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PubMed2001

[Glucose homeostasis in children. I. Regulation of blood glucose].

The amount of glucose in the circulation depends on its absorption from the intestine, uptake by and release from the liver and uptake by peripheral tissues. Insulin and glucagon together control the metabolities required by peripheral tissues and both are involved in maintaining glucose homeostasis. Insulin is considered to be an anabolic hormone in that it promotes the synthesis of protein, lipid and glycogen. The key target tissues for insulin are liver, muscles and adipose tissue. Glucagon acts largely to increase catabolic processes. Between meals or during fast, the most tightly regulated process is the release of glucose from the liver. During fasting glucose is produced from glycogen and is formed by enzymes on the gluconeogenic pathway. Fetal metabolism is directed to ensure anabolism with formation of glycogen, fat and protein. Glucogen is stored in the liver and serves as the immediate source of new glucose during first few hours after birth. Glucose is the most important substrate for brain metabolism. Due to the large size of neonatal brain in relation to body weight cerebral glucose consumption is particularly high. Postnatal hormonal changes have a central role in regulating glucose mobilization through glycogenolysis and gluconeogenesis. The initial glucagon surge is the key adaptive change which triggers the switch to glucose production. The control of insulin and glucagon secretion is of fundamental importance during first hours after birth. Children have a decreased tolerance to starvation when compared with adults, they are more prone to develop hypoglycaemia after short fasting. The faster rate in the fall of blood glucose and gluconeogenic substrates and rapid rate of ketogenesis are characteristic features of fasting adaptation in children.

Adaptation, Physiological↗

PubMed1998

Regional differences in effects of 4-aminopyridine within the sinoatrial node.

4-Aminopyridine (4-AP)-sensitive transient outward current (Ito) has been observed in the sinoatrial node, but its role is unknown. The effect of block of Ito by 5 mM 4-AP on small ball-like tissue preparations (diameter approximately 0.3-0.4 mm) from different regions of the rabbit sinoatrial node has been investigated. 4-AP elevated the plateau, prolonged the action potential, and decreased the maximum diastolic potential. Effects were greater in tissue from the periphery of the node than from the center. In peripheral tissue, 4-AP abolished the action potential notch, if present. 4-AP slowed pacemaker activity of peripheral tissue but accelerated that of central tissue. Differences in the response to 4-AP were also observed between tissue from more superior and inferior regions of the node. In the intact sinoatrial node, 4-AP resulted in a shift of the leading pacemaker site consistent with the regional differences in the response to 4-AP. It is concluded that 4-AP-sensitive outward current plays a major role in action potential repolarization and pacemaker activity in the sinoatrial node and that its role varies regionally.

4-Aminopyridine↗

PubMed2004

Immunosuppression in renal cancer: differential expression of signal transduction molecules in tumor-infiltrating, near-tumor tissue, and peripheral blood lymphocytes.

Alterations in the expression of signal activation molecules, such as the T-cell receptor (TCR) zeta and epsilon chains and p56lck tyrosine kinase, are described in tumor-infiltrating lymphocytes (TIL). The aim of this study was to ascertain if such molecules were present in near-tumor-tissue lymphocytes (NTTL) and peripheral blood lymphocytes (PBL), as well as TIL, of renal cell carcinoma patients, to verify whether this tumor induces immunosuppression only locally or affects distant lymphocytes as well. Tissue from the tumor and from healthy nearby sites, as well as blood samples, were obtained from 27 consecutive patients who had undergone radical nephrectomy for renal cell carcinoma. Phenotype analysis and immunohistochemical staining of the TCR zeta and epsilon chains and p56lck were performed with standard techniques on TIL, NTTL, and PBL, and values were compared for each patient. Low expression of the TCR zeta chain and an almost complete absence of TCR epsilon chain and p56lck expression was observed in TIL (median values: 10% for zeta chain and 0% for epsilon and p56lck). In NTTL, these signal transduction molecules were expressed by a higher percentage of cells (60%, 50%, and 60%, respectively; p=0.000 vs. TIL), whereas PBL showed an almost normal expression of zeta and epsilon chains (80% and 90%, respectively; p=0.000 vs. TIL). Conversely, p56lck was detected in a greater proportion of NTTL than PBL (50% vs. 10%; p=0.001). The absence or the very low expression of signaling activation molecules in TIL compared with NTTL and PBL in renal cancer patients suggest that tumor-induced immunosuppression generally occurs or starts locally.

