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Objectives: Eosinophilic chronic rhinosinusitis (ECRS) is known to recur after surgery. The treatment choice for recurrent ECRS, such as oral steroids or biological agents, must be chosen carefully, and identifying the lesion location may be useful. This study aimed to evaluate the postoperative course of ECRS patients and assess the relationship between endoscopic lesion location and postoperative oral steroid use. Methods: Patients with chronic rhinosinusitis who underwent bilateral endoscopic sinus surgery from April 2018 to March 2020 were divided into two groups based on the presence or absence of oral steroid use after surgery. The primary endpoint was the lesion location on endoscopic findings during surgery: middle turbinate, middle meatus, superior turbinate, superior meatus, nasal septum, and sphenoethmoidal recess. Subjective symptoms, blood tests, and computerized tomography (CT) findings (Lund‐Mackay score) were evaluated as secondary endpoints. Results: Among 264 patients, 88 were diagnosed histologically with ECRS (mean 48.98 ± 1.40 years, 67 males/21 females). Twenty‐three patients were steroid‐using, 65 were steroid‐free, and six stopped attending their appointments. Patients with sphenoethmoidal recess lesions were significantly more likely to require steroids (p = 0.019). There was a significant association between steroid use and younger age (p = 0.041), olfactory dysfunction (p = 0.021), and all sinuses (Frontal sinus: p < 0.001, Anterior ethmoid sinus: p = 0.002, Posterior ethmoid sinus: p = 0.011, Maxillary sinus: p = 0.018, Sphenoid sinus: p = 0.034, Total score: p < 0.001). Conclusion: A sphenoethmoidal recess lesion was a risk factor for requiring postoperative steroids. Young age, olfactory dysfunction, and preoperative severe CT findings were also significant risk factors. Level of Evidence: 3 Laryngoscope, 133:2511–2516, 2023 [ABSTRACT FROM AUTHOR]

B Background: b Emerging evidence suggests the prognostic impact of the tumor microenvironment (TME) in peripheral T-cell lymphomas (PTCLs). THE GENETIC SUBTYPES AND THE TUMOR MICROENVIRONMENT SIGNATURES ARE ASSOCIATED WITH DISTINCT OUTCOMES IN PERIPHERAL T-CELL LYMPHOMA Ninety-two nTFHLs included 85 angioimmunoblastic T-cell lymphomas (AITLs), four nPTCL with TFH phenotypes, two follicular T-cell lymphomas, and one unclassifiable nTFHL. [Extracted from the article]

Positive interactions are known to play important roles in ecological divergence but have received less attention than negative interactions in studies on intertidal communities. Here, we show that growth of the mat‐forming green alga Pseudocladophora conchopheria on the shells of a intertidal gastropod (Lunella coreensis) provides them with benefits for living in intertidal rocky habitats. We found that P. conchopheria covered a large proportion of the shell surface in all L. coreensis inhabiting an exposed rocky shore habitat, but none or only a small proportion of the shell surface in L. coreensis inhabiting a damp boulder shore habitat. Thermal exposure experiment showed that L. coreensis originating from the boulder shore habitat had a higher mortality rate and temperatures inside the shell than those originating from the exposed rocky shore habitat. These differences disappeared when P. conchopheria was removed from the shell or was dried out, indicating that an increased coverage and dampness of the alga suppressed the increase in temperature inside the shell. These support the hypothesis that the growth of P. conchopheria on L. coreensis shells suppresses thermal stress in the hosts; the benefits of P. conchopheria may enable the hosts to exploit habitats where considerable thermal stress is present during air exposure. This paper reveals that algae Pseudocladophora conchopheria on the shells of intertidal gastropods (Lunella coreensis) suppress thermal stress in the hosts, allowing them to live in stressful environments and enabling them to utilize a diverse range of habitats. [ABSTRACT FROM AUTHOR]

