Vogels en mensen in Nederland 1500-1920

Dam, P.J.E.M. van [Promotor]Siepel, H. [Promotor

Helpende burgers: wegsturen of niet?

Burgers helpen ten tijde van crises. Slachtoffers helpen, verkeer regelen: alles wat op dat moment nodig is om de situatie het hoofd te bieden. Wat betekent dat voor de hulpdiensten als die ter plekke komen? Burgers hun gang laten gaan? Instrueren? Of juist wegsturen

High detection rate of adenomas in familial colorectal cancer

Item does not contain fulltextBACKGROUND AND AIMS: Subjects with one first-degree relative (FDR) with colorectal cancer (CRC) 1) adenomas. Men were more often found to have an adenoma than women (24% vs 14.3%; p=0.01). Adenomas were more frequent in group B compared with group A (22.0% vs 15.6%; p=0.09). CONCLUSION: The yield of colonoscopic surveillance in familial CRC is substantially higher than the yield of screening reported for the general population

Demyelination and axonal dystrophy in alpha A-crystallin transgenic mice

Homozygous mice transgenic for αA-crystallin, one of the structural eye lens proteins, developed hindlimb paralysis after 8 weeks of age. To unravel the pathogenesis of this unexpected finding and the possible role of αA-crystallin in this pathological process, mice were subjected to a histopathological and immunohistochemical investigation. Immunohistochemistry showed large deposits of αA-crystallin in the astrocytes of the spinal cord, and in the Schwann cells of dorsal roots and sciatic nerves. Additionally, microscopy showed dystrophic axons in the spinal cord and digestion chambers as a sign of ongoing demyelination in dorsal roots and sciatic nerves. Apart from a few areas with slight αA-crystallin-immunopositive structures, the brain was normal. Because the αA-crystallin protein expression appeared in specific cells of the nervous system (astrocytes and Schwann cells), the most plausible explanation for the paralysis is a disturbance of cell function caused by the excessive intracytoplasmic accumulation of the αA-crystallin protein. This is followed by a sequence of secondary changes (demyelination, axonal dystrophy) and finally arthrosis. In conclusion, αA-crystallin transgenic mice develop a peripheral and central neuropathy primarily affecting spinal cord areas at the dorsal side, dorsal root and sciatic nerve