MTH1 enzyme belongs to the family of Nudix hydro-lases, which can prevent the oxidative damage of nucleic acid by cleaning up oxidized purine nucleotides .Close relationships were found between the activity of MTH 1 and neurodegenerative dis-eases, anti-aging et al.In recent years, MTH1 has been regar-ded as a new promising target for cancer treatment , because it plays an essential role in tumor growth , survival , invasion and metastasis.The transcription and translation , structure, catalyt-ic mechanism, detection and application of MTH1 were de-scribed, as well as various MTH1 inhibitors.

Objective To construct eukaryotic expression plasmid pEGFP-N1/EPO and to detect its expression in vitro in order to provide experimental evidence for further study on the treatment of hypoxic-ischemic brain damage.Methods The total RNA was extracted from rat kidney.EPO cDNA fragment was obtained by RT-PCR amplication,inserted into pEGFP-N1 vector and identified by restriction endonuclease digestion and nucleotide sequencing.MSCs cells were transfected with the plasmid using Lipofectamine 2000.The expression of EPO protein was detected by immunohistochemistry technique and RT-PCR.Results Confirmed by restriction endonuclease digestion and sequencing,the recombinant plasmid contained the sequence of rat EPO gene was successfully constructed.After transfection with the plasmid,EPO protein could be expressed in MSCs cells.Conclusion The constructed eukaryotic expression vector pEGFP-N1/EPO can express rat EPO in vitro.

Objective To observe the effects of chemical compounds exposure and hyperthermal environment to pregnant rats on the hippocampus neuronal morphology and neurobehavioral development of their offsprings. MethodsPregnant rats were divided into 4 groups randomly: the control group; chemical compounds exposure group, chemical compounds combined hyperthermal exposure group and hyperthermal group. The control group was living in normal condition; the chemical compounds exposure group in a cabin with benzene (20.26?0.80) mg/m3, toluene (39.66?4.23) mg/m3, dimethylbenzene (42.40?2.85) mg/m3, and formaldehyde (23.13?1.30) mg/m3; the hyperthermal group was kept in an atmosphere of 38.5 ℃; and the combined group was exposed to the chemical compounds and high temperature at the same time. All animals were treated respectively 2 h per day for 10 d since their pregnancy. Their offspring were lived in normal condition. The development of brain and changes of hippocampus neuronal morphology were observed just or 1 month after born. The primary reflex activity of new-born rats was also examined. ResultsThere was no abnormality in the brain of new born rats from 4 groups. In the chemical compounds exposure and the combined exposure groups, the number of degeneration and necrosis neurons in CA1 region of hippocampus were significantly more than those in control and hyperthermal groups (P

Objective To investigate the myelination of rat brain at different developmental stages.Methods Luxol fast blue staining,immunohistochemistry and Western blotting were applied to determine the distribution and alternation of myelin sheath in the brains of SD rats at different developmental stages.Results Negative LFB and MBP staining were shown at the stages of embryonicage 18 d(E18),postnatal age 0 d(P0) and P2.At P7,the corpus callosum was weakly stained by LFB.The positive stain of LFB and MBP occurred in P15 on the corpus callosum.With the development going on,the stain turned out stronger,especially in P30,which was similar with that in P90 and P720.The results of Western blot analysis showed the expression of MBP in rat brain was gradually increased with the development of rat brain.Conclusion The myelination starts before P15 in rat brain and becomes mature in P30.The optimal observation time of myelin is 30 d born after.

BACKGROUND:There is a close relationship between epilepsy and apoptosis. The appearance of epilepsy can lead to the loss of neurons in the hippocampus, triggering a series of programmed cel death. OBJECTIVE:To investigate the effect of bone marrow stromal stem cel transplantation on apoptosis in epilepsy. METHODS:After modeled to be of epilepsy 45, Sprague-Dawley model rats were randomly divided into three groups, fol owed by given no intervention (moldel group), normal saline (normal saline group) or bone marrow stromal stem cel transplantation (transplantation group). At 1, 2 and 4 weeks after modeling, the number of Bax-positive cel s, Bcl-2-positive cel s and Bax/Bcl-2 were detected by immunohistochemistry. RESULTS AND CONCLUSION:The number of Bax-positive cel s, Bcl-2-positive cel s and Bax/Bcl-2 presented no obvious changes in the normal saline group at different time points. However, the number of Bax-positive cel s and Bax/Bcl-2 in the transplantation group was significantly decreased, while the number of Bcl-2-positive cel s significantly increased compared with the other two groups at 1, 2 and 4 weeks after modeling (P<0.05). Moreover, the above indicators varied significantly in the transplantation group at different time points after modeling (P<0.05). These results show that bone marrow stromal stem cel transplantation can affect the apoptosis and effectively reduce the apoptosis in rats with epilepsy by up-regulating the number of Bax-positive cel s and down-regulating the number of Bcl-2-positive cel s.

