviruses infection in men with genital warts in Shanghai.

Human papillomaviruses (HPV) infected men causes continued transmission of HPV to women. The prevalence of 15 high-risk HPV strains (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66 and 68) and 6 low-risk HPV strains (HPV6, 11, 42, 43, 44 and CP8304) were evaluated in 935 males with genital warts. Of the 447 (447/935, 47.8%) HPV DNA positive subjects, 230 (24.6%), 356 (38.1%) and 139 (14.9%) were infected by high-risk, low-risk and both high and low-risk HPV respectively. Of the 356 low-risk HPV infected subjects, 333(93.5%) were infected by single HPV strain; 203 (57.0%), 147 (41.3%), 24 (6.7%) and 5 (1.4%) were infected with HPV genotype 6, 11, CP8304 and 44 respectively; population with age ≤ 20 showed the highest infection rate. High-risk HPV are also highly prevalent in our patients, genotype 16, 58, 51, 39, 52 and 53 are the top five prevalent genotypes with infection rates of 27.4%, 18.7%, 14.3%, 13.9%, 12.6% and 12.6% respectively; only 68.3% subjects were sole infection; subjects with 41 ≤ age ≤ 50 showed the highest infection rate. Both high and low-risk HPV are highly prevalent in men with genital warts, its impact on women HPV control and prevention need further evaluation.

Microwave-Assisted Synthesis of Glutathione-Capped CdTe/CdSe Near-Infrared Quantum Dots for Cell Imaging.

These glutathione (GSH)-conjugated CdTe/CdSe core/shell quantum dot (QD) nanoparticles in aqueous solution were synthesized using a microwave-assisted approach. The prepared type II core/shell QD nanoparticles were characterized by UV-Vis absorption, photoluminescence (PL) spectroscopy, X-ray powder diffraction (XRD) and high-resolution transmission electron microscopy (HR-TEM). Results revealed that the QD nanoparticles exhibited good dispersity, a uniform size distribution and tunable fluorescence emission in the near-infrared (NIR) region. In addition, these nanoparticles exhibited good biocompatibility and photoluminescence in cell imaging. In particular, this type of core/shell NIR QDs may have potential applications in molecular imaging.