Background Several gene variants identified in bronchial asthmatic patients are associated with a decrease in pulmonary function. The effects of this intervention on pulmonary function have not been fully researched. Objective We determined the effects of high-dose inhaled corticosteroids ( ICSs) on decreased pulmonary function in asthmatic Japanese patients with variants of IL13 and STAT4 during long-term treatments with low to mild doses of ICS. Methods In this study, 411 patients with bronchial asthma who were receiving ICSs and living in Japan were recruited, were genotyped, and underwent pulmonary function tests and fibreoptic examinations. The effects of 2 years of high-dose ICSs administered to asthmatic patients who were homozygous for IL13 AA of rs20541 or STAT4 TT of rs925847 and who progressed to airway remodelling were investigated. Results High-dose ICS treatment increased the pulmonary function of patients homozygous for IL13 AA of rs20541 but not of patients homozygous for STAT4 TT of rs925847. The increased concentrations of the mediators IL23, IL11, GMCSF, hyaluronic acid, IL24, and CCL8 in bronchial lavage fluid ( BLF) were diminished after high-dose ICS treatment in patients homozygous for IL13 AA of rs20541. Conclusion and Clinical Relevance IL13 AA of rs20541 and STAT4 TT of rs925847 are potential genomic biomarkers for predicting lower pulmonary function. The administration of high-dose ICSs to asthmatic patients with genetic variants of IL13 AA may inhibit the advancement of airway remodelling. The genetic variants of STAT4 TT did not respond to high-dose ICSs. Therefore, using medications other than ICSs must be considered even during the initial treatment of bronchial asthma. These genetic variants may aid in the realization of personalized and phenotype-specific therapies for bronchial asthma. [ABSTRACT FROM AUTHOR]

Amoebiasis has rarely been reported in patients undergoing hematopoietic stem cell transplantation, although it is a world-wide infection and extremely common. We present a case of intestinal amoebiasis unexpectedly revealed by colonoscopy after allogeneic bone marrow transplantation from a human leukocyte antigen-mismatched unrelated donor for acute myeloid leukemia arising from chronic myelomonocytic leukemia and successfully treated by metronidazole. [ABSTRACT FROM AUTHOR]

Understanding the molecular mechanism of the regulation of glucagon secretion is critical for treating the dysfunction of α cells observed in diabetes. Glucagon-like peptide (GLP)-1 analogues reduce plasma glucagon and are assumed to contribute to their action to lower blood glucose. It has previously been demonstrated that the central administration of brain-derived neurotrophic factor ( BDNF) improves glucose metabolism by a mechanism independent of feeding behaviour in obese subjects. Using male rats, we examined whether BDNF influences glucagon secretion from α cells via the the central nervous system. We investigate whether: (i) the central infusion of BDNF stimulates glucagon and/or insulin secretion via the pancreatic efferent nerve from the hypothalamus; (ii) the intraportal infusion of GLP-1 regulates glucose metabolism via the central and peripheral nervous system; and (iii) BDNF receptor and/or BDNF-positive fibres are localised near α cells of islets. The portal glucagon level decreased with the central administration of BDNF (n = 6, in each; P < 0.05); in contrast, there was no significant change in portal insulin, peripheral glucagon and insulin levels with the same treatment. This reduction of glucagon secretion was abolished by pancreatic efferent denervation (n = 6, in each; P < 0.05). In an immunohistochemical study, pancreatic α cells were stained specifically with BDNF and tyrosine-related kinase B, a specific receptor for BDNF, and α cells were also co-localised with BDNF. Moreover, intraportal administration of GLP-1 decreased glucagon secretion, as well as blood glucose, whereas it increased the BDNF content in the pancreas; these effects were inhibited with the central infusion of BDNF antibody (n = 6, in each; P < 0.05). BDNF and GLP-1 affect glucose metabolism and modulate glucagon secretion from pancreatic α cells via the central and peripheral nervous systems. [ABSTRACT FROM AUTHOR]

Epitaxial growth of high-quality Mg x Zn1- xO films on Zn faces of single crystal ZnO substrates was achieved by a plasma-assisted reactive evaporation method using ZnMg alloys. The composition of Mg of Mg x Zn1- xO films grown by using this method strongly depended on the composition of Mg of ZnMg alloys. Mg composition of Mg x Zn1- xO films increased with increase in the composition of Mg of ZnMg alloys with 7.5-30 wt%. The maximum value of ( x) of the Mg x Zn1- xO films was 0.24. The peak position of XRD from Mg x Zn1- xO (0002) of a wurtzite structure shifted to a high angle with increase of Mg composition of Mg x Zn1- xO films. The full-width at half-maximum value of the XRD pattern of ω scans of Mg0.17Zn00.83O (0002) was 40 arcsec. The root mean square roughness of the surface of Mg x Zn1- xO films was 1.0 nm or less, and flat terraces and steps with a height of two monolayers were observed. Room temperature photoluminescence spectra of Mg x Zn1- xO films showed a strong near band-edge (NBE) emission and very weak emission in visible regions. The peak of NBE emissions of Mg x Zn1- xO films shifted to higher energy with increase of Mg composition of Mg x Zn1- x O films. The band-gap energy estimated from reflectance spectra increased from 3.38 to 3.83 eV with increase of composition ( x) of Mg x Zn1- xO films from 0.01 to 0.24. This new growth method is useful for preparation of devices based on ZnO and its related compounds. (© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [ABSTRACT FROM AUTHOR]

