Objective To observe the injury effect of ionizing radiation on bone marrow derived c-kit+ cells.Methods Via-bility of c-kit+ cells was measured by bioluminescence;the level of c-kit+ cells reactive oxygen species was measured by DCFH-DA, the ability of colony-forming units was reflected by CFU-GM;proliferation and apoptosis of c-kit+ cells were measured by flow cy-tometry;the variation of pathway was detected by arrays of gene chip.Results Compared to control group(0 Gy).It had a decrease of c-kit+ cells′cell viability and the ability of colony-forming units after the cells receipt irradiation with the dose of 1 Gy and 4 Gy;and the level of cell reactive oxygen species,ratio of apoptosis cells increased.After 1 Gy irradiation exposure,the ratio of prolifera-tion(S/G2/M phase)cells increased compared to control group.However,when the c-kit+ cells were receipt 4 Gy irradiation expo-sure,the ratio of proliferation(S/G2/M phase)cells decreased.After 4 Gy irradiation exposure,the up-regulate genes contained Srxn1,Psmb5,Cdkn1a,Smc1b,Bcl2l1,Lrdd and so on;the down-regulate genes contained Mpo,Mtf1,Chek1,Rcc1 Ebag9,Ciapin1 and so on.Conclusion There was injury effect of ionizing radiation on c-kit+ cells,and it could induce variation of many pathways.

The fourth generation poly( amidoamine) dendrimers ( G4. 0 PAMAM) functionalized multiwalled carbon nanotube ( G4 . 0-MWCNTs ) was prepared by amidation between carboxylated multiwalled carbon nanotube (MWCNTs) and G4. 0 PAMAM. Then a novel hydrogen peroxide (H2O2) sensor was fabricated by electrodepositing Pd nanoparticles (NPs) on a glassy carbon electrode (GCE) modified with G4. 0-MWCNTs composites. The modified electrode was characterized by field emission scanning electron microscopy ( FESEM) , cyclic voltammetry ( CV) and electrochemical impedance spectroscopy ( EIS) . A large amounts of highly dispersion PdNPs could be well loaded on the surface of the G4. 0-MWCNTs, and the modified electrode exhibited excellent electrocatalytic activity towards the reduction of H2 O2 . Under the optimized conditions, the reduction peak currents of H2 O2 were linear to their concentrations in the range from 1. 0 × 10-9 mol/L to 1. 0×10-3 mol/L and the limit of detection of 2. 3×10-8 mol/L was obtained. The recovery of standard addition for human serum samples was 96 . 7%-103 . 1%.

he herpes simplex virus type1 (HSV 1) was used for study on tracing neuronal connections of the cerebellum in the rat. The anterior or posterior lobe of the cerebellum in total 23 rats was injected by HSV 1 (HK 2 strain, from Institute of Virology, Chinese Academy of Preventive Medicine) with the titer of 10 -7 in a volume of 10 15?l for each case. Following a postoperative survival period of 1 5 or 10 days, the animals were perfused and their brains and spinal cords were sectioned and stained immunohistochemically by polycolonal antibodies raised in rabbit against HSV 1. Under the LM, the HSV 1 labelled neurons were shown to be a Golgi like appearance, with clearly labelled cell body and dendrites. It showed that the distributions of the labelled neurons in the CNS depended on the postoperative periods and injection sites. 1. After posterior lobe injection, the labelling was limited in the cerebellum, especially in Purkinje cells and the deep nuclei in 1 day of survival time. Two days later, the labelling could be seen in the vestibular, pontive nuclei and inferior olive nucleus. Anterogradely transneuronal labelling in the ventrolateral thalamic nuclus became apparant 3 days after injetions; 2. After anterior lobe injection, the red nucleus, cuneate nucleus, cuniform nucleus and interstitial nucleus of cajal were labelled after 3 days, in addition to the labelling as shown in those cases with injections in the posterior lobe. The results proved that HSV 1 (HK 2 strain) could be transported both retrogradely and anterogradely in CNS, while the transneuronal transport would mainly occur anterogradely. The distances of HSV 1 transport in neuronal pathways would depend upon the postoperative survival times. This indicates that HSV 1 (HK 2 strain) is a powerful tool for demonstrating the chains of synaptically connected neurons in CNS.

Objective To observe the effect of electric-impulse stimulation to Jiaji points (EX-B2) on spinal cord injury (SCI). Methods Totally 126 eligible SCI patients were randomized into a treatment group and a control group, 63 cases in each group. The control group was intervened by conventional rehabilitation training plus acupuncture, while based on which the treatment group additionally received electric-impulse stimulation to Jiaji points (EX-B2). The spasticity, function, and activities of daily living (ADL) were evaluated 90 d later. Results The spasticity score was significantly changed after intervention in the treatment group(P＜0.01). Tendon reflex and spasticity score were significantly changed in the control group (P＜0.01). After intervention, there was a significant difference between the two groups in comparing spasticity score (P＜0.01). The changes of motor function and sensory function scores in the treatment group were significantly different from that in the control group (P＜0.01, P＜0.05). The Barthel Index (BI) scores were significantly changed in both groups after intervention (P＜0.05). There was a significant difference in comparing the BI score between the two groups after intervention (P＜0.05). Conclusion Electric-impulse stimulation to Jiaji (EX-B2) plus conventional rehabilitation training can significantly improve spasticity, and the motor and sensory functions, and promote the recovery of activities of daily living.

