Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 6 de 6
Mais filtros

Base de dados
Intervalo de ano de publicação
Front Pharmacol ; 10: 92, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30814950


Objective: To evaluate therapeutic efficacy of different combined antimicrobial treatments against Acinetobacter baumannii ventilator-associated pneumonia (VAP). Methods: Clinical outcomes were retrospectively analyzed to elucidate the efficacy of four combined antimicrobial regimens. The chessboard and micro broth dilution methods determined the minimum inhibitory concentrations (MICs) of four antiseptic drugs singly used and combined two drugs against 36 isolates of multidrug-resistant (MDR) A. baumannii. Results: The incidence of VAP was approximately 6.9% (237/3424) between January 1, 2015 and December 31, and 35.9% (85/237) of the cases were caused by A. baumannii. Among these cases, 60 belonged to AB-VAP, for whom antimicrobial treatment plan was centralized and clinical data was complete. Moreover, all 60 strains of A. baumannii were MDR bacteria from reports microbiological laboratory. Resistance rate was lowest for amikacin (68.3%) and ampicillin sulbactam (71.7%). Resistance rate for imipenem increased from 63.2 to 90.9% during the 3 years. However, in these 60 cases of AB-VAP, the combination between 4 antibiotics was effective in most cases: the effective rate was 75% (18/24) for sulbactam combined with etilmicin, 71.4% (10/14) for sulbactam combined with levofloxacin, 72.7% (8/11) for meropenem combined with etilmicin, and 63.6% (7/11) for meropenem combined with levofloxacin. There was no statistical difference between four regimens (P > 0.05). Sulbactam combined with etilmicin decreased 1/2 of MIC50 and MIC90 of sulbactam while the decreases in etilmicin were more obviously than single drug. When adopting meropenem combined with levofloxacin or etilmicin, the MIC of meropenem reduced to 1/2 of that in applying single drug. As for sulbactam or meropenem combined with levofloxacin, it also lessened the MIC50 of levofloxacin to 1/2 of that for single drug. FIC results suggested that the effects of four combined antimicrobial regimens were additive or unrelated. When sulbactam was combined with etimicin, the additive effect was 63.89%. Conclusion: Drug combination sensitivity test in vitro may be helpful for choosing antimicrobial treatment plans. Sulbactam or meropenem as the basis of treatment regimens can function as the alternatives against AB-VAP. Sulbactam combined with etimicin has been regarded as a recommended regimen in Suizhou, Hubei, China.

R Soc Open Sci ; 6(1): 181557, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30800391


A facile one-step hydrothermal synthesis approach was proposed to prepare nitrogen and chlorine co-doped carbon dots (CDs) using l-ornithine hydrochloride as the sole precursor. The configuration and component of CDs were characterized by transmission electron microscopy and X-ray photoelectron and Fourier transform infrared spectroscopies. The obtained CDs (Orn-CDs) with a mean diameter of 2.1 nm were well monodispersed in aqueous solutions. The as-prepared CDs exhibited a bright blue fluorescence with a high yield of 60%, good photostability and low cytotoxicity. The emission of Orn-CDs could be selectively and effectively suppressed by Fe3+. Thus, a quantitative assay of Fe3+ was realized by this nanoprobe with a detection limit of 95.6 nmol l-1 in the range of 0.3-50 µmol l-1. Furthermore, ascorbic acid could recover the fluorescence of Orn-CDs suppressed by Fe3+, owing to the transformation of Fe3+ to Fe2+ by ascorbic acid. The limit of detection for ascorbic acid was 137 nmol l-1 in the range of 0.5-10 µmol l-1. In addition, the established method was successfully applied for Fe3+ and ascorbic acid sensing in human serum and urine specimens and for imaging of Fe3+ in living cells. Orn-CD-based sensing platform showed its potential to be used for biomedicine-related study because it is cost-effective, easily scalable and can be used without additional functionalization and sample pre-treatment.

