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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G. Habasha, F., M. Al- Jeddah i A. M. Al-Darraji. "MORPHOLOGICAL HI8STOPATHOLOGICAL CHANGES IN SOME LIVER DISEASES IN CATTLE". Iraqi Journal of Veterinary Medicine 12, nr 1 (31.12.1988): 207–20. http://dx.doi.org/10.30539/hksj1912.
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Liver biopsies were taken from (89) cattle slaughtered at modern Baghdad abattoir. Macroscopic examination of livers showed that (28.11%) of cases were infected with chronic fascioliasis, while (1.12%) of livers showed acute fascioliasis and (2.24%) of livers showed chronic fascioliasis with hydatidosis. Hydatid cysts were present in (6.74%) of inspected livers, telangiectasis of the livers found in (3.37%) of cases, focal hepatic necrosis (Saw dust) was observed in (19.1%), liver abscesses constituted (1.12%) and (38.2%) of livers had no significant gross lesions. The diagnosis of liver diseases in cattle using liver biopsy technique was more successful when the lesion was extensively diffuse in the liver.
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Hyun, Jeongeun, Seh-Hoon Oh, Richard T. Premont, Cynthia D. Guy, Carl L. Berg i Anna Mae Diehl. "Dysregulated activation of fetal liver programme in acute liver failure". Gut 68, nr 6 (22.01.2019): 1076–87. http://dx.doi.org/10.1136/gutjnl-2018-317603.
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ObjectiveUncertainty about acute liver failure (ALF) pathogenesis limits therapy. We postulate that ALF results from excessive reactivation of a fetal liver programme that is induced in hepatocytes when acutely injured livers regenerate. To evaluate this hypothesis, we focused on two molecules with known oncofetal properties in the liver, Yes-associated protein-1 (YAP1) and Insulin-like growth factor-2 RNA-binding protein-3 (IGF2BP3).DesignWe compared normal liver with explanted livers of patients with ALF to determine if YAP1 and IGF2BP3 were induced; assessed whether these factors are upregulated when murine livers regenerate; determined if YAP1 and IGF2BP3 cooperate to activate the fetal programme in adult hepatocytes; and identified upstream signals that control these factors and thereby hepatocyte maturity during recovery from liver injury.ResultsLivers of patients with ALF were massively enriched with hepatocytes expressing IGF2BP3, YAP1 and other fetal markers. Less extensive, transient accumulation of similar fetal-like cells that were proliferative and capable of anchorage-independent growth occurred in mouse livers that were regenerating after acute injury. Fetal reprogramming of hepatocytes was YAP1-dependent and involved YAP1-driven reciprocal modulation of let7 microRNAs and IGF2BP3, factors that negatively regulate each other to control fate decisions in fetal cells. Directly manipulating IGF2BP3 expression controlled the fetal-like phenotype regardless of YAP1 activity, proving that IGF2BP3 is the proximal mediator of this YAP1-directed fate.ConclusionAfter acute liver injury, hepatocytes are reprogrammed to fetal-like cells by a YAP1-dependent mechanism that differentially regulates let7 and IGF2BP3, identifying novel therapeutic targets for ALF.
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Ebrahim, Nesrine, Omnia A. M. Badr, Mohamed M. Yousef, Amira Hassouna, Dina Sabry, Ayman Samir Farid, Ola Mostafa i in. "Functional Recellularization of Acellular Rat Liver Scaffold by Induced Pluripotent Stem Cells: Molecular Evidence for Wnt/B-Catenin Upregulation". Cells 10, nr 11 (20.10.2021): 2819. http://dx.doi.org/10.3390/cells10112819.
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Background. Liver transplantation remains the only viable therapy for liver failure but has a severely restricted utility. Here, we aimed to decellularize rat livers to form acellular 3D bio-scaffolds suitable for seeding with induced pluripotent cells (iPSCs) as a tool to investigate the role of Wnt/β-catenin signaling in liver development and generation. Methods. Dissected rat livers were randomly divided into three groups: I (control); II (decellularized scaffolds) and III (recellularized scaffolds). Liver decellularization was established via an adapted perfusion procedure and assessed through the measurement of extracellular matrix (ECM) proteins and DNA content. Liver recellularization was assessed through histological examination and measurement of transcript levels of Wnt/β-catenin pathway, hepatogenesis, liver-specific microRNAs and growth factors essential for liver development. Adult rat liver decellularization was confirmed by the maintenance of ECM proteins and persistence of growth factors essential for liver regeneration. Results. iPSCs seeded rat decellularized livers displayed upregulated transcript expression of Wnt/β-catenin pathway-related, growth factors, and liver specification genes. Further, recellularized livers displayed restored liver-specific functions including albumin secretion and urea synthesis. Conclusion. This establishes proof-of-principle for the generation of three-dimensional liver organ scaffolds as grafts and functional re-establishment.
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Sun, Lulu, i Lijian Hui. "Progress in human liver organoids". Journal of Molecular Cell Biology 12, nr 8 (1.04.2020): 607–17. http://dx.doi.org/10.1093/jmcb/mjaa013.
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Abstract Understanding the development, regeneration, and disorders of the liver is the major goal in liver biology. Current mechanistic knowledge of human livers has been largely derived from mouse models and cell lines, which fall short in recapitulating the features of human liver cells or the structures and functions of human livers. Organoids as an in vitro system hold the promise to generate organ-like tissues in a dish. Recent advances in human liver organoids also facilitate the understanding of the biology and diseases in this complex organ. Here we review the progress in human liver organoids, mainly focusing on the methods to generate liver organoids, their applications, and possible future directions.
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Ge, Chenliang, Changguo Ma, Jiesheng Cui, Xingbo Dong, Luyang Sun, Yanjiao Li i An Yu. "Rapamycin suppresses inflammation and increases the interaction between p65 and IκBα in rapamycin-induced fatty livers". PLOS ONE 18, nr 3 (3.03.2023): e0281888. http://dx.doi.org/10.1371/journal.pone.0281888.
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Rapamycin treatment significantly increases lifespan and ameliorates several aging-related diseases in mice, making it a potential anti-aging drug. However, there are several obvious side effects of rapamycin, which may limit the broad applications of this drug. Lipid metabolism disorders such as fatty liver and hyperlipidemia are some of those unwanted side effects. Fatty liver is characterized as ectopic lipid accumulation in livers, which is usually accompanied by increased inflammation levels. Rapamycin is also a well-known anti-inflammation chemical. How rapamycin affects the inflammation level in rapamycin-induced fatty liver remains poorly understood. Here, we show that eight-day rapamycin treatment induced fatty liver and increased liver free fatty acid levels in mice, while the expression levels of inflammatory markers are even lower than those in the control mice. Mechanistically, the upstream of the pro-inflammatory pathway was activated in rapamycin-induced fatty livers, however, there is no increased NFκB nuclear translocation probably because the interaction between p65 and IκBα was enhanced by rapamycin treatment. The lipolysis pathway in the liver is also suppressed by rapamycin. Liver cirrhosis is an adverse consequence of fatty liver, while prolonged rapamycin treatment did not increase liver cirrhosis markers. Our results indicate that although fatty livers are induced by rapamycin, the fatty livers are not accompanied by increased inflammation levels, implying that rapamycin-induced fatty livers might not be as harmful as other types of fatty livers, such as high-fat diet and alcohol-induced fatty livers.
