Histology and histopathology Vol.22, nº 2 (2007)
Permanent URI for this collection
Browse
Browsing Histology and histopathology Vol.22, nº 2 (2007) by Issue Date
Now showing 1 - 12 of 12
Results Per Page
Sort Options
- PublicationOpen AccessImmunohistochemical analyses on serum proteins in nephrons of protein-overload mice by in vivo cryotechnique(Murcia : F. Hernández, 2007) Zhou, D.S.; Ohno, N.; Terada, N.; Li, Z.; Morita, H.; Inui, K.; Yoshimura, A.; Ohno, S.Immunohistochemical analyses on local distributions of serum proteins in living mouse kidneys are usually difficult to examine with conventional preparation methods. By using our “in vivo cryotechnique” combined with freeze-substitution, we have checked immunolocalizations of the serum proteins in nephrons of bovine serum albumin (BSA)-overload mice, and compared them with those obtained by the conventional preparation methods. In two days of daily BSA-injected mice, the immunolocalization of BSA could be observed in Bowman’s space and urinary tubules with their overt proteinuria, where another endogenous mouse albumin was similarly immunolocalized. The leakage of BSA and mouse albumin in Bowman’s space and their reabsorption into proximal tubules were detected in 55% of nephrons, where no leakage of immunoglobulin G1 (IgG1) was detected. However, the leakage of IgG1, in addition to BSA and mouse albumin, was detected in the other nephrons. By carefully examining immunolocalizations of BSA and IgG1, they were obviously different from those obtained by the conventional preparation methods without normal blood circulation into the kidneys. The immunolocalizations of both BSA and mouse serum proteins could be directly analyzed with the “in vivo cryotechnique”, suggesting that functional damage to glomerular filtration barriers are different at early stages of the BSA-overload mouse model, depending on each nephron of living mice.
- PublicationOpen AccessChromosome instability and kinetochore dysfunction(Murcia : F. Hernández, 2007) Tomonaga, T.; Nomura, F.Chromosomal instability (CIN) has been recognized as a hallmark of human cancer and is caused by continuous chromosome missegregation during mitosis. Proper chromosome segregation requires a physical connection between spindle microtubules and centromeric DNA and this attachment occurs at proteinaceous structures called kinetochore. Thus, defect in kinetochore function is a candidate source for CIN and the generation of aneuploidy. Recently, a number of kinetochore components have been shown to be mutated and/or aberrantly expressed in human cancers, which suggests an important role of kinetochore for CIN and carcinogenesis. In this article, we will discuss about how kinetochore dysfunction causes CIN and might lead to the development of cancer.
- PublicationOpen AccessHigh prevalence of human papillomavirus 16 in penile carcinoma(Murcia : F. Hernández, 2007) Pascual, A.; Pariente, M.; Godínez, J.M.; Sánchez-Prieto, R.; Atienzar, M.; Segura, M.; Poblet Martínez, Enriquef Human Papillomavirus (HPV) in penile carcinoma, we studied 49 patients with penile carcinoma. Formalin-fixed, paraffin-embedded tissue samples were collected from 64 samples of penile carcinoma from the Hospital General Universitario (Albacete, Spain). Cases were histologically classified and the polymerase chain reaction (PCR) method was used to detect the presence of HPV. Two sets of consensus primers were used, the My09/My11, and the GP5+/GP6+. All positive cases were sequenced in order to establish the implicated genotype. Our results showed that 38 of the 49 cases were positive for HPV (77,5%). HPV16 appeared in 32 (84,2 %) of the 38 positive cases and HPV18 in 4 (10,5%). Our data demonstrate that the My09/My11 primers are more sensitive than GP5+/GP6+ primers, although the combination of the two sets of primers notably increased the total number of HPV positive cases detected.
