Bibliografie tematiche / Hepatocyte

Letteratura scientifica selezionata sul tema "Hepatocyte"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 4 maggio 2024

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Articoli di riviste sul tema "Hepatocyte"

1

Skuratov, A. G., D. R. Petrenyov e A. N. Kondrachuk. "EXPRESSION OF MARKER GENES BY HEPATOCYTE-LIKE CELLS differentiated from mesenchymal stem cells". Health and Ecology Issues, n. 3 (28 settembre 2013): 105–10. http://dx.doi.org/10.51523/2708-6011.2013-10-3-22.

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Objective: to investigate the expression of marker genes by hepatocyte-like cells differentiated from mesenchymal stem cells (MSCs). Materials and methods. Wistar white rats, bone marrow MSCs, isolated hepatocytes of the rats were obtained by enzymatic perfusion of liver; differentiation of MSCs in hepatocyte direction; light microscopy; investigation of expression of genes by polymerase chain reaction (PCR). Results. The observed changes in the gene expression profile during the stages of differentiation indicate the presence of the cells differentiated into hepatocytic direction in MSCs culture. The expression of Carbox, Krt18, Krt19 Cyt1A1 genes depends on the composition of the medium and is not permanent and inducible in nature. It is important to go on searching for the molecular markers of MSCs differentiation in the hepatocytic direction. These results demonstrate the necessity to systematize the available data on the changes in the levels of gene expression during MSCs differentiation into hepatocytes to unify the conditions of assessment of the gene expression profiling.
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2

Gómez-Aristizábal, Alejandro, e John Edward Davies. "The effects of human umbilical cord perivascular cells on rat hepatocyte structure and functional polarity". Biochemistry and Cell Biology 91, n. 3 (giugno 2013): 140–47. http://dx.doi.org/10.1139/bcb-2012-0079.

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Hepatocyte culture is a useful tool for the study of their biology and the development of bioartificial livers. However, many challenges have to be overcome since hepatocytes rapidly lose their normal phenotype in vitro. We have recently demonstrated that human umbilical cord perivascular cells (HUCPVCs) are able to provide support to hepatocytes. In the present study we go further into exploring the effects that HUCPVCs have in the functional polarization, and both the internal and external organization, of hepatocytes. Also, we investigate HUCPVC–hepatocyte crosstalk by tracking both the effects of HUCPVCs on hepatocyte transcription factors and those of hepatocytes on the expression of hepatotrophic factors in HUCPVCs. Our results show that HUCPVCs maintain the functional polarity of hepatocytes ex vivo, as judged by the secretion of fluorescein into bile canaliculi, for at least 40 days. Transmission electron microscopy revealed that hepatocytes in coculture organize in an organoid-like structure embedded in extracellular matrix surrounded by HUCPVCs. In coculture, hepatocytes displayed a higher expression of C/EBPα, implicated in maintenance of the mature hepatocyte phenotype, and HUCPVCs upregulated hepatocyte growth factor and Jagged1 indicating that these genes may play important roles in HUCPVC–hepatocyte interactions.
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3

Fan, J. Y., G. Dama, Y. L. Liu, W. Y. Guo e J. T. Lin. "Combinational Overexpression of <i>Foxa3</i> and <i>Hnf4a</i> Enhance the Proliferation and Prolong the Functional Maintenance of Primary Hepatocytes". Молекулярная биология 57, n. 4 (1 luglio 2023): 668–70. http://dx.doi.org/10.31857/s0026898423040031.

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In an in vitro culture system, primary hepatocytes usually display a low proliferation capacity, accompanied with a decrease of viability and a loss of hepatocyte-specific functions. Previous studies have demonstrated that the combination introductions of certain hepatocyte-specific transcription factors are able to convert fibroblasts into functional hepatocyte-like cells. However, such combinational usage of transcription factors in primary hepatocytes culture has not yet sufficiently studied. The forkhead box protein A3 (FoxA3) and hepatocyte nuclear factor 4α (Hnf4α) are liver-enriched transcription factors that play vital roles in the differentiation, and maintenance of hepatocytes. Thus, we simultaneously overexpressed the two genes, Foxa3 and Hnf4a, in rat hepatocytes and observed that the combinational augmentation of these two transcription factors have enhanced the proliferation and stabilized the hepatocyte-specific functions of primary hepatocytes over a long-term culture period.
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4

Mason, William S., Chunxiao Xu, Huey Chi Low, Jeffry Saputelli, Carol E. Aldrich, Catherine Scougall, Arend Grosse, Richard Colonno, Sam Litwin e Allison R. Jilbert. "The Amount of Hepatocyte Turnover That Occurred during Resolution of Transient Hepadnavirus Infections Was Lower When Virus Replication Was Inhibited with Entecavir". Journal of Virology 83, n. 4 (10 dicembre 2008): 1778–89. http://dx.doi.org/10.1128/jvi.01587-08.

