Objective: Previous studies have discovered a correlation between cigarette smoking and cortical thickness and surface area, but the causal relationship remains unclear. The objective of this investigation is to scrutinize the causal association between them. Methods: To derive summary statistics from a genome-wide association study (GWAS) on cortical thickness, surface area, and four smoking behaviors: 1) age of initiation of regular smoking (AgeSmk); 2) smoking initiation (SmkInit); 3) smoking cessation (SmkCes); 4) cigarettes per day (CigDay). Linkage disequilibrium score regression (LDSC) was employed to examine genetic association analysis. Furthermore, for traits with significant genetic associations, Mendelian randomization (MR) analyses were conducted. Results: The LDSC analysis revealed nominal genetic correlations between AgeSmk and right precentral surface area, left caudal anterior cingulate surface area, left cuneus surface area, left inferior parietal surface area, and right caudal anterior cingulate thickness, as well as between CigDay and left caudal middle frontal surface area, between SmkCes and left entorhinal thickness, and between SmkInit and left rostral anterior cingulate surface area, right rostral anterior cingulate thickness, and right superior frontal thickness (rg=-0.36–0.29, p<0.05). MR analysis showed a unidirectional causal association between left caudal middle frontal surface area and CigDay (βIVW=0.056, pBonferroni=2×10-4). Conclusion Left caudal middle frontal surface area has the potential to serve as a significant predictor of smoking behavior.

Objective To investigate the mechanism of astragalus polysaccharide(APS)in inhibiting the proliferation and metastasis of osteosarcoma cells.Methods Cell counting kit-8(CCK8)assay was used to detect the inhibitory effect of APS on the proliferation of osteosarcoma cell lines U2OS,HOS,MG63 and osteoblast cell line hFOB1.19,the cell line with the most significant inhibitory effect of APS on osteosarcoma cells was selected for subsequent experiments.Osteosarcoma cells were divided into control group(NC group),APS group,APS+sh-SP1 co treatment group with transfected SP1 knockdown plasmid(APS+sh-SP1),and APS+oe SP1 co treatment group with transfected SP1 overexpression plasmid(APS+oe SP1 group).Western blotting was used to detect the expression of SP1 protein in each group.CCK8 assay was used to detect the proliferation ability of each group.Transwell assay was used to detect the metastatic ability of cells in each group.TOP/FOP Flash assay was used to detect the activity of Wnt/β-catenin signaling pathway.The protein expressions of Wnt3a,β-catenin,CyclinD1,cMYC,matrix metalloproteinase 2(MMP2)and Snail were detected by western blotting.Result After 48h of APS treatment,the cell proliferation inhibition rates of osteosarcoma cells U2OS,HOS,MG63 and osteoblast cells hFOB1.19 were 62.93%±4.79%,20.66%±1.10%,39.31%±3.20%and 5.97%±0.72%,respectively.Compared with osteoblast hFOB1.19,APS significantly inhibited the proliferation of osteosarcoma cells,and the difference was statistically significant(F=208.400,P<0.001),and the inhibitory effect on osteosarcoma U2OS cells was the most significant(t=20.380,P<0.001).Compared with NC group,SP1 protein expression,cell proliferation ability,number of transmembrane cells,Wnt/β-catenin signaling pathway activity in cells,Wnt/β-catenin signaling pathway key proteins Wnt3a,β-catenin,downstream proliferation-related protein CyclinD1,cMYC,and downstream metastasis related proteins MMP2 and Snail in the APS group were decreased,and the differences were statistically significant(t=9.740～90.780,all P<0.05).Compared with the APS group,the expression of SP1 protein,cell proliferation ability,the number of transmembrane cells,the activity of Wnt/β-catenin signaling pathway and the expression of Wnt/β-catenin signaling pathway related proteins in the APS+sh-SP1 group were further decreased,and the differences were statistically significant(t=3.032～12.940,all P<0.05).Compared with the APS group,the expression of SP1 protein,cell proliferation ability,the number of transmembrane cells,the activity of Wnt/β-catenin signaling pathway and the expression of Wnt/β-catenin signaling pathway related proteins in the APS+oe-SP1 group were increased,and the differences were statistically significant(t=3.350～22.450,all P<0.05).Conclusion APS inhibits the proliferation and metastasis of osteosarcoma cells by targeting SP1/Wnt/β-catenin signaling axis.

