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Artykuły w czasopismach na temat "Necrosis"

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Jeican, Ionuț Isaia, Patricia Inișca, Bogdan Alexandru Gheban, Vlad Anton, Costel Vasile Siserman, Codrin Rebeleanu, Maria Aluaș, Carmen Bianca Crivii, Silviu Albu i Veronica Trombitaș. "Asymptomatic Esophageal Necrosis in a Patient with Recent COVID-19: The First Case Diagnosed through Autopsy". Medicina 59, nr 1 (12.01.2023): 154. http://dx.doi.org/10.3390/medicina59010154.

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Acute esophageal necrosis is a rare condition, characterized by a distinctive endoscopic/necropsic image–circumferential black area of the esophagus. This paper presents a case of a 78-year-old patient with recent history of a severe form of COVID-19 (2 months previously), with multiple comorbidities, which presents sudden death in hospital. Anatomic-pathological autopsy showed extensive esophageal necrosis, pulmonary thromboses, and coronarian and aortic atherosclerosis. The histopathological examination revealed necrosis of the esophageal mucosa and phlegmonous inflammation extended to the mediastinum, chronic pneumonia with pulmonary fibrosis, viral myocarditis, papillary muscle necrosis, and pericoronary neuritis. Thromboses and necroses were identified also in the liver, pancreas, and adrenal glands. Post-COVID-19 thromboses can manifest late, affecting various vascular territories, including esophageal ones. Their clinical picture may be diminished or absent in elderly and/or diabetic patients.
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Tejido Sandoval, C., F. Baiocchi Ureta i S. Zarraquiños Martínez. "Acute esophageal necrosis". Revista Andaluza de Patología Digestiva 44, nr 1 (3.03.2021): 30–32. http://dx.doi.org/10.37352/2021441.8.

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Resumen La necrosis esofágica aguda es una patología infrecuente y frecuentemente infradiagnosticada. Es importante su sospecha para realizar un diagnóstico y tratamiento precoces. La manifestación más frecuente es la hemorragia digestiva alta. Presentamos el caso de un paciente con necrosis esofágica aguda a consecuencia del desarrollo de una cetoacidosis diabética.
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Yamasaki, K., i C. Itakura. "Aseptic necrosis of bone in ICR mice". Laboratory Animals 22, nr 1 (1.01.1988): 51–53. http://dx.doi.org/10.1258/002367788780746601.

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Aseptic bone necrosis was observed in the tibia of 23 ICR mice. Histological changes were characterized by a loss of marrow tissue with proliferation of connective tissue and bone necrosis with empty osteocytic lacunae. Focal necrosis was confined beneath the articular cartilage. Extensive necrosis was present in half or all of the epiphysis. Massive necrosis was noted in the diaphysis of one animal. It was considered that focal necrosis might be related to degenerative osteoarthritis, and that extensive and massive necroses might have been caused by a disturbance of the blood supply.
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Maher, Névile, J. Piot, Sylvie Bastien, Jessica Vallance, Patrice Rey i Lucia Guérin-Dubrana. "Wood necrosis in esca-affected vines: types, relationships and possible links with foliar symptom expression". OENO One 46, nr 1 (31.03.2012): 15. http://dx.doi.org/10.20870/oeno-one.2012.46.1.1507.

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<p style="text-align: justify;"><strong>Aims</strong>: Esca disease of grapevine is characterised by foliar symptoms associated with the development of various internal wood necroses. The aims of the present study are to determine the type and the quantity of necroses in the various woody compartments of vines, the relationships between them and the links between necroses and severity of foliar symptoms.</p><p style="text-align: justify;"><strong>Methods and results</strong>: Symptomatic and asymptomatic vines cv Cabernet- Sauvignon were cross-sectioned to quantify the different types of internal necrosis in the scions (cordons, heads, and trunks) and rootstocks. Five necrosis « variables » were accounted for: central necrosis, sectorial necrosis, mixed necrosis, white rot, altered perimeter and in addition to the variable healing cone. In the scion, for all types of necrosis variables, a significant correlation between compartments was found. Vines with acute foliar form of esca had very advanced peripheral tissue degradations in the xylem and cambial zones. Chronic foliar expression of esca was associated with quantity of internal necroses higher than those obtained for asymptomatic vines. A logistic model indicated that white rot in the cordons was the best predictor for the chronic form of esca.</p><p style="text-align: justify;"><strong>Conclusion</strong>: Necroses formed a continuum within the plant. The scion is like a single unit with a volume of necroses useful to determine the health status of vines.</p><p style="text-align: justify;"><strong>Significance and impact of the study</strong>: A quantitative analysis of vine internal necroses would open up new possibilities for esca-epidemic approaches.</p>
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Cicák, A., i I. Mihál. "Can artificial wounding of beech stems induce necroses?" Journal of Forest Science 51, No. 12 (10.01.2012): 559–63. http://dx.doi.org/10.17221/4588-jfs.