Aged↗

PubMed2004

Distribution of neutral amino acid transporter ASCT 1 in the non-neuronal tissues of mice.

Distribution of ASCT1, a neutral amino acid transporter, in non-neuronal peripheral tissues of adult and developing mice was examined by immunohistochemistry and immunoelectron microscopy. Immunoreactivity for ASCT1 in the digestive system was localized in basal cells of stratified squamous epithelia from oral parietes to nonglandular region of the stomach, chief cells of the glandular stomach, acinar cells of the salivary gland and exocrine pancreas, and Paneth's cells of the small intestine, in all of which the basolateral membrane was selectively immuno-labeled. In the liver of adult mice, ASCT1 immunoreactivity was detected on the plasma membrane of hepatocytes surrounding central veins, and a temporal expansion of immunoreactive hepatocytes was observed in the embryonic and CCl4-treated adult livers. ASCT1 was also localized on the plasma membranes of proximal uriniferous tubule epithelial cells in the kidney of adult mice, and those of supporting cells in the medulla of adrenal gland. These results suggest that ASCT1 is expressed in various non-neuronal peripheral tissues in mice, and it contributes to the amino acid transport throughout non-neuronal tissues.

Adrenal Glands↗

PubMed1984

Effects of positive end-expiratory pressure on tissue gas tensions and oxygen transport.

To determine whether positive end-expiratory pressure (PEEP) impairs peripheral tissue oxygenation, hemodynamic variables including blood and subcutaneous tissue gas tensions were measured at 0, 5, 10, 15, and 20 cm H2O of PEEP, in 9 patients who were being mechanically ventilated for acute pulmonary failure. Increasing the level of PEEP produced parallel decreases in cardiac output and oxygen delivery (DO2 = cardiac output X arterial oxygen content); however, there were no significant changes in mean arterial blood pressure (MAP), oxygen consumption (VO2), mixed-venous oxygen tension (PvO2), pH, or base excess. Subcutaneous tissue oxygen (PtO2) and carbon dioxide (PtCO2) tensions, which were directly measured in the femoral region by a mass spectrometer, also remained at their baseline levels (zero end-expiratory pressure). We concluded that peripheral tissue oxygenation is not impaired up to the level of 20 cm H2O of PEEP, even though DO2 significantly decreases.

Acute Disease↗

PubMed1991

3 beta-Hydroxysteroid dehydrogenase activity in glandular and extraglandular human fetal tissues.

The expression of 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) in steroidogenic tissues is an absolute requirement for mammalian reproduction, fetal growth, and life maintenance. We sought to identify extraglandular tissue sites in the human fetus where 3 beta HSD is expressed. To this effect, we conducted in vitro studies by use of homogenates prepared from second trimester fetal tissues. To facilitate the determination of 3 beta HSD activity, an abbreviated technique was developed that consisted in the use of [3 alpha-3H]dehydroepiandrosterone [( 3 alpha-3H]DHEA) as the substrate and NAD+ as the cofactor. With these reagents, the enzymatic reaction leads to the production of both nonradiolabeled androstenedione and NAD3H in equimolar amounts, and the radioactivity associated with NAD3H is used for quantification of 3 beta HSD activity. The kinetic isotope effect introduced by substitution of tritium for hydrogen at the C-3 alpha position of DHEA, determined with six different tissues, was 2.5 +/- 0.7 (mean +/- SD). The specific activities of the enzyme in peripheral tissues and ovary were relatively low, in the range of 0.03 nmol/mg protein.h for stomach (n = 2) to 0.18 +/- 0.14 nmol/mg protein.h for liver (mean +/- SD; n = 13), while in fetal testis and placenta the specific activities were relatively high, viz. 3.4 +/- 0.7 nmol/mg protein.h (mean +/- SD; n = 4) and 2.8 +/- 1.8 nmol/mg protein.h (mean +/- SD; n = 13), respectively. The findings of this study serve to demonstrate that 3 beta HSD is distributed widely among tissues of the human fetus. Although the enzymatic activity was easily demonstrated in peripheral tissues by the use of radiolabeled DHEA as the substrate, 3 beta HSD protein was not readily detected by Western analysis.