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ABSTRACT Transient hepadnavirus infections can involve spread of virus to the entire hepatocyte population. In this situation hepatocytes present following recovery are derived from infected hepatocytes. During virus clearance antiviral cytokines are thought to block virus replication and formation of new covalently closed circular DNA (cccDNA), the viral transcriptional template. It remains unclear if existing cccDNA is eliminated noncytolytically or if hepatocyte death and proliferation, to compensate for killing of some of the infected hepatocytes, are needed to remove cccDNA from surviving infected hepatocytes. Interpreting the relationship between hepatocyte death and cccDNA elimination requires knowing both the amount of hepatocyte turnover and whether cccDNA synthesis is effectively blocked during the period of immune destruction of infected hepatocytes. We have addressed these questions by asking if treatment of woodchucks with the nucleoside analog inhibitor of viral DNA synthesis entecavir (ETV) reduced hepatocyte turnover during clearance of transient woodchuck hepatitis virus (WHV) infections. To estimate hepatocyte turnover, complexity analysis was carried out on virus-cell DNA junctions created by integration of WHV and present following recovery in the livers of WHV-infected control or ETV-treated woodchucks. We estimated that, on average, 2.2 to 4.8 times less hepatocyte turnover occurred during immune clearance in the ETV-treated woodchucks. Computer modeling of the complexity data suggests that mechanisms in addition to hepatocyte death were responsible for elimination of cccDNA during recovery from transient infections.
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Flendrig, L. M., D. Sommeijer, N. C. J. J. Ladiges, A. A. Te Velde, M. A. W. Maas, G. G. A. Jörning, J. Daalhuisen e R. A. F. M. Chamuleau. "Commercially Available Media for Flushing Extracorporeal Bioartificial Liver Systems Prior to Connection to the Patient's Circulation: An in vitro Comparative Study in Two and Three Dimensional Porcine Hepatocyte Cultures". International Journal of Artificial Organs 21, n. 8 (agosto 1998): 467–72. http://dx.doi.org/10.1177/039139889802100803.

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Extracorporeal bioartificial liver (BAL) systems based on hepatocytes need to be flushed before clinical application, as hepatocyte culture media are not approved for medical use. Commercially available 0.9% NaCl solution and hemofiltration solution (both supplemented with 10% human albumin) were investigated in vitro to test their potential to wash BAL systems with minimal stress for the cultured hepatocytes. After a 2 hour incubation, the lidocaine metabolising capacity and release of liver enzymes were assessed. As hepatocytes have been cultured in bioreactors in either two or three dimensional cell configurations, we tested the media in respectively hepatocyte monolayers cultures and in our newly developed bioreactor in which hepatocytes reorganise as small hepatocyte aggregates. The three dimensional hepatocyte cultures tolerated both media well, and no significant differences were seen compared with hepatocytes cultured in Williams’ E (reference hepatocyte culture medium). The two dimensional hepatocyte cultures tolerated the supplemented hemofiltration solution and the reference medium equally well, but the condition of the porcine hepatocytes monolayer cultures was significantly impaired when incubated with the supplemented physiological saline solution. In conclusion, as a supplemented physiological saline solution may have detrimental effects on the condition of the hepatocytes, the more complex hemofiltration solution (bicarbonate buffered, glucose, essential minerals) was considered the better alternative for flushing bioartificial liver systems.
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Naruse, K., Y. Sakai, I. Nagashima, G. X. Jiang, M. Suzuki e T. Muto. "Comparisons of Porcine Hepatocyte Spheroids and Single Hepatocytes in the Non-Woven Fabric Bioartificial Liver Module". International Journal of Artificial Organs 19, n. 10 (ottobre 1996): 605–9. http://dx.doi.org/10.1177/039139889601901008.

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We previously developed a new bioreactor of the bioartificial liver composed of non-woven fabric. We have also experimented with hepatocyte spheroids, with the aim of improving the efficiency of this NWF bioreactor. In this study, we compared the efficiencies of NWF bioreactors employing hepatocyte spheroids versus single hepatocytes. Hepatocytes were isolated from a whole pig liver by Seglen's method. 1.0 × 1010 single hepatocytes were immobilized in the NWF bioreactor. Another 1.0 × 1010 hepatocytes were allowed to form spheroids by 24 hr suspension culture in a 4-L culture vessel, before being immobilized in the bioreactor. Hepatocyte spheroids were found to be functionally superior, on a per-cell basis, to single hepatocytes in the NWF bioreactor. However, the NWF bioreactor employing hepatocyte spheroids exhibited lower efficiency than that employing single hepatocytes, because the total number of the hepatocytes had decreased during the 24 hr suspension culture.
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7

Zhu, Y. X., L. Zhu, Y. F. Chen, J. M. Xu, Z. L. Shen, R. J. Liu, J. Zou, Mingqing Yuan, Fan Ye e Qingqi Zeng. "Luteoloside Ameliorates Palmitic Acid-Induced in Vitro Model of Non-alcoholic Fatty Liver Disease via Activating STAT3-Triggered Hepatocyte Regeneration". Folia Biologica 67, n. 3 (2021): 126–33. http://dx.doi.org/10.14712/fb2021067030126.

