Objective To detect the serum levels of tumor necrosis factor-alpha (TNF-α) and interferengamma (IFN-γ) in brucellosis patients and to study the Th1 immune response in acute and chronic patients.Method Serum levels of TNF-alpha and IFN-gamma of 110 brucellosis patients,including 58 acute brucellosis patients and 52 chronic brucellosis patients,were measured by enzyme linked immunosorbent assay (ELISA) from 2014 to 2015 in Zhangjiakou Infectious Disease Hospital.Results The serum levels of TNF-alpha and IFN-gamma of 58 acute brucellosis patients were (38.2± 3.6) pg/L and (31.3 ± 3.7) ng/L,respectively;the serum levels of TNF-alpha and IFN-gamma of 52 chronic brucellosis patients were (12.4 ± 2.6) pg/L and (8.8 ± 3.4) ng/L,respectively.The differences were statistically significant between acute and chronic patients (t =43.216,33.809,all P ＜ 0.05).The early cure rate,early base cure rate,improvement rate and inefficiency rate were 36.2％ (21/58),32.7％ (19/58),25.9％ (15/58)and 5.2％ (3/58),respectively in acute patients.Inversely,they were 17.3％ (9/52),13.5％ (7/52),15.4％ (8/52)and 53.8％ (28/52),respectively in chronic patients.The therapeutic effect was better in acutepatients than chronic patients (x2 =4.937,5.657,all P ＜ 0.05).Conclusion It seems that acute brucellosis patients have a higher serum levels of TNF-alpha and IFN-gamma and a better prognosis due to effective Th1 immune response,and chronic brucellosis patients are associated with poor outcome due to deficiency of Th1 immune response.

Aging associated cognitive decline has been linked to dampened neural stem/progenitor cells (NSC/NPCs) activities manifested by decreased proliferation, reduced propensity to produce neurons, and increased differentiation into astrocytes. While gene transcription changes objectively reveal molecular alterations of cells undergoing various biological processes, the search for molecular mechanisms underlying aging of NSC/NPCs has been confronted by the enormous heterogeneity in cellular compositions of the brain and the complex cellular microenvironment where NSC/NPCs reside. Moreover, brain NSC/NPCs themselves are not a homogenous population, making it even more difficult to uncover NSC/NPC sub-type specific aging mechanisms. Here, using both population-based and single cell transcriptome analyses of young and aged mouse forebrain ependymal and subependymal regions and comprehensive "big-data" processing, we report that NSC/NPCs reside in a rather inflammatory environment in aged brain, which likely contributes to the differentiation bias towards astrocytes versus neurons. Moreover, single cell transcriptome analyses revealed that different aged NSC/NPC subpopulations, while all have reduced cell proliferation, use different gene transcription programs to regulate age-dependent decline in cell cycle. Interestingly, changes in cell proliferation capacity are not influenced by inflammatory cytokines, but likely result from cell intrinsic mechanisms. The Erk/Mapk pathway appears to be critically involved in regulating age-dependent changes in the capacity for NSC/NPCs to undergo clonal expansion. Together this study is the first example of using population and single cell based transcriptome analyses to unveil the molecular interplay between different NSC/NPCs and their microenvironment in the context of the aging brain.
Aging ; genetics ; Animals ; Astrocytes ; cytology ; metabolism ; Brain ; cytology ; metabolism ; Cell Differentiation ; genetics ; Cell Division ; genetics ; Cell Proliferation ; genetics ; Gene Expression Regulation ; genetics ; Mice ; Neural Stem Cells ; metabolism ; Single-Cell Analysis ; Stem Cells ; cytology ; metabolism ; Transcriptome ; genetics