205 research outputs found

    Automated 3D generation and rendering of stylized building designs

    Get PDF
    Thesis (S.B. in Art and Design)--Massachusetts Institute of Technology, Dept. of Architecture, 2011.Cataloged from PDF version of thesis.Includes bibliographical references (p. 29).The entertainment industry relies fairly heavily on computer-generated imagery to depict built environments in current films, video games, and other forms of simulated reality. These often involve highly complex geometries that take a long time to hand-model and are too difficult or costly for many productions' rendering capacities, both in computational costs as well as time. Procedural modeling and the automation of these geometries is one option to solve these problems. Many modeling programs involve a script or procedural modeling component. This thesis explores the use of CityEngine, a commercially available software that is specialized to generate geometries for buildings in urban environments. By using the CGA Shape Grammar built into CityEngine, this project seeks to generate geometries based on complex architectural precedents using a procedural modeling system based on shape grammar and computational design principles. Results are generated and discussed, as well as applications and future work.by Anisha V. Deshmane.S.B.in Art and Desig

    Umbilical Metastasis as the Manifestation of an Asymptomatic Gallbladder Carcinoma

    Get PDF
    Sister Mary Joseph's nodule (SMJN) is an eponym used to describe the metastatic lesion of the umbilicus. Umbilical metastases are rare and its occurrence as a first manifestation of an asymptomatic primary malignancy is very rare. The gallbladder is the source of SMJN in 2%-3% of cases. SMJN can present in any one of the following ways; first manifestation of an occult primary malignancy, an indication of recurrence in a patient with a previous malignancy, or as progression of an underlying symptomatic primary disease. Our study emphasizes the importance of identifying this very useful and easily applicable clinical sign by careful physical examination of the abdomen, and also the need for proper clinical evaluation of any umbilical lesion, and the histological diagnosis. In the present study we report on a case of Sister Mary Joseph's Nodule as the presentation of an asymptomatic gallbladder carcinoma, and review the relevant literature

    STABILITY INDICATING RP-HPLC METHOD DEVELOPMENT AND VALIDATION FOR SIMULTANEOUS ESTIMATION OF AMLODIPINE AND HYDROCHLOROTHIAZIDE IN PHARMACEUTICAL DOSAGE FORM

    Get PDF
    The Aim of present work is to develop a simple, selective and precise, stability indicating RP-HPLC method for the simultaneous estimation of Amlodipine and Hydrochlorothiazide. The chromatographic separation of the two drugs was achieved on a reverse phase Hypersil Gold, C18, 250 × 4.6 mm, 5μm column using mobile as Potassium dihydrogen buffer – Acetonitrile in ratio of 600:400 v/v (pH adjusted to 3.2±0.05 using orthophosphoric acid) with flow rate of 1.0 ml/min with injection volume 20 μl and the detection was carried out at 237 nm using UV detector. The retention time of amlodipine (Amlo) and hydrochlorothiazide (HCT) were found to be 3.80 and 6.48 min respectively. The linear regression analysis data for the calibration plots showed good linear relationship in the concentration range of 0.84-1.98 μg/ml for hydrochlorothiazide and 4.2-9.8 μg/ml for amlodipine. The method was validated for precision, linearity, LOD and LOQ, specificity, accuracy, system suitability and ruggedness as per ICH guidelines and the results were found to be within the limits. The developed method was used for the stability studies. The validated method can be used for routine quality control testing for HCT and Amlo combine dosage form

    STABILITY INDICATING RP-HPLC METHOD DEVELOPMENT AND VALIDATION FOR SIMULTANEOUS ESTIMATION OF AMLODIPINE AND HYDROCHLOROTHIAZIDE IN PHARMACEUTICAL DOSAGE FORM

