Gotowe bibliografie tematyczne / Liver

Gotowa bibliografia na temat „Liver”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 31 lipca 2024

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Artykuły w czasopismach na temat "Liver"

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Quintana, Fernando G. "Measurement of Liver Size by Ultrasound Unveils Large Livers in Overweight Children". Diabetes & Obesity International Journal 4, nr 4 (2019): 1–7. http://dx.doi.org/10.23880/doij-16000210.

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Purpose: To analyze the relationship between Body Mass Index (BMI) percentile and liver size and to predict the probabilities of fatty liver and hepatomegaly for overweight and obese boys and girls among Mexican-American children. Methods: One thousand two hundred fourteen reports of children visiting a South Texas pediatric clinic from 2011 to 2018 were analyzed. Ultrasonography was requested for patients whenever the patient was gaining excessive weight and the readings for alkaline phosphatase levels were 2 SD above the normal population; or when liver enzymes were elevated, Aspartate Aminotransferase (AST) above 50/46, Alanine Aminotransferase (ALT) above 47/41, and Gammaglutamyl transferase (GGT) above 32/28 for boys and girls respectively. The data was analyzed using linear regression and logistic regression models. Results: The results of the analysis support that the probability of fatty liver and hepatomegaly increase exponentially as BMI percentile increases. There is also a positive linear relationship between liver size and BMI percentile. Conclusion: The logistic regression analysis predicts that as BMI percentile increases the probability of fatty liver and hepatomegaly increases.
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Deepa P Bindhu, Gnana. "Burnout and Lived Experiences among Caregivers of Chronic Liver Disease Patients". International Journal of Science and Research (IJSR) 12, nr 7 (5.07.2023): 178–88. http://dx.doi.org/10.21275/sr23628110920.

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Kulkarni, Pavan, i Sheela Devi C S. "Study of Liver Biopsy in Chronic Liver Diseases". Annals of Pathology and Laboratory Medicine 5, nr 11 (24.11.2018): A900–910. http://dx.doi.org/10.21276/apalm.2272.

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Diehl, Anna Mae. "Recent Events in Alcoholic Liver Disease V. Effects of ethanol on liver regeneration". American Journal of Physiology-Gastrointestinal and Liver Physiology 288, nr 1 (styczeń 2005): G1—G6. http://dx.doi.org/10.1152/ajpgi.00376.2004.

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Liver regeneration is necessary to recover from alcoholic liver injury. Herein, we review evidence that ethanol interferes with liver regeneration. Briefly, alcoholic fatty livers demonstrate increased rates of hepatocyte death. The latter provides a regenerative stimulus. However, unlike mature hepatocytes in healthy adult livers, most surviving mature hepatocytes in alcoholic fatty livers cannot replicate. Therefore, less mature cells (progenitors) must differentiate to replace dead hepatocytes. Little is known about the general mechanisms that modulate the differentiation of liver progenitors in adults. Delineation of these mechanisms and clarification of how ethanol influences them might suggest new therapies for alcoholic liver disease.
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Binnerts, W. T., H. A. Das i T. C. Viets. "Liver selenium analysis in cows with a fast method of neutron activation reveals deficiency areas in the Netherlands". Netherlands Journal of Agricultural Science 41, nr 1 (1.03.1993): 47–57. http://dx.doi.org/10.18174/njas.v41i1.633.

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A total of 230, 100-g freeze-dried liver samples from the caudal lobe of cows from 13 slaughterhouses in the Netherlands were analysed by irradiating with neutrons in a high flux generator for 5 s followed by measurement of the short-lived isotope 77mSe in a rigid time sequence, under fully automated conditions. Liver Se ranged from 0.16 to 1.82 mg/kg DM and did not appear to relate to geography. 3% of the livers contained Se less than 0.25 mg/kg DM, which is considered critical for development of Se deficiency. Another 20% with less than 0.4 mg/kg DM was considered borderline Se deficiency. There was no evidence of Se toxicity. Liver Se positively correlated with liver copper, which may be obtained via feed, but not with liver zinc. It was concluded that animals at risk to Se deficiency are those not fed on concentrates, particularly heifers suffering from retained placentas at delivery. The feeding of Se fortified feeds is recommended.
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Baruah, Prabahita, i Pradipta Ray Choudhury. "ANOMALIES OF LIVER MORPHOLOGY: A STUDY ON CADAVERIC LIVER". International Journal of Anatomy and Research 4, nr 4.3 (31.12.2016): 3284–88. http://dx.doi.org/10.16965/ijar.2016.462.