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Luteoloside (Lute), a bioactive natural ingredient, widely exists in nature and possesses hepatoprotective and hepatocyte proliferation-promoting properties. This study aimed to investigate whether Lute could counteract non-alcoholic fatty liver disease (NAFLD)-caused hepatocyte damage via its stimulation of hepatocyte regeneration efficacy and to explore the involved mechanism. LO2 cells and primary hepatocytes were used to examine the hepatocyte proliferation effects of Lute under physiological conditions and in the palmitic acid (PA)- induced in vitro model of NAFLD. STAT3 and cell cycle-related proteins (cyclin D1, c-myc and p21) were evaluated by Western blot. Under physiological conditions, LO2 cells and primary hepatocytes treated with various concentration of Lute for 12 and 24 h showed increased hepatocyte proliferation, especially with 20 μM treatment for 24 h. More notably, under the model conditions, co-incubation with 20 μM of Lute also markedly reversed PA-induced inhibition of cell proliferation and viability in primary hepatocytes. Mechanistically, Lute could activate STAT3 and subsequently increase cyclin D1 and cmyc expression, which positively regulates cell cycle progression, and decrease expression of p21, an inhibitor of cell cycle progression. Furthermore, Luteinduced hepatocyte proliferation-promoting efficacy was abolished by STAT3 inhibitor stattic. Collectively, Lute can alleviate PA-induced hepatocyte damage via activating STAT3-mediated hepatocyte regeneration.
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Afford, Simon C., Satinder Randhawa, Aristides G. Eliopoulos, Stefan G. Hubscher, Lawrence S. Young e David H. Adams. "CD40 Activation Induces Apoptosis in Cultured Human Hepatocytes via Induction of Cell Surface Fas Ligand Expression and Amplifies Fas-mediated Hepatocyte Death during Allograft Rejection". Journal of Experimental Medicine 189, n. 2 (18 gennaio 1999): 441–46. http://dx.doi.org/10.1084/jem.189.2.441.

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We propose that a novel mechanism of hepatocyte apoptosis, involving a cooperative interaction between CD40 and Fas, is involved in the hepatocyte loss of chronic liver allograft rejection. We detected increased hepatocyte expression of Fas, Fas ligand (FasL), and CD40 associated with dropout of centrilobular (acinar zone 3) hepatocytes in chronic allograft rejection. Expression of CD40 ligand (CD40L) was also increased but was largely restricted to CD68+ macrophages. A functional role for CD40 and Fas in hepatocyte apoptosis was demonstrated in vitro using primary human hepatocytes and the HepG2 cell line in both of which apoptosis was induced, not only by cross-linking Fas directly but also via CD40 activation. Our data suggest that CD40 activation induces apoptosis via Fas because (a) ligation of CD40 upregulated hepatocyte FasL expression, and (b) apoptosis induced via activation of CD40 was prevented by a neutralizing monoclonal antibody to FasL. Thus, CD40 engagement triggers apoptosis of human hepatocytes and might amplify Fas-dependent hepatocyte apoptosis in chronic rejection and other inflammatory liver diseases in which Fas-mediated apoptosis is involved.
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Pastor, Catherine M., e Valérie Vilgrain. "Steatosis Alters the Activity of Hepatocyte Membrane Transporters in Obese Rats". Cells 10, n. 10 (13 ottobre 2021): 2733. http://dx.doi.org/10.3390/cells10102733.

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Fat accumulation (steatosis) in ballooned hepatocytes alters the expression of membrane transporters in Zucker fatty (fa/fa) rats. The aim of the study was to quantify the functions of these transporters and their impact on hepatocyte concentrations using a clinical hepatobiliary contrast agent (Gadobenate dimeglumine, BOPTA) for liver imaging. In isolated and perfused rat livers, we quantified BOPTA accumulation and decay profiles in fa/+ (normal) and fa/fa hepatocytes by placing a gamma counter over livers. Profiles of BOPTA accumulation and decay in hepatocytes were analysed with nonlinear regressions to characterise BOPTA influx and efflux across hepatocyte transporters. At the end of the accumulation period, BOPTA hepatocyte concentrations and influx clearances were not significantly different in fa/+ and fa/fa livers. In contrast, bile clearance was significantly lower in fatty hepatocytes while efflux clearance back to sinusoids compensated the low efflux into canaliculi. The time when BOPTA cellular efflux impacts the accumulation profile of hepatocyte concentrations was slightly delayed (2 min) by steatosis, anticipating a delayed emptying of hepatocytes. The experimental model is useful for quantifying the functions of hepatocyte transporters in liver diseases.
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Rivas, Pedro A., Alfredo J. Fabrega, Daniel Schwartz, William Dagiantis, Michael G. Ward, Jacqueline Blanchard e Raymond Pollak. "Transplantation of Hepatocytes: An In-Vitro and In-Vivo Study in Canines". Cell Transplantation 3, n. 2 (marzo 1994): 193–201. http://dx.doi.org/10.1177/096368979400300208.

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We isolated and transplanted hepatocytes in the canine, large animal model to evaluate hepatocyte yield and purity as well as the optimal site for hepatocyte engraftment (i.e., the spleen or the portal bed). We obtained viable, pure, single hepatocyte suspensions that were readily preserved at 4°C in University of Wisconsin (UW) solution for up to 3 days. Both intrasplenic and portal vein injection were well tolerated, with minimal recipient morbidity and mortality when 1-2 × 109 hepatocytes were injected into immunosuppressed allogeneic hosts. We noted the embolization of hepatocytes into the parenchyma of the native liver within 7 days of intrasplenic transplantation that produced a mild reversible derangement of liver function and histology. These results warrant consideration prior to clinical trials of hepatocyte transplantation in man.
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Tesi sul tema "Hepatocyte"

1

Vroemen, Joseph Pieter Anna Maria. "Hepatocyte transplantation". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5364.

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2

Hannoun, Zara. "Role of SUMO modification in hepatocyte differentiation". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5917.

