Objective:To explore CT and MRI features of the endolymphatic sac tumor (ELST).Methods:The CT and MRI morphology confirmed by surgical pathology for 19 patients with ELST were retrospectively analyzed from June 2011 to May 2019 in Eye & ENT Hospital of Fudan University. The features of CT and MRI included location, size, adjacent structures invasion, CT values, bone destruction, features of T 1WI and T 2WI, enhancement distribution characteristics, dynamic enhancement curve morphology, DWI signal characteristics. The ADC values of the lesions and ipsilateral medial pterygoid muscles were compared using a paired t test. Results:Nineteen ELST patients (one with bilateral diseases) were included. Totally 20 ears (right 9 and left 11) of 13 females and 6 males were studied. The masses with slightly high-density and obscure boundary were located around the vestibular aqueduct at the posterior edge of the petrosal bone. Bone destruction involved mastoid process of the middle ear (16 ears), jugular foramen (11 ears), semicircular canal (10 ears), facial nerve canal (7 ears) and internal auditory canal (9 ears). A large amount of residual bone could be found in the interior of nineteen masses. The CT value was (78.6±21.9) HU. The lesion showed central iso-intensity and peripheral hyperintensity on T 1WI and T 2WI in 16 ears, while no obvious hyperintensity on T 1WI in the other 4 ears. The hyperintensity on T 1WI was around the margin of the lesion in 10 ears, situated at lateral side in 5 ears and all over the lesion in 1 ear. Flow voids signals could be seen in 9 ears as well. Liquid-liquid plane was seen on T 2WI in 2 ears. The solid mass portion which showed iso-intensity on both T 1WI and T 2WI presented marked enhancement on contrast-enhanced T 1WI, while other part of the mass no enhancement. DWI of 14 ears illustrates no evidence of restricted diffusion, and the ADC value [(1.25±0.08)×10 -3 mm 2/s] was slightly higher than that of the medial pterygoid muscles ( t=4.437, P=0.001). The style of time-signal intensity curves of the dynamic contrast-enhanced MRI was rapidly ascending followed by descending curves in 2 ears. Conclusion:Imaging findings of ELST have some characteristics, including located around the vestibular aqueduct at the posterior edge of the petrosal bone, bone destruction, peripheral hyperintensity on T 1WI and no restricted diffusion, which is helpful for its diagnosis.

21-hydroxylase deficiency(21-OHD) is mainly characterized by cortisol deficiency with or without aldosterone deficiency and hyperandrogenemia.The disease requires lifelong exogenous glucocorticoid/salt supplementation.Excessive doses of exogenous glucocorticoids are often needed to control hyperandrogenemia, but the effect is not satisfactory.Corticotropin releasing factor (CRF) type 1 receptor antagonist can directly block the production of adrenocorticotropin, inhibit the generation of adrenogenic androgen, reduce the dose of glucocorticoid therapy, and thus lower the incidence of adverse reactions.In this article, the current research progress on 21-OHD therapy and CRF1 receptor antagonist was reviewed.

BACKGROUND:High-methionine diet can cause liver injury in Cbs+/-mice,and hyperhomocystinemia is related to the occurrence and progression of various liver-related diseases,such as hepatic steatosis,autoimmune hepatitis,and alcoholic fatty liver disease.MicroRNAs(miRNAs)are involved in various cellular processes including cell survival,differentiation and autophagy,which are of great significance. OBJECTIVE:To investigate the critical role of miR-144-3p on Cbs+/-mouse hepatocyte autophagy induced by high methionine die. METHODS:(1)Ten male cystathione-β-synthase normal(Cbs+/+)mice and another 10 male mice with single gene knockout(Cbs+/-)of similar body mass,4 weeks of age,were fed a high-methionine diet and executed after 12 weeks to take liver tissue.(2)Human hepatocytes(HL-7702)were cultured in vitro and divided into control[0 μmol/L homocysteine(Hcy)],Hcy(100 μmol/L Hcy),mimic-NC(transfected with mimic-NC),mimic-NC + Hcy(mimic-NC transfecton+100 μmol/L Hcy),miR-144-3p mimic(transfected with miR-144-3p mimic),and miR-144-3p mimic + Hcy(miR-144-3p mimic transfection+100 μ mol/L Hcy),inhibitor-NC(transfected with inhibitor-NC),inhibitor-NC + Hcy(inhibitor-NC transfection + 100 μmol/L Hcy),miR-144-3p inhibitor(transfected with miR-144-3p inhibitor),and miR-144-3p inhibitor + Hcy(miR-144-3p inhibitor transfection + 100 μmol/L Hcy).Quantitative real-time PCR was used to detect the expression of miR-144-3p in liver tissue and hepatocytes.After transfection of miR-144-3p mimic or inhibitor,quantitative real-time PCR and western blot were used to detect the transfection efficiency of miR-144-3p and its effect on the expression of autophagy-related proteins LC3B and p62.The levels of alanine transferase and aspartate aminotransferase in hepatocyte supernatants were determined by enzyme linked immunosorbent assay.The correlation between the expression of miR-144-3 in hepatocyte and the levels of alanine transferase and aspartate aminotransferase in hepatocyte supernatants were analyzed by Pearson correlation analysis. RESULTS AND CONCLUSION:Compared with the Cbs+/+ group and control group,the expression of miR-144-3p in the liver tissue of the Cbs+/-group and in hepatocytes of the Hcy group was decreased(P<0.01).The expression of LC3B-Ⅱ/Ⅰ was decreased in hepatocyte after transfection of miR-144-3p mimic,while the protein expression of p62 was increased(P<0.01).The opposite results were obtained after transfection of miR-144-3p inhibitor(P<0.01).Compared with the mimic-NC group,the levels of alanine transferase and aspartate aminotransferase were decreased in the miR-144-3p mimic group(P<0.01),while the opposite results were obtained in the inhibitor-NC group(P<0.01).The expression of miR-144-3p in hepatocytes was negatively correlated with the levels of alanine transferase(P<0.01,r=-0.887 6)and aspartate aminotransferase(P<0.01,r=-0.829 9)in the supernatant of hepatocytes.To conclude,Hcy promotes hepatocyte autophagy by inhibiting the expression of miR-144-3p,which subsequently aggravates liver injury.