bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human brain somatostatin release from isolated cortical nerve endings and its modulation through GABAB receptors
Authors: Bonanno Giambattista , Gemignani Anita , Schmid Giovanna , Severi Paolo , Cavazzani Paolo , Raiteri Maurizio 
Published: July 2012

The release of somatostatin‐like immunoreactivity (SRIF‐LI) in the human brain was studied in synaptosomal preparations from fresh neocortical specimens obtained from patients undergoing neurosurgery to remove deeply sited tumours.
The basal outflow of SRIF‐LI from superfused synaptosomes was increased about 3 fold during exposure to a depolarizing medium containing 15 mM KCl. The K+‐evoked overflow of SRIF‐LI was almost totally dependent on the presence of Ca2+ in the superfusion medium.
The GABAB receptor agonist, (—)‐baclofen (0.3–100 μm), inhibited the overflow of SRIF‐LI in a concentration‐dependent manner (EC50 = 1.84 ± 0.20 μm; maximal effect: about 50%). The novel GABAB receptor ligand, 3‐aminopropyl(difluoromethyl)phosphinic acid (CGP 47656) mimicked (—)‐baclofen in inhibiting the SRIF‐LI overflow (EC50 = 3.06 ± 0.52 μm; maximal effect: about 50%), whereas the GABAA receptor agonist, muscimol, was ineffective up to 100 μm.
The inhibition by 10 μm (—)‐baclofen of the K+‐evoked SRIF‐LI overflow was concentration‐dependently prevented by two selective GABAB receptor antagonists, 3‐amino‐propyl (diethoxymethyl)‐phosphinic acid (CGP 35348) (IC50 = 24.40 ± 2.52 μm) and [3‐[[(3,4‐dichlorophenyl) methyl]amino]propyl] (diethoxymethyl) phosphinic acid (CGP 52432) (IC50 = 0.06 ± 0.005 μm).
The inhibition of SRIF‐LI overflow caused by 10 μm CGP 47656 was abolished by 1 μm CGP 52432.
When human synaptosomes were labelled with [3H]‐GABA and depolarized in superfusion with 15 mM KCl, the inhibition by 10 μm (—)‐baclofen of the depolarization‐evoked [3H]‐GABA overflow was largely prevented by 10 μm CGP 47656 which therefore behaved as an autoreceptor antagonist.
In conclusion: (a) the characteristics of SRIF‐LI release from synaptosomal preparations of human neocortex are compatible with a neuronal origin; (b) the nerve terminals releasing the neuropeptide possess inhibitory receptors of the GABAB type; (c) these receptors differ pharmacologically from the GABAB autoreceptors present on human neocortex nerve terminals since the latter have been shown to be CGP 35348‐insensitive but can be blocked by CGP 47656.
B1 bradykinin receptors and sensory neurones
Authors: Davis C.L. , Naeem S. , Phagoo S.B. , Campbell E.A. , Urban L. , Burgess G.M. 
Published: July 2012

