The homology analysis of internal transcribed spacer sequence of ribosomal DNA in common dermatophytes

In order to analyze the sequences of the internal transcribed spacer (ITS) including the 5.8 S ribosomal DNA (rDNA) of common dermatophytes, so as to obtain a rapid and accurate method to identify the species of dermatophytes and to establish the phylogenetic tree of these species to understand their relationship,16 strains of dermatophytes were collected and preliminarily identified by morphological characteristics. General primers for fungi ITS1 and ITS4 were used to amplify the ITS rDNA of each strains with PCR. The PCR products after purification were sequenced directly and were analyzed through internet. In the results,11 strains were identified by means of morphological features, among which 5 strains were Trichophyton,5 strains were Microsporum and 1 was Epidermaphyton, which was consistent with the results by molecular biology. In the 5 unidentifiable strains, 1 strain was proved to be Chrysosporium by molecular biology. These strains studied could be divided into 3 different classes as indicated in the analysis of the phylogenetic tree of the sequences in ITS, which were quite different from those of morphological classification. It is evident from the above observations that the molecular method of analysis on the ITS sequences is a rapid, highly sensitive and accurate approach for the detection of dematophyte species, however, it still exhibits some limitations needing the supplementation with morphological identification.

Integrated Skin Microbiome-Metabolome Analysis Reveals Altered Bacterial Community Composition and Metabolites in Psoriasis

Objective:Current theories highlight the role of the microbiome in the pathogenesis of psoriasis.Additionally,abnormal metabolism can alter disease processes in terms of occurrence,progression,and prognosis.Therefore,an integrative microbiome and metabolome analysis of the skin may aid in understanding the disease pathogenesis and identify therapeutic targets for psoriasis.Methods:We recruited 22 patients with psoriasis and 22 age-and sex-matched healthy controls.Skin swabs were collected from the participants’scalps.All samples underwent amplicon sequencing of the internal transcribed spacer 1 and V3V416S rRNA regions and metabolome analysis.For amplicon data,analysis of the alpha diversities,microbial community structures and principal coordinate analysis were performed.Differential metabolites and pathway enrichment were analyzed for metabolome data.Studentt test and Wilcoxon rank sum test were used for statistical analysis.Results:The psoriatic lesions were characterized by higher bacterial diversity,significantly higher abundances ofCorynebacterium(P<0.001)andStaphylococcus(P=0.012),and a lower abundance ofCutibacterium(P<0.001)compared with healthy controls.However,no significant alterations in the fungal diversity or fungal taxonomies were detected.Metabolome analysis revealed that prostaglandin-related metabolites,nucleotides,and cysteine-and methionine-related metabolites were significantly enriched in patients with psoriasis,and these metabolites were positively correlated with the disease-associated bacteriaStaphylococcus andCorynebacterium.Conclusions:We demonstrated significant alterations in the skin microbiome and metabolome in patients with psoriasis compared with healthy controls.

CircRNA-SORE mediates sorafenib resistance in hepatocellular carcinoma by stabilizing YBX1

Sorafenib is the first-line chemotherapeutic therapy for advanced hepatocellular carcinoma(HCC).However,sorafenib resistance significantly limits its therapeutic efficacy,and the mechanisms underlying resistance have not been fully clarified.Here we report that a circular RNA,circRNA-SORE(a circular RNA upregulated in sorafenib-resistant HCC cells),plays a significant role in sorafenib resistance in HCC.We found that circRNA-SORE is upregulated in sorafenib-resistant HCC cells and depletion of circRNA-SORE substantially increases the cell-killing ability of sorafenib.Further studies revealed that circRNA-SORE binds the master oncogenic protein YBX1 in the cytoplasm,which prevents YBX1 nuclear interaction with the E3 ubiquitin ligase PRP19 and thus blocks PRP19-mediated YBX1 degradation.Moreover,our in vitro and in vivo results suggest that circRNA-SORE is transported by exosomes to spread sorafenib resistance among HCC cells.Using different HCC mouse models,we demonstrated that silencing circRNA-SORE by injection of siRNA could substantially overcome sorafenib resistance.Our study provides a proof-of-concept demonstration for a potential strategy to overcome sorafenib resistance in HCC patients by targeting circRNA-SORE or YBX1.

