Objective To explore the characteristic appearance of MR imaging of atypical craniopharyngioma and improve the diagnostic accuracy.Methods 8 atypical craniopharyngioma were analyzed retrospectively by MR imaging,which had been confirmed by pathology.Results 3 atypical craniopharyngiomas were cystic lesions, 2 were solid lesions, and rest 3 were solid-cystic lesions.The cystic lesion presented variable intensities on T1-weighted imaging (T1WI);and the wall was remarkably enhanced and uniform in thickness.The solid lesions presented hypointense on diffusion weighted imaging (DWI), and reticular enhancement.Solid-cystic tumors presented heterogeneous enhancement.In these lesions,4 lesions in sellar and suprasellar regions were misdiagnosed as pituitary macroadenoma,because of the unclear boundary between the lesions and pituitary gland.2 lesions in superasellar region were misdiagnosed as germinoma, for the remarkable enhancement.And 2 cases in superasellar region were misdiagnosed as pilocytic astrocytoma,for indistinct boundary between lesions and pituitary stalk and optic chiasma.Conclusion The MR imaging characteristics can help distinguish atypical craniopharyngioma from pituitary macroadenoma,sellar germinoma and pilocytic astrocytoma.

Objective To investigate the application value of multi-slice CT enterography (MSCTE)in diagnosing intestinal tuberculosis (ITB)and Crohn’s disease (CD).Methods MSCTE findings were retrospectively analyzed in 25 patients with ITB and in other 25 patients with CD diagnosed through endoscopy,pathologic examination and clinical follow-up.Statistical analysis was performed to find out the difference in CT findings between the ITB and CD.Results 25 patients with CD included the involved ileum in 23,involved duode-num and jejunum in 8,multiple segmental lesions in 20,asymmetrically thickened intestinal wall in 20,hierarchical reinforcement in 1 9,mesenteric vascular hyperplasia in 20,fibrofatty hyperplasia in 18,peritoneal abscess or fistula in 8,anal fistula in 1,and pseu-do-diverticulum formation in the intestinal wall on the opposite side of the mesentery in 2.Meanwhile,the other 25 patients with ITB included the involved terminal ileum in 25,symmetrically thickened intestinal wall in 23,annular enhancement of lymph nodes in 11,thickened peritoneum and omentum together with distinct enhancement,or intestinal adhesion,or ascites appeared in 15.The CD was more likely to represent multiple segmental lesions,asymmetrically thickened intestinal wall,hierarchical reinforcement,mesenteric vascular hyperplasia,fibrofatty hyperplasia,and peritoneal abscess or fistula formation (P <0.05).Meanwhile,the ITB was more likely to represent the lesion only in ileum,symmetrically thickened intestinal wall,and annular enhancement of lymph nodes (P <0.05).Conclusion MSCTE shows promising clinical application in diagnosis and differential diagnosis of CD and ITB.

Objective To examine brain regions with a functional connection to posterior cingulate cortex (PCC) in a relapsing-remitting multiple sclerosis (RRMS) group compared with matched control subjects,and to employ resting-state functional MRI (rs-fMRI) to PCC connectivity gathered by investigating synchronic low frequency fMRI signal fluctuations of default mode network with seed-based correlation analysis (SCA).Methods Twenty-seven patients with RRMS (RRMS group) and 27 age-,and sexmatched healthy controls (HC group) were examined by resting-state fMRI,DTI and 3D-T1 on Siemens Trio Tim 3.0T.The fMRI data preprocessing and processing was performed using Data Processing Assistant for Resting-State fMRI Advanced Edition (DPARSFA) based on Matlab 2012a,and PCC (-5,-49,40)was selected as seed.An SCA approach was used to analyze the rs-fMRI data.We examined the differences in SCA-derived connectivity metrics in patients with RRMS and healthy controls,and analyzed correlations between connectivity correlation coefficient of the differences regions and MRI-derived metrics (brain parenchymal fraction,T2 lesion load),as well as clinical metrics (expanded disability status scale,paced auditory serial addition test,and disease duration) of the disease.Results The SCA via functional connectivity of PCC showed that the temporal correlation between the blood-oxygen-level-dependent signals of the default mode network was reliable spatial patterns of activation in patients with RRMS.The lower connectivity in right superior frontal gyrus within default mode network,and higher connectivity in right posterior lobe of cerebellum,right crus of cerebellum,right medial frontal gyrus,right medial occipital gyrus,left precuneus/cingulate gyrus,right angular gyrus and right cingulate gyrus were found in our study.Significant negative-related was observed between the paced auditory serial addition test and functional connectivity in right middle temporal gyrus (0.387 ± 0.216) of RRMS patients (r =-0.59,P =0.001).Significant negative correlation also was observed between the course of disease and functional connectivity in right superior frontal gyrus (0.039 ± 0.293) in patients (r =-0.39,P =0.041).There was no significant correlations between other regions with different functional connectivity and expanded disability status scale,disease duration,or brain atrophy.The connectivity in right superior frontal gyrus,left medial occipital gyrus,left precentral gyrus was decreased; and connectivity in right cerebellum anterior lobe (dentate),right frontal lobe white matter was significantly increased.Significant positive correlation was observed between the course of disease and functional connectivity in left precentral gyrus (-0.924 ± 0.253),right cerebellum anterior lobe (dentate ;0.217 ± 0.208) of RRMS patients (r =0.650,P =0.000;r =0.436,P =0.023),respectively.Conclusion These findings reveal the compensatory mechanism of the brain in response to structural damage,by means of increased activation or synchronization of default mode network,which seems to be finite.

Precancerous lesions of gastric cancer （PLGC） are a group of pathological changes caused by abnormalities in the structure， morphology， and differentiation of gastric mucosal epithelial cells. Since the early symptoms are hidden and non-specific， PLGC is not easy to be diagnosed and it has often developed into intermediate or advanced gastric cancer once being diagnosed and missed the best time for treatment. Accordingly， the incidence of this disease is increasing year by year， which lifts a heavy burden on the patients. The pathogenesis of PLGC is complex， involving inflammatory microenvironment， bile reflux， glycolysis， autophagy， and apoptosis. Currently， PLGC is mainly treated with anti-inflammatory and endoscopic therapies， which are difficult to curb the development of PLGC. Therefore， seeking a safe and effective therapy is an important topic of modern research. Traditional Chinese medicine （TCM）， characterized by treatment based on syndrome differentiation and a holistic view， exerts effects via multiple pathways， mechanisms， and targets. Recent studies have confirmed that TCM can regulate the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR）， Wnt/β-catenin， Sonic Hedgehog， nuclear factor-κB （NF-κB）， Janus kinase/signal transducer and activator of transcription （JAK/STAT）， hypoxia-inducible factor-1α （HIF-1α）， neurogenic locus notch homolog protein （Notch）， nuclear factor E₂-related factor 2 （Nrf2） and other signaling pathways. By targeting these pathways， TCM can inhibit aerobic glycolysis， reduce oxidative stress， repair the inflammatory microenvironment， regulate cellular autophagy， and promote vascular normalization， thereby delaying or reversing PLGC. However， few researchers have systematically summarized the TCM regulation of PLGC-associated pathways. By reviewing the relevant articles at home and abroad， this paper summarized the roles of the above signaling pathways in the development of PLGC and the research progress in the regulation of signaling pathways by TCM in the treatment of PLGC， with a view to providing a new theoretical basis for the clinical research on PLGC and the drug development for this disease.