SCNP( single cell network profiling) assay can depict the characters of signal pathway network without isolating the dif-ferent cells in advance in complex tissues. It will promote the disease mechanism elucidating, disease classification, diagnosis, and therapeutic regimen at cell level. Drug screening and ration-al personalized treatment will also be improved.

Pulmonary fibrosis can severely disrupt lung functions, but its etiology and pathogenesis remain unclear. Animal models of lung fibrosis play an important role in investigation of the mechanism by which pulmonary fibrosis develops. This review summarizes the characteristics, advantages, and disadvantages of widely used and newly established animal models of lung fibrosis.

Lifelong blood cell production is achieved by the capacity of hematopoietic stem cell(HSC) to differentiate and self-renew.A growing body of evidence suggest that DNA damage induced HSC senescence may be the principal mechanism of aging and HSC exhaustion in response to the stress exposure.Understanding the mechanisms of HSC senescence will help to find new therapeutics that can ameliorate HSC injury induced by chemo-and radiotherapy,elucidate the molecular mechanisms whereby leukemia/cancer stem cell arise and evade cancer therapy by escaping senescence,and identify the novel molecular targets for intervention.

Currently, about 300 million people worldwide are affected by asthma. Most of these sufferers inhale immunosuppressants (ie corticosteroids) and beta-adrenergic receptor agonists for their asthma treatment. However, about 5%-10% of patients of asthma have poor response to such treatment. Investigation of kinase signaling pathway and nuclear transcription factor as a target molecule in the treatment of allergic asthma has been the concern of scholars home and abroad. This paper reviewed inhibitors of kinase signaling pathway and nuclear transcription factors for the treatment of asthma.

As for the ? opioid receptor, there are some disputes about the domains involved in the selective recognition of ligands, the relative spatial orientation of the amino acids within the TM affect the affinities of selective ligands. Regulation of opioid receptor activities does not appear to involve in their ability to promote the association of GTP onto the G proteins and the subsequent dissociation of heterotrimers. It is not very clear if phosphorylation correlates with agonist induced receptor desensitization. The celluar processing of ? opioid receptors requires the formation of multiple protein complexes, it is clear that interactions of ubiquitous transcriptional factors determine gene transcription.

Objective To observe the effect of sesamol on the hematopoietic system in mice exposed to 4 Gy irradiation. Method Twenty C 57 BL/6 mice were randomly divided into control group, sesamol group, irradiated group and irradiated+sesamol group (n=5). Mice of control and sesamol group received sham irradiation, and the rest exposed to 4 Gy total body irradiation, dose rate 1.01 Gy/min. Mice in sesamol group and irradiated+sesamol group received a dose of 10 mg/kg sesamol administered by gavage every day for 7 days after irradiation exposure. Mice of other two groups were treated with vehicle solution. After 4 Gy irradiation 7 day, the peripheral bloods were collected. The levels of colony forming units-granulocyte-macrophage (CFU-GM) were detected. Results Compared to irradiation group, the level of WBC、cell count of BMNCs and CFU-GM significantly decreased in the irradiated mice, decreased in the irradiated mice (P<0.05). Compared to irradiation group, cell count of BMNCs and CFU-GM in the irradiated+sesamol group increased significantly (P<0.05). Conclusion Sesamol has a certain impact on the radiation-induced changes in hematopoietic system. The mechanism need to be further explored.

Objective To investigate the protective effect of sesamol on radiation injury mouse bone marrow c-kit+cell,and further explore its possible mechanism.Methods Mouse bone marrow c-kit+cells were collected by immunomagnetic cell sorting method.There were 2 groups in the study:single dosing group and radiation plus drug group(doses of irradiation included 1 Gy and 4 Gy),and 10 -8 ~10 -3 mol/L sesamol were co-cultured with mouse bone marrow c-kit+cell half hour before irradiation exposure,cells were then cultured for 18 hours under the conventional culture conditions (37℃ and 5% CO2 ).The viability of mouse bone marrow c-kit+cells were measured by bioluminescence.The ability of colony-forming units were detected by CFU-GM and apoptotic rate of c-kit+cells were detected by Annexin V/PI antiapoptotic assay. Results Compared with control group,after 1 Gy and 4 Gy irradiated,cell viability of mouse bone marrow c-kit+cells were decreased 59.52% and 79.35%,respectively(P<0.05),the number of colony-forming were decreased 40.38% and 87.69%,respectively(P<0.05 ).Cell viability of c-kit+cells and the number of colonies formed were significantly increased with sesamol concentration between 10 -8 ~10 -6 mol/L,but not improve apoptosis rate.Conclusion Sesamol has protective effect on irradiation-induced injury in mouse bone marrow c-kit+cells,the mechanism of which may be related to the ability of hematopoietic progenitor cells proliferation.

Objective To observe the protective effect of N-acetyl-cysteine (NAC) on the injury of irradiation-in-duced bone marrow mononuclear cells (BMMNCs), and explore the possible mechanism. Methods There were 3 groups in the study:control group, irradiation group (doses of irradiation were 1 Gy and 4 Gy) and irradiation with NAC group (NAC was cocultured with BMMNCs half hour before irradiation). The 2×106/mL BMMNCs and the RPMI-1640 medium or 2×10-5 mol/L NAC were added into the 2 mL EP tubes according to the different requirement of groups. The tubes were then cul-tured in the 37℃CO2 incubator for 30 min and irradiated with 1 Gy and 4 Gy. The viability of BMMNCs was measured by bioluminescence. The level of reactive oxygen species (ROS) was measured by DCFH-DA, and the ability of colony-forming units was detected by CFU-GM. Results After 4 Gy irradiation exposure, the cell viability of BMMNCs was significantly lower in irradiation group (284 296.7±16 541.2) than that of control group (848 586.7±61 404.4). After 1 Gy irradiation expo-sure, the level of ROS was higher in irradiation group (6 750.0±103.5) than that of control group (5 710.7±56.2). The number of colony-forming units per 105 cells after irradiation exposure was (626.7±51.3), which was significantly lower than that of control group (986.7±100.7). Compared to irradiation group, the cell viability of BMMNCs increased to (352 770.0±23 466.1) in irradiation with NAC group. The level of ROS decreased to (5 430.0±61.0), and the number of colony-forming units per 105 cells increased to (773.3 ± 49.3). Conclusion NAC has protective effect on irradiation-induced injury in BMMNCs, which may be related with the decreased level of ROS. NAC can play the role of positive control for the following work.

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.