Erythroid cells in the marrow express CD71, transferrin receptor, and reticulocytes released from the marrow lose their expression during maturation. The immature reticulocyte fraction, the proportion of reticulocytes with the highest content of RNA, has been determined by hematology analysis. In the present study, we examined CD71 expression on immature reticulocytes by flow cytometry (FCM) in paroxysmal nocturnal hemoglobinuria (PNH) patients with reticulocytosis. We modified ‘reticulocyte-gated FCM’ to multi-color FCM, i.e. RNA/CD71, RNA-CD59 or CD59/CD71/CD45. In PNH, in addition to the increased number of immature reticulocytes (%CD71-positive), a more immature phenotype in regard to both CD71 intensity and RNA content levels was demonstrated. In seven PNH patients studied, %CD71-positive reticulocytes were significantly increased at 32.2 ± 11.9% ( n = 10, normal 10.4 ± 3.5%, P = 0.002). RNA content levels (assessed by mean fluorescence index, MFI) in CD71-positive reticulocytes were significantly increased at 812.0 ± 215.2 MFI in PNH ( n = 10, normal 508 ± 86.1 MFI, P = 0.002). These data indicate that stimulated erythropoietic conditions induce the release of more immature reticulocytes to the peripheral blood than ordinary erythropoietic conditions. CD71 intensity on immature reticulocytes was well correlated with their RNA content levels, indicating the usefulness of CD71 as an immature reticulocyte marker. [ABSTRACT FROM AUTHOR]

Regional comparisons of interannual variations in springtime lower trophic-level ecosystems were made for northern subarctic regions, and for southern Tsushima Current regions of the Japan Sea, based on archival hydrographic and biological data sets collected from the mid-1960s to the early 1990s. Variations related to the Pacific Decadal Oscillation were detected for plankton biomass in both northern and southern regions, although there were regional differences with respect to mechanisms and timing. Springtime stratification increased after the late 1970s in the north, roughly coinciding with the northern Pacific regime shift in 1976/77. Stratification also increased due to warming in the south in the early 1980s, several years after the 1976/77 regime shift. Responding to the increase in stratification, springtime biomass of phytoplankton and zooplankton increased in the north and decreased in the south. Principal component analysis revealed that hydrographic conditions during spring, rather than winter, determined springtime phytoplankton biomass. In northern regions, spring phytoplankton production may be enhanced by increased light availability, due to mixed layer stabilization. In the south, where background nutrient concentration within the water column was low, increases in stratification were likely to limit nutrient supply to the surface layer, resulting in decreases in phytoplankton production. A positive relationship between phytoplankton and zooplankton biomass suggested bottom-up control of secondary production in northern regions. The nature of the links between phytoplankton and zooplankton production was not clear in southern regions, where hydrographic conditions during winter seemed to be responsible for variations in springtime secondary production. [ABSTRACT FROM AUTHOR]

7 The regulation by angiotensin II (Ang II) formed locally on nerve-stimulated purinergic and adrenergic components of double-peaked vasoconstrictions in the canine splenic artery and Ang II receptor subtypes involved were investigated. 2 The perfusion of the precursor angiotensin I (Ang I, 0.1–1 n m) did not affect the vasoconstrictor responses to noradrenaline (NA, 0.03–1 nmol) and adenosine 5′-triphosphate (ATP, 0.03–1 μmol). The second component vasoconstrictor response to nerve stimulation was dose dependently potentiated by Ang I (0.1–1 n m). The first peaked constriction was slightly, but insignificantly increased. The potentiating effects of Ang I were abolished by KRH-594 (10 n m), a selective AT1 receptor antagonist, but not by PD 123319 (1–10 n m), an AT2 receptor antagonist. KRH-594 (10 n m) or PD 123319 (10 n m) never affected the vasoconstrictions to either NA or ATP. 3 The treatment with KRH-594 (1–10 n m) produced a greater inhibition on the second peaked response than the first one, although both of them were dose dependently inhibited. PD 123319 (1–10 n m) did not affect the vasoconstrictor responses induced by nerve stimulation. 4 Inhibition of angiotensin-converting enzyme with 10 n m enalaprilat reduced the second peaked response, having no significant inhibition on the first peaked response. A higher dose of enalaprilat (100 n m) produced a greater inhibition of the second peak than the first one. It reduced the second peak by approximately 65%, while the first peak was decreased approximately 35%. After treatment with enalaprilat, Ang I (1 n m) failed to enhance the neuronal vascular response. Enalaprilat at doses used did not affect the vasoconstrictions to either NA or ATP. 5 The present results indicate that endogenously generated Ang II may produce a more marked potentiation of adrenergic transmission than purinergic transmission via activation of prejunctional AT1 receptors. [ABSTRACT FROM AUTHOR]

