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Objective:To evaluate the effects of wearing N95 mask on the quality of chest compression and fatigue.Methods:A total of 80 participants from Zhongnan Hospital with basic life support (BLS) certification conferred by American Heart Association (AHA) within two years were enrolled. After reviewing the key points of cardiopulmonary resuscitation (CPR) and grasping the operation on the manikin, they were randomized (random number) into two groups: wearing surgical masks (SM group, n=40) and wearing N95 masks (N95 group, n=40) during CPR. Each participant performed a 2-minute chest compression-only CPR on the manikin. Participants' height, body weight, Borg scores and physiological parameters before and after CPR were recorded. The quality of chest compression (including compression depth, compression rate, adequate depth proportions, adequate rate proportions, hand position and complete chest recoil) were recorded by Laerdal QCPR ? software. Student's t test and Mann-Whitney test were used to compare the differences of chest compression quality indexes between the two groups. Results:Compared with the SM group, participants in the N95 group had significantly increased median of Borg scores after CPR (16 vs 14, P=0.027), and decreased quality of chest compression, including the decline in compression depth (mean 47 mm vs 52 mm, P=0.020), compression rate (107 times/min vs 118 times/min, P=0.004), complete chest recoil rate (89.8% vs 98.1%, P=0.046), adequate depth proportions (67.4% vs 89.6%, P<0.01) and adequate rate proportions (60.6% vs 74.8%, P<0.01). Conclusions:Wearing N95 masks during CPR decreases the quality of chest compression and aggravates rescuers’ fatigue. Therefore, it is necessary to exchange rescuers more frequently to ensure the quality of chest compression when wearing N95 masks.
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Aim To investigate the effect of BMS- 345541 on the repair of DNA DSBs induced by VP-16 in AML cells and its possible mechanism. Methods The effects of BMS-345541 on the sensitivity of AML cells to VP-16 were determined by MTT. Flow cytome-try ( FCM) was applied to test the level of DNA dam-age, cell cycle progression and apoptosis in AML cells. High content analysis ( HCA) was used to verify the amount ofγ-H2AX,p-ATM,RAD51 in AML cells. Results BMS-345541 could significantly inhibit the proliferation of AML cells induced by VP-16 . BMS- ＜br> 345541 increased the amount of RAD51 foci and p-ATM foci in AML cells treated with VP-16 after 6 hours , which led to increased numbers of cells in the G2/M phases of the cell cycle,then induced apoptotic cell death. Conclusion BMS-345541 sensitizes AML cells to VP-16 via selective inhibition of homologous recombinational repair of DNA double-strand breaks.
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Objective To explore the therapeutic effects of combined application of survivin antisense nucleic acid and taxol in subcutaneous xenograft mouse model of Balb/c and to preliminarily investigate the mechanism of the anticancer effects.Methods The model of subcutaneous tumor was established by hypodermic injection of C26 cells into Bal b/c mice.The mice were then randomly divided into five groups through the internal tumor injection:the blank group (C),lipo2000 group (L),paclitaxel group (T),survivin antisense nucleic acid group (A),and survivin antisense nucleic acid combined with paclitaxel group (A+T).We observed tumor growth,determined cell apoptosis by TUNEL method,and detected the expression of survivin by Western blot.Results ① All treatment groups had T/C<60%,which was significantly different from that of group L (P <0.05);the intervention was proved effective in vivo .The tumor inhibition rate of mice tumor weight showed that there were significantly curative effects in groups T,A and A+ T compared with that in group C (P < 0.05 ).The antitumor activity of paclitaxel (tumor inhibition rate of 21.82%±0.84%)could be improved by more than 59% through combination therapy (tumor inhibition rate of 54.1 6% ± 0.32%)concerning inhibition of tumor weight growth.② TUNEL method detected apoptotic cells:The tumor cells hardly had apoptosis in the blank group while T group and A group had a certain number of apoptotic cells.The experiment results suggested that PTX could promote tumor cell apoptosis,and that not only A+T strengthened the effect in killing tumor cells,but also the synergy of both could influence tumor resistance and ultimately make the effect in promoting tumor cell apoptosis conspicuous.③ The expression of survivin protein:The results showed that the expression of survivin protein in group A + T was obviously decreased without the expression of β-actin affected;it did not change significantly in group C compared with group L.The ratio of the A-value in groups T,A and A+T was 0.895 ±0.01 1,0.704 ±0.121 and 0.345 ± 0.01 9,respectively.Analysis of variance t-test showed that the expression level in group A+T obviously differed from that in groups C,L,A and T (P <0.05).Conclusion The combined therapy of survivin antisense nucleic acid and taxol can promote tumor cell apoptosis by downregulating the expression of survivin protein,reduce the body’s resistance to drugs and create synergetic effects.