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Primary human hepatocytes are a scarce resource with variable function, which diminishes with time in culture. As a consequence their use in tissue modelling and therapy is restricted. Human embryonic stem cells (hESCs) could provide a stable source of human tissue due to their properties of self-renewal and their ability to give rise to all three germ layers. hESCs have the potential to provide an unlimited supply of hepatic endoderm (HE) which could offer efficient tools for drug discovery, disease modelling and therapeutic applications. In order to create a suitable environment to enhance HE formation, hESC culture needed to be standardised. As such, a media trail was carried out to define serum free media capable of maintaining hESC in a pluripotent undifferentiated state. We also ensured hESC cultured in the various media could be directly differentiated to HE in a reproducible and efficient manner. The project then focused on the effect of post-translational modifications (PTMs), specifically SUMOylation, in hepatocyte differentiation and its subsequent manipulation to enhance HE viability. SUMOylation is a PTM known to modify a large number of proteins that play a role in various cellular processes including: cell cycle regulation, gene transcription, differentiation and cellular localisation. We hypothesised that SUMO modification may not only regulate hESC self renewal, but also maybe required for efficient hESC differentiation. We therefore interrogated the role of SUMOylation in hESC differentiation to hepatic endoderm (HE). hESC were differentiated and the cellular lysates were analysed by Western blotting for key proteins which modulate the conjugation and de conjugation of SUMO. We demonstrate that peak levels of SUMOylation were detectable in hESC populations and during cellular differentiation to definitive endoderm (DE), day 5. Following commitment to DE we observed a decrease in the level of SUMO modified proteins during cellular specialisation to a hepatic fate, corresponding with an increase in SENP 1, a SUMO deconjugation enzyme. We also detected reduced levels of hepatocyte nuclear factor 4 α (HNF4α), a critical regulator of hepatic status and metabolic function, as SUMOylation decreased. As a result, we investigated if HNF4α was SUMOylated and if this process was involved in modulating HNF4α’s critical role in HE. HNF4α is an important transcription factor involved in liver organogenesis during development and is a key regulator for efficient adult liver metabolic functions. We observed a decreasing pattern of HNF4α expression at day 17 of our differentiation protocol in conjunction with a decrease in SUMO modified proteins. In order to further investigate and validate a role of SUMOylation on HNF4α stability Immunoprecipitation (IP) was employed. HNF4α protein was pulled down and probed for SUMO 2. Results show an increase in the levels of SUMO2 modification as the levels of HNF4α decrease. Through deletion and mutation analysis we demonstrated that SUMO modification of HNF4α was restricted to the C-terminus on lysine 365. Protein degradation via the proteasome was responsible for the decrease in HNF4α, demonstrated by the use of a proteasome 26S inhibitor MG132. Additionally, a group at the University of Dundee has shown that polySUMOylation of promyelocytic leukaemia protein (PML) leads to its subsequent ubiquitination via RNF4, an ubiquitin E3 ligase, driving its degradation. Using an in vitro ubiquitination assay, we show that polySUMOylated HNF4α is preferentially ubiquitinated in the presence of RNF4. Overall polySUMOylation of HNF4α may reduce its stability by driving its degradation, hence regulating protein activity. In conclusion, polySUMOylation of HNF4α is associated with its stability. HNF4α is subsequently important for HE differentiation both driving the formation of the hepatocytes and in maintaining a mature phenotype, in agreement with a number of different laboratories. Creating the ideal environment for sustaining mature functional hepatocytes, primary and those derived from hESCs and iPSCs, is essential for further use in applications such as drug screening, disease modelling and extracorporeal devices.
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Schuster, Susanne, e Antje Garten. "Resveratrol Differentially Regulates NAMPT and SIRT1 in Hepatocarcinoma Cells and Primary Human Hepatocytes". Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142581.

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Resveratrol is reported to possess chemotherapeutic properties in several cancers. In this study, we wanted to investigate the molecular mechanisms of resveratrol-induced cell cycle arrest and apoptosis as well as the impact of resveratrol on NAMPT and SIRT1 protein function and asked whether there are differences in hepatocarcinoma cells (HepG2, Hep3B cells) and non-cancerous primary human hepatocytes. We found a lower basal NAMPT mRNA and protein expression in hepatocarcinoma cells compared to primary hepatocytes. In contrast, SIRT1 was significantly higher expressed in hepatocarcinoma cells than in primary hepatocytes. Resveratrol induced cell cycle arrest in the S- and G2/M- phase and apoptosis was mediated by activation of p53 and caspase-3 in HepG2 cells. In contrast to primary hepatocytes, resveratrol treated HepG2 cells showed a reduction of NAMPT enzymatic activity and increased p53 acetylation (K382). Resveratrol induced NAMPT release from HepG2 cells which was associated with increased NAMPT mRNA expression. This effect was absent in primary hepatocytes where resveratrol was shown to function as NAMPT and SIRT1 activator. SIRT1 inhibition by EX527 resembled resveratrol effects on HepG2 cells. Furthermore, a SIRT1 overexpression significantly decreased both p53 hyperacetylation and resveratrol-induced NAMPT release as well as S-phase arrest in HepG2 cells. We could show that NAMPT and SIRT1 are differentially regulated by resveratrol in hepatocarcinoma cells and primary hepatocytes and that resveratrol did not act as a SIRT1 activator in hepatocarcinoma cells.
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Matz-Soja, Madlen, e Rolf Gebhardt. "Hepatic Hedgehog signaling contributes to the regulation of IGF1 and IGFBP1 serum levels". Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142560.

