220 research outputs found

    Triage for coronary artery bypass graft surgery in Canada: Do patients agree on who should come first?

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    <p>Abstract</p> <p>Background</p> <p>The extent to which clinical and non-clinical factors impact on the waiting-list prioritization preferences of patients in the queue is unknown. Using a series of hypothetical scenarios, the objective of this study was to examine the extent to which clinical and non-clinical factors impacted on how patients would prioritize others relative to themselves in the coronary artery bypass surgical queue.</p> <p>Methods</p> <p>Ninety-one consecutive eligible patients awaiting coronary artery bypass grafting surgery at Sunnybrook Health Sciences Centre (median waiting-time duration prior to survey of 8 weeks) were given a self-administered survey consisting of nine scenarios in which clinical and non-clinical characteristic profiles of hypothetical patients (also awaiting coronary artery bypass surgery) were varied. For each scenario, patients were asked where in the queue such hypothetical patients should be placed relative to themselves.</p> <p>Results</p> <p>The eligible response rate was 65% (59/91). Most respondents put themselves marginally ahead of a hypothetical patient with identical clinical and non-clinical characteristics as themselves. There was a strong tendency for respondents to place patients of higher clinical acuity ahead of themselves in the queue (P < 0.0001). Social independence among young individuals was a positively valued attribute (P < 0.0001), but neither age per se nor financial status, directly impacted on patients waiting-list priority preferences.</p> <p>Conclusion</p> <p>While patient perceptions generally reaffirmed a bypass surgical triage process based on principals of equity and clinical acuity, the valuation of social independence may justify further debate with regard to the inclusion of non-clinical factors in waiting-list prioritization management systems in Canada, as elsewhere.</p

    Renal Cell Carcinoma with Unusual Metastasis to the Small Intestine Manifesting as Extensive Polyposis: Successful Management with Intraoperative Therapeutic Endoscopy

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    We present here a rare clinical case of a 53-year-old gentleman with metastasis from renal cell carcinoma (RCC) to the small intestine presenting with extensive polyposis and massive gastrointestinal bleeding which was successfully managed with intraoperative endoscopic polypectomy and segmental small bowel resection. The patient presented with melena 2 weeks after right nephrectomy for RCC. Capsule endoscopy found extensive polyposis throughout the small bowel, and the histological features confirmed the diagnosis of metastatic RCC. The patient eventually underwent laparotomy with intraoperative endoscopy of the entire small bowel. Most of the polyps were removed by snare polypectomy. Three segments of the small bowel with extensive transmural involvement had to be resected with primary anastomosis. In the 2 months following his surgery, the patient had no further evidence of gastrointestinal bleeding. The decision of meticulously removing close to 100 polyps by intraoperative endoscopy prevented the patient from requiring total small bowel resection and lifelong dependence on parenteral nutrition. In conclusion, gastrointestinal bleeding in a patient with known RCC should always trigger full gastrointestinal work-up including capsule endoscopy and, if necessary, double balloon enteroscopy

    Versican G3 Promotes Mouse Mammary Tumor Cell Growth, Migration, and Metastasis by Influencing EGF Receptor Signaling

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    Increased versican expression in breast tumors is predictive of relapse and has negative impact on survival rates. The C-terminal G3 domain of versican influences local and systemic tumor invasiveness in pre-clinical murine models. However, the mechanism(s) by which G3 influences breast tumor growth and metastasis is not well characterized. Here we evaluated the expression of versican in mouse mammary tumor cell lines observing that 4T1 cells expressed highest levels while 66c14 cells expressed low levels. We exogenously expressed a G3 construct in 66c14 cells and analyzed its effects on cell proliferation, migration, cell cycle progression, and EGFR signaling. Experiments in a syngeneic orthotopic animal model demonstrated that G3 promoted tumor growth and systemic metastasis in vivo. Activation of pERK correlated with high levels of G3 expression. In vitro, G3 enhanced breast cancer cell proliferation and migration by up-regulating EGFR signaling, and enhanced cell motility through chemotactic mechanisms to bone stromal cells, which was prevented by inhibitor AG 1478. G3 expressing cells demonstrated increased CDK2 and GSK-3β (S9P) expression, which were related to cell growth. The activity of G3 on mouse mammary tumor cell growth, migration and its effect on spontaneous metastasis to bone in an orthotopic model was modulated by up-regulating the EGFR-mediated signaling pathway. Taken together, EGFR-signaling appears to be an important pathway in versican G3-mediated breast cancer tumor invasiveness and metastasis

    Radiation and breast cancer: a review of current evidence

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    This paper summarizes current knowledge on ionizing radiation-associated breast cancer in the context of established breast cancer risk factors, the radiation dose–response relationship, and modifiers of dose response, taking into account epidemiological studies and animal experiments. Available epidemiological data support a linear dose–response relationship down to doses as low as about 100 mSv. However, the magnitude of risk per unit dose depends strongly on when radiation exposure occurs: exposure before the age of 20 years carries the greatest risk. Other characteristics that may influence the magnitude of dose-specific risk include attained age (that is, age at observation for risk), age at first full-term birth, parity, and possibly a history of benign breast disease, exposure to radiation while pregnant, and genetic factors

    Shedding Light on The Role of Keratinocyte-Derived Extracellular Vesicles on Skin-Homing Cells

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    Extracellular vesicles (EVs) are secretory lipid membranes with the ability to regulate cellular functions by exchanging biological components between different cells. Resident skin cells such as keratinocytes, fibroblasts, melanocytes, and inflammatory cells can secrete different types of EVs depending on their biological state. These vesicles can influence the physiological properties and pathological processes of skin, such as pigmentation, cutaneous immunity, and wound healing. Since keratinocytes constitute the majority of skin cells, secreted EVs from these cells may alter the pathophysiological behavior of other skin cells. This paper reviews the contents of keratinocyte-derived EVs and their impact on fibroblasts, melanocytes, and immune cells to provide an insight for better understanding of the pathophysiological mechanisms of skin disorders and their use in related therapeutic approaches

