• 정보처리학회논문지B
• /
• 제18B권6호
• /
• pp.389-396
• /
• 2011

현대 사회에서 식습관의 변화, 스트레스, 음주 등으로 인해 다양한 간 질환이 발생되거나 악화되어 가고 있다. 따라서 본 논문에서는 간 질환이 음성에 미치는 영향을 연구하여 간 질환을 조기에 진단할 수 있는 방법론을 제안하였다. 이를 위해 간 질환자를 대상으로 입원했을 때와 치료로 인해 정상적으로 퇴원했을 때의 음성을 각각 수집하여 음성 분석 요소를 적용한 실험을 수행하였다. 특히, 한의학적으로 간(肝)과 관련 있는 발음인 아음(牙音)에 대한 분석 실험으로 제3포먼트 주파수 대역폭과 발음 요소값을 적용한 실험을 수행하였으며 이를 통해 간 질환이 공명강과 발성에 미치는 영향을 객관적 지표로 출력하는 연구를 행하였다. 또한 실험 결과를 기반으로 u-Health 환경에서 간 기능을 모니터링하는 시스템 설계에 관한 연구를 수행하였다.

• Genomics & Informatics
• /
• 제21권4호
• /
• pp.45.1-45.11
• /
• 2023

Nonalcoholic fatty liver disease (NAFLD) is a common type of chronic liver disease, with severity levels ranging from nonalcoholic fatty liver to nonalcoholic steatohepatitis (NASH). The extent of liver fibrosis indicates the severity of NASH and the risk of liver cancer. However, the mechanism underlying NASH development, which is important for early screening and intervention, remains unclear. Weighted gene co-expression network analysis (WGCNA) is a useful method for identifying hub genes and screening specific targets for diseases. In this study, we utilized an mRNA dataset of the liver tissues of patients with NASH and conducted WGCNA for various stages of liver fibrosis. Subsequently, we employed two additional mRNA datasets for validation purposes. Gene set enrichment analysis (GSEA) was conducted to analyze gene function enrichment. Through WGCNA and subsequent analyses, complemented by validation using two additional datasets, we identified five genes (BICC1, C7, EFEMP1, LUM, and STMN2) as hub genes. GSEA analysis indicated that gene sets associated with liver metabolism and cholesterol homeostasis were uniformly downregulated. BICC1, C7, EFEMP1, LUM, and STMN2 were identified as hub genes of NASH, and were all related to liver metabolism, NAFLD, NASH, and related diseases. These hub genes might serve as potential targets for the early screening and treatment of NASH.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• 제24권2호
• /
• pp.119-126
• /
• 2021

The aim of our paper was to present current knowledge, review literature and available practice guidelines of international hepatological associations regarding the effect of severe acute respiratory syndrome coronavirus 2 coronavirus on the liver, patients with underline liver disease, awaiting on liver transplantation (LTx) or being after LTx in the pandemic coronavirus disease 2019 area.

• Journal of Ginseng Research
• /
• 제48권2호
• /
• pp.122-128
• /
• 2024

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease characterized by hepatic fat accumulation, while nonalcoholic steatohepatitis (NASH) is an advanced form of NAFLD characterized by hepatic inflammation, fibrosis, and liver injury, resulting in liver cirrhosis and hepatocellular carcinoma (HCC). Given the evidence that ginseng and its major bioactive components, ginsenosides, have potent anti-adipogenic, anti-inflammatory, anti-oxidative, and anti-fibrogenic effects, the pharmacological effect of ginseng and ginsenosides on NAFLD and NASH is noteworthy. Furthermore, numerous studies have successfully demonstrated the protective effect of ginseng on these diseases, as well as the underlying mechanisms in animal disease models and cells, such as hepatocytes and macrophages. This review discusses recent studies that explore the pharmacological roles of ginseng and ginsenosides in NAFLD and NASH and highlights their potential as agents to prevent and treat NAFLD, NASH, and liver diseases caused by hepatic steatosis and inflammation.

