SIRT1 (Sirtuin type 1 ), a member of histone deacetylase, dependents on nicotinamide adenine dinucleotide ( NAD + ). It involves in the covalent modification of histones, participates in tumor development and progression through transcription, translation and post-translational modification and so on. Therefore, the expression of SIRT1 in tumor cells or abnormal function could be one of the important mechanisms of tumor development, and may become a new potential therapeutic target for neoplasms.

Objective To evaluate the effect of the autogenous split-thickness cranial bone grafts on treatment of deformity of oral and maxillofacial regions. Methods The split-thickness cranial bone was harvested through the coronal incisions or the parietotemporal region incisions. The bone graft was then fashioned to the appropriate size and configuration and fixed to the regions of defects and deformities. The cranial bone was used to reconstruct facial bone framework or as sustaining bone graft for facial augmentation. Results 31 patients with the oral and maxillofacial deformities or bone defects were repaired with the cranial bone grafts, including 17 cases of orbital floor defects, 6 cases of malunion of the zygoma fractures, 5 cases of secondary deformity after ankylosis of temporomandibular joint, 2 cases of bone reconstruction after tumor resection and 1 case of cleft palate deformity. The followed-up period ranged from 6 months to 7 years, averaging 11 months. There were no complications of infection and extrusion, no obvious bone resorption was observed, and the facial appearance were greatly improved. Only one patient had a small ectropion which persisted three months. After six-month, the ectropion was not obvious. Conclusion Autogenous bone grafts used to reconstruct the defect and deformity of oral and maxillofacial regions can reduce the risks of infection and extrusion, and there is less visible scar and less bone resorption. Skull bone is an ideal source of bone graft material in the oral and maxillofacial deformity.

Objective To study the expression of S1RT1 in breast cancer with diabetes mellitus,and analyze the correlation between SIRT1 and p53,and analyze blood lipid differences in breast cancer tissue without diabetes mellitus and breast cancer tissue with diabetes mellitus,and to research its relation with type 2 diabetes mellitus and assesse the clinical value.Methods Immunohistochemistry was used to examine the expressions of SIRT1 and p53 in 30 breast cancer patients with diabetes mellitus and 30 breast cancer patients without diabetic mellitus,and their correlation was analyzed.Results The positive rate of SIRT1 in breast cancer tissue with diabetes mellitus was significantly lower than that in breast cancer tissue without diabetic mellitus(P ＜0.05).In SIRT1 positive tissue,the expression level of p53 was significantly higher than that in SIRT1 negative tissue(P ＜ 0.05 ).The expression of SIRT1 was significantly positively related with p53 expression in breast cancer tissue with diabetes( P ＜ 0.05).BMI and TG in breast cancer group with diabetes mellitus were significantly higher than those in breast cancer group without diabetic mellitus( P ＜ 0.05 ),but HDL was lower( P =0.05 ).However,CHO and LDL had no significant differences in both groups( P ＞0.05 ).Conclusions SIRT1 is up-regulated in breast cancer,but the posltive rate of SIRT1 in breast cancer tissue with diabetes mellitus is significantly lower than that in breast cancer tissue without diabetic,and is associated with the progression of diabetes mellitus.SIRT1 protein is significantly positively correlated to p53 expression and it may be involved in the adjustment process of blood lipids,SIRT1 might be a new biological target in diabetes and breast cancer.

[Objective] To screen and identify the new Y-STR loci from the Y chromosome and examine the polymorphism of these Y-STR loci. [Method] To seek and locate the position of 5 Y-STR loci, including DYS709, DYS720, DYS721, DYS722, and DYS723, and perform sequencing of these 5 Y-STR loci. Then to investigate the polymorphism in unrelated Chinese Han males. [Results] Five Y-STR loci were identified from Y chromosome sequence. By scrutinizing the physical position on Y chromosome of previously reported Y-STRs, we found that three loci were novel and two loci overlapped with two loci published only online. All loci could be male-specifically amplified with a product size ranging from 185 bp to 278 bp. After 108 males of the Chinese Han Population (Guangzhou) were examined, we found 5 DYS709, 11 DYS720 alleles, 4 DYS721 alleles, 6 DYS722 alleles, and 6 DYS723 alleles. A total of 95 haplotypes were identified, 84 of which were unique, and with a haplotype diversity of 0.997 2±0.001 2(HD±SE). [Conclusion] This set of Y-STRs can be used as Y chromosome genetic makers in related fields.

