Histology and histopathology Vol.22, nº10 (2007)
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- PublicationOpen AccessThe melanogenic system of the liver pigmented macrophages of Rana esculenta L. - Tyrosinase activity(Murcia : F. Hernández, 2007) Gallone, A.; Sagliano, A.; Guida, G.; Ito, S.; Wakamatsu, K.; Capozzi, V.; Perna, G.; Zanna, P.; Cicero, R.The enzyme system responsible for Amphibian Kupffer Cell (KC) melanogenesis has not been entirely elucidated. This research demonstrates that the KC melanosomes of Rana esculenta L. possess a tyrosine-hydroxylase (TH) activity, showing that a tyrosinase is the enzyme involved in the melanogenesis. The TH reaction depends on catalytic Dopa as a cofactor and is not affected by catalase or H2O2, showing that it is catalysed by the tyrosinase and not by the peroxidase present in the melanosomes. The TH reaction is activated by Cu2+ ions but not by other tyrosinase activators such as limited proteolysis, protein ageing, and Sodium Dodecyl Sulphate (SDS). SDS inhibited the KC TH activity even below the critical micelle concentration. All these results suggest that the KC-tyrosinase differs in structure from other known tyrosinases. Using anti-KC-tyrosinase antobodies, we observed that the sites of the tyrosinase location within the cell are the same as those described in the melanocytes. In the immunoblots, the anti-KC-tyrosinase antibodies also recognised two protein bands, at the higher molecular weight ranges, in the protein electrophoretic pattern. Moreover, the tyrosinase activity was limited to the highest molecular weight band of about 260 kDa, suggesting that the enzyme activity could depend on a molecular aggregate. The melanin produced in the liver was found to be a 5,6-dihydroxyindole-rich eumelanin similar to the Sepia melanin.
- PublicationOpen AccessExperimental change on dopaminergic neurons in striatum of Parkinson disease rats(Murcia : F. Hernández, 2007) Chen, X.Y.; Li, Jiang; Qi, W.Q.; Shen, S.H.Background: Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by selective and progressive demise of dopaminecontaining neurons in the midbrain. In this study, we observe the expression of c-Jun in the striatum of rats with 6-hydroxydopamine (6-OHDA)-lesions after apomorphine (APO) intraperitoneal injection (ip) in substantia nigra compacta (SNc), and to study the mechanism of the rotations behavior. Design: The 6- OHDA was unilaterally injected into rat right SNC. The APO- induced abnormal rotations were investigated on the 1st, 4th, 7th, 14th, 21st days after lesion, respectively. Meanwhile dopaminergic degeneration and c-Jun expression were observed with microscope. Nissl’s body staining and immunohistochemical method (ABC) were employed to study the changes of tyrosine hydroxylase (TH) and c-Jun in DA neurons. Results: We found that the number of dopaminergic neurons decreased gradually in the lesioned site and those neurons’ electron-microscopic structure was severe damaged. There were over 75% of dopaminergic neurons lost, contralateral rotations over 7 turns per minute and c-Jun expressing in the ipsilateral striatum. Conclusion: Dopaminergic neurons deletion may be linked to upregulation of c-Jun.
- PublicationOpen AccessCurrent concepts in human prion protein (Prp) misfolding, Prnp gene polymorphisms and their contribution to Creutzfeldt-Jakob Disease (CJD)(Murcia : F. Hernández, 2007) Michalczyk, K.; Ziman, M.Transmissible spongiform encephalopathies are a group of neural degenerative diseases that may be infectious, sporadic, or hereditary and are associated with an abnormally folded prion protein. Unfortunately at the current time it is not at all clear what the normal structure of the prion protein actually is or how it is toxic to cells. Extensive research on prion diseases has led to a dramatic increase in understanding of the pathogenesis of prion disorders, which will hopefully lead to the development of effective treatments. The inability to detect the disease in blood using current technology has made screening difficult. While fortunately there has been a decline in the number of clinical cases of transmissible variant CJD, evidence indicates that very long incubation periods can occur in humans so there may be a long slow, gradual epidemic. In particular, clinical cases in genotypes other than those homozygous for methionine at codon 129 of PRNP have not yet occurred, but such cases might be expected to have longer incubation periods and show differences in pathology to those seen to date. proportion of infected animals develop sub-clinical disease. Moreover, results from a large prevalence study in humans show that several cases test positive but do not develop clinical disease. It is possible therefore that further cases of secondary transmission could occur by iatrogenic spread, which could result in vCJD persisting in the UK at low levels for many years, highlighting the importance of continued vigilance.
