Objective To explore the effect of MMP-1, TIMP-1 on burn wound healing and hypertrophic scar (HS) forming. Methods Normal human full-thickness skin grafts were transplanted to the back of nude (athymic) mice, after these grafts survived, deep Ⅱ degree burn wounds were made in the middle of these grafts. During the process of burn wound healing and HS formation, the expressions of MMP-1 and TIMP-1 were detected by immunohistochemical staining. Results MMP-1 expression was first noted by day 2 after burns and became more prominent from day 3 to day 15, and then decreased rapidly. Immunostaining for MMP-1 was markedly increased at boundary regions marked by connective tissue fluidity. Immunoreactive TIMP-1 was also detected by day 2 but rapidly assumed the same interface expression pattern as described for MMP-1. Compared with MMP-1, immunostaining of TIMP-1 was irregular, but was obvious around vascular tissues. Conclusions The balance between MMP-1 and TIMP-1 during the inflammation and granulation phases might be important for the regulation of collagen proteins degradation. Within the remodeling phase, the inhibition of MMP-1 by TIMP-1 and the decrease of collagen degradation might lead to HS forming. The striking immunolocalization of MMP-1 and TIMP-1 to epithelial-dermal, eschar-dermal, and vascular-dermal interfaces suggested that they might play a particularly significant role at boundary regions marked by connective tissue fluidity.

Objective: To observe the expression of transient receptor potential channel-1—large conductance Ca2+-activated K+channel (TRPC1-BK) signal complex in aortic smooth muscle tissue in experimental mice of atherosclerosis (AS). Methods: Our research included in 2 groups: Control group, wild C57BL/6J mice were fed by normal diet and AS group, ApoE-/- mice were fed by high fat diet to establish AS model. All animals were treated for 10 weeks, n=10 in each group. The total RNA and protein were extracted from aortic smooth muscle tissue in sacrificed mice. The mRNA and protein expressions of TRPC1, BKα and BKβ1 subunit were measured by RT-PCR, Western blot analysis and immunohistochemistry staining. Results: By RT-PCR examination, compared with Control group, AS group showed increased mRNA expression of TRPC1, P<0.05 and decreased mRNA expressions of BKα and BKβ1 subunit, both P<0.01. By Western blot analysis, compared with Control group, AS group had elevated protein expression of TRPC1, P<0.05 and reduced protein expressions of BKα and BKβ1 subunit, both P<0.01; by immunohistochemistry staining, AS group had the higher protein expression of TRPC1, P<0.01 and the lower protein expressions of BKα and BKβ1 subunit, both P<0.05. Conclusion: The mRNA and protein expressions of TRPC1-BK signal complex were affected in aortic smooth muscle tissue in AS mice, which speculated that TRPC1-BK signal complex might be become a new target for treating the relevant vascular disease.

This study examined the effects of arsenic trioxide on apoptosis and interleukin4 release in T cells of asthmatic patients in vitro and investigated the role of Bcl2 in the active mechanism. Tcells were isolated from asthmatic patients (n=21) and healthy controls (n=20), and then treated with arsenic trioxide and dexamethasone. Cell apoptosis was measured using fluorescence microscopy, flow cytometry and a cytochrome c ELISA kit. Interleukin4 levels in the serum and in supernatants from T cells were quantified by ELISA. Flow cytometric analysis and immunofluorescence studies were performed to determine Bcl 2 expression. Tcells of the asthmatic patients (I.e. without treatment) exhibited decelerated spontaneous apoptosis after 24 h incubation in vitro when compared to T cells of the healthy controls. With dexamethasone treatment, an increase in apoptosis of Tcells was not significantly different between both groups, irrespective of the method used. Arsenic trioxide treatment, however, significantly increased the apoptosis of T cells of the asthmatic group and showed a slight effect on the control group. In asthmatic patients, elevated levels of interleukin 4 and upregulated Bcl 2 expression were detected. Moreover, in vitro, T cells of asthmatic patients spontaneously released more interleukin4 and exhibited more Bcl 2 expression than T cells from the control group. Arsenic trioxide treatment significantly decreased interleukin4 release and downregulated Bcl 2 expression in asthmatic patients, while it only slightly affected healthy controls. Dexamethasone treatment decreased interleukin4 release in both groups examined. It did not significantly influence Bcl2 expression. These results suggest that arsenic trioxide induces T cell apoptosis and decreases interleukin4 release in T cells of asthmatic patients in vitro and that downregulation of Bcl2 expression may be an important mechanism.

