Histology and histopathology Vol.20, nº 2 (2005)
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- PublicationOpen AccessCorneal endothelial cell density decreases with age in emmetropic eyes(Murcia : F. Hernández, 2005) Sanchis-Gimeno, J.A.; Lleó-Pérez, A.; Alonso, L.M.; Rahhal, M.S.; Martínez Soriano, F.Purpose: To analyze the corneal endothelial cell density in healthy adult emmetropic subjects. Methods: We analyzed the corneal endothelial cell density of a group made up of 225 emmetropic subjects (n=225). As age-matched control groups we analyzed two other groups, one made up of myopic subjects (n=209) and the other made up of hyperopic subjects (n=203). We recorded the mean of three consecutive measurements of the corneal endothelial cell density using the Topcon SP-2000P non-contact specular microscope (Topcon Corp., Tokyo, Japan). Results: The mean age was 38.6±11.8 years, 40.7±12.2 years, and 39.2±10.5 years for emmetropic, myopic and hyperopic subjects respectively (p=0.994). No significant differences (p=0.920) in endothelial cell density values were found between emmetropic (2985±245 cells/mm2), myopic (2936±258 cells/mm2) and hyperopic eyes (2946±253 cells/mm2). Lower corneal endothelial cell density values were found in older emmetropic (p<0.001), myopic (p<0.001), and hyperopic subjects (p<0.001). A significant correlation between endothelial cell density and age was found in emmetropic (r= -0.958; p<0.001), myopic (r= -0.954; p<0.001) and hyperopic subjects (r= -0.948; p<0.001). Conclusions: In healthy emmetropic subjects there is a reduction in corneal endothelial cell density with age although there are no differences in corneal endothelial cell density values between emmetropic, myopic and hyperopic subjects.
- PublicationOpen AccessEffects of single, double or triple combinations of octreotide, galanin and serotonin on a human pancreatic cancer cell line(Murcia : F. Hernández, 2005) Tjomsland, V.; El-Salhy, M.The human pancreatic cancer cell line (SW 1990) was exposed to 0.2 µg/ml of octreotide, galanin or serotonin as single, double or triple combinations. The tumor cells were checked at 3, 6 and 12 hours. In order to determine the number of viable cancer cells, the MTTassay was used. Proliferation, apoptosis and the expression of epidermal growth factor were detected with immunohistochemistry using the avidin-biotin complex method. In addition, apoptosis was also detected with (TUNEL) method. The primary antibodies used were proliferating cell nuclear antigen (PCNA), anti-poly (ADP-ribose) polymerase (PARP) and antihuman epidermal growth factor. Single treatment with octreotide or serotonin reduced, the number of viable cells and the proliferation index at all observation times. Galanin increased the number of viable cells and the proliferation index. Whereas double treatments containing octreotide reduced the number of viable cells, those containing galanin increased the number. The effect of single, double or triple treatment on the apoptotic index obtained with both TUNEL method and PARP expression varied depending on the combination and the observation time. Octreotide did not affect the tumor cell expression of EGF. Galanin and serotonin, on the other hand, increased the expression of EGF Whereas triple combination increased the expression of EGF after 6 h, all the other double combinations decreased this expression. It has been concluded that treatment with a combination of octreotide and serotonin may be useful in clinical settings.