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Aim To investigate the role of miR-125 b and its DNA methylation in homocysteine ( Hcy )-in-duced vascular smooth muscle cells( VSMCs) prolifera-tion. Methods VSMCs were stimulated with 0,50, 100, 200, 500 μmol · L-1 Hcy respectively. Then qRT-PCR was used to detect the mRNA levels of miR-125b,and nested-touchdown methylation-specific PCR ( ntMS-PCR) was used to detect the methylation levels of miR-125b. VSMCs were transfected with miR-125b precursor or the inhibitor of miR-125b ,then 3-(4,5-dimethylthiazol-2-yl)-2-5-diphenyl tetrazolium bromide ( MTT ) assay was used to reflect the proliferation of VSMCs. The distribution of CpG islands of miR-125b promoter region was analyzed by bioinformatics meth-ods. VSMCs were stimulated with 100 μmol·L-1 Hcy and transfected with or without DNA methylation inhib-itors 5-nitrogen impurity cytidine ( AZC) , then the ex-pression of miR-125b was detected by qRT-PCR. Re-sults The mRNA levels of miR-125 b were decreased in 100,200,500 μmol·L-1 Hcy group compared with 0 μmol·L-1 Hcy group. The precursor of miR-125b could inhibit the proliferation activity and the inhibitor of miR-125 b could increase the proliferation activity of VSMCs cells. Bioinformatics analysis indicated that MiR-125 b promoter region had a CpG island whose length was 792 bp ( 1881-2672 ) . The miR-125 b pro-moter region methylation levels increased after Hcy in-tervention ( P <0. 01 ) . The expression level of miR-125 b increased after AZC intervention ( P <0. 05 ) . Conclusions ① Hcy promotes vascular smooth mus-cle cell proliferation maybe by down-regulating the ex-pression of miR-125b. ② Hcy down-regulates the ex-pression of miR-125 maybe by up-regulating the methy-lation levels of miR-125b promoter region.
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Aim To investigate the possible mecha-nisms of the levels of NO decrease induced apoptosis in human placental trophoblast cells. Methods Human placental trophoblast cells ( HTR-8 ) were cultured in 5 ml DMEM-F12 culture medium with 37℃ 5% CO2 . Then, the old culture medium was discarded and re-placed with 10,100,500,1 000 μmol·L-1 L-NAME, and the group without L-NAME was set as the control group, cultured for 48h. The effects of L-NAME on the survival of cells were detected by methylthiazolyldiphe-nyl tetrazolium bromide ( MTT); the content of NO in cells was tested by nitrate reductive enzymatic;trans-mission electron microscopy, flow cytometry analysis and Annexin-V FITC dyeing were used to test the effects of L-NAME on apoptosis in HTR-8 cells;restore Fe3+ colorimetric assay was applied for detection of to-tal antioxidant capacity ( T-AOC ) , xanthine oxidase for detection of superoxide dismutase ( SOD) activity, and thiobarbituric acid colorimetry for determination of content of MDA. Results Compared with the control group, the survival rate of HTR-8 cells and the levels of NO in 100,500,1 000 μmol·L-1 L-NAME group were significantly reduced(P<0.05,P<0.01). Flow analysis and Annexin-V FITC staining showed that L-NAME could induce cell apoptosis in a dose-dependent manner. The number of cell apoptosis was negatively correlated with the content of NO ( r = -0.5210 ) in HTR-8 cells. Transmission electron microscopy results showed that compared with the control group, the ex-perimental group's cell nucleus shape was irregular, nuclear pyknosis in irregular shape, the chromatin ag-glutination or side the collection, mitochondrial swell-ing or enrichment, crest fracture or dissolved, even vanished, forming the vacuole, especially in 100 μmol ·L-1 L-NAME group, the apoptotic bodies obviously appeared. At the same time, T-AOC, SOD levels in HTR-8 cells decreased ( P <0.05 ) , and the MDA content increased ( P<0.05 ) . The number of cell ap-optosis was negatively correlated with the level of T-AOC ( r= -0.3212 ) , SOD ( r= -0.2779 ) in HTR-8 cells , while positively correlated with the content of MDA(r=0.2807). Conclusion Oxidative stress may play an important role in the levels of NO decrease in-duced apoptosis in human placental trophoblast cells.
