If you've named one you've named them all!
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Asia, Western↗
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A&E nursing. Naming names.
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Emergency Nursing↗
Physicians. Public Citizen names names.
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Clinical Competence↗
Krever can name names, Supreme Court rules.
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Blood Transfusion↗
[Prescription by common name (generic name): rational or economical?].
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Canada↗
Long-term administration of D-NAME induces hemodynamic and structural changes in the cardiovascular system.
N(G)-nitro-D-arginine-methyl ester (D-NAME) is considered to be an inactive enantiomer of L-NAME and is generally used as the negative control for NO synthase inhibition with L-NAME. With the aim to compare the effects of 4-week L-NAME and D-NAME treatments on hemodynamic and cardiovascular structural parameters, four groups of male Wistar rats were investigated: the controls and groups administered 40 and 20 mg/kg/day of L-NAME and 40 mg/kg/day of D-NAME. At the end of the experiment, myocardial NO synthase activity decreased by 42, 24 and 25%; aortic NO synthase activity decreased by 35, 15 and 13% vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The DNA concentrations in the myocardium and the aorta increased significantly after L-NAME and D-NAME treatments. The inhibition of NO synthase was accompanied by a significant elevation in systolic blood pressure in all three groups. The LVW/BW ratio increased by 27, 14 and 13% vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. The aortic wall mass, measured as the cross-sectional area, increased by 45, 17 and 25% vs. controls in the L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. Myocardial fibrosis represented 0.94% in the controls, but 7.96, 4.70 and 5.25% in L-NAME 40, L-NAME 20 and D-NAME 40 groups, respectively. It is concluded that D-NAME, although less affective than L-NAME, inhibits NO synthase activity resulting in hemodynamic and structural changes in the cardiovascular system similar to the changes induced by half the dose of L-NAME. Thus, the consideration of D-NAME as an inactive enantiomer and its use as the negative control needs to be reevaluated.
Animals↗
Involvement of K+ channel permeability changes in the L-NAME and indomethacin resistant part of adenosine-5'-O-(2-thiodiphosphate)-induced relaxation of pancreatic vascular bed.
1. We have previously demonstrated that adenosine-5'-O-(2-thiodiphosphate) (ADPbetaS), a potent P2Y-purinoceptor agonist, relaxed pancreatic vasculature not only through prostacyclin (PGI2) and nitric oxide (NO) release from the endothelium but also through other mechanism(s). In this study, we investigated the effects of an inhibitor of the Na+/K+ pump, of ATP-sensitive K+ (K(ATP)) channels and of small (SK(Ca)) or large (BK(Ca)) conductance Ca2+-activated K+ channels. Experiments were performed at basal tone and during the inhibition of NO synthase and cyclo-oxygenase. 2. In control conditions, ADPbetaS (15 microM) induced an initial transient vasoconstriction followed by a progressive and sustained vasodilatation. In the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME, 200 microM) the transient vasoconstriction was reversed into a one minute vasodilator effect, which was then followed by a progressive and sustained vasodilatation similar to that observed with ADPbetaS alone. The addition of indomethacin (10 microM) did not significantly modify the profile of ADPbetaS-induced vasodilatation. 3. Ouabain (100 microM) decreased basal pancreatic flow rate and did not modify ADPbetaS-induced relaxation. This inhibitor of the Na+/K+ pump increased the pancreatic vasoconstriction induced by L-NAME or by the co-administration of L-NAME and indomethacin. Ouabain did not modify either the L-NAME or the L-NAME/indomethacin resistant part of the ADPbetaS vasodilatation. 4. The K(ATP) inhibitor tolbutamide (185 microM) did not significantly modify basal pancreatic flow rate and ADPbetaS-induced relaxation. This inhibitor which did not change L-NAME-induced vasoconstriction, significantly diminished the L-NAME resistant part of ADPbetaS-induced vasodilatation. Tolbutamide intensified the vasoconstriction induced by the co-administration of L-NAME and indomethacin. In contrast, the L-NAME/indomethacin resistant part of ADPbetaS vasodilatation was not changed by the closure of K(ATP). 