3-Hydroxysteroid Dehydrogenases↗

PubMed2005

T cell priming by tissue-derived dendritic cells: new insights from recent murine studies.

Dendritic cells (DCs) act as sentinels in peripheral tissues, continuously scavenging for antigens in their immediate surroundings. Their involvement in T cell responses is generally thought to consist of a linear progression of events, starting with capture of antigen in peripheral tissues such as the skin followed by migration to draining lymphoid organs and MHC-restricted presentation of antigen-derived peptide to induce T cell priming. The role of tissue-derived DCs in the direct priming of immune responses has lately been challenged. It now appears that, at least in some instances, a non-migratory subtype of DCs in the secondary lymphoid tissue presents tissue-derived antigen to T cells. Here, we review recent developments in research on DC function in the priming of immune responses.

Animals↗

PubMed1993

Peripheral-type benzodiazepine receptors.

Since their first description as anomalous high affinity diazepam binding sites in rat peripheral tissues, the peripheral-type benzodiazepine receptor (PBR) has been increasingly studied to better understand nonneural effects of the benzodiazepines. The mammalian PBR is ubiquitously distributed with high concentrations in the outer mitochondrial membrane of secretory tissues. In regions of the brain, the density of PBR can equal or exceed the density of central-type benzodiazepine receptors. High affinity PK 11195 binding is diagnostic for the receptor while the affinity for benzodiazepines is species dependent. Recent cDNA cloning of a PBR component, the isoquinoline binding protein (IBP), shows no apparent sequence homology with any GABAA receptor subunits known to comprise central benzodiazepine receptor subtypes. The PBR seems at best only distantly related to CBRs. Recent advances in the pharmacology, biochemistry and molecular biology of the PBR are reviewed.

Amino Acid Sequence↗

PubMed2001

Growth hormone, insulin-like growth factor-I and the cortisol-cortisone shuttle.

In peripheral tissues, corticosteroid hormone action is determined, in part, through the activity of 11beta-hydroxysteroid dehydrogenases (11beta-HSD), two isozymes of which interconvert hormonally active cortisol (F) and inactive cortisone (E). 11beta-HSD type 2 (11beta-HSD2) inactivates F to E in the kidney, whilst 11beta-HSD type 1 (11beta-HSD1) principally performs the reverse reaction activating F from E in the liver and adipose tissue. Alteration in expression of these 11beta-HSD isozymes in peripheral tissues modifies corticosteroid action: loss of 11beta-HSD2 activity in the kidney results in cortisol-induced mineralocorticoid excess, and loss of hepatic 11beta-HSD1 activity improves insulin sensitivity through a reduction in cortisol-induced gluconeogenesis and hepatic glucose output. Conversely, overexpression of 11beta-HSD1 in omental adipose tissue can stimulate glucocorticoid-induced adipocyte differentiation which may lead to central obesity. Patients with hypopituitarism have many clinical features in common with patients with Cushing's syndrome--notably visceral obesity, insulin resistance, osteoporosis and increased vascular mortality. Our hypothesis was that many of these features may be explained by an effect of growth hormone (GH) on the 11beta-HSD isozymes. As assessed by urinary free cortisol/urinary free cortisone ratios and endorsed through in vitro studies, neither GH nor insulin-like growth factor (IGF)-I affect 11beta-HSD2 activity. Patients with acromegaly show a reduction in hepatic-derived metabolites of cortisol/cortisone - levels return to normal when GH concentrations are normalized. Conversely, patients with GH deficiency in the setting of hypopituitarism demonstrate an increased cortisol/cortisone metabolite ratio and reduction in circulating cortisol concentrations in patients on hydrocortisone replacement. Treatment with low-dose GH replacement reverses these abnormalities. These clinical data suggest that GH (and/or IGF-I) inhibits 11beta-HSD1 (i.e. E to F conversion) (parallel in vitro studies suggest that IGF-I and not GH inhibits 11beta-HSD1). These findings have important clinical ramifications. Firstly, the GH-mediated increase in cortisol metabolism (mediated via reduced E to F conversion) may precipitate adrenal insufficiency in hypopituitary patients with partial adrenocorticotropic hormone deficiency commencing GH therapy. Secondly, many of the phenotypic features of hypopituitarism can be explained by an alteration in 11beta-HSD1 activity: GH deficiency effectively increases cortisol production in key target tissues including liver and adipose tissue, promoting insulin resistance and visceral adiposity. Thirdly, the reported beneficial effects of GH on cardiovascular risk factors in patients with hypopituitarism may be an indirect effect via alterations in cortisol metabolism. Finally, the GH/IGF-I modulation of cortisol metabolism may underpin the pathogenesis of common diseases such as central obesity and idiopathic osteoporosis. Patients with central obesity but with no evidence of hypopituitarism have relative GH deficiency and it is exciting to speculate that low-dose GH treatment in this group, by inhibiting cortisol generation within omental fat, may offer a novel therapeutic approach.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗

