Objective: To investigate the ethical decision-making process of breaking confidentiality when counselors dealing with self-inflicted injury and suicide issues in college situation. Methods: A semi-structural interview was addressed to 10 counselors from 7 college counseling centers in Beijing, among whom with (10 ± 8) years of experience on average in this field. Content analysis method was used to transcription of the interviewing data. Results: Totally 8 counselors had received ethical training more or less, and attached great importance to ethical codes. There were still some conflicts between school regulations and confidentiality rules in 7 university counseling centers. Different counselors varied greatly in decision-making on breaking confidentiality when facing college students' self-inflicted injury and suicide. Faced with conflicts between college demands and confidentiality principles, counselors could take the professional standpoint and consider more of the interests of students. Conclusion: The decision-making process on self-inflicted injury and suicide confidentiality breakthrough needs to be standardized. College's attention and support to the counseling work should be strengthen and enhance ethical awareness.

Objective: To construct an aromatase-overexpressing breast cancer cell model and observe the real-time apoptosis of breast cancer cells induced by the aromatase inhibitor, letrozole. Methods: The lentivirus-mediated gene transfection method was used to construct the MCF-7-VC3AI and ZR7530-VC3AI cell lines,which stably expressed the apoptotic fluorescent indicator protein VC3AI.Simultaneously,letrozole-induced apoptosis models of the MCF-7-VC3AI and ZR7530-VC3AI breast cancer cell lines were also constructed.Real-time quantitative PCR(qPCR)and Western blot methods were used to detect the mRNA and protein levels of aroma-tase in the cells.Cell proliferation ability was measured using MTT.The proliferation of cells in vitro under testosterone,estradiol,or letrozole combined with testosterone treatments were also observed.Results:qPCR results showed that the expression of the aroma-tase mRNA was significantly higher in both the MCF-7 and ZR7530 cell models when compared to the MCF-7-VC3AI and ZR7530-VC3AI cell models.Western blot results showed that the expression of the aromatase protein was significantly increased in both cell models. MTT assay results showed that the proliferation of a cell model could be promoted by testosterone and estrogen stimulation.Under 100 nmol/L testosterone,the proliferation rate of over-expressed aromatase MCF-7-VC3AI cells was about 1.2 times than that of the control group(P<0.01)and the proliferation rate of ZR7530-VC3AI cells was about 1.5 times than that of the control group(P<0.01). However,letrozole inhibited the proliferation induced by testosterone in a dose-dependent manner.Under the effect of letrozole at 10 μmol/L,the proliferation rate of over-expressed aromatase MCF7-VC3AI cells was 80% of the control group(P<0.05),while the prolifer-ation rate of over-expressed aromatase ZR7530-VC3AI cells was 68% of the control group(P<0.05).Conclusions:The successful estab-lishment of cell models that can detect letrozole-induced apoptosis provides an important foundation for further investigating the mechanism of letrozole.

Testicular adrenal rest tumor (TART) is frequently complicated by congenital adrenal hyperplasia, which is a benign tumor of the testes frequently found in adolescents and adults.Palpation and scrotal ultrasound are the main diagnostic methods for TART.Poorly managed TART often results in testicular dysfunction or even infertility due to tumor compression.This article reviews the pathogenesis, epidemiology, clinical features, diagnosis, differential diagnosis and treatment of TART, thus improving the understanding of the disease to achieve early diagnosis, early treatment, and improved prognosis.

Objective To investigate the effects of FOXA2 on the proliferation of hepatocellular carcinoma cells and the tumorigenesis of nude mice, and to explore the effect of FOXA2 on the development of hepatocellular carcinoma. Methods Immunohistochemistiy and real-time quantitative PCR were used to detect the expression of FOXA2 in 35 pairs of hepatocellular carcinoma tissues and their matched paracancerous tissues. 293 T cells were used as controls to detect the expression level of FOX A 2 in hepatocellular carcinoma cell lines (HepG2, SMMC-7721 and SK-Hep1) by real-time quantitative PCR. The lentivirus was transfected into HepG2 cells, and there were 3 groups including no virus group (Mock group) , negative control virus group (NC group) and FOXA2-transfected over-expression virus group (FOXA2 group). Plate clone assays were used to detect the effect of FOXA2 on the proliferation of HepG2 cells in vitro and nude mice tumor and formation assays to detect the tumor weight and tumor weight inhibition rate after FOX A2-transfected overexpression of lentivirus-infected cells. Results The results of immunohistochemistry and real-time quantitative PCR showed that the expression of FOXA2 in cancer tissues was significantly lower than that in adjacent tissues (P < 0.01) , And the expression of FOXA2 in hepatoma cell lines (HepG2, SMMC-7721, SK-Hepl) was significantly lower than that of 293 T cells (P < 0.0001). After the lentivirus was transfected into HepG2 cells, the number of clones in the FOXA2 group was significantly less than that in the Mock group and the NC group (P < 0.05). The tumor formation of nude mice showed that the tumor weight of FOXA2 group was smaller than that of the corresponding blank control group and negative control group (P < 0.01).Conclusion FOXA2 is lowly expressed in hepatocellular carcinoma tissues and cells, which has the effect of inhibiting the proliferation of HepG2 cells in vitro and the growth of tumors in nude mice in vivo.