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The paper presents data on the induction of necroses after small injuries to beech stems caused by electrodes during measuring cambium electric resistance. Altogether 121 beech stems of tree class 1&ndash;3 (according to Kraft) were evaluated. Among 2,904 mechanical injuries in 121 stems evaluated (24 per stem), 155 injuries induced necroses, hence each 19<sup>th</sup> injury induced necrosis. Most stems (33.06%) showed one necrosis, few stems (4.96%) showed even four necroses. 28.93% of stems did not show any necrosis. In order to prevent the infection of wounds and subsequent induction of necroses the authors recommend to treat any wounds with a suitable fungicide after using an equipment causing even negligible wounds of stems.
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Wang, Michael X., Timothy Morgan, William Lungo, Lina Wang, Gloria Z. Sze i Samuel W. French. "“Piecemeal” Necrosis: Renamed Troxis Necrosis". Experimental and Molecular Pathology 71, nr 2 (październik 2001): 137–46. http://dx.doi.org/10.1006/exmp.2001.2397.

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Prasad, Dr C. S. B. R. "New insights into programmed necrosis". JOURNAL OF CLINICAL AND BIOMEDICAL SCIENCES 04, nr 4 (15.12.2014): 339–40. http://dx.doi.org/10.58739/jcbs/v04i4.11.

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Kerschbaumer, Johannes, Matthias Demetz, Aleksandrs Krigers, Meinhard Nevinny-Stickel, Claudius Thomé i Christian F. Freyschlag. "Risk Factors for Radiation Necrosis in Patients Undergoing Cranial Stereotactic Radiosurgery". Cancers 13, nr 19 (22.09.2021): 4736. http://dx.doi.org/10.3390/cancers13194736.

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Purpose: single-staged stereotactic radiosurgery (SRS) is an established part of the multimodal treatment in neuro-oncology. Radiation necrosis after high-dose irradiation is a known complication, but there is a lack of evidence about the risk factors. The aim of this study was to evaluate possible risk factors for radiation necrosis in patients undergoing radiosurgery. Methods: patients treated with radiosurgery between January 2004 and November 2020 were retrospectively analyzed. The clinical data, imaging and medication were gathered from electronic patient records. The largest diameter of the tumors was measured using MRI scans in T1 weighted imaging with gadolinium and the edema in T2 weighted sequences. The diagnosis of a radiation necrosis was established analyzing imaging criteria combined with clinical course or pathologically confirmed by subsequent surgical intervention. Patients developing radiation necrosis detected after SRS were compared to patients without evidence of an overshooting irradiation reaction. Results: 388 patients were included retrospectively, 61 (15.7%) of whom developed a radiation necrosis. Median follow-up was 24 (6–62) months with a radiation necrosis after 8 (6–12) months. The most frequent tumors were metastases in 47.2% of the cases, followed by acoustic neuromas in 32.2% and meningiomas in 13.4%. Seventy-three (18.9%) patients already underwent one or more previous radiosurgical procedures for different lesions. The mean largest diameter of the tumors amounted to 16.3 mm (±6.1 mm). The median—80%—isodose administered was 16 (14–25) Gy. Of the radiation necroses, 25 (43.1%) required treatment, in 23 (39.7%) thereof, medical treatment was applied and in 2 (3.4%) cases, debulking surgery was performed. In this study, significantly more radiation necroses arose in patients with higher doses (HR 1.3 [CI 1.2; 1.5], p < 0.001) leading to a risk increment of over 180% between a radiation isodose of 14 and 20 Gy. The maximum diameter was a second significant risk factor (p = 0.028) with an HR of 1065 for every 1 mm increase in multivariate analysis. Conclusion: large diameter and high doses were reliable independent risk factors leading to more frequent radiation necroses, regardless of tumor type in patients undergoing radiosurgery. Alternative therapeutic procedures may be considered in lesions with large volume and an expected high radiation doses due to the increased risk of developing radiation necrosis.
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Thomas, Austin, Athira Jayan, Yusuf Chang, Reese Svetgoff, Saumil Datar, Vinayak Memula, Michael Huang, Laura Winikka i Jeffrey Chen. "Pembrolizumab-associated acral necrosis and esophageal necrosis". Current Problems in Cancer: Case Reports 8 (grudzień 2022): 100193. http://dx.doi.org/10.1016/j.cpccr.2022.100193.

