Meta-analysis of comparison for efficacies between surgical plus radio(chemo)therapy and non-surgery chemoradiotherapy treatment strategies for advanced hypopharyngeal cancer / 中华耳鼻咽喉头颈外科杂志

Meta-analysis was used to compare the long-term efficacy and laryngeal function preservation rate of patients with advanced hypopharyngeal cancer treated with surgery plus radio(chemo)therapy (SRT) or non-surgery chemoradiotherapy (CRT). We searched publicly published articles on case-control studies of surgical and non-surgical comprehensive treatment of advanced hypopharyngeal cancer in PubMed, the Cochrane Library, Wanfang Database, Chinese Journal Full-text Database, and Chinese Science and Technology Periodical Database. The search language was limited to Chinese and English, and the period was from 1990 to 2018. These literatures were rigorously screened by inclusion and exclusion criteria. The data needed for this study were extracted and the Meta analysis was performed using RevMan 5.3 software. A total of 13 literatures were included, and the overall quality of the literature was relatively high, and no significant publication bias was suggested. A total of 1 994 subjects, including 720 in the SRT group and 1 274 in the CRT group. The average 3-year overall survival rates were 42.9% in SRT group and 44.8% in CRT group,with no significant difference (1.14, 95: 0.62-2.06, 0.68). The average 5-year overall survival rate (1.42, 95: 1.10-1.84, 0.01), 5-year local recurrence-free survival rate (1.68, 95: 1.11-2.55, 0.01) and 5-year local control rate (2.17, 95: 1.52-3.12, 0.01) of SRT group were 46.4%, 47.4% and 71.2%, respectively, which were higher than those of non-surgical group (37.9%, 32.0%, and 52.2% respectively). The average laryngeal function preservation rate was 19.8%,being significantly lower than 80.6% of the non-surgical group(0.03, 95: 0.01-0.07, 0.01). SRT has better long-term efficacy, while CRT has better preservation of laryngeal function.

Resveratrol increases sirtuin 1 expression in peripheral blood mononuclear cells of premature infants and inhibits the oxidative stress induced by hyperoxia in vivo / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the effect of resveratrol on the levels of sirtuin 1 (SIRT1) and reactive oxygen species (ROS) in peripheral blood mononuclear cells (PBMCs) of premature infants exposed to hyperoxia.</p><p><b>METHODS</b>Peripheral blood and isolated PBMCs from premature infants (gestational age<32 weeks) without oxygen supplement were collected and were randomly assigned into four groups: control, air+resveratrol, hyperoxia, and hyperoxia+resveratrol. The PBMCs were cultured in vitro for 48 hours, then the ROS content in PBMCs was measured by laser scanning confocal microscopy. Malondialdehyde (MDA) content in the medium was measured by the whole spectrum spectrophotometer. SIRT1 positioning was assessed by immunofluorescence. SIRT1 expression levels in PBMCs were measured by Western bolt.</p><p><b>RESULTS</b>Compared with the control group, the level of SIRT1 in the air+resveratrol group increased significantly (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate in the hyperoxia group increased significantly, while the expression level of SIRT1 decreased significantly compared with the control group (P<0.05). The levels of ROS and MDA and the SIRT1 transposition rate decreased significantly (P<0.05), and the expression level of SIRT1 increased significantly in the hyperoxia+resveratrol group (P<0.05).</p><p><b>CONCLUSIONS</b>Resveratrol can increase SIRT1 expression in PBMCs and inhibit SIRT1 shuttle from nucleus to cytoplasm in order to increase the ability of antioxidative stress in premature infants exposed to hyperoxia, thereby reducing the oxidative stress injury in premature infants.</p>

