Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the morphology of cortical microvessels in the brains of 10 patients who had died after receiving a traumatic head injury (THI). Scanning electron microscopy (SEM) of vascular corrosion casts, confocal microscopy of histological sections after immunocytochemistry, and detection of apoptosis by terminal dUTP nick end labeling (TUNEL) were used. Microvascular casts showed an angioarchitectonic distribution that was defined as normal according to results obtained in a previous, nontraumatic series of subjects. However, when we compared them with previous works, the cast surface of some of the microvessels showed three types of morphological alterations: longitudinal folds, sunken surfaces with craters, and a significant flattening with reduction of lumen. The vessels that were primarily affected were the arterioles and capillaries of the middle and deep cortical vascular zones. Immunostaining with the monoclonal antibody MAS-336 against endothelial cells also showed the presence of longitudinal folds with a thinning of the vascular lumen, cytoplasmic round bodies, and a thickening of the endothelial cell membrane. The TUNEL technique revealed a positive staining of some endothelial cells. The structural alterations we observed indicate that microvessels undergo endothelial cell damage after THI. We suggest that this kind of lesion and the secondary functional injury to the blood-brain barrier (BBB) could play an important role in the development of the secondary lesions that these patients show in the subacute phase.
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PMID:Morphological features in human cortical brain microvessels after head injury: a three-dimensional and immunocytochemical study. 1280 43

We conducted a series of experiments to elucidate the behavior of the human precorneal tear film (PCTF) during blinking and horizontal and vertical saccades. Methodology included video-interferometry with subsequent image cross-correlation (tear film lipid layer [TFLL]) and video-microscopy (mucoaqueous subphase [MAS]). We observed that the TFLL interference pattern deteriorates rapidly with successive blinks and degrades slowly with repeated horizontal saccades during blink suppression when dark arcs of thinning appear in the fluorescein-stained PCTF. Furthermore, after full downgaze and a return to the primary position, a transient horizontal bright band appears, deep to the spreading TFLL. It may be followed by local disturbances in the interference pattern. Two horizontal dark bands form in the stained PCTF after the return saccade. PCTF disruption may occur below the lower band during blink suppression. We concluded that shearing during horizontal saccades is insufficient to disturb the tear film structure greatly. The MAS and TFLL move together as a fluid shell. The dark arcs/bands are caused by meniscus-induced thinning, imprinted onto the PCTF at the lid margin. Their stability during blink suppression suggests that the MAS has gel-like properties. The horizontal bright bands are probably due to transient corneal indentation in downgaze. In downgaze, the disturbance of the TFLL and MAS below the dark bands is possibly due to shearing across the MAS in the return phase. This could cause desiccating stress in everyday activities, such as working at a computer.
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PMID:The precorneal tear film as a fluid shell: the effect of blinking and saccades on tear film distribution and dynamics. 2528 71