Glioblastoma (GBM) is a clinically common type of glioma with a very poor prognosis and complex drug resistance mechanisms, high mortality, short survival time; invasiveness and recurrence are the main obstacles to treatment. Ferroptosis is an iron-dependent regulated cell death associated with massive lipid peroxidation that is related with the development and treatment response of various types of tumors. Cancer cells rely on their strong antioxidant capacity to avoid ferroptosis, therefore, exploring ferroptosis may be an effective strategy to prevent tumor proliferation and invasion. This article mainly reviews the mechanism of ferroptosis in GBM, as well as the research status and progress of ferroptosis as a potential therapeutic target.

Objective: Bioinformatics methods were used to annotate the suspicious pathogenic genes of congenital microtia in detail, and construct the protein-protein interaction (PPI) networks to clarify the function and interaction of pathogenic genes, so as to predict the potential pathogenic genes. Methods: The pathogenic genes of congenital microtia were searched using the mouse genome informatics (MGI). The results were summarized into the STRING database to construct PPI networks. The Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were carried out. Results: Sixty-eight congenital microtia-related pathogenic genes such as FGF8, EYA1 and HOXA2 were searched by MGI. The PPI network contained 65 nodes and 174 edges. The average node degree was 5.35. The clustering coefficient was 0.437 and the PPI enrichment P = 0. The key node proteins were screened in PPI networks. The top ten were CTNNB1, FGF8, EGFR, BCL2, PAX6, FGF3, FGF10, WNT5A, FGFR1 and MAPK1. GO analysis and KEGG pathway analysis showed: the pathogenic genes were involved in the biological process of ear morphogenesis, ear development and embryonic organ morphogenesis. They also get involved in the molecular regulation, including sequence-specific DNA binding and regulatory region DNA binding. Expression of different genes were located in nucleus and other sub-microscopic cell components. Pathogenic genes were also involved in cancer pathway, melanoma, MAPK signaling pathways, RAS signaling pathways and other signaling pathways. Conclusions By using bioinformatics tools, we constructed the PPI networks of the congenital microtia pathogenic genes, and obtained detailed GO enrichment and KEGG pathway data. The key nodes contained the confirmed pathogenic genes of congenital microtia, which preliminarily proved the feasibility of the bioinformatics method in this study. We found some nodes were closely linked with FGF and WNT, which may be potential mutant genes of congenital microtia, although further study is needed.

Objective: To identify a pig model with bilateral external ear defects accompanied by aural atresia and investigate its application in plastic surgery. Methods: Erhualian×Shaziling F₂ pig inbreeding population was introduced, and examination of external ear morphology was conducted in all individuals. Temporal computed tomography scanning and mutational detection of HOXA1 gene were conducted in one affected and one normal individuals. Results: In Erhualian×Shaziling F₂ pig inbreeding population, there were 57 normal and 18 affected individuals among the 75 pigs. Affected subjects presented bilateral external ear defects accompanied by aural atresia; temporal computed tomography scanning showed bilateral aural atresia and dysplasiaof middle ear; and gene detection identified homozygous mutation of HOXA1 gene. Conclusions Pig model with HOXA1 gene homozygous mutation resembles human microtia at different levels. Our findings provide the theoretical basis for its application to study further pathological mechanism for human microtia.

Objective To study the clinical application value of microsurgery in treatment of tentorium meningioma.Methods 53 patients with tentorium meningioma were chosen,they all underwent microsurgical treatment,the extent of resection of the tentorium meningioma and treatment efficacy were observed.The mortality,causes of death of tentorium meningioma patients after microsurgery were analyzed.Spitzer index was compared before and after treatment,the life quality of the patients was evaluated.Results There was no death after microsurgical treatment.The tentorium meningioma tumor removal rate was huge tumor ＜ tumors ＜ medium-sized tumors ＜ small tumor.There were 9 cases excellent,14 cases good in Spitzer index before treatment,26 cases excellent,14 cases good after treatment,there was significant difference between them (x2 =19.15,P ＜ 0.01).Conclusion Microsurgical treatment for the patients with tentorium meningioma has better clinical efficacy and can greatly improve patients' quality of life,which is worthy of further clinical research and promotion.

Objective To observe the application of the mini-mental status examination (MMSE)cognitive assessment in the patients with brain glioma before and after surgery. Methods Using MMSE,36 pastients with primary brain glioma were subjected to the cognitive assessment before surgery, after surgery,and 3 monthsr after surgery. Results The quantitative cognitive assessments with MMSE before surgery revealed the hidden cognitive dysfunction patients.The quantitative cognitive assessments after surgery showed that surgeons might need to protect the non-function area and to form the idea of cognitive function in patients with glioma.Conclusion MMSE assessment is a simple,understandably,and convenient method having good compliance of patient. It may be effectively used to assess cognitive impairment for patients with glioma and worth being studied continuously and used widely in the clinic practice.