- PublicationOpen AccessChronic ethanol feeding alters the epithelial cell proliferation and apoptosis in rat gastric mucosa(Murcia : F. Hernández, 2007) Ge, Y. B.; Du, J.; Fan, L.L.; Li, Y.C.; Gu, L.We developed a chronic drinking rat model to investigate the long-term effects of ethanol feeding on cell proliferation and apoptosis in rat stomach. Adult male Sprague-Dawley (SD) rats received either an isocaloric control or drinking water containing 6% (v/v) ethanol as their only water intake for 1, 3, 7, 14 and 28 days. At the end of each feeding period, animals were sacrificed and the stomach was dissected for the sample preparation. The cell proliferation and apoptosis in gastric mucosa of rats in different groups were analyzed by flow cytometer, immunohistochemistry and computer image analysis. In the flow cytometric study, compared with the control, the cell apoptosis in gastric mucosa of the rats was enhanced during the exposure to the ethanol in 3rd to 28th day. Otherwise the cell proliferation was increased in 3rd to 14th days, and decreased in 28th days, respectively. The results were confirmed by immunohistochemistry and computer image analysis studied. This finding suggested that short-term chronic adequate alcohol intake may enhance the cell turnover of gastric mucosa. Long-term stimulus with the low concentration ethanol may cause the impairment of the cell turnover function of the gastric mucosa and may be one of the mechanisms underlying the gastric pathology associated with alcohol abuse.
- PublicationOpen AccessLeptin secretion by white adipose tissue and gastric mucosa(Murcia : F. Hernández, 2007) Cammisotto, P.G.; Bendayan, M.Leptin is a hormone that plays a central role in the regulation of food intake and energy expenditure. Originally discovered in mature white adipocytes, it was subsequently isolated from the gastric mucosa. This tissue contains a large number of epithelial endocrine and exocrine cells secreting leptin in the blood stream and in the gastric lumen, respectively. Light and electron microscopy have shown that adipocytes and gastric epithelial cells contain leptin along their rough endoplasmic reticulum-Golgi-granules secretory pathway. Both tissues synthesize a soluble form of the leptin receptor that is secreted bound to leptin in the blood and into the gastric juice. This soluble receptor protect leptin and enhances its half-life. Despite the similarities in the mechanisms of leptin secretion by adipocytes and gastric epithelial cells, they are in fact radically different. In gastric cells leptin follows a rapid regulated secretion pathway whereas adipocytes secrete leptin in a constitutive slow fashion. These differences can be explained by the specific roles play by leptin originating from these two different tissues. Gastric leptin is involved in the short-term regulation of digestion, including delay of gastric emptying, absorption of nutrients by the intestinal wall and secretion of gastric, intestinal and pancreatic hormones. On the other hand, leptin secreted by white adipocytes acts primarily on the hypothalamus for the long-term regulation of food intake. Therefore, the coordination of adipose and gastric leptins ensures the proper management of food processing and energy storage.
- PublicationOpen AccessDifferential distribution of transforming growth factor beta and receptors in the hyper or hypoproliferative gastric mucosa of developing and adult rats(Murcia : F. Hernández, 2007) Alvares, E.P.; Jordão, L.R.; Gama, P.Transforming growth factor ß (TGFß) isoforms are known for their antiproliferative effect on epithelial cells in vitro, but the role of each isoform in vivo is poorly understood, mainly when non-pathological conditions are considered. We correlated the presence and distribution of isoforms and receptors to physiological changes in gastric cell proliferation in developing and adult rats. We used fasting to induce either the hyper (14-day-old pups) or hypoproliferation (60-day-old rats) of the gastric epithelium. In 14-d-old pups fasting reduced only TGFß3 labelling in the gland. Conversely, in 60-d-old rats there was an increase of TGFß1 and TGFß3 immunolabelled cells. Receptors were detected at both ages. Therefore, the changes induced by fasting in the constitutive TGFß expression can be correlated to the differential epithelial proliferation in the stomach of developing and adult rats. These results suggest that one of the functional roles of TGFß in vivo is to locally regulate cell proliferation.
- PublicationOpen AccessDevelopment of new RNAi therapeutics(Murcia : F. Hernández, 2007) Liu, G.; Wong-Staal, F.; Li, Q.X.RNAi-mediated gene inactivation has become a cornerstone of the present day gene function studies that are the foundation of mechanism and target based drug discovery and development, which could potentially shorten the otherwise long process of drug development. In particular, the coming of age of “RNAi drug” could provide new promising therapeutics bypassing traditional approaches. However, there are technological hurdles need to overcome and the biological limitations need to consider for achieving effective therapeutics. Major hurdles include the intrinsic poor pharmacokinetic property of siRNA and major biological restrictions include off-target effects, interferon response and the interference with endogenous miRNA. Recent innovations in nucleic acid chemistry, formulations and delivery methods have gradually rendered it possible to develop effective RNAi-based therapeutics. Careful design based on the newest RNAi/miRNA biology can also help to minimize the potential tissue toxicity. If successful with systemic application, RNAi drug will no doubt revolutionize the whole drug development process. This review attempts to describe the progress in this area, including applications in preclinical models and recent favorable experience in a number of human trials of local diseases, along with the discussion on the potential limitations of RNAi therapeutics.