Objective To explore the possible effects on differentiation of SHI-1 cells induced by puerariae radix flavones(PRF)in vitro.Methods SHI-1 cells were treated with PRF in various concertration,then the inhibitory effects of cell proliferation were detected by MTT assay,the cell cycles were analyzed by flow cytometry(FCM),the cells reduction rates were detected by NBT reduction test,and the expression of CD11b and CD14 were tested by FCM.Results 10-50 μg/ml PRF could inhibit the proliferation of SHI-1 cells in a time-and dose-dependent manner,and the cell cycles were arrested in S phase.When SHI-1 cells were treated with 10,30 and 50 μg/ml PRF in 48 houres respectively,the NBT reduction rates of cells were increased in a dose-dependent with PRF(P＜0.05),and the expression of cells surface differentiation antigen CD14 was also increased along with the concentration of PRF.Conclusion The SHI-1 cells could be induced to differentiation partially after treated with 10,30 and 50 μg/ml PRF in vitro.

Objective To investigate differences of ctinicopathologic features in breast cancer patients with or without Type 2 Diabetes Mellitus(DM).Methods The general conditions and elinicopathologic features of the hospitalized breast cancer patients with or without type 2 diabetes were analyzed using a case-control study.Results The average age,fasting blood-glucose,BMI and TG were(58.4 ± 7.80),(8.15 ± 2.80)mmol/L,(27.72 ± 3.47)mmol/L and(2.36 ± 1.18)mmol/L in patients with DM,and(51.6 ± 9.90),(5.13 ±0.63)mmol/L,(24.15 ± 4.95)mmol/L and(1.32 ± 0.59)mmol/L in patients without DM.There were significantdifference between the two groups(t =2.968,P =0.004; t =5.757,P ＜ 0.001 ; t =3.235,P =0.002; t =4.330,P ＜0.001,respectively).HDL-C in patients with DM was(1.39 +0.20)mmol/L,which was significantly lower than that of(1.50 ± 0.24)mmol/L in patients without DM(t =2.000,P =0.05).TC and LDL-C was(4.89 ± 1.16)mmol/L and(3.02 ±0.90)mmol/L in patients with DM,which were not significantly different with those of(4.79 ±0.85)mmol/L and(2.97 +0.61)mmol/L in patients without DM(t =0.396,P =0.693,and t =0.255,P =0.800,respectively).More patients were in the menopausal status in breast cancer patients with Type 2 DM compared to the other group(x2 =11.835,P =0.001).The expression of Her-2 was 76.7％(23/30)in breast cancer patients with Type 2 DM,which was significantly higher than that of 50.8％(33/65)in patients without DM(x2 =5.689,P =0.017).Conclusion The average age was higher in breast cancer patients with Type 2 DM and most of them were in their menopausal status,furthermore the higher body mass index and worse prognosis were observed in this group,so the breast cancer patients with diabetes should choose the more reasonable treatment.

[Objective] To propose a criterion for making conclusions on paternity tests based on STR genotyping. [Method] To use binomial distribution formula to calculate minimal numbers of STR loci that must be tested for different scenarios in paternity testing. [ Results ] We proposed a set of criteria for making STR paternity testing conclusions. For triplet tests, concluded "paternity positive" for the following four cases when the cumulative paternity index (PI) was greater than 10 000: 1) no inconsistent STR locus was detected in 15 loci (PE > 0.571 4/locus) or 2) only one inconsistent STR locus was detected in 19 loci or 3) only two inconsistent STR loci were detected in 28 loci or 4) only three inconsistent STR loci were detected in 35 loci; otherwise, concluded "paternity negative" when at least four inconsistent STR loci had been detected. For single parent tests, concluded "paternity non-exclusive" for the following cases when the cumulative PI was greater than 10 000: 1) no inconsistent STR locus was detected in 18 loci (PE>0.411/locus) or 2) only one inconsistent STR locus was detected in 29 loci or 3) two inconsistent STR loci were detected in 41 loci; concluded "paternity negative" when three or more inconsistent loci were detected. [Conclusion] Our experience has proven that these criteria are robust in STR paternity testing.

