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PubMed1988

The release of histamine from nasal polyp tissue and peripheral blood when challenged with antihuman IgE, house dust mite extract and mixed grass pollen extract and compared with positive skin tests.

Nasal polyps are a condition of uncertain aetiology but are associated with diseases of the lower respiratory tract, in particular, asthma and cystic fibrosis. Asthma may be mediated by mast cell reactions and the commonest allergen to degranulate mast cells is house dust mite. Mast cells have been shown to be degranulated in nasal polyps. This study looks at thirty-six patients who had nasal polypectomy and of whom fourteen were asthmatic to see if histamine was released from polyp tissue and peripheral blood when they were challenged with antihuman IgE and extracts of house dust mite and mixed grass pollens. These results were compared with skin tests to these allergens. A release of above 15 per cent of the total histamine was considered positive. Eight patients released histamine from polyp tissue but only three patients released histamine with both anti IgE and allergen extracts. The release from blood compared well with positive skin tests (p greater than 0.05 corrected chi square). Although allergy may cause mast cell degranulation in polyp tissue, this study suggests that it is unlikely to be a common cause of nasal polyps.

Animals↗
PubMed1985

Pirenzepine distinguishes between muscarinic receptor-mediated phosphoinositide breakdown and inhibition of adenylate cyclase.

Subtypes of muscarinic cholinergic receptors have been proposed to exist, but the biochemical responses mediated by the putative subtypes are unknown. In the present study, muscarinic receptor-mediated phosphoinositide breakdown and inhibition of adenylate cyclase activity were characterized in rat brain as well as rat parotid and heart. To study whether these responses are mediated by separate subtypes of muscarinic receptors, the potencies of agonists and antagonists were determined in both assays. Antagonist potencies were calculated by Schild analysis. In the brain, the putatively selective muscarinic receptor antagonist, pirenzepine, exhibited Ki values of 21 nM in the assay of phosphoinositide breakdown and 310 nM in the assay of adenylate cyclase activity. Similarly, using radioligand binding techniques, it distinguished two binding sites with Kd values of 12 and 168 nM. The antagonist, atropine, on the other hand, was equipotent in the two biochemical assays and the radioligand binding assay with Ki values of approximately 1 to 2 nM. In peripheral tissues with robust muscarinic receptor-mediated phosphoinositide (parotid) and adenylate cyclase (heart) responses, pirenzepine exhibited a similar selectivity (19-fold) for the phosphoinositide assay that was seen in the brain, but it was 6- to 7-fold less potent in both peripheral tissues than in the central nervous system. In addition, the potencies of pirenzepine in binding and functional studies in each tissue were not as well correlated as in the brain. Atropine and other antagonists were 4- to 9-fold selective for inhibiting oxotremorine-stimulated phosphoinositide breakdown in the peripheral tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1982

Cellular and subcellular localization of protein I in the peripheral nervous system.

The cellular and subcellular distribution of protein I, a major brain phosphoprotein, has been studied in the peripheral nervous system. The levels of protein I in various peripheral nerves and innervated peripheral tissues were determined by radioimmunoassay and radioimmunolabeling of polyacrylamide gels. The results indicated tha protein I is present throughout the peripheral nervous system. Denervation studies of adrenal medulla and iris suggested that the protein I contained in peripheral tissues is localized to the neuronal elements innervating those tissues. Protein I was found to be enriched in neurotransmitter vesicle fractions of peripheral nervous tissue. Moreover, protein I appeared to be transported from cell bodies to axons terminals at least partly in association with neurotransmitter vesicles.

Adrenal Glands↗
PubMed1993

Effects of tachykinins on phosphoinositide metabolism in the hypothalamus: is the NK1 receptor involved?