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Johnson, Cheryl D., i Donna K. Hathaway. "The Lived Experience of End-Stage Liver Failure and Liver Transplantation". Journal of Transplant Coordination 6, nr 3 (wrzesień 1996): 130–33. http://dx.doi.org/10.1177/090591999600600306.

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This phenomenological study examined the lived experience of an individual who underwent end-stage liver failure and liver transplantation. The participant was asked to respond to the question, What was it like for you having experienced end-stage liver failure and liver transplantation? Permission was granted to tape-record the interview. Themes derived from the data analysis were identified, analyzed, and sorted. As a result, four categories were delineated: (1) uncertainty, (2) control, (3) social support, and (4) spirituality. Categories and themes contributing to a description of one individual's experience with end-stage liver failure and liver transplantation may provide direction for interventional studies designed to effect change in the lived experiences of those undergoing similar phenomena.
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Serrano Rodriguez, Pablo, Alfred Sidney Barritt IV, David Allen Gerber i Chirag Sureshchandra Desai. "Liver Transplant for Unusually Large Polycystic Liver Disease: Challenges and Pitfalls". Case Reports in Transplantation 2018 (2018): 1–5. http://dx.doi.org/10.1155/2018/4863187.

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Patients with polycystic liver disease are described in the literature as both recipient and donor for liver transplant. Due to well-preserved liver function, it is often difficult for these patients to receive an organ. Livers of these patients are often large and heavier than a normal organ. We describe two cases who had exceedingly large livers, weighing 14 and 19 kg. To the best of our knowledge and search, these are some of the heaviest explanted livers, and one of the patients incidentally received a liver from a donor with ADPKD. The aim of this report is to discuss the challenges and pitfalls of evaluating and listing, technical aspect of the transplant, possibility of transplanting a liver from a donor with a genetic cystic disease to a cystic disease recipient, and the related literature with some highlights on the facts from UNOS/OPTN data.
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McConnon, Aili. "Liver-on-chip models mimic in vivo livers, liver disease". Scilight 2021, nr 42 (15.10.2021): 421108. http://dx.doi.org/10.1063/10.0006843.

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Fingerote, RJ, VG Bain i RN Fedorak. "Liver Transplants for Alcoholic Liver Disease". Canadian Journal of Gastroenterology 5, nr 6 (1991): 195–98. http://dx.doi.org/10.1155/1991/567452.

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Alcohol related end-stage liver disease is a principal cause of liver failure. The scarcity of donor livers and the predominance of alcohol related end-stage liver disease has raised the issue of including alcoholics as candidates for liver transplantation. In rationalizing the arguments for and against the treatment of alcoholic end-stage liver disease with transplantation, factors such as recidivism, resource allocation and principles of medical practice must be considered. Public confidence in organ transplantation depends on the scientific validity and moral integrity of the policies adopted. Sound policies will prove defensible while policies based on perceptions or prejudices will, in the long run, harm the process.
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Rozprawy doktorskie na temat "Liver"

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Tian, Yinghua. "Liver and partial liver transplantation : new models and mechanisms of partial liver graft regeneration /". Zürich, 2005. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253387.

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Tector, A. Joseph. "Discordant liver xenotransplantation in recipients with liver failure". Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84439.

