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PubMed1992

The ventriculus terminalis and filum terminale of the human spinal cord.

Serial sections of the conus medullaris and the filum terminale of 23 randomly selected human spinal cords were studied by light and electron microscopy, and following immunoperoxidase staining for glial fibrillary acidic protein (GFAP), vimentin, neuron-specific enolase (NSE), amyloid beta protein, and S-100 protein. The intradural portion of the filum contains bundles of GFAP-positive glial fibers, scattered silver- and NSE-positive neurons, segments of peripheral nerve, blood vessels, fibrous connective tissue, and fat. Glial cell clusters varying from five to 100 cell layers thick at times constitute the bulk of the filum. The periependymal glial cells possess moderate amounts of eosinophilic cytoplasm and relatively uniform round to ovoid nuclei containing evenly distributed chromatin. They are distributed diffusely with no specific pattern of organization, although some of them showed a tendency to form acinar structures. A minority of the glial cells showed GFAP immunoreactivity, and some were immunoreactive for vimentin. Electron microscopy demonstrated the presence of periependymal cells showing cilia, microvilli, and the formation of intercellular junctional complexes, as well as cells containing bundles of glial filaments within the cytoplasm. Degenerated NSE-positive neurons and degenerated neurites resembling neuritic plaques were also demonstrated. However, immunoperoxidase staining for amyloid beta protein was negative in these structures. Thus, the filum terminale is endowed with an abundance of glial cells and neurons and is not simply a fibrovascular tag. Periependymal glial cells in the filum terminale should not be mistaken for neoplasm. The presence of neuropil with profuse astroglial and neuronal components within the filum terminale suggests a possible functional role for these structures.

Adolescent↗
PubMed1991

Hyperdynamic circulation in cirrhosis: a role for nitric oxide?

Hypotension, low systemic vascular resistance, and a reduced sensitivity to vasoconstrictors are features of cirrhosis. These cardiovascular changes might be the result of increased synthesis of a vasodilator. Nitric oxide (NO), a potent vasodilator, is synthesised in and released from peripheral blood-vessels in man. Studies in animals indicate that bacterial endotoxin and cytokines induce NO synthase expression in vessel walls, with sustained NO release and consequent hypotension. Endotoxaemia is a common feature of cirrhosis; persistent induction of NO synthase may account for the associated haemodynamic changes.

Amino Acid Oxidoreductases↗
PubMed2004

Rat model of orthotopic gastric transplantation.

INTRODUCTION: We tried to find a better surgical procedure of reconstruction after total gastrectomy. Seventy rats were operated to establish a model of orthotopic gastric transplantations which may also be important for abdominal multivisceral transplantation. OBJECTIVE: To establish a rat model of orthotopic gastric transplantation. METHODS: In the donor operation; after the spleen was resected and the proper hepatic artery ligated, the stomach was infused with cold (0 degrees C to 4 degrees C) sodium lactate Ringer's solution via the aorta. The stomach was resected with its peripheral blood vessels-the celiac trunk, the left gastric artery, the splenic artery, the common hepatic artery, the gastroepiploic artery, and the portal vein. In the recipient operation; after the stomach and the spleen were resected, the donor stomach was implanted. An end-to-side anastomosis was performed for the portal veins. After the end-to-end anastomosis between the donor celiac trunk and the recipient left gastric artery, the blood flow was opened. Then the anastomoses of the duodenum, and donor cardia to the recipient esophagus were performed in end-to-end style. RESULTS: Thirty five operations were performed, in which the success rate in the last 20 cases was 80% (16/20). The average operative time was 2.35 hours. The longest survival time was over 3 months. CONCLUSION: A rat model of orthotopic gastric transplantation was successfully established and provides a method to study abdominal multivisceral transplantation. It also provides a new way for reconstruction after the total gastrectomy.

Animals↗
PubMed2006

The presence of human papillomavirus 16 in neural structures and vascular endothelial cells.

