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Pathogen在摘要中的描述方法 abstract

Plant Physiol. 2009 February; 149(2): 1017–1027

Pathogen-induced stomatal closure is part of the plant innate immune response. Phytopathogens using stomata as a way of entry into the leaf must avoid the stomatal response of the host.

Adult Urethral Stricture Disease after Childhood Hypospadias Repair abstract

Adv Urol. 2008; 2008: 150315.

Conclusion. Urethral stricture may occur decades after initial hypospadias surgery. It can be the most severe form of anterior urethral stricture, and may eventually require salvage treatment such as a perineal urethrostomy. Patients undergoing hypospadias surgery should receive lifelong follow-up protocol to detect latent urethral strictures. 三句话:第一句是结论,第二句是解释机制,第三种是结果

Hepatocyte Growth Factor Exerts Its Anti-Inflammatory Action by Disrupting Nuclear Factor-κB Signaling abstract

Am J Pathol. 2008 July; 173(1): 30–41.

Renal inflammation, characterized by the influx of inflammatory cells, is believed to play a critical role in the initiation and progression of a wide range of chronic kidney diseases.第一句概况目前的基本情况,流行趋势。 Here, we show that hepatocyte growth factor (HGF) inhibited renal inflammation and proinflammatory chemokine expression by disrupting nuclear factor (NF)-κB signaling. 第二句本文的结论!In vivo,(接下来告诉读者本文的思路,第一步是in vivo研究)HGF gene delivery inhibited interstitial infiltration of inflammatory T cells and macrophages, and suppressed expression of both RANTES (regulated on activation, normal T cell expressed and secreted) and monocyte chemoattractant protein-1 in a mouse model of obstructive nephropathy. In vitro(第二步是in vitro研究), HGF abolished RANTES induction in human kidney epithelial cells, which was dependent on NF-κB signaling. HGF did not significantly affect the phosphorylation or degradation of IκBα; it also did not influence the phosphorylation or nuclear translocation of p65 NF-κB. However, HGF prevented p65 NF-κB binding to its cognate cis-acting element in the RANTES promoter. HGF action was dependent on the activation of the phosphoinositide 3-kinase/Akt pathway, which led to the phosphorylation and inactivation of glycogen synthase kinase (GSK)-3β. Suppression of GSK-3β activity mimicked HGF and abolished RANTES expression, whereas ectopic expression of GSK-3β restored RANTES induction. HGF also induced renal GSK-3β phosphorylation and inactivation after obstructive injury in vivo.最终的结论与结果说明的问题。These observations suggest that HGF is a potent anti-inflammatory cytokine that inhibits renal inflammation by disrupting NF-κB signaling and may be a promising therapeutic agent for progressive renal diseases.

Interleukin-1 Receptor Type I Signaling Critically Regulates Infarct Healing and Cardiac Remodeling abstract

Am J Pathol. 2008 July; 173(1): 57–67.

The proinflammatory cytokine interleukin (IL)-1 signals exclusively through the type I IL-1 receptor (IL-1RI). IL-1 expression is markedly induced in the infarcted heart; however, its role in cardiac injury and repair remains controversial. We examined the effects of disrupted IL-1 signaling on infarct healing and cardiac remodeling using IL-1RI−/− mice. After reperfused infarction IL-1RI-null mice exhibited decreased infiltration of the infarcted myocardium with neutrophils and macrophages and reduced chemokine and cytokine expression. In the absence of IL-1 signaling, suppressed inflammation was followed by an attenuated fibrotic response. Infarcted IL-1RI−/− mice had decreased myofibroblast infiltration and reduced collagen deposition in the infarcted and remodeling myocardium. IL-1RI deficiency protected against the development of adverse remodeling; however, infarct size was comparable between groups suggesting that the beneficial effects of IL-1RI gene disruption were not attributable to decreased cardiomyocyte injury. Reduced chamber dilation in IL-1RI-null animals was associated with decreased collagen deposition and attenuated matrix metalloproteinase (MMP)-2 and MMP-3 expression in the peri-infarct area, suggesting decreased fibrotic remodeling of the noninfarcted heart. IL-1β stimulated MMP mRNA synthesis in wild-type, but not in IL-1RI-null cardiac fibroblasts. In conclusion, IL-1 signaling is essential for activation of inflammatory and fibrogenic pathways in the healing infarct, playing an important role in the pathogenesis of remodeling after infarction. Thus, interventional therapeutics targeting the IL-1 system may have great benefits in myocardial infarction.

Gelatinase (MMP-2 and -9) expression介绍 abstract

Reproductive Biology and Endocrinology 2008, 6:66

Various molecules participate in implantation and maintaining endometrial function during gestation. The remodeling of endometrial matrices is a necessary process in the coordination of gestational progress. Matrix-metalloproteinases (MMPs) like gelatinases (MMP-2 and -9) and collagenase (MMP-1) are considered to play important roles in this process. We examined MMP-2 and -9 expression using zymography, in situ hybridization, real-time PCR, and microarray analysis to clarify their roles in the bovine endometrium during gestation.