PLoS One ; 7(10): e46508, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-23094025


BACKGROUND: Many epidemiological studies have found a positive association between periodontal disease (PD) and risk of chronic obstructive pulmonary disease (COPD), but this association is varied and even contradictory among studies. We performed a meta-analysis to ascertain the relationship between PD and COPD. METHODS: PubMed and Embase database were searched up to January 10, 2012, for relevant observational studies on the association between PD and risk of COPD. Data from the studies selected were extracted and analyzed independently by two authors. The meta-analysis was performed using the Comprehensive Meta-Analysis software. RESULTS: Fourteen observational studies (one nested case-control, eight case-control, and five cross-sectional) involving 3,988 COPD patients were yielded. Based on random-effects meta-analysis, a significant association between PD and COPD was identified (odds ratio = 2.08, 95% confidence interval = 1.48-2.91; P<0.001), with sensitivity analysis showing that the result was robust. Subgroups analyses according to study design, ethnicity, assessment of PD/COPD, and adjusted/unadjusted odds ratios also revealed a significant association. Publication bias was detected. CONCLUSIONS: Based on current evidence, PD is a significant and independent risk factor of COPD. However, whether a causal relationships exists remains unclear. Morever, we suggest performing randomized controlled trails to explore whether periodontal interventions are beneficial in regulating COPD pathogenesis and progression.

Doenças Periodontais/epidemiologia , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Análise de Variância , Estudos de Casos e Controles , China/epidemiologia , Estudos Transversais , Bases de Dados Bibliográficas , Progressão da Doença , Europa (Continente)/epidemiologia , Feminino , Humanos , Índia/epidemiologia , Masculino , Pessoa de Meia-Idade , Razão de Chances , Doenças Periodontais/complicações , Doenças Periodontais/patologia , Viés de Publicação , Doença Pulmonar Obstrutiva Crônica/complicações , Doença Pulmonar Obstrutiva Crônica/patologia , Fatores de Risco , Estados Unidos/epidemiologia
Life Sci ; 88(5-6): 233-8, 2011 Jan 31.
Artigo em Inglês | MEDLINE | ID: mdl-21147132


AIMS: Investigation of the response of mesenchymal stem cells (MSCs) to vascular mechanical forces is very important in the field of cardiovascular intervention. Ser/Thr-protein kinase Pim-1 is a novel transducer of cell survival and the cell cycle that promotes signals in the hematopoietic cell system. Current studies aim to foster an understanding of Pim-1 expression and regulation in MSCs in response to different durations and strengths of laminar shear stress (SS) and to investigate the role of Pim-1 in SS-induced cell proliferation. MAIN METHODS: A parallel-plate flow chamber was used to control the strength and duration of SS. Proliferation was measured with the BrdU cell proliferation assay. The expressions of Pim-1 mRNA and protein were evaluated by reverse transcription-polymerase chain reaction and western blotting, respectively. RNA interference was used to knock down the Pim-1 gene. KEY FINDINGS: The results showed that SS up-regulation of Pim-1 mRNA and protein was time-dependent. Pim-1 induction was SS strength-dependent, and the expression level reached a maximum at 30 dynes/cm(2). Inhibitors of p38MAPK and ERK attenuated the SS-induced expression of Pim-1. In addition, SS significantly increased BrdU-uptake, which was effectively blocked by the silencing of Pim-1. SIGNIFICANCE: These results demonstrated that Pim-1 is expressed in MSCs and plays an important role in the SS-induced proliferation of MSCs.

Células-Tronco Mesenquimais/citologia , Células-Tronco Mesenquimais/metabolismo , Proteínas Proto-Oncogênicas c-pim-1/metabolismo , Estresse Mecânico , Regulação para Cima , Animais , Western Blotting , Proliferação de Células , Células Cultivadas , RNA Mensageiro/metabolismo , Ratos , Reação em Cadeia da Polimerase Via Transcriptase Reversa
Zhongguo Fei Ai Za Zhi ; 12(7): 747-52, 2009 Jul 20.
Artigo em Chinês | MEDLINE | ID: mdl-20719149


