Objective:To evaluate the contour and functional restoration in segmental defects of mandibles with three-dimensional CT(3D-CT) reconstrction.Methods: Twenty-four patients(16 males,8 females) underwent mandibular reconstruction by using nonvascularized bone grafts.In 24 patients,nonvascularized grafts from the iliac crests(n=11),the ribs(n=10),and the autogenous mandibular bones(AMB)(n=3)were used.`The length of segmental bone grafts ranged from 6 to 20 cm,with an average of 9.8 cm,for the defects with 5 to 20 cm.Both contour and functional effects with reconstructed mandible were determined and analysed via 3D-CT.Results: All free bone grafts were successfully healed.Among them,17 patients showed better soft tissue contour.Only 14 patients were satisfied for skeletal contour.All patients could wear a conventional denture after reconstruction.Conclusion:Facial contour can be achieved via mandibular reconstruction with iliac,rib and AMB.3D-CT can provide anatomy position for the surgical planning.It is an important mean to compensate inadequate of general X-ray and convention CT.Meanwhile it can be used for estimating the reconstruction effects while follow-up.

Objective To investigate the protective mechanism of ischemic preconditioning for myocardial ischemic reperfusion injury (MI/RI) rats. Methods Eighteen male Sprague–Dawley (SD) rats were randomly separated into Sham operation,ischemic reperfusion (IR) and ischemic preconditioning (IP) groups (6 rats in each group). Peripheral blood and cardiac muscle were collected after the establishment of the above 3 animal models. ELISA was employed to determine proinflammatory cytokines TNF-? and IL-1? production in sera of these animals. RT-PCR and Western blot analysis was used to assay the transcriptional level and protein level of Toll-like receptor 4 (TLR4) in cardiac muscle tissue with pathological change,respectively. Results Compared with IR group,ischemic preconditioning effectively decreased the expression levels of TNF-? and IL-1? in sera of rats in IP group (P

Objective　To observe the therapeutic effects and safety of angiotensin-converting enzym e (ACE)-inhibitors in the treatment of the secondary erythromatosis following ren al transplantation.Methods　Twenty-four patients with erythromatosis following renal transplantation recei ved the treatment with ACE-inhibitors. During the administration of ACE-inhibi tors, the hemoglobin, hematocrit and the side effects were observed. Results　All the patients were recovered except one who ha d to be stopped the treatment of ACE-inhibitors because of the depressing of th e blood pressure. The time of producing the effects was 7-20 days. The side effe cts included lower blood pressure accompanied by dizzy in 3 cases, anemia in 2 cases and damage to renal function in 2 cases. Conclusions　ACE-inhibitors were effective in the treatme nt of secondary erythromatosis following renal transplantation. It was important to monitor the hemogram and the renal function of the patients.

The morphogenesis of Valsalva's sinus of semilunar valves in chick embryo was studied with SEM and LM. The sinus began to develop at stage 30 and was basically formed at stage 34 (based on H-H staging). The endothelial cells on arterial and ventricular surfaces of the valve were morphologically different. Mesenchymal cells beneath the endothelium were distributed loosely or densely on different parts of the valve in accordance with the morphological changes of the endothelial cells. The study suggests that the formation of the sinus is associated with not only the growth of endothelial cells on the arterial surface of the valve into underneath mesenchyme, but also with the mesenchyme which is loosing and presents some cavities.