PubMed2001

Postprandial lipoproteins and atherosclerosis.

During the postprandial state, dietary lipid is transported from the intestine to peripheral tissues by plasma lipoproteins called chylomicrons. In the capillary beds of peripheral tissues, chylomicron triglycerides are lipolyzed by the enzyme, lipoprotein lipase, allowing the delivery of free fatty acids to the cells. As a result, this produces a new particle of smaller size and enriched with cholesteryl ester referred to as chylomicron remnants. These particles are rapidly removed from the blood primarily by the liver. The liver has a complex chylomicron remnant removal system which is comprised of a combination of different mechanisms that include the low-density-lipoprotein receptor (LDLR) and the LDLR-related-protein (LRP). Furthermore, it has been suggested that there is a sequestration component whereby chylomicron remnants bind to heparan sulfate proteoglycans (HSPG) and/or hepatic lipase; this is then followed by transport to one or both of the above receptors for hepatic uptake. Over the years, a major concern has arisen about the association of chylomicron remnants and coronary heart disease (CHD) in man. Slow removal of chylomicron remnants, as reflected by a prolonged postprandial state, is now commonly observed in patients with CHD and those that have abnormal lipid disorders such as hypertriglyceridemia, familial hypercholesterolemia, familial combined hyperlipidemia and non-insulin-dependent-diabetes-mellitus. The present review will focus on (a) the details of the metabolic pathway (exogenous pathway) that describes the two-step processing of postprandial lipoproteins, (b) the role of the liver, the receptors, and the importance of efficient removal of chylomicron remnants from the blood circulation, and (c) the potential atherogenic effects of chylomicron remnants on the arterial wall.

Animals↗

PubMed1997

Corticotropin-releasing factor in antinociception and inflammation.

Corticotropin-releasing factor (CRF) plays a major role at the level of the hypothalamus and pituitary to control the body's response mechanisms to stressful stimuli. The recent discovery of CRF outside the central nervous system suggests that CRF may well play a similar role in peripheral tissues, most likely in a paracrine manner. While its effects in many other peripheral tissues is not known yet, CRF and its receptors are upregulated in inflammatory pain states pointing to a key role under these circumstances. Indeed, locally expressed CRF seems to act on CRF receptors on immune cells which have migrated into the area of the inflamed tissue, and induce the release of opioid peptides synthesized within these immune cells. These opioids subsequently act on peripheral opioid receptors located on peripheral sensory nerves to inhibit the transmission of painful stimuli. CRF may also affect the inflammatory response; however, these data are still controversial. The peripheral paracrine effects of CRF may be similar to those of hypothalamic CRF, i.e., to counterbalance local stressful events, such as inflammation and pain, so that they do not threaten the homeostasis of the body. Interestingly, CRF-like peptides have been identified not only in mammalians, but also in species such as the frog (Stenzel-Poore et al., 1992, Mol. Endocrinol. 6, 1716) and the teleost fish (Okawara et al., 1988, Proc. Natl. Acad. Sci. USA 85, 8439) indicating that this is a peptide that has been conserved over a long period (200 million years) across species (Lederis et al., 1990, Prog. Clin. Biol. Res. 342, 467) and that the release of ACTH-like peptides by peptides of the CRF family may represent an ancestral type of stress response (Ottaviani et al., 1992, Gen. Comp. Endocrinol. 87, 354; Tran et al., 1990, Gen. Comp. Endocrinol. 78, 351).

