Histology and histopathology Vol.17, nº 1 (2002)
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- PublicationOpen AccessMorphological changes in the mink area postrema during growth and under different stages of sexual activity(Murcia : F. Hernández, 2002) Aleman, N.; Cerutti, P.; Guerrero, F.The histological features of the area postrema (AP) of mink brains of both sexes were investigated at different ages and physiological conditions with light and electron microscopy. The mink AP was a twin-winged structure located at the dorsal surface of the medulla oblongata and consisted of neurons, glial cells, and both continuous and fenestrated capillaries enmeshed in a rich neuropil. The ventricular surface of the mink AP was covered by a single layer of tanycytes except at its most caudal part that was covered by a basal membrane derived from the pia mater. Supraependymal cells and intraventricular axons were also a common finding over the apical poles of tanycytes. However, our study demonstrates that the mink AP acquires the above general features at an advanced postnatal time and that, once fully developed, it undergoes morphological changes that can be directly linked to the aging process and sexual activity of the animals.
- PublicationOpen AccessDiabetic nephropathy: The central role of renal proximal tubular cells in tubulointerstitial injury(Murcia : F. Hernández, 2002) Phillips, A.O.; Steadman, R.Diabetic nephropathy is now the commonest cause of end stage renal disease and accounts for 30- 40% of all patients requiring renal replacement therapy. Furthermore, the incidence of diabetic nephropathy continues to increase, in part due to the improved survival of type 2 diabetic patients as the cardiovascular mortality in this group declines (Ritz and Stefanski, 1996). Clinically incipient nephropathy is first manifest by the onset of persistent microalbuminuria, after which, overt diabetic nephropathy is heralded by the appearance of persistent proteinuria. Subsequently, there is a progressive decline in glomerular filtration rate (GFR) resulting, within 5 years, in end stage renal disease in 50% of patients (Hasslacher et al., 1989). The pathology of the renal lesions are similar in type I and II diabetes ( Taft et al., 1994), although it has been suggested that there is more heterogeneity in type II diabetes (Chihara et al., 1986). Studies analysing structural-functional relationships have demonstrated that the development of proteinuria correlates with the degree of mesangial expansion (Mauer et al., 1984; White and Bilous, 2000). Although diabetic nephropathy was traditionally considered a primarily glomerular disease, it is now widely accepted that the rate of deterioration of function correlates best with the degree of renal tubulointerstitial fibrosis (Mauer et al., 1984, Bohle et al., 1991). This suggests that although in the majority of patients the primary event is a condition manifest by glomerular changes resulting in proteinuria, the long-term outcome is determined by events in the renal interstitium. Wi t h the increasing awareness of the importance of these pathological interstitial changes, interest has focused on the role of cells, such as the epithelial cells of the proximal tubule (PTC) or the interstitial myofibroblast, in the initiation of fibrosis. The aim of the present review is to analyse the available data supporting the role for the PTC in orchestrating renal interstitial fibrosis in diabetic nephropathy as a result of glucose-dependent alterations in PTC function. The potential for subsequent e ffects on PTC-fibroblast cross-talk will also be considered.
- PublicationOpen AccessGenetic and epigenetic alterations of tumor suppressor and tumor-related genes in gastric cancer(Murcia : F. Hernández, 2002) Tamura, G.Both genetic and epigenetic alterations of tumor suppressor and tumor-related genes involved in the pathogenesis of gastric cancer are reviewed here, and molecular pathways of gastric carcinogenesis are proposed. Gastric carcinomas are believed to evolve from native gastric mucosa or intestinal metaplastic mucosa that undergoes genetic and epigenetic alterations involving either the suppressor pathway (defects in tumor suppressor genes) or mutator pathway (defects in DNA mismatch repair genes). Methylation of E - c a d h e r i n in native gastric mucosa results in undifferentiated carcinomas (suppressor pathway), while methylation of hMLH1 results in differentiated foveolartype carcinomas (mutator pathway). The majority of d i fferentiated gastric carcinomas however, arise from intestinal metaplastic mucosa and exhibit structural alterations of tumor suppressor genes, especially p 5 3. They appear to be related to chronic injury, perhaps due to Helicobacter pylori infection. Approximately 20% of differentiated carcinomas (ordinary-type) have evidence of mutator pathway tumorigenesis. Mutations of E - c a d h e r i n are mainly involved in the progression of d i fferentiated carcinomas to undifferentiated tumors. The molecular pathways of gastric carcinogenesis depend on the histological background, and gastric carcinomas show distinct biological behaviors as a result of discernible cellular genetic and epigenetic alterations.
- PublicationOpen AccessHistological study of timing and embryology of notochordal abnormalities in rat exposed in utero to Doxorubicin(Murcia : F. Hernández, 2002) Menegola, E.; Broccia, M.L.; Di Renzo, F.Experimental Doxorubicin-exposure in utero is correlated with foetal oesophageal atresia, tracheooesophageal fistula, axial alterations. While gastrointestinal and respiratory defects have been larg e l y investigated, only sporadic data have been published to date on notochordal and vertebral defects. The aim of this work was the study of the genesis of chordal and vertebral abnormalities in rat embryos and foetuses exposed to Doxorubicin and the study of their correlation with oesophageal and tracheal defects. For this purpose, pregnant rats were i.p. injected with saline (control) or with 4mg/Kg b.w. Doxorubicin on days 9.5 and 10.5 of gestation. Embryos and foetuses were morphologically analysed on days 10.5-15 and 16, 18, 20 of gestation respectively, fixed in formaldehyde and histologically processed. Slides were routinely stained with haematoxylin-eosin (11-15 days post coitum embryos and all foetuses) or specifically stained with aniline blue for the staining of basal laminae (10.5 days post coitum embryos). Moreover, some foetuses at term (20 days post coitum) were processed for bone and cartilage staining. The data obtained in the present work confirm the specificity of Doxorubicin in inducing gastro-intestinal and tracheal defects, describe the genesis of these defects step by step, describe the type and the genesis of notochordal abnormalities and their fate and exclude the role of Doxorubicin in inducing axial skeletal malformations.
- PublicationOpen AccessUltrastructural abnormalities of muscle spindles in the rat masseter muscle with malocclusion-induced damage(Murcia : F. Hernández, 2002) Bani, D.; Bergamini, M.Human temporomandibular disorders due to disturbed occlusal mechanics are characterized by sensory, motor and autonomic symptoms, possibly 1 related to muscle overwork and fatigue. Our previous study in rats with experimentally-induced malocclusion due to unilateral molar cusp amputation showed that the ipsilateral masseter muscles undergo morphological and biochemical changes consistent with muscle hypercontraction and ischemia. In the present study, the masseter muscle spindles of the same malocclusionbearing rats were examined by electron microscopy. Sham-operated rats were used as controls. In the treated rats, clear-cut alterations of the muscle spindles were observed 26 days after surgery, when the extrafusal muscle showed the more severe damage. The fusal alterations affected predominantly capsular cells, intrafusal muscle fibers and sensory nerve endings. These results suggest that in the malocclusion-bearing t rats, an abnormal reflex regulation of the motor activity of the masticatory muscles may take place. They also allow us to hypothesize that muscle spindle alterations might be involved in the pathogenesis of human temporomandibular disorders.