Summary 1 The vasoconstrictor response to periarterial nerve electrical stimulation (PNS) and neurotransmission by ATP are discussed and illustrated, using canine isolated and perfused splenic arterial preparations. 2 The conditions for appearance of dominant purinergic constrictor response to PNS are discussed. 3 Modulation of the purinergic vasoconstrictor responses to PNS by several kinds of presynaptic receptor agonists and antagonists is reviewed. 4 Influences of purinergic responses to PNS by guanethidine, reserpine, tetrodotoxin (TTX) or ω -conotoxin GVIA (ω CTX) are also reviewed. 5 Effects of imipramine and removal of the endothelium are discussed. 6 Evidence is presented for selective inhibition of purinergic responses to PNS by an adequate cold storage of the vessel. 7 The roles of ATP released by PNS in isolated canine splenic arteries are proposed. [ABSTRACT FROM AUTHOR]

Summary 1 The present study attempted to pharmacologically characterize the subtypes of α-adrenoceptors mediating the vasoconstriction in the isolated and perfused canine vesical artery. 2 Noradrenaline (NA) and phenylephrine (PE, an α[sub 1]-adrenoceptor agonist) induced a dose-dependent vasoconstriction, whereas xylazine (an α[sub 2]-agonist) did not induce any clear vascular constrictor response. 3 Prazosin at 0.01 μ m and rauwolscine at 0.1 μ m failed to affect the NA-induced vasoconstriction. Prazosin at 0.1 μ m antagonized the vasoconstrictor responses to NA, with pK[sub B] value of 7.8. 4 WB 4101 at 0.01–0.1 μ m dose-dependently inhibited the responses to NA, with a pK[sub B] value of 8.9. The vasoconstrictor responses to NA were not significantly affected by chloroethylclonidine (10–30 μ m) or BMY 7378 (0.1 μ m). 5 The present results indicate that the canine vesical arteries dominantly contain α[sub 1]-adrenoceptors but have no α[sub 2]-adrenoceptors, and the functional subtype of α[sub 1]-adrenoceptor is characterized as an α[sub 1A]-adrenoceptor subtype. [ABSTRACT FROM AUTHOR]

Summary 1 The effects of neuropeptide Y (NPY) upon the isolated vasculature are reviewed. 2 The vasconstrictor responses to periarterial nerve stimulation (PNS) and neurotransmission by noradrenaline (NA) and ATP are discussed and illustrated using canine isolated perfused splenic artery. 3 Modulation of the vascular responses to PNS by NPY via pre- and post-junctional NPY Y[sub 2] and Y[sub 1] receptors is discussed. 4 Evidence is presented for different α[sub 1]-adrenoceptor subtypes mediating vasoconstriction to exogenous and endogenously released NA and their different locations in the neurovascular junction and extrajunctional regions. 5 Activation of NPY Y[sub 1]-receptors potentiates sympathetic nerve activated α[sub 1]-adrenoceptor vasoconstriction. The proposal that the postjunctional α[sub 1B] adrenoceptor may be linked to the NPY Y[sub 1]-receptor and is responsible for co-operation between sympathetic and NPYergic interactions in the vasculature is discussed. [ABSTRACT FROM AUTHOR]