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Liver xenotransplantation could eliminate the liver donor shortage, but currently it is not possible because of a lack of understanding of liver xenograft rejection. Hyperacute xenograft rejection is initiated by the binding of preformed naturally occurring xenoreactive antibodies (XNA) to the xenograft endothelium. The XNA bind to the xenograft endothelium, leading to complement-mediated endothelial injury.
Liver xenotransplantation will be initially offered to patients with severe liver failure as a bridge to a human liver transplantation. The hypothesis tested in this thesis is that hyperacute rejection of liver xenografts placed into recipients with liver failure will be diminished because of the complement deficiency that accompanies liver failure. The experiments described in this thesis detail the development of an in vitro pig-to-human liver xenotransplant model incubating cultured pig hepatic endothelial cells (PHEC) and human serum in culture. We showed that either classical or alternative complement pathways could initiate endothelial injury. Next we developed the dog-to-pig liver xenograft model and characterized the lethal coagulopathy that results from hyperacute rejection. The coagulopathy results from the lack of function of platelets as well as their disappearance from the circulation. We then used the galactosamine induced liver injury model in porcine recipients of canine liver xenografts to demonstrate that hyperacute rejection in the setting of liver failure is diminished. We showed that; tissue injury, coagulopathy and platelet defect, and endothelial injury were diminished. Our experiments suggested that the cause of the decreased injury was the lack of complement in the pigs with galactosamine induced liver injury since the XNA levels were no different than in control animals. Our final experiments evaluated serum from patients with liver failure and compared the injury caused by incubation with PHEC. Serum from the liver failure patients had similar levels of XNA when compared with normal subjects, but had less complement activity, and less C3 and C4. Incubation of liver failure serum with PHEC caused much less injury and complement activation than serum from control subjects. The results in this thesis suggest that liver failure will have a significant impact on liver xenograft rejection, helping to diminish hyperacut
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He, Qing. "Liver regeneration in rats after liver resection and small for size liver transplantation from living donors". [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=972086595.

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Lindfelt, Jan O. W. "Hepatic nerves in hemostasis and glucose metabolism :". Lund : Dept. of Surgery, Lund University, 1993. http://catalog.hathitrust.org/api/volumes/oclc/39654187.html.

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Hart, Nils Arnaud 't. "Improving liver preservation new strategies in liver procurement and preservation /". [S.l. : Groningen : s.n. ; University Library Groningen] [Host], 2007. http://irs.ub.rug.nl/ppn/30406856X.

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Bikhchandani, Jai. "Extracorporeal liver perfusion as liver support device : a pilot study". Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/11038.

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Introduction: A liver support device can bridge a patient in acute liver failure safely to transplant. An extracorporeal perfused porcine liver (ECLP) circumvents the limitations of hepatocyte based bioartificial liver, but its clinical application has been limited so far due to the potential risk of transmission of porcine endogenous retroviruses. Aim of this study was to develop an ECLP model that can provide artificial hepatic support across a semi-permeable membrane which should block porcine viruses due to its pore size. Methods: 50-60 Kg white landrace pigs treated with standard abattoir animal procedures were used as donors. The liver was perfused with normothermic autologous oxygenated blood using Medtronic BioMedicus BP560 driven centrifugal pump for 6 hours. This ECLP system was used to support a surrogate patient circulation across the filter Evaclio EC4A. Substances like galactose, ammonia, midazolam and para-aminobenzoic acid, were infused into the surrogate patient and their clearance was calculated. The study was designed as test (n=15) vs. control (n=5); with control experiments having no liver in the circuit. Results: After the optimization phase (n=23), we successfully perfused 15 porcine livers with the mean hepatic artery pressure of 87 mm Hg and flows of 1.2 L /min. Retention of Indocyanine green at 15 minutes was 11% in test and 96% in controls. Mean ammonia clearance of 945 mg/min/kg, galactose Vmax of 111.7 mg/min/Kg, hippurate ratio of 91% and a variable midazolam clearance was seen in the test experiments. Conclusion: The study was successful in proving the feasibility of an ECLP model based on abattoir animals that can be utilised for future research work. This model was able to provide adequate support to the surrogate patient across a hollow filter. Further work is needed to show that an ECLP system can be used in an anhepatic animal prior to application in human trials.
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Triantafyllou, Evangelos. "Mechanisms of immune-mediated liver injury in acute liver failure". Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/mechanisms-of-immunemediated-liver-injury-in-acute-liver-failure(e3e4fdce-9d38-4bdf-b1b4-979f35aef0ae).html.

