Academic literature on the topic 'Donation of organs, tissues, etc – France'

IntroductionKidney transplantation in Ecuador began in 1976, it was limited until 2011, when the Organic Law of Donation and Transplantation of Organs, Tissues and Cells became valid. This is indicated in end-stage renal failure, in adult and pediatric patients; and, compared to peritoneal and renal dialysis, it is less expensive for the health system. In 2015, in Ecuador, at least 30,000 people suffered from end-stage kidney disease; 45% of them could die without treatment. The objective of this study was to determine the current situation in Ecuador regarding kidney transplantation. MethodologyA descriptive, retrospective study. INDOT statistics were reviewed from 2007 to August 2019, to determine the total number of transplants and kidney transplants, type of transplant, effective donors, rate of donors per million population (pmp), transplanted organ rate (pmp), evolution of the national waiting list, survival rate, etc. Results From 2007 to 2019, 6134 transplants were performed: 25.4% renal. Most donors were male (68.1%). The donor rate (pmp) between 2009 and 2019 was 4.2 (SD: ± 2.1). The mean rate of transplanted organs was 8.1 (SD: ± 3.6) (pmp) from 2007 to 2019. In this period 1560 kidney transplants were performed: 83.1% with cadaveric donors (88.1% adults; 11.9% pediatric) and 16.9% with living donors (72.4% adults; 27.6% pediatric). The one-year survival rate after cadaveric and living donor kidney transplantation was 0.94 and 0.97 in adults; and 0.90 and 0.97 in pediatrics, respectively. Currently there are only 5 accredited centers for kidney transplantation in adults and one for pediatric kidney transplantation .ConclusionsKidney transplantation has made significant progress in Ecuador, however, it is still below the World Health Organization (WHO) goal established for the proper management of patients with chronic kidney failure.

Arsenic and Protein Expression: It might help to know the mechanism of As toxicity is described Introduction One of the largest public health problems at present is the drinking of water containing levels of Inorg-As that are known to be carcinogenic. The chronic ingestion of Inorg-As can results in skin cancer, urinary bladder cancer, lungs cancer, kidneys cancer, liver cancer, and cancer of other human organs 1-6. The molecular mechanisms of the carcinogenicity and toxicity of inorganic arsenic are not well understood 7–9. Many mechanisms of arsenic toxicity and carcinogenicity have been suggested 1, 7, 10 including chromosome abnormalities 11, oxidative stress 12, 13, altered growth factors 14, cell proliferation 15, altered DNA repair 16, altered DNA methylation patterns 17, inhibition of several key enzymes 18, gene amplification 19 etc. Some of these mechanisms result in alterations in protein expression. Proteomics is a powerful tool developed to enhance the study of complex biological system 20. This technique has been extensively employed to investigate the proteome response of cells to drugs and other diseases 21, 22. A proteome analysis of the Na-As (III) response in cultured lung cells found in vitro oxidative stress-induced apoptosis 23. In one of the study, hamsters were exposed to sodium arsenite (173 mg As/L) in drinking water for 6 days and several protein spots were over expressed and several were under expressed in the livers and urinary bladders of hamsters (Fig.) 24, 25. Hamsters were exposed to sodium arsenite (173 mg As/L) in drinking water for 6 days. The control hamsters were given tap water. The spot pairs of (A) equally expressed, (B) overexpressed, and (C) under expressed proteins in the liver tissues were shown. The amount of the protein is proportional to the volume of the protein peak. Transgelin was down-regulated, and GST-pi was up-regulated in the urinary bladder tissues of hamsters. In the liver tissues ornithine aminotransferase (OAT) was up-regulated, and senescence marker protein 30 (SMP 30), and fatty acid binding protein (FABP) were