    Metabolic Syndrome and Cardiovascular Disease after Hematopoietic Cell Transplantation: Screening and Preventive Practice Recommendations from the CIBMTR and EBMT

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    Metabolic syndrome (MetS) is a constellation of cardiovascular risk factors that increases the risk of cardiovascular disease, diabetes mellitus, and all-cause mortality. Long-term survivors of hematopoietic cell transplantation (HCT) have a substantial risk of developing MetS and cardiovascular disease, with an estimated prevalence of MetS of 31% to 49% among HCT recipients. Although MetS has not yet been proven to impact cardiovascular risk after HCT, an understanding of the incidence and risk factors for MetS in HCT recipients can provide the foundation to evaluate screening guidelines and develop interventions that may mitigate cardiovascular-related mortality. A working group was established through the Center for International Blood and Marrow Transplant Research and the European Group for Blood and Marrow Transplantation with the goal to review literature and recommend practices appropriate to HCT recipients. Here we deliver consensus recommendations to help clinicians provide screening and preventive care for MetS and cardiovascular disease among HCT recipients. All HCT survivors should be advised of the risks of MetS and encouraged to undergo recommended screening based on their predisposition and ongoing risk factors

    Understanding Communication of Sustainability Reporting: Application of Symbolic Convergence Theory (SCT)

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    The purpose of this paper is to investigate the nature of rhetoric and rhetorical strategies that are implicit in the standalone sustainability reporting of the top 24 companies of the Fortune 500 Global. We adopt Bormann’s (Q J Speech 58(4):396–407, 1972) SCT framework to study the rhetorical situation and how corporate sustainability reporting (CSR) messages can be communicated to the audience (public). The SCT concepts in the sustainability reporting’s communication are subject to different types of legitimacy strategies that are used by corporations as a validity and legitimacy claim in the reports. A content analysis has been conducted and structural coding schemes have been developed based on the literature. The schemes are applied to the SCT model which recognizes the symbolic convergent processes of fantasy among communicators in a Society. The study reveals that most of the sample companies communicate fantasy type and rhetorical vision in their corporate sustainability reporting. However, the disclosure or messages are different across locations and other taxonomies of the SCT framework. This study contributes to the current CSR literature about how symbolic or fantasy understandings can be interpreted by the users. It also discusses the persuasion styles that are adopted by the companies for communication purposes. This study is the theoretical extension of the SCT. Researchers may be interested in further investigating other online communication paths, such as human rights reports and director’s reports

    Relevance of genetic testing in the gene-targeted trial era: the Rostock Parkinson\u27s disease study

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    \ua9 The Author(s) 2024. Estimates of the spectrum and frequency of pathogenic variants in Parkinson’s disease (PD) in different populations are currently limited and biased. Furthermore, although therapeutic modification of several genetic targets has reached the clinical trial stage, a major obstacle in conducting these trials is that PD patients are largely unaware of their genetic status and, therefore, cannot be recruited. Expanding the number of investigated PD-related genes and including genes related to disorders with overlapping clinical features in large, well-phenotyped PD patient groups is a prerequisite for capturing the full variant spectrum underlying PD and for stratifying and prioritizing patients for gene-targeted clinical trials. The Rostock Parkinson’s disease (ROPAD) study is an observational clinical study aiming to determine the frequency and spectrum of genetic variants contributing to PD in a large international cohort. We investigated variants in 50 genes with either an established relevance for PD or possible phenotypic overlap in a group of 12 580 PD patients from 16 countries [62.3% male; 92.0% White; 27.0% positive family history (FH+), median age at onset (AAO) 59 years] using a next-generation sequencing panel. Altogether, in 1864 (14.8%) ROPAD participants (58.1% male; 91.0% White, 35.5% FH+, median AAO 55 years), a PD-relevant genetic test (PDGT) was positive based on GBA1 risk variants (10.4%) or pathogenic/likely pathogenic variants in LRRK2 (2.9%), PRKN (0.9%), SNCA (0.2%) or PINK1 (0.1%) or a combination of two genetic findings in two genes (∼0.2%). Of note, the adjusted positive PDGT fraction, i.e. the fraction of positive PDGTs per country weighted by the fraction of the population of the world that they represent, was 14.5%. Positive PDGTs were identified in 19.9% of patients with an AAO ≤ 50 years, in 19.5% of patients with FH+ and in 26.9% with an AAO ≤ 50 years and FH+. In comparison to the idiopathic PD group (6846 patients with benign variants), the positive PDGT group had a significantly lower AAO (4 years, P = 9 7 10−34). The probability of a positive PDGT decreased by 3% with every additional AAO year (P = 1 7 10−35). Female patients were 22% more likely to have a positive PDGT (P = 3 7 10−4), and for individuals with FH+ this likelihood was 55% higher (P = 1 7 10−14). About 0.8% of the ROPAD participants had positive genetic testing findings in parkinsonism-, dystonia/dyskinesia- or dementia-related genes. In the emerging era of gene-targeted PD clinical trials, our finding that ∼15% of patients harbour potentially actionable genetic variants offers an important prospect to affected individuals and their families and underlines the need for genetic testing in PD patients. Thus, the insights from the ROPAD study allow for data-driven, differential genetic counselling across the spectrum of different AAOs and family histories and promote a possible policy change in the application of genetic testing as a routine part of patient evaluation and care in PD
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