The location of the B1 bradykinin receptors involved in inflammatory hyperalgesia was investigated.
No specific binding of the B1 bradykinin receptor ligand [3H]‐des‐Arg10‐kallidin was detected in primary cultures of rat dorsal root ganglion neurones, even after treatment with interleukin‐1β (100 iu ml−1).
In dorsal root ganglion neurones, activation of B2 bradykinin receptors stimulated polyphosphoinositidase C. In contrast, B1 bradykinin receptor agonists (des‐Arg9‐bradykinin up to 10 μm and des‐Arg10‐kallidin up to 1 μm) failed to activate polyphosphoinositidase C, even in neurones that had been treated with interleukin‐1β (100 iu ml−1), prostaglandin E2 (1 μm) or prostaglandin I2 (1 μm).
Dorsal root ganglion neurones removed from rats (both neonatal and 14 days old) that had been pretreated with inflammatory mediators (Freund's complete adjuvant, or carrageenan) failed to respond to B1 bradykinin receptor selective agonists (des‐Arg9‐bradykinin up to 10 μm and des‐Arg10‐kallidin up to 1 μm).
Bradykinin (25 nM to 300 nM) evoked ventral root responses when applied to peripheral receptive fields or central terminals of primary afferents in the neonatal rat spinal cord and tail preparation. In contrast, des‐Arg9‐bradykinin (50 nM to 500 nM) failed to evoke ventral root depolarizations in either control rats or in animals that developed inflammation following ultraviolet irradiation of the tail skin.
The results of the present study imply that the B1 bradykinin receptors that contribute to hypersensitivity in models of persistent inflammatory hyperalgesia are located on cells other than sensory neurones where they may be responsible for releasing mediators that sensitize or activate the nociceptors.
The involvement of the endothelium in the relaxation of the leopard frog (Rana pipiens) aorta in response to acetylcholine
Authors: Knight Gillian E. , Burnstock Geoffrey 
Published: July 2012

The vasodilator response to acetylcholine (ACh) was investigated in the aortic arches of the leopard frog (Rana pipiens).
With adrenaline pre‐constricted preparations, both ACh and sodium nitroprusside (SNP) caused concentration‐dependent relaxations. Damage to the endothelial layer abolished relaxations to ACh, or reduced them greatly, but had no effect on vasodilatation to SNP.
NG‐Nitro‐L‐arginine methyl ester (L‐NAME; 1–100 μm) concentration‐dependently inhibited relaxations in response to ACh, but had no effect on the ability of SNP to induce vasodilatation.
L‐Arginine (L‐Arg; 100–200 times the concentration of L‐NAME) failed to reverse the inhibitory effect of L‐NAME (1–100 μm) apart from one isolated instance.
In summary, this study has shown endothelium‐dependent vasodilatation to ACh in an amphibian blood vessel that appears to be mediated via nitric oxide (NO). The response to ACh differs from many mammalian preparations in that the inhibitory effect of L‐NAME could not be overcome by L‐Arg, in addition to L‐NAME itself having no direct effect upon the tone of the vessel.
The effect of S‐(+)‐boldine on the α1‐adrenoceptor of the guinea‐pig aorta
Authors: Chuliá Susana , Moreau Joëlle , Naline Emmanuel , Noguera M. Antonia , Ivorra M. Dolores , D'Ocón M. Pilar , Advenier Charles 
Published: July 2012

The cardiovascular activity of S‐(+)‐boldine, an aporphine alkaloid structurally related to papaverine, was determined. The work includes functional studies on guinea‐pig isolated aorta contracted with noradrenaline, caffeine, KCl or Ca2+, and on guinea‐pig trachea contracted with acetylcholine or histamine.
S‐(+)‐boldine inhibited in a concentration‐dependent manner the contractile reponse evoked by noradrenaline (10 μm) in guinea‐pig aorta (IC50 = 1.4 ± 0.2 μm) while the KCl depolarizing solution (60 mM)‐ or the Ca2+ (1 mM)‐induced contractions were only partially affected by boldine up to 300 μm. In contrast, papaverine relaxed noradrenaline (NA), KCl or Ca2+ induced contractions showing similar IC50 values in all cases. S‐(+)‐boldine had a greater potency on the contraction elicited by NA whereas papaverine acted in a non‐selective manner.
S‐(+)‐boldine was found to be an α1‐adrenoceptor blocking agent in guinea‐pig aorta as revealed by its competitive antagonism of noradrenaline‐induced vasoconstriction (pA2 = 5.64 ± 0.08), and its potency was compared with that of prazosin (pA2 = 8.56 ± 0.24), a known potent α1‐adrenoceptor antagonist. In contrast, papaverine caused rightward shifts of the NA concentration‐response curves with depression of maximal response indicating that it acts as a non‐competitive antagonist.
Contraction of guinea‐pig aorta induced by caffeine (60 mM) in a Ca2+‐containing Krebs solution was not affected by a 60 min incubation period with different doses of S‐(+)‐boldine (1–300 μm). Papaverine inhibited partially this caffeine‐induced contraction at the maximal dose used (100 μm).
Inositol phosphates formation induced by noradrenaline (10 μm) in guinea‐pig thoracic aorta was inhibited by S‐(+)‐boldine (30 μm but not by papaverine (10 μm).
Contractions of guinea‐pig trachea caused by acetylcholine (100 μm) or histamine (10 μm) were not modified by S‐(+)‐boldine (0.1–100 μm).
These results provide evidence that S‐(+)‐boldine, an aporphine alkaloid, has interesting properties as an α1‐adrenoceptor blocker in vascular smooth muscle, and acts as a competitive antagonist of the α1‐adrenoceptor present in the guinea pig aorta.
Enhancement of homomeric glycine receptor function by longchain alcohols and anaesthetics
Authors: Mascia Maria Paola , Machu Tina K. , Harris R. Adron 
Published: July 2012