    Get PDF
    Objective: The aim of present work is to develop a simple, selective and precise, stability indicating RP-HPLC method for the simultaneous estimation of Amlodipine and Hydrochlorothiazide. Methods: The chromatographic separation of the two drugs was achieved on a reverse phase Hypersil Gold, C18, 250 × 4.6 mm, 5μm column using mobile as Potassium dihydrogen buffer–Acetonitrile in ratio of 600:400 v/v (pH adjusted to 3.2±0.05 using orthophosphoric acid) with flow rate of 1.0 ml/min with injection volume 20 μl and the detection was carried out at 237 nm using UV detector. Results: The retention time of amlodipine (Amlo) and hydrochlorothiazide (HCT) were found to be 3.80 and 6.48 min respectively. The linear regression analysis data for the calibration plots showed good linear relationship in the concentration range of 0.84-1.98 μg/ml for hydrochlorothiazide and 4.2-9.8 μg/ml for amlodipine. Conclusion: The method was validated for precision, linearity, LOD and LOQ, specificity, accuracy, system suitability and ruggedness as per ICH guidelines and the results were found to be within the limits. The developed method was used for the stability studies. The validated method can be used for routine quality control testing for HCT and Amlo combine dosage form

    GLINT: GlucoCEST in neoplastic tumors at 3 T—clinical results of GlucoCEST in gliomas

    Get PDF
    Objective: Clinical relevance of dynamic glucose enhanced (DGE) chemical exchange saturation transfer (CEST) imaging has mostly been demonstrated at ultra-high field (UHF) due to low effect size. Results of a cohort study at clinical field strength are shown herein. // Materials and methods: Motion and field inhomogeneity corrected T1ρ‐based DGE (DGE⍴) images were acquired before, during and after a D-glucose injection with 6.3 s temporal resolution to detect accumulation in the brain. Six glioma patients with clear blood–brain barrier (BBB) leakage, two glioma patients with suspected BBB leakage, and three glioma patients without BBB leakage were scanned at 3 T. // Results: In high-grade gliomas with BBB leakage, D-glucose uptake could be detected in the gadolinium (Gd) enhancing region as well as in the tumor necrosis with a maximum increase of ∆DGE⍴ around 0.25%, whereas unaffected white matter did not show any significant DGE⍴ increase. Glioma patients without Gd enhancement showed no detectable DGE⍴ effect within the tumor. // Conclusion: First application of DGE⍴ in a patient cohort shows an association between BBB leakage and DGE signal irrespective of the tumor grade. This indicates that glucoCEST corresponds more to the disruptions of BBB with Gd uptake than to the molecular tumor profile or tumor grading

    Interleukin-17D and Nrf2 mediate initial innate immune cell recruitment and restrict MCMV infection.

    Get PDF
    Innate immune cells quickly infiltrate the site of pathogen entry and not only stave off infection but also initiate antigen presentation and promote adaptive immunity. The recruitment of innate leukocytes has been well studied in the context of extracellular bacterial and fungal infection but less during viral infections. We have recently shown that the understudied cytokine Interleukin (IL)-17D can mediate neutrophil, natural killer (NK) cell and monocyte infiltration in sterile inflammation and cancer. Herein, we show that early immune cell accumulation at the peritoneal site of infection by mouse cytomegalovirus (MCMV) is mediated by IL-17D. Mice deficient in IL-17D or the transcription factor Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), an inducer of IL-17D, featured an early decreased number of innate immune cells at the point of viral entry and were more susceptible to MCMV infection. Interestingly, we were able to artificially induce innate leukocyte infiltration by applying the Nrf2 activator tert-butylhydroquinone (tBHQ), which rendered mice less susceptible to MCMV infection. Our results implicate the Nrf2/IL-17D axis as a sensor of viral infection and suggest therapeutic benefit in boosting this pathway to promote innate antiviral responses

    The complex TIE between macrophages and angiogenesis

    Get PDF
    Macrophages are primarily known as phagocytic immune cells, but they also play a role in diverse processes, such as morphogenesis, homeostasis and regeneration. In this review, we discuss the influence of macrophages on angiogenesis, the process of new blood vessel formation from the pre-existing vasculature. Macrophages play crucial roles at each step of the angiogenic cascade, starting from new blood vessel sprouting to the remodelling of the vascular plexus and vessel maturation. Macrophages form promising targets for both pro- and anti-angiogenic treatments. However, to target macrophages, we will first need to understand the mechanisms that control the functional plasticity of macrophages during each of the steps of the angiogenic cascade. Here, we review recent insights in this topic. Special attention will be given to the TIE2-expressing macrophage (TEM), which is a subtype of highly angiogenic macrophages that is able to influence angiogenesis via the angiopoietin-TIE pathway

