2. Effects of TREM-1 gene silencing on lipopolysaccharide-induced inflammatory factor secretion from mice macrophage cell lines RAW264.7
Chinese Pharmaceutical Journal 2013;48(9):695-699
OBJECTIVE: To investigate the role of TREM-1 in tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) secretion from lipopolysaccharide-induced mice macrophage cell lines RAW264.7. METHODS: Designing and synthesizing small interfering RNA (siRNA) with high intangerference ratio, then constructing pLKO1.1-puro-TREM-1 The mice macrophage cell lines RAW264.7 were divided into four groups: control group (control); lipopolysaccharide group (LPS); empty plasmid group (pLKO1.1) - just transfected with pLKO1.1; interference group (siRNA) - transfected with pLKO1.1-puro-TREM1.24 h after stimulation with LPS, real-time PCR was used to detect the mRNA levels of TREM-1, TNF-α and IL-1β respectively. The concentrations of TNF-α and IL-1β were assayed by ELISA. RESULTS: In siRNA group, the mRNA levels of TREM-1, TNF-α and IL-1β were decreased significantly (P<0.01): moreover, the concentrations of TNF-α and IL-1β were lower than other groups significantly (P<0.01). CONCLUSION: Small interfering RNA may reduce TNF-α, IL-1β secretion in LPS-induced macrophage 264.7 through inhibiting the expression of TREM-1 gene.
3.Imaging Features of Primary Bone Lymphoma
Yuefen ZOU ; Yang FENG ; Hai XU
Journal of Practical Radiology 2001;0(08):-
Objective To discuss X-ray, CT and MR findings of primary bone lymphoma. Methods The X-ray, CT and MR findings of 6 cases with non-Hodgkin lymphoma of bone proved pathologically were retrospectively analysed.Results The average age of 6 cases was 51 years old and the lesions all localized at long bone(especially the metadiaphysis) and pelvis. Imaging findings included: osteolytic or moth-eaten bone destruction,surrounding soft tissue mass formation which generally exceeded the extents of bony changes, the cortex bone was destructed and discontinuity.Conclusion primary bone lymphoma has prevalent age and certain imaging specificity.
4.Report of one patient of cerebral infarction associated with methamphetamine and a review of pertinent literature
Meijuan XIAO ; Hai ZOU ; Weiyong YIN
Chinese Journal of General Practitioners 2014;(6):492-494
A case of methamphetamine-related cerebral infarction was reported and the relevant databases of CBMdisc and Medline were searched.Among 14 cases of ischemic stroke , the ratio of male:female was 9∶5 and the age range 19-45 years.There were anterior circulation lesions ( n=13,92.8%) and 10 of them (71.3%) had cerebral vascular occlusion or stenosis.And the predominant manifestation was hemiplegia (85.7%);among 34 cases of hemorrhagic stroke ,the ratio of male: female was 12∶5 and the age range 16-60 years.And 28 cases (82%) were≤45 years.Cerebral hemorrhage was the most common (85%).The major manifestations were headache ( n =26, 76%) and disturbance of consciousness (n=21,62%).The methamphetamine-related stroke occurs frequently in young males.And ischemic stroke tends to involve anterior circulation and cause hemiplegia.Yet hemorrhagic stroke has extensive attack sites and headache and disturbance of consciousness are quite common.
9.Effect of intraspinal grafting of adenovirus-mediated brain derived neurotrophic factor ex vivo transgene myoblasts cells and methylprednisolone on expression of caspase-3 after spinal cord injury
Qiang ZHANG ; Dewei ZOU ; Yong HAI ; Huasong MA ; Yongjun WANG
Chinese Journal of Trauma 2003;0(10):-
Objective To investigate the effect of intraspinal grafting of brain derived neurotrophic factor (BDNF) ex vivo transgene myoblasts cells and methylprednisolone on caspase-3 expression after spinal cord injury (SCI). Methods A total of 120 experimental rats were divided into Group A (spinal cord contusion injury group), Group B (grafting of BDNF ex vivo transgene myoblasts cells group), Group C (methylprednisolone intravenous injection group) and Group D (grafting of BDNF ex vivo transgene myoblasts cells and methylprednisolone intravenous injection group). At days 1, 3, 7, 14 and 28 respectively after SCI, the expression of caspase-3 was measured immunohistochemically for quantitative analysis via a computer image analysis system. The motion functional recovery of the rats was observed by praxiologic and electrophysiologic examination. Results Positive expression cells of caspase-3 were found in all groups, with number from the highest to the lowest in order of Group A, Group B, Group C and Group D (P
10.Influence of tamoxifen on the level of cellular proliferation on cultured human pituitary adenoma cells and its mechanism
Ziying ZOU ; Chengliang YUAN ; Hai HUANG ; Bi ZHAO ; Xiaoli HU
Chinese Pharmacological Bulletin 1986;0(05):-
Aim To investigate the effects of tamoxifen on the proliferation and DNA synthesis of cultured human pituitary adenoma cells and make a further investigation of the mechanism of the inhibitory effect of tamoxifen on the proliferation of pituitary adenoma cells. Methods The techniques of MTT colorimetry, 3H-TdR, flow cytometry, PKC activity detection and cAMP/ cGMP levels detection were used to detect or observe the effects of tamoxifen on proliferation, DNA synthesis, cell cycle, PKC activity and cAMP/ cGMP levels of cultured human pituitary adenoma cells, respectively.Results ①Tamoxifen (0.1,1 and 10 ?mol?L -1) inhibited the proliferation and DNA synthesis of cultured human pituitary adenoma cells in a dose-dependent manner.② tamoxifen (1,10 and 20 ?mol?L -1) increased the ratio of G_1 phase of pituitary adenoma cells, and decreased the ratio of S and G_2 phase markedly;②compared with control, PMA, a PKC activator, increased the activity of membrane and total PKC in human pituitary adenoma cells. However, after a 15-min treatment with tamoxifen (10 ?mol?L -1),a significant reduction of the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells was observed;③tamoxifen (1 and 10 ?mol?L -1) increased the amount of cAMP in the cytoplasm of human pituitary adenoma cells, but had no effect on that of cGMP. Conclusion These data provide an important clue to explore the molecular mechanisms of the inhibitory effect of tamoxifen on the proliferation of pituitary adenoma cells, and suggest that the modulating effect of tamoxifen on the proliferation of pituitary adenoma cells results from interactions of several cellular signaling pathways.