Female ; Fluoroscopy ; Humans ; Intubation, Intratracheal ; Male ; Middle Aged ; Tracheotomy ; methods

Objective To investigate the expressions of receptor for advanced glycation endproducts (RAGE) and nuclear factor κB(NF-κB) in brain hippocampus of rat with chronic fluorosis,and to reveal the mechanism of brain damage resulted from chronic fluorosis.Methods Sixty clean grade SD rats were randomly divided to three groups(20 rats in each group,10 female and 10 male) fed with different contents of fluoride,control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group(10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group(50 mg/L fluoride) for six months.Then the rats were killed by femoral artery bleeding and hippocampus was removed.Protein and mRNA levels of RAGE and NF-κB in the hippocampus were determined by Western blotting and quantitative real time PCR,respectively.Results As compared to the control groups[(100.00 ± 2.60)％,(100.00 ± 7.80)％],the expressions of RAGE and NF-κB at protein level in the hippocampus were significantly increased in the small dosage of fluoride exposure groups [(205.00 ± 15.30)％,(156.00 ± 12.20)％] and the large dosage of fluoride exposure groups[(232.00 ± 10.90)％,(162.00 ± 9.80)％,all P ＜ 0.05]; for the mRNA level of RAGE and NF-κB,the expressions were higher in the small dosage of fluoride exposure groups(1.27 ± 0.09,0.83 ± 0.15) and the large dosage of fluoride exposure groups (2.60 ± 0.19,1.27 ± 0.19) than those of the control groups(0.66 ± 0.18,0.32 ± 0.08,all P＜ 0.05).Conclusions The increased expressions of RAGE and NF-κB in the hippocampus of rat brain are caused by chronic fluorosis,and these changes may be associated with the mechanism of nerve injury.

Objective Aim of the study is to investigate the expression of syndecan-4 and nuclear factor κB(NF-κB) in the kidney of rat with chronic fluorosis,and to reveal the mechanism of kidney damage resulted from the toxicity of excessive amount of fluoride.Methods According to body mass and sex,sixty SD rats were randomly divided to three groups according to body mass and fed with different contents of fluoride:control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group (adding 10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group (50 mg/L fluoride) for six months.The protein level of syndecan-4 and NF-κB in the kidney was detected by Western blotting and syndecan-4 mRNA level by quantitative real time PCR.Results As compared to the control group[(100.0 + 8.1)％],the expression of syndecan-4 at protein level in the kidney of rat was significantly increased in the small dosage of fluoride exposure group [(198.5 + 5.6)％,P ＜ 0.05] and large dosage of fluoride exposure group [(209.2 + 13.0)％,P ＜ 0.05]; the protein levels of NF-κB in the small dosage of fluoride exposure group[(284.4 + 11.1)％,P ＜ 0.05] and in the large dosage of fluoride exposure group[(343.2 + 2.9)％,P ＜ 0.05] were significantly increased than that of the control group[(100.0 ± 10.7)％].The mRNA levels of syndecan-4 in the kidney in the small dosage of fluoride exposure group and large dosage of fluoride exposure group(0.431 + 0.058 and 0.453 ± 0.065,both P ＜ 0.05,respectively) were significantly increased than that of the control(0.128 + 0.026).Conclusions The increased expression of NF-κB in the kidney is induced by increased expression of syndecan-4,which may be involved in kidney damage of chronic fluorosis.

20 % . In both groups CH was induced with infusion of 0.01 % NTP at a rate 0.5-6.0 ?g?kg-1?min-1 to maintain MAP at 55-65 mm Hg. MAP, HR, CVP and CO were continuously monitored. Arterial lactate concentration was measured by enzyme assay. Arterial and mixed venous blood gases were analyzed, and oxygen delivery (DO2 ) and consumption (VO2) were calculated before AHH (T0) after AHH was performed (T1), 30 min after CH was induced (T2) and 30 min after termination of CH (T3) in group Ⅰ and in group Ⅱ before CH (T1), 30 min after induction of CH (T2) and 30 rain after termination of CH (T3 ) .ResultsIn group Ⅰ(AHH + CH) compared with the baseline values (T0 ) HR significantly decreased while CVP significantly increased after AHH (T1 ) ; cardiac output (CO) significantly increased after AHH (T1 ) and during CH (T2) while DO2 was significantly decreased after AHH (T1) and CH (T3 ) but arterial lactate concentration was significantly decreased during and after CH (T2, T3). In group Ⅱ (CH alone) compared with the baseline values (T1) HR significantly increased while CVP significantly decreased during and after CH (T2, T3 ) ; there was no significant change in CO and DO2 at T2 and T3 but arterial lactate concentration significantly increased during and after CH (T2, T3). There was significantly less blood loss during operation in group I than in group Ⅱ . ConclusionThere was tissue deoxygenation during and after deliberate hypotension as shown by increased arterial lactate concentration while AHH combined with CH can improve tissue perfusion and oxygenation. AHH can also maintain hemodynamic stability during CH.