Objective To investigate the assessment of multi-detector spiral CT on the cardiac function after bioprosthetic valve replacement with mitral valve preservation.Methods Thirty-five patients suitable for undergoing bioprosthetic mitral valve replacement in our hospital from May 2012 to February 2014 were randomly divided into 2 groups:group A(experimental group,intraoperative preservation of mitral valve and subvalvular structure during,n=16) and group B (control group,without intraoperative preservation of subvalvular structure of mitral valve,n=19).MDCT before operation and on postoperative 10 d was performed for evaluating the left ventricular function.Results In the comparison of preoperative MDCT,the end diastolic velocity(EDV),end systolic velocity(ESV),ejection fraction(EF) and stroke volume(SV) had no statistical difference between the group A and B.In MDCT results on postoperative 10 d,EDV,ESV and EF in the group A were 113.42±9.22)mL,(38.63±3.40)mL and (51.63±4.71) ％,which in the group B were(113.42 ± 9.22) mL,(38.63 ± 3.40) mL and (51.63 ± 4.71) ％ respectively,the difference was statistically significant(P＜0.05),but SV had no statistical difference between the two groups(P＞0.05).Conclusion The bioprosthetic valve replacement with mitral valve preservation is safe and feasible in technology,moreover effectively protects the postoperative left ventricular function.

Objective To evaluate the role of hippocampal mammalian target of rapamycin (mTOR) signaling pathway in inflammatory pain in rats.Methods Sixty adult male Sprague-Dawley rats,weighing 180-240 g,were randomly divided into 4 groups (n=6 each) by using a random number table:control group (group C),inflammatory pain group (group IP),dimethyl sulfoxide (DMSO) group and rapamycin (inhibitor of mTOR) group (group R).Inflammatory pain was produced by injection of honey bee venom 50 μl into the plantar surface of the left hindpaw.While the equal volume of normal saline was given instead in group C.In group D,2％ DMSO was injected through a gastric tube into stomach 1 ml per day lasting for 3 days,and inflammatory pain was produced at 1 h after the last injection on 3rd day.In group R,rapamycin 10 mg/kg (in 2％ DMSO) was injected through a gastric tube into stomach 1 ml per day lasting for 3 days,and inflammatory pain was produced at 1 h after the last injection on 3rd day.At 2 h after the model was established,the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured.Rats were sacrificed after measurement of pain threshold,and hippocampal tissues were obtained for detection of the expression of mTOR,phosphorylated mTOR (p-mTOR),ribosomal S6 kinase (S6K) and phosphorylated S6K (p-S6K).Results Compared to group C,the MWT was significantly decreased,TWL was shortened,the expression of p-mTOR and p-S6K was up-regulated,and no significant change was found in the expression of mTOR and S6K in IP and DMSO groups,and no significant change was found in group R in the MWT,TWL and expression of p-mTOR,mTOR,p-S6K and S6K.Compared to group IP,no significant change was found in group DMSO in the MWT,TWL and expression of p-mTOR,mTOR,p-S6K and S6K,and the MWT was significantly increased,TWL was prolonged,the expression of p-mTOR and p-S6K was down-regulated,and no significant change was found in the expression of mTOR and S6K in group R.Conclusion Hippocampal mTOR signaling pathways are involved in the development of inflammatory pain in rats.

Aim To investigate the expression and im-plication of HIF-1α, ROCK-2 , FoxM1 in PC12 cell in-jury induced by lead acetate. Methods PC12 cells were treated with lead acetate at the doses of 100 , 200 and 400 μmol·L-1 . The cell viability was determined by MTT reduction assay and LDH assay, the intracellu-lar production of oxygen species was measured by as-sessing SOD and MDA levels, cell apoptosis was deter-mined by Hoechst 33342 staining, the expressions of HIF-1α, ROCK-2 , FoxM1 , Bcl-2 and Bax were deter-mined by immunoblotting analysis. Results Lead ac-etate induced cell injury in PC12 cells in a dose-de-pendent manner, and it potentiated oxygen radical pro-duction and cell apoptosis. In addition, lead acetate enhanced HIF-1α and ROCK-2 expressions, increased Bax/Bcl-2 ratio and decreased FoxM1 expression. Conclusion Lead acetate can induce PC12 cell apop-tosis, which may be related with the expressions of HIF-1α, ROCK-2 and FoxM1 . Cellular oxidative stress may contribute to the injury as well.