A total of 473 patients of diabetic nephropathy (DN) with normal serum creatinine were recruited.Blood routine,blood lipids and urine albumin/creatinine ratio (UACR) were measured.They were divided into microalbuminuria group (DN1,n =246 ) and macroalbuminuria group (DN2,n =227 ).The white blood cell (WBC) count,monocyte count and CRP significantly increased with the progression of DN in the DN2 group versus those in the DNI group [ (6.8 ± 1.7 ) × 109/L vs.(6.3 ± 1.5 ) × 109/L,(0.49±0.23) ×109/Lvs.(0.32 ±0.21) ×109/L,(4.1 ±1.1)mg/Lvs.(1.7±0.3) mg/L,all P＜ 0.05].According to multiple linear regression analysis,WBC,monocyte,low density lipoproteincholesterol and lymphocyte were found to be independent influencing factors for the elevation of UACR.

Objective To investigate the effects of uncoupling protein 2 (UCP-2) gene a 45 bp insertion/deletion (Ins/Del) polymorphism in the 3'-untranslated (3'-UTR) of its exon 8 on macroangiopathy in diabetes mellitus.Methods A total of 182 patients were selected,80 cases with macroangiopathy( A group), 102 cases without macroangiopathy(B group) ,UCP-2 gene polymorphism was confirmed by electrophoresis after PCR with 3% agarose,then compared genotype and allele gene frequency. Results The 3'-UTR Ins/Del polymorphism of UCP-2 gene in A group ( II:6. 25% 、ID: 18. 75% 、DD:75.00% ) and B group( II:9. 80% 、ID:23.53%、 DD: 66. 67% ) had no significant difference ( P ＞ 0. 05 ), and there was also no difference of alleles frequencies in two groups ( I: 15.63 %、 D: 84. 37 % )and(I:21.57% 、D:78.43%)(P ＞0.05). Conclusion No relationship of the 3'-UTR a 45bp Ina/Del polymorphism in exon 8 of the UCP-2 gene was found with macroangiopathy in diabetes mellitus.

Objective To study the impairment and the expression of receptor of advanced glycation endproduct (RAGE) in cultured rat glomerular mesangial cells ( GMC ) induced by constant and intermittent high glucose, and to investigate the pathogenesis of diabetic nephropathy. Methods After being cultured under constant and intermittent high glucose with different concentrations for 24 and 48 hours, the morphological changes of rat mesangial cells were observed, the proliferation of GMC was detected by MTT assay, the activity of superoxide dismutase (SOD)and the level of malondialdehyde (MDA)in supernatant were measured by spectrophotometer,and the expressions of RAGE mRNA were evaluated by RT-PCR. Results ( 1 ) Compared with the control group,the cellular morphology was changed in case of constant and intermittent high glucose. The damage of GMC with intermittent high glucose concentrations was more serious. (2)The activity of SOD was decreased and the level of MDA was raised in case of intermittent high glucose concentrations compared with the constant high glucose concentrations (P＜0.05). (3)The expression of RAGE mRNA with intermittent high glucose concentrations was significantly higher than that with constant high glucose concentrations ( P＜0. 01 ). Conclusions The damaging effects and increased expression of RAGE in cultured rat GMC induced by blood glucose fluctuation was much worse than that with constant high glucose. The blood glucose fluctuation may be one of the causes that induce diabetic nephropathy.

Objective To investigate the relationship between serum transforming growth factor- β1(TGF- β1) levels and early diabetic nephropathy and clarify whether valsartan plays a role in renal protection by reducing the level of serum TGF-β1. Methods The study subjects were divided into four groups:control group (30 cases); normal albuminuria group 1 (NA1 group with 12 cases, U MA/Cr < 10 μg/mg combined with type 2 diabetes);normal albuminuria group 2 (NA2 group with 19 cases,UMA/Cr 10-30 μg/mg combined with type 2 diabetes); microalbuminuria group ( MA group with 35 cases, U MA/Cr 31-300 μg/mg combined with type 2 diabetes). All these type 2 diabetic patients were suffering from diabetic retinopathy, and valsartan ( 80 mg/d) were medicated for those combined with hypertension. The serum TGF-β1 levels were measured by enzyme-linked immunosorbent assay in all subjects. Results Serum TGF- β1 levels in three diabetes groups were (7.41 ± 2.68 ), ( 10.52 ± 4.10), (22.98 ± 43.74) ng/L, respectively, all of which were higher than those in control group [(4.25 ± 5.82) ng/L] (P < 0.05). There were significant differences in serum TGF- β1 levels among MA group, NA2 group and NA1 group (P < 0.05 ). Serum TGF-β1 levels in NA1 group with valsartan treatment significantly decreased compared with those without valsartan treatment (P < 0.05), whereas there was no significant reduction in NA2 and MA group with valsartan treatment (P > 0.05). Conclusions High serum TGF-β1 level may be associated with type 2 diabetes and early diabetic nephropathy. Early intervention of valsartan may be delay the onset and development of diabetic nephropathy by decreasing the serum TGF-β1 level.

A total of 169 patients with short-duration type 2 diabetic mellitus (DM) were divided into atherosclerosis (AS) group and non-AS group according to the intima-media thickness (IMT) of three conducting arteries.The level of serum amyloid A (SAA) was assayed by ELISA.The results showed that SAA level of type 2 DM patients increased significantly, patients in AS group showed higher SAA level than that in non-AS group, and SAA level was positively correlated with age, body mass index, waist hip ratio and IMT of common carotid artery.Age, C-reactive protein and SAA level are the major risk factors for IMT of common carotid artery.