Substance P (SP) has been shown to stimulate the hydrolysis of inositol phospholipids in peripheral tissues and in the brain. In mammalian peripheral tissues, three tachykinin receptor subclasses, neurokinin 1 (NK1), neurokinin 2 (NK2) and neurokinin 3 (NK3), have been identified. The purpose of our study was to pharmacologically characterize the SP receptors in the hypothalamus using phosphoinositide breakdown as a functional response. SP, previously described as a NK1 agonist, and Neurokinin A (NKA), previously described as a NK2 agonist, stimulated phosphoinositide breakdown in the hypothalamus in a dose-dependent fashion, with SP being more potent than NKA. The NK2-selective antagonist L-659,877, at a dose of 10(-6) M, abolished the effect of SP (10(-8) M) without affecting basal phosphoinositide breakdown. However, this NK2-selective antagonist did not inhibit the NKA-induced stimulation in phosphoinositide metabolism. The NK1-selective antagonist L-668,169 stimulated phosphoinositide metabolism at a concentration of 10(-6) M, but not at 10(-8) M. This NK1-receptor antagonist did not significantly inhibit the effect of SP on phosphoinositide metabolism. Spantide II, another NK1-selective antagonist, also stimulated phosphoinositide metabolism at a dose of 10(-6) M. Like L-668,169, spantide II failed to inhibit the SP-induced stimulation of phosphoinositide metabolism, and even potentiated the response to SP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Colonic acetate in the circulating acetate pool of the infant pig.

To identify potential sites of acetate utilization and synthesis, we studied the contribution of colonic acetate to the circulating acetate pool in six neonatal pigs by the simultaneous i.v. infusion of [3H]acetate and colonic infusion of [14C]acetate. In the fasting state, the mean (+/- SEM) acetate concentration was 17 +/- 1 mumol/L in peripheral venous blood, 28 +/- 4 mumol/L in the femoral artery, and 46 +/- 4 mumol/L in portal blood. This concentration gradient implies that acetate was utilized either by peripheral tissues alone or by both liver and peripheral tissues. At the end of the 2-h intracecal acetate infusion, mean acetate concentration increased in the femoral artery to 186 +/- 20 mumol/L and in the portal vein to 333 +/- 31 mumol/L. In the fasted state, mean acetate concentration in the portal vein was on average 63% higher than the acetate concentration of the femoral artery, whereas specific radioactivity of the [3H]acetate in the portal vein was only 5% of that in the femoral artery. It is possible, therefore, that a high proportion of the arterial input of acetate is utilized by the portal-drained viscera. Our study identified the gastrointestinal tract as an important site of acetate utilization in the fasted state. Further, it showed that colonic acetate was efficiently absorbed and utilized in the gastrointestinal tract of infant pigs.

Acetates↗
PubMed2001

The effect of antigen stimulation on the migration of mature T cells from the peripheral lymphoid tissues to the thymus.

Although the maturation and export of T cells from the thymus has been extensively studied, the movement of cells in the opposite direction has been less well documented. In particular, the question of whether T cells which have been activated by antigen in the periphery are more likely to return to the thymus had been raised but not clearly answered. We examined this issue by activating T cells present in the periphery with their cognate antigen, and assessing migration to the thymus. TCR-transgenic cells from OT-I mice (Thy1.2+), which recognise the ovalbumin peptide OVA257-264 in the context of H-2Kb, were transferred into otherwise unmanipulated Thy1.1+ C57BL/6 mice. Recipient mice were injected i.v. with 5 microg peptide (SIINFEKL) approximately 24 hours later. The numbers of donor-derived (Thy1.2+) cells in the thymus and peripheral lymphoid tissue were determined. The results clearly show increased numbers of transgenic cells in the thymus 3 days after antigenic stimulation. However, since numbers of transgenic cells increased in the spleen and LN in about the same proportion, the data do not support the notion that there is highly increased selective migration of activated T cells to the thymus. Rather, they suggest that a sample of peripheral cells enters the thymus each day, and that the mature immigrants detected in the thymus merely reflect the contents of the peripheral T cell pool.

Animals↗
PubMed1993

Dietary marine fish oils and insulin action in type 2 diabetes.

