scholarly journals Effects of primary suture and fibrin sealant on hemostasis and liver regeneration in an experimental liver injury

2008 ◽  
Vol 14 (1) ◽  
pp. 81 ◽  
Author(s):  
Arif Hakan Demirel ◽  
Ozgur Taylan Basar ◽  
Ali Ulvi Ongoren ◽  
Erkut Bayram ◽  
Mustafa Kisakurek
2003 ◽  
Vol 164 (1) ◽  
pp. 57-63 ◽  
Author(s):  
María C. Tovar ◽  
Miguel A. Sanchez-Valverde ◽  
Amalia Agut ◽  
Francisco G. Laredo ◽  
José Murciano

Kanzo ◽  
1974 ◽  
Vol 15 (8) ◽  
pp. 463-471
Author(s):  
Setsuro FUJII ◽  
Hiromichi OKUDA

1976 ◽  
Vol 71 (1) ◽  
pp. 118-122 ◽  
Author(s):  
Yasuyuki Arakawa ◽  
David M. Bull ◽  
Chester F. Schott ◽  
Charles S. Davidson

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Bernat Córdoba-Jover ◽  
Altamira Arce-Cerezo ◽  
Jordi Ribera ◽  
Montse Pauta ◽  
Denise Oró ◽  
...  

Abstract Background and aims Cerium oxide nanoparticles are effective scavengers of reactive oxygen species and have been proposed as a treatment for oxidative stress-related diseases. Consequently, we aimed to investigate the effect of these nanoparticles on hepatic regeneration after liver injury by partial hepatectomy and acetaminophen overdose. Methods All the in vitro experiments were performed in HepG2 cells. For the acetaminophen and partial hepatectomy experimental models, male Wistar rats were divided into three groups: (1) nanoparticles group, which received 0.1 mg/kg cerium nanoparticles i.v. twice a week for 2 weeks before 1 g/kg acetaminophen treatment, (2) N-acetyl-cysteine group, which received 300 mg/kg of N-acetyl-cysteine i.p. 1 h after APAP treatment and (3) partial hepatectomy group, which received the same nanoparticles treatment before partial hepatectomy. Each group was matched with vehicle-controlled rats. Results In the partial hepatectomy model, rats treated with cerium oxide nanoparticles showed a significant increase in liver regeneration, compared with control rats. In the acetaminophen experimental model, nanoparticles and N-acetyl-cysteine treatments decreased early liver damage in hepatic tissue. However, only the effect of cerium oxide nanoparticles was associated with a significant increment in hepatocellular proliferation. This treatment also reduced stress markers and increased cell cycle progression in hepatocytes and the activation of the transcription factor NF-κB in vitro and in vivo. Conclusions Our results demonstrate that the nanomaterial cerium oxide, besides their known antioxidant capacities, can enhance hepatocellular proliferation in experimental models of liver regeneration and drug-induced hepatotoxicity.


1990 ◽  
Vol 110 (8) ◽  
pp. 604-611 ◽  
Author(s):  
Yujiro NIIHO ◽  
Takashi YAMAZAKI ◽  
Yoshijiro NAKAJIMA ◽  
Hiroshi ITOH ◽  
Takashi TAKESHITA ◽  
...  

2007 ◽  
Vol 40 (4) ◽  
pp. 191-197 ◽  
Author(s):  
Hiroyuki Yoneyama ◽  
Yoshiro Kai ◽  
Jun Koyama ◽  
Kenji Suzuki ◽  
Hiroshi Kawachi ◽  
...  

Author(s):  
Tetsuo Takehara ◽  
Naoki Mizutani ◽  
Hayato Hikita ◽  
Yoshinobu Saito ◽  
Yuta Myojin ◽  
...  

Grb2-associated binder 1 (Gab1) is an adaptor protein that is important for intracellular signal transduction by receptor tyrosine kinases that are receptors for various growth factors and plays an important role in rapid liver regeneration after partial hepatectomy and during acute hepatitis. On the other hand, mild liver regeneration is induced in livers of individuals with chronic hepatitis, where hepatocyte apoptosis is persistent; however, the impact of Gab1 on such livers remains unclear. We examined the role of Gab1 in chronic hepatitis. Gab1 knockdown enhanced the decrease in cell viability and apoptosis induced by ABT-737, a Bcl-2/-xL/-w inhibitor, in BNL.CL2 cells, while cell viability and caspase activity were unchanged in the absence of ABT-737. ABT-737 treatment induced Gab1 cleavage to form p35-Gab1. p35-Gab1 was also detected in the livers of mice with hepatocyte-specific Mcl-1 knockout (KO), which causes persistent hepatocyte apoptosis. Gab1 deficiency exacerbated hepatocyte apoptosis in Mcl-1 KO mice with posttranscriptional downregulation of Bcl-XL. In BNL.CL2 cells treated with ABT-737, Gab1 knockdown posttranscriptionally suppressed Bcl-xL expression, and p35-Gab1 overexpression enhanced Bcl-xL expression. Gab1 deficiency in Mcl-1 KO mice activated STAT3 signaling in hepatocytes, increased hepatocyte proliferation, and increased the incidence of liver cancer with the exacerbation of liver fibrosis. In conclusion, Gab1 is cleaved in the presence of apoptotic stimuli and forms p35-Gab1 in hepatocytes. In chronic liver injury, the role of Gab1 in suppressing apoptosis and reducing liver damage, fibrosis, and tumorigenesis is more important than its role in liver regeneration.


2018 ◽  
Vol 9 ◽  
Author(s):  
Bu-Gao Zhou ◽  
Hai-Mei Zhao ◽  
Xiu-Yun Lu ◽  
Wen Zhou ◽  
Fu-Chun Liu ◽  
...  

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