Objective To summarize the imaging features of intracranial solitary fibrous tumors (ISFT).Methods Ten patients with ISFT proven histopathologically were collected.Four cases had CT data and all cases had MR data.The imaging features and pathological results were retrospectively analyzed.Results All cases were misdiagnosed as meningioma at pre-operation.All lesions arose from intracranial meninges including 5 lesions above the tentorium,4 lesions beneath the tentorium and 1lesion growing around the tentorium.The margins of all the masses were well defined,and 8 lesions presented multilobular shape.CT demonstrated hyerattenuated masses in all 4 lesions,smooth erosion of the basicranial skull in 1lesion,and punctiform calcification of the capsule in 1lesion.T1WI showed most lesions with isointense or slight hyperintense signals including homogeneous in 4 lesions and heterogeneous in 6 lesions.T2WI demonstrated isointense or slight hyperintense in 2 lesions,mixed hypointense and hyperintense signals in 4,cystic portion in 2,and two distinct portion of hyperintense and hypointense signal,so called “yin-yang”pattern,in 2.Strong enhanced was found in all lesions,especially in 8 lesion with heterogeneous with the low T2 signal.“Dural tail” was found in 4 lesions.Conclusions ISFI has some specific CT and MR features including heterogeneous signal intensity on T2WI,strong enhancement of areas with low T2 signal intensity,slight or no “dural tail”,without skull thickening,and the typical “yin-yang” pattern.

Objective: To explore the correlation between gross motor development and physical activity level of preschool children at different altitudes, so as to provide exercise basis for the development of gross motor ability. Methods: A total of 188 preschool children living in the 3 240 m high plateau (Hi group) in Tashkurgan County, 175 children living in the 1 290 m low plateau (SubHi group) in Kashgar District and 191 children living in the 450 m high plateau (Pla group) in Gaochang District of Turpan were selected as subjects. The children were assessed for gross motor development and tested for physical activity. Results: With the increase of age, the scores of MPA, VPA, MVPA and gross movement of preschoolers in each test group showed an upward trend. The above indexes in SubHi group were significantly higher than those in Hi group at 5 years old, and those in Pla group at 5 years old were significantly higher than those in Hi group ( P <0.05). The level of MPA in SubHi group and Pla group was significantly higher than that in Hi group at 4 years old, and the MVPA in SubHi group at 5 years old was significantly higher than that in Hi group ( P <0.05). SubHi group and Pla group were significantly higher than Hi group at 5 years of age, and Pla group was significantly higher than SubHi group at 4 years of age ( P <0.05). There were no significant differences in the related indexes of gross motor among girls at different altitude groups ( P >0.05). The LPA of the Hi group and the SubHi group was positively correlated with the operational movement score ( r =0.60,0.44), and the LPA of the Pla group was positively correlated with the displacement movement score ( r =0.69).There was a positive correlation between MPA and displacement score of Hi group ( r =0.53), displacement score and gross movement total score of SubHi group ( r =0.45,0.59), and gross movement scores of Pla group ( r =0.69, 0.52 , 0.73). Except the displacement score and gross movement total score of the Pla group, VPA was positively correlated with the gross movement scores of each group ( P <0.05). Conclusion There is a certain correlation between gross motor development and physical activity level in children aged 3-6 years.MVPA can be used as an effective means to improve the development of rough movements of 3-6 year old children.

