Objective To investigate the dose-response of micronuclei (MN) frequency in the lymphocytes irradiated with or without combination of α-particles and γ-rays. Methods Human lymphoblast cells HMy2.CIR were irradiated with 0 - 1 Gy of α-particles,0 - 5 Gy of γ-rays,and 0.025 -0.5 Gy of α-particles followed by different doses of γ-rays,respectively.The micronuclei (MN) in the irradiated cells were measured with the cytokinesis block technique,and the dose-responses of MN were established under different irradiation conditions.Results For γ-ray irradiation,the dose-response of MN was well-fit by the linear-quadratic model with an equation Y =c + αD + βD2.For α-particle irradiation,the MN induction increased linearly with the dose less than 0.250 Gy. But when the dose of α-particles increased continually,the dose-response curve bended and could be well fit with the BaD model Y =c + αD + σ[ 1 - exp( - δD) ] exp( - βD) where radiation-induced bystander effect (RIBE) was indicated.For the combined exposure,the dose-response of MN was similar to that of γ-irradiation when the dose of α-particles was lower than 0.1 Gy,but it was similar to that of α-irradiation when the dose of α-particles was higher.When the dose of α-particles was 0.2 and 0.5 Gy,MN induced by the mixed radiation were significantly higher than the sum of corresponding irradiation alone ( t =5.22 - 11.86,P ＜ 0.05 ).Conclusions The radiation damage of α-particles differs from that of γ-rays,where RIBE may be involved.The combination irradiation of α-particles and γ-rays has a synergistic effect on radiation damage of lymphoblast cells.

Objective To investigate the effect of equol on ERK mediated signal transduction pathway and to clarify its mechanism of proliferation inhibition on human ovarian carcinoma cell line SKOV-3. Method SKOV-3 cells were treated with 10-8,10-7,10-6,10-5,5?10-5,10-4 mol/L equol for 24,48 and 72h. After pretreatment with 10 ?mol/L U0126 an ERK signaling pathway inhibitor or ICI182,780,estrogen receptor inhibitors for 1h,then treatment with 50 ?mol/L equol for 2h,the cell viability was examined and the expressions of ERK and p-ERK protein were determined using Western blotting. Results Equol was demonstrated to inhibit SKOV-3,proliferation time-and dose-dependently. The expression of p-ERK protein was decreased in dose-dependent manner,while the expression of total ERK was unchanged. Both the single use of U0126,or ICI182,780,and combined with equol could decrease the expression of p-ERK protein. Conclusion Equol could inhibit proliferation in ovarian carcinoma cell lines SKOV-3. Its inhibitory effect appears to be due to down-regulation of p-ERK protein.

Phosphorylation is the most common way of p 53 post-translational modifications .However , gaps still exist in our knowledge regarding the role and mechanism of phosphorylation of p 53 at Ser392 in carcinogenesis and cancer prevention.In the present study, we summarized the effect of phos-p53-Ser392 to wild-type and mutant p53, the regulation by DNA damage agents and protein kinase , and the significance of phosphorylation of p 53-Ser392 in cancer treatment .

OBJECTIVE:To observe the effect of Compound glycyrrhizin on serum VEGF of patients with alopecia areata. METHODS:36 alopecia areata patients were selected as trial group and treated with Compound glycyrrhizin(50 mg/time,3 times/d) for 3 months. Double-antibody sandwich ELISA method was adopted to determine the content of VEGF in serum before and after treatment. 36 healthy volunteers were included in control group,and serum content of VEGF in control group was compared with trial group. RESULTS:Compared with control group,the serum content of VEGF was lower in trial group,with statistical signifi-cance(t=5.863,P<0.05). After treatment,the serum VEGF levels of trial group increased,with statistical significance(t=4.351, P<0.05);there was no statistical significance in VEGF levels between trial group and control group after treatment(t=1.678,P>0.05). CONCLUSIONS:Compound glycyrrhizin can cure alopecia areata through increasing serum level of VEGF.

Adolescent ; Adult ; Child ; Deubiquitinating Enzyme CYLD ; Female ; Humans ; Male ; Neoplastic Syndromes, Hereditary ; genetics ; Pedigree ; Skin Neoplasms ; genetics ; Tumor Suppressor Proteins ; genetics ; Young Adult

Humans ; Male ; Middle Aged ; Pedigree ; Porokeratosis ; genetics

Adult ; Female ; Humans ; Male ; Pedigree ; Tuberous Sclerosis ; diagnosis