832 research outputs found

    Popliteal venous thrombosis in juvenile arthritis with Baker cysts: report of 3 cases

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    Three pediatric patients with different illnesses leading to knee arthritis and large Baker cysts and additional calf swelling are reported. Calf swelling was due to true popliteal venous thrombosis and not to the much more common cause of pseudothrombophlebitis. Careful ultrasound examination can differentiate these two causes of calf swelling. Even though all our patients had risk factors for thrombophilia, we do not recommend routine thrombophilia work-up for all arthritis patients in the absence of thrombosis

    Primary cardiac sarcoma presenting as acute left-sided heart failure

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    Primary cardiac sarcomas are rare malignant tumors of the heart. Clinical features depend on the site of tumor and vary from symptoms of congestive heart failure to thromboembolism and arrhythmias. Echocardiography is helpful but definitive diagnosis is established by histopathology. Surgical resection is the mainstay of treatment, and the role of chemotherapy and radiotherapy is unclear. We report a case of primary cardiac sarcoma which presented with signs and symptoms of acute left-sided heart failure

    Reverse mathematics of matroids

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    Matroids generalize the familiar notion of linear dependence from linear algebra. Following a brief discussion of founding work in computability and matroids, we use the techniques of reverse mathematics to determine the logical strength of some basis theorems for matroids and enumerated matroids. Next, using Weihrauch reducibility, we relate the basis results to combinatorial choice principles and statements about vector spaces. Finally, we formalize some of the Weihrauch reductions to extract related reverse mathematics results. In particular, we show that the existence of bases for vector spaces of bounded dimension is equivalent to the induction scheme for \Sigma^0_2 formulas

    Estimating the within-household infection rate in emerging SIR epidemics among a community of households

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    This paper is concerned with estimation of the within household infection rate λL for a susceptible → infective → recovered epidemic among a population of households, from observation of the early, exponentially growing phase of an epidemic. Specifically, it is assumed that an estimate of the exponential growth rate is available from general data on an emerging epidemic and more-detailed, household-level data are available in a sample of households. Estimates of λL obtained using the final size distribution of single-household epidemics are usually biased owing to the emerging nature of the epidemic. A new method, which accounts correctly for the emerging nature of the epidemic, is developed by exploiting the asymptotic theory of supercritical branching processes and proved to yield a strongly consistent estimator of λL as the population and sampled households both tend to infinity in an appropriate fashion. The theory is illustrated by simulations which demonstrate that the new method is feasible for finite populations and numerical studies are used to explore how changes to the parameters governing the spread of an epidemic affect the bias of estimates based on single-household final size distributions

    Identification of the initial molecular changes in response to circulating angiogenic cells-mediated therapy in critical limb ischemia

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    BackgroundCritical limb ischemia (CLI) constitutes the most aggressive form of peripheral arterial occlusive disease, characterized by the blockade of arteries supplying blood to the lower extremities, significantly diminishing oxygen and nutrient supply. CLI patients usually undergo amputation of fingers, feet, or extremities, with a high risk of mortality due to associated comorbidities.Circulating angiogenic cells (CACs), also known as early endothelial progenitor cells, constitute promising candidates for cell therapy in CLI due to their assigned vascular regenerative properties. Preclinical and clinical assays with CACs have shown promising results. A better understanding of how these cells participate in vascular regeneration would significantly help to potentiate their role in revascularization.Herein, we analyzed the initial molecular mechanisms triggered by human CACs after being administered to a murine model of CLI, in order to understand how these cells promote angiogenesis within the ischemic tissues.MethodsBalb-c nude mice (n:24) were distributed in four different groups: healthy controls (C, n:4), shams (SH, n:4), and ischemic mice (after femoral ligation) that received either 50 mu l physiological serum (SC, n:8) or 5x10(5) human CACs (SE, n:8). Ischemic mice were sacrificed on days 2 and 4 (n:4/group/day), and immunohistochemistry assays and qPCR amplification of Alu-human-specific sequences were carried out for cell detection and vascular density measurements. Additionally, a label-free MS-based quantitative approach was performed to identify protein changes related.ResultsAdministration of CACs induced in the ischemic tissues an increase in the number of blood vessels as well as the diameter size compared to ischemic, non-treated mice, although the number of CACs decreased within time. The initial protein changes taking place in response to ischemia and more importantly, right after administration of CACs to CLI mice, are shown.ConclusionsOur results indicate that CACs migrate to the injured area; moreover, they trigger protein changes correlated with cell migration, cell death, angiogenesis, and arteriogenesis in the host. These changes indicate that CACs promote from the beginning an increase in the number of vessels as well as the development of an appropriate vascular network.Institute of Health Carlos III, ISCIII; Junta de Andaluci