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Schoonderwoerd, K., A. J. Verhoeven i H. Jansen. "Rat liver contains a limited number of binding sites for hepatic lipase". Biochemical Journal 302, nr 3 (15.09.1994): 717–22. http://dx.doi.org/10.1042/bj3020717.
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The binding of hepatic lipase to rat liver was studied in an ex vivo perfusion model. The livers were perfused with media containing partially purified rat hepatic lipase or bovine milk lipoprotein lipase. The activity of the enzymes was determined in the perfusion media before and after passage through the liver. During perfusion with a hepatic-lipase-containing medium the lipase activity in the medium did not change, indicating that there was no net binding of lipase by the liver. In contrast, more than 80% of the lipoprotein lipase was removed from the medium. This lipoprotein lipase activity could be recovered into the perfusion medium completely by heparin perfusion of the liver. If livers, first depleted of hepatic lipase by heparin, were subsequent perfused with a hepatic-lipase-containing medium, 90 +/- 24 m-units of the lipase activity was bound per g of liver (up to 1000 m-units/total liver). However, heparin treatment of the liver decreases the ability of the liver to re-bind hepatic lipase by 80%. Perfusion of rat livers with 0.3 M NaCl released 60% of the lipase activity into the medium. Upon subsequent perfusion of these livers with hepatic-lipase-containing media, 541 +/- 164 m-units of hepatic lipase could be bound per g of liver (up to 5000 m-units/total liver). The binding of hepatic lipase was also studied in livers of corticotropin (ACTH)-pre-treated rats. In these rats also, hepatic lipase bound only to livers which had been pre-perfused with heparin or 0.3 M NaCl. After heparin pre-perfusion, 88 +/- 12 m-units of hepatic lipase could be bound per g of liver, similar to that with livers of control rats not treated with ACTH. After prior salt perfusion, however, the capacity of the livers of ACTH-pre-treated rats to bind hepatic lipase was 212 +/- 60 m-units/g of liver. This is less than in livers of control rats (541 +/- 164 m-units/g of liver). These results indicate that in rat liver the binding of hepatic lipase is heterogeneous in character and consists of heparin-resistant and heparin-sensitive components. The hepatic-lipase binding capacity of the liver is saturable and fully utilized under various conditions. The heparin-sensitive binding capacity is lowered in ACTH-treated rats, whereas the heparin-resistant binding is unaffected. We postulate that the functional hepatic lipase activity can be regulated by changes in the binding capacity of the liver.
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Mergental, Hynek, Darius Mirza, Simon Afford i Ricky Bhogal. "The Emerging Importance of Liver Sinusoidal Endothelial Cells in Regulating Injury during Machine Perfusion of Deceased Liver Donors". Seminars in Liver Disease 38, nr 03 (24.07.2018): 252–59. http://dx.doi.org/10.1055/s-0038-1661371.
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AbstractWhile majority of liver transplants worldwide continue to be performed using deceased donor organs, the demands for donor livers continues to exceed the current supply. In an attempt to maximize the number of potentially usable donor livers and expand the current donor pool, there is intense global research by various groups exploring the role of machine perfusion in the liver transplantation, particularly with respect to the machine perfusion of extended-criteria liver donors. In this review, the authors summarize the current field of machine perfusion strategies as applied to deceased donor liver transplantation and how therapeutic targeting of the liver sinusoidal endothelial cell may improve the quality of donor livers.
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Johnson, Cheryl, i Donna 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/10.7182/prtr.1.6.3.r735490753203252.
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Belaschk, Elisa, Susanne Rohn, Ramla Mukiibi, Anja Reutzel-Selke, Peter Tang, Birgit Sawitzki, Johann Pratschke, Igor M. Sauer i Martina T. Mogl. "Isolation, Characterization and Cold Storage of Cells Isolated from Diseased Explanted Livers". International Journal of Artificial Organs 40, nr 6 (23.05.2017): 294–306. http://dx.doi.org/10.5301/ijao.5000594.
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Introduction Livers discarded after standard organ retrieval are commonly used as a cell source for hepatocyte transplantation. Due to the scarcity of organ donors, this leads to a shortage of suitable cells for transplantation. Here, the isolation of liver cells from diseased livers removed during liver transplantation is studied and compared to the isolation of cells from liver specimens obtained during partial liver resection. Methods Hepatocytes from 20 diseased explanted livers (Ex-group) were isolated, cultured and stored at 4°C for up to 48 hours, and compared to hepatocytes isolated from the normal liver tissue of 14 liver lobe resections (Rx-group). The nonparenchymal cell fraction (NPC) was analyzed by flow cytometry to identify potential liver progenitor cells, and OptiPrep™ (Sigma-Aldrich) density gradient centrifugation was used to enrich the progenitor cells for immediate transplantation. Results There were no differences in viability, cell integrity and metabolic activity in cell culture and survival after cold storage when comparing the hepatocytes from the Rx-group and the Ex-group. In some cases, the latter group showed tendencies of increased resistance to isolation and storage procedures. The NPC of the Ex-group livers contained considerably more EpCAM+ and significantly more CD90+ cells than the Rx-group. Progenitor cell enrichment was not sufficient for clinical application. Conclusions Hepatocytes isolated from diseased explanted livers showed the essential characteristics of being adequate for cell transplantation. Increased numbers of liver progenitor cells can be isolated from diseased explanted livers. These results support the feasibility of using diseased explanted livers as a cell source for liver cell transplantation.
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Yagi, Shintaro, Masaaki Hirata, Yosuke Miyachi i Shinji Uemoto. "Liver Regeneration after Hepatectomy and Partial Liver Transplantation". International Journal of Molecular Sciences 21, nr 21 (9.11.2020): 8414. http://dx.doi.org/10.3390/ijms21218414.
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The liver is a unique organ with an abundant regenerative capacity. Therefore, partial hepatectomy (PHx) or partial liver transplantation (PLTx) can be safely performed. Liver regeneration involves a complex network of numerous hepatotropic factors, cytokines, pathways, and transcriptional factors. Compared with liver regeneration after a viral- or drug-induced liver injury, that of post-PHx or -PLTx has several distinct features, such as hemodynamic changes in portal venous flow or pressure, tissue ischemia/hypoxia, and hemostasis/platelet activation. Although some of these changes also occur during liver regeneration after a viral- or drug-induced liver injury, they are more abrupt and drastic following PHx or PLTx, and can thus be the main trigger and driving force of liver regeneration. In this review, we first provide an overview of the molecular biology of liver regeneration post-PHx and -PLTx. Subsequently, we summarize some clinical conditions that negatively, or sometimes positively, interfere with liver regeneration after PHx or PLTx, such as marginal livers including aged or fatty liver and the influence of immunosuppression.
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Garg, Pinky, Saroj Choudhary, Montosh Chakraborty i Karthikeyan P. "INDICES OF OXIDATIVE STRESS AND LIVER INJURY IN ALCOHOLIC LIVER DISEASE". International Journal of Integrative Medical Sciences 4, nr 5 (5.09.2017): 488–92. http://dx.doi.org/10.16965/ijims.2017.107.
