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The present study was conducted to evaluate sublethal effects of B-azolemiteacrylic on the two-spotted spider mite, Tetranychus urticae Koch (Acari: Tetranychidae). Female adults of T. urticae were exposed to LC10 and LC30 of the acaricide, and the effects on treated females and their offspring were evaluated. The results showed that the fecundity of F0 female adults treated with LC10 and LC30 of B-azolemiteacrylic was reduced by 30.9 and 39.2%, respectively. Longevity and oviposition period of the females were significantly reduced as well. The developmental duration of egg and deutonymph stage of the F1 generation were not significantly different from that of the control. The protonymph stage after LC30 treatment lasted significantly longer, whereas the larva, deutonymph and female stage were significantly shorter than the control. The oviposition period of the F1 generation was significantly shortened, the fecundity of each female decreased significantly, and the ratio of female-to-male was reduced too. Moreover, the average generation period of T. urticae after LC10 and LC30 treatments was shorter than that of the control, and the net production rate (R0), intrinsic rate of increase (rm) and finite rate of increase (λ) were all reduced by 33.3, 7.5 and 1.9% (LC10 treatment) and by 51.3, 14.8 and 3.6% (LC30 treatment), respectively. The population doubling time was prolonged by 7.5 and 14.8% after LC10 and LC30 treatments, respectively, compared with the control. These results indicate that B-azolemiteacrylic may effectively inhibit the development rate of the F0 and F1 populations of T. urticae, which will help design integrated strategies for the comprehensive control of T. urticae and rational use of pesticides in the field.
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Acaricides , Life History Traits , Tetranychidae , Animals , Demography , Female , Male , OvipositionABSTRACT
Objective:To analyze the level and latent categories of the training needs of the nursing staff of the social volunteer teams in Jiangsu Province, and to provide basis for the targeted training.Methods:From March to July in 2018, 224 elderly care teachers from 13 social volunteer teams of 100 Red Cross societies in Jiangsu Province were surveyed for the knowledge of the care for the aged and the needs of training by the self-designed questionnaires. A total of 207 valid questionnaires were collected, with an effective recovery rate of 92.4%. SPSS 21.0 and Latent GOLD 5.1 software were used for description analysis, hierarchical clustering and latent category analysis.Results:The number of answer of "very need" to knowledge and skills among the aged care teachers for the elderly, such as psychological care, elderly volunteer services and recreational activities for the elderly, was 196, 196 and 193, with a proportion of 94.7%, 94.7% and 93.2%, respectively. Cluster analysis showed that training needs could be divided into four aspects: life care knowledge and skills, health care knowledge and skills, psychological care knowledge and skills, and spiritual comfort knowledge and skills. The results of latent category analysis showed that the aged care teachers could be divided into three groups based on their different training needs: high demand group for overall knowledge and skills, partial demand group for overall knowledge and skills, and high demand group for medical care and psychological care knowledge and skills. The corresponding latent probability of the three groups were 80.2%, 13.0%, 6.8%, respectively.Conclusion:The training for the aged care of social volunteer teams should pay attention to the teaching of spiritual comfort knowledge and skills for the elderly. The training program should be oriented to the multi-level and individualized needs of the teachers, so as to meet the needs of the aged care teachers for their own development.