Analgesia↗

PubMed1975

Progesterone, 20 alpha-dihydroprogesterone and 20 beta-dihydroprogesterone in mother and child at birth.

In 14 healthy pregnant women at term progesterone (P) and 20 alpha-dihydroprogesterone (20 alpha-DHP) were determined by radioimmunoassay both in the maternal and foetal compartments. The average concentrations were as follows (ng/ml blood or ng/g wet weight tissue): peripheral maternal blood P 56 +/- 26, 20 alpha-DHP 16 +/- 8; placental tissue P 2514 +/- 1516, 20 alpha-DHP 429 +/- 412; placental blood P 365 +/- 160, 20 alpha-DHP 35 +/- 18; blood of the umbilical vein P 388 +/- 121, 20 alpha-DHP 33 +/- 15; blood of the umbilical arteries P 162 +/- 62, 20 alpha-DHP 28 +/- 10. In 5 healthy pregnant women at term progesterone (P), 20 alpha-dihydroprogesterone (20 alpha-DHP) and 20 beta-dihydroprogesterone (20 beta-DHP) were also determined by gas-liquid chromatography both in the maternal and foetal compartments. The average concentrations were as follows (ng/ml plasma or ng/g wet weight tissue): peripheral maternal plasma P 129 +/- 49, 20 alpha-DHP 15 +/- 15, 20 beta-DHP 1.7 +/- 0.9; placental tissue P 5060 +/- 1435, 20 alpha-DHP 230 +/- 158, 20 beta-DHP 38 +/- 30; placental plasma P 723 +/- 245, 20 alpha-DHP 24 +/- 13, 20 beta-DHP 1.0 +/- 0.1; plasma of the umbilical vein P 740 +/- 227, 20 alpha-DHP 17 +/- 3, 20 beta-DHP 1.2 +/- 0.3; plasma of the umbilical arteries P 324 +/- 94, 20 alpha-DHP 17 +/- 5, 20 beta-DHP 2.6 +/- 2.1. These results show that, contrary to the progesterone concentrations, no significant difference exists in the concentrations of 20 alpha-DHP and 20 beta-DHP between the blood from the umbilical vein and arteries. Furthermore, no significant difference could be found in the concentrations of P and 20 alpha-DHP between the sexes in either the blood from the umbilical vein or from the umbilical arteries.

20-alpha-Dihydroprogesterone↗

PubMed2005

Mapping PrPSc propagation in experimental and natural scrapie in sheep with different PrP genotypes.