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Siegal, Deborah M., Richard J. Cook i Theodore E. Warkentin. "Acute Hepatic Necrosis and Ischemic Limb Necrosis". New England Journal of Medicine 367, nr 9 (30.08.2012): 879–81. http://dx.doi.org/10.1056/nejmc1207074.

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Rozprawy doktorskie na temat "Necrosis"

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Bridges, James. "Necrosis in colorectal cancer /". Leeds : University of Leeds, School of Computer Studies, 2008. http://www.comp.leeds.ac.uk/fyproj/reports/0708/Bridges.pdf.

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Albataineh, Eman Mohammad. "Studies of tumour necrosis factor receptor-1 in tumour necrosis factor receptor associated periodic sysndrome (TRAPS)". Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537655.

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Dry, P. R. "Primary bud-axis necrosis of grapevines /". Title page, contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09A/09ad798.pdf.

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Naylor, Michael Stuart. "Tumour necrosis factor and ovarian cancer". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332896.

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Braidwood, Luke Anthony. "Engineering resistance to maize lethal necrosis". Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/273678.

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Modern agriculture is dependent on both global supply chains and crop monocultures. These features aid the evolution and spread of novel plant pathogens. Limited genetic diversity in commercial crop lines can result in widespread susceptibility to emerging pathogens. Pathogen resistance may be developed through conventional breeding approaches, or a number of transgenic strategies. This thesis focuses on the characterisation of an emerging maize disease, Maize lethal necrosis (MLN), and engineering resistant maize lines using an artificial microRNA (amiRNA) approach. MLN is a synergistic viral disease caused by the interaction of Maize chlorotic mottle virus (MCMV) with any maize-infecting member of the potyviridae. I used next-generation RNA sequencing to characterise the MLN outbreak in East Africa, discovering that local and Chinese strains of the potyvirus Sugarcane mosaic virus (SCMV) typically coinfect with MCMV. A first global MCMV phylogeny was constructed using these samples combined with new Sanger sequencing of samples in Ecuador and Hawaii. The phylogeny supported previous hypotheses of a link between the Chinese and African outbreaks, and suggested a novel link between the Hawaiian and Ecuadorian outbreaks. The SCMV sequences generated demonstrated strong evidence of extensive recombination, in line with previous reports on SCMV and potyviruses. These data also produced first reports of a number of RNA viruses in East Africa, and five novel viral-like sequences, with their presence confirmed by RT-PCR. RNA silencing is an important component of the plant immune response to viral infection. amiRNAs can be used to generate specific and effective viral resistance through Watson- Crick base pairing between the amiRNA and the (RNA) viral genome. Previous amiRNA approaches have targeted invariable genomic regions using consensus sequences. However, the high mutation rate of RNA viruses means single cells contain a variety of mutant genomes, collectively called a quasispecies. To deter the evolution of resistance breaking I devised a novel strategy to include intra-sample variation from NGS data in amiRNA design, and constructs, each containing five of these amiRNAs, were transformed into tropical maize lines. RNA silencing may be hampered by the expression of viral suppressors of silencing (VSRs). Local VSR assays demonstrated that there are no local VSRs in the MCMV genome, while systemic VSR assays showed a possible systemic VSR role for the unique P32 protein, and an interesting link between photoperiod and systemic silencing more generally.
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Björnberg, Flemming. "Processing of TNF-receptors to soluble receptor forms in myeloid cells". Lund : Dept. of Hematology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39176479.html.

