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Association of the Cellular Apoptosis Susceptibility Protein with HBV Infection in Hepatocellular Carcinoma

proliferation and apoptosis associated CSE1L/CAS gene in hepatitis and liver neoplasms: correlation with tumor progression. Int J Mol Med 2001;7(5):489-494. 5. Scherf U, Pastan I, Willingham MC, Brinkmann U. The human CAS protein which is homologous to the CSE1 yeast chromosome segregation gene product is associated with microtubules and mitotic spindle. Proc Natl Acad Sci USA 1996; 93(7):2670-2674. 6. Brinkmann U, Brinkmann E, Gallo M, Pastan I. Cloning and characterization of a cellular apoptosis susceptibility gene, the human homologue to

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The mechanism of HBx protein to promote the initiation and progression of hepatocellular carcinoma

transformation process, HBx promoted the expression of AFP in hepatocytes. The AFP then stimulated the expression of some protooncogenes in hepatocytes by activating the phosphatidylinositol-3 kinase (PI3K)/protein kinase -A (AKT) signaling pathway. Subsequently, intracellular apoptosis signals were inhibited and growth signals were activated, resulting in the survival of the HBV-infected hepatocytes in the body [ 9 ]. In addition, the HBx-induced overexpression of AFP in hepatocytes can stimulate the body to produce inflammatory cytokines, especially interleukin-6 (IL-6

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Different Effects of Plasma from Patients with Acute on Chronic Liver Failure on the Proliferation and Biotransformation Function of C3A Cells


Objective To investigate the effects of plasma from patients with acute on chronic liver failure on the proliferation and biotransformation function of C3A cells in vitro, and provide experimental data for C3A cells to be efficiently used in the bioartificial liver system.

Methods C3A cells were incubated in 100% normal human plasma (NHP) and 100% abnormal plasma (AP) from patients with acute on chronic liver failure. Growth morphology of the two groups were observed under inverted microscope and scanning electron microscope. The method of methyl thiazolyl tetrazolium (MTT) was conducted for the proliferation activities of C3A cells. The cellular apoptosis rates were assessed by the flow cytometer. The biotransformation function of cells was evaluated through diazepam metabolic amount assay. The concentrations of epithelial growth factor (EGF), transforming growth factor-α (TGF-α) and interleukin-1 (IL-1) were detected in plasma of the two groups.

Results A: The proliferation activities of C3A cells incubated in 100% AP for 24, 48, 72, 96 and 120 hours were significantly higher than that in 100% NHP (P < 0.01). B: Observation under the inverted microscope indicated that the cells in 100% AP were growing faster than those in 100% NHP after cells attached to the plastic at 24 and 48 hours. The same phenomena was observed under the scanning electronic microscope. C: The C3A cells cultured in both groups of plasma showed the same apoptosis rate at 48 hours and there was no statistical difference. D: The diazepam metabolic value of C3A cells incubated in 100% AP for 24, 72 and 120 hours were lower than that in 100% NHP and were statistically different (P < 0.01). E: The concentrations of TGF-α, EGF and IL-1 in AP were significantly higher than that in NHP (P < 0.01).

Conclusions Compared with normal human plasma, the plasma from patients with acute on chronic liver failure has more obvious effect to facilitate the proliferation of C3A cells, but also decreases partial biotransformation function of C3A cells.

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NADPH promotes the rapid growth of the tumor

normal cell metabolism process and has different effects on cells according to its concentration. Low levels of ROS can promote cell proliferation and survival, while high levels of ROS can damage biological macromolecules, induce cell senescence and apoptosis [ 4 ] and cause harmful oxidative stress, leading to cell death. Cells producing antioxidant molecules, such as NADPH, can reduce the level of ROS to offset the negative impact of it [ 5 ]. The antioxidant systems rely on the reduction of NADPH to urge regeneration of antioxidant activity. NADPH not only can act

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Research progress on immune response of B lymphocytes and anti-Mycobacterium tuberculosis infection

