Mitochondrial protein UCP1 mediates liver injury induced by LPS through EKR signaling pathway.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Mitochondrial protein UCP1 mediates liver injury induced by LPS through EKR signaling pathway, by P. Liu, J. Yang, Z.-Y. Chen, P. Zhang, G.-J. Shi, published in Eur Rev Med Pharmacol Sci 2017; 21 (16): 3674-3679-PMID: 28925474" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13284.

[A restricted view on the identification of litigation cases of traditional Chinese medicine in the Republic of China: a case study of Yan Yulin].

Medical appraisal is one of the important means to determine whether there are faults in medical behavior and to deal with medical disputes. The issue of whether the medical lawsuit of traditional Chinese medicine should be submitted to traditional Chinese medicine, western medicine or forensic identification began to be debated since the Republic of China. With the efforts of the traditional Chinese medicine community, the Prescription Appraisal Committee of the National Medical Center of the Republic of China was established, which obtained the peer appraisal right for the lawsuit of traditional Chinese medicine. This paper takes the case of Yan Yulin's negligence causing death, which was sent by Shandong High Court to the National Medical Center in 1937, as an example, to explore the general situation of the identification system of the traditional Chinese medicine litigation in the period of the Republic of China, in order to provide reference for the establishment of the judicial identification system of medical damage in traditional Chinese medicine.

[The establishment and influence of the Prescription Appraisal Committee of the Central National Physician Pavilion].

The Prescription Appraisal Committee of the Central National Physician Pavilion was established on November 8, 1935. It specializes in handling cases where the parties entrusted by the Court have applied for re-identification against the identification of the local Chinese Medicine branch or medical group.The statutes of the Prescription Appraisal Committee stipulate the entrusted appraisers, the scope of appraisal, the appraisers, the appraisal process, and the signing and service of the appraisal opinions for the re-identification of TCM cases. To a certain extent, it played a role in improving the medical service environment of Chinese medicine at that time, safeguarding the common interests of doctors and patients, and promoting the institutionalized development of appraisal of Chinese medicine lawsuits in the Republic of China. However, due to historical reasons and limitations, it also had inherent limitations such as the uneven geographical distribution of appraisal candidates, the lack of strict identification procedures, and the inconsistency of appraisal standards.

LncRNA H19 promotes the development of hepatitis B related hepatocellular carcinoma through regulating microRNA-22 via EMT pathway.

OBJECTIVE: To explore the relationship between long non-coding RNA (lncRNA) H19 expression and prognosis of hepatitis B-related hepatocellular carcinoma (HBV-related HCC), and its underlying mechanism. PATIENTS AND METHODS: Expression level of lncRNA H19 in 36 HBV-related HCC tissues and para-cancerous tissues was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The relationship between lncRNA H19 expression and prognosis of HBV-related HCC was analyzed by Kaplan-Meier method. Serum DNA levels of HBV were detected by fluorescence quantitative polymerase chain reaction (FQ-PCR). For in vitro experiments, lncRNA H19 expression in HCC cell line, HBV-related HCC cell line and normal liver cell line was detected by qRT-PCR. After plasmids construction, the effects of lncRNA H19 on cell viability, migration, and invasion were detected by cell counting kit-8 (CCK-8), colony formation and transwell assay, respectively. Finally, protein levels of epithelial-mesenchymal transition (EMT) pathway-related genes were detected by Western blot. RESULTS: LncRNA H19 was highly expressed in HBV-related HCC tissues. The expression of lncRNA H19 was positively correlated with lymph node metastasis and distant metastasis, whereas negatively correlated with the overall survival of HBV-related HCC patients. Results of in vitro experiments showed that lncRNA H19 knockdown significantly downregulated cell proliferation and invasion. However, lncRNA H19 knockdown significantly upregulated apoptosis of HBV-related HCC cells. Western blot results demonstrated that lncRNA H19 remarkably decreased the protein expressions of EMT pathway-related genes, including N-cadherin, Vimentin, ß-catenin and MMP-9. In addition, rescue experiments demonstrated that lncRNA H19 remarkably promoted malignant development of HBV-related HCC via regulating microRNA-22. CONCLUSIONS: LncRNA H19 promotes malignant development of HBV-related HCC through regulating microRNA-22 via EMT pathway.

Mitochondrial protein UCP1 mediates liver injury induced by LPS through EKR signaling pathway.

OBJECTIVE: Mitochondria are abundant in liver. The roles of mitochondrial protein in liver injury and related signaling pathways are still unclear. UCP1 is a novel mitochondrial transmembrane protein. Its expression pattern and function in liver still needs further investigation. MATERIALS AND METHODS: A mouse model of liver injury was established by the treatment of LPS. UCP1 expression in the liver tissue was detected by Western blot and qRT-PCR. ERK signaling activity was tested by enzymatic activity kit. ATP production was evaluated by flow cytometry. Cell apoptosis was determined by Western blot and flow cytometry. ERK signaling pathway inhibitor, U0126, was used to pre-treat mice. Liver tissue from sepsis patients was collected from the surgery. RESULTS: Our data showed that the level of UCP1 was upregulated, ERK signaling was activated, ATP production was reduced, and cell apoptosis was enhanced in mice with liver injury model caused by LPS. U0126 intervention significantly suppressed UCP1 expression, inhibited ERK signaling pathway, enhanced ATP production, and restrained liver cell apoptosis in mice liver injury model. UCP1 increased, ERK signaling activated, and cell apoptosis elevated in the liver tissue of sepsis patients. CONCLUSIONS: UCP1 plays a role in the liver tissue of mouse liver injury model and sepsis patients through the modulation of mitochondrial ATP production and cell apoptosis by ERK signaling pathway.