In the last decade, we have seen a growth of Compassionate Communities and Cities (CCC) at the end of life. There has been an evolution of organizations that help construct Community-Based Palliative Care programs. The objective is to analyze the implementation, methodology and effectiveness of the CCC models at the end of life. We conducted a systematic review following PRISMA ScR Guideline. The protocol was registered on PROSPERO (CRD42017068501). Five databases (MEDLINE, EMBASE, Web of Science, CINAHL and Google Scholar) were searched for studies (from 2000 to 2018) using set eligibility criteria. Three reviewers screened full-texts articles and extracted study data. Outcomes were filled in a registration form which included a narrative synthesis of each article. We screened 1975 records. We retrieved 112 articles and included 31 articles for the final analysis: 17 descriptive studies, 4 interventions studies, 4 reviews and 6 qualitative studies. A total of 11 studies regard the development models of CCC at the end of life, 15 studies were about evaluation of compassionate communities' programs and 5 studies were about protocols for the development of CCC programs. There is poor evidence of the implementation and evaluation models of CCC at the end of life. There is little and low-/very low-quality evidence about CCC development and assessment models. We found no data published on care intervention in advance disease and end of life. A global model for the development and evaluation of CCC at the end of life seems to be necessary.
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http://dx.doi.org/10.3390/ijerph17176271 | DOI Listing |
Life (Basel)
December 2024
Molecular Oncology and Viral Pathology Group, Research Centre of IPO Porto (CI-IPOP), Pathology and Laboratory Medicine Department, Clinical Pathology SV/RISE@CI-IPOP (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Centre (Porto. CCC), 4200-072 Porto, Portugal.
Ovarian cancer (OC) presents daunting lethality rates worldwide, with frequent late-stage diagnosis and chemoresistance, highlighting the need for improved prognostic approaches. Venous thromboembolism (VTE), a major cancer mortality factor, is partially driven by endothelial dysfunction (ED). ED's pro-inflammatory state fosters tumour progression, suggesting a VTE-independent link between ED and cancer.
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Department of Nutrition, Chung Shan Medical University, Taichung 402, Taiwan.
Spinocerebellar ataxia type 3 (SCA3), caused by the abnormal expansion of polyglutamine (polyQ) in the ataxin-3 protein, is one of the inherited polyQ neurodegenerative diseases that share similar genetic and molecular features. Mutant polyQ-expanded ataxin-3 protein is prone to aggregation in affected neurons and is predominantly degraded by autophagy, which is beneficial for neurodegenerative disease treatment. Not only does mutant polyQ-expanded ataxin-3 increase susceptibility to oxidative cytotoxicity, but it also hampers antioxidant potency in neuronal cells.
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January 2025
Center for Cell and Gene Therapy, Clinical Research Center for Cell-based Immunotherapy, Shanghai Pudong Hospital, State Key Laboratory of Genetic Engineering, School of Life Sciences, Human Phenome Institute, Fudan University, Shanghai, 200433, China.
Ampullary adenocarcinoma (AMPAC) is a rare and heterogeneous malignancy. Here we performed a comprehensive proteogenomic analysis of 198 samples from Chinese AMPAC patients and duodenum patients. Genomic data illustrate that 4q loss causes fatty acid accumulation and cell proliferation.
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January 2025
IQ Health Science Department, Radboud University Medical Center, Nijmegen, The Netherlands.
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January 2025
Institute of Endocrine and Metabolic Diseases, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230027, China. Electronic address:
Nonalcoholic fatty liver disease (NAFLD) is a progressive condition characterized by ectopic fat accumulation in the liver, for which no FAD-approved drugs currently exist. Emerging evidence highlights the role of liver kinase B1 (LKB1), a key metabolic regulator, has been proposed in NAFLD, particularly in response to excessive nutrient levels. However, few agents have been identified that can prevent the progression of nonalcoholic steatohepatitis (NASH) by targeting LKB1 deacetylation.
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