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Green, Ian R. "Studies on ovine tumour necrosis factor alpha". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/29788.

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Tumour necrosis factor alpha (TNFα), a mediator of inflammatory responses and pathologies of a wide variety of diseases, has been extensively studied in humans and mice. However, little has previously been known about this cytokine in the sheep, a species of value not only to the agricultural industry, but also as a laboratory animal. In this work, the cDNA encoding ovine TNFα has been amplified, cloned, sequenced and used to express recombinant ovine TNFα (rovTNFα). The latter has been partially purified, characterised and used to raise both poly- and mono- clonal antibodies. The sequence of ovine TNFα shows a high degree of homology to those of other species. Certain regions, which are known to be structurally or functionally important to the mRNA and/or protein, are particularly well conserved. Consequently, rovTNFα displays several biological activities previously noted for TNF'sα of other species, including cytotoxicity, enhancement of thymocyte and fibroblast profileration and cartilage-degrading and anti-viral activities. However, whilst rovTNFα is active in assays on ovine cells at concentrations comparable to those observed in similar assays for other species, it is 1000 fold less active than recombinant human TNFα (rhTNFα) in cytotoxicity assays on TNF-sensitive murine (L929) cells, whose general lack of species specificity allows their use in detecting TNF'sα from many sources. A monoclonal antibody raised to rovTNFα detects a glycoprotein of appropriate size for mature ovine TNFα in the supernatants of stimulated ovine cell cultures. As in other species both ovine TNFα mRNA and protein are rapidly inducible. Such supernatants repeatedly have no activity in cytotoxicity assays (sensitive to 30pg rhTNFα/ml) on L929 cells, in spite of many containing >1ng ovine TNFα/ml.
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Stewart, Victoria C. "Human renal lipoxygenases : implications for papillary necrosis". Thesis, University of Aberdeen, 1995. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU078660.

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The long-term administration or abuse of analgesics and therapeutic doses of non-steroidal anti-inflammatory drugs have been implicated in renal papillary necrosis (RPN). Several drugs implicated in RPN undergo metabolic activation, via prostaglandin synthetase (PGS) and / or lipoxygenase (LO) systems in papilla, forming potentially damaging free radicals, providing an attractive theory to account for the necrosis. This thesis demonstrated interspecies and intrarenal variation in terms of renal PGS and LO activities. PGS was primarily responsible for arachidonic acid (AA)-dependent metabolism of xenobiotics in rabbit, while in a combination of PGS and LO catalysed drug cooxidation in rat kidney. In contrast in man, AA-dependent cooxidation of drugs in renal tissue occurred via the 5-lipoxygenase, which was predominately located in the papilla. These results indicated that the commonly used laboratory animals, rabbit and rat, are not suitable models for studying RPN in man. These studies also offer a potential explanation for a long-standing anomaly. PGS was thought to be central to the development of RPN but it has been difficult to equate the involvement of PGS with the fact that many papillotoxic compounds are also PGS inhibitors (eg, indomethacin, mefenamic acid). However, this study suggests that 5-LO may be responsible for RPN, either by metabolic activation of drugs or production of pro-inflammatory 5-LO products, altering the renal eicosanoid balance and subsequently renal haemodynamics, thereby precipitating necrosis. This hypothesis was further strengthened by the increased activity of renal 5-LO noted in animal models of both diabetic- and chemically-induced papillotoxicity. Unfortunately, administration of 5-LO inhibitors did not protect against this chemically-induced papillotoxicity. It is possible that inhibitors of 5-LO may provide protection against, or reverse, drug- or disease-induced nephropathy.
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Schobesberger, Martina. "Oligodendroglial degeneration in distemper : apoptosis or necrosis? /". [S.l.] : [s.n.], 1998. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Jaramillo, Martinez Diana. "Epidemiology and pathogenesis of Nervous Necrosis Virus". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13088.

