HIV-assodated dementia (HAD) is a public health problem and is particularly prevalent in drug abusers. The neuropathogenesis of human immunodeficiency virus (HIV) infection involves a complex cascade of inflammatory events, including monocyte/macrophage infiltration in the brain, glial immune activation and release of neurotoxic substances. In these events, astrocytic-derived monocyte chemoattractant protein-1 (MCP-1) plays an important role, whose release is elevated by HIV transactivator of transcription (HIV tat) and could be further elevated by opiates. This review will also consider some critical factors and events in MCP-1 enhancement induced by the interactions of opiate and HIV tat, including the mediating role of mu opioid receptor (MOR) and CCR2 as well as the possible signal transduction pathways within the cells. Finally, it will make some future perspectives on the exact pathways, new receptors and target cells, and the vulnerability to neurodegeneration with HIV and opiates.

The current global pandemic, known as COVID-19, poses challenges to healthcare systems worldwide. At the same time, it has provoked a collective focus on new and disruptive technology and stimulated the application of such technologies to disease control and containment efforts. Some of the innovations that have played the most significant roles have come from the fields of artificial intelligence, big data analytics, and communications technology. The current situation provides a good opportunity to relook how medical people engage with technological advances. This narrative review attempts to provide a historical context to the adoption of technology and of technical developments in Singapore and discusses the impact of disruptive technology in healthcare.

ObjectiveTo investigate the postoperative analgesic activity offlurbiprofen to intracranial aneurysm patients who went under endovascular treatment with propofol and remifentanil anesthesia.Methods Totally 40 ASA physical status Ⅰ - Ⅱ intracranial aneurysm patients were randomly scheduled flurbiprofen group (group F, 20 cases) and control group (group C, 20 cases). The patients in group F were given flurbiprofen 1 mg/kg respectively at 10 min before operation and at the end of the operation; while the patients in group C were given fat milk at the same time. The patients' circulation of the two groups before and after operation,the headache visual analog scores (VAS) and body comfort score (BCS) were observed.ResultsThe mean arterial pressure(MAP) in group C after operation 1,2 and 3 h were significantly higher than that before operation (P ＜ 0.05 ); the heart rate in group C after operation had no significantly difference compared with before operation (P ＞0.05). The MAP and the beart rate in group F had no significantly differences before and after operation(P ＞ 0.05 ). The VAS of postoperation headache after operation 1,2 and 3 h were (0.30 ± 0.65 ), (0.30 ± 0.57) and (0.25 ± 0.44) scores in group F, which were significantly lower than those in group C [ (3.25 ± 1.58), (3.00 ± 1.56) and (2.90 ± 1.48 ) scores](P ＜ 0.05 ) ; the BCS after operation in group F after operation 1,2 and 3 h were (3.30 ±0.86), (3.45 ±0.86) and(3.62 ±0.86)scores, which were significantly higher than those in group C [ ( 1.20 ± 1.00), ( 1.45 ± 0.94) and ( 1.50 ±1.00)scores](P＜ 0.05 ). ConclusionFlurbiprofen can reduce intracranial aneurysm patient's postoperative headache under endovascular treatment.

Neonatal sepsis is a systemic infection in which bacteria or fungi invade blood circulation and grow in it in the neonatal period,caused by toxin produce from bacteria or fungi.Currently sepsis is the major causing morbidity and mortality in neonatal infectious diseases,its clinical manifestation is not obvious and this brings us a range of clinical problems.In this review,we discussed these characteristics epidemiology,etiology,pathophysiology,clinical features of neonatal sepsis and septic shock in adults,to deepen the understanding of neonatal sepsis.

