AIM To study the adaptive cytoprotection of H 2O 2 preconditioning against oxidative stress damage in PC12 cell and the relationships between brain derived neurotrophic factor (BDNF) and the adaptive cytoprotection of H 2O 2 preconditioning. METHODS The viability of PC12 cells was evaluated by MTT assay. Apoptosis was detected by PI stain flow cytometer. Expression of BDNF was analyzed by immuo flow cytometer. RESULTS After H 2O 2 preconditioning, the survival of PC12 cells exposure to H 2O 2 (20～60 ?mol?L -1 ) was increased and the apoptosis of PC12 cells induced by H 2O 2 (20 or 30 ?mol?L -1 ) was inhibited and the expression of BDNF in PC12 cells was enhanced. CONCLUSION H 2O 2 preconditioning is protective against the damage of PC12 cells induced by H 2O 2 and its mechanisms may involve up modulation of the expression of BDNF.

OBJECTIVE: To study the expression of CD68 antibody marked tumor associated macrophage TAMs and matrix solution element MMP-7 in laryngeal squamous carcinoma tissue and the relationship with clinicopathological parameters, so that to explore the relationship between the expression of the two molecular markers and laryngeal cancer tissue microvascular density (MVD). METHOD: Immunohistochemical method was employed to detect the expression of CD68 and MMP-7 in 65 cases (laryngeal squamous carcinoma tissue in 45 cases; peritumoral nontumor tissue in 20 cases) and CD 34 antibody marked MVD expression. RESULT: CD68 positive rate in squamous carcinoma tissue (82.2%, 37/45) is obviously higher than that in the peritumoral tissue (15%, 3/20) (P < 0.05), and MMP-7 positive rate in squamous carcinoma tissue is significantly different from that in peritumoral tissue (71.1%; 25%) (P < 0.05). The expression rate of CD34-MVD in laryngeal squamous carcinoma tissue( 26.52 +/- 6.36 )is higher than that in peritumoral tissue (12.23 +/- 4.01) (P < 0.05). In lymph node metastasis group, the positive expression rates of CD68 and MMP-7 are higher than those in the group without lymph node metastasis. MMP-7 showed no correlation with cancer stage, and CD68 was related with cancer stage; CD68, MMP-7 and CD34- MVD have positive correlation. CONCLUSION The high level of expression of TAMs and MMP-7 in laryngeal cancer tissue and the positive correlation with MVD illustrate that both of the markers play important roles in promoting laryngeal squamous carcinoma tissue metastasis and angiogenesis, which can be used as important markers to evaluate the invasion and metastasis of laryngeal cancer.
Adult ; Aged ; Antigens, CD ; metabolism ; Antigens, CD34 ; metabolism ; Antigens, Differentiation, Myelomonocytic ; metabolism ; Carcinoma, Squamous Cell ; blood supply ; metabolism ; pathology ; Humans ; Laryngeal Neoplasms ; blood supply ; metabolism ; pathology ; Lymphatic Metastasis ; Macrophages ; cytology ; metabolism ; Male ; Matrix Metalloproteinase 7 ; metabolism ; Microvessels ; Middle Aged ; Neoplasm Staging ; Neovascularization, Pathologic

Ferroptosis is a nonapoptotic form of cell death and differs considerably from the well-known forms of cell death in terms of cell morphology,genetics,and biochemistry.The three primary pathways for cell ferroptosis are system Xc-/glutathione peroxidase 4(GPX4),lipid metabolism,and ferric metabolism.Since the discovery of ferroptosis,mounting evidence has revealed its critical regulatory role in several diseases,especially as a novel potential target for cancer therapy,thereby attracting increasing attention in the fields of tumor biology and anti-tumor therapy.Accordingly,broad prospects exist for identifying ferroptosis as a potential therapeutic target.In this review,we aimed to systematically summarize the activation and defense mechanisms of ferroptosis,highlight the therapeutic targets,and discuss the design of nanomedicines for ferroptosis regulation.In addition,we opted to present the advantages and disadvantages of current ferroptosis research and provide an optimistic vision of future directions in related fields.Overall,we aim to provide new ideas for further ferroptosis research and inspire new strategies for disease diagnosis and treatment.