Human papillomavirus (HPV) is known as a strictly epitheliotropic pathogen. Our results raised the possibility that HPV 16 is present in neural cells and in the vascular endothelium. By in situ hybridization, we have detected HPV 16 E6 ORF sequence in small blood vessels and peripheral nerves adjacent to oral and cervical cancers. The same structures have clearly shown immunohistochemical reactivity for the E6 oncoprotein. These results were verified by PCR applied to E6 and L1 ORFs following microscopic laser dissection of the immunohistochemically positive nerves and vessels. These observations suggest that HPV 16 DNA and protein are present in neurons and endothelial cells in the vicinity of HPV-associated tumors. The HPV 16 genome presumably exists in a non-replicating form in the neurons and constitutively produces high levels of E6 and E7 proteins with an unknown neuropathological outcome.

Base Sequence↗
PubMed1998

Alpha 2-adrenergic receptor activation inhibits calcitonin gene-related peptide expression in cultured dorsal root ganglia neurons.

Calcitonin gene-related peptide (CGRP), a potent vasodilator, is produced in dorsal root ganglia (DRG) neurons which extend nerves peripherally to blood vessels and centrally to the spinal cord. We previously reported that neuronal CGRP expression is significantly reduced in the spontaneously hypertensive rat (SHR) which could contribute to the elevated BP. Other studies suggest that the enhanced activity of the sympathetic nervous system in the SHR may mediate, at least in part, this reduction in neuronal CGRP expression via activation of alpha 2-adrenoreceptors (alpha 2-AR) on DRG neurons. To test this hypothesis in vitro we employed primary cultures of adult rat DRG neurons. Neuronal cultures were initially exposed (24 h) to either the alpha 2-AR agonist UK 14,304 (10(-6) M) or vehicle; however, no changes in CGRP mRNA content or immunoreactive CGRP (iCGRP) release were observed. Using the rationale that in vivo DRG neurons receive a continuous supply of target tissue derived nerve growth factor (NGF), which stimulates CGRP synthesis, the cultured neurons were treated (24 h) with either vehicle, NGF (25 ng/ml) alone, or NGF plus UK. NGF treatment increased CGRP mRNA accumulation 5.5 +/- 0.9-fold (p < 0.001) and iCGRP release 2.9 +/- 0.4-fold (p < 0.001) over control levels. The stimulatory effects of NGF were markedly attenuated, but not abolished, by UK (NGF + UK vs. control, CGRP mRNA, 2.9 +/- 0.4-fold, p < 0.05; iCGRP, 1.7 +/- 0.2-fold, p < 0.05). These values were also significant (p < 0.05) when compared to NGF treatment alone. Experiments performed using the alpha 2-antagonist yohimbine confirmed that the effects of UK were mediated by the alpha 2-AR. These results, therefore, demonstrate that alpha 2-AR activation attenuates the stimulatory effects of NGF on CGRP expression in DRG neurons.

Adrenergic alpha-Agonists↗
PubMed1997

Inhibitory mechanisms of beta-adrenoceptor agonists for immunoglobulin E-mediated experimental allergic reactions in rats.

Inhibitory mechanisms of isoproterenol and clenbuterol for immunoglobulin E (IgE)-mediated experimental allergic reactions in rats were studied. IgE-mediated passive cutaneous anaphylaxis, histamine-induced cutaneous reaction and serotonin-induced cutaneous reaction were evoked at the same time in the same rats. Isoproterenol administered intravenously immediately before challenge inhibited all these reactions significantly. Clenbuterol administered intravenously 0-3 h before challenge also significantly inhibited the three cutaneous reactions. The inhibition was maximum when the drug was given 1 h before challenge. Passive cutaneous anaphylaxis was always inhibited more potently than histamine-induced cutaneous reaction and serotonin-induced cutaneous reaction by these beta-adrenoceptor agonists. Passive peritoneal anaphylaxis was caused by injecting an antigen intravenously. Isoproterenol administered intravenously immediately before challenge inhibited the reaction significantly. Clenbuterol administered intravenously 0-3 h before challenge also significantly inhibited passive peritoneal anaphylaxis, maximally so when given 1 h before challenge. In vitro IgE-dependent histamine release from sensitized peritoneal mast cells or mesenteric mast cells was not affected by isoproterenol and clenbuterol. Mouse monoclonal IgE, a foreign protein, administered intravenously decreased rapidly in the circulation. About 50% of the mouse IgE given disappeared in 20 min. The decrease of mouse IgE was partly but significantly inhibited by the beta-adrenoceptor agonists, and the inhibition was abolished by simultaneous treatment with propranolol. These results indicate that direct inhibition of mast cell activation does not contribute to the potent inhibition of in vivo allergic reactions in rats by beta-adrenoceptor agonists, and that inhibition of the allergic cutaneous reaction is partially explained by the inhibition of vascular permeability increases caused by mast cell mediators. Penetration of intravenously administered antigen from blood vessels to peripheral tissues to cause mast cell activation might be inhibited by beta-adrenoceptor agonists, and this could play some role in inhibiting intravenous antigen-induced allergic reactions in rats. Clenbuterol exhibited its maximum action with some latency in vivo, suggesting that some time-requiring process may be involved in the manifestation of its action.