Supplementation of omega-3 fish oils (n-3 FO) usually worsens the glycemic control in type 2 diabetic subjects. This may be a dose-related phenomenon and is reversed after discontinuation of the n-3 FO supplementation. An increase in the daily caloric intake, due to the fat content of n-3 FO supplements, and a consequent weight gain may contribute to the increase in hyperglycemia. Mechanisms of the increase in hyperglycemia include: (1) n-3 FO may interfere with insulin secretion from the pancreas, and this in turn can cause an increase in the hepatic glucose output and/or a decrease in the glucose uptake by the peripheral tissues; (2) n-3 FO may primarily decrease the sensitivity of liver to insulin action and consequently increase gluconeogenesis and/or glycogenolysis and/or decrease the glycogenesis; (3) n-3 FO may primarily affect the sensitivity of peripheral tissues to insulin, resulting in decreased glucose-uptake; (4) n-3 FO may increase the availability of gluconeogenic substrates by directly altering the partitioning of the metabolic fuels for different pathways in the liver. [formula: see text] Direct experimental testing of these possibilities has been difficult, because n-3 FO affects the carbohydrate metabolism differently in animal models than in humans. The available data suggest that n-3 FO inhibits insulin secretion in response to glucose load, mixed meal, and glucagon but not at the fasting state. Hepatic glucose output is increased. Sensitivity of the peripheral tissues to insulin is not changed. An encouraging observation is that the hyperglycemic effect of n-3 FO may decrease with time even when therapy is continued. Proper use of this treatment modality requires careful evaluation of the risk/benefit ratio for every individual patient.

Blood Glucose↗
PubMed1988

The diabetic intrauterine milieu has a long-lasting effect on insulin secretion by B cells and on insulin uptake by target tissues.

From our previous work, it appears that fetal development in the abnormal intrauterine milieu of a mother with diabetes results in impaired glucose tolerance in adult life. In adult Wistar rats that were the offspring of mildly or severely diabetic mothers, in vitro islet stimulation and in vivo insulin uptake studies were undertaken to distinguish between alterations in glucose sensitivity and insulin secretion at the B cell level and alterations in insulin sensitivity and uptake at the level of the peripheral tissues. Insulin output after glucose stimulation by isolated islets was lower than normal in the rats of mothers with mild diabetes and higher than normal in the animals of severely diabetic mothers, confirming the results of previous in vivo studies. Insulin binding by the liver was normal in both groups. Insulin uptake by the kidney was normal in rats with mildly diabetic mothers but was increased in rats of severely diabetic mothers, suggesting decreased uptake of insulin by the peripheral tissues. Impaired glucose tolerance in rats of mildly diabetic mothers, resulting from decreased responsiveness to glucose, is interpreted as a consequence of hyperactivity of these B cells during the intrauterine life. Impaired glucose tolerance in rats of severely diabetic mothers, associated with insulin hypersecretion and decreased insulin uptake by the peripheral tissues might result from intrauterine alterations of the peripheral receptor or postreceptor system induced by the abnormal intrauterine milieu. These data on experimental diabetes in the rat demonstrate that the maternal diabetic environment exerts a diabetogenic influence on the offspring.

Animals↗
PubMed1995

Protein metabolism in human colon carcinomas: in vivo investigations using a modified tracer technique with L-[1-13C]leucine.

