ABSTRACT
After ischemic stroke, the key to reduce the mortality and disability rate is to restore the blood supply of brain tissue as soon as possible. However, the cerebral ischemia-reperfusion injury (CIRI) caused by blood flow restoration is also an important cause of brain tissue structural damage and dysfunction. Studies in recent years have shown that the activation of mitophagy at CIRI stage can reduce the volume of cerebral infarction and protect neurons from CIRI, while excessive or insufficient mitophagy can aggravate CIRI. This suggests that inducing moderate mitophagy may be a potential therapeutic target for neuroprotection after stroke. However, the neuroprotective mechanism of mitophagy has not yet been fully elucidated. This article reviews the neuroprotective mechanism and potential application of mitophagy in stroke, and discusses some problems of mitophagy as a therapeutic target for stroke.
ABSTRACT
Ischemic stroke is one of the main causes of disability and death. Although intravenous thrombolysis and endovascular mechanical thrombectomy can achieve cerebral vascular recanalization, most patients with ischemic stroke leave serious neurological deficits due to missed treatment window. Neural plasticity is the basis of neural function repair. Recent studies have shown that microRNAs play an indispensable role in regulating neural plasticity. This article reviews the regulatory role of microRNAs on neural plasticity in ischemic stroke, in order to provide reference for the treatment of ischemic stroke.
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Background:Small bowel capsule endoscopy(SBCE)has become a first-line procedure for examining small bowel diseases. Aims:To evaluate the diagnostic value of SBCE in patients with mid-gastrointestinal bleeding(MGIB). Methods:MGIB patients who underwent SBCE from Jan. 2012 to Dec. 2014 at the Third People’s Hospital of Bengbu were enrolled. Diagnostic value of SBCE in MGIB was analyzed. Re-bleeding was followed up by outpatient visit and telephone. Results:Forty-four consecutive MGIB patients underwent SBCE procedures,the detection rate was 95. 5% and the positive rate was 65. 9% . Vascular abnormality(37. 9% ),inflammation(31. 0% )and tumor(20. 7% )were the three major etiology in SBCE positive patients. Follow-up results showed that re-bleeding rate in SBCE positive group was significantly higher than in non-positive group(41. 4% vs. 13. 3% ,P < 0. 05). Conclusions:Vascular abnormality is still the most major etiology of MGIB,meanwhile the proportions of inflammation and tumor are increasing. SBCE has a high detection rate and positive rate in initial screening of MGIB,and the risk of re-bleeding in patients with negative SBCE is low.
ABSTRACT
Early exercise training after stroke is a therapeutic strategy that has been paid w idespread attention. A series of studies found that early exercise training after stroke can increase expression of neurotrophic factors and maintain the integrity of the blood-brain barrier by inhibiting acute neuroinflammation and apoptosis, and reduce brain damage. This artice reviews the neuroprotective roles of early exercise training after stroke and their possible molecular mechanisms.
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Objective To investigate the effect of early rehabilitation on rats' motor performance after moderate or severe experimental traumatic brain injury (TBI).Methods After adult Sprague-Dawley rats had received moderate or severe TBI,they were randomly assigned to either a 24 hour exercise group (group A),a 3-day exercise group (group B),a 7-day exercise group (group C) or a control group.Each group was composed of 8 rats.The exercise group endured forced treadmill training on an electric treadmill for 14 consecutive days initiated 24 hours,3 days or 7 days post TBI.The foot-fault and cylinder tests were performed on the 6th,12th,18th,24th and 28th day post injury.On the 28th day the rats were sacrificed and the brains were removed and frozen.The frozen coronal brain sections were stained with cresyl violet (CV) for quantitative evaluation of cortical lesion volume.Results The rats in groups B and C showed significant decreases in the percentage of left forelimb foot faults compared with the control group at the 18th,24th and28th day after injury.In addition,the rats of group C demonstrated significant decreases in the percentage of left forelimb foot-fault at the 12th day after injury.There was no significant difference between group A and the control group in terms of foot fault scores in any of the subsequent test sessions.In the cylinder test the forelimb use asymmetry scores of neither group A nor group B were significantly different from the control group.Group C showed marked locomotor asymmetry improvement at day 28 post-injury.There was no significantly different loss of hemispheric tissue between those groups.Conclusion After treadmill exercise for 14 consecutive days initiated at 3 or 7 days following moderate or severe TBI,rats' motor function improved.The cortical lesion volume was not associated with recovery of motor function.