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Doi, Hiroshi, Hiroya Shiomi, Norihisa Masai, Daisaku Tatsumi, Takumi Igura, Yasuharu Imai i Ryoong-Jin Oh. "Threshold doses and prediction of visually apparent liver dysfunction after stereotactic body radiation therapy in cirrhotic and normal livers using magnetic resonance imaging". Journal of Radiation Research 57, nr 3 (1.06.2016): 294–300. http://dx.doi.org/10.1093/jrr/rrw008.
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Abstract The purpose of the present study was to investigate the threshold dose for focal liver damage after stereotactic body radiation therapy (SBRT) in cirrhotic and normal livers using magnetic resonance imaging (MRI). A total of 64 patients who underwent SBRT for liver tumors, including 54 cirrhotic patients with hepatocellular carcinoma (HCC) and 10 non-cirrhotic patients with liver metastases, were analyzed. MRI was performed 3−6 months after SBRT, using gadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid-enhanced T1-weighted sequences. All MRI datasets were merged with 3D dosimetry data. All dose distributions were corrected to the biologically effective dose using the linear–quadratic model with an assumed α/β ratio of 2 Gy. The development of liver dysfunction was validly correlated with isodose distribution. The median biologically effective dose (BED 2 ) that provoked liver dysfunction was 57.3 (30.0−227.9) and 114.0 (70.4−244.9) Gy in cirrhotic and normal livers, respectively ( P = 0.0002). The BED 2 associated with a >5% risk of liver dysfunction was 38.5 in cirrhotic livers and 70.4 Gy in normal livers. The threshold BED 2 for liver dysfunction was not significantly different between Child−Pugh A and B patients ( P = 0.0719). Moreover, the fractionation schedule was not significantly correlated with threshold BED 2 for liver dysfunction in the cirrhotic liver ( P = 0.1019). In the cirrhotic liver, fractionation regimen and Child−Pugh classification did not significantly influence the threshold BED 2 for focal liver damage after SBRT. We suggest that the threshold BED 2 for liver dysfunction after SBRT is 40 and 70 Gy in the cirrhotic and normal liver, respectively.
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Popa, Alexandru, Ioan Sporea, Felix Bende, Alina Popescu, Renata Fofiu, Andreea Borlea, Victor Bâldea i in. "The Non-Invasive Ultrasound-Based Assessment of Liver Viscosity in a Healthy Cohort". Diagnostics 12, nr 6 (13.06.2022): 1451. http://dx.doi.org/10.3390/diagnostics12061451.
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Liver fibrosis is the most significant prognostic factor in chronic liver disease (CLD). Clinical practice guidelines recommend the use of non-invasive techniques, such as two-dimensional shear-wave elastography (2D-SWE), to assess liver stiffness as a marker of fibrosis. Several other factors influence liver stiffness in addition to liver fibrosis. It is presumed that changes due to necro-inflammation modify the propagation of shear waves (dispersion). Therefore, new imaging techniques that investigate the dispersion properties of shear waves have been developed, which can serve as an indirect method of measuring liver viscosity (Vi PLUS). Defining the reference values in healthy subjects among different age groups and genders and analyzing the factors that influence these values is essential. However, published data on liver viscosity are still limited. This is the first study that aimed to assess the normal range of liver viscosity values in subjects with healthy livers and analyze the factors that influence them. One hundred and thirty-one consecutive subjects with healthy livers were enrolled in this prospective study. The results showed that Vi PLUS is a highly feasible method. Liver stiffness, age and BMI influenced the liver viscosity values. The mean liver viscosity by Vi PLUS in subjects with healthy livers was 1.59 Pa·s.
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Li, Chang Xian, Hong Wei Wang, Wang Jie Jiang, Gao Chao Li, Yao Dong Zhang, Chen Huan Luo i Xiang Cheng Li. "The Inhibition of Aldose Reductase Accelerates Liver Regeneration through Regulating Energy Metabolism". Oxidative Medicine and Cellular Longevity 2020 (28.02.2020): 1–11. http://dx.doi.org/10.1155/2020/3076131.
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Objectives. Our previous study showed that aldose reductase (AR) played key roles in fatty liver ischemia-reperfusion (IR) injury by regulating inflammatory response and energy metabolism. Here, we aim to investigate the role and mechanism of AR in the regeneration of normal and fatty livers after liver surgery. Methods. The association of AR expression with liver regeneration was studied in the rat small-for-size liver transplantation model and the mice major hepatectomy and hepatic IR injury model with or without fatty change. The direct role and mechanism of AR in liver regeneration was explored in the AR knockout mouse model. Results. Delayed regeneration was detected in fatty liver after liver surgery in both rat and mouse models. Furthermore, the expression of AR was increased in liver after liver surgery, especially in fatty liver. In a functional study, the knockout of AR promoted liver regeneration at day 2 after major hepatectomy and IR injury. Compared to wild-type groups, the expressions of cyclins were increased in normal and fatty livers of AR knockout mice. AR inhibition increased the expressions of PPAR-α and PPAR-γ in both normal liver and fatty liver groups after major hepatectomy and IR injury. In addition, the knockout of AR promoted the expressions of SDHB, AMPK, SIRT1, and PGC1-α in liver, which regulated mitochondrial biogenesis and energy metabolism. Conclusions. The knockout of AR promoted the regeneration of normal and fatty livers through regulating energy metabolism. AR may be a new potential therapeutic target to accelerate liver regeneration after surgery.
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Ibarra, R., J.-E. Dazard, Y. Sandlers, F. Rehman, R. Abbas, R. Kombu, G.-F. Zhang, H. Brunengraber i J. Sanabria. "Metabolomic Analysis of Liver Tissue from the VX2 Rabbit Model of Secondary Liver Tumors". HPB Surgery 2014 (2.03.2014): 1–12. http://dx.doi.org/10.1155/2014/310372.
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Purpose. The incidence of liver neoplasms is rising in USA. The purpose of this study was to determine metabolic profiles of liver tissue during early cancer development. Methods. We used the rabbit VX2 model of liver tumors (LT) and a control group consisting of sham animals implanted with Gelfoam into their livers (LG). After two weeks from implantation, liver tissue from lobes with and without tumor was obtained from experimental animals (LT+/LT−) as well as liver tissue from controls (LG+/LG−). Peaks obtained by Gas Chromatography-Mass Spectrometry were subjected to identification. 56 metabolites were identified and their profiles compared between groups using principal component analysis (PCA) and a mixed-effect two-way ANOVA model. Results. Animals recovered from surgery uneventfully. Analyses identified a metabolite profile that significantly differs in experimental conditions after controlling the False Discovery Rate (FDR). 16 metabolites concentrations differed significantly when comparing samples from (LT+/LT−) to samples from (LG+/LG−) livers. A significant difference was also shown in 20 metabolites when comparing samples from (LT+) liver lobes to samples from (LT−) liver lobes. Conclusion. Normal liver tissue harboring malignancy had a distinct metabolic signature. The role of metabolic profiles on liver biopsies for the detection of early liver cancer remains to be determined.
