Natural blackcurrant extract contained gelatin hydrogel with photothermal and antioxidant properties for infected burn wound healing.

Burns represent a prevalent global health concern and are particularly susceptible to bacterial infections. Severe infections may lead to serious complications, posing a life-threatening risk. Near-infrared (NIR)-assisted photothermal antibacterial combined with antioxidant hydrogel has shown significant potential in the healing of infected wounds. However, existing photothermal agents are typically metal-based, complicated to synthesize, or pose biosafety hazards. In this study, we utilized plant-derived blackcurrant extract (B) as a natural source for both photothermal and antioxidant properties. By incorporating B into a G-O hydrogel crosslinked through Schiff base reaction between gelatin (G) and oxidized pullulan (O), the resulting G-O-B hydrogel exhibited good injectability and biocompatibility along with robust photothermal and antioxidant activities. Upon NIR irradiation, the controlled temperature (around 45-50 °C) generated by the G-O-B hydrogel resulted in rapid (10 min) and efficient killing of Staphylococcus aureus (99 %), Escherichia coli (98 %), and Pseudomonas aeruginosa (82 %). Furthermore, the G-O-B0.5 hydrogel containing 0.5 % blackcurrant extract promoted collagen deposition, angiogenesis, and accelerated burn wound closure conclusively, demonstrating that this well-designed and extract-contained hydrogel dressing holds immense potential for enhancing the healing process of bacterial-infected burn wounds.

Cadmium Hydroxyl Chloride with Balanced Band Gap and Second-Harmonic-Generation Response.

Ultraviolet (UV) nonlinear-optical (NLO) materials are crucial in laser technology due to their ability to modulate light frequency. In this work, when d10 cations, hydroxyl groups, and Cl atoms were combined, a cadmium double salt, Cd(OH)Cl, was synthesized by a simple hydrothermal method. It has a large phase-matched second-harmonic-generation (SHG) response at 1064 nm (2.5 × KDP) with a short UV-cutoff edge (260 nm), which can be applied in a solar-blind UV band. Theoretical calculations suggest that [Cd(OH)3Cl3] groups lead to a large SHG response. Our work may shed light on the exploration of new NLO materials in metal hydroxyl chlorides.

A hyaluronic acid / chitosan composite functionalized hydrogel based on enzyme-catalyzed and Schiff base reaction for promoting wound healing.

The healing of full-thickness skin defect has been a clinical challenge. Hydrogels with multiple functions inspired by extracellular matrix are expected to be used as wound dressing. In this paper, dopamine-grafted oxidized hyaluronic acid was blended with quaternary ammonium chitosan to form a composite functionalized hydrogel by enzyme-catalyzed cross-linking and Schiff base reaction. The hydrogel has convenient preparation, good biocompatibility, antibacterial and antioxidant, high adhesion and self-healing properties. The results in vivo show that the hydrogel can effectively close the wound and accelerate the speed of wound healing by up-regulating the expression of angiogenic protein and promoting the distribution of collagen deposition more uniform and regular. It is expected that this composite functionalized hydrogel dressing has great potential in wound regeneration.

New insights into balancing wound healing and scarless skin repair.

Scars caused by skin injuries after burns, wounds, abrasions and operations have serious physical and psychological effects on patients. In recent years, the research of scar free wound repair has been greatly expanded. However, understanding the complex mechanisms of wound healing, in which various cells, cytokines and mechanical force interact, is critical to developing a treatment that can achieve scarless wound healing. Therefore, this paper reviews the types of wounds, the mechanism of scar formation in the healing process, and the current research progress on the dual consideration of wound healing and scar prevention, and some strategies for the treatment of scar free wound repair.

Cadmium phosphates with two types of fundamental building units and a wide ultraviolet transparency window.

