Organizing Pneumonia in A Patient Double-Positive for ANCA and Anti-GBM Antibodies:A Case Report

Both anti-glomerular basement membrane(GBM)disease and the anti-neutrophil cytoplasmic antibody(ANCA)-associated vasculitis(AAV)are common causes of pulmonary-renal syndrome.Organizing pneumonia(OP),a special pattern of interstitial lung disease,is extremely rare either in AAV or anti-GBM disease.We report an old woman presented with OP on a background of co-presentation with both ANCA and anti-GBM antibodies.

Effects of Glucocorticoid?Induced Transcript 1 Gene Deficiency on Glucocorticoid Activation in Asthmatic Mice

Background: Glucocorticoid (GC) is the first?line therapy for asthma, but some asthmatics are insensitive to it. Glucocorticoid?induced transcript 1 gene (GLCCI1) is reported to be associated with GCs efficiency in asthmatics, while its exact mechanism remains unknown. Methods: A total of 30 asthmatic patients received fluticasone propionate for 12 weeks. Forced expiratory volume in 1 s (FEV1) and GLCCI1 expression were detected. Asthma model was constructed in wild?type and GLCCI1 knockout (GLCCI1?/?) mice. Glucocorticoid receptor (GR) and mitogen?activated protein kinase phosphatase 1 (MKP?1) expression were detected by polymerase chain reaction and Western blotting (WB). The phosphorylation of p38 mitogen?activated protein kinase (MAPK) was also detected by WB. Results: In asthmatic patients, the change of FEV1 was well positively correlated with change of GLCCI1 expression (r = 0.430, P = 0.022). In animal experiment, GR and MKP?1 mRNA levels were significantly decreased in asthmatic mice than in control mice (wild?type: GR: 0.769 vs. 1.000, P = 0.022; MKP?1: 0.493 vs. 1.000, P < 0.001. GLCCI1?/?: GR: 0.629 vs. 1.645, P < 0.001; MKP?1: 0.377 vs. 2.146, P < 0.001). Hydroprednisone treatment significantly increased GR and MKP?1 mRNA expression levels than in asthmatic groups; however, GLCCI1?/?.asthmatic mice had less improvement (wild?type: GR: 1.517 vs. 0.769, P = 0.023; MKP?1: 1.036 vs. 0.493, P = 0.003. GLCCI1?/?: GR: 0.846 vs. 0.629, P = 0.116; MKP?1: 0.475 vs. 0.377, P = 0.388). GLCCI1?/? asthmatic mice had more obvious phosphorylation of p38 MAPK than wild?type asthmatic mice (9.060 vs. 3.484, P < 0.001). It was still higher even though after hydroprednisone treatment (6.440 vs. 2.630, P < 0.001). Conclusions: GLCCI1 deficiency in asthmatic mice inhibits the activation of GR and MKP?1 and leads to more obvious phosphorylation of p38 MAPK, leading to a decremental sensitivity to GCs.

Using posterior part of the deltoid muscle as receptor and quality control with intra-operative electrophysiological examination in targeted muscle reinnervation for high-level upper extremity amputees

To the Editor:Targeted muscle reinnervation(TMR)is a surgical technique of multiple nerve transfers,providing a potential of improved intuitive prosthetic control via surface electromyography(sEMG)in the high-level upper extremity amputees.[1]However,there is a risk that some of the reinnervations might be unsuccessful,especially for the ulnar nerve.[2]Both the quality control of nerve stumps and the receptor are important factors for the surgery.Assessing the nerve stumps during the surgery and finding more muscles as receptor might address the problem.Biceps,triceps,and brachialis muscles were mostly chosen as receptors for reinnervation in the trans-humeral amputees.Pectoralis major and pectoralis minor were mostly chosen as receptors for reinnervation in the shoulder disarticulation patients.