Histology and histopathology Vol.15, nº 2 (2000)
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- PublicationOpen AccessCharacterization of inflammatory reaction in upper airways of cystic fibrosis patients(Murcia : F. Hernández, 2000) Lesprit, E.; Escudier, E.; Roger, G.; Pruliere, V.; Lenoir, G.; Reinert, Ph.; Coste, A.Inflammatory cell populations have not been yet precisely evaluated in cystic fibrosis (CF) airways. We intended to characterize morphological modifications, inflammatory cell infiltration and cell proliferation in nasal tissues obtained from 15 CF patients and from 6 non-CF patients with nasal polyposis. Morphological analysis showed an intense inflammatory infiltration in CF and non-CF tissues with only few modifications in the epithelium from CF tissues. Inflammatory cell populations characterized by specific immunolabeling were quantified, showing a predominance of macrophages and T- and B-lymphocytes and only moderate numbers of neutrophils in CF tissues; in non-CF polyps, lymphocytes and eosinophils were abundant. Proliferating cell percentages quantified after proliferating cell nuclear antigen immunolabeling were 5.3+4.1% (mean t SD) in CF polyps and 3.1?1.2% in non-CF polyps in epithelium but were very low in lamina propria. Intense inflammation in nasal tissues from CF patients is therefore dominated by macrophages and lymphocytes rather than by neutrophils. While morphology is preserved, proliferation is high in epithelium from CF polyps. These findings should be regarded in the future for a better understanding of inflammation in CF airway disease.
- PublicationOpen AccessGain of function properties of mutant p53 proteins at the mitotic spindle cell cycle checkpoint(Murcia : F. Hernández, 2000) Hixon, M.L.; Flores, A.; Wagner, M.; Gualberto, A.Mutations in the p53 tumor suppressor gene locus predispose human cells to chromosomal instability. This is due in part to interference of mutant p53 proteins with the activity of the mitotic spindle and postmitotic cell cycle checkpoints. Recent data demonstrates that wild type p53 is required for postmitotic checkpoint activity, but plays no role at the mitotic spindle checkpoint. Likewise, structural dominant p53 mutants demonstrate gain-of-function properties at the mitotic spindle checkpoint and dominant negative properties at the postmitotic checkpoint. At mitosis, mutant p53 proteins interfere with the control of the metaphase-toanaphase progression by up-regulating the expression of CKsl, a protein that mediates activatory phosphorylation of the anaphase promoting complex (APC) by Cdc2. Cells that carry mutant p53 proteins overexpress CKsl and are unable to sustain APC inactivation and mitotic arrest. Thus, mutant p53 gain-of-function at mitosis constitutes a key component to the origin of chromosomal instability in mutant p53 cells.
- PublicationOpen AccessNeonatal treatment with monosodium glutamate MSG structure of the TSH-immunoreactive pituitary cells(Murcia : F. Hernández, 2000) Miskowiak, B.; Partyka, M.Glutamic acid represents the most abundant stimulatory neurotransmitter in the central nervous system. Monosodium glutamate (MSC), subcutaneously administered to newborn rats in the perinatal period, induces lesions in 80 to 90% of the neurocytes of arcuate nuclei in the hypothalamus. These nuclei are the site of production of numerous stimulatory and inhibitory hormones including growth hormone releasing hormone (GHRH). The present studies were performed on male Wistar strain rats, subcutaneously injected on days 2, 4, 6, 8, and 10 of postnatal life with MSC at a dose of 4 mglg body weight. Eighteen-month-old rats were additionally treated with Ambinon. When the animals reached the ages of 6 or 12 months, their body weight, body length and weight of pituitary were determined. On parafrin sections, using imrnunohistochemical techniques, TSHimmunoreactive cells were detected and characterised by computerised image analysis. The results were subjected to statistical analysis using Student's t test. The rats which were perinatally treated with MSC and examined after 6 or 12 months of life were obese and shorter than control rats by 7% and 10% respectively. They also exhibited a reduction in the weight of the pituitary of 30% and 40% respectively in the two age groups. The proportion of TSH-immunoreactive cells in the pituitary remained unchanged and amounted to 4.5% in the 6-month-old and 5.4% in the 12-month-old rats respectively. The number of TSH-positive cells per mm 2 area remained unchanged. The area and circumference of the cells in the 12-month-old rats were reduced by 22% and 18%, respectively. Perinatal injury to hypophyseal arcuate nuclei induced by monosodium glutamate injection, was not associated with any significant alterations in pituitary structure, as defined by the proportion of pituitary volume occupied by TSH-immunoreactive cells.