Owing to diverse crystal structures and intriguing properties, metal phosphates have attracted much attention in recent studies. In this work, two cadmium phosphates, KCd6P7O24 and KCd3P3O11, were obtained by the high-temperature solution method. In the crystal structure, both the title compounds contain two types of P-O fundamental building units. Thermal and spectral analyses were carried out on the title compounds, indicating that both of them have good thermal stability and short UV cut-off edges. In addition, the relationship between the electronic structures and optical properties was studied by theoretical calculations.

M(NH2SO3)2·xH2O (M = Ca, Pb, x = 0, 1, 4): Effect of Hydrogen Bonding on Structural Transformations and Second Harmonic Generation of Metal Sulfamates.

Nonlinear optical (NLO) crystals are very important for laser technology, but the performances of available NLO crystals are still insufficient for increasing demand. Recently, the exploration of new NLO crystals in non-π-conjugated systems with the heteroatomic tetrahedra is attracting a lot of interest. In this work, we systematically explore the metal sulfamates containing [NH2SO3] groups and four metal sulfamates, namely, Ca(NH2SO3)2·4H2O, Ca(NH2SO3)2·H2O, Pb(NH2SO3)2·H2O, and Pb(NH2SO3)2 were synthesized by aqueous solution and hydrothermal methods. Notably, these metal sulfamates exhibit different crystal structures and optical properties owing to the diverse arrangement of the functional groups in their structures. In addition, due to hydrogen bond regulation, the centrosymmetric (CS) compound Ca(NH2SO3)2·4H2O can transform into noncentrosymmetric (NCS) Ca(NH2SO3)2·H2O, leading to NLO activity. Experimental characterizations and theoretical analysis reveal that these metal sulfamates are ultraviolet transparent and suitable for developing new NLO materials.

MicroRNA-149-Mediated MAPK1/ERK2 Suppression Attenuates Hair Follicle Stem Cell Differentiation.

Hair follicle stem cells (HFSCs) are responsible for hair growth and hair follicle regeneration. MicroRNAs have been demonstrated to be involved in the differentiation of HFSCs. Thus, this study aimed to explore the potential role of miR-149 in the differentiation of HFSCs. The isolated HFSCs were identified by flow cytometric sorting. miR-149 expression was determined during differentiation of HFSCs. Gain- and loss-of-function approaches were conducted to explore the roles of miR-149, MAPK1/ERK2, and FGF2/c-MYC in colony formation and proliferation of HFSCs. Furthermore, in vivo assays were undertaken in miR-149 knockout mice to confirm their roles in HFSC differentiation. miR-149 was found to be downregulated during HFSC differentiation, and overexpressed miR-149 restricted the proliferation and differentiation of HFSCs. miR-149 was confirmed to target and inhibit MAPK1/ERK2, which was highly expressed in and positively associated with HFSC differentiation. The MAPK1/ERK2 promotion in HFSC differentiation was achieved by augmenting expression of FGF2 and c-MYC. The in vitro effects of miR-149 were validated in in vivo experiments. Taken together, upregulated miR-149 restricted HFSC differentiation and hair growth by targeting MAPK1/ERK2 to reduce expression of FGF2 and c-MYC, which sheds light on the underlying molecular mechanism of hair growth.

Long non-coding RNA PICSAR knockdown inhibits the progression of cutaneous squamous cell carcinoma by regulating miR-125b/YAP1 axis.

