Objective To study the apoptosis pathway of human lung adenocarcinoma cell line A549 induced by 1-β-D-arabinofuranosylcytosine (Ara-C) in vitro. Methods A549 cells were incubated with Ara-C for 72hours in vitro. Biological changes of apoptotic cells were studied by TUNEL staining. Morphological changes of the A549 cells treated with Ara-C were observed by transmission electron microscope. The expressions of p53 and p73 were investigated by Western blotting. Results 1.Apoptotic rates of A549 cells exposure to Ara-C studied by TUNEL staining were higher than that of the control (P＜0.01). 2.Apoptosis body was apparently observed by transmission electron microscope. 3.Endogenous p73 but not p53 was induced and activated in dose-dependent manner upon Ara-C treatment by Western blotting.Conclusion Ara-C can effectively induce apoptosis of A549 cells. DNA damage-induced apoptosis of A549 cells treated by Ara-C is independent of functional p53.Up-regulation of p73 may play an important role that enhances the sensitivity of A549 cells to Ara-C and be partly responsible for p53-independent apoptosis.

Objective To investigate the clinical efficacy of photodynamic therapy with red and blue light in the treatment of facial acne. Methods Ninety-two cases of facial acne in dermatology outpatient hospital were randomly divided into the test group and the control group, with 46 cases in each group. Patients in the test group received the photodynamic therapy, and patients in the control group received red plus blue light treatment for eight weeks, respectively. Results Before treatment, patients in the test group and the control group had no significant differences in acne, papules, pustules, nodules, cysts and gags score. After 8-week treatment, the comedones, papules, pustules, nodules cyst number, gags score of patients in the test group were significantly less than or lower than those of patients in the control group (P < 0.05, respectively). The healing rate was 84.78% in the test group, which was higher than that of 65.22%in the control group of (P<0.05). The total efficiency was 97.83%in the test group and 93.48% in the control group, with no significant difference. The adverse reaction rate was 10.87% in the test group and was 23.91% in the control group, with no significant difference. Conclusion The effect of photodynamic therapy for facial acne is better than red plus blue light treatment ,with a less incidence of adverse reactions.

Purpose To investigate clinicopathological features, diagnosis and differential diagnosis of non-sebaceous lymphadenoma of the parotid gland. Methods The histopathological morphology, immunohistochemical profiles and clinicopathological features were an-alyzed in two cases of NSL, along with review the related literatures. Results Two patients were female adults. Microscopically, The tumor was a well-circumscribed mass surrounded by a fibrous capsule of variable thickness and comprised a mixture of proliferating epi-thelium accompanied by a prominent lymphoid component, reactive lymphoid follicles were found in lymphoid stroma. The epithelial component took the form of anastomosing trabeculae, glands, solid basaloid islands or cyst formation. The cysts and glands were lined with luminal cells and abluminal cells, filled with eosinophilic secretions with occasional histiocytes. The epithelial cell was no seba-ceous differentiation, significant cytological atypia and mitotic activity. A fibrous capsule with subcapsular sinus was seen around the mass in one case. Immunohistochemically, the abluminal cells were positive for p63, CK34βE12 and CK5/6, while the epithelial cells were positive for CK(AE1/AE3) and CK7. Conclusion NSL is a very rare benign of salivary gland, which occuring in the lymph node lesions are less reported, knowledge of the wide histological spectrum of this rare tumor is important in order to avoid misdiagno-sis, particularly as malignant tumor.

Objective To study the effect of selection of indications in percutaneous laser disc decompression(PLDD).Methods Lumbar disc herniation treated by PLDD with satisfactory and unsuited indications in 34 cases respectively were matched studied.Results The curative effect was 85.3% and 55.9% in satisfactory indication group and unsuited indication group respectively (?~2=5.06,P

Objective To investigate the the clinical effect and immune regulatory mechanism of red-blue light combined with Niuhuang Shangqing capsules for the moderate-severe acne.Methods A total of 180 patients with moderate to severe acne treated in People's Hospital of Nanhai District in Foshan City from June 2014 to June 2016 were randomly divided into 2 groups with each group 90 patients. The control group was treated with red and blue light, and observation group was treated with the combination of red and blue light andNiuhuang-Shangqingcapsules. The levels of SP(Substance P), IL-1 and IL-6 in peripheral blood were observed and analyzed. The recurrence rates and adverse events were observed.Results After treatment, the SP (657.4 ± 36.6 pg/mlvs.799.9 ± 60.2 pg/ml,t=19.188), IL-1(61.8 ± 24.7pg/L vs.92.1 ± 23.5 pg/L,t=8.431), IL-6 (38.7 ± 10.3pg/mlvs.66.7 ± 14.1pg/ml, t=12.421) of the observation group were significantly better than those of the control group (allPs<0.01). The total effect rate of the observation group were 91.11% (82/90), which were significantly higher than 70.00% (63/90) of control group (χ2=12.804,P<0.01). Conclusions The Red-blue light combined withNiuhuang-Shangqing capsules for treating moderate-severe acne, has significant effect and can reduce the serum levels of SP, IL-1 and IL-6, with fewer adverse events and lower recurrence rates. They can be used as a safe and effective treatment of acne.

