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: 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.

Liver cancer has high morbidity and mortality worldwide.Traditional morphological imaging can offer crucial anatomical information for the diagnosis and treatment of liver cancer,and when combined with the functional data shown by PET imaging,the diagnostic accuracy of tumors can be further improved and assisted in treatment selection.Fibroblast activation protein(FAP),a signature protein of cancer-associated fibroblasts,is highly expressed in a variety of malignant tumors of epithelial origin and is an important target for tumor diagnosis and treatment.Compared with routinely applied 18F-fluorodeoxyglucose(FDG)PET imaging,FAP inhibitor(FAPI)PET imaging has the advantages of high image contrast and independence from blood glucose.In recent years,a variety of radiopharmaceuticals targeting FAP have been continuously expanded in the diagnosis,staging and targeted therapy of different liver cancer types,and the progress of their related applications is reviewed in this paper.

Objective:To investigate the relationship between 1p/16q loss of heterozygosity (LOH) and 1p gain in Wilms tumor and their clinicopathologic characteristics and prognosis.Methods:A total of 175 Wilms tumor samples received from the Department of Pathology, Beijing Children′s Hospital from September 2019 to August 2022 were retrospectively analyzed. The histopathologic type and presence of lymph node involvement were evaluated by two pathologists. The clinical data including patients′gender, age, tumor location, preoperative chemotherapy, and tumor stage were summarized. Fluorescence in situ hybridization (FISH) was done to detect 1p/16q LOH and 1p gain and their correlation with the clinicopathological features and prognosis were analyzed.Results:Among the 175 samples, 86 cases (49.1%) were male and 89 (50.9%) were female. The mean age was (3.5±2.9) years, and the median age was 2.6 years. There were 26 (14.9%) cases with 1p LOH, 28 (16.0%) cases with 16q LOH, 10 (5.7%) cases of LOH at both 1p and 16q, and 53 (30.3%) cases with 1q gain. 1q gain was significantly associated with 1p LOH ( P<0.01) and 16q LOH ( P<0.01). There were significant differences ( P<0.01) between 1q gain, 1p LOH and 16q LOH among different age groups. The rate of 16q LOH in the high-risk histopathological subtype (50.0%) was significantly higher than that in the intermediate-risk subtype (13.6%, P<0.05). The frequency of 1q gain, 1p LOH, and 16q LOH in children with advanced clinical stages (Ⅲ and Ⅳ) was significantly higher than that in children with early clinical stages (Ⅰ and Ⅱ). 1q gain, 1p LOH, and 16q LOH showed no significant correlation with gender, unilateral or bilateral disease, chemotherapy, or lymph node metastasis. The progression-free survival (PFS) time for patients with 1q gain and 1p LOH was significantly shorter than those without these aberrations ( P<0.05). Additionally, the PFS time of patients with 16q LOH was slightly shorter than those with normal 16q, although the difference was not statistically significant. Patients with stage Ⅲ to Ⅳ disease exhibiting 1q gain or 1p LOH had a significantly higher relative risk of recurrence, metastasis, and mortality. Conclusions:1p/16q LOH and 1q gain are associated with age, high-risk histological type, and clinical stage in Wilms tumor. 1q gain and 1p LOH are significantly correlated with the prognosis of Wilms tumor.

Objective:To observe the expression of microRNA (miRNA)-7159-5p in gastric cancer tissues, and explore its effect on the proliferation and invasion of gastric cancer cells and its molecular mechanism.Methods:The cancer tissues and adjacent tissues of 29 patients with gastric cancer who underwent surgical resection in Hubei 672 Orthopedic Hospital of Integrated Traditional Chinese and Western Medicine from March 2018 to November 2019 were collected. Fluorescence real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-7159-5p in gastric cancer tissues and adjacent tissues, gastric cancer cell lines and normal gastric epithelial cell lines. Select the cell line with the lowest expression of miR-7159-5p, set the control group and the experimental group, and be transfected with control and miR-7159-5p mimics respectively. qRT-PCR was used to detect the expression of miR-7159-5p in transfected cells. The lymphocyte proliferation test (MTS method) was used to detect the proliferation of transfected cells, and the Transwell chamber method was used to detect the invasion activity of transfected cells. The miRNAMap database and dual luciferase reporter gene experiment were used to predict and verify the target genes of miR-7159-5p. qRT-PCR and Western blot were used to detect the expression of target genes in transfected cells.Results:The expression of miR-7159-5p in gastric cancer tissues was lower than that in adjacent tissues ( P<0.01), the expression of miR-7159-5p in gastric cancer cell lines was lower than that of normal gastric epithelial cells (all P<0.01), and the expression of miR-7159-5p was the lowest in SGC7901 cells ( P<0.01). After transfection, the expression of miR-7159-5p in SGC7901 cells of the experimental group was significantly higher than that in the control group ( P<0.01). After transfection, the proliferation activity and the cell invasion activity of the experimental group was significantly lower than that of the control group (all P<0.01). The target gene of miR-7159-5p was tripartite motif 26 (TRIM26). After transfection, the expression of TRIM26 mRNA in SGC7901 cells of the experimental group was significantly lower than that in the control group ( P<0.01). Western blot showed that after transfection, the expression of TRIM26, c-Myc, cyclin D1, β-catenin protein were lower than those in the control group (all P<0.05). Conclusions:The expression of miR-7159-5p is low in gastric cancer tissues, and miR-7159-5p can inhibit the proliferation and invasion of SGC7901 cells by down-regulating the expression of TRIM26.