AIMS: The purpose of this study was to explore the precise role and mechanism of p38 inhibiting cutaneous squamous cell carcinoma associated lincRNA (PICSAR) in CSCC. MATERIALS AND METHODS: The expression levels of PICSAR, microRNA-125b (miR-125b) and yes-associated protein1 (YAP1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis and invasion were evaluated by Cell Counting Kit-8 (CCK-8) assay, flow cytometry, transwell assay, respectively. The interaction between miR-125b and PICSAR or YAP1 was predicted by bioinformatics software and confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Western blot was employed to detect the protein expression of YAP1. The mice xenograft model was established to investigate the role of PICSAR in vivo. KEY FINDINGS: PICSAR was upregulated in CSCC tissues and cells. PICSAR knockdown inhibited cell proliferation and invasion and induced apoptosis in CSCC cells. Moreover, miR-125b could directly bind to PICSAR and its inhibition reversed the effect of PICSAR knockdown on proliferation, invasion and apoptosis in CSCC cells. In addition, YAP1 was a direct target of miR-125b and its overexpression attenuated the anti-cancer role of miR-125b in CSCC cells. Furthermore, YAP1 expression was positively regulated by PICSAR and negatively regulated by miR-125b. Besides, interference of PICSAR suppressed tumor growth by upregulating miR-125b and downregulating YAP1. SIGNIFICANCE: PICSAR knockdown suppressed cell proliferation and invasion and promoted apoptosis in CSCC cells by regulating miR-125b/YAP1 axis, providing new sights for treatment of CSCC.

DNMT1-mediated methylation inhibits microRNA-214-3p and promotes hair follicle stem cell differentiate into adipogenic lineages.

BACKGROUND: Dysfunction of the DNA methylation was associated with stem cell reprogramming. Moreover, DNA methyltransferase 1 (DNMT1) deficiency was involved in the differentiation of hair follicle stem cell (HFSc), but the molecular mechanisms remain unknown. METHODS: HFSc from human scalp tissues were isolated and cultured. The oil red O staining was used to observe the adipogenesis. The interaction relationship between microRNA (miR)-214-3p and mitogen-activated protein kinase 1 (MAPK1) was accessed by dual-luciferase reporter gene assay. The methylation level of miR-214-3p promoter was detected by methylation-specific PCR and the enrichment of DNMT1 in miR-214-3p promoter by chromatin immunoprecipitation assay. A mouse model of trauma was established to observe the skin regeneration at 0, 6, and 14 days. RESULTS: Expression of DNMT1 and MAPK1 was increased in the HFSc, while the expression of miR-214-3p was reduced. Moreover, DNMT1 inhibited the expression of miR-214-3p by promoting the promoter methylation of miR-214-3p. Overexpression of DNMT1 could reduce the expression of miR-214-3p, but increase the expression of MAPK1 and the extent of extracellular signal regulated kinase (ERK)1/2 phosphorylation, leading to enhanced adipogenic differentiation. Importantly, DNMT1 promoted skin regeneration in vivo. Conversely, overexpression of miR-214-3p could reverse the effects of DNMT1 on adipogenesis of HFSc. CONCLUSION: DNMT1 promotes adipogenesis of HFSc by mediating miR-214-3p/MAPK1/p-ERK1/2 axis. This study may provide novel biomarkers for the potential application in stem cell therapy.

EZH2-mediated inhibition of microRNA-22 promotes differentiation of hair follicle stem cells by elevating STK40 expression.

Hair follicle stem cells (HFSCs) contribute to the regeneration of hair follicles (HFs), thus accelerating hair growth. microRNAs (miRs) are potential regulators in various cellular processes, including HFSC proliferation and differentiation. This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40 (STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis. Gain- and loss-of-function approaches were adopted to explore the roles of EZH2, miR-22, and STK40 in the proliferation and apoptosis of HFSCs, along with the functional relevance of MEF2-ALP activity. STK40 was elevated during HFSC differentiation, which was found to facilitate HFSC proliferation, but impede their apoptosis by activating MEF2-ALP. Mechanically, miR-22 targeted and inversely regulated STK40, which inhibited MEF2-ALP activity to impede HFSC proliferation and differentiation. Moreover, EZH2 elevated the STK40 expression by repressing miR-22 to promote the proliferation and differentiation of HFSCs. Furthermore, in vivo experiments further validated the roles of EZH2 and STK40 on hair follicle neogenesis and hair growth. Collectively, EZH2 elevated the STK40 expression by downregulating miR-22, consequently accelerating differentiation of HFSCs and hair growth, which sheds light on the underlying molecular mechanism responsible for hair growth.