Objective Toinvestigatetheexpressionof SIRT1anditsassociationwith clinicopathologic features in breast carcinoma with type 2 diabetes mellitus.MethodsThe expression of SIRT1 in 30 breast cancer with type 2 diabetes mellitus,65 samples of breast cancer without diabetes mellitus and 18 samples of corresponding normal breast tissues was investigated using immunohistochemistry.ResultsThe positive rate of SIRT1 in breast cancer tissues was significantly higher than that breast cancer with type 2 diabetes mellitus and normal breast tissue (P ＜0.05). In breast cancer with type 2 diabetes mellitus group.The positive rate of SIRT1 was significantly higher than that normal breast tissue(P ＜0.05).The expression of SIRT1 was positively correlated with the number of lymph node(P =0.011),pTNM tumor stage (P =0.028), p53 (P =0.003) and Her-2 (P =0.031) in breast cancer with type 2 diabetes mellitus group. The expression level of SIRT1 in lymph node-positive group was higher than that in lymph node-negative group (P ＜0.05).The expression level of SIRT1 was in lymph node-positive group was higher than that in lymph node-negative group(P ＜0.05).ConclusionSIRTI was up-regulated in breast cancer with type 2 diabetes mellitus,but its expression was lower than that breast cancer without diabetes mellitus,and was associated with the progression of diabetes mellitus. SIRT1 was positively correlated with lymph node, pTNM tumor stage,p53 and Her-2, SIRT1 may be a novel biological parameter to evaluate the malignant degree of breast carcinoma and to predict prognosis of breast cancer.

AIM: To clarify the effects of specific and non-specific cyclooxygenase-2 (COX-2) inhibitors on gastric epithelial cell proliferating and gastric healing following acid-induced damage. METHODS: Male Sprague-Dawley rats were given 1 mL of 0.6 mol/L hydrochloric acid (HCl) into the stomach. Ten minutes after the administration of the acid,the animals were given NS-398 (COX-2 inhibitor) or indomethacin. Levels of COX-1 and COX-2 in the gastric mucosa before and after HCl-administration were analyzed using western blotting and immunohistochemical staining. Proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry for epithelial cell proliferation. Gastric lesion index (LI) was assessed using planimetry. RESULTS: Expression of COX-2 was enhanced mainly in surface epithelial cells and neck cells following HCl-administration. At 24 h following acid administration,PCNA labeling index (PCNA-LI) was (22.72?4.33) % and (21.98?5.18) % in the groups treated with 40 mg/kg of NS-398 and indomethacin respectively,which was significantly lower than that in the control group [ (34.46?3.61) %,P

AIM: To clarify the effects of gastrin on t he expression of cyclooxygenase (COX) and several growth factors in rat gastric mu cosa. METHODS: Male Sprague Dawley rats were fasted for 24 hours and s ubcutaneously injected with saline or gastrin 17 at doses of 1 ?g/kg, 10 ?g/kg and 100 ?g/kg, respectively. The expression of COX-1, COX-2, heparin-binding e p idermal growth factor-like growth factor (HB-EGF) and hepatocyte growth factor ( HGF) in the gastric mucosa were examined using Western blotting and immunohistoc hemical staining. Effects of a potent gastrin receptor antagonist YM022 on the e xpression of COX-1, COX-2, HB-EGF and HGF in gastric mucosa were also evaluated. RESULTS: Gastrin dose-dependently increased the expression of C OX-2 and HB-EGF in rat gastric mucosa while the expression of COX-1 and HGF did not change significantly after treatment with gastrin. However, pretreatment wit h YM022 dose-dependently abolished the up-regulation of COX-2 and HB-EGF express ion induced by gastrin. CONCLUSIONS: This study demonstrates that gastrin up-regulates C OX-2 and HB-EGF expression in rat gastric mucosa, indicating that COX-2 and HB-E GF are involved in pathogenesis of the gastrin-related gastric mucosal hyperplas ia and carcinoma of stomach.