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Σάββατο 26 Μαΐου 2018

Turning cancer's metabolic plasticity into fragility- an evolving paradigm

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SOCIO-ECOLOGICAL CORRELATES OF EXERCISE AT CARDIAC REHABILITATION COMPLETION

Objectives To describe: (1) the amount of physical activity (PA) in cardiac rehabilitation (CR) graduates by sex, and (2) the correlates of their PA. Design Secondary analysis of baseline data from a randomized trial was undertaken. Graduates were recruited from 3 CR programs. Participants completed a questionnaire which assessed constructs from the Socio-ecological model (i.e., individual-level, social and physical-environmental levels). PA was measured objectively using an ActiGraph GT3X accelerometer. Multi-level modeling was performed. Results 255 patients consented, of which 200 (78.4%) completed the survey and provided valid accelerometer data. Participants self-reported engaging in a mean of 184.51±129.10 (standard deviation) minutes of moderate-to-vigorous-intensity PA (MVPA) per week (with men engaging in more than women, p<.05 accelerometer data revealed participants engaged in minutes of mvpa with meeting recommendations. the mixed models socio-ecological correlate significantly related to greater self-reported was self-regulation accelerometer-derived neighborhood aesthetics conclusions approximately one-quarter cr program completers are achieving recommendations although two-thirds perceive they are. programs should exploit accelerometry and promote skills namely self-monitoring goal-setting positive reinforcement time management relapse prevention. patients be encouraged exercise pleasing locations. funding: this work supported by a grant-in-aid from heart stroke foundation canada ontario award number: prof. grace her toronto general western hospital peter munk cardiac centre university health network. stephanie prince is funded fellowship canadian institute research an endowed strategic ottawa foundation. funders played no role design study collection analysis or interpretation writing manuscript. conflict interest: authors declare that have interest. statement human rights: has been approved appropriate institutional national ethics committee performed accordance ethical standards as laid down declaration helsinki its later amendments comparable standards. on welfare animals: article does not contain any studies animals authors. informed consent: consent obtained all individual corresponding author: sherry l. phd. school kinesiology science bethune york keele street m3j ip3 canada. email: sgrace copyright wolters kluwer inc. rights reserved.>

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Pronator Syndrome: An Uncommon Median Nerve Entrapment Syndrome

Not Applicable for Visual Vignette Correspondence: Ying Liang LOW, National University Hospital, 5 Lower Kent Ridge Road, Singapore 119074, Email: ying_liang_low@nuhs.edu.sg Author Disclosures: There are no competing interests; no funding, grants or equipment provided for the project from any source; and no financial benefits to the authors. This article has not been presented in any form previously. Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.

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(OA48) Prospective In-Silico Quality Assurance Study of Contouring Target Volumes in Thoracic Tumors Within a Cooperative Group Setting

Target delineation variability is a significant technical impediment in multi-institutional, including cooperative group, trials which employ intensity modulated radiotherapy (IMRT), as there is real potential for clinically meaningful variance in radiotherapy plans submitted to future studies. However, little is known how best to optimize protocols to account for multimodality imaging (e.g. PET, 4DCT) in the treatment planning process. The goal of this study is to determine the variability of target delineation among observers from different institutions as part of SWOG Radiotherapy Committee's multi-institutional in-silico quality assurance study of target delineation in patients with superior sulcus tumors.

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Accelerated vascular aging and persistent cognitive impairment in older female breast cancer survivors