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Viral Nervous Necrosis (VNN) is a globally distributed disease that affects a large number of finfish species, causing significant economic losses on affected farms. The causative agent is a small single stranded RNA virus called Nervous Necrosis Virus (NNV) from the genus Betanodavirus. NNV is neurotropic; clinical signs involve abnormal behaviour and high mortality associated with histopathological findings of vacuolating necrosis in the central nervous system and retina. In Australia, NNV has been isolated from Australian bass (Macquaria Novemaculeata) and barramundi (Lates calcarifer) populations recurrently for the past 10 and 25 years, respectively. However, the prognosis of NNV infection is highly variable. Although NNV became notorious for mass mortalities in marine fish hatcheries, it is often detected in apparently healthy individuals in the absence of clinical signs or histopathological lesions. Current knowledge on NNV epidemiology and pathogenesis is fragmentary. It is still unclear how the virus is transmitted between hosts and why some individuals are susceptible to VNN while others are not. The aim of this work was to study the epidemiology and pathogenesis of NNV in Australian native species with a focus on transmission and disease determinants to provide a basis for the development of prevention and control strategies. In Chapter 3, a partially retrospective study was conducted on the occurrence of NNV at the Darwin Aquaculture Centre (DAC), a barramundi hatchery. Observations on NNV detection frequency and distribution provided clues to the possible transmission pathways of the virus, including the potential role of broodstock as reservoirs, and the age-dependency of the disease. To assess the NNV exposure distribution among populations of adult fish, an indirect antibody detection ELISA was developed (Chapter 4). The assay was optimized and compared with a competitive ELISA format to provide the best discriminatory power between sera from immunized and non-immunized populations. After defining the best antibody detection protocol (the indirect ELISA), the diagnostic accuracy of the assay was assessed in naturally exposed subjects using a Bayesian approach in the absence of a gold standard (Chapter 5). After validation of the ELISA, a single point and repeated cross sectional analysis of NNV seroprevalence was conducted on native Australian adult fish populations (barramundi, Australian bass and groupers Epinephelus sp.) (Chapter 6). Survey results discredited the role of broodstock as NNV reservoirs based on the lack of correspondence between NNV seroprevalence and the occurrence of NNV outbreaks at the hatchery level. Results also suggested that the exposure of adult fish to NNV antigens must be progressive as seroconversion was often observed and the seroprevalence tended to be higher in older fish populations. From this and previous accumulated epidemiological evidence, horizontal transmission of NNV was considered most likely. An environmental reservoir outside the hatcheries has yet to be investigated. In Chapter 7, the factors influencing the pathogenesis of NNV in barramundi were explored. Juveniles of different ages were challenged by immersion to analyse the influence of the age of the host on VNN disease expression. Additionally, to test the influence of the virus isolate, juveniles were challenged with two inoculums obtained from NNV outbreaks in barramundi populations with different disease presentation (clinical and subclinical). Results showed that fish from all the age groups tested (range 20 to 63 days post hatch) were susceptible to NNV infection. However, the survival of the fish following NNV challenge was highly influenced by the age of the host. Juveniles of 5 weeks of age and older showed no clinical signs and their survival odds were the same as the non-challenged controls, whereas younger fish developed clinical disease. No significant effect on disease severity was noted between different NNV isolates. In Chapter 8, the factors influencing the pathogenesis of NNV in Australian bass were explored. In addition to the age of the host and the isolate factor, the influence of the dose of the virus and the water temperature on VNN expression was examined. As with barramundi, the disease expression in Australian bass was age dependent. The severity of the disease was affected by the water temperature in younger fish but it did not affect the outcome in fish above 5 weeks of age. The dose of the virus influenced the incidence of infection but not the severity of the disease expression. Again, no significant effect on disease severity was noted between the two isolates tested. From the experimental challenge of barramundi and Australian bass, further observations on NNV pathogenesis were provided: incubation period, minimum infectious dose, tissue distribution, shedding and humoral immune response. The results from this study narrow the knowledge gap on NNV transmission mechanisms and provide important insights into the virus pathogenesis in barramundi and Australian bass. The virus is most likely being transmitted horizontally and VNN disease expression as distinct from infection with NNV is highly age dependent. From this evidence, recommendations are made on the direction of efforts to control VNN at the farm level.
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Książki na temat "Necrosis"

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McCall, Kimberly, i Charles Klein, red. Necrosis. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-383-1.