- PublicationOpen AccessMüllerianosis(Murcia : F. Hernández, 2007) Batt, R.E; Smith, R.A.; Buck Louis, G.M.; Martin, D.C.; Chapron, C.; Koninckx, P.R.; Yeh, J.Müllerianosis may be defined as an organoid structure of embryonic origin; a choristoma composed of müllerian rests - normal endometrium, normal endosalpinx, and normal endocervix - singly or in combination, incorporated within other normal organs during organogenesis. A choristoma is a mass of histologically normal tissue that is “not normally found in the organ or structure in which it is located” (Choristoma, 2006). Müllerian choristomas are a subset of non-müllerian choristomas found throughout the body. Histologically, endometrial-müllerianosis and endometriosis are both composed of endometrial glands and stroma, but there the similarity ends. Their pathogenesis is different. Sampson faced the same difficulty with pathogenesis and nomenclature when he wrote: “The nomenclature of misplaced endometrial or müllerian lesions is a difficult one to decide upon.” “The term müllerian would be inclusive and correct, but unfortunately it suggests an embryonic origin.” Sampson then divided “misplaced endometrial or müllerian tissue” into “four or possibly five groups, according to the manner in which this tissue reached its ectopic location” (Sampson, 1925). Sampson’s classification of heterotopic or misplaced endometrial tissue is based on pathogenesis: 1) “direct or primary endometriosis” [adenomyosis]; “a similar condition occurs in the wall of the tube from its invasion by the tubal mucosa” [endosalpingiosis]; 2) “peritoneal or implantation endometriosis;” 3) “transplantation endometriosis;” 4) “metastatic endometriosis;” and 5) “developmentally misplaced endometrial tissue. (I admit the possibility of such a condition, but have never been able to appreciate it.)” (Sampson, 1925). It is precisely this condition “developmentally misplaced endometrial tissue,” [müllerianosis] that is the subject of this review.
- PublicationOpen AccessThe absence of one or both nidogens does not alter basement membrane composition in adult murine kidney(Murcia : F. Hernández, 2007) Gersdorff, N.; Otto, S.; Roediger, Matthias; Kruegel, J.; Miosge, NicolaiNidogen-1 and nidogen-2 are major components of all basement membranes and are considered to function as link molecules between laminin and collagen type IV networks. Surprisingly, the knockout of one or both nidogens does not cause defects in all tissues or in all basement membranes. In this study, we have elucidated the appearance of the major basement membrane components in adult murine kidney lacking nidogen-1, nidogen-2, or both nidogens. To this end, we localized laminin-111, perlecan, and collagen type IV in knockout mice, heterozygous (+/-) or homozygous (-/-) for the nidogen-1 gene, the nidogen-2 gene, or both nidogen genes with the help of light microscopic immunostaining. We also performed immunogold histochemistry to determine the occurrence of these molecules in the murine kidney at the ultrastructural level. The renal basement membranes of single knockout mice contained a similar distribution of laminin-111, perlecan, and collagen type IV compared to heterozygous mice. In nidogen double-knockout animals, the basement membrane underlying the tubular epithelium was sometimes altered, giving a diffuse and thickened pattern, or was totally absent. The normal or thickened basement membrane of double-knockout mice also showed a similar distribution of laminin-111, perlecan, and collagen type IV. The results indicate that the lack of nidogen-1, nidogen-2, or both nidogens, plays no crucial role in the occurrence and localization of laminin-111, collagen type IV, and perlecan in murine tubular renal basement membranes
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