BACKGROUND: Matrine, one of the major alkaloid components of the traditional Chinese medicine Sophora roots, has a wide range of pharmacological effects including anti-inflammatory activities, growth inhibition and induction of cell differentiation and apoptosis. Motigen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) has found to be a crucial signaling pathway in endothelial cells. The aim of this study is to investigate the role of Matrine and MAPK/ERK signal transduction in the inhibition of the proliferation and migration of human umbilical veins endothelial cells (HUVECs) induced by lung cancer cells. METHODS: HUVECs were cultured with A549CM. Mat or PD98059 (i.e PD), specific inhibitor of MAPK/ERK, was added into the A549CM. The proliferation of the HUVECs was measured by cell counting. The migration of the HUVECs was observed by wound healing assay. The expression levels of ERK and p-ERK protein were detected by Western Blot analysis. RESULTS: On 24 hours after intervention, the A549CM significantly stimulated the proliferation, migration and expression of p-ERK of HUVECs. Compared with the A549CM group, Mat significantly inhibited the proliferation, migration and p-ERK expression of HUVECs induced by A549CM. While PD only decreased the proliferation and p-ERK expression of HUVECs induced by A549CM. PD had no effect in the migration of HUVECs. CONCLUSIONS: The results demonstrated that Mat and PD98059 can effectively decrease proliferation and expression of p-ERK of HUVECs induced by A549CM. Furthermore Mat can also inhibit migration of HUVECs induced by A549CM that did not changed by PD98059. These data implied that suppressing MAPK/ERK signal transduction may play the crucial role in resisting lung cacinoma angiogenesis with Mat.

Zhonghua Jie He He Hu Xi Za Zhi ; 28(4): 263-7, 2005 Apr.
Artigo em Chinês | MEDLINE | ID: mdl-15854440


OBJECTIVE: To investigate the effect of human angiotensin II (AngII) type 1 receptor (AT(1)R) antisense cDNA (ahAT(1)) on migration, proliferation, and apoptosis of cultured human pulmonary artery smooth muscle cells (PASMC). METHODS: Two recombinant adenoviral vectors, AdCMVahAT(1) containing full length antisense cDNA targeting to human AT(1)R mRNA, and AdCMVLacZ containing LacZ, were constructed by orientation clone technology and homologous recombination. The PASMC was divided into 3 groups (DMEM, AdCMVLacZ, AdCMVahAT(1)) and different interventions were given to different groups. AT(1)R expression was detected by RT-PCR and immunohistochemistry method; migration of PASMC was measured by Boyden's Chamer method. Other PASMC was divided into 4 groups (DMEM, AngII, AdCMVLacZ + AngII and AdCMVahAT(1) + AngII), and only the last 2 groups were respectively transfected with AdCMVLacZ and AdCMVahAT(1) before administration of AngII. From 6 h to 96 h after stimulation by AngII (10(-7) mol/L), proliferation index (PI) and apoptosis of PASMC were determined by flow cytometry. RESULTS: At the 48 h the level of AT(1)R mRNA was significantly less in PASMC transfected AdCMVahAT(1) than that in group DMEM and in group AdCMVLacZ. The protein level showed a same difference (P < 0.01). At 24 h the migration distance of PASMC also was significantly less in group AdCMVahAT(1) than that in group DMEM and Group AdCMVLacZ (P < 0.01). Stimulated by AngII for 48 h, in group AngII the PI of PASMC markedly increased (P < 0.01 vs group DMEM). But in Group AdCMVahAT(1) + AngII PI of PASMC clearly decreased (P < 0.01 vs group AngII and group DMEM respectively). There was no statistic difference of PI between group AdCMVLacZ + AngII and group AngII. Moreover, apoptosis peak emerged only in group AdCMVahAT(1) + AngII. The rate of apoptosis in those PASMC used AdCMVahAT(1) and AngII was 24.70 +/- 4.04 (P < 0.01 vs the other 3 groups respectively). CONCLUSIONS: These results indicate that AngII stimulates proliferation via AT(1) receptors in human PASMC, and antisense cDNA targeting to human AT(1)R transfection mediated by adenoviral vector has powerful inhibitory effects on AngII-induced migration and proliferation of human PASMC by attenuating AT(1)R mRNA and protein expression. Also, it can promote apoptosis of human PASMC. That demonstrate that AT(1)R antisense cDNA is a potent inhibitors of the actions of AngII on PASMC. Antisense inhibition targeting to AT(1)R has therapeutic potential for the treatment of pulmonary vascular diseases.

Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/metabolismo , Artéria Pulmonar/metabolismo , Receptor Tipo 1 de Angiotensina/genética , Adenoviridae , Apoptose , Diferenciação Celular , Proliferação de Células , Células Cultivadas , DNA Antissenso/genética , DNA Complementar/genética , Vetores Genéticos , Humanos