Aim To investigate the role of HIF-1 αin PC1 2 cell injury induced by quinolinic acid.Methods PC1 2 cells were treated with quinolinic acid at the do-ses of 2.5,5 and 1 0 mmol·L -1 ,the cell viability was determined by MTT reduction assay and LDH as-say,the intracellular levels of oxygen species was measured by assessing SOD and MDA levels,cell ap-optosis was determined by Hoechst 33258 staining,the intracellular distribution of HIF-1 αwas examined by HIF-1 αimmunostaining,and the expressions of HIF-1 α,Akt,p-Akt,Bcl-2 and Bax were determined by im-munoblotting analysis.Results Quinolinic acid in-duced cell injury in PC1 2 cells in a dose-dependent manner,and potentiated oxygen radical production and cell apoptosis.In addition,quinolinic acid enhanced HIF-1 αexpression and accumulation in nuclei.The p-Akt expression and Bax/Bcl-2 ratio was increased by quinolinc acid in PC1 2 cells.Conclusions HIF-1 αand Akt mediate qunolinc acid-induced cell apoptosis in PC1 2 cells.And cellular oxidative stress may con-tribute to the injury as well.

OBJECTIVES: This study is conducted to estimate the cost paid by the public suffering from disease possibly caused by chemical and to examine the effect on public health. METHODS: Cost-benefit analysis is an important factor in analysis and decision-making and is an important policy decision tool in many countries. Cost-of-illness (COI), a kind of scale-based analysis method, estimates the potential value lost as a result of illness as a monetary unit and calculates the cost in terms of direct, indirect and psychological costs. This study estimates direct medical costs, transportation fees for hospitalization and outpatient treatment, and nursing fees through a number of patients suffering from disease caused by chemicals in order to analyze COI, taking into account the cost of productivity loss as an indirect cost. RESULTS: The total yearly cost of the diseases studied in 2012 is calculated as 77 million Korean won (KRW) per person. The direct and indirect costs being 52 million KRW and 23 million KRW, respectively. Within the total cost of illness, mental and behavioral disability costs amounted to 16 million KRW, relevant blood immunological parameters costs were 7.4 million KRW, and disease of the nervous system costs were 6.7 million KRW. CONCLUSIONS: This study reports on a survey conducted by experts regarding diseases possibly caused by chemicals and estimates the cost for the general public. The results can be used to formulate a basic report for a social-economic evaluation of the permitted use of chemicals and limits of usage.
Cost of Illness ; Cost-Benefit Analysis ; Efficiency ; Fees and Charges ; Hospitalization ; Humans ; Nervous System ; Nursing ; Outpatients ; Public Health ; Transportation

ObjectiveTo explore the effects of recombinant human growth hormone(rhGH)on myocardial inflammatory cytokine expression and heart function in rats with acute myocardial infarction (AMI). MethodsRats with AMI induced by left anterior descending coronary branch ligation were randomized to rhGH and control groups compared with sham-operated group. The effects of 4 weeks of therapy with GH starting 24 hours after myocardial infarction on myocardial cytokines expression and heart function were studied. Myocardial inflammation was examined by analyzing the myocardial cytokine production including the pro-inflammatory cytokines: interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α and the anti-inflammatory cytokine: IL-10. Echocardiography was used to evaluate heart function. ResultsThe levels of TNF-α, IL-1β, IL-6 and IL-10 in the infarcted and non-infarcted region of control group were markedly elevated compared to sham-operated group (all P＜0.05). After 4 weeks therapy, rhGH reduced the expression of TNF -α, IL-1β, IL-6 and increased IL-10 expression in the infarcted and non-infarcted region of rhGH group compared to control group (all P＜0. 05 ). Echocardiography showed that rhGH markedly improved left heart function (P＜0. 05 ). ConclusionsEarly rhGH treatment can improve heart function and myocardial inflammatory cytokine expression after AMI. One of immunopharmacologic mechanisms underlying the beneficial effects of rhGH on heart function improvement may involve the attenuation of pro-inflammatory cytokines and the increase of anti-inflammatory cytokine levels in cardiac myocytes.