Roles of PKCβ/P66Shc oxidative stress signal pathway in mediating hyperoxia-induced ROS production in alveolar epithelial cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the roles of PKCβ/P66Shc oxidative stress signal pathway in mediating hyperoxia-induced reactive oxgen species (ROS) production in alveolar epithelial cells (A549) and the protective effects of PKCβ inhibitor on hyperoxia-induced injuries of alveolar epithelial cells.</p><p><b>METHODS</b>A549 cells were cultured in vitro and randomly divided into three groups: control, hyperoxia and PKCβ inhibitor LY333531 treatment. The hyperoxia group was exposed to a mixture of O2 (950 mL/L) and CO2 (50 mL/L) for 10 minutes and then cultured in a closed environment. The LY333531 group was treated with PKCβ inhibitor LY333531 of 10 µmol/L for 24 hours before hyperoxia induction. Cells were collected 24 hours after culture and the levels of PKCβ, Pin1, P66Shc and P66Shc-Ser36 were detected by Western blot. The intracellular translocation of P66Shc, the production of ROS and cellular mitochondria membrane potential were measured using the confocal microscopy.</p><p><b>RESULTS</b>Compared with the control group, the levels of PKCβ, Pin1, P66Shc and P-P66Shc-Ser36 in A549 cells 24 hours after culture increased significantly in the hyperoxia group. These changes in the hyperoxia group were accompanied with an increased translocation rate of P66Shc from cytoplasm into mitochondria, an increased production of mitochondrial ROS, and a reduced mitochondrial membrane potential. Compared with the hyperoxia group, the levels of Pin1, P66Shc and P66Shc-Ser36 in A549 cells, the translocation rate of P66Shc from cytoplasm into mitochondria and the production of mitochondrial ROS decreased significantly, while the mitochondrial membrane potential increased significantly in the LY333531 treatment group. However, there were significant differences in the above mentioned measurements between the LY333531 treatment and control groups.</p><p><b>CONCLUSIONS</b>Hyperoxia can increase the expression of PKCβ in alveolar epithelial cells and production of mitochondrial ROS and decrease mitochondrial membrane potential. PKCβ inhibitor LY333531 can partially disrupt these changes and thus alleviate the hyperoxia-induced alveolar epithelial cell injury.</p>

Silencing of Pin1 suppresses hyperoxia-induced apoptosis of A549 cells / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the effect of silence of Pin1 expression on hyperoxia-induced apoptosis in alveolar epithelial cells A549.</p><p><b>METHODS</b>A549 cells were divided into four groups: control, hyperoxia, negative lentivirus and Pin1-shRNA hyperoxia. The hyperoxia group was exposed to a mixture of 95%O2 and 5%CO2 for 10 minutes. Then cells were cultured in a closed environment. After 24 hours, the changes of morphology were observed under an inverted microscope. Cell apoptosis was detected by flow cytometry (FCM). The expression of X-linked inhibitor of apoptosis protein (XIAP) and Caspase-9 were detected by immunohistochemistry. The production of reactive oxygen species (ROS) and cellular mitochondria membrane potential (△Ψm) were determined by fluorescence microscopy.</p><p><b>RESULTS</b>Under the inverted microscope, the A549 cells grew slowly and the changes in morphology of the cells were most obvious in the hyperoxia and negative lentivirus groups. The changes in morphology of A549 cells were obviously improved in the Pin1-shRNA hyperoxia group. The FCM results showed that the apoptosis rate of A549 cells increased, Caspase-9 expression increased, XIAP expression decreased, mitochondrial ROS production increased and mitochondrial membrane potential decreased in the hyperoxia and negative lentivirus groups compared with the control group (P<0.05). Compared with the hyperoxia and negative lentivirus groups, the apoptosis rate of A549 cells decreased, Caspase-9 expression decreased, XIAP expression increased, mitochondrial ROS production decreased and mitochondrial membrane potential increased in the Pin1-shRNA hyperoxia group (P<0.05), although the levels of the indexes did not reach to those of the control group.</p><p><b>CONCLUSIONS</b>Silencing of Pin1 could suppress hyperoxia-induced apoptosis of A549 cells.</p>

Expressions of Caveolin-1 and Transforming growth factor betal 1 in A549 cells exposed to hyperoxia and their relationship / 中华实用儿科临床杂志