We studied the binding properties of KRH-594, a new selective antagonist of angiotensin II (AII) type 1 (AT[sub 1]) receptors, to rat liver membranes and to recombinant AT[sub 1] and AT[sub 2] receptors. Preincubation of rat liver membranes with KRH-594 produced maximal inhibition of [[sup 125]I]-AII binding when the preincubation time was 1-2 h. Preincubation with KRH-594 for 2 h decreased the B[sub max] value and increased the K[sub d] value. For human AT[sub 1], human AT[sub 2], rat AT[sub 1A] and rat AT[sup 1B] receptors, the K[sub i] values for KRH-594 were 1.24, 9360, 0.67, and 1.02 nM, respectively. The rank order of K[sub i] values for human AT[sub 1] receptors was KRH594 >> EXP3174 > candesartan = AII. The order of specificities for human AT[sub 1] and AT[sub 2] receptors was candesartan > EXP3174 > KRH-594. Although a 2-h preincubation of human AT[sub 2] receptors with KRH-594 (30 µM) or CGP 42112 (a selective AT[sub 2] receptor antagonist; 0.3 nM) inhibited binding of [[sup 125]I]-AII, the suppression by KRH-594 was not significant. These results indicate that KRH-594 binds potently to AT[sub 1] receptors in an insurmountable manner, and that at a very high dose (30 µM) it may also bind to AT[sub 2] receptors, but in a surmountable manner. [ABSTRACT FROM AUTHOR]

1 The effects of BIIE 0246, a novel and non-peptide neuropeptide Y (NPY) Y[sub 2] receptor antagonist on sympathetic vasoconstriction of the canine splenic artery were investigated. 2 The vasoconstrictor response to periarterial electrical nerve stimulation was described to be a double peaked vasoconstriction consisting of an initial transient, dominantly P2X purinoceptormediated constriction followed by a prolonged, mainly α[sub 1] adrenoceptor-induced response. 3 BIIE 0246 at a concentration of 0.1-1 µM dose-dependently potentiated double peaked constrictions at low frequencies (1 and 4 Hz), whereas at high frequency (10 Hz), it failed to affect these responses. BIIE 0246 (1 µM) also enhanced double peaked responses even in the presence of rauwolscine (0.1 µM). NPY (13-36) (1-100 nM), a selective Y[sub 2] receptor agonist reduced these two peaked responses in a dose-related manner. The vasoconstriction to noradrenaline (0.1-10 nmol) or adenosine triphosphate (0.01-1 µmol) was not significantly influenced by either 1 µM BIIE 0246 or 100 nM NPY (13-36). Exposure of tissues to 1 µM BIIE 0246 almost completely prevented the suppression of double peaked constrictions by NPY (13-36) (10 nM) or by NPY (10 nM). 4 We conclude that NPY inhibits sympathetic purinergic and adrenergic vasoconstrictions through an activation of prejunctional Y[sub 2] receptor subtype in the neurovascular junction of the canine splenic artery. [ABSTRACT FROM AUTHOR]

Abstract Background Hypothalamic neuronal histamine has been shown to increase lipolysis in white adipose tissue. The present study aimed to clarify whether peripheral loading with L-histidine, a precursor of neuronal histamine, may affect lipid metabolism in adipose tissue. Materials and methods The in vivo microdialysis study was used to assess lipolysis in rat epididymal adipose tissue by measuring the release of glycerol in response to administration of L-histidine. In addition, electrophysiological measurements were performed to record changes in activity of sympathetic nerve innervating adipose tissue following histidine treatment. Results Sequential administration of isoproterenol, a β-adrenoceptor agonist, through the microdialysis cannula at concentrations of 10-8 to 10-6 M increased the glycerol concentration in the dialysate dose-dependently (P < 0·05). Intraperitoneal administration of L-histidine at a dosage of 0·35 mmol kg-1 also increased the glycerol concentration compared to that of phosphate buffered saline (P < 0·05). Concomitantly, the administration of histidine increased the serum concentration of free fatty acid compared to control treatment (P < 0·05). The accelerating effects of histidine on lipolysis were mimicked by the infusion of 102 nmol rat-1 L-histamine into the third cerebroventricle (P < 0·05). Electrophysiological measurement demonstrated that administration of histidine at a dosage of 0·35 mmol kg-1 increased the activity of efferent sympathetic nerve, innervating adipose tissue more than the infusion of phosphate buffered saline (P < 0·05). Conclusion The present results indicate that histidine accelerates lipolysis in white adipose tissue through activation of the sympathetic nerve. The regulation of lipolysis may therefore involve histamine neurons in the brain, probably through the conversion of L-histidine to... [ABSTRACT FROM AUTHOR]