To quantify the protein anabolism of tumors it is not sufficient simply to determine the level of protein synthesis. The decisive factor is the net balance. This is the first attempt to establish this parameter in human tumors in vivo. Intraoperative tumor leucine/protein metabolism was studied in 15 patients with resectable malignant colon tumors using a balance model and L[1-13C]leucine as the tracer substance. Comparative measurements were also carried out simultaneously for peripheral tissue (forearm); in addition, protein kinetics parameters were established for the whole body using a proven two-pool model (with the same tracer as above). In view of the frequently conflicting data on amino acid metabolism in tumors, the tumoral and peripheral exchange rates of 20 amino acids were also determined. In tumors, essential and branched-chain amino acid uptakes were found to be 1.68 +/- 0.59 (SE) and 1.52 +/- 0.23 mumol/100 g tissue/min, respectively; in peripheral tissue there was overall an amino acid release [-0.11 +/- 0.06 and -0.05 +/- 0.04 mumol/100 g/min; in either case P < 0.01 (tumor versus periphery)]. Tracer analyses yielded a net retention for the tumors but a protein loss for peripheral tissue (8.941 +/- 3.113 versus -0.557 +/- 0.53 g/kg/24 h; P < 0.01) and for the whole body (-0.363 +/- 0.04 g/kg/24 h). The tumors were divided into two prognostic groups on the basis of their histology. Significant differences were found between the two groups in terms of the net retention rate for 10 amino acids, including leucine; retention was elevated in tumors with an unfavorable prognosis, possibly due to a higher amino acid requirement because of more rapid growth or for export processes (mucus production). The protein balance model used here has proved satisfactory for our purposes and could also be used to directly evaluate dietary measures (e.g., adjuvant parenteral nutrition in connection with chemotherapy).

Aged↗
PubMed2006

Biomechanical characterization of needle piercing into peripheral nervous tissue.

Several neural interfaces have been developed to control neuroprostheses and hybrid bionic systems. Among them, intraneural electrodes are very promising because they represent an interesting trade-off between the needs for high selectivity and for reduced invasiveness. However, in most of the cases, no particular attention has been devoted so far to the design of these systems starting from the mechanical properties of the system to be interfaced. The aim of this paper was to study and characterize in a quantitative way the piercing of peripheral nervous tissue in order to gather useful information to design intraneural interfaces able to reduce (as much as possible) the damages provoked by this task. In particular, attention has been paid to determine the values of force and pressure to carry out the piercing task in different velocity conditions. From the experimental data it was possible to characterize indirectly the tissue sinking under the needle tip. For each experimental velocity (ranging from 1 to 2000 mm/min) a threshold, under which the tissue cannot be pierced, has been calculated. The force magnitude required for piercing was shown to be in the range 0.3-25 mN for the different velocities. Moreover, differences between piercing carried out at very low velocity (multi-piercing) and at low velocity (mono-piercing) have been characterized and correlated with the physical characteristics of the nervous tissue. Experimental data have been integrated with a theoretical analysis of the neural interfaces piercing structures. The problem of buckling, representing for these structures the main cause of tissue piercing impossibility, has been analyzed. The nonlinear theoretical model allows to compare different needle geometries and materials with regard to piercing possibility at different velocities. Moreover, an optimization of piercing elements geometry with regard to amount of used material and space has been provided.

Animals↗
PubMed2002

Distribution and accumulation of PrP in gut-associated and peripheral lymphoid tissue of scrapie-affected Suffolk sheep.

The distribution of disease-associated prion protein (PrP) was investigated in eight animals (20-24 months of age) from a flock of Suffolk sheep that had experienced frequent cases of natural scrapie over a period of several years. Tissue from the central nervous system (CNS), alimentary tract, peripheral nervous system and lymphoreticular system was examined by histopathology and immunohistochemistry. The lymphoid tissues were subjected further to histoblot and immunofluorescence examination. The four clinically affected PrP(ARQ/ARQ) sheep had widespread accumulations of disease-associated PrP in the CNS, lymphoreticular system and peripheral ganglia. In the two PrP(ARQ/ARQ) sheep that did not show clinical signs of scrapie, only limited vacuolation and PrP accumulation were detected in the brain, but the results from the lymphoreticular system and peripheral nervous system were comparable with the clinically affected animals. The remaining PrP(ARR/ARR) and PrP(ARR/ARQ) sheep did not show proteinase K-resistant PrP accumulations in the lymphoid tissues examined and immunohistochemistry did not reveal the presence of disease-associated PrP. In lymphoid tissues of the PrP(ARQ/ARQ) sheep, the dominant localization of disease-associated PrP was in lymphoid nodules and double immunofluorescence labelling for PrP and CD21 provided further support for the role of follicular dendritic cells in scrapie in sheep. A striking finding in the present study was the large accumulations of disease-associated PrP in the lymphoid nodules of the alimentary tract at the late sub-clinical and clinical stage of the infection. The study also identified disease-associated PrP in extra-nodular sites of lymphoid tissues, such as the marginal zone of the spleen, and these observations were used to argue that cells of the mononuclear phagocyte system of sheep may be involved in the uptake, transport, elimination and shedding of the scrapie agent.