5. The SK(Ca) inhibitor apamin (0.1 microM) did not significantly change pancreatic vascular resistance whatever the experimental conditions (in the absence or in presence of L-NAME or L-NAME/indomethacin). In the presence of L-NAME, the closure of SK(Ca) channels changed the one minute vasodilator effect of ADPbetaS into a potent vasoconstriction and thereafter modified only the beginning of the second part of the L-NAME-resistant part of the ADPbetaS-induced vasodilatation. In contrast, the L-NAME/indomethacin resistant part of ADPbetaS-induced relaxation remained unchanged in the presence of apamin. 6. Charybdotoxin (0.2 microM), an inhibitor of BK(Ca), increased pancreatic vascular resistance in the presence of L-NAME/indomethacin. In the presence of L-NAME, the closure of BK(Ca) channels reversed the one minute vasodilator effect of ADPbetaS into a potent vasoconstriction and drastically diminished the sustained vasodilatation. In contrast the L-NAME/indomethacin resistant part of ADPbetaS-induced relaxation was not modified by the presence of charybdotoxin. Under L-NAME/indomethacin/charybdotoxin/apamin infusions, ADPbetaS evoked a drastic and transient vasoconstriction reaching a maximum at the second minute, which was followed by a sustained increase in the flow rate throughout the ADPbetaS infusion. The maximal vasodilator effect of ADPbetaS observed was not modified by the addition of apamin. 7. The results suggest that the L-NAME-resistant relaxation induced by ADPbetaS in the pancreatic vascular bed involves activation of BK(Ca), K(ATP) and to a lesser extent of SK(Ca) channels, but the L-NAME/indomethacin resistant part of ADPbetaS-induced relaxation is insensitive to the closure of K(ATP), SK(Ca) and BK(Ca) channels.
Adenosine Diphosphate↗
Spanish personal name variations in national and international biomedical databases: implications for information retrieval and bibliometric studies.
OBJECTIVES: The study sought to investigate how Spanish names are handled by national and international databases and to identify mistakes that can undermine the usefulness of these databases for locating and retrieving works by Spanish authors. METHODS: The authors sampled 172 articles published by authors from the University of Granada Medical School between 1987 and 1996 and analyzed the variations in how each of their names was indexed in Science Citation Index (SCI), MEDLINE, and Indice Medico Español (IME). The number and types of variants that appeared for each author's name were recorded and compared across databases to identify inconsistencies in indexing practices. We analyzed the relationship between variability (number of variants of an author's name) and productivity (number of items the name was associated with as an author), the consequences for retrieval of information, and the most frequent indexing structures used for Spanish names. RESULTS: The proportion of authors who appeared under more then one name was 48.1% in SCI, 50.7% in MEDLINE, and 69.0% in IME. Productivity correlated directly with variability: more than 50% of the authors listed on five to ten items appeared under more than one name in any given database, and close to 100% of the authors listed on more than ten items appeared under two or more variants. Productivity correlated inversely with retrievability: as the number of variants for a name increased, the number of items retrieved under each variant decreased. For the most highly productive authors, the number of items retrieved under each variant tended toward one. The most frequent indexing methods varied between databases. In MEDLINE and IME, names were indexed correctly as "first surname second surname, first name initial middle name initial" (if present) in 41.7% and 49.5% of the records, respectively. However, in SCI, the most frequent method was "first surname, first name initial second name initial" (48.0% of the records) and first surname and second surname run together, first name initial (18.3%). CONCLUSIONS: Retrievability on the basis of author's name was poor in all three databases. Each database uses accurate indexing methods, but these methods fail to result in consistency or coherence for specific entries. The likely causes of inconsistency are: (1) use by authors of variants of their names during their publication careers, (2) lack of authority control in all three databases, (3) the use of an inappropriate indexing method for Spanish names in SCI, (4) authors' inconsistent behaviors, and (5) possible editorial interventions by some journals. We offer some suggestions as to how to avert the proliferation of author name variants in the databases.