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Zhou, Guang-Peng, Li-Ying Sun i Zhi-Jun Zhu. "The concept of “domino” in liver and hepatocyte transplantation". Therapeutic Advances in Gastroenterology 13 (styczeń 2020): 175628482096875. http://dx.doi.org/10.1177/1756284820968755.
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Although orthotopic liver transplantation remains the only proven treatment for end-stage liver disease and inherited metabolic liver disease, its application has been limited by the scarcity of donor organs available for transplantation. Among feasible approaches developed to expand the donor organ pool, domino liver transplantation is a strategy in which explanted genetically defective livers of liver transplant recipients are used as grafts in other patients. Another promising therapeutic strategy is hepatocyte transplantation, an alternative to liver transplantation for certain groups of patients. However, the availability of primary hepatocytes is also hindered by the shortage of donor liver tissues. Against this background, domino hepatocyte transplantation, a strategy that utilizes the hepatocytes derived from the explanted livers of liver transplant recipients with noncirrhotic inherited metabolic liver diseases as the source of primary hepatocytes, may help increase the supply of liver cells available for transplantation. In this review, we focus on the status quo of domino liver transplantation and domino hepatocyte transplantation. We also describe recent innovative transplant strategies based on domino transplantation.
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Hefler, Joshua, Sanaz Hatami, Aducio Thiesen, Carly Olafson, Kiarra Durand, Jason Acker, Constantine J. Karvellas, David L. Bigam, Darren H. Freed i Andrew Mark James Shapiro. "Model of Acute Liver Failure in an Isolated Perfused Porcine Liver—Challenges and Lessons Learned". Biomedicines 10, nr 10 (6.10.2022): 2496. http://dx.doi.org/10.3390/biomedicines10102496.
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Acute liver failure (ALF) is a rare but devastating disease associated with substantial morbidity and a mortality rate of almost 45%. Medical treatments, apart from supportive care, are limited and liver transplantation may be the only rescue option. Large animal models, which most closely represent human disease, can be logistically and technically cumbersome, expensive and pose ethical challenges. The development of isolated organ perfusion technologies, originally intended for preservation before transplantation, offers a new platform for experimental models of liver disease, such as ALF. In this study, female domestic swine underwent hepatectomy, followed by perfusion of the isolated liver on a normothermic machine perfusion device. Five control livers were perfused for 24 h at 37 °C, while receiving supplemental oxygen and nutrition. Six livers received toxic doses of acetaminophen given over 12 h, titrated to methemoglobin levels. Perfusate was sampled every 4 h for measurement of biochemical markers of injury (e.g., aspartate aminotransferase [AST], alanine aminotransferase [ALT]). Liver biopsies were taken at the beginning, middle, and end of perfusion for histological assessment. Acetaminophen-treated livers received a median dose of 8.93 g (8.21–9.75 g) of acetaminophen, achieving a peak acetaminophen level of 3780 µmol/L (3189–3913 µmol/L). Peak values of ALT (76 vs. 105 U/L; p = 0.429) and AST (3576 vs. 4712 U/L; p = 0.429) were not significantly different between groups. However, by the end of perfusion, histology scores were significantly worse in the acetaminophen treated group (p = 0.016). All acetaminophen treated livers developed significant methemoglobinemia, with a peak methemoglobin level of 19.3%, compared to 2.0% for control livers (p = 0.004). The development of a model of ALF in the ex vivo setting was confounded by the development of toxic methemoglobinemia. Further attempts using alternative agents or dosing strategies may be warranted to explore this setting as a model of liver disease.
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Mansur, Dil Islam, P. Shrestha i S. Maskey. "Morphological Variations in Human Liver: A Cadaveric Study". Nepal Medical College Journal 21, nr 4 (31.12.2019): 249–53. http://dx.doi.org/10.3126/nmcj.v21i4.27612.
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The variations of liver like the accessory fissures and lobes are a potential source of diagnostic errors. The knowledge in the variations may help in diagnosis, treatment planning and minimize the risk of post operative complications. The present study was aimed to observe the morphological variations of livers. The study was done in 70 formalin fixed human livers and was observed for morphological variations. The present study concluded the normal morphology of liver was in 54.28% and anomalies in 45.71% of liver. The most common anomalies were accessory fissures which were found in 32.86% of livers. The second common anomalies were absence or incomplete fissure for ligamentum teres in 15.71% of livers. Then the enlarged papillary process was found in 11.43%, short gall bladder was in 10% and elongated left lobe was in 7.14%. The knowledge of normal and variant liver may contribute to the understanding of the liver disease and to achieve correct preoperative diagnosis; and to avoid intra-operative complications.
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Horslen, Simon P., James M. Hammel, Lance W. Fristoe, Jeff A. Kangas, Dean S. Collier, Debra L. Sudan, Alan N. Langnas i in. "EXTRACORPOREAL LIVER PERFUSION USING HUMAN AND PIG LIVERS FOR ACUTE LIVER FAILURE". Transplantation 70, nr 10 (listopad 2000): 1472–78. http://dx.doi.org/10.1097/00007890-200011270-00014.
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Osawa, Yosuke, Hironari Kawai, Keigo Nakashima, Yuichi Nakaseko, Daisuke Suto, Keisuke Yanagida, Tomomi Hashidate-Yoshida i in. "Sphingosine-1-phosphate promotes liver fibrosis in metabolic dysfunction-associated steatohepatitis". PLOS ONE 19, nr 5 (16.05.2024): e0303296. http://dx.doi.org/10.1371/journal.pone.0303296.
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Aim Metabolic dysfunction-associated steatohepatitis (MASH) is one of the most prevalent liver diseases and is characterized by steatosis and the accumulation of bioactive lipids. This study aims to understand the specific lipid species responsible for the progression of liver fibrosis in MASH. Methods Changes in bioactive lipid levels were examined in the livers of MASH mice fed a choline-deficient diet (CDD). Additionally, sphingosine kinase (SphK)1 mRNA, which generates sphingosine 1 phosphate (S1P), was examined in the livers of patients with MASH. Results CDD induced MASH and liver fibrosis were accompanied by elevated levels of S1P and increased expression of SphK1 in capillarized liver sinusoidal endothelial cells (LSECs) in mice. SphK1 mRNA also increased in the livers of patients with MASH. Treatment of primary cultured mouse hepatic stellate cells (HSCs) with S1P stimulated their activation, which was mitigated by the S1P receptor (S1PR)2 inhibitor, JTE013. The inhibition of S1PR2 or its knockout in mice suppressed liver fibrosis without reducing steatosis or hepatocellular damage. Conclusion S1P level is increased in MASH livers and contributes to liver fibrosis via S1PR2.
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MOORLOCK, GREG, JAMES NEUBERGER, SIMON BRAMHALL i HEATHER DRAPER. "An Empirically Informed Analysis of the Ethical Issues Surrounding Split Liver Transplantation in the United Kingdom". Cambridge Quarterly of Healthcare Ethics 25, nr 3 (27.06.2016): 435–47. http://dx.doi.org/10.1017/s0963180116000086.