Familial glucocorticoid deficiency type 4(FGD4) is a rare autosomal recessive disorder caused by mutations in the nicotinamide nucleotide transhydrogenase(NNT) gene. The article presented clinical data, laboratory results, and genetic mutation findings of a child with FGD4. Additionally, a retrospective analysis of the clinical data of FGD4 patients reported domestically and internationally was conducted, summarizing the types of gene mutations and clinical characteristics. This case identifies novel mutation sites in the NNT gene, providing a basis for the early diagnosis and treatment of FGD4 patients.

Objective: To investigate the effectiveness and safety of intraoperative sac coiling embolization among patients who are athigh-risk developing type-Ⅱ endoleak after endovascular aortic repair(EVAR). Methods: From Jan 2014 to Jan 2018, one hundred and twelve consecutive patients with infra-renal AAA were enrolled for this study, There were 76 patients undergoing standard EVAR (standard-group)and 36 patients doing aneurysmal sac coiling embolization (embo-group). Baseline characteristics, aneurysmal sac parameters, radiological intervention details and follow up results were recorded. Results: Mean follow-up time was 25.9 m for embo-group. During follow-up period, no coils-related complications were noted and no type-Ⅱ endoleak associated secondary interventions were reported. A mean of (2.72±1.16) coils (range 1-7) was used in the embo-group. The incidence of type Ⅱ endoleak was 30.3%(23/76) in standard-group and 11.1%(4/36) in embo-group(χ²=4.90, P=0.027). Logistic multivariate analysis revealed that the independent risk factors of type Ⅱ endoleak after endovascular aortic repair for high-risk patients were those EVAR without sac embolization and sac volume≥128 cm³. In the subgroup analysis (sac volume≥128 cm³), the incidence of type-Ⅱ endoleak was lower in embo-group compared to standard-group (χ²=6.07, P=0.014). Conclusion Intraoperative sac coiling embolization in high-risk patients is safe and effective in prevention of type Ⅱ endoleak. This preventive effect is more significant with large sac aneurysm compared to small sac aneurysm.

Objective: To investigate the mechanisms of miR-375 affecting the proliferation and invasion of hepatoma cells via targeting YAP (Yes-associated protein). Methods: The cancerous tissues and corresponding para-cancerous tissues of 70 patients with hepatocellular carcinoma (HCC) who underwent surgical resection at the Second Affiliated Hospital of Henan University of Traditional Chinese Medicine from January 2015 to December 2016, as well as the hepatoma cell lines SMMC-7721, Hb611, HepG2 and BEL-7405 were collected for this study. qPCR method was used to detect the expression level of miR-375 in collected HCC tissues and different hepatoma cell lines; Dual luciferase reporter gene assay was used to verify the interaction between miR-375 and YAP; The relationship between miR-375 and clinicopathological features of HCC patients was also analyzed; MTT assay was used to detect the effect of miR375 on the proliferation of hepatoma cells; Transwell invasion assay was used to detect the invasive ability of hepatoma cells after inhibiting the expression of miR-375; Western blotting was used to detect the expression of YAP in HepG2 cells. The nude mouse model of subcutaneously transplanted xenograft was established, and the tumor volume and mass of transplanted hepatoma cells were detected after inhibiting the expression of miR-375. The expression of YAP in xenograft of nude mice was detected by immunohistochemistry and Western blotting. Results: The expression of miR-375 and YAP in HCC tissues was significantly higher than that in para-cancerous tissues (all P<0.05). The expression of miR-375 in HepG2 cells was the highest (P<0.05). miR-375 could specifically bind to the 3' UTR of YAP and regulate the expression activity of YAP. After inhibiting the expression of miR-375, the proliferation and invasion abilities of HepG2 cells were reduced (all P<0.05); The tumor volume and mass of transplanted xenografts were significantly reduced (both P<0.05); The expression of YAP protein in the transplanted xenografts was down-regulated (P<0.05). Conclusion: miR-375 plays an important role in the occurrence and development of liver cancer, and can influence the malignant biological behaviors of hepatoma cells by targeting and regulating the expression ofYAP.