Objective To observe the expressions of Caveolin-1 (CAV-1) and transforming growth factor bata 1 (TGF-β1) in human adenocarcinoma of lung A549 cells exposed to hyperoxia,and to explore the changes in CAV-1 and TGF-β1 expressions and the role in hyperoxic lung injury.Methods After the A549 human lung cancer cell lines were resuscitated,the cells were packaged and cultured in 50 mL/L CO2 culture chamber,when approaching to the condition of confluence in CO2 culture chamber(37 ℃,50 mL/L CO2),the cells were randomly divided into control group and hyperoxia group.Eighteen bottles of A549 cells in each group.The hyperoxia group received attacking factor that was mixed with oxygen (950 mL/L)and CO2 (50 mL/L) at a velocity of 3 L/min for 10 min;then the flasks were enclosed and cultured in culture chamber,while those in control group were still exposed to 5 mL/L CO2.After cells were cultured for 12 h,24 h,48 h,the changes in morphology were observed under the inverted microscope,the expressions CAV-1 and TGF-β1 were detected by double immunofluorescence staining technique,followed by laser scanning under the focus microscope.Results In the control group,there was high expression of CAV-1 associated with low expression of TGF-β1 (44.25 ± 3.23,10.18 ± 2.74).Compared with control group,the content of CAV-1 reduced continuously (12 h:35.25 ± 1.88,24 h:20.75 ± 1.68,48 h:9.86 ± 2.80) under prolonged hyperoxia exposure,but TGF-β1 increased gradually(12 h:17.32 ± 1.50,24 h:26.51 ± 1.82,48 h:41.94 ±4.47),and the expression of CAV-1 had highly negative relation to TGF-β1 at the same time (r =-0.91,-0.62,-0.53,-0.88,all P ＜ O.05) in the control group and the hyperoxia group in 12 h,24 h,48 h.Conclusions The reduction of CAV-1 expression can attenuate the inhibitory effect of TGF-β1 and activate TGF-β1 signaling pathway,which may result in hyperoxic lung injury.

Protective effects of mitochondrial ATP-sensitive potassium channel on A549 cell apoptosis induced by hyperoxia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the protective effects of mitochondrial ATP-sensitive potassium channel opener diazoxide on hyperoxia-induced apoptosis of type II alveolar epithelial cells (A549 cells) and possible mechanisms.</p><p><b>METHODS</b>A549 cells were cultured in vitro and divided randomly into control, hyperoxia and diazoxide group. The hyperoxia group was exposed to a mixture of O2 (900 mL/L) and CO2 (50 mL/L) for 10 minutes, then cultured in a closed environment. The diazoxide group was pretreated with diazoxide of 100 μmol/L for 24 hrs before hyperxia induction. The cells were collected 12, 24 and 48 hrs after culture. The morphologic changes of A549 cells were observed under an inverted microscope. A549 cell apoptosis was detected by flow cytometry. The expression of Omi/HtrA2 in the endochylema of A549 cells was determined by immunohistochemistry.</p><p><b>RESULTS</b>A549 cells were damaged and the changes in morphology of the cells were serious in the hyperoxia group. The apoptosis rate of A549 cells and the expression of Omi/HtrA2 in the endochylema increased in the hyperoxia group compared with the control group (P<0.05). The growth and the morphology of A549 cells were greatly improved and the cell injuries were obviously alleviated in the diazoxide group. The expression of Omi/HtrA2 in the endochylema and the apoptosis rate of A549 cells were significantly reduced in the diazoxide group compared with the hyperoxia group (P<0.05).</p><p><b>CONCLUSIONS</b>Diazoxide as an opener of mitoKATP channel can reduce the expression of Omi/HtrA2 and the apoptosis rate of A549 cells, thus relieves the injury of A549 cells induced by hyperoxia.</p>