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Abstract:Surgical advances have allowed for the development of split liver transplantation, providing two recipients with the opportunity to potentially benefit from one donated liver by splitting the liver into two usable parts. Although current data suggest that the splitting of livers provides overall benefit to the liver-recipient population, relatively low numbers of livers are actually split in the United Kingdom. This article addresses the question of whether ethical concerns are posing an unnecessary barrier to further increasing the number of life-saving transplantations. Recognizing that an important aspect of exploring these concerns is gaining insight into how transplant staff and patients regard splitting livers, the article presents the findings of a qualitative study examining the views of senior transplant staff and liver transplant patients in the UK and uses these to inform a commentary on the ethical issues relating to split liver transplantation.
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Lin, Yi-Ling, Chih-Ying Chen, Deng-Jye Yang, Yi-Hsieng Samuel Wu, Yue-Jia Lee, Yi-Chou Chen i Yi-Chen Chen. "Hepatic-Modulatory Effects of Chicken Liver Hydrolysate-Based Supplement on Autophagy Regulation against Liver Fibrogenesis". Antioxidants 12, nr 2 (15.02.2023): 493. http://dx.doi.org/10.3390/antiox12020493.
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Chicken-liver hydrolysates (CLHs) have been characterized as performing several biofunctions by our team. This study aimed to investigate if a CLH-based supplement (GBHP01TM) can ameliorate liver fibrogenesis induced by thioacetamide (TAA) treatment. Our results showed that the TAA treatment caused lower body weight gains and enlarged livers, as well as higher serum ALT, AST, and ALP levels (p < 0.05). This liver inflammatory and fibrotic evidence was ameliorated (p < 0.05) by supplementing with GBHP01TM; this partially resulted from its antioxidant abilities, including decreased TBARS values but increased TEAC levels, reduced GSH contents and catalase/GPx activities in the livers of TAA-treated rats (p < 0.05). Additionally, fewer nodules were observed in the appearance of the livers of TAA-treated rats after supplementing with GBHP01TM. Similarly, supplementing GBHP01TM decreased fibrotic scars and the fibrotic score in the livers of TAA-treated rats (p < 0.05). Moreover, the increased hepatic IL-6, IL-1β, and TNF-α levels after TAA treatment were also alleviated by supplementing with GBHP01TM (p < 0.05). Meanwhile, GBHP01TM could decrease the ratio of LC3B II/LC3B I, but upregulated P62 and Rab7 in the livers of TAA-treated rats (p < 0.05). Taking these results together, the CLH-based supplement (GBHP01TM) can be characterized as a natural agent against liver fibrogenesis.
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Kreisel, Charles, Alexandra Monde, Gregory Carlisle, Jeffrey Toretsky, Michael Terao i Alexandra Monde. "Liver recovery in a child with hemophagocytic lymphohistiocytosis-induced acute liver failure". Journal of Case Reports and Images in Pediatrics 4, nr 2 (21.07.2022): 1–6. http://dx.doi.org/10.5348/100015z19ck2022cr.
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Introduction: Hemophagocytic lymphohistiocytosis is a rare condition with dysregulated multi-organ inflammation that may cause acute liver failure. It often presents with non-specific clinical features and can be difficult to diagnose. Case Report: We present the case of a 2-year-old girl with lethargy, encephalopathy, poor oral intake, vomiting, and jaundice. Her labs indicated acute liver failure with additional findings of bicytopenia and elevated ferritin. Given high concern for hemophagocytic lymphohistiocytosis, we promptly consulted the hematology/oncology, transplant hepatology, and pharmacy services. Bone marrow biopsy initially showed no evidence of hemophagocytosis. Given our high clinical index of suspicion for hemophagocytic lymphohistiocytosis and its high mortality and morbidity, we initiated treatment with high dose dexamethasone, etoposide, and the recently approved biologic drug emapalumab, a monoclonal antibody against interferon gamma, despite not meeting full HLH-2004 diagnostic criteria. One day after treatment initiation, the final review of the bone marrow biopsy showed evidence of hemophagocytosis. Ultimately, with implementation of multidisciplinary rounds, close neurologic examinations, aggressive management of evolving hyperammonemia and cerebral edema, and early initiation of treatment, our patient achieved full liver recovery. Conclusion: This patient’s presentation emphasizes the importance of having a broad differential when a patient presents with liver failure and cytopenias. Our management of this patient showcases the importance of expedient, multidisciplinary management for a complex critically ill pediatric patient. The patient’s survival and complete liver recovery with the treatment protocol given suggests emapalumab should be studied in future clinical trials as an important adjunctive treatment for patients with hemophagocytic lymphohistiocytosis with acute liver failure.
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PD, Gupta. "Liver Cells Can Dedifferentiate and Act as Progenitor Cells for Liver Growth". Journal of Embryology & Stem Cell Research 3, nr 2 (2019): 1–2. http://dx.doi.org/10.23880/jes-16000124.
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Krüger, Melanie, Alicia Ruppelt, Benjamin Kappler, Elke Van Soest, Roos Anne Samsom, Guy C. M. Grinwis, Niels Geijsen i in. "Normothermic Ex Vivo Liver Platform Using Porcine Slaughterhouse Livers for Disease Modeling". Bioengineering 9, nr 9 (14.09.2022): 471. http://dx.doi.org/10.3390/bioengineering9090471.
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Metabolic and toxic liver disorders, such as fatty liver disease (steatosis) and drug-induced liver injury, are highly prevalent and potentially life-threatening. To allow for the study of these disorders from the early stages onward, without using experimental animals, we collected porcine livers in a slaughterhouse and perfused these livers normothermically. With our simplified protocol, the perfused slaughterhouse livers remained viable and functional over five hours of perfusion, as shown by hemodynamics, bile production, indocyanine green clearance, ammonia metabolism, gene expression and histology. As a proof-of-concept to study liver disorders, we show that an infusion of free fatty acids and acetaminophen results in early biochemical signs of liver damage, including reduced functionality. In conclusion, the present platform offers an accessible system to perform research in a functional, relevant large animal model while avoiding using experimental animals. With further improvements to the model, prolonged exposure could make this model a versatile tool for studying liver diseases and potential treatments.
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Heier, A., A. Gröne, J. Völlm, A. Kübber-Heiss i L. N. Bacciarini. "Immunohistochemical Study of Retinol-binding Protein in Livers of Polar Bears (Thalarctos maritimus)". Veterinary Pathology 40, nr 2 (marzec 2003): 196–202. http://dx.doi.org/10.1354/vp.40-2-196.
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Liver tumors of unknown cause have frequently been described in polar bears. Concurrent decrease of vitamin A levels and chronic liver disease are associated with hepatic carcinogenesis in humans. More than 90% of the body's vitamin A is stored in the liver, where it is bound to an intracellular retinol-binding protein (RBP). Therefore, in this retrospective study, RBP was assessed by immunohistochemistry in liver sections of 11 polar bears. Two of these polar bears had hepatocellular carcinoma, four showed other chronic liver changes, and five had normal livers. In normal livers, the cytoplasm stained diffusely positive with intensely staining cytoplasmic granules. RBP staining was evaluated and the abundance of diffuse cytoplasmic staining and intracytoplasmic large granules was determined. All cases with pathologic liver changes had markedly decreased staining intensities for RBP compared with normal livers. The findings of this study suggest that in polar bears, as in humans, vitamin A metabolism may play a role in hepatic carcinogenesis.