Objective    To compare the clinical effects of segmentectomy and lobectomy for ≤2 cm lung adenocarcinoma with micropapillary and solid subtype negative by intraoperative frozen sections. Methods    The patients with adenocarcinoma who received segmentectomy or lobectomy in multicenter from June 2020 to March 2021 were included. They were divided into two groups according to a random number table, including a segmentectomy group (n=119, 44 males and 75 females with an average age of 56.6±8.9 years) and a lobectomy group (n=115, 43 males and 72 females with an average of 56.2±9.5 years). The clinical data of the patients were analyzed. Results    There was no significant difference in the baseline data between the two groups (P>0.05). No perioperative death was found. There was no statistical difference in the operation time (111.2±30.0 min vs. 107.3±34.3 min), blood loss (54.2±83.5 mL vs. 40.0±16.4 mL), drainage duration (2.8±0.6 d vs. 2.6±0.6 d), hospital stay time (3.9±2.3 d vs. 3.7±1.1 d) or pathology staging (P>0.05) between the two groups. The postoperative pulmonary function analysis revealed that the mean decreased values of forced vital capacity and forced expiratory volume in one second percent predicted in the segmentectomy group were significantly better than those in the lobectomy group (0.2±0.3 L vs. 0.4±0.3 L, P=0.005; 0.3%±8.1% vs. 2.9%±7.4%, P=0.041). Conclusion    Segmentectomy is effective in protecting lungs function, which is expected to improve life quality of patients.

Objective:To investigate the expression of long non-coding RNA (lncRNA) ALMS1-IT1 in colorectal cancer tissues and the molecular mechanism of its effect on the proliferation and migration of colorectal cancer HT-29 cells in vitro.Methods:The cancer tissue specimens and paracancerous tissue (>5 cm from the edge of the tumor) specimens were collected from 40 colorectal cancer patients who were diagnosed by pathological examination after surgical resection in Hubei 672 Orthopedic Hospital of Integrated Traditional Chinese and Western Medicine from July 2018 to November 2020. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of ALMS1-IT1 in colorectal cancer tissues and paracancerous tissues, when the relative expression of ALMS1-IT1 was higher than or equal to its median relative expression, ALMS1-IT1 was highly expressed, and the correlation of ALMS1-IT1 expression with the clinicopathological characteristics of patients was analyzed. HT-29 cells were infected with the empty lentivirus and the lentivirus carrying the ALMS1-IT1 silence sequence, and named control group and si-ALMS1-IT1 group. qRT-PCR was used to detect the expression of ALMS1-IT1 in the two groups of HT-29 cells. CCK-8 method and Transwell experiment were used to detect the proliferation and migration ability of the two groups of HT-29 cells. The starBase v2.0 online database was used to predict ALMS1-IT1 interacting molecules, and qRT-PCR and Western blot were used to detect the expression of these molecules.Results:The relative expression of ALMS1-IT1 in colorectal cancer tissues was higher than that in paracancerous tissues (4.54±0.61 vs. 1.19±0.31, t = 34.89, P < 0.01). The median relative expression of ALMS1-IT1 in cancer tissues of 40 patients was 2.93, and the high expression rate of ALMS1-IT1 was 50.0% (20/40). The high expression rate of ALMS1-IT1 in cancer tissues of TNM stage Ⅲ patients was higher than that in TNM stage Ⅰ-Ⅱ patients, the high expression rate of ALMS1-IT1 in poorly-differentiated patients was higher than that in well- and moderately-differentiated patients, and the high expression rate of ALMS1-IT1 in patients with lymph node metastasis was higher than that in patients without lymph node metastasis (all P < 0.01). The cell proliferation capacity (absorbance value) of HT-29 cells in the si-ALMS1-IT1 group after cultured for 2, 3, 4, and 5 days was lower than that in the control group (all P < 0.05). The number of cell migration at 24 h in HT-29 cells of the si-ALMS1-IT1 group was less than that of the control group (45±7 vs. 112±18, t = 3.45, P < 0.05). Using starBase v2.0 online database to predict that the target gene of ALMS1-IT1 may be miRNA-889-3p (miR-889-3p), and the target gene of miR-889-3p may be ATAD2. Compared with the control group, the relative expression of miR-889-3p in HT-29 cells of the si-ALMS1-IT1 group increased (4.24±0.46 vs. 1.01±0.11, t = 6.81, P < 0.01). Compared with the control group, ATAD2 mRNA ( P < 0.01) and protein expression levels in the si-ALMS1-IT1 group were reduced. Conclusions:ALMS1-IT1 is highly expressed in colorectal cancer tissues, and the ALMS1-IT1 expression is related to the TNM stage, degree of tumor differentiation and lymph node metastasis of patients. Down-regulation of ALMS1-IT1 in vitro may inhibit the proliferation and migration of colorectal cancer HT-29 cells by regulating the miR-889-3p-ATAD2 axis. ALMS1-IT1 may be a therapeutic target for colorectal cancer.