Objective:To observe the clinical efficacy of back-Shu and front-Mu points combination needling on balance and walking function in patients after stroke and its mechanism. Methods:A total of 79 patients with post-stroke balance and walking dysfunction were randomly divided into a control group and an observation group.Both groups received conventional treatments such as dietary guidance and oral medications as well as rehabilitation training.On this basis,the control group was treated with additional conventional acupuncture,and the observation group was treated with additional back-Shu and front-Mu points combination needling.Both groups were treated for 4 consecutive weeks.The thickness of abdominal muscle group(transverse abdominal muscle,rectus abdominis,obliquus internus abdominis,and obliquus externus abdominis),the scores of Berg balance scale(BBS),Fugl-Meyer assessment(FMA),and functional ambulation categories(FAC),and walking velocity and stride were compared between the two groups. Results:During the trial,there was 1 dropout case in the control group and 4 dropout cases in the observation group.Before treatment,there were no statistical differences in the abdominal muscle group thickness,scores of BBS,FMA,and FAC,and walking velocity and stride between the two groups(P>0.05).After 4 weeks of treatment,the thickness of abdominal muscle groups,scores of BBS,FMA,and FAC,and walking velocity and stride in both groups were improved(P<0.01),and the observation group was superior to the control group(P<0.05). Conclusion:Both conventional acupuncture and back-Shu and front-Mu points combination needling are conducive to the improvement of balance and walking function in patients after stroke.The back-Shu and front-Mu points combination needling method has better curative efficacy.Strengthening the core muscle group strength may be one of the mechanisms of back-Shu and front-Mu points combination needling treatment.

Background Growth factor-induced proliferation and migration of retinal pigment epithelium (RPE) cells are the major pathological changes of proliferative vitreoretinopathy (PVR).Arsenic trioxide ( As2O3 ) is an active ingredient of Chinese traditional medicines,which has an inhibition on proliferation and migration of tumor cells.However,it is not clear whether As2O3 could inhibit growth factor-induced proliferation and migration of RPE cells. Objective This study was to explore the effects of As2O3 on epidermal growth factor (EGF)-induced proliferation and migration of ARPE-19 cells. Methods RPE cell line (ARPE-19 cells) were cultured.Different concentrations of As2O3(0,0.5,1.0,2.0,5.0,10.0,20.0 μmol/L) were added in the culture plate to treat ARPE-19 cells with or without 10 mg/L EGF in serum-free group for 24 and 48 hours,respectively.The MTT colorimetric assay was used to check the cell viability and evaluate the drug toxicity.The effects of As2O3 on EGF-induced proliferation of ARPE-19 cells were analyzed to get an effective and avirulent concentrations of As2O3.The effects of As2O3 on EGF-induced migration of ARPE-19 cells were observed by scratch-wound assay and the Boyden chamber assay.Results MTT assay showed that the A values were gradually declined with the increase of As2O3 concentrations after As2O3 treatment without EGF for 24 hours and 48 hours ( Fgroup =38.269,P =0.000 ; Ftime =0.874,P =0.358 ).Compared with the control group,no significant differences were seen in the A values of ARPE-19 cells in 0.5-5.0 μmol/L groups (all P＞0.05).Meantime,As2O3 reduced the A values of ARPE-19 cell with 10 mg/L EGF in dose- and time-dependent manner ( Fgroup =152.155,P =0.000 ; Ftime =51.649,P =0.000 ).There were not significant differences in 10 mg/L EGF-induced cell growth after 0.5,1.0,2.0 μmol/L As2O3 was added for 24 and 48 hours ( Fgroup =2.215,P =0.126 ;Ftime =2.230,P =0.155).However,when 5.0-20.0 μmol/L As2O3 added,the A values of 10 mg/L EGF-induced ARPE-19 cells lowed,showing a significant difference in comparison with the control groups ( all P＜0.05),with the cellular inhibiting rate 12％,32％,37％ in 24 hours and 39％,44％ and 53％ in 48 hours.Scratch-wound assay showed that EGF-induced horizontal migration of ARPE-19 cells was slow after 0.5-2.0 μmol/L As2O3 treated,and the same results also appeared in cell lognitudinal migration by Boyden chamber assay,with the inhibitory rates 22％,33％ and 46％ respectively. Conclusions As2O3 is avirulent on ARPE-19 cells within definite concentration range.At ≤ 2.0 μmol/L concentrations,As2O3 dose not affect EGF-induced proliferation of ARPE-19 cells,but it suppresses EGF-induced cell migration.At ≥ 5.0 μmol/L concentrations,As2O3 plays an inhibitory role to EGF-induced proliferation of ARPE-19 cells.