Cure of condyloma acuminata covering the glans penis using aminolevulinic acid/photodynamic therapy.

Condyloma acuminata are a type of verrucous hyperplasia in the genital and perianal areas caused by human papilloma virus (HPV) infection. Traditional treatment methods for condyloma acuminata, such as topical medications, carbon dioxide (CO2) laser, cryotherapy, and surgical excision, can be effective at removing warts, however, they do not eliminate subclinical and latent HPV infection, resulting in a high recurrence rate and even leaving trauma and scars. We report a case of condyloma acuminata covering the glans penis, considering our patient had a singular, large lesion, thus, to reduce the risk of recurrence and minimize the trauma caused by treatment, we chose ALA/photodynamic therapy (ALA-PDT). We provided eight rounds of ALA-PDT at a treatment interval of 7 days, the skin lesion disappeared completely, leaving a chapped, flushed glans without scarring. There was no recurrence during the 6-month follow-up period. Thus, we firmly believe that ALA-PDT is an effective, safe, and curative treatment, and is worth popularizing in clinical practice.

A crucial role of fibroblast growth factor 2 in the differentiation of hair follicle stem cells toward endothelial cells in a STAT5-dependent manner.

Fibroblast growth factor (FGF2) is reported to affect the proliferation, differentiation, and survival abilities of stem cells. In this study, we hypothesize that FGF2 might promote the differentiation of hair follicle stem cell (HFSCs) into endothelial cells (ECs), in a manner dependent on STAT5 activation. We first treated human HFSCs with recombinant human FGF2 to determine the involvement of FGF2 in the differentiation of HFSCs. Then the expression of EC-specific markers including von Willebrand factor (vWF), VE-cadherin, CD31, FLT-1, KDR and Tie2 was evaluated using immunofluorescence and flow cytometry, while the expression of HFSC-specific markers such as K15, K19, Lgr5, Sox9 and Lhx2 was determined by flow cytometry. Next, in vitro tube formation was performed to confirm the function of FGF2, and low-density lipoprotein (LDL) uptake by ECs and HFSCs was studied by Dil-acetylated LDL assay. In addition, we transduced FGF2-treated HFSCs with constitutive-active or dominant-negative STAT5A adenovirus vectors. FGF2 up-regulated the expression of EC-specific markers, and promoted the differentiation of HFSCs into ECs, tube formation and LDL uptake. The phosphorylated STAT5 was translocated into the nucleus of HFSCs after FGF2 treatment, but this translocation was blocked by the dominant-negative STAT5A mutant. FGF2 increased the differentiation potential through the activation of STAT5 in vivo. Taken together, we find that FGF2 promotes the differentiation of HFSCs into ECs via activated STAT5, which gives a new perspective on the role of FGF2 in the development of ischemic vascular disease.

BMP2-mediated PTEN enhancement promotes differentiation of hair follicle stem cells by inducing autophagy.

The proliferation and differentiation of hair follicle stem cells (HFSCs) is regulated by several signaling pathways, including BMP and PTEN. Therefore, this study intended to clarify the potential effects of two such regulators, BMP2 and PTEN, on HFSC differentiation. HFSCs were subjected to BMP2, noggin (BMP2 ligand inhibitor), rapamycin (Rapa, autophagy inducer), 3-methyladenine (3-MA, autophagy inhibitor), or shRNA against PTEN. The differentiation of HFSCs was evaluated using oil red O staining and autophagy was assessed using the transmission electron microscope. Then expression of epidermal differentiation marker (K10 and involucrin), adipogenic markers (PPAR-γ2, aP2, perilipin2, and Adipoq), keratinocyte-specific marker (K15), proliferation-related markers (PCNA and Ki67) and autophagy-related factors (Atg5, Atg7, Atg12, Beclin-1 and LC3-II/LC3-I) was examined by RT-qPCR and Western blot analysis. Next, HFSCs were treated with 3-MA, or shRNA against Atg5 or Atg7 to verify the effect of autophagy on differentiation of BMP2-treated HFSCs. Finally, the effect of BMP2 on HFSC differentiation was verified by a mouse wound model. HFSCs overexpressing BMP2 exhibited elevated expression of epidermal differentiation marker, adipogenic markers and autophagy-related factors but inhibited expression of keratinocyte-specific marker and proliferation-related markers. Furthermore, we found that PTEN promoted the differentiation of BMP2-treated HFSCs by inducing autophagy. In vivo experiments further confirmed the roles of BMP2/PTEN on differentiation of HFSCs. Taken together, BMP2 up-regulated PTEN and consequently induced autophagy to facilitate HFSC differentiation.

