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The effect of zinc deficiency on the membrane skeleton of red blood cells from rats was examined through composition analysis and extractability evaluation of spectrin from rats kept on a zinc-deficient diet. Results showed that zinc deficiency did not modify spectrin oligomeric form and extractability. It did, however, reduce protein R5 composition of spectrin. This alteration in the composition of the membrane skeleton suggests a structural or compositional modification not indicated by spectrin extractability and oligomeric analysis.

Background and Purpose: Cerebral microinfarcts (CMI) are associated with intracerebral hemorrhage due to small vessel disease (SVD) in studies not including an ischemic etiologic workup. We aimed to determine their incidence and potential causes in a large ischemic stroke (IS) cohort.Methods: Consecutive patients with MRI-confirmed IS within 72 hours of onset were enrolled. Subjects had either single high-risk embolic source (cardioembolic or large vessel disease) or no embolic source. CMIs were classified by their relationship to the primary infarct as within or outside the same vascular territory. White matter hyperintensities (WMH) and microbleeds were markers SVD severity. Multivariable regression tested the association between CMIs and potential etiologies.Results: We analyzed 946 IS patients, mean age 69 ± 15 years, 46% female. We detected CMI (≤5 mm) on diffusion-weighted imaging in 269 (28%) subjects, 190 (71%) within the vascular territory of the primary infarct. Large-vessel atherosclerosis (P <.001), cardioembolic source (P <.001), higher WMH (P = .032) and lower systolic blood pressure (SBP, P = .024) were independently associated with the presence of CMI. While SBP was associated with CMI in any location (P <.05), WMH was only associated with CMI outside the territory of the primary infarct (P = .033), and large vessel atherosclerosis with CMI within the primary infarct territory (P = .004).Conclusions: CMIs occurring within the vascular territory of a larger infarct are more likely embolic, but those occurring outside are probably related to SVD. Our findings suggest a role for SVD in pathogenesis of CMIs and emphasize the importance of etiologic workup to identify alternate etiologies. [ABSTRACT FROM AUTHOR]

Background: Glycogen phosphorylase is the key enzyme that breaks down glycogen to yield glucose-1-phosphate in order to restore depleted energy stores during cerebral ischaemia. We sought to determine whether plasma levels of glycogen phosphorylase BB (GPBB) isoform increased in patients with acute ischaemic stroke (AIS).Methods: We studied plasma GPBB levels within 12 hours and again at 48±24 hours of symptom onset in 172 patients with imaging-confirmed AIS and 133 stroke-free individuals. We determined the ability of plasma GPBB to discriminate between cases and controls and examined the predictive value of plasma GPBB for 90-day functional outcome, 90-day survival and acute lesion volumes on neuroimaging.Results: The mean (SD) GPBB levels were higher in cases (46.3±38.6 ng/mL at first measurement and 38.6±36.5 ng/mL at second measurement) than in controls (4.1±7.6 ng/mL, p<0.01 for both). The area under the receiver operating characteristic (ROC) curve for case-control discrimination based on first GPBB measurement was 0.96 (95% CI 0.93 to 0.98). The sensitivity and specificity based on optimal operating point on the ROC curve (7.0 ng/mL) were both 93%. GPBB levels increased in 90% of patients with punctate infarcts (<1.5 mL) and in all patients admitted within the first 4.5 hours of onset. There was no correlation between GPBB concentration and either clinical outcome or acute infarct volume.Conclusion: GPBB demonstrates robust response to acute ischaemia and high sensitivity for small infarcts. If confirmed in more diverse populations that also include stroke mimics, GPBB could find utility as a stand-alone marker for acute brain ischaemia. [ABSTRACT FROM AUTHOR]