Twenty-one orally inoculated and seven naturally infected sheep with scrapie were examined for PrP(Sc) in peripheral tissues and in the central nervous system (CNS), using immunohistochemistry. In the inoculated group, VRQ (valine at codon 136, arginine at codon 154 and glutamine at codon 171)/VRQ sheep generally had a greater accumulation of the pathologic form of prion protein (PrP(Sc)) in peripheral tissues, as compared with VRQ/ARQ (alanine at codon 136, arginine at codon 154, and glutamine at codon 171) animals at corresponding time points after inoculation. PrP(Sc) was not detected in the ileal Peyer's patch, the spleen, the superficial cervical lymph node, and peripheral nervous tissues of several inoculated VRQ/ARQ animals. All inoculated VRQ/VRQ sheep, but only one of eight inoculated VRQ/ARQ animals, were PrP(Sc)-positive in the CNS. Thus, the propagation of PrP(Sc) seemed slower and more limited in VRQ/ARQ animals. Tissue and cellular localization of PrP(Sc) suggested that PrP(Sc) was disseminated through three different routes. PrP(Sc)-positive cells in lymph node sinuses and in lymphatics indicated spreading by lymph. The sequential appearance of PrP(Sc) in the peripheral nervous system and the CNS, with satellite cells as early targets, suggested the periaxonal transportation of PrP(Sc) through supportive cells. Focal areas of vascular amyloid-like PrP(Sc) in the brain of five sheep, suggested the hematogenous dissemination of PrP(Sc). There was a poor correlation between the amount of PrP(Sc) in the CNS and clinical signs. One subclinically affected sheep showed widespread PrP(Sc) accumulation in the CNS, whereas three sheep had early clinical signs without detectable PrP(Sc) in the CNS. A VV(136) (homozygous for valine at codon 136) sheep inoculated with ARQ/ARR (alanine at codon 136, arginine at codon 154, and arginine at codon 171) tissue succumbed to disease, demonstrating successful heterologous transmission. Less susceptible sheep receiving VRQ/VRQ or ARQ/ARR material were PrP(Sc)-negative by immunohistochemistry, enzyme-linked immunosorbent assay, and western blot.

Amino Acid Substitution↗

PubMed2002

T-cell activation occurs simultaneously in local and peripheral lymphoid tissue following oral administration of a range of doses of immunogenic or tolerogenic antigen although tolerized T cells display a defect in cell division.

How the mucosal immune system promotes active immunity against harmful organisms but tolerance to commensal bacteria or dietary antigens is poorly understood. Thus, the antigen-presenting cell (APC), site of antigen presentation, and effector mechanisms responsible for oral priming and tolerance remain unclear. Characterizing differences between oral priming and tolerance may improve the exploitation of oral tolerance for therapeutic applications and aid the design of oral vaccines. To address these questions we compared the mucosal and systemic activation and localization of antigen-specific T cells during the induction of oral priming and tolerance. Activation marker expression and cell division by tg T cells was determined in conjunction with their anatomical location. These studies show that after feeding, T cells are activated in both peripheral and local lymphoid tissues within 6 hr, irrespective of the presence of adjuvant. Subsequently, T-cell accumulation can be detected simultaneously in peripheral and mesenteric lymph nodes and Peyer's patches within 24 hr of feeding, but only after 3 days post feeding in the lamina propria. Primed and tolerized T cells adopted similar phenotypes as assessed by activation marker expression. However, within the mesenteric lymph nodes (MLN) tolerized T cells underwent significantly fewer divisions than primed T cells. Thus, T-cell activation and expansion occurs throughout the animal after feeding a range of doses of antigen, irrespective of whether priming or tolerance is the eventual outcome. However, the presence of an adjuvant enhances clonal expansion in the MLN while tolerized T cells display defective cell division.

Administration, Oral↗

PubMed1995

A widespread amino acid polymorphism at codon 905 of the glycogen-associated regulatory subunit of protein phosphatase-1 is associated with insulin resistance and hypersecretion of insulin.

The regulatory G-subunit of the glycogen-associated form of protein phosphatase 1 (PP1) plays a crucial part in muscle tissue glycogen synthesis and breakdown. As impaired insulin stimulated glycogen synthesis in peripheral tissues is considered to be a pathogenic factor in subsets of non-insulin-dependent diabetes mellitus (NIDDM) and obesity, the G-subunit of PP1 should be viewed as a candidate gene for inherited insulin resistance. When applying heteroduplex formation analysis and nucleotide sequencing of PP1G-subunit cDNA from 30 insulin resistant white NIDDM patients two cases were identified as heterozygous carriers of an Asp905 --> Tyr substitution. The carrier prevalence of the PP1G-subunit variant was 18% in 150 healthy subjects and 13% in 313 NIDDM subjects (chi 2 = 1.94, p = 0.16). Twenty-seven healthy subjects volunteered for a 4 h euglycaemic, hyperinsulinaemic clamp in combination with indirect calorimetry in order to elucidate the potential impact of the Tyr905 substitution on the whole body glucose metabolism. Interestingly, the Tyr905 variant was associated with altered routing of glucose: a decreased insulin stimulated non-oxidative glucose metabolism of peripheral tissues (glycogen synthesis) (p < 0.04) and an increased basal glucose oxidation rate (p < 0.04) when compared with wild type carriers. A population-based sample of 380 unrelated young healthy Caucasians was examined during a combined intravenous glucose and tolbutamide test to address whether the Asp905/Tyr905 polymorphism was associated with alterations in insulin secretion which might be secondary to the insulin resistance of skeletal muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Base Sequence↗