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Background Hedgehog signaling plays an important role in embryonic development, organogenesis and cancer. In the adult liver, Hedgehog signaling in non-parenchymal cells has been found to play a role in certain disease states such as fibrosis and cirrhosis. However, whether the Hedgehog pathway is active in mature healthy hepatocytes and is of significance to liver function are controversial. Findings Two types of mice with distinct conditional hepatic deletion of the Smoothened gene, an essential co-receptor protein of the Hedgehog pathway, were generated for investigating the role of Hedgehog signaling in mature hepatocytes. The knockout animals (KO) were inconspicuous and healthy with no changes in serum transaminases, but showed a slower weight gain. The liver was smaller, but presented a normal architecture and cellular composition. By quantitative RT-PCR the downregulation of the expression of Indian hedgehog (Ihh) and the Gli3 transcription factor could be demonstrated in healthy mature hepatocytes from these mice, whereas Patched1 was upregulated. Strong alterations in gene expression were also observed for the IGF axis. While expression of Igf1 was downregulated, that of Igfbp1 was upregulated in the livers of both genders. Corresponding changes in the serum levels of both proteins could be detected by ELISA. By activating and inhibiting the transcriptional output of Hedgehog signaling in cultured hepatocytes through siRNAs against Ptch1 and Gli3, respectively, in combination with a ChIP assay evidence was collected indicating that Igf1 expression is directly dependent on the activator function of Gli3. In contrast, the mRNA level of Igfbp1 appears to be controlled through the repressor function of Gli3, while that of Igfbp2 and Igfbp3 did not change. Interestingly, body weight of the transgenic mice correlated well with IGF-I levels in both genders and also with IGFBP-1 levels in females, whereas it did not correlate with serum growth hormone levels. Conclusions Our results demonstrate for the first time that Hedgehog signaling is active in healthy mature mouse hepatocytes and that it has considerable importance for IGF-I homeostasis in the circulation. These findings may have various implications for mouse physiology including the regulation of body weight and size, glucose homeostasis and reproductive capacity.
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Kolatsi, Maria. "Hepatocyte growth factor and renal morphogenesis". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243452.

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Aravinthan, Aloysious Dominic. "Hepatocyte senescence in chronic liver disease". Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708050.

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Powers, Mark J. (Mark James). "Substratum control of hepatocyte aggregate morphology". Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/43328.

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Ainscow, Edward Keith. "Control and regulation of hepatocyte metabolism". Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624775.

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Dunlay, Samantha, e Jonathan M. Peterson. "CTRP3 Prevents ETOH- Induced Hepatocyte Apoptosis". Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/127.

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McCullough, Christian Thomas. "IFNγ-mediated apoptosis in the primary hepatocyte". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/24935.

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This thesis describes the establishment of a primary cell culture system to investigate IFN-γ-induced hepatocyte apoptosis. We hypothesised that the hepatocyte response to IFN signalling is context-dependent, influenced by both external stimuli, such as growth factors, and the internal state of the cell. This was tested using a dual approach; firstly to assess the importance of known genes, IRF-l, p53 and p21 on apoptosis in this system and the contribution of known apoptotic inducers, such as CD95 and c-myc, to IFN-γ signalling. Secondly, to assess the feasibility of a functional gene trap assay in primary cells to identify unknown effectors of IFNγ-induced apoptosis. The results show that IFNΔ induces primary hepatocyte apoptosis in the context of serum- deprivation, an effect requiring IRF-1 but not p53. A deficiency of p21 potentiated apoptosis. Rather than generating a single outcome, the cellular response to IFNγ is modulated by external factors. IFNγ-induced apoptosis was inhibited by specific cytokines, while IFNγ potentiated primary hepatocyte apoptosis induced by death receptor signalling and DNA damage, in an IRF-1-dependent manner. Further, thyroid hormone potentiated IFNγ-induced apoptosis via MAPK- mediated phosphorylation of STAT1 at serine 727. This occurred via an extra-nuclear, that is non-genomic, signalling pathway. For the first time in primary hepatocytes it is demonstrated that IFNγ-mediated apoptotic signalling required the cell surface interaction of CD95 and its ligand and that IFNγ induces soluble CD95 ligand release from hepatocyte monolayers. The characteristics of IFNγ-mediated apoptosis identified in this research led to a hypothesis that c-myc contributes to IFNγ-induced apoptosis.
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Libri sul tema "Hepatocyte"

1

Stock, Peggy, e Bruno Christ, a cura di. Hepatocyte Transplantation. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6506-9.

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Dhawan, Anil, e Robin D. Hughes, a cura di. Hepatocyte Transplantation. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-201-4.

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1931-, Mito Michio, e Sawa Masayuki, a cura di. Hepatocyte transplantation. Basel: Karger Landes Systems, 1997.

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Berry, Michael N., e Anthony M. Edwards, a cura di. The Hepatocyte Review. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-3345-8.

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N, Berry Michael, e Edwards Anthony M, a cura di. The hepatocyte review. Dordrecht: Kluwer Academic Publishers, 2000.

