ObjectiveThe aim of this study was to determine the effect of exposure to different antithyroid drugs during pregnancy on the incidence of neonatal congenital malformations.MethodsA meta-analysis was performed to compare the incidence of neonatal congenital malformations after exposure to different antithyroid drugs during pregnancy. Twelve studies that met the inclusion criteria were included in this meta-analysis. PubMed, Embase, and CENTRAL databases were searched from inception until January 2017. Study designs included case–control studies, prospective cohort studies, and retrospective cohort studies.ResultsTwelve studies involving 8028 participants with exposure to different antithyroid drugs during pregnancy were included in this study; however, only 10 studies involving 5059 participants involved exposure to different antithyroid drugs exactly during pregnancy. Our results indicated that exposure to methimazole (MMI)/carbimazole (CMZ) only during pregnancy significantly increased the risk of neonatal congenital malformations compared to no antithyroid drug exposure (OR 1.88; 95%CI 1.33 to 2.65; P = 0.0004). No differences were observed between propylthiouracil (PTU) exposure and no antithyroid drug exposure only during pregnancy (OR 0.81; 95%CI 0.58 to 1.15; P = 0.24). Exposure to MMI/CMZ only during pregnancy significantly increased the risk of neonatal congenital malformations compared to that associated with exposure to PTU (OR 1.90; 95%CI 1.30 to 2.78; P = 0.001).ConclusionFor pregnant women with hyperthyroidism, exposure to MMI/CMZ significantly increased the incidence of neonatal congenital malformations compared to exposure to PTU and no antithyroid drug exposure; however, no differences were observed between PTU exposure and no antithyroid drug exposure.

Purpose To compare the multimodal techniques (including neuronavigation, intraoperative MRI [iMRI], and neuromonitoring [IONM]) and conventional approach (only guided by neuronavigation) in removing glioblastoma (GBM) with corpus callosum (CC) involvement (ccGBM), their effectiveness and safety were analyzed and compared. Methods Electronic medical records were retrospectively reviewed for ccGBM cases treated in our hospital between January 2016 and July 2020. Patient demographics, tumor characteristics, clinical outcomes, extent of resection (EOR), progression-free survival (PFS), and overall survival (OS) were obtained and compared between the multimodal group (used multimodal techniques) and the conventional group (only used neuronavigation). Both groups only included patients that had maximal safe resection (not biopsy). Postoperative radiochemotherapy was also performed or not. Univariate and multivariate analyses were performed to identify significant prognostic factors and optimal EOR threshold. Results Finally 56 cases of the multimodal group and 21 cases of the conventional group were included. The multimodal group achieved a higher median EOR (100% versus 96.1%, P = 0.036) and gross total resection rate (60.7% versus 33.3%, P = 0.032) and a lower rate of permanent motor deficits (5.4% versus 23.8%, P = 0.052) than the conventional approach. The multimodal group had the longer median PFS (10.9 versus 7.0 months, P = 0.023) and OS (16.1 versus 11.6 months, P = 0.044) than the conventional group. Postoperative language and cognitive function were similar between the two groups. In multivariate analysis, a higher EOR, radiotherapy, and longer cycles of temozolomide chemotherapy were positive prognostic factors for survival of ccGBM. An optimal EOR threshold of 92% was found to significantly benefit the PFS (HR = 0.51, P = 0.036) and OS (HR = 0.49, P = 0.025) of ccGBM. Conclusion Combined use of multimodal techniques can optimize the safe removal of ccGBM. Aggressive resection of EOR > 92% using multimodal techniques combined with postoperative radiochemotherapy should be suggested for ccGBM.