Animals↗
PubMed1993

Peripheral metabolism of branched-chain keto acids in patients with chronic renal failure.

Peripheral tissue metabolism of branched-chain amino acids (BCAA) and branched-chain keto acids (BCKA) in the postabsorptive state was evaluated in 8 patients with chronic renal failure (CRF) and 7 controls by measuring the arterial-deep forearm venous differences for BCAA and BCKA. Arterial whole blood levels of BCAA and BCKA were also measured in an additional 7 patients and 11 controls. In CRF, total BCKA levels are reduced owing to a decrease in ketoisocaproic acid (KICA) and ketoisovaleric acid (KIVA) levels, parallel to changes in BCAA levels, whereas levels of ketomethylvaleric acid (KMVA) are not different from controls. Both in normal conditions and in patients, arterial levels of individual BCAA are directly correlated with arterial levels of the corresponding BCKA. However, in CRF, the ratios of leucine to KICA and of isoleucine to KMVA are increased. A direct correlation between KICA and HCO3- levels is observed. In CRF, the release of leucine and valine as well as of KICA and KMVA from peripheral tissues is reduced, whereas KIVA is neither released nor taken up by the forearm. The lack of KICA release from peripheral tissues likely accounts for its low circulating levels. The depressed peripheral release of leucine associated with the lack of KICA release suggests an increased degradation of leucine which proceeds beyond the transamination step.

Adult↗
PubMed1985

Regional blood flow distribution during the Cushing response: alterations with adrenergic blockade.

Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood flow (CBF) decreased 50%, coronary blood flow (CoBF) increased 120%, and peripheral tissue blood flow was reduced only in the kidneys (18%) and the intestines (small 22%, large 35%). Blood flow to the other viscera, skin, and skeletal muscle was unchanged. CO (16%) and heart rate (HR, 38%) decreased, and total peripheral resistance (TPR, 68%) and stroke volume (SV, 38%) increased. In BB, CBF decreased 50%, CoBF decreased 20%, and blood flow was reduced 40-80% in all peripheral tissues. CO (69%) and HR (62%) decreased, TPR increased 366%, and SV was unchanged. We conclude that the Cushing response in UB animals combines an alpha-receptor-mediated vasoconstriction with a beta-receptor cardiac stimulation. The beta-mechanism is neither necessary nor sufficient for the hypertension. However, the combination of alpha- and beta-adrenergic mechanisms maintains cardiac output and peripheral tissue blood flow relatively constant while producing a systemic hypertension.

Adrenergic alpha-Antagonists↗
PubMed1991

Calcium deficiency enhances cadmium accumulation in the central nervous system.

Weanling male rats were administered 1 of 4 diets for 40 days: control (CONT), low Ca (LOCA), control plus Cd (CONT + Cd) or low Ca plus Cd (LOCA + Cd). After 40 days, Cd was analyzed in 7 brain regions, spinal cord, serum, liver, kidney, muscle and femur by atomic absorption spectrophotometry with Zeeman background correction. No significant difference in Cd between CONT and LOCA was found except in femur, where it was increased. In CONT + Cd rats, peripheral tissues showed an increase in Cd of 30-71 fold above CONT rats. Brain regions exhibited a more modest 7-10 fold change, and serum Cd was 8.5 times above control. LOCA + Cd rats showed a 25-fold increase of Cd above LOCA in serum, 25-100 fold in peripheral tissues, and a 14-20 times in brain. These findings show that brain Cd is increased during Ca deficiency, but that central nervous system Cd changes less than peripheral tissue Cd. This increase in brain Cd could alter brain function.

Animals↗
PubMed2004

Structure, chemical composition, and xylanase degradation of external layers isolated from developing wheat grain.