Adrenergic beta-Agonists↗
PubMed2002

Aggregation of antigen-specific T cells at the inoculation site of mature dendritic cells.

Cellular immune responses are initiated by direct interaction of naive T cells with professional antigen-presenting cells, i.e., dendritic cells. In general, this interaction takes place in secondary lymphoid organs to which both naive T cells and mature dendritic cells preferentially home. This physiologic scenario differs substantially, however, from therapeutic dendritic-cell-based vaccinations used to treat human cancer. In fact, only a small fraction of intradermally injected dendritic cells migrate to the draining lymph node and the majority of cells remain at the site of inoculation. These sites are characterized by a distinct oligoclonal T cell infiltrate comprising both L-Selectin+/CD45RA+ and L-Selectin+/CD45RA- cells. Blood vessels expressing peripheral lymph node addressin represent possible entry channels for such naive and central memory T cells, the former probably attracted by dendritic cell-CK1 produced by the injected dendritic cells. In situ staining with multimeric peptide/major histocompatibility complex class I complexes revealed that infiltrating T cells specifically recognize peptide epitopes presented by the injected dendritic cells. Thus, the fraction of dendritic cells not migrating to secondary lymphatic tissue after therapeutic inoculation nevertheless seem to be involved in a specific immune modulation.

Antigens, Neoplasm↗
PubMed1988

[Color-coded Doppler sonography of kidney transplants].

A prospective study was carried out in 81 patients to compare the ability of colour coded Doppler sonography (angiodynography) and Tc bolus examination for demonstrating renal blood supply. In patients with normal transplant function both methods performed equally well. In anuric patients angiodynography was superior to the Tc bolus examination: In three cases angiodynography was able to provide important additional information such as absence of blood flow in peripheral intrarenal vessels or missing blood supply of a transplant pole. Angiodynography seems to be able to replace the Tc bolus examination; this statement excludes very obese patients until low-frequency probes for angiodynography will be available.

Anuria↗
PubMed2003

TTF-1 phosphorylation is required for peripheral lung morphogenesis, perinatal survival, and tissue-specific gene expression.

Thyroid transcription factor-1 (TTF-1) is a 43-kDa, phosphorylated member of the Nkx2 family of homeodomain-containing proteins expressed selectively in lung, thyroid, and the central nervous system. To assess the role of TTF-1 and its phosphorylation during lung morphogenesis, mice bearing a mutant allele, in which seven serine phosphorylation sites were mutated, Titf1PM/PM, were generated by homologous recombination. Although heterozygous Titf1PM/+ mice were unaffected, homozygous Titf1PM/PM mice died immediately following birth. In contrast to Titf1 null mutant mice, which lack peripheral lung tissues, bronchiolar and peripheral acinar components of the lung were present in the Titf1PM/PM mice. Although lobulation and early branching morphogenesis were maintained in the mutant mice, abnormalities in acinar tubules and pulmonary hypoplasia indicated defects in lung morphogenesis later in development. Although TTF-1PM protein was readily detected within the nuclei of pulmonary epithelial cells at sites and abundance consistent with that of endogenous TTF-1, expression of a number of known TTF-1 target genes, including surfactant proteins and secretoglobulin 1A, was variably decreased in the mutant mice. Vascular endothelial growth factor mRNA was decreased in association with decreased formation of peripheral pulmonary blood vessels. Genes mediating surfactant homeostasis, vasculogenesis, host defense, fluid homeostasis, and inflammation were highly represented among those regulated by TTF-1. Thus, in contrast to the null Titf1 mutation, the Titf1PM/PM mutant substantially restored lung morphogenesis. Direct and indirect transcriptional targets of TTF-1 were identified that are likely to play important roles in lung formation and function.