Databases, Bibliographic↗
[Effect of nitric oxide synthase inhibitor L-NAME on the induction of brain ischemic tolerance in rats].
To explore the role of NO in the induction of brain ischemic tolerance (BIT) in vivo, the effect of nitric oxide synthase (NOS) inhibitor L-NAME on the induction of BIT induced by cerebral ischemic preconditioning (CIP) was investigated in the hippocampal CA1 subfield in CIP and ischemic insult models established by rat four-vessel occlusion using brain tissue section and thionine staining methods. Fifty-four male Wistar rats were divided into 6 groups: (1) sham-operated group (n=6): bilateral common arteries were separated without occluding the cerebral blood flow; (2) ischemia group (n=6): an ischemic insult for 10 min was given; (3) CIP+ischemia group (n=6): 3-min CIP was preformed 72 h prior to 10-min ischemic insult; (4) L-NAME group (total n=24, n=6 for each subgroup): L-NAME (5 mg/kg, i.p.) was administered 1 h prior to CIP and 1, 12 and 36 h after CIP, respectively. Other procedures were the same as those for the CIP+ischemia group; (5) L-NAME+L-Arg group (n=6): L-NAME (5 mg/kg, i.p.) and L-Arg (300 mg/kg, i.p.) were administered 1 h prior to CIP, other procedures were the same as those for the L-NAME group; (6) L-NAME+ischemia group (n=6): L-NAME (5 mg/kg, i.p.) was administered 72 h before the 10-min ischemic insult. The results showed that (1)10-min ischemic insult resulted in an increase in the histological grade (indicating a more serious tissue injury) and a decrease in pyramidal neuronal density (P<0.01); (2) the histological grade and neuronal density in hippocampal CA1 in the CIP+ischemia group were similar to those in the sham-operated group (P>0.05); (3) in the L-NAME group, administration of L-NAME brought about an increase in the histological grade and a decrease in neuronal density (P<0.01), suggesting that L-NAME blocked the protection of CIP; (4) the neuronal damage in L-NAME+L-Arg group was slighter than that in the L-NAME group, but still more serious than that in the CIP+ischemia group, suggesting that L-Arg partly reversed the blocking effect of L-NAME; (5) the morphological representations in L-NAME+ischemia group were basically similar to those in the ischemia group. The results mentioned above indicate that NO is involved in the induction of BIT in vivo. The blocking effect of L-NAME administered at 36 h after CIP was obviously weaker than the effects of L-NAME administered 1 h prior to CIP, and 1 or 12 h after CIP. It is suggested that NO is involved in the induction of BIT at an early stage and that the involvement might take place via activating cascades of the events.
Animals↗
Brain potentials related to seeing one's own name.
Subjects were assigned an assumed name and then shown a series of statements of the form, "My name / is / X", where X was the assumed name, their own first name, or one of a set of other false names. Their task was to respond positively to the "assumed" name and reject as false all other names, including their own. An N380 feature of the averaged task-related brain potentials, considered to be inversely related to the degree of contextual priming, was greatly enhanced for the false names compared to the assumed name. The N380 to one's own name was more similar to that of the false than the assumed name, indicating that the sentence context's priming of various names was under the subjects' attentional control, and that the late negativity could be modulated by this attention. In contrast, a large P510 feature distinguished one's own name from the false name, and this difference was unaffected by practice. Even in cases, then, where the context allows anticipation of one verbal event (here, the assumed name), a highly overlearned and salient stimulus such as one's own name continues to produce a distinctive neural response.
Adolescent↗
Category-specific cortical mapping: color-naming areas.