down-regulated. Down-regulation of transgelin has been noted in the urinary bladders of rats having bladder outlet obstruction 26. Ras-dependent and Ras-independent mechanisms can cause the down regulation of transgelin in human breast and colon carcinoma cell lines and patient-derived tumor samples 27. The loss of transgelin expression has been found in prostate cancer cells 28 and in human colonic neoplasms 29. It has been suggested that the loss of transgelin expression may be an important early event in tumor progression and a diagnostic marker for cancer development 26-29. Figure. Three-dimentional simulation of over-and under expressed protein spots in the livers of hamsters using Decyder software. Over-expression of GST-pi has been found in colon cancer tissues 30. Strong expression of GST-pi also has been found in gastric cancer 31, malignant melanoma 32, lung cancer 33, breast cancer 34 and a range of other human tumors 35. GST-pi has been up-regulated in transitional cell carcinoma of human urinary bladder 36. OAT has a role in regulating mitotic cell division and it is required for proper spindle assembly in human cancer cell 37. Ornithine amino transferase knockdown in human cervical carcinoma and osteosarcoma cells by RNA interference blocks cell division and causes cell death 37. It has been suggested that ornithine amino transferase has a role in regulating mitotic cell division and it is required for proper spindle assembly in human cancer cells 37. SMP 30 expressed mostly in the liver. By stimulating membrane calcium-pump activity it protects cells against various injuries 38. High levels of saturated, branched chain fatty acids are deleterious to cells and resulting in lipid accumulation and cytotoxicity. FABP expression has protected the cells against branched chain saturated fatty acid 39. Proteomics would be a powerful tool to know the unknown cellular mechanisms of arsenic toxicity in humans. References. NRC (National Research Council). (2001). Arsenic in Drinking Water. Update to the 1999 Arsenic in Drinking Water Report. National Academy Press, Washington, DC. Chen, C. J., Chen, C. , Wu, M. M., Kuo, T. L. (1992). Cancer potential in liver, lung, bladder, and kidney due to ingested inorganic arsenic in drinking water. Br. J. Cancer 66, 888-892. Hopenhayn-Rich, C., M.L. Biggs, A. Fuchs, et al. 1996. Bladder cancer mortality with arsenic in drinking water in Argentina. Epidemiology 7: 117–124. International Agency for Research on Cancer. (1987). In IARC Monograph on the Evaluation of Carcinogenicity Risk to Humans. Overall Evaluation of Carcinogenicity:An Update of IARC Monographs 1–42 (Suppl. 7). Lyon, France: International Agency for Research on Can-cer, pp. 100–106. Rossman, T.G., Uddin, A.N., and Burns, F.J. (2004). Evidence that arsenite acts as a cocarcinogen in skin cancer. Toxicol. Appl. Pharmacol. 198: 394–404. Smith, A.H., Hopenhayn-Rich, C., Bates, M.N., et al. (1992). Cancer risks from arsenic in drinking water. Environ. Health Perspect. 97: 259–267. Aposhian, H.V. & Aposhian, M.M. (2006). Arsenic toxicology: five questions. Chem. Res. Toxicol. 19: 1–15. Goering, P.L., Aposhian, H.V., Mass, M.J., et al. (1999). The enigma of arsenic carcinogenesis: role of metabolism. Toxicol. Sci. 49: 5–14. Waalkes, M.P., Liu, J., Ward, J.M., et al. (2004). Mechanisms underlying arsenic carcinogenesis: hypersensitivity of mice exposed to inorganic arsenic during gestation. Toxicology 198: 31–38. Kitchin, K. T., Recent advances in arsenic carcinogenesis: modes of action, animal model systems, and methylated arsenic metabolites. Appl. Pharmacol. 2001, 172, 249-261. Beckman, G., Beckman, L., Nordenson, I., Chromosome aberrations in workers exposed to arsenic. Environ. Health Perspect. 1977, 19, 145-146. Yamanaka, K., Hoshino, M., Okanoto, M., Sawamura, R., et al., Induction of DNA damage by dimethylarsine, a metabolite of inorganic arsenics, is for the major part likely due to its peroxyl radical. Biophys. Res. Commun. 