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Teixeira, Andreza Correa, Fernanda Fernandes Souza, Gustavo de Assis Mota, Ana de Lourdes Candolo Martinelli, Ajith Kumar Sankarankutty i Orlando de Castro e Silva. "Liver transplantation: expectation with MELD score for liver allocation in Brazil". Acta Cirurgica Brasileira 21, suppl 1 (2006): 12–14. http://dx.doi.org/10.1590/s0102-86502006000700003.
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Liver transplantation represents the most effective therapy for patients suffering from chronic end-stage liver disease. Until very recently, in Brazil, liver allocation was based on the Child-Turcotte-Pugh score and the waiting list followed a chronological criterion. In February 2002 the Model for End-stage Liver Disease (MELD) score was adopted for the allocation of donor livers in the US. After that change, an increased number of patients with more severe liver disease was observed, although there was no difference in 1-year patient and graft survival. A reduction in waiting-list mortality was also observed. In Brazil, the MELD score was adopted on May 31st, 2006. Good results are expected regarding the new criterion for allocation.
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van Cooten, Véronique V., Daan J. de Jong, Frank J. Wessels, Pim A. de Jong i Madeleine Kok. "Liver Enhancement on Computed Tomography Is Suboptimal in Patients with Liver Steatosis". Journal of Personalized Medicine 11, nr 12 (25.11.2021): 1255. http://dx.doi.org/10.3390/jpm11121255.
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This study’s aim was twofold. Firstly, to assess liver enhancement quantitatively and qualitatively in steatotic livers compared to non-steatotic livers on portal venous computed tomography (CT). Secondly, to determine the injection volume of contrast medium in patients with severe hepatic steatosis to improve the image quality of the portal venous phase. We retrospectively included patients with non-steatotic (n = 70), the control group, and steatotic livers (n = 35) who underwent multiphase computed tomography between March 2016 and September 2020. Liver enhancement was determined by the difference in attenuation in Hounsfield units (HU) between the pre-contrast and the portal venous phase, using region of interests during in three different segments. Liver steatosis was determined by a mean attenuation of ≤40 HU on unenhanced CT. Adequate enhancement was objectively defined as ≥50 ΔHU and subjectively using a three-point Likert scale. Enhancement of non-steatotic and steatotic livers were compared and associations between enhancement and patient- and scan characteristics were analysed. Enhancement was significantly higher among the control group (mean 51.9 ± standard deviation 11.5 HU) compared to the steatosis group (40.6 ± 8.4 HU p for difference < 0.001). Qualitative analysis indicated less adequate enhancement in the steatosis group: 65.7% of the control group was rated as good vs. 8.6% of the steatosis group. We observed a significant correlation between enhancement, and presence/absence of steatosis and grams of iodine per total body weight (TBW) (p < 0.001; adjusted R2 = 0.303). Deduced from this correlation, theoretical contrast dosing in grams of Iodine (g I) can be calculated: g I = 0.502 × TBW for non-steatotic livers and g I = 0.658 × TBW for steatotic livers. Objective and subjective enhancement during CT portal phase were significantly lower in steatotic livers compared to non-steatotic livers, which may have consequences for detectability and contrast dosing.
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Norman, Douglas J. "ALLOCATION OF LIVERS FOR LIVER TRANSPLANTATION". Clinics in Liver Disease 1, nr 2 (sierpień 1997): 281–86. http://dx.doi.org/10.1016/s1089-3261(05)70271-3.
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Ozaki, Michelle K., Yi Zhang, Zheng Xi i Pepper Schedin. "Abstract A046: Liver involution generates a pro-metastatic niche in a murine model of postpartum breast cancer liver metastasis". Cancer Research 84, nr 3_Supplement_1 (1.02.2024): A046. http://dx.doi.org/10.1158/1538-7445.advbc23-a046.
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Abstract Postpartum breast cancer (PPBC), cases diagnosed within 10 years of childbirth, has increased risk of liver metastases. Our lab has shown that the liver undergoes growth during pregnancy and lactation to support milk production, and upon weaning, undergoes involution. We have previously shown the actively involuting liver supports breast cancer liver metastasis in rodent models of PPBC, yet the mechanisms are poorly understood. Here, we performed RNAseq analysis in mouse livers across a lactation/wean cycle, and identify stromal alterations that may contribute to the “involution-educated” metastatic niche. During involution, RNA seq analysis reveals increased signatures for apoptotic cell death, catabolic metabolism, regulatory immune cell abundance, and extracellular matrix remodeling consistent with fibroblast activation. Using liver perfusion methods in live animals, we isolated viable stromal cells from livers of nullip or involution mice and validated these cells as highly enriched for fibroblasts by quantitative PCR. Liver fibroblasts were then mixed 1:1 with mouse mammary tumor cells, and injected into host mice at the flank site. We found fibroblasts from involuting livers generated larger tumors (n=28 tumors/group p=0.013), with decreased caspase 3 staining. Further, involution fibroblast tumors had increased ECM deposition as measured by trichrome staining, consistent with involution liver fibroblasts being more activated. Combined these data suggest that involution liver fibroblasts support tumor growth by suppressing tumor cell death, and by providing a pro-tumor collagen matrix when compared to nulliparous liver fibroblasts. These data implicate fibroblasts as components of the involution-educated metastatic niche in the postpartum liver. RNAseq analysis of involuting livers also identified gene signatures correlated with immature myeloid cells that associate with immune suppression and worse prognosis in numerous cancers. We thus evaluated for immature myeloid cells by multiplex immunohistochemistry in healthy mouse livers across a reproductive cycle, and identified increased abundance of immature myeloid cells (CD45+, CD11b+, Gr-1+) specifically during involution (n=6/group, p<0.05). Further, our data suggest liver involution may have a durable impact on immune composition of breast cancer liver metastases, as we find evidence for increased immature myeloid cells (CD45+, CD11b+, CD33+, CD68-, CD66b-, Cd56-, CD11c-, CD20-) in liver metastases of PPBC patients compared to non-PPBC patients. These data implicate immature myeloid cells as another component of the involution-educated liver metastatic niche. In sum, we find physiological involution of the liver post-wean alters the liver stromal microenvironment in a manner consistent with establishing a metastatic niche. Our findings may lead to the identification of liver stromal targets that can be exploited for prevention and or treatment strategies for PPBC liver metastasis. Citation Format: Michelle K Ozaki, Yi Zhang, Zheng Xi, Pepper Schedin. Liver involution generates a pro-metastatic niche in a murine model of postpartum breast cancer liver metastasis [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Advances in Breast Cancer Research; 2023 Oct 19-22; San Diego, California. Philadelphia (PA): AACR; Cancer Res 2024;84(3 Suppl_1):Abstract nr A046.
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Ye, Shicheng, Jochem W. B. Boeter, Louis C. Penning, Bart Spee i Kerstin Schneeberger. "Hydrogels for Liver Tissue Engineering". Bioengineering 6, nr 3 (5.07.2019): 59. http://dx.doi.org/10.3390/bioengineering6030059.
