Background Androgenetic alopecia in male is increasing in incidence every year. And hair transplantation with hair follicle unit extraction (FUE) is becoming increasingly accepted as a suitable treatment for these male patients. Methods A retrospective study was conducted, encompassing 158 male patients with androgen alopecia, of whom were diagnosed and operated in January 2016 to December 2020 in the medical cosmetology department of The First Affiliated Hospital of Xi 'an Medical University. Demographic data and treatments characteristics were recorded and analyzed. clinical curative effect,operation related complications ,satisfaction rate and life quality score of the patients were scored and analyzed. Results After FUE hair transplantation, the hair follicle survival rate of 158 patients was more than ninety percent, in addition, more than eighty-five percent of patient hair follicle survival rate was over ninety-five percent at 12 months, the patient satisfaction rate was higher than ninety-eight percent, but the complication rate was less than six percent. Conclusion Our data show that FUE is a minimally invasive hair transplant technique that has high hair follicle survival rate and ideal hair density, which is an effective method to treat male androgen alopecia and is worthy of clinical application.

Background Currently, the clinically used immune biomarkers for non-small cell lung cancer (NSCLC) are programmed death ligand 1 (PD-L1) and tumor mutation burden (TMB). However, they cannot accurately predict the effectiveness of immunotherapy. Identifying appropriate biomarkers that can differentiate between beneficiary groups is imperative. Methods We identified LRP1B as a potential biomarker for immunotherapy by analyzing clinical data, combined with bioinformatics analysis. The effects of LRP1B on ferroptosis were assessed using qRT-PCR, Western blotting, CCK-8 assay, and flow cytometry. The potential mechanism underlying the regulation of ferroptosis by LRP1B was elucidated using qRT-PCR, Western blotting, ChIP, and dual-luciferase reporter gene assays. Results Through the collection and analysis of clinical data, we had established that LRP1B mutation is a highly promising biomarker for immunotherapy. Bioinformatics analysis revealed significant differences in the expression levels of PD-L1 and TMB between patients with LRP1B mutation and wild-type patients in lung adenocarcinoma (LUAD), while in lung squamous cell carcinoma (LUSC), only the level of TMB showed a significant difference. Furthermore, we observed that patients with LRP1B mutation in LUAD had significantly higher levels of tumor-infiltrating lymphocytes (TILs), including CD4+ T cells and M1 macrophages, than wild-type patients, whereas in LUSC, no such differences were detected. In addition, we found that patients with LRP1B mutation in LUAD had significantly prolonged progression-free survival (PFS) compared to wild-type patients, but no PFS benefit was observed in patients with LRP1B mutation in LUSC. These findings provided strong evidence that LRP1B mutation was a potential biomarker for immunotherapy in LUAD. Moreover, our in vivo experiments indicated that knockdown of LRP1B enhanced the efficacy of mPD-1, and mechanistic studies revealed that LRP1B regulated the sensitivity of cells to ferroptosis by modulating the expression of SLC7A11 through altering the phosphorylation level of STAT3. Importantly, LRP1B alterations also affected the sensitivity of cells to ferroptosis induced by IFN-γ. Further analysis revealed that LRP1B knockdown promoted immunotherapy in vivo. Conclusions Our results confirmed that LRP1B affected the efficacy of immunotherapy by modulating the sensitivity of NSCLC cells to ferroptosis.

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