• 생명과학회지
• /
• 제21권12호
• /
• pp.1795-1803
• /
• 2011

현대인의 고지방 식습관과 당뇨와 비만인구 증가로 인한 비 알코올성 지방간(nonalcoholic fatty liver)의 유병률(prevalence rate)은 나날이 증가하고 있는 추세이며, 특히 남성과 폐경기 여성에게서 두드러진다. 이런 성 특이적(sex-specific) 간질환의 차이는 여성 호르몬인 에스트로겐(estrogen)의 보호 역할 때문일 것으로 추정되고 있으나, 에스트로겐의 보호 기작을 포함한 지방간의 만성 간질환으로의 진행 메커니즘이 규명되어 있지 않기 때문에 간질환의 효과적인 예방 및 치료책이 없는 실정이다. 그런데 최근에 간 섬유화(fibrosis)를 포함한 만성 간질환의 진행에서 헤지호그(hedgehog) 신호전달계가 주요한 역할을 함이 보고되면서 손상된 간의 회복과 간질환 진행메커니즘 조절을 위한 연구대상으로서 주목 받고 있다. 헤지호그는 발생 및 분화를 조절하는 모포젠(morphogen)으로 성인의 건강한 간에서는 발현되지 않으나, 손상된 간에서 손상 정도에 비례하게 재 발현되며, 섬유화 유발세포인 근섬유아세포(myofibroblasts) 및 간 줄기세포(hepatic progenitor cells)의 활성 및 증식인자로 작용하여 지나친 간 섬유화를 일으킨다. 이에 반해, 에스트로겐은 간 성상세포(hepatic stellate cells)가 근섬유아세포로 활성화되는 것을 억제함으로써 간 섬유화를 막는 것으로 보고되고 있다. 간 섬유화에 대한 헤지호그와 에스트로겐의 상반된 역할 사이의 관련성은 아직 밝혀지지 않고 있으나, 간 섬유화 유발 물질인 오스테오폰틴(osteopontin) 발현에 대한 에스트로겐의 억제효과와 헤지호그에 의한 오스테오폰틴 발현 유도는 오스테오폰틴에 의해 매개되는 에스트로겐과 헤지호그 신호전달계 사이의 연관성을 시사한다. 따라서, 에스트로겐에 의한 헤지호그 신호전달계 조절 메커니즘을 규명하는 것은 간질환 환자에서의 간 섬유화 및 만성 질환으로의 진행을 억제할 수 있는 치료제 개발에 대한 기초 지식을 제공할 수 있다. 이를 위해 간 섬유화에 대한 헤지호그와 에스트로겐의 역할을 확실하게 이해하고, 상호 관련성 및 조절 기작을 밝히는 연구가 선행되어야 할 것이다.

• Journal of Yeungnam Medical Science
• /
• 제2권1호
• /
• pp.167-174
• /
• 1985

1985년 5월부터 1985년 11월까지 영남대학병원 내과에 입원한 간질환 환자 255예를 대상으로 간질환에 동반된 피부 증상을 관찰하여 다음과 같은 결론을 얻었다. 1. 255예중 161예 (63%)에서 피부증상을 동반하였다. 2. 피부증상은 황달 및 소양증 (43.1%), 혈관의 변화 (39.6%), 알레르기성 변화 (10.6%), 조갑변화 (5.1%), 호르몬에 의한 변화 (4.3%), 색소변화 (3.5%), 기타 (2.4%)의 순으로 많았다. 3. 피부증상을 상기 7개 군으로 분류할때 간경화증에서 가장 않은 피부 증상을 동안 하였고 (1.6군), 만성 활동성 간염(0.7군)과 급성 바이러스성 간염 (0.8군)에서 적었다. 4. 알레르기성 변화는 주로 급성 바이러스성 간염(AVH) 환자에 서 나타났고, serum sickness-like prodrome의 증상은 3예였다. 5. 혈관의 변화, 조갑의 변화, 호르몬에 의한 변화, 색소 변화 등은 주로 만성 간질환에서 관찰 되었다.