    Computability and Complexity

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    We study the uniform computational content of the Vitali Covering Theorem for intervals using the tool of Weihrauch reducibility. We show that a more detailed picture emerges than what a related study by Giusto, Brown, and Simpson has revealed in the setting of reverse mathematics. In particular, different formulations of the Vitali Covering Theorem turn out to have different uniform computational content. These versions are either computable or closely related to uniform variants of Weak Weak K\H{o}nig's Lemma.Comment: 13 page

    The developmental regulator Pax6 is essential for maintenance of islet cell function in the adult mouse pancreas

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    The transcription factor Pax6 is a developmental regulator with a crucial role in development of the eye, brain, and olfactory system. Pax6 is also required for correct development of the endocrine pancreas and specification of hormone producing endocrine cell types. Glucagon-producing cells are almost completely lost in Pax6-null embryos, and insulin-expressing beta and somatostatin-expressing delta cells are reduced. While the developmental role of Pax6 is well-established, investigation of a further role for Pax6 in the maintenance of adult pancreatic function is normally precluded due to neonatal lethality of Pax6-null mice. Here a tamoxifen-inducible ubiquitous Cre transgene was used to inactivate Pax6 at 6 months of age in a conditional mouse model to assess the effect of losing Pax6 function in adulthood. The effect on glucose homeostasis and the expression of key islet cell markers was measured. Homozygous Pax6 deletion mice, but not controls, presented with all the symptoms of classical diabetes leading to severe weight loss requiring termination of the experiment five weeks after first tamoxifen administration. Immunohistochemical analysis of the pancreata revealed almost complete loss of Pax6 and much reduced expression of insulin, glucagon, and somatostatin. Several other markers of islet cell function were also affected. Notably, strong upregulation in the number of ghrelin-expressing endocrine cells was observed. These findings demonstrate that Pax6 is essential for adult maintenance of glucose homeostasis and function of the endocrine pancreas

    Valvular heart disease: what does cardiovascular MRI add?

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    Although ischemic heart disease remains the leading cause of cardiac-related morbidity and mortality in the industrialized countries, a growing number of mainly elderly patients will experience a problem of valvular heart disease (VHD), often requiring surgical intervention at some stage. Doppler-echocardiography is the most popular imaging modality used in the evaluation of this disease entity. It encompasses, however, some non-negligible constraints which may hamper the quality and thus the interpretation of the exam. Cardiac catheterization has been considered for a long time the reference technique in this field, however, this technique is invasive and considered far from optimal. Cardiovascular magnetic resonance imaging (MRI) is already considered an established diagnostic method for studying ventricular dimensions, function and mass. With improvement of MRI soft- and hardware, the assessment of cardiac valve function has also turned out to be fast, accurate and reproducible. This review focuses on the usefulness of MRI in the diagnosis and management of VHD, pointing out its added value in comparison with more conventional diagnostic means

    Insulin and IGF1 signalling pathways in human astrocytes <i>in vitro</i> and <i>in vivo</i>; characterisation, subcellular localisation and modulation of the receptors.

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    Background The insulin/IGF1 signalling (IIS) pathways are involved in longevity regulation and are dysregulated in neurons in Alzheimer’s disease (AD). We previously showed downregulation in IIS gene expression in astrocytes with AD-neuropathology progression, but IIS in astrocytes remains poorly understood. We therefore examined the IIS pathway in human astrocytes and developed models to reduce IIS at the level of the insulin or the IGF1 receptor (IGF1R). Results We determined IIS was present and functional in human astrocytes by immunoblotting and showed astrocytes express the insulin receptor (IR)-B isoform of Ir. Immunocytochemistry and cell fractionation followed by western blotting revealed the phosphorylation status of insulin receptor substrate (IRS1) affects its subcellular localisation. To validate IRS1 expression patterns observed in culture, expression of key pathway components was assessed on post-mortem AD and control tissue using immunohistochemistry. Insulin signalling was impaired in cultured astrocytes by treatment with insulin + fructose and resulted in decreased IR and Akt phosphorylation (pAkt S473). A monoclonal antibody against IGF1R (MAB391) induced degradation of IGF1R receptor with an associated decrease in downstream pAkt S473. Neither treatment affected cell growth or viability as measured by MTT and Cyquant® assays or GFAP immunoreactivity. Discussion IIS is functional in astrocytes. IR-B is expressed in astrocytes which differs from the pattern in neurons, and may be important in differential susceptibility of astrocytes and neurons to insulin resistance. The variable presence of IRS1 in the nucleus, dependent on phosphorylation pattern, suggests the function of signalling molecules is not confined to cytoplasmic cascades. Down-regulation of IR and IGF1R, achieved by insulin + fructose and monoclonal antibody treatments, results in decreased downstream signalling, though the lack of effect on viability suggests that astrocytes can compensate for changes in single pathways. Changes in signalling in astrocytes, as well as in neurons, may be important in ageing and neurodegeneration
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