Percutaneous injection of a low-concentration alkaline solution targeting hepatocellular carcinoma.

Tamai, Tsutomu; Seki, Takaomi; Imamura, M; Nakagawa, Tomoe; Wakabayashi, Masayuki; Nishimura, Akira; Yamashiki, Noriyo; Shiro, Tomohiro; Inoue, Kazuko; Okamura, Atsushi; Harada, K

doi:10.3892/or.7.4.719

Cited by 5 publications

(4 citation statements)

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“…Hepatitis C patients who drink alcohol typically show a pattern of hepatic injury that is more characteristic of chronic viral hepatitis than alcohol-induced injury, suggesting that alcohol enhances the pathogenic effects of HCV rather than exerting its independent effects on liver (6). Several clinical studies have correlated increased serum and intrahepatic HCV titer with the amount of alcohol consumed (2,4,5).…”

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confidence: 99%

Ethanol Enhances Hepatitis C Virus Replication through Lipid Metabolism and Elevated NADH/NAD+

Seronello

Ito

Wakita

et al. 2010

Journal of Biological Chemistry

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Ethanol has been suggested to elevate HCV titer in patients and to increase HCV RNA in replicon cells, suggesting that HCV replication is increased in the presence and absence of the complete viral replication cycle, but the mechanisms remain unclear. In this study, we use Huh7 human hepatoma cells that naturally express comparable levels of CYP2E1 as human liver to demonstrate that ethanol, at subtoxic and physiologically relevant concentrations, enhances complete HCV replication. The viral RNA genome replication is affected for both genotypes 2a and 1b. Acetaldehyde, a major product of ethanol metabolism, likewise enhances HCV replication at physiological concentrations. Ethanol consumption is a well-known risk factor for chronic liver diseases. Ethanol is also a key cofactor in the pathogenesis induced by hepatitis C virus (HCV), 2 and it decreases the efficacy of anti-HCV treatments (1, 2). Likewise, HCV infection exacerbates liver damage caused by prolonged alcohol abuse (2). It has also been reported that patients with a history of alcohol abuse are more likely to be infected with HCV than the rest of the population (1). In addition, ethanol has been suggested to exacerbate HCVinduced liver diseases in part by affecting the viral titer (2-5). Hepatitis C patients who drink alcohol typically show a pattern of hepatic injury that is more characteristic of chronic viral hepatitis than alcohol-induced injury, suggesting that alcohol enhances the pathogenic effects of HCV rather than exerting its independent effects on liver (6). Several clinical studies have correlated increased serum and intrahepatic HCV titer with the amount of alcohol consumed (2, 4, 5). Abstinence or moderation of alcohol consumption could reduce the HCV titer in some patients (2, 5). Furthermore, in vitro studies suggest that ethanol increases HCV RNA levels in Huh7 human hepatoma replicon cell lines that continuously support the HCV RNA replication without virus production (3,7,8). These studies suggest that ethanol enhances HCV replication both in the presence and absence of the complete viral replication cycle. HCV replicon systems and more recent virus-producing cell culture models have increased our understanding of HCV and provide us with tools for studying potential interactions between HCV and pathological cofactors, such as ethanol (9).Nevertheless, whether ethanol directly enhances HCV production in the context of the complete viral replication cycle has not been demonstrated. Furthermore, the mechanism by which ethanol modulates HCV RNA replication remains controversial as reactive oxygen species (ROS) and lipid peroxidation products, which can be generated during ethanol metabolism, can suppress, rather than increase, HCV RNA replication in cells, suggesting the involvement of other metabolites of ethanol (10 -14). Oxidative hepatic ethanol metabolism is a multistep process (4). Alcohol dehydrogenase, the predominant ethanol-metabolizing enzyme, is found in the cytosol and produces acetaldehyde and NADH. Ethanol-inducible cyto...

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confidence: 99%

Ethanol Enhances Hepatitis C Virus Replication through Lipid Metabolism and Elevated NADH/NAD+

Seronello

Ito

Wakita

et al. 2010

Journal of Biological Chemistry

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“…Other fluids are being investigated, such as alkaline solutions 184 and acetic acid. Acetic acid has a higher penetrating power than ethanol, resulting in a more homogeneous diffusion.…”

Section: Other Injection Therapiesmentioning

confidence: 99%

Interstitial ablative techniques for hepatic tumours

Erce

Parks

2003

British Journal of Surgery

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“…11) Sodium hydroxide has also been used in multiple studies of animal models. 12,13) In this study, the sodium hydroxide pinpoint pressing permeation (SHPPP) method was used to construct an SSS damage model in rats. The success rate, heart rate (HR), and electrophysiology index of sinus node were determined and recorded and then compared with the FPPP method and traditional thoracotomy method.…”

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confidence: 99%

Sodium Hydroxide Pinpoint Pressing Permeation Method for the Animal Modeling of Sick Sinus Syndrome

et al. 2015

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Sodium hydroxide pinpoint pressing permeation (SHPPP) was investigated in order to build a rat model of sick sinus syndrome (SSS), which is easy to operate and control the degree of damage, with fewer complications and applicable for large and small animals.Thirty healthy Wistar rats (15 males and 15 females, weighing 250-350 g) were randomly divided into 3 groups, namely a formaldehyde thoracotomy wet compressing group (FTWC), formaldehyde pinpoint pressing permeation group (FPPP) group, and SHPPP group. The number of surviving rats, heart rate (HR), sinoatrial node recovery time (SNRT), corrected SNRT (CSNRT), and sinoatrial conduction time (SACT) were recorded 3 days, one week, and two weeks after modeling.The achievement ratio of modeling was 10% in the FTWC group, 40% in the FPPP group, and 70% in the SHPPP group, and the differences were statistically significant (χ(2) = 7.250, P = 0.007). Meanwhile, the HR was reduced by about 37% in these 3 groups 3 days after modeling, while the reduction was maintained only in SHPPP (P > 0.05) and the HR was re-elevated in the FTWC and FPPP groups 2 weeks after modeling (P < 0.05). Additionally, the SNRT, cS-NRT, and SACT were significantly prolonged compared with pre-modeling in all 3 groups (P < 0.01).SHPPP was the best method with which to build an SSS model with stable and lasting low HR and high success rate of modeling, which might be helpful for further studies on the SSS mechanisms and drugs.

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Percutaneous injection of a low-concentration alkaline solution targeting hepatocellular carcinoma.

Cited by 5 publications

References 0 publications

Ethanol Enhances Hepatitis C Virus Replication through Lipid Metabolism and Elevated NADH/NAD+

Ethanol Enhances Hepatitis C Virus Replication through Lipid Metabolism and Elevated NADH/NAD+

Interstitial ablative techniques for hepatic tumours

Sodium Hydroxide Pinpoint Pressing Permeation Method for the Animal Modeling of Sick Sinus Syndrome

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