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Goodpasture’s syndrome (GPS) is a rare but severe vasculitis disease, characterized by rapidly progressive glomerulonephritis (RPGN), diffuse pulmonary hemorrhage in the presence of anti-glomerular basement membrane antibody (anti-GBM antibody). Central nervous system (CNS) was rarely involved, especially in the absence of anti-neutrophil cytoplasmic antibodies (ANCA). Typically, CNS vasculitis was one of important causes. Herein we present a case of GPS presenting RPGN, clonic-tonic seizures and bloody sputum. She underwent renal puncture and bleeding complication occurred afterwards. Due to the insufficiency of conservative therapy including transfusion, fluid infusion, selective renal arteriography embolization was then employed. Angiogram results showed beading changes of renal artery. Brain CT scan was found negative, but MRA imaging demonstrated the obvious involvement of cranial vessels. The changes of renal and cranial vascular involvement were highly suspicious of nervous vasculitis based on the primary disease. The patient was treated with corticoids and plasma exchange. Patient’s condition improved quickly and anti-GMB antibodies proved to be negative, but renal failure persisted, dependent on long-term hemodialysis. We described for the first-time association of Goodpasture’s syndrome with both renal and nervous vascular involvements.

Background. The development of lung adenocarcinoma (LUAD) involves the interactions between cell proliferation and death. Autophagy-dependent ferroptosis, a distinctive cell death process was implicated in a multitude of diseases, whereas no research revealing the relationship between autophagy-dependent ferroptosis and LUAD pathogenesis was reported. Thus, the primary objective was to explore the role and potential function of the autophagy-dependent ferroptosis-related genes in LUAD.Methods. Clinical information and transcriptome profiling of patients with LUAD were retrieved and downloaded from open-source databases. Autophagy-dependent ferroptosis-related genes were screened by published articles. The key gene was identified as the intersection between the differentially expressed genes and prognosis-related genes. Patients were divided into high- and low-risk groups using the expression level of the key gene. The validity of the key gene prognosis model was verified by survival analysis. The correlation between the clinical characteristics of LUAD and the expression level of the key gene was analyzed to explore the clinical significance and prognosis value. And the roles of the key gene in response to chemotherapy, immune microenvironment and tumor mutation burden were predicted. The validation of key gene expression levels were further performed by quantitative real-time PCR and immunohistochemistry staining.Results. FANCD2, a key autophagy-dependent ferroptosis-related gene by searching database, was confirmed as an independent prognostic factor for LUAD occurrence. The high expression level of FANCD2 was associated with an advantaged TNM stage, a less chemotherapy sensitivity, a low ImmuneScore, which indicated a deactivation status in immune microenvironment, a high tumor mutation burden, and a poor survival for LUAD patients. Pathway enrichment analysis showed that FANCD2 were involved in response to oxidative stress and neutrophil mediated immunity. Quantitative real-time PCR and immunohistochemistry staining showed that the expression level of FANCD2 is higher in LUAD patients than normal tissue samples, which was in accordance with the database report.Conclusion. FANCD2, a key gene related to autophagy-dependent ferroptosis, could work as a biomarker, which predicts the survival, chemotherapy sensitivity, tumor immunity and mutation burden of LUAD. Research of autophagy-dependent ferroptosis and targeting the FANCD2 may offer a new perspective for the treatment and improvement of prognosis in LUAD.

Background Although previous studies have discussed whether the minimally invasive esophagectomy (MIE) is superior to open surgery, the data concerning esophageal squamous cell carcinoma (ESCC) patients underwent neoadjuvant treatment followed by radical resection is limited. The purpose of our study was to compare the short- and long-term clinical outcomes of the two surgical approaches in treating ESCC patients. Methods Between January 2010 and December 2016, ESCC patients who had received neoadjuvant therapy and underwent Mckeown esophagectomy at our institute were eligible. The baseline characteristics, pathological data, short-and long-term outcomes of these patients were collected and compared based on the surgical approach. Results A total of 195 patients was included in the current study. Compared to patients underwent open surgery, patients underwent MIE had shorter operative time and less intraoperative bleeding (390 min vs 330 min, P = 0.001; 204 ml vs 167 ml, P = 0.021). In addition, the risk of anastomotic leakage was decreased in MIE group (20.0% vs 3.3%, P P = 0.013). Conclusion Minimally invasive Mckeown esophagectomy is safe and feasible for ESCC patients who underwent neoadjuvant therapy. MIE approach presented better perioperative results than open esophagectomy. The effect of surgical approaches on survival was depending on the scheme of neoadjuvant treatment.

Background Chemotherapy often causes chemotherapy-induced peripheral neuropathy (CIPN), but effective prevention measures are still lacking. Whether vitamin E can prevent peripheral neurotoxicity caused by chemotherapy is inconclusive. Therefore, we collected related randomized controlled trials (RCTs) and conducted a meta-analysis to examine whether vitamin E could prevent CIPN. Methods We searched PubMed, EMBASE and the Cochrane databases in November 2019 for eligible trials. Two reviewers conducted the analysis independently when studies were homogeneous enough. Results Eight RCTs, involving 555 patients, were identified. Upon pooling these RCTs, patients who received vitamin E supplementation of 600 mg/day had a significantly lower incidence of peripheral neuropathy (RR 0.31; 95% CI 0.14 to 0.65; P = 0.002) induced by chemotherapy compared with the placebo group. Vitamin E played a key role in decreasing the incidence of peripheral neuropathy in the cisplatin chemotherapy group (RR 0.28; 95% CI 0.14 to 0.54; P = 0.0001). With regard to improvements in sural amplitude, vitamin E supplementation significantly decreased patients’ sural amplitude after three rounds of chemotherapy (RR -2.66; 95% CI -5.09 to -0.24; P =0.03) in contrast with that of placebo supplementation, while no significant difference was observed when patients were treated with vitamin E after six rounds of chemotherapy. In addition, the vitamin E group had better improvement in the neurotoxicity score (RR -2.65; 95% CI -4.01to -1.29; P = 0.0001) and a lower incidence of reflexes and distal paraesthesias (RR 0.50; 95% CI 0.29 to 0.87; P = 0.01) compared to the control group. Conclusion Available data included in this meta-analysis showed that vitamin E supplementation can confer modest improvement in the prevention of CIPN. However, large-scale, well-designed RCTs are needed to confirm the exact role of vitamin E supplementation in the prevention of CIPN.