It has long been acknowledged that there is a link between inflammation and cancer, but its molecular mechanism remains unclear. A key player in inflammation is nuclear transcription factor NF-?B, that activity is triggered in response to infectious agents and proinflammatory cytokines via the I?B kinase. In parenchyma cells, inflammation through I?B kinase/NF-?B pathway suppresses apoptosis, accelerates cell cycle, then promote tumorigenesis. In mesenchyma cells inflammation through I?B kinase/NF-?B pathway produces cytokines and chemokines that may serve as tumor growth factors. To sum up, I?B kinase/NF -?B pathway represents a critical molecular link between inflammation and cancer.

Objective To investigate the effect of glucagon-like peptide-1 (GLP-1) on glycolipid metabolism in 3T3-L1 adipocytes and explore the mechanism. Methods 3T3-L1 adipocytes were treated with GLP-1, insulin, or both for 24 h, and Western blotting was used to analyze the expression levels of adipose triglyceride lipase (ATGL), glucose transporter type 4 (GLUT4), Akt1, Akt2 and phosphorylated Akt in the cells. Immunofluorescence was used to observe lipid content in 3T3-L1 adipocytes. Results Akt1 and Akt2 were not activated by insulin stimulation in 3T3-L1 adipocytes. Akt was phosphorylated by GLP-1 stimulation, which inhibited the expression of ATGL and increased the translocation of GLUT4 from the intracellular membranes to plasma membranes. These changes were more obvious under the synergistic effect of insulin in 3T3-L1 adipocytes. Conclusion GLP-1 decreases lipolysis by inhibiting the expression of ATGL and improves insulin resistance by increasing the translocation of GLUT4 in 3T3-L1 adipocytes.

Objective To investigate the effect of glucagon-like peptide-1 (GLP-1) on glycolipid metabolism in 3T3-L1 adipocytes and explore the mechanism. Methods 3T3-L1 adipocytes were treated with GLP-1, insulin, or both for 24 h, and Western blotting was used to analyze the expression levels of adipose triglyceride lipase (ATGL), glucose transporter type 4 (GLUT4), Akt1, Akt2 and phosphorylated Akt in the cells. Immunofluorescence was used to observe lipid content in 3T3-L1 adipocytes. Results Akt1 and Akt2 were not activated by insulin stimulation in 3T3-L1 adipocytes. Akt was phosphorylated by GLP-1 stimulation, which inhibited the expression of ATGL and increased the translocation of GLUT4 from the intracellular membranes to plasma membranes. These changes were more obvious under the synergistic effect of insulin in 3T3-L1 adipocytes. Conclusion GLP-1 decreases lipolysis by inhibiting the expression of ATGL and improves insulin resistance by increasing the translocation of GLUT4 in 3T3-L1 adipocytes.

OBJECTIVETo investigate the effect of glucagon-like peptide-1 (GLP-1) on glycolipid metabolism in 3T3-L1 adipocytes and explore the mechanism.

METHODS3T3-L1 adipocytes were treated with GLP-1, insulin, or both for 24 h, and Western blotting was used to analyze the expression levels of adipose triglyceride lipase (ATGL), glucose transporter type 4 (GLUT4), Akt1, Akt2 and phosphorylated Akt in the cells. Immunofluorescence was used to observe lipid content in 3T3-L1 adipocytes.

RESULTSAkt1 and Akt2 were not activated by insulin stimulation in 3T3-L1 adipocytes. Akt was phosphorylated by GLP-1 stimulation, which inhibited the expression of ATGL and increased the translocation of GLUT4 from the intracellular membranes to plasma membranes. These changes were more obvious under the synergistic effect of insulin in 3T3-L1 adipocytes.

CONCLUSIONGLP-1 decreases lipolysis by inhibiting the expression of ATGL and improves insulin resistance by increasing the translocation of GLUT4 in 3T3-L1 adipocytes.

3T3-L1 Cells ; Adipocytes ; cytology ; metabolism ; Animals ; Cell Membrane ; metabolism ; Down-Regulation ; Drug Synergism ; Glucagon-Like Peptide 1 ; pharmacology ; Glucose Transporter Type 4 ; metabolism ; Insulin ; pharmacology ; Insulin Resistance ; Intracellular Membranes ; metabolism ; Lipase ; metabolism ; Mice ; Phosphorylation ; Protein Transport ; drug effects ; Proto-Oncogene Proteins c-akt ; metabolism

The update of multi-omics technology is a key means to promote the rapid development of accurate health model in the whole life cycle.It can formulate dynamic and accurate nursing measures and provide massive data information from the perspective of nursing biology of health and disease.At present,clinical nursing research faces many challenges such as insufficient application and transformation ability of multi-omics technology.This paper introduces the multi-omics technology,reviews the application status of multi-omics technology in cancer nursing,maternal and child nursing,chronic metabolic disease nursing and symptom management,and puts forward the cross integration and prospect of multi-omics technology and nursing research,so as to strengthen the information mining ability of nurses at different levels of health and disease,and provide an important basis for accelerating the clinical transformation of precision nursing.

Cornelia de Lange syndrome (CdLS) is a genetic syndrome with severe neurodevelopmental disorders as the main manifestation. Its clinical manifestations included mental retardation, typical facial features, intrauterine and postnatal developmental delay, and deformity in multiple organs and systems, with an incidence rate of about 1/10000 to 1/30000. International CdLS Consensus Group was established in 2017 and issued the first international consensus on CdLS, i.e., "Diagnosis and management of Cornelia de Lange syndrome: first international consensus statement", in July 2018. Being developed through a modified Delphi consensus process, this consensus provides guidance on the diagnosis and management of children with CdLS. This article gives an interpretation of this consensus, aiming to help clinicians with early identification, diagnosis, standard follow-up, and management of this disease.
Consensus ; De Lange Syndrome ; Humans