Objective:To investigate the impact of excessive fluoride exposure on the expression profile of microRNA (miRNA) in mouse testes, and elucidate the reproductive toxicity mechanism of fluoride.Methods:A total of 24 8-week-old C57BL/6J male mice weighing (23 ± 1) g were randomly divided into a control group [0 mg/L sodium fluoride (NaF)] and a fluoride exposure group (50 mg/L NaF) using a random number table method, with 12 mice in each group. After 90 days of treatment, the mice were anesthetized and euthanized. Sperm samples were collected to assess their quantity, viability, and deformity rate. Additionally, testicular tissue was stained with hematoxylin-eosin (HE). RNA was extracted from testicular tissue, and high-throughput sequencing technology was employed to analyze the effect of fluoride on the expression profile of mouse testicular miRNA. Deferentially expressed miRNA was screened and its target genes were predicted, and functional annotation and pathway enrichment analysis were performed. Real-time fluorescence quantitative PCR (qRT-PCR) was used to verify the expression level of deferentially expressed miRNA.Results:Compared with the control group [number of sperm: (11.30 ± 2.52) × 10 6/ml; viability rate: (90.07 ± 4.34)%; deformity rate: (15.49 ± 3.25)%], the number of sperm of mice exposed to fluoride [(9.01 ± 2.25) × 10 6/ml] and the viability rate [(84.34 ± 4.21)%] decreased ( P = 0.041, 0.003), while deformity rate [(22.36 ± 6.51)%] increased ( P = 0.003). Furthermore, in the fluoride exposure group, the interstitial distance of testis increased, the number of sperm in the spermatogenic tubule decreased, and the cell arrangement was disordered. Through sequencing, 34 deferentially expressed miRNAs were identified in the testes of mice exposed to fluoride. According to qRT-PCR verification, compared with the control group, the expression levels of mmu-miR-29b-1-5p ( P < 0.001), mmu-miR-196a-5p ( P = 0.002), and mmu-miR-196b-5p ( P = 0.031) in the testes of mice exposed to fluoride were significantly increased, and the expression levels of mmu-let-7a-2-3p ( P < 0.001) and mmu-miR-466n-3p ( P = 0.018) were significantly decreased, consistent with the sequencing results. By KEGG enrichment of deferentially expressed miRNA target genes, it was found that fluoride exposure could change the axon guidance signal pathway, olfactory transduction pathway, neuroactive ligand-receptor interaction pathway, and lysosome signal pathway, etc., in mouse testes. Conclusions:Fluoride exposure may induce testicular injury by altering the expression profile of miRNA in the testes and by mediating the post-transcriptional regulatory signal pathway. Testicular miRNA may be a potential biomarker of fluoride reproductive toxicity, which may provide a new idea and perspective for exploring the mechanism of fluoride poisoning.

Objective To investigate the correlation between the expression of Hsa_circ_0026352 and the clinical characteristics of breast cancer(BC) patients, to evaluate the value of Hsa_circ_0026352 as a diagnostic marker of breast cancer. Methods Human circRNA microarray was used to screen the different expression of circRNAs in BC tissues. qRT-PCR was used to verify the expression of Hsa_circ_0026352 in BC tissue and peripheral blood. CircRNA structure were performed by circPrimer1.2 software. T-test, ANOVA analysis, curve regression analysis and ROC curve analysis were performed to determine the diagnostic values of Hsa_circ_0026352. Results Hsa_circ_0026352 was significantly down-regulated in both breast cancer tissues and peripheral blood (P < 0.01). The AUC of Hsa_circ_0026352 were 0.881 in tissues and 0.826 in peripheral blood (both P < 0.01). The relative expression of Hsa_circ_0026352 in peripheral blood of BC cancer patients was negatively correlated with CA153 level (P < 0.05). The AUC of Hsa_circ_0026352 in peripheral blood of patients with ER positive, early stage breast cancer and breast neoplasm metastasis were 0.710, 0.771 and 0.722 (all P < 0.01), respectively. Conclusion Hsa_circ_0026352 could be a novel predictive biomarker for diagnosis of BC.