The external layers of wheat grain were investigated during maturation with respect to chemical and structural features and xylanase degradability. Cytochemical changes were observed in the isolated peripheral tissues of the wheat grain at four defined stages following anthesis. Marked chemical changes were highlighted at 11 days after anthesis, for which protein and lipid contents varied weakly. The profile of esterified ferulic acid showed large variation in the maturing peripheral layers of grain in contrast to the deposition of ferulate dimers, p-coumaric and sinapic acids. Lignin was monitored at the latest stages of ripening, which corresponds to the cessation of reserve accumulation in the grain. Arabinoxylans (AX) reached a maximum at 20 days and did not display any significant change in arabinosyl substitution proportion until ripeness. When submitted to xylanase, all outer layers were similarly altered in the proportion of soluble AX except for the peripheral tissues of the 11-day-aged wheat grain that had very little AX. Aleurone and nucellar layers were mostly degraded, whereas pericarp stayed intact at all stages of maturation. This degradation pattern was connected with the preferential immunolocalization of xylanase in aleurone and nucellar layers irrespective of the developmental stages. Further chemical examination of the enzyme-digested peripheral tissues of the grain supports the facts that ferulic ester is not a limiting factor in enzyme efficiency. Arabinose branching, ferulic dimers, and ether-linked monomers that are deposited early in the external layers would have more relevance to the in situ degradability of AX.

Carbohydrates↗
PubMed2001

MHC class II-regulated central nervous system autoaggression and T cell responses in peripheral lymphoid tissues are dissociated in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis.

We dissected the requirements for disease induction of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis in MHC (RT1 in rat) congenic rats with overlapping MOG peptides. Immunodominance with regard to peptide-specific T cell responses was purely MHC class II dependent, varied between different MHC haplotypes, and was linked to encephalitogenicity only in RT1.B(a)/D(a) rats. Peptides derived from the MOG sequence 91-114 were able to induce overt clinical signs of disease accompanied by demyelinated CNS lesions in the RT1.B(a)/D(a) and RT1(n) haplotypes. Notably, there was no detectable T cell response against this encephalitogenic MOG sequence in the RT1(n) haplotype in peripheral lymphoid tissue. However, CNS-infiltrating lymphoid cells displayed high IFN-gamma, TNF-alpha, and IL-4 mRNA expression suggesting a localization of peptide-specific reactivated T cells in this compartment. Despite the presence of MOG-specific T and B cell responses, no disease could be induced in resistant RT1(l) and RT1(u) haplotypes. Comparison of the number of different MOG peptides binding to MHC class II molecules from the different RT1 haplotypes suggested that susceptibility to MOG-experimental autoimmune encephalomyelitis correlated with promiscuous peptide binding to RT1.B and RT1.D molecules. This may suggest possibilities for a broader repertoire of peptide-specific T cells to participate in disease induction. We demonstrate a powerful MHC class II regulation of autoaggression in which MHC class II peptide binding and peripheral T cell immunodominance fail to predict autoantigenic peptides relevant for an autoaggressive response. Instead, target organ responses may be decisive and should be further explored.

Alleles↗
PubMed2003

Correlation between the avidity maturation of anti-HSP70 IgG autoantibody and recombination activating gene expressions in peripheral lymphoid tissues of Toxoplasma gondii-infected mice.

The avidity maturation of anti-TgHSP70 IgG antibody produced by B-2 cells of BALB/c mice (a resistant strain) and that of anti-mHSP70 IgG autoantibody produced by B-1 cells of C57BL/6 mice (B6; a susceptible strain) was observed after Toxoplasma gondii infection. Recombination-activating genes (RAGs) were predominantly expressed in B-1 cells from peritoneal exudate cells (PECs) of T. gondii-infected B6 mice, while RAGs were expressed in B-2 cells from PECs of BALB/c mice. These results suggest that the involvement of RAG gene activations in the peripheral lymphoid tissues in the avidity maturation of anti-TgHSP70 IgG antibody and anti-mHSP70 IgG autoantibody in T. gondii-infected mice.

Animals↗