- PublicationOpen AccessRapid microglial activation induced by traumatic brain injury is independent of blood brain barrier disruption(Murcia : F. Hernández, 2007) Koshinaga, M.; Suma, T.; Fukushima, M.; Tsuboi, I.; Aizawa, S.; Katayama, Y.Following CNS injury, microglia respond and transform into reactive species exhibiting characteristic morphological changes that have been termed “activated” or “ameboid” microglia. In an attempt to establish that microglial reactions induced immediately after injury are caused by intrinsic mechanisms rather than infiltration of blood and its constituents, oxygenized Ringer’s solution was perfused into the cerebral circulation of rats so that the circulating blood could be eliminated prior to injury induction. Under artificial respiration, a catheter was inserted from the cardiac apex into the ascending aorta, and oxygenized Ringer’s solution was immediately perfused with a pulsatile blood pump, resulting in wash out of the circulating blood from the brain within 1 min. Subsequently, a cortical contusion was induced in the unilateral parietal cortex using a controlled cortical impact (CCI) device. At 5 min following the injury, the brain was fixed by perfusion of fixative through the catheter and removed. Coronal vibratome sections were then processed for CR3 immunohistochemistry to examine the microglial activation. It appeared that microglial activation with both morphological transformation and an increase in CR3 immunoreactivity was induced throughout the hemisphere ipsilateral to the injury side exclusively, even in rats with elimination of circulating blood. The microglial reactions did not differ substantially from those observed in the control rats with extensive BBB disruption. The present results thus provide direct evidence that the microglial activation induced immediately after injury is independent of infiltration of circulating blood induced by concurrent BBB disruption.
- PublicationOpen AccessCerebral ß-amyloid angiopathy in aged squirrel monkeys(Murcia : F. Hernández, 2007) Elfenbein, H.A.; Rosen, R.F.; Stephens, S.L.; Switzer, R.C.; Smith, Y.; Pare, J.; Mehta, P.D.; Warzok, R.; Walker, L.C.Cerebral ß-amyloid angiopathy (CAA) is an age-related disorder of the brain vasculature that is involved in up to 20% of non-traumatic cerebral hemorrhage in humans. CAA is a risk factor for cognitive decline, and may exacerbate the dementia of Alzheimer's disease. Progress in discovering the cause and potential therapies for this disorder has been hindered by the paucity of animal models, particularly models of idiopathic CAA. The squirrel monkey (Saimiri spp) develops significant CAA in the natural course of aging. To evaluate the suitability of Saimiri as a model of human CAA, we studied the distribution and composition of Aß subtypes in CAA and parenchymal (senile plaque) deposits in the brains of aged squirrel monkeys, as well as the relationship between vascular ßamyloid deposition and comorbid vasculopathies that occur in aged humans. Our findings show that: 1) CAA consists ultrastructurally of classical amyloid fibrils and is the principal type of cerebral ß-amyloidosis in squirrel monkeys; 2) The two primary isoforms of Aß (Aß40 and Aß42) coexist in most microvascular and parenchymal lesions of Saimiri, although Aß40 tends to predominate in larger arterioles; 3) CAA and parenchymal plaques overlap to a considerable degree in most affected brain areas, and are distributed symmetrically in the two hemispheres; 4) Both CAA and plaques are particularly abundant in rostral regions and comparatively sparse in the occipital lobe; 5) Capillaries are especially vulnerable to CAA in squirrel monkeys; and 6) When CAA is severe, it is associated with a small, but significant, increase in other vasculopathies, including microhemorrhage, fibrinoid extravasation and focal gliosis. These findings, in the context of genetic, vascular and immunologic similarities between squirrel monkeys and humans, support the squirrel monkey as a biologically advantageous model for studying the basic biology of idiopathic, age-related CAA, and for testing emerging therapies for human ß-amyloidoses such as Alzheimer's disease.