OBJECTIVE: To investigate the role of high mobility group protein 1(HMGB1) in toluene diisocyanate(TDI) induced nucleotide-binding oligomerization domain like receptor family pyrin domain-containing 3(NLRP3) inflammasome activation in human bronchial epithelial cells(HBECs). METHODS: i) The TDI-human serum albumin(HSA) stimulation experiment: the HBECs in logarithmic growth phase were randomly divided into control group, low-, medium-and high-dose groups that were pretreated with TDI-HSA with the final concentration of 0.00, 40.00, 80.00 and 120.00 mg/L for 12 hours. ii) The HMGB1 expression inhibition experiment: the HBECs in logarithmic growth phase were divided into control group, TDI-HSA group, TDI-HAS+negative-siRNA group, and TDI-HAS+HMGB1-siRNA group. The cells in TDI-HAS+negative-siRNA group and TDI-HAS+HMGB1-siRNA group were infected with HBECs with negative-siRNA lentivirus and HMGB1-siRNA lentivirus, respectively. Cells in these two groups and the TDI-HSA group were treated with 120.00 mg/L of TDI-HSA for 12 hours. The cells in the control group were not treated with TDI-HAS. iii) The expression of HMGB1, NLRP3, apoptosis-associated speck-like protein containing CARD(ASC), pro-caspase-1 and caspase-1 p20 proteins in all groups were detected by Western blot. The number of NLRP3 and caspase-1 inflammasome in TDI-HSA stimulation experiment was observed by immunofluorescence method. RESULTS: i) TDI-HSA stimulation experiment: the relative protein expression of HMGB1 and ASC was higher in HBECs of medium-and high-dose groups than that of control group(all P values were <0.01). The relative protein expression of NLRP3 and casepase-1 p20 and the number of NLRP3-caspase-1 inflammasome were higher in HBECs of 3 dose groups than that of control group(all P values were <0.01). The number of NLRP3-caspase-1 inflammasome in HBECs increased obviously in low-, medium-and high-dose groups as compared to the control group(all P values were <0.05). The number of NLRP3-caspase-1 inflammasome in HBECs increased with the increase of TDI-HSA dose(all P values were <0.01). ii) The HMGB1 expression inhibition experiment: the relative protein expression of HMGB1, NLRP3, ASC, pro caspase-1 and caspase-1 p20 in HBECs were higher in the TDI-HSA group and TDI-HSA + negative-siRNA group than those of the control group(all P values were <0.01). The above indexes of HBECs were lower in the TDI-HAS + HMGB1-siRNA group than those in the TDI-HSA group and TDI-HSA + negative-siRNA group(all P values were <0.01).CONCLUSION: TDI treatment in HBECS can induce the increase of HMGB1 protein expression and activate NLPR3 inflammasome. Inhibition of HMGB1 expression can down-regulate the expression of NLPR3 and its related proteins.

Hearing loss has become increasingly prevalent and causes considerable disability, thus gravely burdening the global economy. Irreversible loss of hair cells is a main cause of sensorineural hearing loss, and currently, the only relatively effective clinical treatments are limited to digital hearing equipment like cochlear implants and hearing aids, but these are of limited benefit in patients. It is therefore urgent to understand the mechanisms of damage repair in order to develop new neuroprotective strategies. At present, how to promote the regeneration of functional hair cells is a key scientific question in the field of hearing research. Multiple signaling pathways and transcriptional factors trigger the activation of hair cell progenitors and ensure the maturation of newborn hair cells, and in this article, we first review the principal mechanisms underlying hair cell reproduction. We then further discuss therapeutic strategies involving the co-regulation of multiple signaling pathways in order to induce effective functional hair cell regeneration after degeneration, and we summarize current achievements in hair cell regeneration. Lastly, we discuss potential future approaches, such as small molecule drugs and gene therapy, which might be applied for regenerating functional hair cells in the clinic.
Infant, Newborn ; Humans ; Hair Cells, Auditory, Inner/physiology* ; Ear, Inner/physiology* ; Hair Cells, Auditory/physiology* ; Regeneration/genetics* ; Stem Cells