BACKGROUND/AIMS: MicroRNAs (miRNAs) were reported to be responsible for intestinal permeability in diarrhea-predominant irritable bowel syndrome (IBS-D) rats in our previous study. However, whether and how miRNAs regulate visceral hypersensitivity in IBS-D remains largely unknown. METHODS: We established the IBS-D rat model and evaluated it using the nociceptive visceral hypersensitivity test, myeloperoxidase activity assay, restraint stress-induced defecation, and electromyographic (EMG) activity. The distal colon was subjected to miRNA microarray analysis followed by isolation and culture of colonic epithelial cells (CECs). Bioinformatic analysis and further experiments, including dual luciferase assays, quantitative real-time polymerase chain reaction, western blot, and enzyme-linked immunosorbent assay, were used to detect the expression of miRNAs and how it regulates visceral hypersensitivity in IBS-D rats. RESULTS: The IBS-D rat model was successfully established. A total of 24 miRNAs were differentially expressed in the distal colon of IBS-D rats; 9 were upregulated and 15 were downregulated. Among them, the most significant upregulation was miR-200a, accompanied by downregulation of cannabinoid receptor 1 (CNR1) and serotonin transporter (SERT). MiR-200a mimic markedly inhibited the expression of CNR1/SERT. Bioinformatic analysis and luciferase assay confirmed that CNR1/SERT are direct targets of miR-200a. Rescue experiments that overexpressed CNR1/SERT significantly abolished the inhibitory effect of miR-200a on the IBS-D rats CECs. CONCLUSIONS: This study suggests that miR-200a could induce visceral hyperalgesia by targeting the downregulation of CNR1 and SERT, aggravating or leading to the development and progression of IBS-D. MiR-200a may be a regulator of visceral hypersensitivity, which provides potential targets for the treatment of IBS-D.
Animals ; Blotting, Western ; Colon ; Computational Biology ; Defecation ; Diarrhea ; Down-Regulation ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells ; Hyperalgesia ; Hypersensitivity ; Irritable Bowel Syndrome ; Luciferases ; Microarray Analysis ; MicroRNAs ; Models, Animal ; Permeability ; Peroxidase ; Rats ; Real-Time Polymerase Chain Reaction ; Receptors, Cannabinoid ; Serotonin Plasma Membrane Transport Proteins ; Serotonin ; Up-Regulation

BACKGROUND: The switch/sucrose nonfermentable chromatin-remodeling (SWI/SNF) complex is a pivotal chromatin remodeling complex, and the genomic alterations (GAs) of the SWI/SNF complex are observed in several cancer types, correlating with multiple biological features of tumor cells. However, their role in liver metastasis of non-small cell lung cancer (NSCLC) remains unclear. Our study aims to investigate the role and potential mechanisms underlying NSCLC liver metastasis induced by the GAs of SWI/SNF complex. METHODS: The GAs of SWI/SNF complex in NSCLC cell lines (H1299, H23 and H460) were identified by whole-exome sequencing (WES). ARID1A knockout H1299 cell was constructed with the CRISPR/Cas9 technology. The mouse model of liver metastasis from NSCLC was established to simulate lung cancer liver metastasis and observe the metastasis rate under different gene mutation conditions. RNA sequencing and Western blot were conducted for differential gene expression analysis. Immunohistochemistry (IHC) analysis was used to assess protein expression levels of SWI/SNF-regulated target molecules in mouse liver metastases. RESULTS: WES analysis revealed intracellular gene mutations. The animal experiments demonstrated a correlation between the GAs of SWI/SNF complex and a higher liver metastasis rate in immunodeficient mice. Transcriptome sequencing and Western blot analysis showed upregulated expression of ALDH1A1 and APOBEC3B in SWI/SNF-mut cells, particularly in ARID1A-deficient H460 and H1299 sgARID1A cells. IHC staining of mouse liver metastases further demonstrated elevated expression of ALDH1A1 in the H460 and H1299 sgARID1A group. CONCLUSIONS This study underscores the critical role of the GAs of SWI/SNF complex, such as ARID1A and SMARCA4, in promoting liver metastasis of lung cancer cells. The GAs of SWI/SNF complex may promote liver-specific metastasis by upregulating ALDH1A1 and APOBEC3B expression, providing novel insights into the molecular mechanisms underlying lung cancer liver metastasis.
Animals ; Mice ; Carcinoma, Non-Small-Cell Lung/genetics* ; Lung Neoplasms/genetics* ; Mutation ; Liver Neoplasms/genetics*