Effects of Ucf-101 on expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the expression of serine protease Omi/HtrA2 in kidneys of postasphyxial neonatal rats, and to study the effects of Ucf-101 on apoptosis and the expression of Omi/HtrA2 in these rats.</p><p><b>METHODS</b>Seventy-two neonatal Wistar rats of 7-10 days old were randomly divided into 3 groups: control, postasphyxial model, Ucf-101-treated postasphyxialThe postasphyxial model was established by normobaric asphyxiaExpression of Omi/HtrA2 was determined with streptavidin-peroxidase immunohistochemistry 2, 24 and 48 hrs after asphyxia. Terminal deoxynuleotidyl-mediated nick end labeling (TUNEL) was used to ascertain the apoptosis of renal cells.</p><p><b>RESULTS</b>Compared with the control group, OmiHtrA2 expression in renal cells began to increase 2 hrs after asphyxia and peaked at 24 hrs. The expression of Omi/HtrA2 in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group (P<0.01). TUNEL-positive cells began to increase 2 hrs after asphyxia and peaked at 24 hrs in the postasphyxial model group when compared with the control group. The number of TUNEL-positive cells in the Ucf-101-treated postasphyxial group was significantly lower than that in the postasphyxial model group at all time points (P<0.01).</p><p><b>CONCLUSIONS</b>The expression of Omi/HtrA2 in kidneys is increased in postasphyxial neonatal rats. The increased Omi/HtrA2 expression may play an important role in the development of postasphyxial renal injury. Treatment with Ucf-101 can reduce the expression of Omi/HtrA2 in kidneys of postasphyxial neonatal rats and thus reduce renal tububar epithelial cell apoptosis.</p>

Viral Etiological Analysis of 104 Cases of Infantal Viral Pneumonia / 实用儿科临床杂志

Objective To explore the etiology,clinical manifestations of infantal viral pneumonia in Luzhou area.Methods Five viral specific serum IgM antibodies were detected by enzyme-linked immunosorbent assay(ELISA) in acute period of viral pneumonia.Five kinds of virus were separated,as respiratory syncytial virue(RSV),influenza virus(IFV),adenovirus(ADV),cytonegalo virus(CMV),and parainfluenza virus(PIV).Serum specific IgM was positive,C-reactive protein(CRP) was less than 8 mg/L,and there was no(clini-)cal and laboratory proof of other pathogenic infection detected in 221 infants with pneumonia.Results 1.One hundred and four cases of viral infection were detected from 221 infants with pneumonia.The viral positive detected rate was 47.1%,and there were 75 cases of single viral infection(72.1%) and 29 cases of mixed viral infection(27.9%) among them.2.In the single viral infection,RSV was the first,IFV,ADV,PIV and CMV being the second,the third,the fourth,and the fifth respectively.3.The types of likely infection virus were different in different age-stage and seasons in infants.Conclusions The etiology of infantal pneumonia is complicated.The types of viral infection are various besides germ infection and the epidemic season peak;clinical manifestations are different.Earlier detection of(etiology) in infection will make clear the etiology and then take appropriate treatment measures to improve curative effect.

Protective Effects of Diazoxide on Injury of Human Renal Tubular Cell Induced by Serum Obtained from Neonates with Asphyxia / 实用儿科临床杂志

Objective To explore the protective effects of diazoxide on injury of human renal tubular cell(HK-2)induced by serum obtained from neonates with asphyxia.Methods HK-2 cells was used as the target cel1.The attacking concentration of serum obtained from neonates with asphyxia was 200 mL/L.The experiment was designed as 3 groups.HK-2 cells were divided into control group,asphyxia group,and diazoxide group.Control group:joined nutrient fluid including 100 mL/L embryo cow blood serum.Asphyxia group:joined nutrient fluid including the isometric 200 mL/L serum obtained from neonates with asphyxia.Diazoxide group:the diazoxide was joined nutrient including the isometric 200 mL/L serum obtained from neonates with asphyxia fluid.The diazoxide density finally was 100 ?mol/L.Then the change of morphology was observed and photographed under inverted microscope,and the cell viability was measured by methyl thiazolyl tetrazolium method,and the leakage rate oflactate dehydrogenase(LDH)was determined by biochemical methods.Results Under inverted microscopy,HK-2 cells in control group pastes the wall to be good,assumes the paving stone type,into flat polygon,fission many,the cell arrangement was close,connection large expanse,quantity were many.Compared with control group,the HK-2 cell to suffer injury obviously,the shape changed,become the anomalous circular or the ellipse by the model flat polygonal cell,the intercellular space crevice enlarged,the connection was loose,intercellular space obviously many cell fragmented.Living cell quantity reduced obviously,the cell vigor dropped,and the leakage rate of LDH increased significantly in asphyxia group(P