- PublicationOpen AccessFunctional aspects of the somatostatinergic system in the retina and the potential therapeutic role of somatostatin in retinal disease(Murcia : F. Hernández, 2005) Casini, G.; Catalani, E.; Dal Monte, M.; Bagnoli, P.The somatostatinergic system of the retina has been investigated in a variety of studies. A considerable amount of experimental evidence is available concerning the patterns of expression of somatostatin (SRIF) and its receptors in vertebrate retinas. However the functional roles of this peptidergic system in retinal physiology are far from being elucidated. Nonetheless, data have been provided concerning the regulatory action of SRIF on the excitability of different retinal cell types and on the modulation of ion channels in different vertebrate retinas. The present review is focused on recent and unpublished investigations of the mouse retina relative to the involvement of specific SRIF receptors in the regulation of ion channels and transmitter release, the transduction pathways coupled to SRIF receptors, and the mechanisms regulating the expression of SRIF and its receptors as derived from studies in transgenic animal models. In these models, altered expression levels of SRIF or of specific SRIF receptors have also been found to affect the morphology of retinal cell types (namely the rod bipolar cells) and to result in functional alterations at the level of both ion channel regulation and transmitter release. These new pieces of evidence constitute an important step forward in the understanding of the functional actions of the retinal somatostatinergic system, although our current knowledge is far from being exhaustive. The ultimate goal of understanding SRIF functional actions in the retina is concerned with the possibility of using SRIF or its analogs as therapeutic agents to cure retinal diseases. Indeed, encouraging results are being obtained in clinical investigations focused on the use of SRIF analogs to treat diabetic retinopathy, a retinal disease with high social impact and originating as a complication of diabetes. The closing part of the present paper examines the evidence supporting SRIF as a promising therapeutic agent in this disease.
- PublicationOpen AccessImmunodetection of aldose reductase in normal and diseased human liver(Murcia : F. Hernández, 2005) Brown, K.E.; Broadhurst, K.A.; Mathahs, M.M.; Kladney, R.D.; Fimmel, C.J.; Srivastava,S.K.; Brunt, E.M.Aldose reductase is an NADPH-dependent aldo-keto reductase best known as the rate-limiting enzyme of the polyol pathway that is implicated in the complications of diabetes. Aldose reductase appears to be involved in a variety of disease states other than diabetes, presumably due to its ability to catalyze the reduction of a broad spectrum of aldehydes, including some cytotoxic products of lipid peroxidation. Although the data regarding expression of aldose reductase in normal liver are conflicting, prior studies have suggested that the enzyme may be induced in diseased liver. The goal of these studies was to characterize expression of aldose reductase in normal and diseased human liver, using RT-PCR, Western analysis and immunohistochemistry. Aldose reductase transcripts and protein were detected at low levels in control human livers. In contrast, levels of aldose reductase mRNA and protein were increased in chronically diseased human livers. Immunohistochemistry demonstrated localization of aldose reductase in sinusoidal lining cells; dual immunofluorescence confocal microscopy with the macrophage marker, CD68, confirmed that the aldose reductase-positive sinusoidal lining cells were Kupffer cells. Abundant aldose reductase-positive, CD68- positive cells were present in the fibrous septa of cirrhotic livers, accounting for the increase in Immunostaining of human lung, spleen and lymph node revealed that macrophages in those tissues also express aldose reductase. These data are the first to demonstrate that aldose reductase is expressed by human macrophages in various tissues and suggest that this enzyme may play a role in immune or inflammatory processes.
- PublicationOpen AccessHuman and animal spongiform encephalopathies are the result of chronic autoimmune attack in the CNS: A novel medical theory supported by overwhelming experimental evidence(Murcia : F. Hernández, 2005) Ting Zhu, BaoSpongiform encephalopathies, also called "prion diseases", are fatal degenerative diseases of the central nervous system which can occur in animals (such as the "mad cow disease" in cattle) and also in humans. This paper presents a novel medical theory concerning the pathogenic mechanisms for various human and animal spongiform encephalopathies. It is hypothesized that various forms of prion diseases are essentially autoimmune diseases, resulting from chronic autoimmune attack of the central nervous system. A key step in the pathogenic process leading towards the development of spongiform encephalopathies involves the production of specific autoimmune antibodies against the disease-causing prion protein (PrPsc) and possibly other immunogenic macromolecules present in the brain. As precisely explained in this paper, the autoimmune antibodies produced against PrPsc are responsible for the conversion of the normal cellular prion protein (PrPc) to PrPsc, for the accumulation of PrPsc in the brain and other peripheral tissues, and also for the initiation of an antibody-mediated chronic autoimmune attack of the central nervous system neurons, which would contribute to the development of characteristic pathological changes and clinical symptoms associated with spongiform encephalopathies. The validity and correctness of the proposed theory is supported by an overwhelming body of experimental observations that are scattered in the biomedical literature. In addition, the theory also offers practical new strategies for early diagnosis, treatment, and prevention of various human and animal prion diseases.