MiR-125b-5p and miR-181b-5p inhibit keratinocyte proliferation in skin by targeting Akt3.

MicroRNAs (miRNAs) have been widely accepted to play important roles in the regulation of keratinocyte functions. Here, we aimed to further explore the role and underlying mechanism of miR-125b-5p and miR-181b-5p in psoriasis. The expression levels of miR-125b-5p, miR-181b-5p and Akt3 mRNA were detected by qRT-PCR assay. Cell proliferation ability was determined by MTT assay and BrdU incorporation assay. Dual-luciferase reporter assay and RNA Immunoprecipitation assay were used to confirm the targeted interaction between miR-125b-5p or miR-181b-5p and Akt3 in human epidermal keratinocytes (HEKs). The levels of ki-67, Akt3 protein, Akt, p-Akt, mTOR and p-mTOR were measured by Western blot. Our study indicated that miR-125b-5p and miR-181b-5p were downregulated (about 61.3% with miR-125b-5p and 60.4% with miR-181b-5p) and Akt3 was upregulated (about 2.68-fold) in psoriasis. Upregulation of miR-125b-5p or miR-181b-5p resulted in about a 33% or 40% reduction of HEKs proliferation in vitro, while Akt3 overexpression triggered a 1.3-fold enhancement on HEKs proliferation. Akt3 was a direct target of miR-125b-5p or miR-181b-5p. Moreover, HEKs proliferation ability in cotransfection of miR-125b-5p mimics (or miR-181-5p mimics) and vector-Akt3 group was about 2-fold (or 1.98-fold) that in the miR-125b-5p mimics (or miR-181-5p mimics) alone group. Akt/mTOR signaling was involved in miR-125b-5p mimics- or miR-181b-5p mimics-mediated inhibition effect on HEKs proliferation. Our study suggested that the upregulation of miR-125b-5p or miR-181b-5p inhibited HEKs proliferation at least partly by targeting Akt3, providing novel mechanisms of miRNAs involved in psoriasis.

Up-regulated lncRNA5322 elevates MAPK1 to enhance proliferation of hair follicle stem cells as a ceRNA of microRNA-19b-3p.

Hair follicle stem cells (HFSCs), located in the bulge region of the follicle, maintain hair follicle growth and cycling. Long non-coding RNAs (lncRNAs), non-protein coding transcripts, are widely known to play critical roles in differentiation and proliferation of stem cells. Therefore, the current study aimed to explore the regulatory roles of lncRNA5322 in HFSCs proliferation and the underlying regulatory mechanisms. Initially, the expression patterns of lncRNA5322 and microRNA-19b-3p (miR-19b-3p) in HFSCs were detected. Subsequently, gain-and loss-of-functions analyses were conducted to explore the roles of lncRNA5322, miR-19b-3p and mitogen-activated protein kinase 1 (MAPK1) in cell proliferation, colony formation and apoptosis of HFSCs, with the expression of cyclin-dependent kinase (CDK)1 and CDK2 examined. Also, the interaction relationships among lncRNA5322, miR-19b-3p and MAPK1 were explored. Furthermore, a mouse model was established to detect the roles of lncRNA5322, miR-19b-3p, and MAPK1 in wound contraction and epidermal regeneration. Over-expressed lncRNA5322 was found to promote proliferation, colony formation ability but inhibit apoptosis of HFSCs, in addition to up-regulation of the expression of CDK1 and CDK2. LncRNA5322 was found to act as a ceRNA of miR-19b-3p which directly targeted MAPK1. Furthermore, up-regulation of lncRNA5322 enhanced wound contraction and epidermal regeneration in vivo by increasing the expression of MAPK1 through functioning as a ceRNA of miR-19b-3p. In summary, the results in this study suggested that lncRNA5322 serves as a ceRNA of miR-19b-3p to elevate the expression of MAPK1, ultimately promoting HFSCs proliferation, wound contraction and epidermal regeneration of mouse model.