Circulating endothelial cells (CEC) are endothelial cells which are detected in the peripheral blood. There are very few CEC in healthy adults while the number is obviously increasing in patients with arthrosclerosis, diabetes mellitus, lupus erythematosus, et al. Nowadays, flow cytometry analysis and immunomagnetic isolation for CEC are employed successfully in clinic and scientific research. Several research findings have confirmed that there is intimate relation between CEC and tumorigenesis. Because of the important role in angiogenesis and tumor growth, CEC would be a perspective tumor marker in antiangiogenesis and would also predict the chemotherapy efficacy.

HIV-associated dementia (HAD) is a public health problem and is particularly prevalent in drug abusers. The neuropathogenesis of human immunodeficiency virus (HIV) infection involves a complex cascade of inflammatory events, including monocyte/macrophage infiltration in the brain, glial immune activation and release of neurotoxic substances. In these events, astrocytic-derived monocyte chemoattractant protein-1 (MCP-1) plays an important role, whose release is elevated by HIV transactivator of transcription (HIV tat) and could be further elevated by opiates. This review will also consider some critical factors and events in MCP-1 enhancement induced by the interactions of opiate and HIV tat, including the mediating role of mu opioid receptor (MOR) and CCR2 as well as the possible signal transduction pathways within the cells. Finally, it will make some future perspectives on the exact pathways, new receptors and target cells, and the vulnerability to neurodegeneration with HIV and opiates.

HIV-associated dementia (HAD) is a public health problem and is particularly prevalent in drug abusers. The neuropathogenesis of human immunodeficiency virus (HIV) infection involves a complex cascade of inflammatory events, including monocyte/macrophage infiltration in the brain, glial immune activation and release of neurotoxic substances. In these events, astrocytic-derived monocyte chemoattractant protein-1 (MCP-1) plays an important role, whose release is elevated by HIV transactivator of transcription (HIV tat) and could be further elevated by opiates. This review will also consider some critical factors and events in MCP-1 enhancement induced by the interactions of opiate and HIV tat, including the mediating role of mu opioid receptor (MOR) and CCR2 as well as the possible signal transduction pathways within the cells. Finally, it will make some future perspectives on the exact pathways, new receptors and target cells, and the vulnerability to neurodegeneration with HIV and opiates.

Cellular signal transduction plays an important role in pathogenesis of myocardial ischemia reperfusion(MIR) injury. During this process, extracellular signal molecules, membrance receptors and intracellular signal paths are involved. There are many cross talkings in signal pathways at many levels. The present article reviews cellular signal transduction mechanisms in MIR. The exploration of MIR's cellular pathogenesis may be beneficial for us to prevent and cure the heart damage in clinic. Furthermore, it may provide a new way of thinking in mechanism research of medicine.

Aim To explore the effects of Shuangshen tongguan(SSTG) drug serum on Calcium-Calmodulin(CaM)-Calcium/CaM dependent kinaseⅡsignal system in cardiomyocytes injury induced by hypoxia and reoxgyenization.Methods The cardiomyocytes were deprived of oxygen and glucose to mimic hypoxia reoxygenation injury.Intracellular calcium concentration,calmodulin(CaM) and calcium/calmodulin dependent kinaseⅡ?(CaMPKⅡ?) mRNA were measured by fluorospectrophotometry and reverse transcription-polymerase chain reaction(RT-PCR)respectively.Results After hypoxia/reoxygenation,intracellular calcium concentration,CaM and CaMPKⅡ? expression were enhanced(P

Aim To explore the effects of shuang shen tong guan(SSTG) drug serum on calcium and NOS-NO system in cardiomyocytes injured by hypoxia and reoxgyenization.Methods The cardiomyocytes were deprived of oxygen and glucose to mimic hypoxia reoxygenation injury.Intracellular calcium concentration was determined by Fluorospectrophotometry.NOS activity and NO contents were detected using colorimetric method.Results Intracellular calcium concentration,NOS activity and NO content were increased after hypoxia and reoxygenation injury.SSTG drug serum inhibted the upwards of intracellular calcium concentration,activity of total NOS,indusive NOS and NO content due to hypoxia/reoxygenation injury significantly(P