- PublicationOpen AccessAn immunohistochemical analysis of the temporal and spatial expression of growth factors FGF 1, 2 and 18, IGF 1 and 2, and TGFß1 during distraction osteogenesis(Murcia : F. Hernández, 2007) Haque, T.; Amako, M.; Nakada, S.; Lauzier, D.; Hamdy, R.C.Distraction osteogenesis (DO) is a well established surgical technique that generates new bone by gradual distraction of two bony segments. In this study, we investigated the temporal and spatial profile of FGF 1, 2 and 18, IGF 1 and 2, and TGFß1 during distraction osteogenesis using immunohistochemistry. An osteotomy was performed on the right tibia of 13 white male New Zealand rabbits. After a delay of 7 days, distraction was started at a rate of 0.25mm/12hrs for 3 weeks which was followed by a 3 week period of consolidation. Immunohistochemical analysis was performed on a weekly interval to determine the expression of the growth factors. Staining of all growth factors was apparent at various levels in the centre and callus region in fibroblasts and chondrocyte cells. FGF2 however, showed continued high expression in osteoblasts. Within two weeks after the end of distraction all growth factors showed a reduction in expression except for FGF18 which maintained high levels of expression (up to 100% staining) throughout the distraction and consolidation phases. The study suggests that in comparison to the other investigated growth factors, FGF18 may play in important role throughout the entire process of distraction osteogenesis.
- PublicationOpen AccessPituitary tumor transforming gene: An important gene in normal cellular functions and tumorigenesis(Murcia : F. Hernández, 2007) Bradshaw, C.; Kakar, S.S.Pituitary tumor transforming gene (PTTG) is an oncogene which is found to be highly expressed in proliferating cells and in most of the tumors analyzed to date. Overexpression of PTTG induces cellular transformation and promotes tumor development in nude mice. PTTG is regulated by various growth factors including insulin and IGF-1. PTTG is a multifunctional and multidomain protein. Some of the functions of PTTG include inhibition of separation of sister chromatids, expression and secretion of angiogenic and metastatic factors. In this review we focus on expression of PTTG in normal and tumor tissues, define its biological function, its role in tumorigenesis, and its interaction with other proteins that may play important role in mediating tumorigenic function of PTTG.
- PublicationOpen AccessSteroid receptors ERa, ERß, PR-A and PR-B are differentially expressed in normal and atrophic human endometrium(Murcia : F. Hernández, 2012-05-21) Mylonas, I.; Jeschke, U.; Shabani, N.; Kuhn, C.; Kunze, Sussane; Dian, D.; Friedl, C.; Kupka, M.S.; Friese, K.Objective: The endometrium expresses estrogen (ER) and progesterone receptor (PR), which are related to autocrine and paracrine processes that respond to estrogen and progesterone. Therefore, the aim of this study was to evaluate the distribution pattern of ERa, ERß, PR-A and PR-B with monoclonal antibodies in normal human endometrial tissue. Study Design: Human endometrial tissue was obtained from 84 premenopausal and 11 postmenopausal patients and immunohistochemically analysed with monoclonal antibodies against ERa, ERß, PR-A and PR-B. Results: ERa, PR-A and PR-B declined significantly (p<0.001, p<0.05, p<0.05 respectively) in glandular epithelium from proliferative to late secretory phase. The ERß immunohistochemical reaction showed a similar significant declining pattern (p<0.05), although the staining intensity was lower than that of ERa. While ERa, ERß and PR-B decrease significantly in atrophic endometrial tissue compared to proliferative endometrium, a significant up-regulation of PR-A was observed compared to late secretory phase (p<0.05). Conclusion: ERa, ERß, PR-A and PR-B were expressed in normal human endometrium with a cyclical variation during the menstrual cycle. In normal postmenopausal endometrial tissue, a down-regulation of ERa, ERß and PR-B occurs with a subsequent higher expression of PRA. These results show the presence of steroid receptors in human epithelium, indicating that these cells respond to estrogen and progesterone, thus playing a significant role in endometrial physiology.