Concentrations, spatial distributions, and congener profiles of polychlorinated dibenzo-p-dioxins and dibenzofurans around original plastic solid waste recovery sites in China.

The concentrations, profiles, and spatial distributions of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in soil and sediment samples from several typical plastic solid waste (PSW) recovery sites (particularly from areas in which PSW is burned openly) in China were investigated. The results showed that burning PSW directly influenced PCDD/F concentrations immediately around the burning area. All of the samples in which soil contained black burning residue, collected from immediately around burning areas, had PCDD/F concentrations (mean 21708 ng kg-1) and toxic equivalent (TEQ) concentrations (mean 2140 ng I-TEQ kg-1 or 1877 ng WHO2006-TEQ kg-1) more than 100 times higher than the concentrations in samples collected away from burning areas (mean 222 ng kg-1, 8.75 ng I-TEQ kg-1, 7.96 ng WHO2006-TEQ kg-1). Principal component analysis and hierarchical cluster analysis indicated that the PCDD/F concentrations in seven soil samples from near PSW burning areas were influenced by PSW burning but that the PCDD/Fs in these soil samples may have had other or multiple sources. PCDD/F distributions at PSW recovery sites have been investigated in few previous studies. The results presented here indicate that appropriate measures should be taken to decrease the ecological risks posed by PSW recovery and to prevent, control, and remediate PCDD/F and other chemical contamination caused by PSW recovery.

Long non­coding RNA regulates hair follicle stem cell proliferation and differentiation through PI3K/AKT signal pathway.

Long non-coding RNAs (lncRNAs) are defined as non-coding transcripts (>200 nucleotides) that serve important roles in the proliferation and differentiation of stem cells. Hair follicle stem cells (HFTs) have multidirectional differentiation potential and are able to differentiate into skin, hair follicles and sebaceous glands, serving a role in skin wound healing. The aim of the present study was to analyze the regulatory role of lncRNA AK015322 (IncRNA5322) in HFTs and the potential mechanism of IncRNA5322­mediated differentiation of HFTs. The results demonstrated that lncRNA5322 transfection promoted proliferation and differentiation in HFTs. It was identified that lncRNA5322 transfection upregulated the expression and phosphorylation of phosphoinositide 3­kinase (PI3K) and protein kinase B (AKT) in HFTs. It was also observed that lncRNA5322 transfection upregulated microRNA (miR)­21 and miR­21 agonist (agomir­21) eliminated lncRNA5322­induced expression and phosphorylation of PI3K and AKT. The present study also demonstrated that agomir­21 blocked IncRNA5322­induced expression and phosphorylation of PI3K and AKT in HFTs. The results indicated that agomir­21 transfection also suppressed the IncRNA5322­induced proliferation and differentiation of HFTs. In conclusion, the results of the present study suggest that lncRNA5322 is able to promote the proliferation and differentiation of HFTs by targeting the miR­21­mediated PI3K­AKT signaling pathway in HFTs.

BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR­204.