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Background: Acute liver failure (ALF) is characterized by overwhelming hepatocyte death and liver inflammation where the infiltration of myeloid cells in areas of necrosis is contrasted by immune cell depletion and dysregulation in the systemic circulation. The mechanisms underlying resolution of acute hepatic inflammation are largely unknown to date. In this thesis, I used both human and murine experimental models in order to investigate the impact of Mer Tyrosine Kinase (MerTK) during ALF and examine how the micro-environmental mediator, Secretory Leukocyte Protease Inhibitor (SLPI), governs this immunological response. Methods: Flow cytometry, immunohistochemistry, confocal imaging and gene expression analyses determined the phenotypic, functional and transcriptomic profile and tissue topography of MerTK+ monocytes and macrophages in ALF, healthy and disease controls. The temporal evolution of macrophage MerTK expression and its impact on hepatic resolution was examined in APAP-induced acute liver injury using wild-type (WT) and Mer-deficient (Mer−/−) mice. Furthermore, SLPI effects on hepatic myeloid cells were determined in vitro and in vivo using APAP-treated WT mice. Results: I demonstrate a significant expansion of resolution-like MerTK+HLA-DRhigh cells in both circulatory and tissue compartments of ALF patients. Compared to WT mice, that show an increase of MerTK+MHCIIhigh hepatic macrophages during the resolution phase in ALF, APAP-treated Mer−/− mice exhibit persistent liver injury and inflammation, characterized by a decreased proportion of liver-resident Kupffer cells and increased number of hepatic neutrophils. Both in vitro and in APAPtreated mice, SLPI reprograms macrophages towards resolution responses through induction of a MerTK+HLA-DRhigh phenotype which promotes neutrophil apoptosis and their subsequent clearance. Conclusions: The work presented in this thesis has identified a prorestorative, MerTK+, macrophage phenotype that evolves during the resolution phase of APAP-induced ALF and represents a novel immunotherapeutic target to promote resolution responses following acute liver injury.
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Foss, Aksel. "Liver regeneration and partial liver transplantation an experimental study in the rat /". Lund : Dept. of Surgery, Lund University, 1992. http://books.google.com/books?id=d_BqAAAAMAAJ.

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Li, Jiangning. "Functional genomics and liver regeneration : transcriptional regulation on rapid liver regeneration /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/6351.

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Kung, Janet Wui Cheung. "Investigating the liver progenitor cell niche in the developing human liver". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25953.

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Liver cirrhosis places an increasing burden on healthcare worldwide. Currently the only treatment is liver transplantation. Whilst liver transplant has a relatively good five-year survival, donor organ shortage costs many lives every year and results in lifelong immunosuppression. Alternative treatments are thus urgently needed. It is with this background that there is understandable interest for the development of stem cell therapies for liver regeneration. The identification of putative liver stem cells has brought closer the previously separate fields of liver ontology, regeneration, and carcinogenesis. Significant overlaps in the regulation of these processes are now being described. For example, studies in embryonic liver development have already provided the basis for directed differentiation of human embryonic stem cells and induced pluripotent stem cells into hepatocyte-like cells. As a result, the understanding of the cell biology of proliferation and differentiation in the liver has been improved. This knowledge can be used to improve the function of hepatocyte-like cells for drug testing, bio-artificial livers, and transplantation. In parallel, the mechanisms regulating cancer cell biology are now clearer, providing fertile soil for novel therapeutic approaches. Recognition of the relationships between development, regeneration, and carcinogenesis, and the increasing evidence for the role of stem cells in all of these areas, has sparked fresh enthusiasm in understanding the underlying molecular mechanisms and has led to new targeted therapies for liver cirrhosis and primary liver cancers. Human liver progenitor cells (LPCs) have therapeutic potential but their in vitro culture results in inadequate differentiation, function, and phenotypic instability reflecting an incomplete understanding of in vivo processes. LPCs can be robustly isolated from second trimester human foetal livers by immunoselection for EpCAM+/CD29+/CD49d+/CD49e–/CD235a–/CD45– cells. Expression profiling of mRNA and microRNA in human foetal LPCs was performed and compared with mature human hepatocytes and human embryonic stem cells undergoing hepatocytic differentiation. Foetal LPCs exhibit a distinct transcriptome profile consistent with a stem cell signature, cell division, and some liver-specific functions. Bioinformatic integration of microRNA and mRNA datasets revealed that microRNAs up-regulated in LPCs targeted genes involved in metabolic processes implying repression of the mature hepatocyte phenotype. Control of LPC gene expression therefore occurs at both transcriptional and, via microRNAs, post-transcriptional levels. Furthermore, transcription factor binding site analyses revealed enriched E2F1 motif in gene and microRNA promoters suggesting feedback control in determining LPC fate. Foetal LPCs were capable of differentiation to a hepatocytic phenotype in the presence of appropriate paracrine signals provided by EpCAM– non-parenchymal cells (NPCs), which consist mainly of endothelial cells and hepatic stellate cells. Fibronectin, despite being produced in abundance by EpCAM– NPCs, had no effect on LPC synthetic function in vitro. The expression of fibronectin in the perisinusoidal space suggests its potential role of modulating cross-talk between hepatoblasts/hepatocytes, liver sinusoidal endothelial cells, and hepatic stellate cells. Fibronectin expression in the portal vein mesenchyme and laminin α5 expression along the ductal plate suggest that both matrix molecules, located in close proximity to LPCs, may be important in supporting the LPC niche. Findings in this work provide insight into the regulation of the human foetal LPC functional phenotype, bringing stem cell-based therapies for liver disease one step closer.
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Książki na temat "Liver"