1990, 168, 58-64. Yamanaka, K., Okada, S., Induction of lung-specific DNA damage by metabolically methylated arsenics via the production of free radicals. Health Perspect. 1994, 102, 37-40. Simeonova, P., Luster, M. I., Mechanisms of arsenic carcinogenicity:Genetic or epigenetic mechanisms? J. Environ. Pathol. Toxicol. Oncol. 2000, 19, 281-286. Popovicova, J., Moser, G. J., Goldsworthy, T. , Tice, R. R., Carcinogenicity and co-carcinogenicity of sodium arsenite in p53+/- male mice. Toxicologist 2000, 54, 134. Li, J. H., Rossman, T. G., Mechanism of co-mutagenesis of sodium arsenite with N-methyl-N-nitrosourea. Bi Trace Elem. 1989, 21, 373-381. Zhao, C. Q., Young, M. R., Diwan, B. A., Coogan, T. P., et , Association of arsenic-induced malignant transformation with DNA hypomethylation and aberrant gene expression. Proc. Natl. Acad. Sci. USA 1997, 94, 10907-10912. Abernathy, C. O., Lui, Y. P., Longfellow, D., Aposhian, H. , et al., Arsenic: Health effects, mechanisms of actions and research issues. Environ. Health Perspect. 1999, 107, 593-597. Lee, T. C., Tanaka, N., Lamb, P. W., Gilmer, T. M., et al., Induction of gene amplification by arsenic. Science 1988, 241, 79-81. Lau, A. T., He, Q. Y., Chiu, J. F. (2003). Proteomic technology and its biomedical applications. Acta Biochim. Bioph Sin. 35, 965-975. Jungblut, P. R., Zimny-Arndt, U., Zeindl-Eberhart, E., Stulik, J., Koupilova, K., Pleissner, K. P., Otto, A., Muller, E. C., Sokolowska-Kohler, W., Grabher, G., Stoffler, G. (1999). Proteomics in human disease: cancer, heart and infectious diseases. Electrophoresis 20, 2100-2110. Hanash, S. M., Madoz-Gurpide, J., Misek, D. E. (2002). Identification of novel targets for cancer therapy using expression proteomics. Leukemia 16, 478-485. Lau, A. T., He, Q. Y., Chiu, J. F. (2004). A proteome analysis of the arsenite response in cultured lung cells: evidence for in vitro oxidative stress-induced apoptosis. J. 382, 641-650. Chowdhury, U. K., Aposhian, H. V. (2008). Protein expression in the livers and urinary bladders of hamsters exposed to sodium arsenite. A N. Y. Acad. Sci. 1140, 325-334. Chowdhury, U.K. Expression of proteins in the tissues of hamsters exposed to sodium arsenite. Int. J. of Toxicol., 2021, 1, 1-8. Kim, H-J., Sohng, I., Kim, D-H., Lee, D-C., et al., 2005. Investigation of early protein changes in the urinary bladder following partial bladder outlet obstruction by proteomic approach. J. Korean Med. Sci. 20, 1000-1005. Shields, J.M., Rogers-Graham, K., Der, C.J., 2002. Loss of transgelin in breast and colon tumors and in RIE-1 cells by Ras deregulation of gene expression through Raf-independent pathways. J. Biol. Chem. 277, 9790-9799. Yang, Z., Chang, Y- J., Miyamoto, H., Ni, J., et al., Transgelin functions as a suppressor via inhibition of ARA54-enhanced androgen receptor transactivation and prostate cancer cell grown. Mol. Endocrinol. 2007, 21, 343-358. Yeo, , Kim, D- K., Park, H. J., Oh, T. Y., et al., Loss of transgelin in repeated bouts of ulcerative colitis-induced colon carcinogenesis. Proteomics 2006, 6, 1158-1165. Tsuchida, S., Sekine, Y., Shineha, R., Nishihira, T., et al., Elevation of the placental glutathione S-transferase form (GST-PI) in tumor tissues and the levels in sera of patients with cancer. Cancer Re 1989, 43, 5225-5229. Tsutsumi, M., Sugisaki, T., Makino, T., Miyagi, N., et al., Oncofetal expression of glutathione S-transferase placental form in human stomach carcinomas. 1987, 78, 631-633. Mannervik, B., Castro, V. M., Danielson, U. H., Tahir, M. K., et , Expression of class Pi glutathione transferase in human malignant melanoma cells. Carcinogenesis (Lond.) 1987, 8, 1929-1932. Di llio, C., Del Boccio, G., Aceto, A., Casaccia, R., et al,. Elevation of glutathione transferase activity in human lung tumor. Carcinogenesis (Lond.) 1988, 9, 335-340. Sreenath, A. S., Ravi, K. K., Reddy, G. V., Sreedevi, B., et al., Evidence for the association of synaptotagmin with glutathione S- transferase: implications for a novel function in human breast cancer. Clinical Biochem. 