    JC Virus T-Antigen Regulates Glucose Metabolic Pathways in Brain Tumor Cells

    Get PDF
    Recent studies have reported the detection of the human neurotropic virus, JCV, in a significant population of brain tumors, including medulloblastomas. Accordingly, expression of the JCV early protein, T-antigen, which has transforming activity in cell culture and in transgenic mice, results in the development of a broad range of tumors of neural crest and glial origin. Evidently, the association of T-antigen with a range of tumor-suppressor proteins, including p53 and pRb, and signaling molecules, such as β-catenin and IRS-1, plays a role in the oncogenic function of JCV T-antigen. We demonstrate that T-antigen expression is suppressed by glucose deprivation in medulloblastoma cells and in glioblastoma xenografts that both endogenously express T-antigen. Mechanistic studies indicate that glucose deprivation-mediated suppression of T-antigen is partly influenced by 5′-activated AMP kinase (AMPK), an important sensor of the AMP/ATP ratio in cells. In addition, glucose deprivation-induced cell cycle arrest in the G1 phase is blocked with AMPK inhibition, which also prevents T-antigen downregulation. Furthermore, T-antigen prevents G1 arrest and sustains cells in the G2 phase during glucose deprivation. On a functional level, T-antigen downregulation is partially dependent on reactive oxygen species (ROS) production during glucose deprivation, and T-antigen prevents ROS induction, loss of ATP production, and cytotoxicity induced by glucose deprivation. Additionally, we have found that T-antigen is downregulated by the glycolytic inhibitor, 2-deoxy-D-glucose (2-DG), and the pentose phosphate inhibitors, 6-aminonicotinamide and oxythiamine, and that T-antigen modulates expression of the glycolytic enzyme, hexokinase 2 (HK2), and the pentose phosphate enzyme, transaldolase-1 (TALDO1), indicating a potential link between T-antigen and metabolic regulation. These studies point to the possible involvement of JCV T-antigen in medulloblastoma proliferation and the metabolic phenotype and may enhance our understanding of the role of viral proteins in glycolytic tumor metabolism, thus providing useful targets for the treatment of virus-induced tumors

    HDL Interfere with the Binding of T Cell Microparticles to Human Monocytes to Inhibit Pro-Inflammatory Cytokine Production

    Get PDF
    BACKGROUND: Direct cellular contact with stimulated T cells is a potent mechanism that induces cytokine production in human monocytes in the absence of an infectious agent. This mechanism is likely to be relevant to T cell-mediated inflammatory diseases such as rheumatoid arthritis and multiple sclerosis. Microparticles (MP) generated by stimulated T cells (MPT) display similar monocyte activating ability to whole T cells, isolated T cell membranes, or solubilized T cell membranes. We previously demonstrated that high-density lipoproteins (HDL) inhibited T cell contact- and MPT-induced production of IL-1beta but not of its natural inhibitor, the secreted form of IL-1 receptor antagonist (sIL-1Ra). METHODOLOGY/PRINCIPAL FINDINGS: Labeled MPT were used to assess their interaction with monocytes and T lymphocytes by flow cytometry. Similarly, interactions of labeled HDL with monocytes and MPT were assessed by flow cytometry. In parallel, the MPT-induction of IL-1beta and sIL-1Ra production in human monocytes and the effect of HDL were assessed in cell cultures. The results show that MPT, but not MP generated by activated endothelial cells, bond monocytes to trigger cytokine production. MPT did not bind T cells. The inhibition of IL-1beta production by HDL correlated with the inhibition of MPT binding to monocytes. HDL interacted with MPT rather than with monocytes suggesting that they bound the activating factor(s) of T cell surface. Furthermore, prototypical pro-inflammatory cytokines and chemokines such as TNF, IL-6, IL-8, CCL3 and CCL4 displayed a pattern of production induced by MPT and inhibition by HDL similar to IL-1beta, whereas the production of CCL2, like that of sIL-1Ra, was not inhibited by HDL. CONCLUSIONS/SIGNIFICANCE: HDL inhibit both MPT binding to monocytes and the MPT-induced production of some but not all cytokines, shedding new light on the mechanism by which HDL display their anti-inflammatory functions
    corecore