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R, Billiar Timothy, e Curran Ronald D, a cura di. Hepatocyte and Kupffer Cell interactions. Boca Raton: CRC Press, 1992.

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Hepatocyte transplantation: Methods and protocols. New York, NY: Humana, 2009.

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8

Vinken, Mathieu, e Vera Rogiers, a cura di. Protocols in In Vitro Hepatocyte Research. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2074-7.

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Boros, Peter. Hepatocyte growth factor: The basic principles. Austin: R.G. Landes, 1999.

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10

1924-, Takahashi Naomi, a cura di. Hepatocyte development in rat liver regeneration. [Kanagawa-ken Kawasaki-shi]: Institute of Science and Technology Meiji University, 1993.

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Capitoli di libri sul tema "Hepatocyte"

1

Olsavsky Goyak, Katy M., Elizabeth M. Laurenzana e Curtis J. Omiecinski. "Hepatocyte Differentiation". In Methods in Molecular Biology, 115–38. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-688-7_6.

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Najimi, Mustapha, Françoise Smets e Etienne Sokal. "Hepatocyte Apoptosis". In Methods in Molecular Biology, 59–74. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-201-4_6.

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Mito, Michio, e Masayuki Sawa. "Hepatocyte transplantation". In Yearbook of Cell and Tissue Transplantation 1996–1997, 127–33. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0165-0_12.

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Sirbu-Boeti, Mirela-Patricia, Kyle Soltys, Alejandro Soto-Gutierrez e Ira J. Fox. "Hepatocyte Transplantation". In Molecular Pathology Library, 309–19. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_21.

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Lima-Quaresma, Katia R. F., Andre Gustavo Bonavita, Matheus Kafuri Cytrangulo, Marcelo Alves Pinto e Luiz Anastácio Alves. "Hepatocyte Xenotransplantation". In Xenotransplantation, 245–49. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-845-0_15.

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Kuo, Calvin J., e Gerald R. Grabtree. "Hepatocyte Differentiation". In Development, 479–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77043-2_33.

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Berry, Michael N. "Isolated hepatocytes: forty years on". In The Hepatocyte Review, 1–9. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-3345-8_1.

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Guillouzo, André, Claire Guyomard, Alain Fautrel e Christophe Chesné. "Storage of isolated hepatocytes". In The Hepatocyte Review, 125–45. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-3345-8_10.

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Meijer, Alfred J. "Hepatocyte swelling: techniques and effects on metabolism". In The Hepatocyte Review, 147–67. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-3345-8_11.

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Declercq, Peter E., e Myriam I. Baes. "Permeabilisation of hepatocytes with α-toxin". In The Hepatocyte Review, 169–80. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-3345-8_12.

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Atti di convegni sul tema "Hepatocyte"

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Toner, Mehmet. "Hepatic Tissue Engineering". In ASME 1996 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1996. http://dx.doi.org/10.1115/imece1996-1212.

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Abstract (sommario):
Abstract Each year, approximately 5000 individuals in the United States develop severe enough hepatic failure to require hepatic support. Of these patients, approximately 2000 will undergo orthotopic liver transplantation, currently the only available method for the clinical management of severe hepatic failure. For patients who are not selected for transplantation, there is no adequate treatment available. Those suffering from cirrhosis fight the seventh-leading cause of death in the United States and those suffering from acute liver failure face a mortality of greater than 80%. Although the replacement of liver function using nonbiological, biological, and semibiological or hybrid approaches his been attempted by many investigators, no means for reliable liver replacement, other than organ transplantation, currently exists. One of the most promising approaches for restoring liver function involves the use of cultured hepatocytes that would be part of an extracorporeal device. For a successful extracorporeal device containing stable and functioning hepatocytes, several critical technologies need further development including techniques for (1) long-term hepatocyte culture and methods for reconstructing “in-vivo-like” liver tissue in vitro (2) hepatocyte cryopreservation, and (3) effect of plasma perfusion or in-vivo like fluids on hepatocytes. In this presentation, we will review some of our most recent progress in these three areas. The following is a brief summary.
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Qureshi, G. D., M. Sun, C. Gervin e H. Evans. "RAT HEPAT0CYTES IN CULTURE INACTIVATE FACTOR Xa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643294.

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Plasma contains zymogens of clotting factors, which under various stimuli are activated to serine proteases. Whereas much knowledge has been gained about the activation of clotting factors, relatively little is known about inactivation of these proteases. Antithrombin III has been shown to inactivate some activated clotting factors in plasma. Studies in intact animals have suggested that activated clotting factors are mainly inactivated in the liver. To investigate more fully the role of liver in inactivating the activated factors, we studied the stability of activated factor X(Xa) in hepatocyte cultures. Monolayer cultures on non-proliferating rat hepatocytes were prepared according to the method of Bissell et al. The culture medium was chemically defined and was free from serum or serum products. After the 24 h stabilization period, 0.5 units/ml of 100% activated bovine factor Xa was co-cultured with hepatocytes for 8 h. Samples were collected at 0, ½, 1 2, 4 and 8 h and tested for Xa activity using chromogenic substrate S-2222. At the end of 8 h only 41.07% of the initial Xa activity remained. Xa inactivation was not affected by a commercially prepared unfractionated heparin (1 unit/ml) and estradiol at 12.5, 25, 125 nM, a potentiator and inhibitor of antithrombin III, respectively. Inactivation of Xa in hepatocyte cultures was inhibited by the addition of cycloheximide (10-4M). Our data suggests that factor Xa is inactivated in hepatocyte cultures by one or more hepatic derived factors which do not meet the functional characteristics of antithrombin III.
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Ingerslev, J., B. Sloth Christiansen, A. Bukh, S. Stenbjerg, T. Munck Jørgensen e C. Munck Petersen. "HUMAN HEPATOCYTES CONTAIN HIGH MOLECULAR WEIGHT POLYPEPTIDES OF FACTOR VIII". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644324.