HOX cofactors expression and regulation 摘要中的方法学描述 abstract

Reproductive Biology and Endocrinology 2008, 6:49

In this study, the expression of HOX cofactors, PBX1, PBX2, and MEIS1/2, were examined by using RT-PCR, immunofluorescence in cultured immortalized human granulosa (SVOG) cells. The distribution of these HOX cofactors in human ovaries was examined by immunohistochemistry. The effects of growth differentiation factor-9 (GDF-9) and follicle-stimulating hormone (FSH) on PBX2 in SVOG cells were investigated by western blot analysis. Binding activities of HOXA7 and PBX2 to the specific sequences in granulosa cells were determined by electrophoretic mobility shift assay (EMSA).

鲑鱼生长抑素克隆,有关它概括和介绍 abstract

Reproductive Biology and Endocrinology 2008, 6:42

Somatolactin (Sl) is a fish specific adenohypophyseal peptide hormone related to growth hormone (Gh). Some species, including salmonids, possess two forms: Sl alpha and Sl beta. The somatolactin receptor (slr) is closely related to the growth hormone receptor (ghr). Sl has been ascribed many physiological functions, including a role in sexual maturation. In order to clarify the role of Sl in the sexual maturation of female Atlantic salmon (Salmo salar), the full length cDNAs of slr, Sl alpha and Sl beta were cloned and their expression was studied throughout a seasonal reproductive cycle using real-time quantitative PCR (RTqPCR).

ABSTRACT 逻辑结构写法 abstract

J. Biol. Chem., Vol. 282, Issue 52, 37429-37435

Brahma (Brm) and Brahma-related gene-1 (Brg1) ATPases share similarities in structure and function, but their presence in human SWI/SNF chromatin remodeling complexes is mutually exclusive. Although Brm and Brg1 can compensate for each other, it is possible that Brm and Brg1 have their unique properties to differentially regulate gene expression in vivo. To explore this, we examined the requirement of Brm and Brg1 for p53-dependent transcription, especially p53-mediated induction of p21 and MDM2, using cell lines in which Brm or Brg1 could be inducibly knocked down. We found that Brg1, but not Brm, is required for p21 induction in MCF7 cells. However, in Brg1-deficient H1299 cells, Brm is also required for p21 induction. Likewise, Brm is necessary for induction of p21 in MCF7 cells in which Brg1 is stably knocked down. In contrast, Brg1 has little, if any, effect on p53-mediated induction of MDM2 in cells that have Brm and vice versa. In addition, we demonstrated that the impaired induction of p21 upon Brg1 knockdown is at least in part due to decreased p53 binding to the p21 promoter. Taken together, we provided evidence that Brg1 is preferentially recruited by p53 for inducing a subset of target genes through chromatin remodeling. Thus, we hypothesize that the potential tumor suppressor function for Brg1 is mediated in part through the p53 pathway. 以上标色是十分严谨的逻辑关系,细细体会!

Genome-wide association yields new sequence variants at seven loci that associate with measures of obesity abstract

Nature Genetics 41, 18 - 24 (2008)

摘要分析(www.medsci.cn评审专家): Obesity results from the interaction of genetic and environmental factors. --肥胖是遗传与环境相互作用的结果,一句话扣紧主题,直接切入到遗传学的研究。同时,也强调肥胖不仅仅是遗传因素。 To search for sequence variants that affect variation in two common measures of obesity, weight and body mass index (BMI), both of which are highly heritable, we performed a genome-wide association (GWA) study with 305,846 SNPs typed in 25,344 Icelandic, 2,998 Dutch, 1,890 European Americans and 1,160 African American subjects and combined the results with previously published results from the Diabetes Genetics Initiative (DGI) on 3,024 Scandinavians. ------这个句子包括了以下信息:研究目的(sequence variants)、研究指标(obesity, weight and body mass index (BMI),)、研究方法(GWA) 、研究范围(305,846 SNPs )、研究人群范围。非常精练!! We selected 43 variants in 19 regions for follow-up in 5,586 Danish individuals and compared the results to a genome-wide study on obesity-related traits from the GIANT consortium. ---典型的用数字说话。这一个句子里有43、19、5586,这是高质量文章的共同特性之一。也是进一步细化整个实验的过程。 In total, 29 variants, some correlated, in 11 chromosomal regions reached a genome-wide significance threshold of P < 1.6 10-7. This includes previously identified variants close to or in the FTO, MC4R, BDNF and SH2B1 genes, in addition to variants at seven loci not previously connected with obesity. ----结果与发现。同样是数字!两句简单的话,将研究发现,创新点全部说明出来。

摘要的结论部分 abstract

Arthritis Res Ther. 2008; 10(3): R53

In this report we examine discontinuation rates in randomized trials of etoricoxib in chronic musculoskeletal conditions. Our prior hypotheses were as follows. First, discontinuation rates would differ between osteoarthritis (OA), rheumatoid arthritis (RA) and other musculoskeletal conditions for lack of efficacy, but probably not because of adverse events. Second, discontinuation rates would differ between shorter and longer trials. Third, discontinuations because of gastrointestinal adverse events would be lower with etoricoxib than with traditional NSAIDs. Finally, higher doses of etoricoxib would produce lower rates of lack of efficacy discontinuations and higher rates of adverse event discontinuations. 这个结论非常清晰.