PubMed1993

[Detection of hemorrhagic fever virus-RNA in renal tissue and peripheral blood in patients with hemorrhagic fever with renal syndrome].

Hemorrhagic fever virus (HFV) RNA in renal tissue and blood samples from 21 patients with epidemic hemorrhagic fever with renal syndrome (HFRS) were examined by either in situ or blot hybridization using digoxigenin labelled HFV-cDNA probe. HFV associated antigen and immune complex (IC) in renal tissue were also investigated simultaneously using immunofluorescence (IF) technique. HFV-RNA was detected in the renal specimen particularly renal tubular in 8/21 HFRS patients mostly of severe type illness. However, the deposition of IC in the renal tissue in this group of patients occurred mainly in the mild type apparently in a different manner of HFV-RNA. We conclude that both the HFV-RNA and immune complexes deposition are contributable to the pathogenesis of renal lesion in HFRS.

Adolescent↗

PubMed2000

Effect of fruits, vegetables, or vitamin E--rich diet on vitamins E and C distribution in peripheral and brain tissues: implications for brain function.

Age-related neurodegenerative conditions are the principal cause of declining cognitive and motor function during aging. Evidence support that fruits and vegetables containing generous amounts of antioxidant nutrients are important for neurological function. We investigated the effect of diets enriched with fruits or vegetables but low in vitamin E and a diet high in vitamin E on the distribution of vitamins C and E in the brain and dopamine release of Fischer 344 rat model, over an 8-month period. The low-vitamin E diet resulted in lowered alpha-tocopherol levels in brain and peripheral tissues, whereas the animals that received a diet enriched in vitamin E showed a significant increase, between 500-900%. Vitamin C concentration in plasma, heart, and liver was reduced in the vitamin E-supplemented group. It is concluded that supplementation or depletion of alpha-tocopherol for 8 months results in marked changes in vitamin E levels in brain tissue and peripheral tissues, and varied distribution of alpha-tocopherol throughout the different brain regions examined. In addition, compared to control group, rats supplemented with strawberry, spinach, or vitamin E showed a significant enhancement in striatal dopamine release. These findings suggest that other nutrients present in fruits and vegetables, in addition to the well-known antioxidants, may be important for brain function.

Aging↗

PubMed1996

Tissue distribution of opioid receptor gene expression in the rat.

The endogenous opioid peptides have multiple physiological actions at both a central and peripheral level which are mediated by 3 main classes of opioid receptors, mu, delta and kappa. The rat mu, delta and kappa opioid receptors have recently been cloned and their distribution of expression in the central nervous system has been mapped. In these studies we have used the reverse transcriptase polymerase chain reaction and Southern blotting to determine the distribution of expression of the mu, delta and kappa opioid receptors in the peripheral tissues of the rat. All 3 opioid receptors were found to be widely expressed in several peripheral tissues including the small intestine, large intestine, adrenal, kidney, lung, spleen, testis, ovary and uterus. In the stomach, delta and kappa but not mu opioid receptor transcripts were detected. Predominantly delta transcripts were detected in the heart, with no mu and only a weak signal for the kappa receptor. In the liver mu and delta but not kappa transcripts were present. Opioid receptor expression was not detected in endothelium or synovium. There is therefore a broad, but tissue specific distribution of opioid receptor expression in the periphery of the rat, suggesting that the endogenous opioid peptides play an endocrine, paracrine, or autocrine role in the regulation of physiology at a peripheral as well as central level.

Animals↗