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Human hepatocytes were isolated by the two-step collagenase technique applied on distal left liver lobe. Homogenous and large cells were isolated revealing hepatocyte characteristics by light-microscopy. Hepatocytes were washed repeatedly in albumine buffer (5%), resuspended in the same buffer and sonicated using a cell density of 0.75 × 106 cells/ml. In some cases cells were separated from non-viable cells by flotation on a linear Percoll gradient. Supernate material after sonication was subjected to ELISA for VIII:Ag using human antibodies and vWf:Ag by polyclonal antibodies. Freshly isolated cells contained at least 0.25 IU/ 0.75 × 106 hepatocytes, whereas the vWf:Ag was below 0.01 IU/ 0.75 × 106 cells. The material obtained from sonication was further studied using fast protein liquid chromatography by Mono-Q HR 5/5 revealing a single peak of VIII: Ag eluting in the same position as the high molecular weight polypeptides of VIII :Ag of high purity FVIII derived from the plasma source. Isolated hepatocytes also were cultivated at 37°C in medium RPMI 1640 supplemented with Ultroser G (4%), glutamine and antibiotics. Cells secreted increasing quantities of albumin, fitrinogpn and protease-inhibitors. The supernatants also contained VIII: Ag in quantities ranging from 0.04 - 0.17 IU/ml after 24 hours, but no further secretion was observed. No vWf: Ag could be detected. Cells harvested and sonicated after 30 hours of culture only contained 0.04 IU/ 0.75 × 106 cells. Our results shows, that VIII :Ag is present in freshly isolated human hepatocytes and that only traces of vWf:Ag is found. A hepatocyte site of production of VIII is speculated. These very preliminary findings do not permit conclusions concerning active synthesis of VIII in hepatocytes. Further studies are underway.
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Eggert, S., F. A. Alexander e J. Wiest. "Enabling 3D hepatocyte spheroids for microphysiometry". In 2017 39th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2017. http://dx.doi.org/10.1109/embc.2017.8037148.

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Fowlkes, P. M., P. K. Lund, M. Blake e J. Snouwaert. "THE REGULATION OF FIBRINOGEN PRODUCTION INVOLVES AT LEAST ONE OTHER HEPATOCYTE GENE". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644317.

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It is currently thought that glucocorticosteriods have a direct effect on the transcription of the alpha, beta and gamma fibrinogen genes. However, our studies indicate that while corticosteriods play a role in fibrinogen production, this role is not due to transcriptional activation via glucocorticosteriod receptors. In initial experiments, we compared the levels of fibrinogen mRNA in hepatocytes isolated from hypophysectomized rats to those from control animals. The levels of mRNA in hypophysectomized rats, which produce little ACTH or corticosteriods, were significantly higher than the levels in control animals. Albumin mRNA levels were unaffected by hypophysectomy. These results are in opposition to those which we had anticipated. Based on previously published data, we had thought that physiologic deprivation of corticosteriods would lead to decreased levels of fibrinogen. We propose that these results are related to the negative feedback that corticosteroids have on Hepatocyte Stimulating Factor (HSF) production through a tightly controlled feedback circuit. To investigate the role of corticosteriods in fibrinogen gene regulation, we have conducted experiments with primary hepatocytes in culture and rat FAZA cells (continuous hepatoma cell line). There is a 4 to 5 fold increase in fibrinogen production when these cells are treated with HSF but no change when these cells are treated with dexamethasone alone. However, there is a marked additional increase in the production of fibrinogen with the combination of dexamethasone and HSF. Data gathered through kinetic analysis of this synergistic interaction suggest that the maximum response to HSF requires another gene product whose production is responsive to dexamethasone. Detailed analysis of the rate of transcription of thegamma fibrinogen gene, its processing and mRNA turnover suggests a specific role for this gene product in regulating fibrinogen synthesis. Characterization of this gene product will lead to greater understanding of the regulation of the Acute Phase Reactants.
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Shi, Gengbei, e Robin N. Coger. "Enhanced Oxygen Delivery to Liver Tissue Equivalent by Perfluorocarbon". In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19190.

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Bioartificial Liver Devices (BALs) have the potential to serve as a bridge strategy for patients awaiting liver transplants, and also show promise as drug testing platforms for the pharmaceutical industry [1]. Yet the limitations of O2 transport through the 3D tissue structures of current designs continue to present engineering challenges. In previous work our group successfully improved O2 availability for hepatocytes by introducing micropathways within the BAL’s cellular space [3–5]. The current study investigates the benefits of increasing O2 availability of the flow medium via perfluorocarbons (PFCs). PFCs were chosen since they have demonstrated effectiveness in increasing the overall oxygen solubility of their carrier liquids, e.g., artificial blood [2]. The study seeks to clarify the effects of PFCs on hepatocyte viability and functional performance under various culture conditions.
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Hsu, MJ, M. Hempel, H. Kühne e B. Christ. "Physical contact between mesenchymal stromal cells and hepatocytes via tunneling nanotubes favor the utilization of hepatocyte lipids". In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677163.