Abstract

Advances in breast cancer treatment have markedly increased survivorship over the past three decades, with over 3.1 million survivors expected to live into their 70s and 80s. Without symptom relief interventions, nearly 35% of these survivors will have life-altering and distressing cognitive symptoms. This pilot study explored associations between serum markers of vascular aging, laterality in cerebral oxygenation, and severity of cognitive impairment in women, 12–18 months after chemotherapy for stage 2/3 invasive ductal breast cancer. Fifteen women (52–84 years) underwent a brief cognitive assessment (Montreal Cognitive Assessment [MOCA]) and blood draws to assess markers of vascular aging (interleukin-6 [IL-6], tumor necrosis factor alpha [TNF-α], C-reactive protein [CRP], and insulin growth factor-1 [IGF-1]). All underwent a computer-based test protocol that is known to increase blood flow within the frontal lobes. Percent cerebral oxyhemoglobin saturation (rcSO2) was recorded during and after testing. Laterality in rcSO2 was defined by ≥ 3% difference between left and right rcSO2 (|rcSO2 meanRIGHT – meanLEFT|). Eight participants had MOCA scores between 21 and 25 points, suggestive of mild cognitive impairment. Neither CRP (r = −.24) nor IL-6 (r = .34) nor TNF-α (r = .002) were associated with MOCA scores. Higher IL-6 was associated with greater laterality (r = .41). MOCA scores were significantly lower in subjects with laterality in rcSO2 than in those without laterality (F(1,14) = 13.5, p = 003). Lower IGF-1 was significantly associated with greater laterality (r = − .66, p = .007) and lower cognitive function (r = .58). These findings suggest that persistent cognitive impairment is associated with phenotypical changes consistent with accelerated vascular aging.



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Hepatocellular nodules in vascular liver diseases

Abstract

Hepatocellular nodules have been recognized in vascular liver diseases for a long time and mostly described and studied in the imaging literature. Some confusions in their identification and overlap in their definitions exist, especially in this specific clinical context. Pathology descriptions report the development of nodular regenerative hyperplasia, large regenerative nodule, and focal nodular hyperplasia, as adaptive responses of the liver parenchyma to the modified blood flow. True neoplastic hepatocellular nodules such as hepatocellular adenoma and hepatocellular carcinoma can also appear, mainly in Budd-Chiari syndrome, and have to be correctly diagnosed. This is more difficult for the radiologist in these diseased livers, leading more frequently to perform liver biopsies. We describe the histology of each type of well-differentiated hepatocellular nodules and provide some clues for their differential diagnosis. A review of the literature gives an historical perspective of the problem and enlightens the frequency and the subtypes of hepatocellular nodules found in the most common vascular liver diseases.



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The long non-coding RNA PTTG3P promotes cell growth and metastasis via up-regulating PTTG1 and activating PI3K/AKT signaling in hepatocellular carcinoma

Abstract

Background

Dysfunctions of long non-coding RNA (lncRNAs) have been associated with the initiation and progression of hepatocellular carcinoma (HCC), but the clinicopathologic significance and potential role of lncRNA PTTG3P (pituitary tumor-transforming 3, pseudogene) in HCC remains largely unknown.

Methods

We compared the expression profiles of lncRNAs in 3 HCC tumor tissues and adjacent non-tumor tissues by microarrays. In situ hybridization (ISH) and quantitative real-time polymerase chain reaction (qRT-PCR) were applied to assess the level of PTTG3P and prognostic values of PTTG3P were assayed in two HCC cohorts (n = 46 and 90). Artificial modulation of PTTG3P (down- and over-expression) was performed to explore the role of PTTG3P in tumor growth and metastasis in vitro and in vivo. Involvement of PTTG1 (pituitary tumor-transforming 1), PI3K/AKT signaling and its downstream signals were validated by qRT-PCR and western blot.

Results

We found that PTTG3P was frequently up-regulated in HCC and its level was positively correlated to tumor size, TNM stage and poor survival of patients with HCC. Enforced expression of PTTG3P significantly promoted cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, PTTG3P knockdown had opposite effects. Mechanistically, over-expression of PTTG3P up-regulated PTTG1, activated PI3K/AKT signaling and its downstream signals including cell cycle progression, cell apoptosis and epithelial-mesenchymal transition (EMT)-associated genes.

Conclusions

Our findings suggest that PTTG3P, a valuable marker of HCC prognosis, promotes tumor growth and metastasis via up-regulating PTTG1 and activating PI3K/AKT signaling in HCC and might represent a potential target for gene-based therapy.



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