AIM To study the possible mechanism of the treatment of arsenic trioxide on asthma. METHODS T cells isolated from 21 asthmatic patients and 20 healthy controls were treated with arsenic trioxide (0.1 mg·L-1) or dexamethasone (5 mg·L-1),in vitro, for 24 h. Interleukin-4 (IL-4) levels in supernatants from T cells were quantified with ELISA. Cell apoptosis was measured by using fluorescence microscopy, flow cytometry and cytochrome c ELISA kit. RESULTS T cells of asthmatic patients spontaneously released more IL-4 than that of healthy controls. Arsenic trioxide significantly decreased IL-4 release of T cells from asthmatic patients, which was more obvious compared with healthy controls. Dexamethasone decreased IL-4 release in both groups. Apoptosis percentage and cytochrome c content in cytoplasm of T cells from asthmatic patients were lower than those from healthy controls. Arsenic trioxide significantly increased the apoptosis percentage and cytochrome c content in cytoplasm of T cells in the asthmatic group, and had slighter effects on that in healthy controls. Dexamathasone increased the apoptosis percentage and cytochrome c content of T cells in both groups. CONCLUSION The mechanism of the treatment of arsenic trioxide on asthma involves the induction of T cell apoptosis and decrease of IL-4 release in asthmatic patients.

Objective To explore the effect of nicotine on rats callus content and maturity in the process of fracture healing.Methods Sixty male Sprague-Dawley rats were randomly divided into model group,mild nicotine group and severe nicotine group (n =20/each group).The 3-mm bone defects fracture models were made in the junction of the lower 1/3 of the rat left radial.Five rats of each group were sacrificed randomly in the 3,7,14,21 days after surgery,respectively.The left radial were collected as the observed object.The callus thickness and maturity of the specimens were detected by HE staining.Results At the 3rd days after modeling,the difference in specimens callus thickness between each treatment group and the model group was not statistically significant (P ＞ 0.05),no difference in the maturity of the callus under the microscope; callus thickness in mild and severe nicotine groups and model group was (1.59 ± 0.09) mm,(1.43 ± 0.12) mm,(1.39 ± 0.09) mm at the 7th day after modeling,(1.98 ± 0.12) mm,(1.78 ± 0.08)mm and (1.68 ± 0.09) mm at the 14th day after modeling,and (2.39 ± 0.09) mm,(1.93 ± 0.11) mm,(1.89 ± 0.09) mm at the 21 st day after modeling; The difference of callus thickness in specimens between each treatment group and the model group had statistical significance (P ＜ 0.05,P ＜0.01),callus thickness and maturity of the treatment group were lower than that in the model group.Conclusions Nicotine affects the proliferation and differentiation of callus,reduces callus formation,inhibits maturity transformation of bone,and delays the healing process of fracture.

Objective:To investigate the expression of CD 163 in the plasma and tumor tissue of non-small cell lung cancer (NSCLC)patients,and the effects of cancer cell migration and proliferation .Methods:35 cases of NSCLC patients in our hospital as the study group,and 35 healthy volunteers as control group ,we used Real-time RCR to detect the expression of CD163 in the plasma and tumor tissue of NSCLC patients.Using small interfering RNA (siRNA) to inhibit the expression of CD163 in MH-2,and co-culture with A549.The level of cancer cell migration was observed by transwell and the level of cell proliferation was observed by CCK -8.Results:The expression of CD163 in the plasma and tumor tissue of NSCLC patients was significantly higher than the control group , the difference was statistically significant (P<0.05);after the expression of CD163 was suppressed in MH-2,the levels of cancer cell migration and proliferation were significantly decreased , the difference was statistically significant ( P<0.05 ) .Conclusion: The expression of CD163 in the plasma and tumor tissue of NSCLC patients is increased ,and may elevate the levels of cancer cell migration and proliferation.

Objective:To investigate the expression of microRNA-Let-7a in the serum and tumor tissue of non-small cell lung cancer( NSCLC) patients and the effects of cancer cell migration and proliferation.Methods: 50 cases of NSCLC patients in our hospital as the study group,50 healthy volunteers were used as control group,we used Real-time RCR to detect the expression of microRNA-Let-7a in the serum and tumor tissue of NSCLC patients.Using microRNA let-7a mimics transfected into A549,the level of cancer cell migration was observed by transwell,the level of cell proliferation was observed by CCK-8,the level of k-Ras was observed by Real-time RCR and Western blot.Results: The expression of microRNA-Let-7a in the serum and tumor tissue of NSCLC patients was significantly higher than the control group,the difference was statistically significant (P<0.05).After microRNA let-7a transfected into A549,the levels of cancer cell migration and proliferation were significantly decreased,the difference was statistically significant (P<0.05),the mRNA and protein levels of k-Ras were reduced inA549 cells,the difference was statistically significant (P<0.05). Conclusion:The expression of microRNA let-7a is low in the serum and tumor tissue of NSCLC patients,and may weaken the levels of cancer cell migration and proliferation through the Ras signaling pathway.