Objective: Previous studies have discovered a correlation between cigarette smoking and cortical thickness and surface area, but the causal relationship remains unclear. The objective of this investigation is to scrutinize the causal association between them. Methods: To derive summary statistics from a genome-wide association study (GWAS) on cortical thickness, surface area, and four smoking behaviors: 1) age of initiation of regular smoking (AgeSmk); 2) smoking initiation (SmkInit); 3) smoking cessation (SmkCes); 4) cigarettes per day (CigDay). Linkage disequilibrium score regression (LDSC) was employed to examine genetic association analysis. Furthermore, for traits with significant genetic associations, Mendelian randomization (MR) analyses were conducted. Results: The LDSC analysis revealed nominal genetic correlations between AgeSmk and right precentral surface area, left caudal anterior cingulate surface area, left cuneus surface area, left inferior parietal surface area, and right caudal anterior cingulate thickness, as well as between CigDay and left caudal middle frontal surface area, between SmkCes and left entorhinal thickness, and between SmkInit and left rostral anterior cingulate surface area, right rostral anterior cingulate thickness, and right superior frontal thickness (rg=-0.36–0.29, p<0.05). MR analysis showed a unidirectional causal association between left caudal middle frontal surface area and CigDay (βIVW=0.056, pBonferroni=2×10-4). Conclusion Left caudal middle frontal surface area has the potential to serve as a significant predictor of smoking behavior.

Objective: Previous studies have discovered a correlation between cigarette smoking and cortical thickness and surface area, but the causal relationship remains unclear. The objective of this investigation is to scrutinize the causal association between them. Methods: To derive summary statistics from a genome-wide association study (GWAS) on cortical thickness, surface area, and four smoking behaviors: 1) age of initiation of regular smoking (AgeSmk); 2) smoking initiation (SmkInit); 3) smoking cessation (SmkCes); 4) cigarettes per day (CigDay). Linkage disequilibrium score regression (LDSC) was employed to examine genetic association analysis. Furthermore, for traits with significant genetic associations, Mendelian randomization (MR) analyses were conducted. Results: The LDSC analysis revealed nominal genetic correlations between AgeSmk and right precentral surface area, left caudal anterior cingulate surface area, left cuneus surface area, left inferior parietal surface area, and right caudal anterior cingulate thickness, as well as between CigDay and left caudal middle frontal surface area, between SmkCes and left entorhinal thickness, and between SmkInit and left rostral anterior cingulate surface area, right rostral anterior cingulate thickness, and right superior frontal thickness (rg=-0.36–0.29, p<0.05). MR analysis showed a unidirectional causal association between left caudal middle frontal surface area and CigDay (βIVW=0.056, pBonferroni=2×10-4). Conclusion Left caudal middle frontal surface area has the potential to serve as a significant predictor of smoking behavior.