The effects of n‐alcohols (ethanol to dodecanol) and anaesthetics on strychnine‐sensitive glycine receptors were studied in Xenopus oocytes expressing homomeric α1 or α2 glycine receptor subunits, with the two electrode voltage‐clamp recording technique.
The glycine‐induced chloride conductance of homomeric α glycine receptors was potentiated by all the alcohols tested when an EC2 concentration of glycine was used. Homomeric α1 and α2 receptors were potentiated similarly by the n‐alcohols, except that low concentrations of ethanol produced greater potentiation with α1, as previously reported.
Increasing the n‐alcohol carbon number has been shown to increase the potency of the alcohols up to decanol at concentrations corresponding to EC50s for producing loss of righting reflex in tadpoles. However, dodecanol was no more potent than decanol, and only modest potentiation (30–60%) was obtained with dodecanol, in contrast to marked (150–200%) potentiation with the other alcohols. Thus, a ‘cut‐off’ occurred at about dodecanol.
Propofol, alphaxalone, pentobarbitone, halothane and enflurane, reversibly potentiated the function of homomeric α1 glycine receptors at concentrations which represent approximately twice the EC50 for production of anaesthesia in mammals, but ketamine and etomidate were ineffective.
Two novel cyclobutane compounds were tested; the anaesthetic compound (1‐chloro‐1,2,2‐trifluorocyclobutane) from 0.5 to 5 mM potentiated the action of glycine in a concentration‐dependent manner; however, the non‐anaesthetic analogue (1,2‐dichloro‐hexfluorocyclobutane) had no effect on glycine receptor function at concentrations (25 to 80 μm) predicted to be anaesthetic, based on the lipid solubility of this compound.
These results suggest that the α subunits of strychnine‐sensitive glycine receptors contain sites of action for n‐alcohols, propofol, alphaxalone, pentobarbitone and volatile anaesthetics, but not for ketamine and etomidate. Potentiation of glycine receptor function may contribute to the anaesthetic action of n‐alcohols and volatile agents.
The effect of GABA stimulation on GABAA receptor subunit protein and mRNA expression in rat cultured cerebellar granule cells
Authors: Piatt Kathleen P. , Zwartjes Raymond E. , Bristow David R. 
Published: July 2012