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Objective To observe the effect of microRNA-155 (miR-155) on the inflammatory response of rat alveolar macrophages induced by lipopolysaccharide (LPS). Methods The alveolar macrophages NR8383 of rat were cultured in vitro, the macrophages in logarithmic growth phase were harvested to conduct experiment. ① The 1 mg/L LPS was used to stimulate the rat alveolar macrophages for 3, 6, 12, and 24 hours, a phosphate buffer solution (PBS) control group was also set up. Enzyme linked immunosorbent assay (ELISA) was used to detect the dynamic changes of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the supernatant, and real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the dynamics expression of miR-155 in the cells, which confirmed the optimal time for LPS stimulation was 12 hours. ② Carboxyfluorescein (FAM) labeled mimic (FAM mimic) and inhibitor (FAM inhibitor) were used to transfect the alveolar macrophage, and the transfection effect was observed under inverted fluorescence microscope 6 hours later to confirm the optimal transfection concentration of mimic was 20 nmol/L, and the optimal transfection concentration of inhibitor was 100 nmol/L. miR-155 mimic and miR-155 inhibitor were transfected to alveolar macrophages respectively at the optimal transfection concentration for 24 hours, and 1 mg/L LPS was used to stimulate the cells for 12 hours. A mimic negative control + LPS group and an inhibitor negative control + LPS group were set up. The expressions of IL-1β and TNF-α in the supernatant were determined by ELISA to observe the regulation of miR-155 on inflammatory response of alveolar macrophages. Results ① After stimulation of 1 mg/L LPS on alveolar macrophages, the contents of IL-1β and TNF-α in the supernatant and the expression of miR-155 in the cells were increased gradually with time prolongation, IL-1β and TNF-α contents peaked at 12 hours, and the expression of miR-155 peaked at 24 hours [as compared with PBS control group, IL-1β (ng/L): 910.43±36.09 vs. 22.66±7.84, TNF-α (ng/L): 3 138.39±394.10 vs. 233.92±8.84, miR-155 (2-ΔΔCt): 7.82±0.30 vs. 1, all P < 0.05]. ② Under inverted fluorescence microscope, after 20 nmol/L FAM mimic or 100 nmol/L FAM inhibitor transfected alveolar macrophages for 6 hours, a large number of cells showed green fluorescence, indicating that the transfection was successful. The expression of miR-155 in the cells transfected with 20 nmol/L miR-155 mimic was up-regulated by (236.73±46.49) times as much as that in the negative control group (P < 0.05), and the levels of IL-1β and TNF-α in the supernatant of the cells stimulated by 1 mg/L LPS for 12 hours were significantly lower than those in the negative control group [IL-1β (ng/L): 324.37±36.59 vs. 799.31±39.44, TNF-α (ng/L): 1 554.01±342.48 vs. 3 020.49±418.30, both P < 0.05]. The miR-155 activity was significantly inhibited in the cells transfected with 100 nmol/L miR-155 inhibitor, and the expression of miR-155 was decreased by (4.00±3.26)% as compared with the negative control group, but the difference was not statistically significant (P > 0.05), and the levels of IL-1β and TNF-α in the supernatant of the cells stimulated by 1 mg/L LPS for 12 hours were significantly higher than those in the negative control group [IL-1β (ng/L): 1 358.98±212.04 vs. 878.68±53.42, TNF-α (ng/L): 4 225.57±281.11 vs. 2 881.32±286.08, both P < 0.05]. Conclusion In LPS induced inflammatory response of alveolar macrophages, miR-155 plays an obvious inhibitory role.
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<p><b>OBJECTIVE</b>To prepare rabbit anti-mouse zona pellucida 2 (mZP2) polyclonal antibodies and test their immunoactivity.</p><p><b>METHODS</b>Recombinant proteins of mZP2 expressed in Rosetta transformant was separated by SDS-PAGE, and the gel strips containing the recombinant mZP2 were cut out and emulsified to immunize New Zealand white rabbits. The antibody response of the antiserum was detected by ELISA, and the specificity of the antiserum was verified by immunohistochemical assay. The effect of the antiserum on the binding of oocytes with acrosomal reacted sperm was tested by sperm-egg binding assay.</p><p><b>RESULTS</b>ELISA results showed that the immunized rabbit produced anti-mZP2 antiserum. The antiserum reacted specifically with the zona pellucida of mouse ovarian sections. Sperm-egg binding assay showed that treatment of the oocytes with the anti-mZP2 antiserum caused decreased binding of zona pellucida with the acrosomal reacted sperm by 43.7%.</p><p><b>CONCLUSION</b>We obtained rabbit anti-mouse ZP2 polyclonal antibodies that can inhibit the binding of oocytes with acrosomal reacted sperm.</p>