Objective To investigate the changes in the expression of macrophage migration inhibitory factor (MIF) mRNA in a rat model of ventilator-induced lung injury.Methods Thirty adult male Sprague-Dawley rats,weighing 2β5-260 g,were randomly divided into 3 groups (n =10 each) using a random number table:control group (group C),small tidal volume (VT) mechanical ventilation group (group S) and large tidal volume mechanical ventilation group (group L).The animals were anesthetized with intraperitoneal ketamine 100 mg/kg,midazolam 0.2 mg/kg and atropine 1.0 mg/kg.The rats were tracheostomized and spontaneous breathing was maintained in group C,while the rats were tracheostomized and mechanically ventilated for 4 h in groups S and L.The tidal volume was 7 ml/kg (group S) or 40 ml/kg (group L),I ∶ E was 1 ∶ 1,RR was 80 bpm and FiO2 was 100％.At 4 h of spontaneous breathing or mechanical ventilation,broncho-alveolar lung lavage fluid (BALF) was collected for determination of the total protein concentration,white blood cell (WBC) counts and concentrations of MIF,IL-6 and IL-1β (by ELISA).Then the rats were sacrificed and the lungs removed for microscopic examination and for determination of wet to dry lung weight ratio (W/D ratio) and expression of MIF mRNA (by RT-PCR).Results Compared with C and S groups,WBC counts,concentrations of total protein,MIF,IL-6 and IL-1β in BALF,and W/D ratio and expression of MIF mRNA in lung tissues were significantly increased in group L (P ＜ 0.05).There was no significant difference in the indexes mentioned above between group C and group S (P ＞ 0.05).The pathological changes occurred in group L.Conclusion The up-regulation of MIF mRNA expression in lung tissues may be involved in the development of ventilator-induced lung injury in rats.

Objective To investigate the role of Toll-like receptor9 (TLR9)-myeloid differentiation factor 88 (MyD88) signal pathway in alveolar macrophages in ventilator-induced lung injury (VILI).Methods 30 adult male Sprague-Dawley (SD) rats were randomly assigned to three groups (with 10 rats in each group).Group A was the control group,with spontaneous respiration after tracheostomy.Rats in group B received mechanical ventilation for 4 hours with normal tidal volume (VT) 7 ml/kg after tracheostomy,and group C rats received mechanical ventilation with VT 40 ml/kg for 4 hours.After termination of ventilation,examination with transmission electron microscopy was performed to observe the ultrastructure changes in alveolar epithelial cell type Ⅱ (AEC Ⅱ) of the lung.Lung wet/dry ratios (W/D) and total protein concentration,the concentration of interleukins (IL-6 and IL-1 β) in bronchoalveolar lavage fluid (BALF) were determined.The protein and mRNA expressions of TLR9,MyD88 and nuclear factor-κB (NF-κB) in alveolar macrophages were assayed by Western Blot and real-time reverse transcription-polymerase chain reaction (RT-PCR).Results The ultrastructure of AEC Ⅱ in the group A and group B was almost normal,whereas the chromatin of the nuclei,the lamellar corpuscles in the cytoplasm,the cell membrane and the microvilli of the AEC Ⅱ in the group C showed injurious changes in various degrees.When the group C was compared with the group A and the group B,it was shown that the W/D ratios (5.54 ± 0.17 vs.4.58 ± 0.17,4.69 ± 0.16) and total protein concentration (g/L:6.33 ± 0.61 vs.0.45 ± 0.05,0.47 ± 0.04),IL-6 (μg/L:1.989 ± 0.103 vs.1.033 ± 0.061,1.010 ± 0.069) and IL-lβ (ng/L:2.79 ±0.25 vs.1.05 ±0.15,1.23 ±0.22) in BALF,the protein expressions of TLR9,MyD88 and NF-κB [TLR9 (A value):0.770 ±0.042 vs.0.300 ±0.027,0.310 ±0.037; MyD88 (A value):0.950 ±0.091 vs.0.560 ±0.082,0.580±0.084; NF-κB(A value):1.020 ±0.076 vs.0.740 ±0.052,0.700 ±0.076] in alveolar macrophages were all increased significantly,and all of which showed significant difference (P＜0.05 or P＜0.01).The mRNA levels of TLR9,MyD88 and NF-κB in alveolar macrophages in the group B were (1.13 ± 0.32),(1.18 ± 0.33),and (1.11 ± 0.22) folds of those of the group A,respectively,but there were no significant differences (all P＞0.05).While the mRNA levels of TLR9,MyD88 and NF-κB of alveolar macrophages in the group C were (8.66 ± 0.69),(6.41 ± 0.53) and (5.29 ± 0.71) folds of those of the group A,respectively,and all of them showed significant difference (all P＜0.01).Conclusion TLR9-MyD88 signaling in alveolar macrophages plays a role in pathogenesis of VILI.

Objective To explore the differences and development of executive function(EF) between cerebral palsy(CP) children and normal children. Methods Forty-eight 4 ～6 years old CP children and fiftyeight normal children were tested by "cool" and "hot" EFs. Results There were significant differences between "cool" EF of CP children(18.34±14.31) and normal children(6.94 ±3. 18) ( t = 3. 83, P<0.01 ) ;and there were significant differences between "hot" EF of CP children(279.67 ±330. 18) and normal children(709.31 ± 304. 13)( t = -4.93, P< 0.01). There were significant age differences on the "cool" EF ( F=8.689, P< 0.01) and "hot" EF ( F=3. 833, P<0.05) of CP children. There were significant age differences on the "cool" EF ( F= 15.469, P<0.01) and on the "hot" EF ( F=8.470, P<0.01) of normal children. There was negative correlation between "cool" EFs and "hot" EFs( r= -0.440, P<0.01). Conclusion "Cool" and "hot" EFs of CP children are lower than those of normal children. "Cool" and "hot" EFs can develop from 4 to 6 years old,but the development of EFs are not absolutely consistent between CP children and normal children. There is correlation between "cool" and "hot" EFs in patients with CP,but not dissociation.

Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00%(6/30), 24.24%(8/33), and 21.05%(16/76), respectively;χ2=0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells. Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00%(6/30), 24.24%(8/33), and 21.05%(16/76), respectively;χ2=0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells. Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.