After 8 days in vitro, rat cerebellar granule cells were exposed to 1 mM γ‐aminobutyric acid (GABA) for periods of 1, 2, 4, 6, 8 and 10 days. The effect of the GABA exposure on GABAA receptor al, a6 and β2,3 subunit protein expression and α1 and α6 subunit steady‐state mRNA levels, was examined using Western blotting and reverse transcriptase‐polymerase chain reaction (RT‐PCR), respectively.
GABA exposure for 2 days decreased α1 (35 ± 10%, mean ± s.e.mean), β2,3 (21±9%) and α6 (28 ± 10%) subunit protein expression compared to control levels. The GABA‐mediated reduction in al subunit expression after 2 days treatment was abolished in the presence of the GABAA receptor antagonist, Ru 5135 (10 μm).
GABA exposure for 8 days increased α1 (26 ± 10%, mean ± s.e.mean) and β2,3 (56 ± 23%) subunit protein expression over control levels, whereas α6 subunit protein expression remained below control levels (by 38 ± 10%). However, after 10 days GABA exposure, a6 subunit protein expression was also increased over control levels by 65 ± 29% (mean ± s.e.mean).
GABA exposure did not change the α1 or α6 subunit steady‐state mRNA levels over an 8 day period, nor did it alter the expression of cyclophilin mRNA over 1–8 days.
These results suggest that chronic GABA exposure of rat cerebellar granule cells has a bi‐phasic effect on GABAA receptor subunit expression that is independent of changes to mRNA levels. Therefore, the regulation of the GABAA receptor expression by chronic agonist treatment appears to involve post‐transcriptional and/or post‐translational processes.
Pharmacological analysis of the CCKB/gastrin receptors mediating pentagastrin‐stimulated gastric acid secretion in the isolated stomach of the immature rat
Authors: Hills David M. , Gerskowitch V. Paul , Roberts Sonia P. , Welsh Nicola J. , Shankley Nigel P. , Black James W. 
Published: July 2012

The CCKB/gastrin receptors mediating pentagastrin stimulation of gastric acid secretion by histamine release and by direct stimulation of oxyntic cells have been characterized in the immature rat isolated stomach assay. This was achieved by estimating antagonist affinity values for competitive antagonists from three distinct chemical classes (L‐365,260, PD 134,308 and JB93190) in the absence and presence of a high concentration of the histamine H2‐receptor antagonist, famotidine (30 μm).
Pentagastrin produced concentration‐dependent stimulation of gastric acid secretion in the absence and presence of famotidine. Famotidine depressed the maximum secretory response to pentagastrin although the degree of depression varied between experimental replicates (25–60%). This variation was attributed to the histamine‐release mediated component of acid secretion, as judged by the consistency of the maximum responses obtained in the presence, but not absence, of famotidine.
All three CCKB/gastrin receptor antagonists behaved as surmountable antagonists in the absence and presence of famotidine. JB93190 (pK∼B∼9.1, ∼8.9, in the absence and presence of famotidine, respectively) was approximately 30 fold more potent than either L‐365,260 (pKB∼7.4, ∼7.1) or PD 134,308 (pKB∼7.6, ∼7.4).
It was assumed that the famotidine treatment converted pentagastrin‐stimulated acid secretion from a combination of an indirect action due to the release of histamine and a direct action on the oxyntic cell to solely a direct action on the oxyntic cell. A simple mathematical model of this two‐receptor system was developed. The direct and indirect components were assumed to sum to produce the total response to pentagastrin obtained in the absence of famotidine. It was found that this model could account quantitatively for the behaviour of the three antagonists without invoking a difference in antagonist affinity for the CCKB/gastrin receptors mediating the direct and indirect actions of pentagastrin. However, a conclusion of receptor homogeneity has to be qualified because the model was also used to generate simulations which indicated that the analysis could only detect antagonist affinity differences of greater than one log‐unit between enterochromaffin‐like (ECL) and oxyntic cell CCKB/gastrin receptor populations.
Antagonism of the effects of (+)‐PD 128907 on midbrain dopamine neurones in rat brain slices by a selective D2 receptor antagonist L‐741,626
Authors: Bowery B.J. , Razzaque Z. , Emms F. , Patel S. , Freedman S. , Bristow L. , Kulagowski J. , Seabrook G.R. 
Published: July 2012

