Blood-Brain Barrier Disruption, Vascular Impairment, and Ischemia/Reperfusion Damage in Diabetic Stroke.

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Term Occurence Count Dictionary
diabetes mellitus 1 endocrinologydiseases
diabetic retinopathy 1 endocrinologydiseases
hyperglycemia 15 endocrinologydiseases
lactic acidosis 1 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
Insulin 4 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
Insulin 23759 stroke.90 However, the mechanisms of DM‐increased I/R injury after stroke are not very clear.High Insulin ResistanceNinety percent to 95% of patients with DM are T2DM.100 Insulin resistance is commonly present
Insulin 23832 stroke are not very clear.High Insulin ResistanceNinety percent to 95% of patients with DM are T2DM.100 Insulin resistance is commonly present in patients with T2DM, hypertensive patients, elderly and obese populations,
Insulin 24966 reported that treatment with tPA in such cases is less efficient compared with other types of stroke.105 Insulin resistance remains a high risk factor for stroke and a potential target for stroke prevention and control.101Experimental
Insulin 25365 volume after stroke was found to be directly proportional to increasing levels of hyperglycemia.106 Insulin resistance has been reported to mediate hindlimb I/R damage in rats via inflammatory responses that
Select Disease Character Offset Disease Term Instance
diabetes mellitus 5879 addition, a higher incidence of poststroke edema was reported in patients with DM.22 Similarly, in type 2 diabetes mellitus (T2DM) mice subjected to stroke, a significant increase in both ipsilateral and contralateral brain
diabetic retinopathy 11648 localized to astrocyte end‐feet.47 DM regulates Aquaporin‐4 expression in the retina and induces diabetic retinopathy .54 Knockdown of Aquaporin‐4 exacerbates retinopathy by increasing retinal vascular permeability, retinal
hyperglycemia 835 costs. Diabetes mellitus (DM) is a chronic, lifelong, severe metabolic health problem characterized by hyperglycemia , attributable to insulin deficiency, insulin resistance, or a combination of both. Patients with DM
hyperglycemia 11142 after stroke.50, 51 Using a model of forebrain ischemia in rats, it has been reported that diabetic hyperglycemia suppresses ischemia‐induced astrocyte activation, increases astrocyte cell death, damages the astrocyte
hyperglycemia 24235 neurological functional outcome while increasing inflammatory responses.102, 103 Another study reported that hyperglycemia during tPA infusion after stroke in rats increased BBB permeability and intracerebral hemorrhage, which
hyperglycemia 25347 with DM, the infarct volume after stroke was found to be directly proportional to increasing levels of hyperglycemia .106 Insulin resistance has been reported to mediate hindlimb I/R damage in rats via inflammatory responses
hyperglycemia 33811 respectively.130 Several studies have indicated that in a majority of patients with acute stroke with admission hyperglycemia , hyperglycemia may be triggered by stress responses in reaction to the extensive brain injury.130, 131
hyperglycemia 33826 studies have indicated that in a majority of patients with acute stroke with admission hyperglycemia, hyperglycemia may be triggered by stress responses in reaction to the extensive brain injury.130, 131 Experimental
hyperglycemia 33964 stress responses in reaction to the extensive brain injury.130, 131 Experimental evidence suggests that hyperglycemia significantly worsens both cortical intracellular brain acidosis and mitochondrial function in the ischemic
hyperglycemia 34274 production.129, 132 While most experimental studies as well as clinical trials have concluded that DM and hyperglycemia are associated with poor outcome poststroke, there are, however, a few reports indicating that hyperglycemia
hyperglycemia 34383 hyperglycemia are associated with poor outcome poststroke, there are, however, a few reports indicating that hyperglycemia may also extend mild protection against neuronal damage.133, 134 Using 2 experimental stroke models
hyperglycemia 34555 damage.133, 134 Using 2 experimental stroke models in rodents, it has been shown that the adverse effects of hyperglycemia in stroke may critically depend on several factors: (1) the extent of collateral blood supply to the
hyperglycemia 34752 blood supply to the injured brain tissue, (2) the extent of local CBF decrease, and (3) the timing of hyperglycemia .134 In the ischemic border tissue, hyperglycemia increases glucose supply and promotes anaerobic metabolism
hyperglycemia 34801 extent of local CBF decrease, and (3) the timing of hyperglycemia.134 In the ischemic border tissue, hyperglycemia increases glucose supply and promotes anaerobic metabolism converting glucose to lactic acid.132, 134
hyperglycemia 35206 expected, in animals subject to stroke with diffuse infarctions in the cortex and subcortical brain, acute hyperglycemia significantly increased neurological deficits and infarction volume.135 However, in lacunar infarction
hyperglycemia 35381 volume.135 However, in lacunar infarction that involves the occlusion of a deep penetrating vessel, hyperglycemia decreases neurological functional deficits without affecting, or even decreasing, subcortical infarction
hyperglycemia 36513 spreading depression near ischemic core regions may be fueled under high glucose conditions.136 Persistent hyperglycemia after stroke is an independent determinant of infarct expansion via recruiting the ischemic penumbra
lactic acidosis 34134 acidosis and mitochondrial function in the ischemic penumbra, while provoking anaerobic metabolism, lactic acidosis , and free radical production.129, 132 While most experimental studies as well as clinical trials have
type 2 diabetes mellitus 5872 addition, a higher incidence of poststroke edema was reported in patients with DM.22 Similarly, in type 2 diabetes mellitus (T2DM) mice subjected to stroke, a significant increase in both ipsilateral and contralateral brain

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