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A, Curley Steven, red. Liver cancer. New York: Springer, 1998.

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Ferrell, Linda D., i Sanjay Kakar. Liver pathology. New York: Demos Medical, 2011.

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Starzl, Thomas E. Liver transplantation. Austin, Tex: Silvergirl, 1988.

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Xiao, Shu-Yuan. Liver pathology. New York: Demos Medical, 2015.

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Chakravarty, K. Dilip. Liver transplantation. New Delhi, India: Jaypee Brothers Medical Publishers, 2010.

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L, Burns J., red. Liver cirrhosis research. New York: Nova Biomedical Books, 2007.

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R, Lucey Michael, Neuberger James i Shaked Abraham, red. Liver transplantation. Georgetown, Tex: Landes Bioscience, 2003.

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ussinger, D. Ha. Liver regeneration. Berlin: de Gruyter, 2011.

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Chao-yu, Tʼang, Wu Meng-chʼao i Hsia Sui-sheng, red. Primary liver cancer. Beijing: China Academic Publishers, 1989.

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National Institute of Diabetes and Digestive and Kidney Diseases (U.S.), red. Liver transplantation. Bethesda, Md.]: U.S. Dept. of Health and Human Services, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, 2010.

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Części książek na temat "Liver"

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Lee, Sung-Gyu, i Deok-Bog Moon. "Live Donor Liver Transplant". W Contemporary Liver Transplantation, 1–20. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-05543-5_5-1.

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Lee, Sung-Gyu, i Deok-Bog Moon. "Live Donor Liver Transplant". W Contemporary Liver Transplantation, 1–20. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-05543-5_5-2.

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Lee, Sung-Gyu, i Deok-Bog Moon. "Live Donor Liver Transplant". W Contemporary Liver Transplantation, 99–117. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-07209-8_5.

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Randone, Bruto, Ronald Matteotti i Brice Gayet. "Liver – Anatomical Liver Resections". W Minimally Invasive Surgical Oncology, 273–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-540-45021-4_22.

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Andronikou, Savvas. "Liver". W See Right Through Me, 463–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-23893-2_18.

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Lencioni, Riccardo, Laura Crocetti i Emanuele Neri. "Liver". W 3D Image Processing, 211–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-59438-0_19.

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de Miranda, Aline Silva, i Ana Cristina Simões e Silva. "Liver". W Angiotensin-(1-7), 191–99. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-22696-1_12.

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Skandalakis, Lee J., i John E. Skandalakis. "Liver". W Surgical Anatomy and Technique, 515–63. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8563-6_13.