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Shirakashi, Ryo, Tomomi Yoshida, Christophe Provin, Kiyoshi Takano, Yasuyuki Sakai e Teruo Fujii. "Steady Measurement of Glucose Metabolism of Hepatocyte". In ASME/JSME 2007 Thermal Engineering Heat Transfer Summer Conference collocated with the ASME 2007 InterPACK Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/ht2007-32750.

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Production of hybrid artificial organs for implantation is one of the main topics of tissue engineering. A large organ consisting of soft tissues requires a high cell density, c.a. 108 cells/mL, to satisfy the same physiological metabolic rate per organ-volume as an organ in vivo. Therefore, the supply of oxygen and nutrition to all the cells composing the soft tissue is always critical problem for the in vitro artificial organ production. Energy metabolic rates, such as oxygen and glucose metabolism rate, of single cell at various temperatures are the basic data for designing the oxygen and nutrition transport in an artificial organ. It is reported that several conditions including pH, temperature, oxygen or glucose concentration have effects on energy metabolism, although these interactions are not clearly quantitatively measured mainly because of the problems of measuring systems. In this study, convenient method to measure glucose consumption rate of hepatocyte (HepG2 cell line) at different temperature and glucose concentration is proposed. A device for the measurement was developed which consists of a small closed chamber with an inlet and an outlet of culture medium at the both ends of the chamber. On the one side of the walls in the chamber, confluent HepG2 on a coverslip was installed. Culture medium supplemented with various concentration of glucose was supplied to the open flow chamber in a constant flow rate. The whole chamber was in a thermostatic bath to keep the temperature in the chamber constant. Glucose consumption rate can be calculated by measuring the difference between glucose concentration of inlet culture medium and outlet culture medium, the flow rate and the number of cells in the chamber. Enzymatic analysis using D-Glucose-HK allows quantification of the sample glucose concentration. The advantages of the proposed method include; 1) small number of cells is required for the measurement, c. a. 105cells, 2) the flow pattern and the glucose supply are in steady state. Especially the latter advantage made it possible to evaluate the effects of different conditions on the glucose consumption rate. Since the most of the metabolic rate were measured under unsteady state, conditions, such as pH, oxygen concentration and glucose concentration, were changed sometime drastically during the measurement. The results provided the several parameters of Michaelis-Menten kinetics at various temperatures.
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Ke, Ling-Yi, Yu-Shih Chen, Jing Liu e Cheng-Hsien Liu. "Cryogenic frozen device for hepatocyte culture and responses". In 2012 7th IEEE International Conference on Nano/Micro Engineered and Molecular Systems (NEMS). IEEE, 2012. http://dx.doi.org/10.1109/nems.2012.6196745.

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Shafigullina, Zlata, e Irina Danilova. "Immunological Regulation of Hepatocyte Apoptosis During Toxic Damage". In 2020 Ural Symposium on Biomedical Engineering, Radioelectronics and Information Technology (USBEREIT). IEEE, 2020. http://dx.doi.org/10.1109/usbereit48449.2020.9117693.

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Rapporti di organizzazioni sul tema "Hepatocyte"

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, marzo 2005. http://dx.doi.org/10.21236/ada435856.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, marzo 2004. http://dx.doi.org/10.21236/ada428439.

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Knudesen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, marzo 2003. http://dx.doi.org/10.21236/ada416620.

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Knudsen, Beatrice S. Hepatocyte Growth Factor and Interleukin-6 in Prostate Cancer Bone Metastasis. Fort Belvoir, VA: Defense Technical Information Center, giugno 2006. http://dx.doi.org/10.21236/ada467982.

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Naseem, Syed M., K. A. Mereish, Rikki Solow e Harry Hines. Toxin-Induced Activation of Rat Hepatocyte Prostaglandin Synthesis and Phospholipid Metabolism. Fort Belvoir, VA: Defense Technical Information Center, aprile 1990. http://dx.doi.org/10.21236/ada221157.

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Siegfried, Jill. Targeting the Hepatocyte Growth Factor Pathway for the Treatment of Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, settembre 1999. http://dx.doi.org/10.21236/ada383623.

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Ross, Bernard A. Adjuvant Action of Hepatocyte Growth Factor in Vitamin D Therapy of Androgen-Unresponsive Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, dicembre 2001. http://dx.doi.org/10.21236/ada401687.

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Lee, Young H. Mechanism of Hepatocyte Growth Factor Inhibition of Angiotensin II-induced Apoptosis in Primary Lung Cells. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2010. http://dx.doi.org/10.21236/ad1013415.

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Mirosevich, Janni. Investigating the Role of Hepatocyte Nuclear Factor-3 (HNF-3) Alpha and Beta in Prostate Cancer and Cellular Differentiation. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2006. http://dx.doi.org/10.21236/ada455964.

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Mirosevich, Janni. Investigating the Role of Hepatocyte Nuclear Factor-3 (HNF-3) Alpha and Beta in Prostate Cancer and Cellular Differentiation. Fort Belvoir, VA: Defense Technical Information Center, gennaio 2005. http://dx.doi.org/10.21236/ada431320.

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