Abstract A high level of geographical variation at an exceptionally fine scale was detected in the mitochondrial 16S ribosomal RNA genes of a land snail species Euhadra quaesita from the Kanto region of Japan. In total, 50 haplotypes were detected from 27 populations, with most sample sites possessing private alleles. In some individual populations the different haplotypes do not fall as a monophyletic group, so that some of the haplotypes are phylogenetically distant, differing from each other by > 10%. In contrast, phylogenetically similar haplotypes were found in separate sites at long distances from their main distribution. Together, these findings strongly suggest that contraction and expansion of populations has occurred repeatedly in the past. The subsequent expansion of populations and migration from different areas may have mixed distant populations. This repetition of isolation and mixing has resulted in an exceptionally fine scale of geographical variation, and the accumulation of high genetic diversity within and between populations of this species. [ABSTRACT FROM AUTHOR]

1 Using the cannula inserting method, vasodilator responses to β-adrenoceptor agonists (isoprenaline, denopamine and procaterol) were investigated in isolated and perfused rat common carotid arteries. 2 Each β-adrenoceptor agonist induced a vasodilation in preparations preconstricted by phenylephrine in a dose-related manner. The potencies were in the order of isoprenaline > procaterol >> denopamine. 3 Denopamine-induced dilations were significantly inhibited by 1 nmol betaxolol (a selective β[sub 1]-adrenoceptor antagonist), but it was not influenced by 1 nmol ICI 118,551 (a selective β[sub 2]-adrenoceptor antagonist). On the other hand, procaterol-induced vasodilations were significantly inhibited by 1 nmol ICI 118,551 but not modified by 10 nmol betaxolol. 4 ACh-induced vasodilations disappeared after intraluminal saponin injection to remove endothelium, but procaterol- and denopamine-induced dilations were not modified by removal of the endothelium. 5 Pretreatment with L-N[sup G]-nitroarginine methyl ester (L-NAME) readily inhibited ACh-induced vasodilations. However, neither procaterol- or denopamine-induced vasodilation was modified by L-NAME treatment. 6 From these results, it is concluded that in the rat common carotid arteries (1) there are abundant β[sub 2]- and a few β[sub 1]-adrenoceptors, and (2) there is no participation of the endothelium-dependent mechanism in β-adrenoceptor mediated vasodilations. [ABSTRACT FROM AUTHOR]

Background This study was designed to evaluate the immunogenic characteristics of enzymatically digested gelatin, ‘FreAlagin’, employing the lymphoproliferative response in subjects with gelatin hypersensitivity. Our purpose was to assess the response of primed lymphocytes to the newly developed FreAlagin and compare it to the response to conventional gelatin. Methods A gelatin-specific lymphocyte proliferation test (LPT) was performed in 110 children with adverse reactions to gelatin-containing vaccines, who showed positive gelatin-specific cell-mediated immunity and were thus diagnosed as having gelatin hypersensitivity. Gelatin-specific IgE was measured in all subjects. The antigenic activity of FreAlagin to lymphocytes was compared with that of conventional bovine gelatin. Positive and negative control specimens were obtained from the patients with anaphylaxis and from subjects inoculated with gelatin-free vaccine who showed no adverse reactions in order to establish the fluorometric ELISA system to determine IgE antibody to gelatin and LPT. Results The lymphocyte activity against FreAlagin was much less than that to Wako gelatin and more than half of the subjects who reacted positively to Wako gelatin had a negative LPT to FreAlagin. Although 47% of the subjects had positive LPTs to FreAlagin, all but two still had lower SIs to FreAlagin compared with Wako gelatin. Conclusion We conclude that the antigenic activity of FreAlagin as measured by the cell-mediated immune response is significantly less than that of conventional bovine gelatin. However, it is still necessary to perform clinical trials to show a reduced or absent clinical reactivity to FreAlagin in sensitized patients to conventional gelatin. [ABSTRACT FROM AUTHOR]

Examines the monophasic vasoconstrictor responses to periarterial purinerguc nerve stimulation. Effects of rauwolscine on vasoconstrictor responses to periarterial electric nerve stimulation; Influence of the pulse trains at low frequency on the activation of purinergic components of sympathetic cotransmission; Role of alpha-adrenergic mechanism on the modulation of adenosine 5-triphosphate release.

Investigates the characteristics of the double peaked vasoconstrictor responses to periarterial electric simulation. Use of prazosin and alpha and beta-methylene adenosine triphosphate (ATP) in the study; Effects of prazosin and alpha and beta-methylene ATP on vasoconstrictor responses; Conclusion that vasoconstrictor responses is induced via an activation of P2X receptors.