225 research outputs found
Macrocranium and macrencephaly in neurofibromatosis
Data were collected on 52 patients (30 males and 22 females) with neurofibromatosis. Using the volumetric method of Gordon, it was found that 44% of the patients had cranial capacities above the 95th percentile (70% were above the 50th percentile). The presence of intracranial tumors and/or hydrocephalus did not influence skull size. Four patients above the 95th percentile had normal pneumoencephalograms and cerebral angiograms, indicating that the cause of the macrocranium, in some instances at least, is macrencephaly. Volumetric measurement of the sella turcica in 27 of the 52 patients gave results which strongly suggest that idiopathic enlargement of the sella in neurofibromatosis is uncommon, if not rare. Skull films of 26 patients with tuberous sclerosis did not show an increase in cranial capacity similar to that found in neurofibromatosis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46770/1/256_2004_Article_BF00347724.pd
Omental and pleural milky spots: different reactivity patterns in mice infected with Schistosoma mansoni reveals coelomic compartmentalisation
In vertebrate animals, pleural and peritoneal cavities are repositories of milky spots (MS), which constitute an organised coelom-associated lymphomyeloid tissue that is intensively activated by Schistosoma mansoni infection. This study compared the reactive patterns of peritoneal MS to pleural MS and concluded from histological analysis that they represent independent responsive compartments. Whole omentum, lungs and the entire mediastinum of 54 S. mansoni-infected mice were studied morphologically. The omental MS of infected animals were highly activated, modulating from myeloid-lymphocytic (60 days of infection) to lymphomyeloid (90 days of infection) and lymphocytic or lymphoplasmacytic (160 days of infection) types. The non-lymphoid component predominated in the acute phase of infection and was expressed by monocytopoietic, eosinopoietic and neutropoietic foci, with isolated megakaryocytes and small foci of late normoblasts and mast cells. Nevertheless, pleural or thoracic MS of infected mice were monotonous, consisting of small and medium lymphocytes with few mast and plasma cells and no myeloid component. Our data indicate that compartmentalisation of the MS response is dependent on the lymphatic vascularisation of each coelomic cavity, limiting the effects or consequences of any stimulating or aggressive agents, as is the case with S. mansoni infection
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