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Objective To observe the sensitivity of myocardium to ischemia/reperfusion (I/R) injury in mechanical trauma rats.Methods The mechanical trauma was established by Noble-Collip drum in the rats that were completely randomized into five groups:sham trauma group,trauma group,sham trauma and sham surgery group,sham trauma and I/R group,trauma and I/R group.The rats were subjected to 30 minutes of ischemia and one hour of reperfusion one week after trauma.The left ventricular systolic pressure (LVSP) and the left ventricular maximum rate of pressure rise and fall ( ± dp/dtmax ) were recorded with BL-410 biological signal recording and analysis system.The levels of serum creatine kinase isoenzyme MB (CK-MB) and cardiac troponinⅠ (cTnI) were detected by double antibody sandwich ABC-ELISA technique.At the end of reperfusion,the heart was excised and stained with Evan' s blue dye and triphenyltetrazolium chloride (TTC) to measure the infarct region with Image-Pro Plus 6.0 image analysis software.Results Compared with the sham traumatic I/R group,the cardiac function in vivo was significantly decreased in the traumatic I/R group ( P ＜ 0.01 ).While the serum CK-MB [ (4 960 ± 588 ) ng/ml:(2 925 ± 426) ng/ml,P ＜ 0.01 ],cTnI [ ( 18.10 ± 3.06 ) ng/ml:( 6.67 ±1.57 ) ng/ml,P ＜ 0.01 ] levels and myocardial infarct size [ ( 36.70 ± 7.42 ) ％:( 22.27 ± 4.54 ) ％,P＜0.01] were obviously higher in the traumatic I/R group compared with the sham traumatic I/R group.Conclusion Mechanical trauma increases the sensitivity of myocardium to I/R injury in rats.
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<p><b>AIM</b>To prepare the working standards of 3-nitrotyrosine (3-NT) and establish a two-antibody-sandwich ELISA for determining the concentration of peroxynitrite in the tissue.</p><p><b>METHODS</b>Nitrated bovine serum albumin was prepared by additions of an alkaline stock solution of peroxynitrite which was synthesized by a quenched-flow reactor. The monoclone anti-3-NT antibody from mouse was used as coating antibody and the polyclone anti-3-NT antibody from as labeling antibody to prepare the standard work curve by orthogonal design. The concentrations of 3-NT in cardiac tissue from rats subjected to myocardial ischemia and reperfusion (MI/R) were analyzed.</p><p><b>RESULTS</b>A two-antibody-sandwich ELISA method for measuring 3-NT content in biological fluids and homogenates was successfully established. The detecting limit was 0.1 ng x ml(-1) and the linear range of standard work curve was 0.15 - 7.50 ng x ml(-1) (r2 = 0.995). The 3-NT concentration in cardiac tissue from rats subjected to MI/R (1022.42 +/- 97.35 ng x mg pro(-1)) was significantly higher than that in the sham group (246.58 +/- 56.52 ng x mg pro(-1), P < 0.01).</p><p><b>CONCLUSION</b>A two-antibody-sandwich ELISA was established for determining the 3-NT concentration in the tissue and conveniently, quickly, accurately quantitative analysis of the content of 3-NT. The assay provides a new method for quantitative analysis of the peroxyinitrite in the future.</p>
Subject(s)
Animals , Male , Rats , Antibodies, Monoclonal , Enzyme-Linked Immunosorbent Assay , Methods , Myocardial Reperfusion Injury , Myocardium , Chemistry , Peroxynitrous Acid , Rats, Wistar , Sensitivity and Specificity , TyrosineABSTRACT
<p><b>OBJECTIVE</b>To investigate the biological effects of anti-beta(3) adrenoceptor (beta(3)-AR) autoantibody in the serum of patients with heart failure, which may contribute to a new therapeutic clue for heart failure.</p><p><b>METHODS</b>The synthetic peptide of the second extracellular loop of the beta(3)-AR was used as the antigen to screen sera of patients with heart failure and of healthy controls by using enzyme-linked immunosorbent assay. IgG in the patients group of positive autoantibody sera was prepared by using a MabTrap Kit (Amersham) following the manufacturer's instructions. The effects of IgG per each group both on contractile response of adult isolated cardiomyocytes and on beating frequency of cultured neonatal rat cardiomyocytes were observed.</p><p><b>RESULTS</b>The positive rate of anti-beta(3)-AR autoantibody was 26.7% (mean antibody titer: 1:43.27 +/- 2.71) or 11.0% (mean antibody titer: 1:14.59 +/- 1.61) in patients or healthy subjects, respectively P < 0.05. Compared with the control group, the autoantibody against beta(3)-AR from the patients group decreased cell shortening amplitude/cell shortening 3.84% +/- 0.33%, the velocity of shortening -0.47 microm/s +/- 0.07 microm/s and relengthening 0.17 microm/s +/- 0.02 microm/s in adult isolated cardiac myocytes, respectively. The autoantibody in the patients group decreased the beating rate in cultured neonatal rat cardiac myocytes by 47.1 beats/min +/- 8.11 beats/min, which could have a 6-hour continuance. This decreasing was not modified by Nadolol (beta(1)-AR and beta(2)-AR antagonist) in pretreating myocytes, but was nearly prevented by Bupranolol (nonselective beta-AR antagonist) or beta(3)-AR specific antigen.</p><p><b>CONCLUSION</b>It seems reasonable to state that a high titer of the autoantibody against beta(3)-AR in the serum in patients with heart failure, which could have a negative inotropic and chronotropic effect, may be a part of pathophysiological mechanisms of heart failure.</p>