Animals↗
PubMed2001

A new locus for autosomal dominant familial exudative vitreoretinopathy maps to chromosome 11p12-13.

We report a new locus for familial exudative vitreoretinopathy (FEVR), on chromosome 11p12-13 in a large autosomal dominant pedigree. Statistically significant linkage was achieved across a 14-cM interval flanked by markers GATA34E08 and D11S4102, with a maximum multipoint LOD score of 6.6 at D11S2010. FEVR is a disease characterized by the failure of development of peripheral retinal blood vessels, and it is difficult to diagnose clinically because of the wide spectrum of fundus abnormalities associated with it. The identification of a new locus is important for genetic counseling and potentiates further studies aimed toward the identification of a gene with an important role in angiogenesis within neuroepithelial tissues. Such a gene may also have a role in the genetic predisposition to retinopathy of prematurity, a sporadic disorder with many clinical similarities to FEVR.

Chromosome Mapping↗
PubMed2006

Acute and chronic hypoxia as well as 7-day recovery from chronic hypoxia affects the distribution of pulmonary mast cells and their MMP-13 expression in rats.

Chronic hypoxia results in pulmonary hypertension due to vasoconstriction and structural remodelling of peripheral lung blood vessels. We hypothesize that vascular remodelling is initiated in the walls of prealveolar pulmonary arteries by collagenolytic metalloproteinases (MMP) released from activated mast cells. Distribution of mast cells and their expression of interstitial collagenase, MMP-13, in lung conduit, small muscular, and prealveolar arteries was determined quantitatively in rats exposed for 4 and 20 days to hypoxia as well as after 7-day recovery from 20-day hypoxia (10% O2). Mast cells were identified using Toluidine Blue staining, and MMP-13 expression was detected using monoclonal antibody. After 4, but not after 20 days of hypoxia, a significant increase in the number of mast cells and their MMP-13 expression was found within walls of prealveolar arteries. In rats exposed for 20 days, MMP-13 positive mast cells accumulated within the walls of conduit arteries and subpleurally. In recovered rats, MMP-13 positive mast cells gathered at the prealveolar arterial level as well as in the walls of small muscular arteries; these mast cells stayed also in the conduit part of the pulmonary vasculature. These data support the hypothesis that perivascular pulmonary mast cells contribute to the vascular remodelling in hypoxic pulmonary hypertension in rats by releasing interstitial collagenase.

Acute Disease↗
PubMed1993

The effect of experimental frost-bite on the responses of the rabbit ear-artery to adrenergic and electrical stimulation.

The aim of the present investigation was to study the effect of sub-zero temperatures on the adrenergic activated, smooth muscle-contraction of a peripheral blood-vessel. The central ear-artery of the rabbit was used for this purpose. The artery was stimulated to contract in vitro by activation of phentolamine sensitive, post-junctional, alpha-adrenoceptors by use of noradrenaline, or by noradrenaline released from noradrenergic nerves in the blood-vessel following electrical field stimulation. The effect of freezing the tissue in vivo for 15 min at sub-zero temperatures (-4, -6 and -9 degrees C) was studied in vitro. Exposure to -4 and -6 degrees C did not alter the apparent affinity (ED50) of noradrenaline significantly, when measured immediately, or 2 or 6 days after exposure. The maximal response to noradrenaline was reduced by approximately 54, 74 and 100% following exposure to -4, -6 and -9 degrees C, respectively. The response was completely restored after 2 and 6 days of regeneration in vivo following exposure to -6 degrees C, whereas the response after exposure to -9 degrees C was restored by only about 8 and 30% after 2 and 6 days regeneration, respectively. The maximal response to electrical field stimulation, which was completely inhibited by tetrodotoxin and phentolamine, was reduced by approximately 92% after exposure for 15 min to -4 and -6 degrees C, while it was completely inhibited after exposure to -9 degrees C. The response was restored by only 15-20% following 2 and 6 days in vivo after exposure to -6 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Responses of noradrenergic nerves in rabbit ear-artery before and after experimental frost-bite.