Objective To evaluate the efficacy and safety of a superpulse-mode fractional carbon dioxide(CO2) laser for the treatment of onychomycosis. Methods Patients with typical clinical manifestations of onychomycosis and positive for direct microscopic examinations of fungi were enrolled into this study, and treated with a superpulse-mode fractional CO2 laser for eight sessions. The scoring clinical index for onychomycosis (SCIO)and onychomycosis severity index (OSI)were calculated according to patients′ age, clinical type of onychomycosis, thickness of nails, area and length of nail involvement before the treatment, at the end of treatment, 1 month and 3 months after completion of treatment. Mycological clearance was also evaluated according to direct microscopy and fungal culture results. Adverse reactions to laser therapy were recorded. Statistical analysis was carried out by using the chi-square test and Wilcoxon signed-rank sum test with the SPSS 17.0 software. Results Totally, 20 patients with onychomycosis were enrolled into this study, and 75 affected nails were treated. Finally, 18 patients with 71 target nails completed the treatment and follow-up. The SCIO and OSI were 13.07 ± 6.47 and 21.11 ± 11.94 in these patients at baseline respectively, both significantly different from those at the end of treatment(9.03 ± 6.14 and 13.63 ± 12.10, respectively, both P < 0.05), 1 month((8.51 ± 6.99 and 14.18 ± 13.65, respectively, both P < 0.05)and 3 months(7.89 ± 7.26 and 13.70 ± 13.93 respectively, both P <0.05)after completion of treatment. No significant differences were observed in mycological clearance rates between the posttreatment time points(57.75%(41/71)at the end of treatment vs. 59.15%(42/71)at 1 month vs. 61.97%(44/71) at 3 months after completion of treatment, P > 0.05). The SCIO and OSI decreased from 12.48 ± 5.41 and 16.44 ± 9.89 at the baseline to 5.01 ± 5.56 and 6.44 ± 8.26 at 3 months after the treatment, respectively, in patients with distal and lateral subungual onychomycosis (DLSO), and from 17.86 ± 3.98 and 34.05 ± 2.56 to 15.88 ± 4.10 and 31.00 ± 7.28 respectively in patients with total dystrophic onychomycosis (TDO). During the treatment, several patients felt transient mild pain, but no subungual hemorrhage or other adverse reactions occurred. Conclusions The fractional CO2 laser in superpulse mode shows a reliable efficacy for the treatment of mild to moderate onychomycosis such as DLSO, especially when the nail plate is superficially invaded and grows rapidly. It directly inhibits and kills fungi, and treatment duration should be prolonged according to conditions.

Objective To explore the effective means and important significance for preventing the born of neonatal patients with severe thalassemia.Methods Among the pregnant women and spouses receiving prenatal examination in our hospital from January 2013 to December 2015 were performed the thalassemia screening and gene diagnosis,49 couples carrying the same type thalassemia were conducted the prenatal amniotic fluid thalassemia gene diagnosis and follow up after prenatal diagnosis.Results In 49 couples carrying the same type thalassemia,the main gene mutation types of α-thalassemia detected by the gene diagnosis were --SEA/aα(50.0％),-α3.7/αa (36.5％) and-α4.2/αa (11.5％),which of β-thalassemia were CD17/N(42.0％),CD41-42/N (26.0％) and IVS-Ⅱ-654/N(22.0％).The results of prenatal diagnosis showed that there were 4 cases of HbH disease,2 cases of Bart's hydrops fetus,10 cases of severe β-thalassemia,19 a-thalassemia carriers,10 β-thalassemia carriers,1 case of co-inheritance of a-and β-thalassemia,and 3 health fetuses.The follow up results were consistent with those of prenatal diagnosis.Conclusion Conducting prenatal screening and diagnosis of thalassemia in pregnant women can effectively prevent the birth of neonatal patients with severe thalassemia.

Objective To investigate the risk factors of pancreatic fistula after pancreaticoduodenectomy (PD).Methods The clinical data of 186 patients who received PD at the Second Affiliated Hospital of Kunming Medical College from May 2000 to May 2010 were retrospectively analyzed.All patients were divided into pancreatic fistula group (39 patients) and non-pancreatic fistula group ( 147 patients).Risk factors of pancreatic fistula after PD were screened out from 20 factors by univariate and multivariate analysis.The univariate analysis was carried out by chi-square test or Fisher exact test,and the muhivariate analysis was done by Logistic regression.Results Thirty-nine patients were complicated with pancreatic fistula,including 26 in grade A,10 in grade B and 3 in grade C.The results of univariate analysis showed that duration of preoperative jaundicc,loss of body weight at 6 months before operation,preoperative total bilirubin level,preoperative albumin level,postoperative albumin level,length of pancreas dissected,pancreatic tube diameter,pancreatic texture and time of abdominal drainage tube pull out were high risk factors of pancreatic fistula ( x2 =34.990,20.480,8.212,10.890,13.561,11.505,13.820,4.539,36.590,P ＜ 0.05).The results of multivariate analysis showed that duration of preoperative jaundice ＞ 8 weeks,loss of body weight at 6 months before operation ≥ 10％,pancreatic tube diameter ＜ 3 mm,soft pancreatic texture and time of abdominal drainage tube pull out ＞ 5 days were the independent risk factors of pancreatic fistula ( OR =2.229,3.383,1.437,1.273,11.939,P ＜ 0.05).Conclusion Duration of preoperative jaundice ＞ 8 weeks,unconscious loss of body weight ≥ 10％ within 6 months before operation,pancreatic tube diameter ＜ 3 mm,soft pancreatic texture,time of abdominal drainage tube pull out ＞ 5 days would increase the risk of pancreatic fistula after PD.