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Bioengineered livers are promising in vitro models for drug testing, toxicological studies, and as disease models, and might in the future be an alternative for donor organs to treat end-stage liver diseases. Liver tissue engineering (LTE) aims to construct liver models that are physiologically relevant. To make bioengineered livers, the two most important ingredients are hepatic cells and supportive materials such as hydrogels. In the past decades, dozens of hydrogels have been developed to act as supportive materials, and some have been used for in vitro models and formed functional liver constructs. However, currently none of the used hydrogels are suitable for in vivo transplantation. Here, the histology of the human liver and its relationship with LTE is introduced. After that, significant characteristics of hydrogels are described focusing on LTE. Then, both natural and synthetic materials utilized in hydrogels for LTE are reviewed individually. Finally, a conclusion is drawn on a comparison of the different hydrogels and their characteristics and ideal hydrogels are proposed to promote LTE.
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Rao, Joseph Sushil, Robert Ivkov i Anirudh Sharma. "Nanoparticle-Based Interventions for Liver Transplantation". International Journal of Molecular Sciences 24, nr 8 (19.04.2023): 7496. http://dx.doi.org/10.3390/ijms24087496.
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Liver transplantation is the only treatment for hepatic insufficiency as a result of acute and chronic liver injuries/pathologies that fail to recover. Unfortunately, there remains an enormous and growing gap between organ supply and demand. Although recipients on the liver transplantation waitlist have significantly higher mortality, livers are often not allocated because they are (i) classified as extended criteria or marginal livers and (ii) subjected to longer cold preservation time (>6 h) with a direct correlation of poor outcomes with longer cold ischemia. Downregulating the recipient’s innate immune response to successfully tolerate a graft having longer cold ischemia times or ischemia-reperfusion injury through induction of immune tolerance in the graft and the host would significantly improve organ utilization and post-transplant outcomes. Broadly, technologies proposed for development aim to extend the life of the transplanted liver through post-transplant or recipient conditioning. In this review, we focus on the potential benefits of nanotechnology to provide unique pre-transplant grafting and recipient conditioning of extended criteria donor livers using immune tolerance induction and hyperthermic pre-conditioning.
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Sumida, K. D., J. H. Urdiales i C. M. Donovan. "Enhanced gluconeogenesis from lactate in perfused livers after endurance training". Journal of Applied Physiology 74, nr 2 (1.02.1993): 782–87. http://dx.doi.org/10.1152/jappl.1993.74.2.782.
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The effects of endurance training (running 90 min/day at 30 m/min, 10% grade) on hepatic gluconeogenesis were studied in 24-h-fasted rats with use of the isolated liver perfusion technique. After isolation, the liver was perfused (single pass) for 30 min with Krebs-Henseleit bicarbonate buffer and fresh bovine erythrocytes (hematocrit 22–24%) with no added substrate. Subsequent to the "washout" period, the reservoir was elevated with various concentrations of lactate and [U-14C]lactate (10,000 dpm/ml) to assess hepatic glucose production. Relative flow rates were not significantly different between trained (1.94 +/- 0.05 ml/g liver) and control livers (1.91 +/- 0.05 ml/g liver). Furthermore, no significant differences were observed in perfusate pH, hematocrit, bile production, or serum alanine aminotransferase effluxing from trained or control livers. At saturating arterial lactate concentrations (> 2 mM), the maximal rate (Vmax) for hepatic glucose production was significantly higher for trained (0.91 +/- 0.04 mumol.min-1 x g liver-1) than for control livers (0.73 +/- 0.02 mumol.min-1 x g liver-1). That this reflected increased gluconeogenesis is supported by a significant elevation in the Vmax for [14C]glucose production from trained (13,150 +/- 578 dpm.min-1 x g liver-1) compared with control livers (10,712 +/- 505 dpm.min-1 x g liver-1). Significant increases were also observed in the Vmax for lactate uptake (25%), O2 consumption (19%), and 14CO2 production (23%) from endurance-trained livers. The Km for hepatic glucose output, approximately 1.05 mM lactate, was unchanged after endurance training. These findings demonstrate that chronic physical activity results in an elevated capacity for hepatic gluconeogenesis, as assessed in situ at saturating lactate concentrations.
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Li, Heliang, Linbin Yang i Erwei Song. "Abstract 628: Liver macrophages promote breast cancer liver metastasis through migrating neutrophils and initiating NETosis". Cancer Research 83, nr 7_Supplement (4.04.2023): 628. http://dx.doi.org/10.1158/1538-7445.am2023-628.
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Abstract Neutrophils extracellular traps (NETs), which are DNA scaffolds in complex with granule proteins, could be detected in the pre-metastatic liver niches and were associated with a poor survival in breast cancer patients. However, the mechanisms of neutrophils infiltration and NETs formation in the pre-metastatic liver tissues remain poorly understood. Here, we dynamically characterized the liver micro-environment of normal and 4T1-bearing BALB/C mouse models with or without liver metastasis by the single cell RNA sequencing. Interestingly, we found that CXCL1 and CXCL2, derived from the liver macrophages, were dramatically elevated in pre-metastatic livers and induced the infiltration of peripheral neutrophils by CXCR2. Besides, liver macrophages were educated by cancer cells-derived cathepsin C to secrete the CXCL1 and CXCL2. Furthermore, we identified that the complement signals were over-activated in pre-metastatic livers and induced neutrophils to NETosis. Therapeutically, targeting CXCL1, CXCL2 and complement signals could inhibit the NET formation and effectively reduce breast cancer liver metastasis. Citation Format: Heliang Li, Linbin Yang, Erwei Song. Liver macrophages promote breast cancer liver metastasis through migrating neutrophils and initiating NETosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 628.
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Poznański, Jarosław, Dariusz Sołdacki, Bożena Czarkowska-Pączek, Arkadiusz Bonna, Oskar Kornasiewicz, Marek Krawczyk, Wojciech Bal i Leszek Pączek. "Cirrhotic Liver of Liver Transplant Recipients Accumulate Silver and Co-Accumulate Copper". International Journal of Molecular Sciences 22, nr 4 (11.02.2021): 1782. http://dx.doi.org/10.3390/ijms22041782.
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Silver-based materials are widely used in clinical medicine. Furthermore, the usage of silver containing materials and devices is widely recommended and clinically approved. The impact on human health of the increasing use of silver nanoparticles in medical devices remains understudied, even though Ag-containing dressings are known to release silver into the bloodstream. In this study, we detected a widespread and sometimes significant silver accumulation both in healthy and sick liver biopsies, levels being statistically higher in patients with various hepatic pathologies. 28 healthy and 44 cirrhotic liver samples were investigated. The median amount of 0.049 ppm Ag in livers was measured in cirrhotic livers while the median was 0.0016 ppm for healthy livers (a more than 30-fold difference). The mean tissue concentrations of essential metals, Fe and Zn in cirrhotic livers did not differ substantially from healthy livers, while Cu was positively correlated with Ag. The serum levels of gamma-glutamyl transpeptidase (GGTP) was also positively correlated with Ag in cirrhotic livers. The increased Ag accumulation in cirrhotic livers could be a side effect of wide application of silver in clinical settings. As recent studies indicated a significant toxicity of silver nanoparticles for human cells, the above observation could be of high importance for the public health.
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Seye C, Ndoye JM, Wade R, Mar NB i Ndiaye Ab. "Morphometric Liver Study in Adults". International Journal of Anatomy and Research 9, nr 3.2 (5.08.2021): 8054–58. http://dx.doi.org/10.16965/ijar.2021.134.