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Animals , Female , Male , Mice , Rabbits , Antibodies , Allergy and Immunology , Antibody Formation , Egg Proteins , Allergy and Immunology , Immune Sera , Membrane Glycoproteins , Allergy and Immunology , Oocytes , Receptors, Cell Surface , Allergy and Immunology , Recombinant Proteins , Allergy and Immunology , Sperm-Ovum Interactions , Spermatozoa , Zona Pellucida GlycoproteinsABSTRACT
ObjectiveTo investigate the protective effect of transfected microRNA-146a (miR-146a) on mice with sepsis-induced acute lung injury (ALI) in vivo.Methods Twenty-four healthy male BALB/C mice were randomly divided into sham group, sepsis group, transfection group and transfection control group, eachn = 6. Mice in transfection group were given miR-146a agomir loaded by in vivo-jetPEITM via airway before reproduction of model, and mice in transfection control group were given negative control loaded by in vivo-jetPEITM only via airway. The septic model was reproduced by cecal ligation and puncture (CLP) 12 hours after transfection , and the mice in the sham group underwent laparotomy and closure only without ligation and puncture of the cecum. The mice of each group were sacrificed at 24 hours post-operation. The expression of miR-146a in lung tissue was determined by real time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and the quantity of tumor necrosis factor-α (TNF-α) in the bronchial alveolar lavage fluid (BALF) was determined with enzyme-linked immunosorbent assay (ELISA). The wet/dry ratio of lung (W/D) was determined. The pathohistological changes in the lung were observed and scored. Results The expression of miR-146a showed a significant increase in sepsis group, transfection group and transfection control group, which were (3.56±0.43), (27.64±3.46) and (3.72±0.54) folds of that in sham group, respectively (P 0.05). Compared with the sham group, higher level of TNF-αin the BALF was found in the sepsis group, transfection group and transfection control group (ng/L: 511.65±43.47, 305.74±34.76, 492.27±42.21 vs. 50.72±7.23, allP< 0.01). The level of TNF-α in transfection group was significantly lower than that in sepsis group and transfection control group (bothP< 0.01). Compared with the sham group, the W/D ratio of lung in sepsis group, transfection group and transfection control group showed a significant increase (6.11±0.32, 5.02±0.29, 6.05±0.43 vs. 4.18±0.10, allP< 0.01). The W/D ratio of lung in transfection group was significantly lower than that of sepsis group and transfection control group (bothP< 0.01). The lung injury score of transfection group was significantly lower than that of sepsis group and transfection control group (6.12±0.75 vs. 10.53±1.52, 9.73±1.08, bothP< 0.01).Conclusions miR-146a agomir loaded by in vivo-jetPEITM instillation into airway was able to increase the expression of miR-146a in the lung tissue of septic mice. Up-regulation of miR-146a inhibit the release of the inflammatory cytokine TNF-α stimulated by sepsis, and alleviate inflammatory reaction and lung tissue injury in mice with sepsis-induced ALI.
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OBJECTIVES: To observe the kinetic changes in microRNA-132 (miR-132) expression in rat alveolar macrophages after lipopolysaccharide (LPS)-induced inflammation, and to investigate initially on the role of miR-132 in alveolar macrophages inflammatory response. METHODS: The rat alveolar macrophages NR8383 cultured without pyrogen in vitro were divided into blank control group and LPS (1 mg/L) stimulated 3, 6, 12, 24 hours groups. Culture supernatants and cell pellets were collected at each time point respectively. Enzyme-linked immunosorbent assay (ELISA) was used to assay the production changes in tumor necrosis factor-α (TNF-α), interleukins (IL-1ß and IL-6) in the supernatant. Real-time quantitative polymerase chain reaction (PCR) was used to detect the expression of miR-132 in the cells. RESULTS: After stimulating rat alveolar macrophages with LPS, the production of TNF-α (ng/L: 364.83 ± 46.29 vs. 34.07 ± 8.62, P<0.01), IL-1ß (ng/L: 153.83 ± 43.67 vs. 32.33 ± 10.62, P<0.05) and IL-6 (ng/L: 183.85 ± 43.52 vs. 42.62 ± 11.21, P<0.05) were all increased significantly at 3 hours post LPS stimulation compared with blank control group, reached the peak at 12 hours (TNF-α: 605.09 ± 57.13, IL-1ß: 377.09 ± 28.55, IL-6: 558.04 ± 77.45, all P<0.01), and descended at 24 hours (TNF-α: 281.95 ± 41.61, IL-1ß: 263.17 ± 51.36, IL-6: 438.74 ± 79.94) but the levels remained significantly higher than blank control group (all P<0.01). The expression of miR-132 started to rise at 3 hours after LPS stimulation compared with blank control group [(1.12 ± 0.11) folds, P=0.995], and presented a gradual increasing trend at 6, 12, 24 hours [(5.98 ± 0.65), (7.64 ± 0.53), (8.92 ± 0.83) folds, all P<0.01]. CONCLUSION: The expression of miR-132 increased gradually over time after LPS-induced inflammation of rat alveolar macrophages, suggesting that miR-132 may be involved in regulation of rat alveolar macrophages inflammatory response.