The research progresses of iron homeostasis and the diagnosis of hereditary iron overload in the 56th American Society of Hematology (ASH) annual meetings were reviewed.Over the last 2 decades,the discovery of mutations in genes leading to hereditary disorders of iron overload,iron deficiency,and iron maldistribution had accelerated our understanding of human iron homeostasis.This article provided an updated overview of the human iron cycle,regulation of iron homeostasis,how perturbations in these homeostatic mechanisms led to iron overload disease and strategies for the diagnosis of hereditary iron overload.

Progress of guidelines for quantifying iron overload in the 56th American Society of Hematology (ASH) annual meetings was reviewed.This article reviewed the use of historical data,serological measures,and MRI to estimate somatic iron burden.Before chelation therapy utilization,transfusional volume was an accurate method for estimating liver iron burden,whereas transferrin saturation reflected the risk of extrahepatic iron deposition.Liver biopsy was invasive and plagued by sampling variability.In the current study,we recommended annual liver iron concentration to be measured by MRI for all patients on chronic transfusion therapy.And it was important to measure cardiac T2* by MRI every 6-24 months depending on the clinical risk of cardiac iron deposition.Recent validation data for pancreas and pituitary iron assessments was also presented,while the further confirmatory data was suggested before these techniques could be recommended for routine clinical use.

New progresses of timing of allogeneic hematopoietic stem cell transplantation (allo-HSCT) for myelodysplastic syndrome (MDS) and aplastic anemia in the 56th ASH annual meetings were reviewed.Allo-HSCT for MDS was a potentially curative procedure,but it was associated with a significant risk of morbidity and mortality.With the recent approval of disease-modifying agents,the appropriate timing of alloHSCT needed to be addressed.For low and intermediate-1 IPSS risk groups,the decision to delay HSCT from the time of diagnosis maximized overall survival.For patients with intermediate-2 and high-risk disease,immediate HSCT at the time of diagnosis was associated with a greater number of life-years than HSCT at a delayed time point.The methods that underwent HSCT were after azacitidine,leukemia-type induction chemotherapy,or both.for severe aplastic anemia (SAA),HSCT was a proven cure,but HLA-matched sibling donors were found in fewer than 25 ％ of newly diagnosed patients.The use of early unrelated donor HSCT was an evolving concept that will became more accepted as improvements in HSCT outcomes continued.Moving forward,HLA-matched related and unrelated donor HSCT will likely become the treatment of choice for most patients with higher-risk MDS and newly diagnosed SAA.

New progress of guidelines for novel targets to iron overload in the 56th American Society of Hematology (ASH) annual meeting was reviewed.β-thalassemia and hereditary hemochromatosis disorders,and inappropriately low levels of the liver hormone hepcidin are responsible for the increased iron absorption,leading to toxic iron accumulation in many organs.Several studies have shown that targeting iron absorption could be beneficial to reducing or preventing iron overload in these 2 disorders.New approaches target Tmprss6.Additional strategies in β-thalassemia are showing beneficial effects in ameliorating ineffective erythropoiesis and anemia.The goal of this review is to discuss the major factors controlling iron metabolism and erythropoiesis and to discuss potential novel therapeutic approaches to reduce or prevent iron overload in these 2 disorders and ameliorate anemia in β-thalassemia.

Gut microbiota plays an important role in the maintenance of physiological function and genesis of some gut diseases. Brain-gut axis,as an important link between brain and gastrointestinal tract,is a requisite of gut microbiota stability. The dysfunction of brain-gut axis may lead to intestinal dysbiosis through activation of intestinal immune activity. Conversely,intestinal dysbiosis can influence nervous system development and may cause dysfunction of brain-gut axis,in which vagus nerve and metabolites in serum may be the critical factors. This article reviewed the advances in study on interaction between gut microbiota and brain-gut axis.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by the accumulation and proliferation of inflammatory cells in the synovial (joint) lining.By investigating RA pathologic processes and also through experimental models where immune complexes (inflammatory sediments) play a fundamental role.Many other autoantibodies have then come to our knowledge to be associated with the disease.Though it remains unknown the autoimmune pathology of B cells and why the clones of autoreactive B cells survive and proliferate in RA patients,but no doubt these autoantibodies represent a very useful tool in both diagnostic and prognostic terms.In joint synovial fulid,B cells also secrete cytokines,which can be interacted with other cells.B cells express IL-13 receptor a1 (IL-13Ra1),IL-13 can induce CD23 expression on B cells and promote proliferation of naive B cells. In addition,IL-13 is a cytokine which is produced mainly by activated T helper cell 2 (Th2 cells),it can inhibit the production of pro-inflammatory factor and chemokines,and has a certain relationship with the differentiation of B cells. Therefore,it is necessary to summarize the mechanims of RA pathogenesis related with B cells and IL-13,which has great significance in the diagnosis,treatment and basic immunology research of autoimmune diseases such as RA.