2005, 38, 436-443. Shea, T. C., Kelley S. L, Henner, W. D., Identification of an anionic form of glutathione transferase present in many human tumors and human tumor cell lines. Cancer Res. 1988, 48, 527-533. Simic, T., Mimic-Oka, J., Savic-Radojevic, A., Opacic, M., et al., Glutathione S- transferase T1-1 activity upregulated in transitional cell carcinoma of urinary bladder. Urology 2005, 65, 1035-1040. Wang, G., Shang, L., Burgett, A. W. G., Harran, P. G., et al., Diazonamide toxins reveal an unexpected function for ornithine d-amino transferase in mitotic cell division. PNAS 2007, 104, 2068-2073. Fujita, T., Inoue, H., Kitamura, T., Sato, N., et a, Senescence marker protein-30 (SMP30) rescues cell death by enhancing plasma membrane Caat-pumping activity in hep G2 cells. Biochem. Biophys. Res. Commun. 1998, 250, 374-380. Atshaves, B. P., Storey, S. M., Petrescu, A., Greenberg, C. C., et al., Expression of fatty acid binding proteins inhibits lipid accumulation and alters toxicity in L cell fibroblasts. A J. Physiol. Cell Physiol. 2002, 283, C688-2703.

Objective: To synthesize evidence from the recent interventions to improve organ donation rates and attitude towards organ donation. The effective intervention is defined as significant increases in the enrollment rate of organ donation and positive changes of attitude. And the second one is to give recommendations on feasible intervention designs based on the specific situation of Mainland China. Methods: A systematic review was conducted through PubMed, Cochrane Library, Google Scholar and reference lists. The quality of the studies was evaluated by CONSORT guideline. Results: Nine randomized control studies were included in this systematic review, and the quality of all these studies was average. The main targets of the studies were religious beliefs, distrust medical system, lack of knowledge and fear of premature death. Using lay health advisors, implementing lecture, presentation and discussion, and exposure to mass media with donation information frequently were all identified as effective components to change the attitude and improve the enrollment rate. Conclusion: Based on this systematic review, discrepant interventions could change the public attitude towards organ donation and improve the enrollment donation rate in the United States. However, given the cultural differences in China, more research is needed to see whether implementation of these interventions could improve the situation of organ donation in China.
published_or_final_version
Public Health
Master
Master of Public Health

Background. Organ transplantation as one of the most effective treatment options for patients with organ failure is challenged by organ shortage around the world. This systematic review aims to summary relevant factors influencing people’s intention and behavior for organ donation. Method. Three databases, namely PUB med, Medline and China knowledge resources integrated database, were applied for literature searching. Fourteen studies, which meet the inclusion criteria and exclusion criteria, are used in this review. Quality assessment was proceeding upon STROBE checklist. Results. Seven factors influencing individuals’ intentions and behavior for organ donation are summarized, including: demographic factors, cultural factors, attitudes towards death and funeral, family influence, information accessibility for organ donation, distrust medical community and legislation for organ donation. In addition, two more factors, acceptance of brain death and effectiveness in receiving donation request, are associated with family consent to organ donation. Conclusion. This review highlights factors could influence individual’s intention and behavior for organ donation. Potential implications could be implemented base on the effect of these factors. Possible interventions, upon demographic characteristics, dealing with Chinese traditional concept and enhancing knowledge and exposure of organ donation, to Chinese population are discussed. Limitations of this systematic review are also mentioned.
published_or_final_version
Public Health
Master
Master of Public Health