Experiments were designed to determine the effects of sub-zero temperatures on the function of the noradrenergic innervation of a peripheral blood-vessel. The central ear-artery of the rabbit was used for this purpose. The ear was exposed to temperatures of -6, -9 or -18 degrees C in vivo for 15 min. After 1 day (24 h) or 6 days in vivo, the central ear-artery was dissected free, incubated in [3H]-noradrenaline (NA) and stimulated in vitro with high potassium (75 mM) for 5 min to evoke release of [3H]-NA. The release of [3H]-NA was Ca(2+)-dependent. One day after exposure to -6, -9 or -18 degrees C, increases of 45-57 and 44-72% and a reduction of 12-35% were observed, respectively, in three successive potassium-evoked NA-releases. After 6 days in vivo an increase of 30-34% was observed following exposure to -6 degrees C, while no alteration was observed after exposure to -9 degrees C. A reduction of 84-89% was recorded after exposure to -18 degrees C. Following this exposure to -18 degrees C, there was also a great reduction in the evoked release of [3H]-NA compared with the spontaneous release, whereas this correlation did not change after exposure to -6 and -9 degrees C. The total uptake of [3H]-NA was unchanged after freezing the tissue at -6 degrees C, but was substantially reduced after exposure to -9 and -18 degrees C. A short period of in vivo restoration (6 days, enhanced the uptake of [3H]-NA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Analysis of the expression of aquaporin-1 and aquaporin-9 in pig liver tissue: comparison with rat liver tissue.

Aquaporins (AQPs) are cellular proteins involved with the movement of water across cell membranes and are fundamentally important to the fluid transport in the bile ducts and ductules of the liver. An immunohistochemical analysis of AQP-1 and AQP-9 was undertaken to describe their expression in fetal and adult pig liver, while immunoreagents specific to some other AQPs were screened for their efficacy on pig liver tissues. Anti-AQP-1 antibody reacted with the bile duct of the portal space and the bile ductules at the periphery of the liver lobules. Histological identification of bile ductules was confirmed by positive reactivity with anti-cytokeratin-7 and antilaminin immunostaining. Anti-AQP-1 signals were also pronounced in the endothelium of the portal space blood vessels and peripheral distributing venules. Antibody to AQP-9 reacted strongly with small ductules peripheral to the liver lobules, but only weakly with the bile ducts of the portal space. Anti-AQP-adipose antibody bound to the smooth muscle cells of the arteries in the portal space and sporadically with certain binucleated cells in the liver lobule. Antibodies to AQP-3, AQP-4, AQP-7, and AQP-8 were nonreactive with any of the tissues of the adult pig liver. For comparative purposes, immunohistochemical analysis of rat liver tissue was done with the anti-AQP-1 and AQP-9 antibodies. Anti-AQP-1 reacted weakly with the rat liver's bile ducts, but robustly with the endothelium of the liver's veins and arteries. It also reacted strongly with the central vein of the rat liver lobules, and, because the staining was continuous with hepatic sinusoids, it appeared that the reactivity was specific to the endothelial cells. Anti-AQP-9 antibodies reacted with rat hepatocytes and was not associated with the canaliculi, as judged by concurrent phalloidin staining of actin. The results indicate that specific AQPs are expressed in the tissues of the pig liver and that AQP-9 expression is distinct from its expression in the rat liver.

Animals↗