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Allen, Derek C., R. Iain Cameron i Maurice B. Loughrey. "Liver". W Histopathology Specimens, 99–110. London: Springer London, 2012. http://dx.doi.org/10.1007/978-0-85729-673-3_10.

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Kelly, Paul J., Derek C. Allen, R. Iain Cameron i Maurice B. Loughrey. "Liver". W Histopathology Specimens, 111–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57360-1_10.

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Streszczenia konferencji na temat "Liver"

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Zhou, Jiayin, Feng Ding, Wei Xiong, Weimin Huang, Qi Tian, Zhimin Wang, Sudhakar K. Venkatesh i Wee Kheng Leow. "Segmentation of liver and liver tumor for the Liver-Workbench". W SPIE Medical Imaging, redaktorzy Benoit M. Dawant i David R. Haynor. SPIE, 2011. http://dx.doi.org/10.1117/12.877927.

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Debbaut, Charlotte, David De Wilde, Christophe Casteleyn, Pieter Cornillie, Manuel Dierick, Luc Van Hoorebeke, Diethard Monbaliu, Ye-Dong Fan i Patrick Segers. "Electrical Analog Models to Simulate the Impact of Partial Hepatectomy on Hepatic Hemodynamics". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14266.

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Due to the growing shortage of donor livers, more patients are waiting for liver transplantation. Efforts to expand the donor pool include the use of living donor liver transplantation (LDLT) and split liver transplantation. LDLT involves a healthy person undergoing a partial hepatectomy to donate a part of his liver to a patient with severe liver failure. Afterwards, the regenerative capacity of the organ allows the livers of both donor and recipient to regrow to normal liver masses. The procedure is not without risk as serious complications may occur (such as cholestasis, ascites, gastrointestinal bleeding and renal impairment). An inadequate liver mass compared to the body mass may result in the small-for-size syndrome (SFSS). In both donor and recipient, LDLT may lead to portal hypertension associated with the elevated intrahepatic resistance of a smaller liver, and an increased portal venous (PV) inflow per gram of liver tissue compared to the total liver before resection. Excessive hyperperfusion and shear stress may damage the sinusoidal endothelial cells and lead to graft dysfunction.
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Kang, Y. B., T. R. Sodunke, J. Cirillo, M. J. Bouchard i H. Noh. "Liver on a chip: Engineering the liver sinusoid". W 2013 Transducers & Eurosensors XXVII: The 17th International Conference on Solid-State Sensors, Actuators and Microsystems (TRANSDUCERS & EUROSENSORS XXVII). IEEE, 2013. http://dx.doi.org/10.1109/transducers.2013.6626762.

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Shevchenko, N., B. Seidl, J. Schwaiger, M. Markert i T. C. Lueth. "MiMed liver: A planning system for liver surgery". W 2010 32nd Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC 2010). IEEE, 2010. http://dx.doi.org/10.1109/iembs.2010.5627120.

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Vorontsov, Eugene, An Tang, Chris Pal i Samuel Kadoury. "Liver lesion segmentation informed by joint liver segmentation". W 2018 IEEE 15th International Symposium on Biomedical Imaging (ISBI 2018). IEEE, 2018. http://dx.doi.org/10.1109/isbi.2018.8363817.

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Kim, Soohyun, Kyoyeong Koo, Taeyong Park i Jeongjin Lee. "ICP Algorithm Based Liver Rigid Registration Method Using Liver and Liver Vessel Surface Mesh". W RACS '23: International Conference on Research in Adaptive and Convergent Systems. New York, NY, USA: ACM, 2023. http://dx.doi.org/10.1145/3599957.3606225.

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Fradsham, Sarah, Edward Britton, Helen Caldwell i Kate Hayden. "P-124 Liver let live: working collaboratively to improve access and care for patients with advanced liver disease". W Accepted Oral and Poster Abstract Submissions, The Palliative Care Congress, Recovering, Rebounding, Reinventing, 24–25 March 2022, The Telford International Centre, Telford, Shropshire. British Medical Journal Publishing Group, 2022. http://dx.doi.org/10.1136/spcare-2022-scpsc.145.