• Parasites, Hosts and Diseases
• /
• 제62권1호
• /
• pp.30-41
• /
• 2024

The dense granule protein of Toxoplasma gondii, inhibitor of signal transducer and activator of transcription 1 (IST) is an inhibitor of signal transducer and activator of transcription 1 (STAT1) transcriptional activity that binds to STAT1 and regulates the expression of inflammatory molecules in host cells. A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-γ and TNF-α, is activated without infection. In relation to inflammatory liver injury, we hypothesized that Toxoplasma gondii inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1/IRF-1 mechanism in liver inflammation. This study used IFN-γ and TNF-α as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1/IRF-1 axis. In stable cells transfected with TgIST, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-κB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9/10/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3/8/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-γ/TNF-α stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.

• Biomolecules & Therapeutics
• /
• 제30권5호
• /
• pp.391-398
• /
• 2022

Polyploidization is a process by which cells are induced to possess more than two sets of chromosomes. Although polyploidization is not frequent in mammals, it is closely associated with development and differentiation of specific tissues and organs. The liver is one of the mammalian organs that displays ploidy dynamics in physiological homeostasis during its development. The ratio of polyploid hepatocytes increases significantly in response to hepatic injury from aging, viral infection, iron overload, surgical resection, or metabolic overload, such as that from non-alcoholic fatty liver diseases (NAFLDs). One of the unique features of NAFLD is the marked heterogeneity of hepatocyte nuclear size, which is strongly associated with an adverse liver-related outcome, such as hepatocellular carcinoma, liver transplantation, and liver-related death. Thus, hepatic polyploidization has been suggested as a potential driver in the progression of NAFLDs that are involved in the control of the multiple pathogenicity of the diseases. However, the importance of polyploidy in diverse pathophysiological contexts remains elusive. Recently, several studies reported successful improvement of symptoms of NAFLDs by reducing pathological polyploidy or by controlling cell cycle progression in animal models, suggesting that better understanding the mechanisms of pathological hepatic polyploidy may provide insights into the treatment of hepatic disorders.

• Journal of Ginseng Research
• /
• 제35권1호
• /
• pp.69-79
• /
• 2011

Hepatocellular carcinoma (HCC) is the fi fth most common malignancy in the world and complicates liver cirrhosis related to hepatitis C virus (HCV) in many cases. We evaluated the therapeutic effect of Korean red ginseng extract (KGE) in patients with chronic liver diseases. Thirty male and female patients with HCC and another thirty with liver cirrhosis were included. Each category was divided into two groups; the first was used as control group, and received medical therapy only and the second group received the medical therapy supplemented with KGE capsules. The treated group with HCC received three KGE capsules/day (900 mg) while the treated group with HCV received two KGE capsules/day (600 mg) for 11 weeks along with their medical therapy. All patients were subjected to clinical examination and laboratory investigations, including liver function tests (at baseline, after 6 weeks of treatment and at the end of the study) and abdominal ultrasonography. Patients showing focal hepatic lesions were subjected to triphasic spiral abdominal computerized tomography and alpha-fetoprotein (AFP). HCV RNA was determined quantitatively by Roche for patients in the HCV group. Results showed that the medical therapy alone failed to normalize the liver enzymes or decrease the virus concentration. KGE administration induced a significant improvement in liver function tests, decreased the tumor marker (AFP) levels, and decreased the viral titers in HCV patients. Thus, KGE demonstrated powerful therapeutic effects against HCV and liver cancer.

• Toxicological Research
• /
• 제30권4호
• /
• pp.243-250
• /
• 2014

Mitochondrial integrity is critical for maintaining proper cellular functions. A key aspect of regulating mitochondrial homeostasis is removing damaged mitochondria through autophagy, a process called mitophagy. Autophagy dysfunction in various disease states can inactivate mitophagy and cause cell death, and defects in mitophagy are becoming increasingly recognized in a wide range of diseases from liver injuries to neurodegenerative diseases. Here we highlight our current knowledge on the mechanisms of mitophagy, and discuss how alterations in mitophagy contribute to disease pathogenesis. We also discuss mitochondrial dynamics and potential interactions between mitochondrial fusion, fission and mitophagy.