Objective To compare genomic copy number variations (CNVs) among different subtypes of breast cancer and analyze specific CNVs in each subtype. Methods AIMS software was used for genotype breast cancer (BasL, Her2, LumA and LumB), and GISTIC2.0 software was used to analyze genome-wide CNVs in tumor tissues from TCGA. We collected and analyzed the information and samples of 324 cases of invasive breast cancer admitted to Jiangmen Central Hospital(JMCH). Fluorescence quantitative PCR was used to detect the CNV of ERBB2, TFDP1, MIR148B, CCND1, MDM2 and MIR139 genes in the tumor tissues, to verify TCGA analysis. Results 13q34 was specifically amplified and 12q13.13 was specifically deleted in BasL-type breast cancer. The 17q12 was specifically amplified in Her2 type. The 12q15 was specifically amplified and 11q13.4 was specifically deleted in LumB type, but LumA type had no specific amplification or deletion of chromosome region. The proportion of TFDP1 amplification or MIR148B deletion in BasL type were 57.8% (TCGA) and 71.4% (JMCH), which were significantly higher than other subtypes (P < 0.001). The proportion of ERBB2 amplification of Her2 type were 55.2% (TCGA) and 86.7% (JMCH), which were significantly higher than other subtypes (P < 0.001). The proportion of LumB type with CCND1 or MDM2 amplification or MIR139 deletion were 47.6% (TCGA) and 61.8% (JMCH), which were significantly higher than other subtypes (P < 0.05). Conclusion At the CNV level of breast cancer, Her2 type is characterized by the amplification of ERBB2, BasL type is characterized by the amplification of TFDP1 or the deletion of MIR148B, LumB type is characterized by the amplification of CCND1 or MDM2 or the deletion of MIR139, but LumA type lacks specific CNV characteristics.

Ferroptosis is a novel form of programmed cell death that relies on the accumulation of intracellular iron ions,causing irreversible damage to cell membranes through extensive lipid peroxidation,ultimately leading to cell death.Ferroptosis is closely associated with various neurodegenerative diseases.The ferroptosis of glial cells can regulate neuronal death by inducing neuroinflammation and affecting oxidative stress,thereby exacerbating the progression of neu-rodegenerative diseases.This review summarizes how ferroptosis occurs in different types of glial cells and its impact on neurons,aiming to deeply understand the effects of glial cell ferroptosis on neurodegenerative diseases and explore the po-tential therapeutic applications of inhibiting this process in treatment.

Objective: To investigate the effect and mechanism of α-lipoic acid(ALA) on the formation of hypertrophic scar(HTS) in rabbit ears. Methods: Eighteen New Zealand white rabbits were randomly divided into normal group, model group and 4%ALA group. After 28 days of treatment, the changes of scar related indexes were evaluated by hematoxylin-eosin(HE) staining, Masson pine(Masson) staining and immunohistochemical staining, the changes of oxidative stress related indexes were evaluated, and the expression of antioxidant pathway related proteins was detected by Western blotting. Results: The color, texture and volume of scar in 4%ALA group were lighter and softer than those in model group. The results of HE, Masson staining and immunohistochemical staining showed that the number of fibrous cells and the degree of fibrosis in the 4%ALA group were less than those in the model group. In the 4%ALA group, the content of malondialdehyde(MDA) was lower than that of the model group(P<0.001), the content of hydroxyproline(Hyp) was lower than that of the model group(P<0.01), the level of glutathione(GSH) was higher than that of the model group(P<0.01), the activity of T-SOD was higher than that of the model group(P<0.001). Western blotting showed that the content of NRF2 and the expression level of downstream antioxidant proteins in the 4%ALA group were higher than those in the model group. Conclusion ALA up-regulates NRF2 signal pathway to reduce the level of oxidative stress in HTS and inhibit scar proliferation in rabbit ears.