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Cortological superficial tin disease is a hemorrhagic neuroimaging marker of cerebral amyloid vascular disease.
fact, cortitry is becoming a powerful independent risk factor for future large-leaf cerebral hemorrhage.
, however, the underlying neuropathological correlation and pathophysiological mechanisms of cortitological light iron insocision remain unclear.
here, researchers used in vivo MRIs, ionosome MRIs, and histopathology methods to assess the neuropathological correlation and vascular pathology of cortical superficial tin disease.
study included 14 autopsies for cerebral amyloid vascular disease (average age of death 73 years, 9 cases for men) and 3 controls (average age of death of 91 years, 1 case for men).
a 3 T MRI scanner to scan the fixed brain hemisphere of Formarin.
the cortitological superficial iron leprosy based on the ionosome gradient echo and turbine spin echo MRI sequence, and compared it with the findings of MRI in vivo.
, 11 representative areas were sampled in four cases in which mrI scans were available for histological pathology of MRI-defined cortical superficial ferret disease.
, the samples were taken from a predetermined standard area of the brain with no knowledge of MRI results.
the continuous slices were dyed with sumo and sulfa and Perls Prussus blue, and immune tissue chemistry was β amyloid and GFAP.
8/14 cases (57%) and 0/3 control of cortological supersethic horn disease were found on ionized MRIs (P s 0.072).
In histopathology, cortical superficial ferropathy corresponds to iron-positive hemoglobin deposition in the lower cavity of the cobweb membrane and in the shallow epithelial layer, indicating chronic bleeding events originating from soft meninges.
increase in the severity of cortical superficial tetring disease was associated with an increase in reactive astrological glial cells.
, in cases of cerebral amyloid vascular disease, a total of 65 Perls-stained slices were evaluated for cortical surface tin disease in combination with MRI positioning and non-location sampling.
Mild to moderate to severe cortitological superficial iron chip disease is associated with congenital cracking of the blood vessel walls of soft meninges (late forms of vascular damage associated with cerebral amyloid vascular disease) (P -lt;0.0001), but the severity of cerebral amyloid vascular disease in cortogenic blood vessels is reduced (P s 0.048).
In the case of secondary tissue damage, moderate to severe cortitological surface iron chip disease was associated with micro-infarction (P s 0.025), but no slight bleeding (P s 0.973).
overall, these data show that cortical superficial tin disease on MRIs corresponds to iron-positive deposits in the shallow epithelial layer, representing a chronic manifestation of soft meningococral hemorrhage attacks.
appears to be the result of late-stage cerebral amyloid vascular disease, which appears to be the result of soft meninges, and may cause secondary ischemic damage at the place of the disease.
origins: Andreas Charidimou, Valentina Perosa, Matthew P Frosch, Neuropathological correlates of the cortical superficial siderosis in cerebral amyloid angiopathy. MedSci Original Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Original" are owned by Mets Medicine and are not authorized to be reproduced by any media, website or individual, and are authorized to be reproduced with the words "Source: Mets Medicine".
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