Objective: Previous studies have discovered a correlation between cigarette smoking and cortical thickness and surface area, but the causal relationship remains unclear. The objective of this investigation is to scrutinize the causal association between them. Methods: To derive summary statistics from a genome-wide association study (GWAS) on cortical thickness, surface area, and four smoking behaviors: 1) age of initiation of regular smoking (AgeSmk); 2) smoking initiation (SmkInit); 3) smoking cessation (SmkCes); 4) cigarettes per day (CigDay). Linkage disequilibrium score regression (LDSC) was employed to examine genetic association analysis. Furthermore, for traits with significant genetic associations, Mendelian randomization (MR) analyses were conducted. Results: The LDSC analysis revealed nominal genetic correlations between AgeSmk and right precentral surface area, left caudal anterior cingulate surface area, left cuneus surface area, left inferior parietal surface area, and right caudal anterior cingulate thickness, as well as between CigDay and left caudal middle frontal surface area, between SmkCes and left entorhinal thickness, and between SmkInit and left rostral anterior cingulate surface area, right rostral anterior cingulate thickness, and right superior frontal thickness (rg=-0.36–0.29, p<0.05). MR analysis showed a unidirectional causal association between left caudal middle frontal surface area and CigDay (βIVW=0.056, pBonferroni=2×10-4). Conclusion Left caudal middle frontal surface area has the potential to serve as a significant predictor of smoking behavior.

Objective: Previous studies have discovered a correlation between cigarette smoking and cortical thickness and surface area, but the causal relationship remains unclear. The objective of this investigation is to scrutinize the causal association between them. Methods: To derive summary statistics from a genome-wide association study (GWAS) on cortical thickness, surface area, and four smoking behaviors: 1) age of initiation of regular smoking (AgeSmk); 2) smoking initiation (SmkInit); 3) smoking cessation (SmkCes); 4) cigarettes per day (CigDay). Linkage disequilibrium score regression (LDSC) was employed to examine genetic association analysis. Furthermore, for traits with significant genetic associations, Mendelian randomization (MR) analyses were conducted. Results: The LDSC analysis revealed nominal genetic correlations between AgeSmk and right precentral surface area, left caudal anterior cingulate surface area, left cuneus surface area, left inferior parietal surface area, and right caudal anterior cingulate thickness, as well as between CigDay and left caudal middle frontal surface area, between SmkCes and left entorhinal thickness, and between SmkInit and left rostral anterior cingulate surface area, right rostral anterior cingulate thickness, and right superior frontal thickness (rg=-0.36–0.29, p<0.05). MR analysis showed a unidirectional causal association between left caudal middle frontal surface area and CigDay (βIVW=0.056, pBonferroni=2×10-4). Conclusion Left caudal middle frontal surface area has the potential to serve as a significant predictor of smoking behavior.

Objective To investigate the mechanism of astragalus polysaccharide(APS)in inhibiting the proliferation and metastasis of osteosarcoma cells.Methods Cell counting kit-8(CCK8)assay was used to detect the inhibitory effect of APS on the proliferation of osteosarcoma cell lines U2OS,HOS,MG63 and osteoblast cell line hFOB1.19,the cell line with the most significant inhibitory effect of APS on osteosarcoma cells was selected for subsequent experiments.Osteosarcoma cells were divided into control group(NC group),APS group,APS+sh-SP1 co treatment group with transfected SP1 knockdown plasmid(APS+sh-SP1),and APS+oe SP1 co treatment group with transfected SP1 overexpression plasmid(APS+oe SP1 group).Western blotting was used to detect the expression of SP1 protein in each group.CCK8 assay was used to detect the proliferation ability of each group.Transwell assay was used to detect the metastatic ability of cells in each group.TOP/FOP Flash assay was used to detect the activity of Wnt/β-catenin signaling pathway.The protein expressions of Wnt3a,β-catenin,CyclinD1,cMYC,matrix metalloproteinase 2(MMP2)and Snail were detected by western blotting.Result After 48h of APS treatment,the cell proliferation inhibition rates of osteosarcoma cells U2OS,HOS,MG63 and osteoblast cells hFOB1.19 were 62.93%±4.79%,20.66%±1.10%,39.31%±3.20%and 5.97%±0.72%,respectively.Compared with osteoblast hFOB1.19,APS significantly inhibited the proliferation of osteosarcoma cells,and the difference was statistically significant(F=208.400,P<0.001),and the inhibitory effect on osteosarcoma U2OS cells was the most significant(t=20.380,P<0.001).Compared with NC group,SP1 protein expression,cell proliferation ability,number of transmembrane cells,Wnt/β-catenin signaling pathway activity in cells,Wnt/β-catenin signaling pathway key proteins Wnt3a,β-catenin,downstream proliferation-related protein CyclinD1,cMYC,and downstream metastasis related proteins MMP2 and Snail in the APS group were decreased,and the differences were statistically significant(t=9.740～90.780,all P<0.05).Compared with the APS group,the expression of SP1 protein,cell proliferation ability,the number of transmembrane cells,the activity of Wnt/β-catenin signaling pathway and the expression of Wnt/β-catenin signaling pathway related proteins in the APS+sh-SP1 group were further decreased,and the differences were statistically significant(t=3.032～12.940,all P<0.05).Compared with the APS group,the expression of SP1 protein,cell proliferation ability,the number of transmembrane cells,the activity of Wnt/β-catenin signaling pathway and the expression of Wnt/β-catenin signaling pathway related proteins in the APS+oe-SP1 group were increased,and the differences were statistically significant(t=3.350～22.450,all P<0.05).Conclusion APS inhibits the proliferation and metastasis of osteosarcoma cells by targeting SP1/Wnt/β-catenin signaling axis.