Background Oxidative damage plays an important role in pathogenesis of age-related macular degeneration( AMD ),and its mechanism is the destroy of blood-retinal barrier.Müller cells is a primary component to stabilize the inner barrier of the blood-retina.Researches showed that epidermal growth factor(EGF) can promote the proliferation and migration of animal Müller cells,but less study was found in the effect of EGF on human Müller cells. Objective The present study was to investigate the effects of EGF on the proliferation and migration of human Müller cells and its molecular mechanism. Methods Human Müller cell line MIO-M1 cells were cultured and incubated,and cultured cells were identified using glial fibrillory acidic protein (GFAP),factor Ⅷ,α-smooth muscle actin( α-SMA ),keratin and S-100.Different concentrations of EGF( 0,1,10,30,100 mg/L)was added in freeserum DMEM,and the positive rate of the cells was calculated using 5-bromo-2-deoxyuridine(BrdU) method.The cells were divided into EGF group,H2 O2 group,EGF + H2 O2 group,glucose oxidase ( GO ) group,GO + EGF group,EGF + LY294002+H2O2 group according to the different intervention,and the effects of LY294002 on the proliferation of Müller cells (A590 )were detected by colorimetric assay for cellular growth and survival( MTT assay).The scratch test of Müller cells was used to assess the influence of EGF(0,1,10,30,100 mg/L)on H2 O2-induced damage of human Müller cell.Western blot was used to detect the cell proliferation under the protection of EGF on co-cultured cells using LY294002 and H2O2 and the activation of Akt signal pathways. Results The proliferative rates of the cells were 28.0％,32.9％,39.0％ in 10,30,100 mg/L EGF groups respectively and obviously higher than those in 0,1 mg/L EGF groups (24.5 ％,26.2 ％ ).Under the H2O2 culture,GO culture,respectively,the A570 value of the Müller cell in high concentrations of EGF groups was significantly increased in comparison with lower concentrations EGF groups with the statistical significance among the groups( F=23.582,P=0.000).Compared with EGF+H2O2 group,the A570value of the Müller cells was lowed in EGF+LY294002+H2O2 group.The maximum migration rate of Müller cells was found in 10 mg/L EGF group.Western blot revealed that the presence of H2O2 reinforced the expression of Akt in Müller cells,however,pretreatment with 100 mg/L EGF antagonized the harmful effect of H2O2 on Müller cells.Meanwhile,pretreatment with EGF and LY294002 reduced the expression of Akt in Müller cells. Conclusions EGF can induce the proliferation and migration of human Müller cells with the strongest effect in 10 mg/L.100 mg/L exogenous EGF has a stronger protection to the Müiller cells against H2O2-induced cell damage by activating the PI3KAkt cell survival pathway.

Objective To establish a reproducible rat model of acute rectal mucosal injury induced by acetic acid. Methods Fifteen healthy Sprague-Dawley rats were randomly divided into the control group (3 rats) and experimental group (12 rats).Acute rectal mucosal injury was induced by 4%acetic acid using a cotton swab inserted into the rat rec-tum for 1 min to a depth of 3 cm.The morphological characteristics were analyzed by the naked eye and histology at 0.5 h and 1, 4, and 6 days after acetic acid intervention.Results All rats survived 6-day study period.The successful rate of model establishment was 100%.From 0.5 h to 1st day after acetic acid intervention, the gross morphology of recta showed congestion, edema and ulcer to ulcer complicated with hemorrhage.The histology showed necrosis and hemorrhage of the epithelial tissue of the mucosa to complete and extensive necrosis of the mucosa.The glandular structure showed partial to complete loss.The submucosa showed edema to edema complicated with hemorrhage and congestion.The interstitial tissues showed vasodilatation and congestion to inflammatory cell invasion.From 4 to 6 days after acetic acid intervention, the rectal mucosal changes were obviously improved.Epithelial and glandular regeneration and inflammatory granulation occurred, but not fully recovered, some edema and redness, partial lack of glands were still present.Conclusions 4%acetic acid for 1 min can be used to successfully induce rat model of acute rectal mucosal injury.This procedure is easy to operate, with a high success rate,reproducible, and the alterations are lasting more than 6 days.This animal model is very suitable for rapid screening of topical drugs for the treatment for rectal mucosal injury.

Objective To study the protective effect of vitamin C on UV-induced photoaged skin structure in rats and provide a basis for clinical medicine and health care.Methods Photoaging skin models were set up by chronic ultraviolet radiation in 24 SPF female Sprague-Dawley rats, irradiated twice weekly for 4 weeks.The rat photoaged skin was induced by exposure to a total dose of 123 J/cm2 UVA and 5 J/cm2 UVB for 4 weeks.Vitamin C was administered by gastric gavage in a dose of 50 mg/kg once daily for 30 days during the model development.We compared the pathological changes in the irradiated skin using HE, Masson’ s trichrome and Victoria blue B staining, and compared the ultrastructural changes by electron microscopy.Results Rat models with photoaged skin were developed successfully.The vitamin C group showed significant reduction of pathological severity including erythema, ulcers, epidermal cell proliferation, epidermal thickness, dermis vasodilation, inflammatory cell infiltration, fibroblast proliferation, endoplasmic reticulum dilatation, mitochondrial swelling and vacuolization, elastic fibers degeneration and focal accumulation, collagen fibers swelling with uneven thickness,compared with the rats of model group at the irradiation site.Conclusions Vitamin C is effective in reducing the structural damage of UV-induced photoaged skin in rats.