Angiogenesis is of great importance to a variety of normal physiological processes and pathological disorders.It is tightly regulated by many mechanisms, among which vascular endothelial growth factor(VEGF) is one of the most potent promoters.VEGF binds and activates its specific receptor tyrosine kinases, especially vascular endothelial growth factor receptor-2(VEGFR-2).VEGFR-2 mediates the key functional and biochemical effects of VEGF in endothelial cells including proliferation, migration, survival, and permeability.Following its binding to VEGF, VEGFR-2 dimerizes and undergoes autophosphorylation on tyrosine residues within its cytoplasmic portion.This creates docking sites for adapter molecules to be recruited through their Src homology domain-2(SH2).These adapter molecules can then initiate the activation of downstream signaling cascades.Further down-stream effector molecules are activated, and regulate the biological effects of endothelial cells.It is also foound that VEGF/VEGFR-2 signaling pathway may negatively regulate the function of human monocyte-derived mature dendritic cells(DCs) as well as the maturation of immature-DCs.Advances in the understanding of the VEGF/VEGFR-2 signaling pathway may contribute to the discovery of kinds of pharmaceutical agents.

Objective To study the cellular immunity function and clinic of HFRS patients treated by cimetidine.Methods CD+_4 T lymphocyte,CD+_8 T lymphocyte and NK cell activity were determined by flow cytometer.Results Treating HFRS patients with cimetidine could shorten fever period(P0.05).Conclusion IFN-? and ribavirin+thymosin can treat HFRS patients effectively,three therapies have equal effect.

Objective To study the cell apoptosis after injecting NS398 in neonatal rat brain injured by hypoxia and ischemia.Methods The model of hypoxic-ischemic brain damage(HIBD)was established in 48 Wistar rats.Intraperitoneal injection of NS398 at dose of 5,20,40 mg/kg respectively was carried out in 36 HIBD rats 30 min before hypoxia.There were also sham operation group in which the normal saline took the place of NS398.Ischemic cortex and hippocampus were sampled for analysis at 24 h,and 7 d after the onset of hypoxic-ischemic damage.The expression and number of apoptotic cells in the cortex and hippocampus were examined with TUNEL.Results The percentage of TUNEL-positive cells in HIBD group was higher than that of sham operation group.The percentage of TUNEL-positive cells in NS398 groups significantly decreased as compared with that of HIBD group.NS398 group at dose of 20 mg/kg was of no difference with NS398 group at dose of 40 mg/kg,but significantly lower than NS398 group at dose 5 mg/kg.Conclusion NS398 can reduce the TUNEL-positive cells,and 20 mg/kg and 40 mg/kg are the more effective dosage.NS398 is of the effective capability to inhibit the brain damage in the growth period when HI happened.

Objective To study the expression of cyclooxygenase 2 (COX-2) in neonatal rats after hypoxic-ischemic brain damage (HIBD). Methods A model of HIBD in the left brain of 7-day-old Wistar rats was established. The ischemic cortex was sampled for analysis at 2, 6, 24, and 72 h, and 7 d after the onset of hypoxic-ischemic damage. The expression and number of the positive cells of COX-2 in the cortex and hippocampus at different time points were observed by immunohistochemistry. Results Low level of COX-2 immunohistochemical expression was observed in the control group. COX-2 positive cells were upregulated in ischemic brain at 2 h and peaked between 6-24 h significantly (P

Objective To investigate the pathogenic factors and the visceral involvement in murine disseminated trichosporonosis caused by Trichosporon asahii. Methods Forty-five mice were immunosuppressed with cyclophospamide 3 days hefore and 7 days after inoculation of T. asahii, and were divided into intravenously inoculated group (n = 15), intradermal inoculated group (n = 7), gastrointestinal infusion group (n = 8), intravenously inoculated + treatment group (n = 15). In the control groups the mice were not immunosuppressed, and were also divided into intravenous, intradermal, and G.I. infusion groups with the same number of mice respectively. In the treatment group the mice were given both liposomal amphotericin B and fluconazole. The main viscera of the mice were examined by mycologic culture and pathologic sections. Results In the intravenous inoculation group of immunized mice, Trichosporon asahii were isolated from at least one organ in 10/12 mice, while T. asahii were only isolated in 2/14 mice in the control group; in 2/7 mice of the intradermal group of immunosuppressed mice, skin lesion appeared at the inoculation site, but no visceral infection was observed. No visceral infection was found in the groups that T. asahii was inoculated by non-intravenous injection in both immunosuppressed and non-immunosuppressed mice. The number of mice died, the number of visceral organs involved and the incidence of systemic infection were significantly less in the treatment group than those in the non-treatment groups (P