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Myllys, M., CH Holland, J. Saez-Rodriquez, W. Murad, A. Zaza, R. Hassan, YA Ahmed i in. "Metabolic reprogramming in livers of mice with chronic liver disease". W 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402167.

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Anderson, Brian, Kristy Brock, Bruno Odisio, Guillaume Cazoulat, Ethan Lin i Sanjay Gupta. "Improvement of liver ablation treatment for colorectal liver metastases". W Image-Guided Procedures, Robotic Interventions, and Modeling, redaktorzy Robert J. Webster i Baowei Fei. SPIE, 2018. http://dx.doi.org/10.1117/12.2294554.

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Yee, Tan Sing, Sarinder K. Dhillon i Amandeep S. Sidhu. "Fuzzy Estimation of Liver Stiffness in Modelling Liver Deformation". W 2014 IEEE International Conference on Bioinformatics and Bioengineering (BIBE). IEEE, 2014. http://dx.doi.org/10.1109/bibe.2014.34.

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Raporty organizacyjne na temat "Liver"

1

Nagarajan, Ganesh. Liver Anatomy. Touch Surgery Publications, wrzesień 2016. http://dx.doi.org/10.18556/touchsurgery/2016.s0131.

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Nagarajan, Ganesh. Liver Laparoscopic Segmentectomy. Touch Surgery Simulations, 2017. http://dx.doi.org/10.18556/touchsurgery/2017.s0107.

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Nagarajan, Ganesh. Open Liver Surgery. Touch Surgery Simulations, 2017. http://dx.doi.org/10.18556/touchsurgery/2017.s0108.

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Nagarajan, Ganesh. Liver Laparoscopic Segmentectomy. Touch Surgery Simulations, 2017. http://dx.doi.org/10.18556/touchsurgery/2018.s0107.

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Nagarajan, Ganesh. Open Liver Surgery. Touch Surgery Simulations, 2017. http://dx.doi.org/10.18556/touchsurgery/2018.s0108.

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Li, Chengcheng, Xin Yang, Yuhang Quan, Yafang Lai, Yifang Wang i Anhao Wu. Network meta-analysis of different liver protective drugs in the treatment of drug-induced liver injury. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2023. http://dx.doi.org/10.37766/inplasy2023.6.0039.

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Wells, Alan. An Organotypic Liver System for Tumor Progression. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2005. http://dx.doi.org/10.21236/ada443204.

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Young, J., Eitan Bogin, Donald Beitz i A. McGillard. Etiology of Fatty Liver of Dairy Cows. United States Department of Agriculture, październik 1986. http://dx.doi.org/10.32747/1986.7566851.bard.

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Ismaiel, Abdulrahman, Ayman Jaaouani, Daniel-Corneliu Leucuta, Stefan-Lucian Popa i Dan-Lucian Dumitrascu. The Visceral Adiposity Index in Non-Alcoholic Fatty Liver Disease and Liver Fibrosis — Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, grudzień 2021. http://dx.doi.org/10.37766/inplasy2021.12.0056.

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Streszczenie:
Review question / Objective: The objective of the study was to compare the mean difference and AUROC of Visceral Adiposity Index (VAI) in NAFLD/NASH/liver fibrosis patients and controls in observational studies. Condition being studied: Nonalcoholic fatty liver disease (NAFLD) is a multi-system disease, being mainly a liver pathology involving excessive hepatic fat accumulation unrelated to alcohol consumption or other secondary causes of hepatic steatosis. It is an emerging cause of concern and increasing clinical burden, imposing a public health challenge. NAFLD is the most common chronic liver disease and is predicted to be the most common indication for a liver transplant in Western countries by 2030, owing to a prevalence of 25% worldwide. The visceral adiposity index (VAI) is a scoring system based on body mass index, triglycerides, high-density lipoproteins (HDLs), and waist circumferences (WCs).
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Ott, Lee W., Frank Witzmann, Camilla A. Mauzy, Claude C. Grigsby, Deirdre A. Mahle i John J. Schlager. Quantifying Biomarkers of Liver Damage Using Shotgun Proteomics. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2006. http://dx.doi.org/10.21236/ada498948.

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