Adult Urethral Stricture Disease after Childhood Hypospadias Repair abstract

Adv Urol. 2008; 2008: 150315.

Results. Mean patient age was 38.9 years old. The lag time of urethral stricture presentation ranged from 25 to 57 years after primary hypospadias surgery, with an average of 36 years. Stricture length ranged from 1 to 17 cm (mean: 10.3 cm). Open graft-based urethroplasties were performed in 4/9 cases. Salvage perineal urethrostomy was performed in 2/9 cases. Another 3 cases chose to undergo repeat urethrotomy or dilatations—none of these patients was cured by such treatment. Complications included one urethrostomy stenosis and one urinary tract infection.

TRAIL-R deficiency in mice enhances lymph node metastasis without affecting primary tumor development abstract

J Clin Invest. 2008 January 2; 118(1): 100–110

TRAIL is a promising anticancer agent due to its ability to selectively induce apoptosis in established tumor cell lines but not nontransformed cells. Herein, we demonstrate a role for the apoptosis-inducing TRAIL receptor (TRAIL-R) as a metastasis suppressor.

EMT,MET的综述 abstract

Cell Research (2009) 19:156–172.

During development and in the context of different morphogenetic events, epithelial cells undergo a process called epithelial to mesenchymal transition or transdifferentiation (EMT). In this process, the cells lose their epithelial characteristics, including their polarity and specialized cell-cell contacts, and acquire a migratory behavior, allowing them to move away from their epithelial cell community and to integrate into surrounding tissue, even at remote locations. EMT illustrates the differentiation plasticity during development and is complemented by another process, called mesenchymal to epithelial transition (MET). While being an integral process during development, EMT is also recapitulated under pathological conditions, prominently in fibrosis and in invasion and metastasis of carcinomas. Accordingly, EMT is considered as an important step in tumor progression. TGF- signaling has been shown to play an important role in EMT. In fact, adding TGF- to epithelial cells in culture is a convenient way to induce EMT in various epithelial cells. Although much less characterized, epithelial plasticity can also be regulated by TGF--related bone morphogenetic proteins (BMPs), and BMPs have been shown to induce EMT or MET depending on the developmental context. In this review, we will discuss the induction of EMT in response to TGF-, and focus on the underlying signaling and transcription mechanisms.

TIM-3 is Expressed on Activated Human CD4+ T Cells and Regulates Th1 and Th17 Cytokines abstract

Eur J Immunol. 2009 September; 39(9): 2492–2501.

以下为MedSci编辑人员剖析: 摘要写法,比较经典。 TIM-3 is a molecule selectively expressed on a subset of murine IFNγ-secreting Th1 cells but not Th2 cells, and regulates Th1 immunity and tolerance in vivo.(一句话概况TIM-3的功能,很经典) At this time little is known about the role of TIM-3 on human T cells. (目前存在的问题和研究不足.) To determine if TIM-3 similarly identifies and regulates Th1 cells in humans, we generated a panel of monoclonal antibodies specific for human TIM-3.(本文研究目的). We report that TIM-3 is expressed by a subset of activated CD4+ cells, and that anti-CD3/28 stimulation increases both the level of expression as well as the number of TIM-3+ T cells. (我们的结果发现之一) We also find that TIM-3 is expressed at high levels on in vitro polarized Th1 cells, and is expressed at lower levels on Th17 cells. (我们的结果发现之二) In addition, human CD4+ T cells secreted elevated levels of IFNγ, IL-17, IL-2, and IL-6, but not IL-10, IL-4, or TNFα, when stimulated with anti-CD3/28 in the presence of TIM-3-specific, putative antagonistic antibodies. This was not mediated by differences in proliferation or cell death, but rather by induction of cytokines at the transcriptional level.(我们的结果发现之三) These results suggest that TIM-3 is a negative regulator of human T cells and regulates Th1 and Th17 cytokine secretion.(结论) 这个摘要写得很地道!!

TIM-3 is Expressed on Activated Human CD4+ T Cells and Regulates Th1 and Th17 Cytokines abstract

Eur J Immunol. 2009 September; 39(9): 2492–2501.

TIM-3 is a molecule uniquely expressed on the surface of murine Th1 cells that negatively regulates IFNγ secretion by inducing cell death by binding to its ligand Galectin-9 MedSci点评:uniquely精妙!

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