UBQLN1 mediates sorafenib resistance through regulating mitochondrial biogenesis and ROS homeostasis by targeting PGCip in hepatocellular carcinoma

The treatment for hepatocellular carcinoma(HCC)is promising in recent years,but still facing critical challenges.The first targeted therapy,sorafenib,prolonged the overall survival by months.However,resistance often occurs,largely limits its efficacy.Sorafenib was found to target the electron transport chain complexes,which results in the generation of reactive oxygen species(ROS).To maintain sorafenib resistance and further facilitate tumor progression,cancer cells develop strategies to overcome excessive ROS production and obtain resistance to oxidative stress-induced cell death.In the present study,we investigated the roles of ROS in sorafenib resistance,and found suppressed ROS levels and reductive redox states in sorafenib-resistant HCC cells.Mitochondria in sorafenib-resistant cells maintained greater functional and morphological integrity under the treatment of sorafenib.However,cellular oxygen consumption rate and mitochondria DNA content analyses revealed fewer numbers of mitochondria in sorafenib-resistant cells.Further investigation attributed this finding to decreased mitochondrial biogenesis,likely caused by the accelerated degradation of peroxisome proliferator-activated receptor y coactivator ip(PGC1P).Mechanistic dissection showed that upregulated UBQLN1 induced PGCip degradation in a ubiquitination-independent manner to attenuate mitochondrial biogenesis and ROS production in sorafenib-resistant cells under sorafenib treatment.Furthermore,clinical investigations further indicated that the patients with higher UBQLN1 levels experienced worse recurrence-free survival.In conclusion,we propose a novel mechanism involving mitochondrial biogenesis and ROS homeostasis in sorafenib resistance,which may offer new therapeutic targets and strategies for HCC patients.

Microwave-assisted synthesis of oxygen vacancy associated TiO_(2)for efficient photocatalytic nitrate reduction

The solar-driven photocatalytic technology has shown great potential in nitrate(NO_(3)^(-))pollutants reduction,however,it has been greatly hindered by the complex preparation and high cost of photocatalysts.Herein,a relatively low-cost photocatalyst,rutile and anatase mixed phase TiO_(2) was synthesized by a facile microwave-hydrothermal method.Meanwhile,oxygen vacancy is successfully generated,leading to an acidic surface for strong adsorption towards NO_(3)^(-),which further improved the reduction activity.Compared with the commercial P25,a higher NO_(3)^(-) conversion of ca.100%and nitrogen(N_(2)) selectivity of 87%were achieved under UV(365 nm)irradiation within 2 h.This research provides a promising strategy for designing efficient noble metal free photocatalyst in the NO_(3)^(-) reduction.

Trichosporon montevideense isolated from the descending colon of a patient with active severe Crohn disease:a case report

To the Editor:A 13-year-old girl with Crohn disease(CD)from Shandong Province transferred to our inflammatory bowel disease(IBD)center during April 2013.Three months previously,the patient presented with hematochezia and fever,but antibiotic treatment was unsuccessful.After admission,a colonoscopy indicated manifestations of segmental lesions,cobble stoning,and stricture[Figure 1 A].Cytomegalovirus,Epstein-Barr virus,Clostridium difficile^and amoebae were excluded as possible causes.There were also no indications of Behcet disease,systemic vasculitis,or other autoimmune diseases.Our initial diagnosis was active severe CD(Vienna typing,A1L3B2).This study was approved by the Ethical Committee of First Hospital of Peking University(No.2019153).An appropriate signed patient consent form was obtained.

CircRNA-SORE mediates sorafenib resistance inhepatocellular carcinoma by stabilizing YBX1

Sorafenib is the first-line chemotherapeutic therapy for advanced hepatocellular carcinoma(HCC).However,sorafenib resistance significantly limits its therapeutic efficacy,and the mechanisms underlying resistance have not been fully clarified.Here we report that a circular RNA,circRNA-SORE(a circular RNA upregulated in sorafenib-resistant HCC cells),plays a significant role in sorafenib resistance in HCC.We found that circRNA-SORE is upregulated in sorafenib-resistant HCC cells and depletion of circRNA-SORE substantially increases the cell-killing ability of sorafenib.Further studies revealed that circRNA-SORE binds the master oncogenic protein YBX1 in the cytoplasm,which prevents YBX1 nuclear interaction with the E3 ubiquitin ligase PRP19 and thus blocks PRP19-mediated YBX1 degradation.Moreover,our in vitro and in vivo results suggest that circRNA-SORE is transported by exosomes to spread sorafenib resistance among HCC cells.Using different HCC mouse models,we demonstrated that silencing circRNA-SORE by injection of siRNA could substantially overcome sorafenib resistance.Our study provides a proof-of-concept demonstration for a potential strategy to overcome sorafenib resistance in HCC patients by targeting circRNA-SORE or YBX1.