- PublicationOpen AccessDuodenal endocrine cells in mice with particular regard to age-induced changes(Murcia : F. Hernández, 2000) Sandstrom, O.; El-Salhy, M.Duodenal endocrine cell types in four age groups of NMRI mice (1, 3, 12 and 24 months old) were identified by immunocytochemistry and quantified by computerized image analysis. Whereas the number of secretin-immunoreactive cells was significantly increased in the 24-month-old group, the number of GIP-immunoreactive cells was reduced in 12-month-old compared with 3-month-old mice. The number of somatostatin-immunoreactive cells was fewer in both the 12- and 24-month-olds vis-a-vis the 3-month-old mice. Whereas serotonin-immunoreactive cells were fewer in both 1-month-old and 12-month-old mice, they were more numerous in 24-month-old mice then in the 3- month-old ones. The number of gastrin/CCK-immunoreactive cells was unaffected by age. The cell secretory index (CSI) of secretin- and serotonin-immunoreactive cells was increased in the 24-month-old mice vis-a-vis the 3-month-old ones and the CSI of GIP- and somatostatin-immunoreactive cells was increased in 12- month-old mice vis-a-vis 3-month-old rnice. In contrast, the CSI of somatostatin- and serotonin-immunoreactive cells in 1-month-old mice was lower than that of 3- month-old-mice. The nuclear volume of secretin-, GIP-, gastrin/CCK- and serotonin-immunoreactive cells was less in 1-month-olds than in 3-month-old mice. Whereas the nuclear volume of somatostatin-immunoreactive cells was decreased in 12-month-old animals, that of gastrin/CCK- and serotonin-immunoreactive cells was greater in 24-month-old mice than in 3-month-old ones. It is concluded that these changes may be secondary to structural and functional changes in the gastrointestinal tract caused by ageing. It is possible that these changes are involved in the development of dysfunction of the gut observed at advanced age.
- PublicationOpen AccessPathophysiology of primary hyperparathyroidism(Murcia : F. Hernández, 2000) Hellman, P.; Carling, T.; Rask, L.; Akerstrom, G.Parathyroid gland is the overall regulatory organ within the systemic calcium homeostasis. Through cell surface bound calcium-sensing receptors external calcium inversely regulates release of parathyroid hormone (PTH). This mechanism, which is voltage independent and most sensitive around physiologic calcium concentrations, is regulated through a 120 kDa calcium sensing receptor, CaR. Inherited inactivation of this receptor is the cause for familial hypocalciuric hypercalcemia (FHH). Parallel research identified the 550 kDa glycoprotein megalin, which also is expressed on the parathyroid cell surface, as another potential calcium sensing protein. Although this protein expresses numerous calcium binding sites on its external domain, its main function may be calcium sensitive binding and uptake of steroid hormones, such as 25-OH-vitamin Dg (bound to vitamin D binding protein) and retinol. In hyperparathyroidism (HPT), excessive PTH is secreted and the calcium sensitivity of the cells reduced, i.e. the set-point, defined as the external calcium concentration at which half-maximal inhibition of PTH release occurs, shifted to the right. Pathological cells have reduced expression of both CaR and megalin, and reduced amount of intracellular lipids, possibly including stored steroid hormones. A number of possible genetic disturbances have been identified, indicating multifactorial reasons for the disease. In postmenopausal women, however, the individual group with highest incidence of disease, a causal relation to reduced effect of vitamin D is possible. An incipient renal insufficiency with age, lack of sunshine in the Northern Hemisphere, and an association to the baT haplotype of the vitamin D receptor supports this theory. This review summarizes data on regulation of PTH release, dysregulation in HM; as well as proliferation of parathyroid cells.