BRAF-activated non-coding RNA (BANCR) is a long non-coding RNA (lncRNA) that contributes to the initiation and development of many solid tumors, including melanoma. However, the BANCR functions and downstream mechanisms are largely unknown. In this study, we aim to investigate how BANCR participates in the proliferation and migration of malignant melanoma and elucidate the underlying mechanism in this process. We found that the expression of the BANCR was low in melanocytic nevus and human melanocytes but high in melanoma tissues and cell lines. Knockdown of BANCR inhibited melanoma cell proliferation and invasion, and induced cell apoptosis. The decreased expression of relative marker proteins further demonstrated the inhibitory effect of BANCR siRNA in cell growth and migration. Then, we detected downregulation of microRNA-204 (miR­204), a suppressor of melanoma growth, in melanoma tissues and cell lines. We identified that miR­204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR­204. BANCR may promote melanoma cell growth through inhibition of miR­204, leading to the activation of Notch2 pathway. By tumorigenicity assay in BALB/c nude mice, we further demonstrated that BANCR knockdown inhibited tumor growth in vivo. Our results suggest the BANCR/miR­204/Notch2 axis mediates melanoma cell proliferation and tumor progression.

Effect of 5-aminolevulinic acid photodynamic therapy on keratinocyte proliferation and apoptosis in condyloma acuminatum.

BACKGROUND: The effect of 5-aminolevulinic acid photodynamic therapy on keratinocyte proliferation and apoptosis in condyloma acuminatum tissues was evaluated. METHODS: An immunohistochemical method and TdT-mediated dUTP nick end labeling were performed to detect the positive expression of the keratinocyte proliferation-related gene Ki-67 and apoptosis, respectively, in condyloma acuminatum tissues. RESULTS: Of 52 cases, 44 showed positive expression of Ki-67 in condyloma acuminatum keratinocytes before the treatment, with a positive expression rate of 84.62% (44/52), an expression strength of mostly ++ - +++, and a Ki-67 proliferation index of 80.26±5.07%. After treatment, 22 cases showed positive expression of Ki-67 in condyloma acuminatum keratinocytes, with a positive expression rate of 42.31% (22/52), an expression strength of mostly - - ++, and a proliferation index of 42.67±3.06%. The differences in the positive expression rate, expression strength, and proliferation index in the before- and after-treatment groups were statistically significant (χ2=20.070, P<0.001). For visible apoptotic cells in condyloma acuminatum keratinocytes before the 5-aminolevulinic acid photodynamic treatment, the expression strength was mostly + - ++, and the average apoptotic index was 13.94±2.35%; after treatment, the expression strength was mostly ++ - +++, and the average apoptotic index was 73.88±7.65%; the difference in the apoptotic index between the before and after treatment groups was statistically significant (P<0.001). CONCLUSION: 5-Aminolevulinic acid photodynamic therapy can inhibit the proliferation and promote the apoptosis of keratinocytes, and represents an effective mechanism for treating condyloma acuminatum.

Gold nanoparticles-decorated graphene field-effect transistor biosensor for femtomolar MicroRNA detection.

Early detection is proven to be the best chance for successful cancer treatment. MiRNAs, as ideal biomarkers, can identify cancer in the early stage. Therefore, development of highly sensitive and selective detection methods for miRNA is still anticipated. Here we report on a gold nanoparticles (AuNPs)-decorated graphene field-effect transistor (FET) biosensor for highly sensitive, selective and label-free detection of miRNA. The AuNPs-decorated graphene FET biosensor was fabricated by drop-casting the reduced graphene oxide (R-GO) suspension onto the sensor surface, and subsequently decorating AuNPs onto the surface of R-GO. After peptide nucleic acid (PNA) probe was immobilized on the AuNPs surface, miRNA detection was carried out via PNA-miRNA hybridization. It was found that the developed FET biosensor was able to achieve a detection limit as low as 10 fM. In addition, the biosensor enabled an accurate distinction of complementary miRNA from one-base mismatched miRNA and noncomplementary miRNA. What's more, this highly sensitive and selective assay was also applied to the detection of miRNA in serum samples, making it a potential method for diagnosis of gene-related diseases.