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Téot, Luc, Sylvie Meaume, Sadanori Akita, William J. Ennis i Veronique del Marmol, red. Skin Necrosis. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1241-0.

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Ting, Adrian T., red. Programmed Necrosis. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8754-2.

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Dominik, Broniek, Kucharski Damian i Fabryka Słów, red. Necrosis: Przebudzenie. Wyd. 5. Lublin: Fabryka Słów, 2016.

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Corti, Angelo, i Pietro Ghezzi. Tumor Necrosis Factor. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592597718.

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National Institutes of Health (U.S.), red. Tumor necrosis factor. [Bethesda, Md.?: National Institutes of Health, 1989.

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National Institutes of Health (U.S.), red. Tumor necrosis factor. [Bethesda, Md.?: National Institutes of Health, 1989.

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Piracha, Kashif. Acute Tubular Necrosis. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-49923-4.

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Munro, A. L. S. Infectious pancreatic necrosis (IPN). Aberdeen: Department of Agriculture and Fisheries for Scotland, Marine Laboratory, 1988.

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Arlet, J., i B. Mazières, red. Bone Circulation and Bone Necrosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-73644-5.

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Części książek na temat "Necrosis"

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Capinera, John L., Marjorie A. Hoy, Paul W. Paré, Mohamed A. Farag, John T. Trumble, Murray B. Isman, Byron J. Adams i in. "Necrosis". W Encyclopedia of Entomology, 2574. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_2158.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea i in. "Necrosis". W Encyclopedia of Psychopharmacology, 822. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_770.

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Lipsker, Dan. "Necrosis". W Clinical Examination and Differential Diagnosis of Skin Lesions, 225–27. Paris: Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0411-8_43.

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Gonzalez, Raul S., i Kay Washington. "Necrosis". W Non-Neoplastic Liver Pathology, 169–80. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-31424-2_11.

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Wallace, Heather M., i Keith R. Pye. "Necrosis". W Encyclopedia of Cancer, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_7231-1.

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Vázquez-Nin, Gerardo H., María Luisa Escobar i Olga M. Echeverría. "Necrosis". W Cell Death in Mammalian Ovary, 111–21. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1134-1_7.

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Wallace, Heather M., i Keith R. Pye. "Necrosis". W Encyclopedia of Cancer, 3033–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_7231.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei i Melinda M. Manore. "Necrosis". W Encyclopedia of Exercise Medicine in Health and Disease, 632. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2742.

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Cuylits, Nicolas, Farida Benhadou i Véronique del Marmol. "Hand Necrosis". W Skin Necrosis, 173–78. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1241-0_29.

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Harms, J. D., C. D’Andréa i N. Fartaoui. "Stonefish Necrosis". W Skin Necrosis, 241–47. Vienna: Springer Vienna, 2014. http://dx.doi.org/10.1007/978-3-7091-1241-0_40.

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Streszczenia konferencji na temat "Necrosis"

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Latre, Marta, Samuel Jesús Martínez, Cristina Victoria Borao, María Concepción Aso, Julia López, María Ortiz de Solorzano, Antonio Aguilar, Enrique Ceamanos, María Hernández i Carlos Sostres. "NECROSIS GÁSTRICA POR CÁUSTICOS". W 44 Congreso de la Sociedad Española de Endoscopia Digestiva. Grupo Pacífico, 2022. http://dx.doi.org/10.48158/seed2022.p220.

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Dzandzygazyan, K. A. "INFECTIOUS NECROSIS OF HEMAPOIETIC TISSUE". W STATE AND DEVELOPMENT PROSPECTS OF AGRIBUSINESS. ООО «ДГТУ-Принт» Адрес полиграфического предприятия: 344003, г. Ростов-на-Дону, пл. Гагарина,1., 2024. http://dx.doi.org/10.23947/interagro.2024.81-86.