. Circulating antibodies to lipoarabinomannan in relation to sputum microscopy, clinical features and urinary anti-lipoarabinomannan detection in pulmonary tuberculosis. Scand J Infect Dis, 2002, 34(2):97-103. 5 Dubaniewicz A, Trzonkowski P, Dubaniewicz-Wybieralska M, et al . Comparative analysis of mycobacterial heat shock proteins-induced apoptosis of peripheral blood mononuclear cells in sarcoidosis and tuberculosis. Clin Immunol, 2006, 26(3):243-50. 6 Maglione PJ, Xu J, Casadevall A, et al . Fc gamma receptors regulate immune activation and susceptibility

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Editorial. The Role of Autophagy in Hepatitis C Virus Infection

viral countermeasures. Biochim Biophys 2009;1793:1478-1484. 6 Feldstein A, Kleiner D, Kravetz D, Buck M. Severe hepatocellular injury with apoptosis induced by a hepatitis C polymerase inhibitor. J Clin Gastroenterol 2009;43:374-381. 7 Dreux M, Chisari FV. Impact of the autophagy machinery on hepatitis C virus infection. Viruses 2011;3:1342-1357. 8 Sir D, Ann DK, Ou JH. Autophagy by hepatitis B virus and for hepatitis B virus. Autophagy 2010;6:4383-4388. 9 Coller KE, Berger KL, Heaton NS, Cooper JD, Yoon

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Effects of Interleukin-18 and Anti-interleukin- 18-mAb on Experimental Immunological Liver Fibrosis Induced by Repeatedly Administered Concanavalin A and Its Mechanism

, Yoon JH, Lee YJ, Yang JI, Kwak MS, Cho EJ, et al. Mesalamine-induced B7-H1 expression on hepatic stellate cells attenuates autoimmune liver injury. Hepatol Res 2011;41(1):79-86. 16. Fujino M, Kawasaki M, Funeshima N, Kitazawa Y, Kosuga M, Okabe K, et al. CrmA gene expression protects mice against concanavalin-A-induced hepatitis by inhibiting IL-18 secretion and hepatocyte apoptosis. Gene Ther 2003;10(20):1781-1790. 17. Ishiwata Y, Yokochi S, Hashimoto H, Ninomiya F, Suzuki T. Protection against concanavalin A-induced murine liver

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The Pathogenesis of Acute on Chronic Hepatitis B Liver Failure

circulating CD4+ CD25+ regulatory T cells (Tregs) in patients with acute-on-chronic liver failure (ACLF). J Tansl Med 2012; 10:193. 4. Schurich A, Khanna P, Lopes AR, Han KJ, Peppa D, Micco L, et al. Roleof the coinhibitory recepyor cytotoxic T lymphocyte antigen-4 on apoptosis-prone CD8+ T in persistent hepatitis B virus infection. Hepatology 2011; 53:1494-1503. 5. Wu W, Shi Y, Li S, Zhang Y, Liu Y, Wu Y, et al. Blockade of Tim-3 signaling restores the virus-specific CD8+ T-cell response in patients with chronic hepatitios B. Eur J Immunol

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The function of HBx in HBV-induced hepatocellular carcinoma

activion 5 , 6 , 7 , 8 , 9 , 10 , 11 , epigenetic regulation 12 , 13 , 14 , apoptosis regulation 15 , DNA repair regulation 16 , 17 , 18 and so on. 2 Correlation between HBx and hepatocellular carcinoma HBx often restructured in the host cell genome 19 . In recent years, more and more significant advancement in the molecular mechanisms about the role of in HCC. Continuous replication in the host is an important process of HCC. In the process of chronic liver disease, the regeneration of infected hepatocytes leads to the integration of HBx into the host gene. It is

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Review of Research on the Prevention of HPV Infection and Cervical Cancer

References 1 Denny L. Cervical cancer prevention: new opportunities for primary and secondary prevention in the 21st century. Int J Gynecol Obstet, 2012, 119(Suppl 1): 80-84. 2 Alam MS, Ali A, Mehdi SJ, et al . HPV typing and its relation with apoptosis in cervical carcinoma from Indian population. Tumour Biol, 2012, 33(1): 17-22. 3 Koliopoulos G, Valasoulis G, Zilakou E. An update review on HPV testing methods for cervical neoplasia. Expert Opinion on Medical Diagnostics, 2009, 3(2): 123-131. 4 Halfon P, Benmoura D, Khiri H, et al

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