Purpose: To explore molecular alterations and their correlation with the survival of patients with glioblastoma (GBM) with corpus callosum (CC) involvement (ccGBM).Methods: Electronic medical records were reviewed for glioma patients tested for molecular alterations and treated at our hospital between January 2016 and July 2020. ccGBM was compared to GBM without CC involvement (non-ccGBM) to identify differences in molecular alterations. Clinical outcomes and survival were compared between ccGBM and non-ccGBM patients, as well as among patients with ccGBM with different molecular alteration statuses. ccGBM was also compared to diffuse midline glioma (DMG) to clarify their correlation in molecular alterations, the progression-free survival (PFS), and overall survival (OS).Results: Thirty ccGBM and 88 non-ccGBM patients were included. PDGFRA amplification (PDGFRAamp, 33.3 vs. 9.1%, P = 0.004) and missense mutation (PDGFRAmut, 20.0 vs. 3.4%, P = 0.011) both had higher incidences in ccGBM than in non-ccGBM. PDGFRA alteration was associated with the occurrence of ccGBM (OR = 4.91 [95% CI: 1.55–15.52], P = 0.007). ccGBM with PDGFRAamp resulted in a shorter median PFS (8.6 vs. 13.5 months, P = 0.025) and OS (12.4 vs. 17.9 months, P = 0.022) than non-ccGBM with PDGFRAnon-amp. ccGBM with PDGFRAamp combined with PDGFRAmut (PDGFRAamp-mut) had a shorter median PFS (7.6 vs. 8.9 months, P = 0.022) and OS (9.6 vs. 17.8 months, P = 0.006) than non-ccGBM with wild-type PDGFRA and no amplification (PDGFRA-w, non-amp). Compared to ccGBM with PDGFRA-w, non-amp, ccGBM with PDGFRAamp and PDGFRAamp-mut both had a shorter median PFS and OS (P < 0.05). The hazard ratios (HRs) of PDGFRAamp for PFS and OS in ccGBM were 3.08 (95% CI: 1.02–9.35, P = 0.047) and 5.07 (1.52–16.89, P = 0.008), respectively, and the HRs of PDGFRAamp-mut for PFS and OS were 13.16 (95% CI: 3.19–54.40, P < 0.001) and 16.36 (2.66–100.70, P = 0.003). ccGBM may have similar incidences of PDGFRAamp or mut (PDGFRAamp/mut) as DMG, and they also had similar median PFS (10.9 vs. 9.0 months, P = 0.558) and OS (16.8 vs. 11.5 months, P = 0.510).Conclusion:PDGFRA alterations are significantly associated with the occurrence and poor prognosis of ccGBM. ccGBM with PDGFRAamp/mut may be classified as a single subtype of GBM that has a similar survival rate to DMG. PDGFR inhibitors may be a promising treatment method for ccGBM.

Introduction: We here evaluated the efficacy of piceatannol (PIC) in high glucose (HG)-induced injury of renal tubular epithelial cells HK-2. Methods: After the establishment of HG-induced cell injury model and the treatment with PIC at both high and low concentrations and/or Acetazolamide (ACZ, the inhibitor of carbonic anhydrase 2 (CA2)), MTT and flow cytometry assays were carried out to confirm the viability and apoptosis of HK-2 cells. The levels of oxidative stress markers lactate dehydrogenase (LDH), malondialdehyde (MDA), and reactive oxygen species (ROS), the ratio of glutathione/oxidized glutathione (GSH/GSSG), and the CA2 activity were determined. Both quantitative reverse-transcription polymerase chain reaction and Western blot were used to calculate the expressions of CA2 (the predicted target gene of PIC via intersecting the data from bioinformatic analyses), and AKT pathway- (Phosphatase and tensin homolog (PTEN), phosphorylated (p)-AKT, AKT) and apoptosis-related proteins (Bcl-2 and cleaved caspase-3). Results: HG suppressed cell viability and the levels of GSH/GSSG ratio, CA2, pThr308-AKT/AKT, pSer473-AKT/AKT, and Bcl-2, while promoting cell apoptosis, the levels of LDH, MDA, and ROS and the expressions of PTEN and cleaved caspase-3. All effects of HG were reversed by PIC at a high concentration. CA2 was predicted and identified as the target of PIC. In HG-treated HK-2 cells, additionally, ACZ reversed the effects of PIC on the viability, apoptosis, and the levels of both oxidative stress markers and AKT pathway- and apoptosis-related factors. Conclusion: PIC protects against HG-induced injury of HK-2 cells via regulating CA2.