The ability of PD 128907 to activate dopamine receptors in the ventral tegmental area, substantia nigra pars compacta, and striatum was investigated by use of in vitro electrophysiological recording and fast cyclic voltammetry. The affinity of a novel D2 selective antagonist L‐741,626 for receptors activated by this agonist was measured to determine if its effects were mediated by D2 or D3 receptors.
The active (+) enantiomer of PD 128907 bound with high affinity and selectivity to rat D3 dopamine receptors. The Ki values for (+)‐PD 128907 were 620 nM at D2, 1 nM at D3 and 720 nM at D4 receptors.
(+)‐PD 128907 inhibited cell firing in both the ventral tegmental area and substantia nigra pars compacta with EC50 values of 33 nM (pEC50 = 7.48 ± 0.10, n= 10) and 38 nM (pEC50 = 7.42 ± 0.15, n = 5), respectively. No effects of (+)‐PD 128907 (100 nM) were observed on glutamate or GABA‐mediated synaptic potentials elicited by focal bipolar stimulation.
L‐741,626 antagonized these effects of (+)‐PD 128907 in a concentration‐dependent and surmountable manner with an affinity, determined from Schild analysis, of 20 nM (pKB = 7.71 ± 0.14) in the ventral tegmental area and 11 nM (pKB = 7.95 ± 0.18) in the substantia nigra pars compacta.
(+)‐PD 128907 also inhibited dopamine release in the caudate‐putamen with an EC50 of 66 nM (n = 5). The affinity of L‐741,626 for these nerve terminal autoreceptors (pKB = 7.71 ± 0.06; =20 nM) was identical to that observed on midbrain dopamine neurones.
These data demonstrate that the D3 receptor ligand (+)‐PD 128907 is a potent agonist on rat midbrain dopamine neurones. However, its lack of regional selectivity, and the high affinity of the selective D2 receptor antagonist L‐741,626 for receptors activated by (+)‐PD 128907, was more consistent with an action on D2 autoreceptors rather than upon a D3 dopamine receptor subtype.
Diagnosis of Common Dermopathies in Dialysis Patients: A Review and Update
Authors: Markova Alina , Lester Jenna , Wang Joanne , Robinson‐Bostom Leslie 
Published: July 2012

AbstractCutaneous abnormalities in patients with end‐stage renal disease (ESRD) receiving hemodialysis or peritoneal dialysis may demonstrate signs of their underlying condition or reveal associated disease entities. While a thorough examination of the scalp, skin, mucosa, and nails is integral to establishing a diagnosis, certain conditions will resolve only with dialysis or improvement of their renal disease and others may not require or respond to treatment. Half and half nails, pruritus, xerosis, and cutaneous hyperpigmentation are common manifestations in ESRD. With hemodialysis, uremic frost is no longer prevalent in ESRD patients and ecchymoses have decreased in incidence. Acquired perforating dermatoses are seen in over one‐tenth of hemodialysis patients. Metastatic calcinosis cutis and calciphylaxis are both rarely reported, although the latter is seen almost exclusively in the setting of hemodialysis. Diagnosis of nephrogenic systemic fibrosis has historically been challenging; as such, new diagnostic criteria have been proposed. Blood porphyrin profiles are needed to differentiate between porphyria cutanea tarda and pseudoporphyria. We will review and provide an update on the aforementioned common cutaneous manifestations of ESRD in patients receiving dialysis.
Sidelined or Mainstreamed? Political Participation and Attitudes of People with Disabilities in the United States
Authors: Schur Lisa , Adya Meera 
Published: July 2012

ObjectiveWe examine whether people with disabilities are part of the political mainstream, or remain outsiders in important respects, by studying political participation and the underexplored topic of how disability relates to attitudes toward politics.MethodWe analyze new disability measures on the 2008 and 2010 Current Population Surveys voting supplements, and two other nationally representative surveys for 2006 and 2007.ResultsCitizens with disabilities remain less likely than nondisabled citizens to vote. While there are few differences in political preferences and party affiliations, people with disabilities tend to favor a greater government role in employment and healthcare, and give lower ratings on government responsiveness and trustworthiness.ConclusionPeople with disabilities continue to be sidelined in important ways. Fully closing the disability gap would have led to 3.0 million more voters in 2008 and 3.2 million more voters in 2010, potentially affecting many races and subsequent public policies.
The Impact of Foreclosures on Neighborhood Disorder Before and During the Housing Crisis: Testing the Spiral of Decay
Authors: Wallace Danielle , Hedberg E. C. , Katz Charles M. 
Published: July 2012