Subject(s)
Inflammation/pathology , Macrophages, Alveolar/metabolism , MicroRNAs/metabolism , Animals , Cell Line , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Lipopolysaccharides/adverse effects , Macrophages, Alveolar/drug effects , Rats , Tumor Necrosis Factor-alpha/metabolismABSTRACT
<p><b>BACKGROUND</b>Novel influenza A viruses of avian-origin may be the precursors of pandemic strains. This descriptive study aims to introduce a novel avian-origin influenza A (H10N8) virus which can infect humans and cause severe diseases.</p><p><b>METHODS</b>Collecting clinical data of three cases of human infection with a novel reassortment avian influenza A (H10N8) virus in Nanchang, Jiangxi Province, China.</p><p><b>RESULTS</b>Three cases of human infection with a new reassortment avian influenza A(H10N8) virus were described, of which two were fatal cases, and one was severe case. These cases presented with severe pneumonia that progressed to acute respiratory distress syndrome (ARDS) and intractable respiratory failure.</p><p><b>CONCLUSION</b>This novel reassortment avian influenza A (H10N8) virus in China resulted in fatal human infections, and should be added to concerns in clinical practice.</p>
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Aged , Female , Humans , Male , Middle Aged , Antiviral Agents , Therapeutic Uses , Fluoroquinolones , Therapeutic Uses , Imipenem , Therapeutic Uses , Influenza A Virus, H10N8 Subtype , Virulence , Influenza, Human , Diagnosis , Drug Therapy , Oseltamivir , Therapeutic UsesABSTRACT
Objective To determine kinetics of TNF-α and miR-146a (microRNA-146a)expressions in lipopolysaccharide (LPS)-induced NR8383 alveolar macrophages (AM) at different intervals and their relationships in order to explore regulatory effect and mechanism of miR-146a on alveolar macrophages inflammatory responses.Methods NR8383 alveolar macrophages were seeded in a 6-well plate,and stimulated with 1 μg/ml of LPS for 0 h,3 h,6 h and 12 h separately after 90 min.Cells were harvested and supernatant were collected 0 h,3 h,6 h and 12 h after incubation.The expressions of miR146a and TNF-α mRNA in cells were detected by real-time qPCR and the levels of TNF-α protein in the supematant of cells were assayed by enzyme-linked immunosorbent assay ( ELISA ).Pearson correlation analysis was used to analyze the correlation between miR-146a and TNF-α mRNA.Results ①The level of TNF-α protein in the supernatant of cell was significantly increased 3 h after LPS challenge ( 359.80 ±57.54) pg/ml (P <0.01 ),and peaked 12 h later (729.22 ±50.40) pg/ml (P<0.01 ) ; ②the expression of TNF-α mRNA peaked 3 h after LPS challenge (67.48 ±24.52) fold,P <0.01 ),and then decreased gradually; ③the expression of miR-146a mRNA increased continuously until 6 h or 12 h after LPS challenge 6 h:(5.33 ±0.81) fold,12 h:(8.21 ±1.19) fold,(P<0.01),and it showed an upward tendency;④ the expression of miR-146a mRNA was negatively correlated with TNF-α mRNA ( r =-0.895,P <0.01).Conclusions The miR-146a mRNA showed a negative correlation with TNF-α mRNA present in lipopolysaccharide-stimulated alveolar macrophages,suggesting miR-146a mRNA involved in regulating the inflammatory response of alveolar macrophages.