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Background: The aim is to study the dimensions of the adult liver in Senegal in order to contribute to the data of the manufacture of a peri-hepatic prosthesis wrapping in the therapeutic means of post-traumatic hemorrhagic lesions of the liver. Materials and methods: This study involved 50 livers of anatomical subjects with an average age of 38 years. We have noted some biometric parameters. On the livers collected, we measured the weight and some dimensions. Results: The intermediate morphotype predomined with 48% of cases. The dorso-petal position of the liver was observed in 84% of the subjects. There was no correlation between the morphotype of the subjects and the orientation of the visceral face of the liver. The average liver weight was 1410 g. The average transverse diameter was 25.77cm while the antero-posterior diameter of the right lobe was 16 cm. The sagittal circumference of the liver in the sickle cell ligament was significantly lower than those measured at the right and left lobes. The sagittal circumferences of the liver in the Breviligneous subject were lower than those of the intermediate and long morphotype subjects. Conclusion: The choke zone between the two lobes of the liver in the sickle cell ligament is a mooring point for the peri-hepatic wrapping prosthesis. However, this can only be segmental for each right and left lobe. The morphotype of the subject, however, affects the weight, thickness and sagittal circumferences of the liver, which are essential for the dimensions of a peri-hepatic prosthesis. KEY WORDS: Liver morphometric, peri-hepatic prosthesis.
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Gandhi, Armin Aabish, Filipe Araujo Hoffmann, Michael LaPorte II, Aaron Havas, Adarsh Rajesh, Andrew Davis, Marcos G. Teneche, Jessica Proulx, Susan Kaech i Peter D. Adams. "Abstract 1407: Investigating the effect of an aged liver microenvironment on immune surveillance and predisposition to cancer". Cancer Research 84, nr 6_Supplement (22.03.2024): 1407. http://dx.doi.org/10.1158/1538-7445.am2024-1407.
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Abstract The incidence of liver cancer is increasing and there is an urgent need for new therapies and preventative strategies. Age is a major risk factor for liver cancer, the reasons for which are not well defined. One of the hallmarks of aging is immune dysfunction which affects liver homeostasis potentially making it prone to cancer. To understand the role of immune dysfunction in aging liver, we analyzed immune cells from young and old livers. As is reported before, in aged livers we observed an increase in CD101+PD1+CD8+ T cell population as well as an increase in an IFNγ+TNFα+ population suggesting an increase in T cell response in an aging liver. We next sought to understand the cause of T cell exhaustion in aged livers. Cell cluster analysis of the young (4-month-old) and old (22 month old) livers by scRNA seq revealed a cell population unique to the aged livers, showing increased expression of immune checkpoint ligands as well as tumor-initiating cell markers. We validated this data by flow cytometry. We next functionally probed the immune environment of aged liver, by testing the effect of cognate antigen expression in young and old hepatocytes on adoptively transferred activated P14 CD8+ T cells isolated from a young P14 mouse. Analysis of the ex vivo activated P14 CD8+ T cells from young and old antigen-expressing livers by flow cytometry and scRNA sequencing revealed increased exhaustion and cytokine-deficiency in old mice as compared to the young mice. This study explores the age-associated alterations in the immune cells in the liver, aiming to alter liver-resident immune cells and their metabolic states in a way that promotes anti-tumor immunity in an aging liver. Citation Format: Armin Aabish Gandhi, Filipe Araujo Hoffmann, Michael LaPorte II, Aaron Havas, Adarsh Rajesh, Andrew Davis, Marcos G. Teneche, Jessica Proulx, Susan Kaech, Peter D. Adams. Investigating the effect of an aged liver microenvironment on immune surveillance and predisposition to cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 1407.
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Lai, Hong-Shiee. "Liver Regeneration and Nutrition". Japanese Journal of SURGICAL METABOLISM and NUTRITION 49, nr 3 (2015): 75. http://dx.doi.org/10.11638/jssmn.49.3_75.
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Adhyatmika, Adhyatmika, Leonie Beljaars, Kurnia S. S. Putri, Habibie Habibie, Carian E. Boorsma, Catharina Reker-Smit, Theerut Luangmonkong i in. "Osteoprotegerin Is more than a Possible Serum Marker in Liver Fibrosis: A Study into Its Function in Human and Murine Liver". Pharmaceutics 12, nr 5 (21.05.2020): 471. http://dx.doi.org/10.3390/pharmaceutics12050471.
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Osteoprotegerin (OPG) serum levels are associated with liver fibrogenesis and have been proposed as a biomarker for diagnosis. However, the source and role of OPG in liver fibrosis are unknown, as is the question of whether OPG expression responds to treatment. Therefore, we aimed to elucidate the fibrotic regulation of OPG production and its possible function in human and mouse livers. OPG levels were significantly higher in lysates of human and mouse fibrotic livers compared to healthy livers. Hepatic OPG expression localized in cirrhotic collagenous bands in and around myofibroblasts. Single cell sequencing of murine liver cells showed hepatic stellate cells (HSC) to be the main producers of OPG in healthy livers. Using mouse precision-cut liver slices, we found OPG production induced by transforming growth factor β1 (TGFβ1) stimulation. Moreover, OPG itself stimulated expression of genes associated with fibrogenesis in liver slices through TGFβ1, suggesting profibrotic activity of OPG. Resolution of fibrosis in mice was associated with decreased production of OPG compared to ongoing fibrosis. OPG may stimulate fibrogenesis through TGFβ1 and is associated with the degree of fibrogenesis. It should therefore be investigated further as a possible drug target for liver fibrosis or biomarker for treatment success of novel antifibrotics.
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Jauregui, Hugo O., Namita Roy Chowdhury i Jayanta Roy Chowdhury. "Use of Mammalian Liver Cells for Artificial Liver Support". Cell Transplantation 5, nr 3 (maj 1996): 353–67. http://dx.doi.org/10.1177/096368979600500302.
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Advances in orthotopic liver transplantation have improved the survival rate of both acute and chronic liver failure patients to nearly 70%. However, the success of this treatment modality has created an international organ shortage. Many patients die while awaiting transplantation in part due to the minimal capacity to store viable transplantable livers beyond 24 h. Additionally, for many areas of the world, routine use of whole liver transplantation to treat liver disease is impractical due to the demands on both financial and technical resources. Potentially, these issues may be alleviated, at least in part, by the use of liver cell transplantation or cellular-based liver assist devices. The well-documented regenerative capacity of the liver may obviate the need for whole organ transplantation in some instances of acute failure, if the patient may be provided temporary metabolic support. Although other patients ultimately may require transplantation, a longer period of time to find a suitable organ for transplantation may be gained by that supportive therapy. The field of liver cell transplantation may offer solutions to patients with inherited metabolic deficiencies or chronic liver disease. The potential to treat an hepatic disorder by using only a fraction of the whole liver would increase the number of whole organs available for orthotopic liver transplantation. Research in the fields of hepatocyte based intra- and extra-corporeal liver support is providing evidence that these therapeutic modalities may ultimately become routine in the treatment of severe liver disease. A historic overview of that technology along with its current status is discussed.