PubMed | Shandong University, Huanhu Hospital, Huazhong University of Science and Technology, Anhui Medical University and 11 more.
Type: Journal Article | Journal: Trials | Year: 2016
Patients with symptomatic internal carotid artery (ICA) or middle cerebral artery (MCA) occlusion with haemodynamic insufficiency are at high risk for recurrent stroke when treated medically.The Carotid or Middle cerebral artery Occlusion Surgery Study (CMOSS) trial is an ongoing, government-funded, prospective, multicentre, randomised controlled trial. The CMOSS will recruit 330 patients with symptomatic ICA or MCA occlusion (parallel design, 1:1 allocation ratio) and haemodynamic insufficiency. Participants will be allocated to best medical treatment alone or best medicine plus extracranial-intracranial (EC-IC) bypass surgery. The primary outcome events are all strokes or deaths occurring between randomisation and 30days post operation or post randomisation and ipsilateral ischaemic stroke within 2years. Recruitment will be finished by December 2016. All the patients will be followed for at least 2years. The trial is scheduled to complete in 2019.The CMOSS will test the hypothesis that EC-IC bypass surgery plus best medical therapy reduces subsequent ipsilateral ischaemic stroke in patients with symptomatic ICA or MCA occlusion and haemodynamic cerebral ischaemia. This manuscript outlines the rationale and the design of the study. CMOSS will allow for more critical reappraisal of the EC-IC bypass for selected patients in China.NCT01758614 with ClinicalTrials.gov. Registered on 24 December 2012.
Ge C.,The 307 Hospital of PLA |
Zang X.-X.,Chinese PLA General Hospital |
Zou J.-C.,The 307 Hospital of PLA |
Yu K.-T.,The 307 Hospital of PLA |
And 2 more authors.
Chinese Journal of Tissue Engineering Research | Year: 2013
BACKGROUND: Pubic symphysis is the same kind of tissue as the temporomandibular joint disc, meniscus or intervertebral disc, but it is rarely reported that pubic symphysis can be used as a donor area of tissue engineering seed cells. OBJECTIVE: To explore the feasibility of the pubic symphysis as the donor area of tissue engineering seed cells. METHODS: Hematoxylin-eosin stain, alcian blue stain and type II collagen immunohistochemical study were used to detect the histological features of the extracellular matrix of rat pubic symphysis tissue. Cells derived from rat pubic symphysis were cultured in three-dimensional alginate scaffold in vitro. Cell viability in scaffold was detected by living cells fluorescence staining. Cells proliferation in the alginate scaffold cultured in vitro for 21 days was observed. Eight pelvis specimens of adult men were used to measure the cartilage volume of the pubic symphysis. RESULTS AND CONCLUSION: Parallel and crossing fibrous bands were spread in the rat pubic symphysis tissue, and between them there were small round or short-fusiform cells in the lacunae, with basophilic cytoplasm. Cells were in pairs or lined up. Sections stained with alcian blue and type II collagen antibody showed positive in the cytoplasm and extracellular matrix surrounding the round lacunae, whereas the matrix farther from cells stained lightly. Alginate gel scaffold displayed a porous structure with (27.0±16.7) μm pore diameter. Cell viability in the scaffold was (72.4±4.5)%. The spheroidal cells in the alginate gel grew into isogenous group after long-term three-dimensional culture in vitro. Cell clusters were observed after cultured for 13 days, and became larger with more cells after 21 days culture. Pubic symphysis cartilage region of adult man was wedge shaped with thick front part and its volume was (1.13±0.21) cm2. It turns out that cells of the rat pubic symphysis have the chondrocyte features as alignment and specific histological stain of cartilage tissue. Cells derived from the pubic symphysis proliferate well in three-dimensional culture in vitro. Volume of adult man pubic symphysis cartilage is large enough as a donor site to supply cartilage mass for cells isolation.
PubMed | Thadweik Academy of Medicine, the 307 Hospital of PLA and Academy of Military Medical science
Type: Journal Article | Journal: Acta pharmacologica Sinica | Year: 2015
To determine whether administration of choline could attenuate brain injury in a rat model of ischemic stroke and the underlying mechanisms.A rat model of ischemic stroke was established through permanent middle cerebral artery occlusion (pMCAO). After the surgery, the rats were treated with choline or choline plus the specific 7 nAChR antagonist methyllycaconitine (MLA), or with the control drug nimodipine for 10 days. The neurological deficits, brain-infarct volume, pial vessel density and the number of microvessels in the cortex were assessed. Rat brain microvascular endothelial cells (rBMECs) cultured under hypoxic conditions were used in in vitro experiments.Oral administration of choline (100 or 200 mgkg(-1)d(-1)) or nimodipine (20 mgkg(-1)d(-1)) significantly improved neurological deficits, and reduced infarct volume and nerve cell loss in the ischemic cerebral cortices in pMCAO rats. Furthermore, oral administration of choline, but not nimodipine, promoted the pial arteriogenesis and cerebral-cortical capillary angiogenesis in the ischemic regions. Moreover, oral administration of choline significantly augmented pMCAO-induced increases in the expression levels of 7 nAChR, HIF-1 and VEGF in the ischemic cerebral cortices as well as in the serum levels of VEGF. Choline-induced protective effects were prevented by co-treatment with MLA (1 mgkg(-1)d(-1), ip). Treatment of rBMECs cultured under hypoxic conditions in vitro with choline (1, 10 and 100 mol/L) dose-dependently promoted the endothelial-cell proliferation, migration and tube formation, as well as VEGF secretion, which were prevented by co-treatment with MLA (1 mol/L) or by transfection with HIF-1 siRNA.Choline effectively attenuates brain ischemic injury in pMCAO rats, possibly by facilitating pial arteriogenesis and cerebral-cortical capillary angiogenesis via upregulating 7 nAChR levels and inducing the expression of HIF-1 and VEGF.