ABSTRACT
Kasabach-Merritt phenomenon (KMP) is a rare disease that is characterized by severe thrombocytopenia and consumptive coagulation dysfunction caused by kaposiform hemangioendothelioma or tufted hemangioma. This condition primarily occurs in infants and young children, usually with acute onset and rapid progression. This review article introduced standardized recommendations for the pathogenesis, clinical manifestation, diagnostic methods and treatment process of KMP in China, which can be used as a reference for clinical practice.
Subject(s)
Kasabach-Merritt Syndrome/diagnosis , Kasabach-Merritt Syndrome/therapy , Child , China/epidemiology , Diagnosis, Differential , Humans , Kasabach-Merritt Syndrome/epidemiology , Standard of CareABSTRACT
Recently, growing evidence has demonstrated Dexmedetomidine (Dex) a promising intervene preventing postoperative cognitive decline (POCD) following surgery, which is associated with neuroinflammation leading to neuronal apoptosis and deregulated neurogenesis. Previous studies suggested the anti-inflammation and anti-neuroapoptosis action of Dex. Therefore we hypothesize the promoting neurogenesis of Dex linked to stimulating BDNF and subsequent p-MPAK production in a rat model of POCD. In the present study, the POCD animal model was established by performing an exploratory laparotomy under isoflurane anaesthesia in old rats, utilizing which Dex response is confirmed by behavioural tests. Inflammatory biomarkers as IL-1ß and TNF-α, mature neuron percentage measured by doublecortin staining (DCX), promoting factors as brain derived growth factor (BDNF), phosphorylated cAMP response element binding protein (CREB) and proteins of kinase A (PKA), MAPK production as p-P38-MAPK protein express were measured. Herein, we showed that surgery reduced DCX-positive neurons and expression of BDNF representing neurogenesis profoundly. As expected, Dex rescued the associated cognitive impairment and inflammatory changes, as well as up-regulated expression of BDNF, PKA, p-CREB/CREB and following p-P38-MAPK regulation. Our results confirmed the protective Dex response and indicated the proneurogenesis role of it as well, suggesting the mechanism of beneficial effects of Dex to prevent POCD.
Subject(s)
Cognitive Dysfunction/prevention & control , Dexmedetomidine/administration & dosage , Neurogenesis/drug effects , Neurons/drug effects , Neuroprotective Agents/administration & dosage , Postoperative Complications/prevention & control , Animals , Cognitive Dysfunction/etiology , Doublecortin Protein , Encephalitis/etiology , Encephalitis/metabolism , Hippocampus/drug effects , Hippocampus/physiology , Male , Neurons/physiology , Rats, Sprague-Dawley , Signal Transduction , Spatial Memory/drug effectsABSTRACT
MicroRNA (miRNA or miR) has been shown to play an important role in the initiation and development in many different cancers. Here, we demonstrated down-regulated expression of miR-27a-3p in hepatocellular carcinoma (HCC) tissues in comparison with that in adjacent normal liver tissues based on the TCGA database. Cells viability and apoptosis was measured by CCK-8 and flow cytometry assay. Cell invasion and migration was measured by Transwell and wound healing assay. The effect of miR-27a-3p on DUSP16 expression was evaluated by luciferase assays, and western blot assay. miR-27a-3p up-regulation by transfection with miR-27a-3p mimics attenuated SMMC-7721 and HepG2 cell viability, invasion as well as migration, obviously. Moreover, we found that dual specificity phosphatase 16 (DUSP16), also known as mitogen-activated protein kinase phosphatase 7 (MKP-7), is a target of miR-27a-3p. DUSP16 expression was obvious decrease by miR-27a-3p at both transcriptional and protein levels in both SMMC-7721 and HepG2 cells. DUSP16 expression in tissues of HCC was up-regulated in comparison with that in tissues of adjacent liver based on the TCGA database. Overexpression of DUSP16 significantly reversed the cell changes in viability, invasion and migration which resulted from miR-27a-3p up-regulation in SMMC-7721 and HepG2 cells. Our findings contribute to current understanding of the functions of miR-27a-3p and suggest a mechanism by which miR-27a-3p plays an anti-tumor role in the development of HCC by targeting DUSP16.
