Inhibition of TREM-1 attenuates inflammation and lipid accumulation in diet-induced nonalcoholic fatty liver disease.

In the liver tissues of obese diabetic or nondiabetic patients, triggering receptor expressed on myeloid cells-1 (TREM-1) is usually found to be upregulated, thus leading to upregulation of various inflammatory cytokines and lipid accumulation. On the other hand, nonalcoholic fatty liver disease (NAFLD), characterized by excess lipid accumulation, and inflammatory injury in liver, is becoming an epidemic disease, globally. In the present study, we aimed to investigate the biological role and the underlying mechanisms of TREM-1 in NAFLD. upregulation of TREM-1 occurred in high-fat diet (HFD)-induced mice NAFLD model and oleic acid-treated HepG2 and primary mouse hepatocytes cell model at messenger RNA and protein levels. Functional studies established that overexpression of TREM-1 displayed hyperlipidemia, and increased in inflammatory indicators and lipid accumulation-related genes, which was ameliorated by knockdown of TREM-1. Our results also showed that obvious lipid accumulation and inflammatory injury occurred in the liver tissue of HFD-fed mice, while treatment with lentiviral vector short hairpin TREM showed marked improvement in tissue morphology and architecture and less lipid accumulation, thus deciphering the mechanism through which knockdown of TREM-1 ameliorated the inflammatory response and lipid accumulation of NAFLD mice through inactivation of the nuclear factor-κB (NF-κB) and PI3K/AKT signal pathways, respectively. In conclusion, TREM-1/NF-κB and TREM-1/PI3K/AKT axis could be an important mechanism in ameliorating the inflammatory response and lipid accumulation, respectively, thus shedding light on the development of novel therapeutics to the treatment of NAFLD.

Faulty blood typing misled by auto anti-D in AIHA.

Pre-transfusion testing is a vital link to enhance patients' safety but may be influenced by heterotypic blood transfusion and disease. Previous history of blood transfusion most of time help us determine the blood type. On the other hand, it can also mislead technicians to a wrong conclusion. Anti-D, which is clinically important in hemolytic transfusion reaction, is either alloimmunized by transfusion, pregnancy or induced in certain diseases. Here, we reported a rare case with false blood identification interfered by heterotypic blood transfusion and auto anti-D in autoimmune hemolytic anemia (AIHA).

PRC1 promotes GLI1-dependent osteopontin expression in association with the Wnt/ß-catenin signaling pathway and aggravates liver fibrosis.

BACKGROUND: PRC1 (Protein regulator of cytokinesis 1) regulates microtubules organization and functions as a novel regulator in Wnt/ß-catenin signaling pathway. Wnt/ß-catenin is involved in development of liver fibrosis (LF). We aim to investigate effect and mechanism of PRC1 on liver fibrosis. METHODS: Carbon tetrachloride (CCl4)-induced mice LF model was established and in vitro cell model for LF was induced by mice primary hepatic stellate cell (HSC) under glucose treatment. The expression of PRC1 in mice and cell LF models was examined by qRT-PCR (quantitative real-time polymerase chain reaction), western blot and immunohistochemistry. MTT assay was used to detect cell viability, and western blot to determine the underlying mechanism. The effect of PRC1 on liver pathology was examined via measurement of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and hydroxyproline, as well as histopathological analysis. RESULTS: PRC1 was up-regulated in CCl4-induced mice LF model and activated HSC. Knockdown of PRC1 inhibited cell viability and promoted cell apoptosis of activated HSC. PRC1 expression was regulated by Wnt3a signaling, and PRC1 could regulate downstream ß-catenin activation. Moreover, PRC1 could activate glioma-associated oncogene homolog 1 (GLI1)-dependent osteopontin expression to participate in LF. Adenovirus-mediated knockdown of PRC1 in liver attenuated LF and reduced collagen deposition. CONCLUSIONS: PRC1 aggravated LF through regulating Wnt/ß-catenin mediated GLI1-dependent osteopontin expression, providing a new potential therapeutic target for LF treatment.

The popularization and application of cold storage red blood cells or whole blood at -80 degrees C of the Rh (D) negative patients in surgical operation.

The efficiency of cold storage red blood cells (CSRBC) or whole blood at -80 degrees C used in 27 Rh (D) negative patients during surgical operation was reported. The Rh (D) negative patients received the transfusion of CSRBC or whole blood stored at -80 degrees C for 180 to 360 days. The changes in the indexes, such as blood TB, DB, K+, Na+, BUN, Cr, urine protein (URPO), UOB, Hb, HCT, serum total protein, relative to hemolytic reaction and blood volume before and after transfusion were observed. The results showed that after transfusion of CSRBC or whole blood 27 cases were negative for urine protein and UOB, and the levels of BUN and Cr were normal (P > 0.05). Blood TB, DB, Hb, and HCT were increased, while pH, blood K+ and blood Na+ was normal with the difference being not significant before and after operation (P > 0.05). Plasma protein was decreased, but there was no significant difference before and after operation (P > 0.05). It was suggested that CSRBC or whole blood at -80 degrees C could be safely infused to the Rh(D) negative patients without side effects during the surgical operation.