ObjectivesThe objectives of this study were to examine whether an increasing number of foreclosures in a neighborhood subsequently increase disorder and whether the temporal relationship between foreclosures and disorder is different before and during the housing crisis.MethodsWe employ longitudinal data to examine the impact of foreclosure on crime in Glendale, Arizona, a city at the epicenter of the nation's foreclosure problem. We rely on three data sources: (1) foreclosure data, (2) Computer‐Aided Dispatch/Police Records Management System data, and (3) U.S. Census and census estimate data.ResultsOur findings suggest that foreclosures do have a short‐term, four‐month effect on overall disorder and social disorder; however, that relationship only holds during the months preceding the housing crisis. During the housing crisis, there is no effect of foreclosures on disorder.ConclusionsOur results suggest that instead of the long‐standing negative impact that foreclosures have on disorder in communities, their negative effect is short lived and limited. Thus, foreclosures during the housing crisis do not signal disorder and decay as expected. A number of communities across the country have enacted prevention, enforcement, and reuse policies and programs aimed at foreclosure for the purpose of reducing disorder and subsequent crime; our results suggest that some of these policies and programs require substantial resources and might not have their desired impact.
The athlete's body and the global condition: Tongan rugby players in Japan
Authors: Besnier Niko 
Published: July 2012

ABSTRACTThe mobility of rugby professionals from Tonga to Japan and points beyond poses new questions about the role of the body as a mediator between the subjective and the objective, which anthropologists and other social scientists have generally examined within the confines of specific societies. Increasingly, mobility across different regimes of valuation offers highly skilled bodies both new possibilities for agency and new constraints on agency. The articulation of athletes’ mobility with economic, social, and ideological dynamics provides a window onto the underexplored aspects of the global condition from the ground up.
Documentary disorders: Managing medical multiplicity in Maputo, Mozambique
Authors: McKay Ramah 
Published: July 2012

ABSTRACTWhat do attempts at documentary standardization in a clinic in Maputo, Mozambique, reveal about transnational medical governance? By following medical and bureaucratic practices in an NGO‐supported public clinic, I illustrate how documentary practices enact and complicate medical authority in Mozambique. In efforts toward standardization, medical documents are made multiple, simultaneously articulating a range of ethical, bureaucratic, and knowledge‐producing activities. Concurrently, medical authority itself is multiplied, as a plurality of agencies and institutions come to intervene in and on practices of documentation, measurement, knowledge production, and care in the clinic. Anthropologists have shown how pluralities of medical care present both predicaments and opportunities for patients and healers; I extend these insights to the material life of postcolonial and transnational medical governance, suggesting that governmental and medical multiplication through the document form presents opportunities as well as challenges for the patients, local health workers, and staff of international organizations who navigate this varied documentary terrain.
The psychic life of biopolitics: Survival, cooperation, and Inuit community
Authors: Stevenson Lisa 
Published: July 2012

ABSTRACTWhat does it mean for Inuit to cooperate with the (disavowed) desires that emerge in a colonial bureaucracy dedicated to improving Inuit lives? In this article, I consider the psychic life of biopolitics in the context of welfare colonialism in the Canadian Arctic. I suggest that the colonial desire that Inuit cooperate in their own survival is haunted by other desires the colonist can never name and that such unspeakable desires are also at work in the response to the contemporary suicide epidemic among Inuit youth. Attention to Inuit naming practices provides an alternate way of linking death, desire, and community in a postcolonial world.