258 research outputs found

    Large aortic aneurysm mimicking a cardiac tumor

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    <p>Abstract</p> <p>Introduction</p> <p>Extrinsic left atrial compression caused by a displaced, crooked descending thoracic aorta is rare. This anomaly may mimic primary cardiac tumors or metastatic neoplasms from the first look.</p> <p>Case presentation</p> <p>We reported a 78-year-old woman presented to our emergency room with back pain, increased exercise intolerance and intermittent angina. She also had one syncopal event 1 month ago and gastric cancer post gastrectomy history. Subsequent chest plain film showed no mediastinum widening.</p> <p>Two-dimensional echocardiography was performed and revealed a heterogeneous mass as large as 2.3 × 2.4 cm occupying the left atrium (LA). Three-dimensional echocardiography vividly demonstrated that LA was constrained between the aortic valve (AV) and a luminal structure with pulsatile character suggestive of the aorta.</p> <p>Conclusions</p> <p>We successfully demonstrated the detailed structure and location of an anomalous descending aorta on the oblique imaging plane of RT-3DE, which may not be readily available by traditional 2D method.</p

    Altered thymic differentiation and modulation of arthritis by invariant NKT cells expressing mutant ZAP70

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    Various subsets of invariant natural killer T (iNKT) cells with different cytokine productions develop in the mouse thymus, but the factors driving their differentiation remain unclear. Here we show that hypomorphic alleles of Zap70 or chemical inhibition of Zap70 catalysis leads to an increase of IFN-gamma-producing iNKT cells (NKT1 cells), suggesting that NKT1 cells may require a lower TCR signal threshold. Zap70 mutant mice develop IL-17-dependent arthritis. In a mouse experimental arthritis model, NKT17 cells are increased as the disease progresses, while NKT1 numbers negatively correlates with disease severity, with this protective effect of NKT1 linked to their IFN-gamma expression. NKT1 cells are also present in the synovial fluid of arthritis patients. Our data therefore suggest that TCR signal strength during thymic differentiation may influence not only IFN-gamma production, but also the protective function of iNKT cells in arthritis

    Association of mitral annulus calcification, aortic valve calcification with carotid intima media thickness

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    BACKGROUND: Mitral annular calcification (MAC) and aortic annular calcification (AVC) may represent a manifestation of generalized atherosclerosis in the elederly. Alterations in vascular structure, as indexed by the intima media thickness (IMT), are also recognized as independent predictors of adverse cardiovascular outcomes. AIM: To examine the relationship between the degree of calcification at mitral and/or aortic valve annulus and large artery structure (thickness). METHODS: We evaluated 102 consecutive patients who underwent transthoracic echocardiography and carotid artery echoDoppler for various indications; variables measured were: systemic blood pressure (BP), pulse pressure (PP=SBP-DBP), body mass index (BMI), fasting glucose, total, HDL, LDL chlolesterol, triglycerides, cIMT. The patients were divided according to a grading of valvular/annular lesions independent scores based on acoustic densitometry: 1 = annular/valvular sclerosis/calcification absence; 2 = annular/valvular sclerosis; 3 = annular calcification; 4 = annular-valvular calcification; 5 = valvular calcification with no recognition of the leaflets. RESULTS: Patient score was the highest observed for either valvular/annulus. Mean cIMT increased linearly with increasing valvular calcification score, ranging from 3.9 ± 0.48 mm in controls to 12.9 ± 1.8 mm in those subjects scored 5 (p < 0.0001). In the first to fourth quartile of cIMT values the respective maximal percentual of score were: score 1: 76.1%, score 2: 70.1%, score 4: 54.3% and score 5: 69.5% (p > 0.0001). CONCLUSION: MAC and AVC score can identify subgroups of patients with different cIMT values which indicate different incidence and prevalence of systemic artery diseases. This data may confirm MAC-AVC as a useful important diagnostic parameter of systemic atherosclerotic disease

    Bruton's tyrosine kinase regulates TLR7/8-induced TNF transcription via nuclear factor-κB recruitment

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    Tumour necrosis factor (TNF) is produced by primary human macrophages in response to stimulation by exogenous pathogen-associated molecular patterns (PAMPs) and endogenous damage-associated molecular patterns (DAMPs) via Toll-like receptor (TLR) signalling. However, uncontrolled TNF production can be deleterious and hence it is tightly controlled at multiple stages. We have previously shown that Bruton's tyrosine kinase (Btk) regulates TLR4-induced TNF production via p38 MAP Kinase by stabilising TNF messenger RNA. Using both gene over-expression and siRNA-mediated knockdown we have examined the role of Btk in TLR7/8 mediated TNF production. Our data shows that Btk acts in the TLR7/8 pathway and mediates Ser-536 phosphorylation of p65 RelA and subsequent nuclear entry in primary human macrophages. These data show an important role for Btk in TLR7/8 mediated TNF production and reveal distinct differences for Btk in TLR4 versus TLR7/8 signalling

    Selective Remodeling: Refining Neural Connectivity at the Neuromuscular Junction

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    A primer on new research by Fuentes-Medel and colleagues explains the important role of non-neural cells in clearing neural debris, which is continuously produced during the normal remodeling processes that establish and maintain neural connectivity
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