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Caucci, Luca, Matthew A. Kupinski, Melanie Freed, Lars R. Furenlid, Donald W. Wilson i Harrison H. Barrett. "Adaptive SPECT for tumor necrosis detection". W 2008 IEEE Nuclear Science Symposium and Medical Imaging conference (2008 NSS/MIC). IEEE, 2008. http://dx.doi.org/10.1109/nssmic.2008.4774505.

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Hwang, Darryl H., Passant Mohamed, Bino A. Varghese, Vinay Duddalwar i Steven Y. Cen. "NecroQuant: quantitative assessment of radiological necrosis". W 13th International Symposium on Medical Information Processing and Analysis, redaktorzy Jorge Brieva, Juan David García, Natasha Lepore i Eduardo Romero. SPIE, 2017. http://dx.doi.org/10.1117/12.2285891.

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Hasanova, S. Y. k. "To the question of the treatment of pancreatic necrosis". W General question of world science. Наука России, 2021. http://dx.doi.org/10.18411/gq-31-07-2021-06.

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The results of surgical treatment of pancreatic necrosis using stem cells, the structure of mortality and complications for the period 2013-2019 were analyzed. It has been shown that the use of cordon blood stem cells after laparotomy in the treatment of pancreatic necrosis can reduce the mortality rate associated with complications of infected pancreatic necrosis and improve the overall results of treatment of acute pancreatitis.
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Tanaka, Norimitsu, Nobukazu Hokamura i Yuji Tachimori. "Abstract 2429: Airway necrosis after salvage esophagectomy." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2429.

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"Simulation of Tumor Necrosis in Primary Melanoma". W 2016 Summer Simulation Multi-Conference. Society for Modeling and Simulation International (SCS), 2016. http://dx.doi.org/10.22360/summersim.2016.scsc.013.

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Chinn, Daniel, Elvis Nditafon, Alvin Yew i Chandrasekhar Thamire. "Thermal Therapy Protocols for Benign Prostatic Hyperplasia". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176764.

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Thermal therapy for treatment of benign prostatic hyperplasia (BPH) is becoming increasingly popular due to the minimally invasive nature of the treatment. Successful management of such therapy requires accurate estimation of thermal dosage. The purpose of this study is to provide correlations for the thermal damage caused by ultrasound, microwave, and infrared devices under a range of operating conditions. A boundary-fitting finite difference method is used to examine the heat transfer in the prostate gland and surrounding tissue. The Pennes bioheat transfer model and a porous media model were utilized to calculate temperature histories. Necrosis zones were determined using published necrosis data for prostatic tissue and cells. Thermal damage correlations for the three different hyperthermia sources along with sample temperature contours and necrosis zones are presented. Results indicate that the applicator power level and heating time are the most important parameters in achieving the desired necrosis zones, while coolant parameters strongly affect the temperatures of the sensitive urethra and serve as constraints for protocol parameters. Out of the three sources evaluated, ultrasound modality appears to be the most capable of causing necrosis in the target zones, with least damage to the surrounding healthy tissues.
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Paolini, Lara, i Chandrasekhar Thamire. "Treatment Protocols for Managing Transurethral Thermal Therapy for Benign Prostatic Hyperplasia". W ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-81421.

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Application of thermal therapy using microwave or ultrasound applicators is becoming increasingly popular as a minimally invasive treatment for benign prostatic hyperplasia (BPH). Successful management of the therapy using such methods requires an accurate estimation of the thermal dosage. The purpose of this study is to theoretically evaluate the thermal damage caused by different heating sources for different values of thermal doses and operating parameters. Using a 3-D finite differences method, the Pennes bio-heat transfer equation is solved for selected operating parameters. Necrosis zones are then determined from published necrosis data for prostatic tumor cells. Sample results are presented in terms of the temperature contours and necrosis zones. Results indicate that heating time and power level are the most important parameters in creating the desired necrosis zones, while coolant parameters strongly affect the temperatures of the sensitive urethra and serve as constraints for protocol parameters.
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James, Melissa K., i Richard N. Kitsis. "Abstract 1729: Mitochondrial necrosis pathway drives tumor progression." W Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1729.

