Objective To compare the T cell receptor recombination excision cycle (TREC) levels in peripheral blood mononuclear cells (PBMC) of systemic lupus erythematosus (SLE) patients with normal age- and gender- matched controls. To investigate the correlations between TREC levels of SLE patients and their clinical features. Methods We studied TREC levels in peripheral blood mononuclear cells (PBMC) of 21 SLE patients and 22 normal age- and sex- matched controls. TREC concentration was determined by real-time quantitative polymerase chain reaction (real-time qPCR) as the number of TREC copies/1000 PBMCs. The clinical features of the SLE patients such as systemic lupus erythematosus disease activity index (SLEDAI) , ESR, C reaction protein (CRP) , ANA, anti-dsDNA and complement levels and organ involvement were recorded and assessed. Results SLE patients had lower TREC levels [ (9.6 ± 7.5 )copies/1000 PBMC] than controls[ (16.1 ±11.1) copies/1000 PBMC,P = 0.033]. There was an inverse correlation between age and TREC levels in controls (r =- 0. 614, P = 0. 002) but not in SLE patients.There was an inverse correlation between SLEDAI and TREC levels in SLE patients(r =-0. 656, P =0. 001) and TREC levels seemed to have relations to skin lesions ( r = - 0. 620, P = 0. 003 ). No other clinical association was observed between TREC levels and clinical and laboratory SLE manifestations.Conclusion SLE patients had lower TREC levels than normal controls and there is a tendency that TREC level is reversely correlated with disease activity. The decrease PBMC TREC level is indicative of a low proportion of recent thymic emigrant (RTE) in SLE and could be caused by decreased RTE output and/or by increased peripheral T cell proliferation in this disease. The under-representation of RTE in the peripheral T cell pool may play a role in the immune tolerance abnormalities observed in SLE.

Objective To investigate the effect of electroacupuncture(EA)in improving the reconstruction of synapse after cerebral ischemia.Methods Forty-five Wistar rats were divided into 3 groups:sham-operated group,ischemia group and EA group.The number density(Nv)of synapses and the surface density(Sv)of synaptic joint band were observed 1 hour,1 day,3 days,1 week and 3 weeks after ischemia and EA, respectively.Heat-coagulation-induced occlusion of the middle cerebral artery was performed to establish the model of focal cerebral ischemia.EA group received EA on the acupoints of Baihui and Dazhui.The changes of synaptie structure,Nv and Sv as well as the influence of EA on the above indexes were observed in different time.Results There existed significant decrease of Nv and Sv 1 hour,1 day and 3 days after establishment of models in the isehemia group(P0.05).Conclusion EA can reduce the cerebral ischemic injury by increasing the synaptic amount and area in the cortex of rat model of cerebral isehemia at early stage,promoting the cerebral recovery after ischemia,which will provide substantial morphological basis for the improvement of synaptic reconstruction and recovery from cerebral isehemia by EA at different time after ischemic cerebral injury.

Glioblastoma (GBM) is a highly aggressive and lethal brain tumor with an immunosuppressive tumor microenvironment (TME). In this environment, myeloid cells, such as myeloid-derived suppressor cells (MDSCs), play a pivotal role in suppressing antitumor immunity. Lipometabolism is closely related to the function of myeloid cells. Here, our study reports that acetyl-CoA acetyltransferase 1 (ACAT1), the key enzyme of fatty acid oxidation (FAO) and ketogenesis, is significantly downregulated in the MDSCs infiltrated in GBM patients. To investigate the effects of ACAT1 on myeloid cells, we generated mice with myeloid-specific (LyzM-cre) depletion of ACAT1. The results show that these mice exhibited a remarkable accumulation of MDSCs and increased tumor progression both ectopically and orthotopically. The mechanism behind this effect is elevated secretion of C-X-C motif ligand 1 (CXCL1) of macrophages (Mφ). Overall, our findings demonstrate that ACAT1 could serve as a promising drug target for GBM by regulating the function of MDSCs in the TME.