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Jilin, China

Coder B.D.,University of North Texas Health Science Center | Wang H.,Jilin Medical College | Ruan L.,Wenzhou University | Su D.-M.,University of North Texas Health Science Center
Journal of Immunology

Thymic involution and the subsequent amplified release of autoreactive T cells increase the susceptibility toward developing autoimmunity, but whether they induce chronic inflammation with advanced age remains unclear. The presence of chronic low-level proinflammatory factors in elderly individuals (termed inflammaging) is a significant risk factor for morbidity and mortality in virtually every chronic age-related disease. To determine how thymic involution leads to the persistent release and activation of autoreactive T cells capable of inducing inflammaging, we used a Foxn1 conditional knockout mouse model that induces accelerated thymic involution while maintaining a young periphery. We found that thymic involution leads to T cell activation shortly after thymic egress, which is accompanied by a chronic inflammatory phenotype consisting of cellular infiltration into non- lymphoid tissues, increased TNF-α production, and elevated serum IL-6. Autoreactive T cell clones were detected in the periphery of Foxn1 conditional knockout mice. A failure of negative selection, facilitated by decreased expression of Aire rather than impaired regulatory T cell generation, led to autoreactive T cell generation. Furthermore, the young environment can reverse age-related regulatory T cell accumulation in naturally aged mice, but not inflammatory infiltration. Taken together, these findings identify thymic involution and the persistent activation of autoreactive T cells as a contributing source of chronic inflammation (inflammaging). Copyright © 2015 by The American Association of Immunologists, Inc. Source

Zhou J.-J.,Dalhousie University | Zhou J.-J.,PLA Fourth Military Medical University | Li M.-S.,Dalhousie University | Li M.-S.,Jilin Medical College | And 2 more authors.
Journal of General Physiology

Rapid chloride permeation through the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel is dependent, on the presence of fixed positive charges in the permeation pathway. Here, we use site-directed mutagenesis and patch, clamp recording to show that the functional role played by one such positive charge (K95) in the inner vestibule of the pore can be "transplanted" to a residue in a different transmembrane (TM) region (Sl141). Thus, the mutant channel K95S/S1141K showed Cl- conductance and open-channel blocker interactions similar to those of wild-type CFTR, thereby "rescuing" the effects of the charge-neutralizing K95S mutation. Furthermore, the function of K95C/S1141C, but not K95C or Sl141C, was inhibited by the oxidizing agent copper(II)-o-phenanthroline, and this inhibition was reversed by the reducing agent dithiothreitol, suggesting disulfide bond formation between these two introduced cysteine side chains. These results suggest that the amino acid side chains of K95 (in TM1) and Sl141 (in TM12) are functionally interchangeable and located closely together in the inner vestibule of the pore. This allowed us to investigate the functional effects of increasing the number of fixed positive charges in this vestibule from one (in wild type) to two (in the S1141K. mutant). The Sl141K mutant had similar Cl- conductance as wild type, but increased susceptibility to channel block by cytoplasmic anions including adenosine triphosphate, pyrophosphate, 5-nitro-2-(3-phenylpropylamino)benzoic acid, and Pt(NO 2)4 2- in inside-out membrane patches. Furthermore, in cell-attached patch recordings, apparent voltagedependent channel block by cytosolic anions was strengthened by the Sl141K mutation. Thus, the Cl- channel function of CFTR is maximal with a single fixed positive charge in this part of the inner vestibule of the pore, and increasing the number of such charges to two causes a net decrease in overall Cl - transport through a combination of failure to increase Cl - conductance and increased susceptibility to channel block by cytosolic substances. © 2010 Zhou et al. Source

Feng X.M.,Jilin Medical College
Zhongguo ji sheng chong xue yu ji sheng chong bing za zhi = Chinese journal of parasitology & parasitic diseases

To inhibit the expression of pyruvate kinase (PK) mRNA in Giardia lamblia by specific hammerhead ribozyme. The constructed hammerhead-GCV vector (pGCV-PKH) which aims to PK mRNA was electroporated into G. lamnblia trophozoites (group A). Electroporated trophozoites (group B) and normal trophozoites (group C) served as control Trophozoites in each group were collected at 24, 48, 72 and 96 h post-electroporation, respectively. The concentrations of trophozoites were calculated and the growth curves were constructed. At 24, 48, 72 and 96 h post-electroporation, mRNA of each group was detected by RT-PCR and real-time PCR, respectively. The PK activity was tested by ultraviolet spectrophotometry. The growth curve showed that the growth of trophozoites was considerably depressed after 96 h post-electroporation. RT-PCR result displayed that the specific ribozyme mRNA was detected in group A from 24 h to 96 h post-electroporation. At 24 and 48 h after transfection, the PK mRNA level of group A decreased to 5% (5 +/- 0.17) and 8% (8 +/- 0.19) of the level in group C, respectively; and the PK activity of group A decreased to 32% (32 +/- 0.64) and 38% (38 +/- 0.65) of the level in group C. PK mRNA expression in G. lamblia has been inhibited by specific hammerhead ribozyme. Source

Zhang F.-Z.,Jilin Medical College
National Medical Journal of China

Objective: To determine the effects of disease activity and other risk factors on bone mineral density (BMD) in untreated systemic lupus erythematosus (SLE). Methods: Lumbar and hip BMD were determined by dual energy X-ray absorptiometry (DXA) in 50 healthy controls and 120 premenopausal SLE females from Department of Rheumatology & Immunology, Third Hospital of Medical College of Jilin University during the period of 2010-2012. The SLE patients were divided into 2 groups, i. e. untreated and treated with glucocorticoid and immunosuppressives. Simple and multiple linear regression analyses were performed to determine the associations between BMD and disease-related variables. To completely eliminate the influences of glucocorticoid treatment on the results, the untreated SLE patients were chosen to investigate the risk factors with regression analysis. Results: In femoral neck, greater trochanter and total hip, both the treated and untreated SLE patients had significantly lower BMD than the healthy controls (P < 0.01). In greater trochanter, the treated SLE group had significantly lower BMD than the untreated group. The BMD of left and right femoral neck of the former were botj -0.06 while that of the later -0.11 and -0.12 respectively (P < 0.05). Regression analysis showed that long disease duration and high (SLE disease activity index) SLEDAI were the risk factors of low BMD (P < 0.05), especially high SLEDAI. Conclusion: SLE itself may result in low BMD, especially in patients with high SLEDAI. Hip joints are predominatly affected. Long disease duration is also closely associated with low BMD in SLE. Source

Guan J.,Jilin Medical College
Zhong yao cai = Zhongyaocai = Journal of Chinese medicinal materials

To investigate the pharmacokinetics and tissue distribution of Schisandra chinensis in mice. Schisandrin in mice plasma and tissues including heart, liver, spleen, lung and kidney was quantitatively determined by HPLC. The concentration-time curve of Schisandra chinensis extract was described by a single compartment model, Cmax was (2.17 +/- 0.27) mg/ mL, t(max) was (1.00 +/- 0.32) h, AUC0-->infinity, was (4.07 +/- 0.62) mg x h/mL. The sequence of distribution of schisandrin in mice body was as follows: liver > plasma > kidney > lung > heart > spleen. The distribution of extract in the body is abroad. Liver has relative high concentration of schisandrin, which is beneficial to the treatment of hepatic disease. Source

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