Objective To investigate the value of a nomogram model constructed from intratumoral and peritumoral magnetic resonance imaging radiomics combined with clinical characteristics in predicting the status of lymphovascular space invasion(LVSI)in cervical cancer.Methods A retrospective analysis was conducted on 178 cervical cancer patients confirmed by postoperative pathology,with 70 cases of LVSI(+)and 108 cases of LVSI(-).The patients were divided into a training set[142 cases,including 54 cases of LVSI(+)and 88 cases of LVSI(-)]and a test set[36 cases,including 16 cases of LVSI(+)and 20 cases of LVSI(-)]at a ratio of 8:2.All underwent magnetic resonance imaging before surgery,and regions of interest were manually delineated layer by layer on the T2WI sequence,with the peritumoral region being uniformly expanded outward.Univariate logistic analysis was performed on clinical factors to select independent factors for cervical cancer LVSI(+).Radiomic features were extracted separately from the intratumoral region,the peritumoral region,and the intratumoral-peritumoral region to construct radiomics models,and the differences between the peritumoral and the intratumoral-peritumoral models were compared.A combined model was established based on the radiomics scores of the optimal intratumoral-peritumoral model and clinical independent predictive factors,and a nomogram was plotted.Receiver operating characteristic curves were used to evaluate the diagnostic performance of each model,and decision curve analysis was used to assess the clinical value of the models.Results The combined model demonstrated the best performance among the various models,with AUC of 0.970 in the training set and 0.803 in the test set.Conclusion Intratumoral and peritumoral magnetic resonance imaging radiomics combined with clinical characteristics can effectively predict LVSI in cervical cancer.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.

Objective:To identify additional loci associated with depression and the hippocampus (HIP) through genome-wide association study.Methods:The depression-related genome-wide association study (GWAS) meta summary data was downloaded from the official website of the Psychiatric Genomics Consortium, which had involved 170 756 cases and 329 443 controls. The left and right hippocampal volume GWAS data sets were downloaded from the UK Biobank, which involved 33 224 participants. The conditional false discovery rate (condFDR) was used to identify novel genetic loci for depression and left and right hippocampal volumes, and a conjunctional false discovery rate (conjFDR) was used to evaluate the enrichment of pleiotropic loci between depression and left and right hippocampal volumes.Results:Respectively, 7, 13, and 12 new loci have been associated with depression, left hippocampal volume and right hippocampal volume, with a significant threshold of condFDR < 0.01. A site of rs1267073 locus was found to be shared by the depression and right hippocampal volume with a threshold of conjFDR < 0.01.Conclusion:Above findings have provided more insights into the genetic mechanisms underlying the volume of hippocampus and the risk for depression. The results may also provide evidence for future clinical trials for treating depression.