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The renin-angiotensin system exerts a profound regulatory effect on the functional features of dendritic cells (DCs), thus suggesting a new target of angiotensin II (Ang II) action in the immune system. This study analyzed whether peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activation in DCs regulated Ang II-induced activation of DCs and exploited the possible molecular mechanisms, especially focused on the signaling pathways of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-kappaB). Ang II stimulation of human monocyte-derived DCs resulted in an intermediate state of DC maturation and function via modulating the balance of the negative or positive regulation of the signaling pathways of extracellular regulated kinase (ERK), p38 MAPK and NF-kappaB, but not c-Jun N-terminal kinase (JNK). Moreover, pretreatment of DCs with the PPAR-gamma agonist pioglitazone reverted these effects of Ang II on DCs via suppression of the MAPK and NF-kappaB signaling pathways at least in part. Collectively, our data support the notion that PPAR-gamma activation in human DCs inhibits the activation of DCs induced by Ang II, with which involves the regulation of MAPK and NF-kappaB signaling pathways. These findings may support the important role of these mediators in the regulation of DC-mediated inflammatory and immunologic processes.
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Angiotensin II/immunology , Dendritic Cells/immunology , Hypoglycemic Agents/pharmacology , MAP Kinase Signaling System/drug effects , Monocytes/immunology , NF-kappa B/immunology , PPAR gamma/agonists , Thiazolidinediones/pharmacology , Cells, Cultured , Extracellular Signal-Regulated MAP Kinases/immunology , Humans , Inflammation/immunology , MAP Kinase Kinase 4/immunology , PPAR gamma/immunology , Pioglitazone , p38 Mitogen-Activated Protein Kinases/immunologyABSTRACT
Objective To study the treatment effect and the mechanism of high volume hemofiltration(HVHF)on acute lung injury(ALl)induced by endotoxin in dogs.Methods Sixteen healthy hybrid male dogs were injected LPS(650?g/kg)via central vein within 30 minutes.After model establishment,all animals were divided into two groups randomly( n=8).One group received the treatment of HVHF,while another group received routine treatment.PH,PaO_2,PaCO_2 in arterial blood were recorded at O h after LPS model establishment and 4h after HVHF.Contents of TNF-?,IL-6,and IL- 10 in plasma were measured by radioirnmunity,mRNA expression of TNF-?,IL-6,and IL-10 in lung tissue homogenate were measured by RT-PCR and NF-?B activity by flow cytometer.Results After injection of LPS,PaO_2 and PaO_2/FiO_2 began to decrease,and PaO_2/FiO_2 value was
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<p><b>OBJECTIVE</b>To observe the effect of tetrandrine on reversion of mice S180's obtained multi-drug resistance tumor cell induced by chemotherapy by PFC. And then discuss the molecular mechanism of it for the use of TCM in clinic to restrain the drug-resistant of chemotherapy, thereby improve the curative effect.</p><p><b>METHOD</b>By the methods of less dosage of chemotherapy PFC, give the mouse cisplatin 3 mg x kg(-1) i.p., once a week; CTX and 5-FU 3 mg x kg(-1) i.g. four weeks, set up the mice models of multi-drug resistance of S180 tumor cell, and then observe the P170, Fas, CD54 and apoposis by flow cytometry.</p><p><b>RESULT</b>Tetrandrine can obviously lower the express of P170 increase the express of Fas and the apoposis of drug resistant tumor cell. And at the same time it can obviously reduce the express of intercellular adhesion molecule (CD54).</p><p><b>CONCLUSION</b>Terandrine, with its adjustment of correlated biotic active matter, can intervene the occurrence of the multi-drug resistance of tumor cells induced by chemotherapy.</p>