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1.
Basic & Clinical Medicine ; (12): 999-1002, 2018.
Article in Chinese | WPRIM | ID: wpr-694024

ABSTRACT

Objective To understand the characteristics of patients with hematological illness and chronic subdural hematoma.,and the effect of blood disease on the treatment of chronic subdural hematoma. To guide the treatment of patients who both with hematological illness and chronic subdural hematoma. Methods Through a retrospective study of the cases of chronic subdural hematoma from January 1, 2000 to June 1, 2017 in Peking Union Medical College Hospital, the following items were investigated. 1).According to whether or not they were associated with blood disorders, the collected cases were divided into the blood disorders group and the non-blood disorders group. And the clinic data of the sex composition, average ages, treatment effect and mortality were compared. 2). Ac-cording to the treatment, the cases with blood disease were divided into the surgical group and the conservative group. And the treatment effect and mortality were compared. Results A total of 433 patients with chronic subdural hematoma were included in this study, including 35 patients associated with hematological illness. 1) Compared to the controls group, the patients group was younger( P<0.01) ;the male ratio was lower ( P<0.01) ; the treatment effect was lower( P<0.001) and the mortality was higher( P<0.001) . 2) Within the patients with hematological illness, the surgical group had the better treatment effect(78.9% vs 31.3%,P<0.01) and the lower mortality (15.8% vs 50.0%,P<0.05). Conclusions 1)The hematological illness group is younger and the male ratio is lower than the non-hematological illness group; 2) The hematological illness is a risk factor for the treatment of chronic subdural hematoma; 3) The patients who both with the hematological illness and the chronic subdural he-matoma should be treated by surgery.

2.
Acta Academiae Medicinae Sinicae ; (6): 33-36, 2016.
Article in English | WPRIM | ID: wpr-289910

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the protective effect of Exosomes from human adipose-derived mesenchymal stem cells (hAMSCs) in neural injury induced by glutamate and its possible mechanism.</p><p><b>METHODS</b>Characteristics of Exosomes from hAMSCs were identified by electron microscopy and Western blot analysis. Cytokines that might play a major role in the protective effect were tested by enzyme-linked immunosorbent assay (ELISA). The protective action of Exosome and its possible signaling pathway were researched by the in vitro neural injury induced by glutamate, including control group (without Glu), Glu group (dealing with Glu), Glu+Exo group (dealing with Glu +100 ng/ml Exo), Glu+Exo+Akt group (dealing with Glu+100 ng/ml Exo+10 μmol/L Akt), Glu+Exo+Erk group (dealing with 100 ng/ml Glu+100 ng/ml Exo+10 μmol/L Erk), and Glu+Exo+TrkB group (dealing with Glu+100 ng/ml Exo +10 μmol/L TrkB).</p><p><b>RESULTS</b>Exosomes from hAMSCs had similar sizes to those isolated from other kinds of cells, and expressed the characteristic proteins such as CD63, CD81, HSP70, and HSP90. Cytokines that had neurotrophic effects on Exosomes were mainly insulin-like growth factor and hepatocyte growth factor, with the concentration being 9336.49±258.63 and 58,645.50±16,014.62, respectively; brain derived neurotrophic factor, nerve growth factor,and vascular endothelial growth factor had lower levels, with the concentration being 1928.25±385.47, 1136.94±5.99, and 33.34±9.43, respectively. MTS assay showed that the PC12 cell survival rates were 0.842±0.047, 0.306±0.024, 0.566±0.026, 0.461±0.016, 0.497±0.003, and 0.515±0.034 in the control group, Glu group, Glu+Exo group, Glu+Exo+Akt group, Glu+Exo+Erk group, and Glu+Exo+TrkB group; obviously, it was significantly lower in Glu group than in control group (P=0.02), significantly higher in Glu+Exo group than in Glu group (P=0.01), and significantly lower in Glu+Exo+Akt group than in Glu+Exo group (P=0.01).</p><p><b>CONCLUSION</b>Exosomes secreted from hAMSCs have protective effect against neuron damage induced by glutamate, which may be mediated through activating the PI3/K-Akt signalling pathway.</p>


Subject(s)
Animals , Humans , Rats , Central Nervous System , Wounds and Injuries , Exosomes , Glutamic Acid , Mesenchymal Stem Cells , PC12 Cells , Vascular Endothelial Growth Factor A
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