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Raporty organizacyjne na temat "Necrosis"

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Wise, Kiersten, Daren Mueller, Adam Sisson, Martin Chilvers, Albert Tenuta, Carl Bradley, Loren Giesler i in. Soybean Vein Necrosis Virus. United States: Crop Protection Netework, maj 2015. http://dx.doi.org/10.31274/cpn-20190620-025.

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Larrick, James W., Vera Morhenn, Yawen L. Chiang i Tim Shi. Activated Langerhans Cells Release Tumor Necrosis Factor. Fort Belvoir, VA: Defense Technical Information Center, styczeń 1988. http://dx.doi.org/10.21236/ada206646.

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Vakharia, Vikram, Shoshana Arad, Yonathan Zohar, Yacob Weinstein, Shamila Yusuff i Arun Ammayappan. Development of Fish Edible Vaccines on the Yeast and Redmicroalgae Platforms. United States Department of Agriculture, luty 2013. http://dx.doi.org/10.32747/2013.7699839.bard.

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Betanodaviruses are causative agents of viral nervous necrosis (VNN), a devastating disease of cultured marine fish worldwide. Betanodavirus (BTN) genome is composed of two single-stranded, positive-sense RNA molecules. The larger genomic segment, RNA1 (3.1 kb), encodes the RNA-dependent RNA polymerase, while the smaller genomic segment, RNA 2 (1.4kb), encodes the coat protein. This structural protein is the host-protective antigen of VNN which assembles to form virus-like particles (VLPs). BTNs are classified into four genotypes, designated red-spotted grouper nervous necrosis virus (RGNNV), barfin flounder nervous necrosis virus (BFNNV), tiger puffer nervous necrosis virus (TPNNV), and striped jack nervous necrosis virus (SJNNV), based on phylogenetic analysis of the coat protein sequences. RGNNV type is quite important as it has a broad host-range, infecting warm-water fish species. At present, there is no commercial vaccine available to prevent VNN in fish. The general goal of this research was to develop oral fish vaccines in yeast and red microalgae (Porphyridium sp.) against the RGNNV genotype. To achieve this, we planned to clone and sequence the coat protein gene of RGNNV, express the coat protein gene of RGNNV in yeast and red microalgae and evaluate the immune response in fish fed with recombinantVLPs antigens produced in yeast and algae. The collaboration between the Israeli group and the US group, having wide experience in red microalgae biochemistry, molecular genetics and large-scale cultivation, and the development of viral vaccines and eukaryotic protein expression systems, respectively, was synergistic to produce a vaccine for fish that would be cost-effective and efficacious against the betanodavirus infection.
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Ristow, Sandra S., Jeanene M. Arnzen i JoAnn Ching Leong. Research Studies on the Life Cycle of Infectious Hematopoietic Necrosis Virus. Office of Scientific and Technical Information (OSTI), listopad 1990. http://dx.doi.org/10.2172/5915687.

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Zhang, Hui-Mei, Xiao-Bing Huo, Hua-Long Wang i Chen Wang. Recurrent glioma and radiation necrosis: a meta-analysis of MRI diagnosis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, grudzień 2021. http://dx.doi.org/10.37766/inplasy2021.12.0028.

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Leong, JoAnn Ching. Evaluation of a Subunit Vaccine to Infectious Hematopoietic Necrosis Virus, 1986 Annual Report. Office of Scientific and Technical Information (OSTI), wrzesień 1986. http://dx.doi.org/10.2172/758122.

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Gao, Li-nan, Lian-gang Ge, Ming-zhe Zhu i Xin-xin Yao. Association between tumor necrosis factor α and uterine fibroids: a protocol of systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, lipiec 2020. http://dx.doi.org/10.37766/inplasy2020.7.0010.

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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Related Apoptosis-Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2008. http://dx.doi.org/10.21236/ada486929.

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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Related Apoptosis-Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2009. http://dx.doi.org/10.21236/ada508266.

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Leong, JoAnn Ching. Evaluation of a Subunit Vaccine to Infectious Hematopoietic Necrosis (IHN) Virus, 1984 FY Annual Report. Office of Scientific and Technical Information (OSTI), lipiec 1985. http://dx.doi.org/10.2172/758121.

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