OBJECT: It has been hypothesized that a certain degree of specialization exists within language areas, depending on some specific lexical repertories or categories. To spare hypothetical category-specific cortical areas and to gain a better understanding of their organization, the authors studied patients who had undergone electrical stimulation mapping for brain tumors and they compared an object-naming task with a category-specific task (color naming). METHODS: Thirty-six patients with no significant preoperative language deficit were prospectively studied during a 2-year period. Along with a reading task, both object- and color-naming tasks were used in brain mapping. During color naming, patients were asked to identify 11 visually presented basic colors. The modality specificity of the color-naming sites found was subsequently tested by asking patients to retrieve the color attributes of objects. High individual variability was observed in language organization among patients and in the tasks performed. Significant interferences in color naming were found in traditional language regions-that is, Broca (p < 0.003) and Wernicke centers (p = 0.05)--although some color-naming areas were occasionally situated outside of these regions. Color-naming interferences were exclusively localized in small cortical areas (< 1 cm2). Anatomical segregation of the different naming categories was apparent in 10 patients; in all, 13 color-specific naming areas (that is, sites evoking no object-naming interference) were detected in the dominant-hemisphere F3 and the supramarginal, angular, and posterior parts of the temporal gyri. Nevertheless, no specific brain region was found to be consistently involved in color naming (p > 0.05). At five sites, although visually presented color-naming tasks were impaired by stimulation, auditory color naming (for example, "What color is grass?") was performed with no difficulty, showing that modality-specific areas can be found during naming. CONCLUSIONS: Within language areas, a relative specialization of cortical language areas for color naming can be found during electrical stimulation mapping.
Adult↗
Identification of famous faces and famous names in early Alzheimer's disease. Relationship to anterograde episodic and general semantic memory.
We assessed remote memory in 33 patients with dementia of Alzheimer's type (DAT) with Mini-Mental State Examination (MMSE) scores between 17 and 30, and 30 matched controls using a Famous Faces Test and Famous Names Test designed to assess face recognition, identification and naming, and name recognition and identification, respectively, together with a range of anterograde episodic and semantic memory tests. Patients with DAT were impaired on all components of the remote memory tests, i.e. famous face recognition, identification and naming, and famous name recognition and identification. There was also evidence of a modest temporal gradient, with relatively greater impairment of more recent memory, which may be artefactual resulting from the very insidious onset of their anterograde amnesia. In contrast to the uniform impairment of anterograde memory, there was considerable heterogeneity in performance on remote memory. Although the DAT patient group's performance on remote memory measures was impaired with respect to controls, some patients had significant impairment on all measures, whereas others had intact remote memory. Overall, there was only a weak correlation between dementia severity and remote memory, and no correlation between performance on the Faces and Names tests and measures of anterograde memory. At a cognitive level, the deficit in face and name processing in DAT involved recognition, identification and naming. This would suggest that so called 'face and name recognition units', semantic knowledge of famous persons and post-semantic processing are all affected by the disease. There was also supporting evidence for the concept that recognition of famous faces and names both draw on common sources. Similar results were found for face and name identification. This suggests that face and name recognition units are closely linked, and that identification of a face or name accesses the same central pool of semantic knowledge regarding the famous person. Performance on famous names tests correlated, to a limited degree, with that on general semantic tests, suggesting that knowledge of famous people, at least as accessed by names, is associated with general semantic memory. By contrast, no correlation was found between performance on the famous faces and on other general semantic tasks.
Aged↗
Proper name anomia: a case with sparing of the first-letter knowledge.
In this article we describe the case of GC, a woman affected by severe proper name anomia due to progressive brain atrophy that mainly affected the left temporal pole. Proper name comprehension and semantic knowledge about the people she was unable to name were normal. GC showed a sparing of initial letter knowledge of proper names, while other phonological characteristics were not equally available. At a later stage of her illness, the naming impairment began to affect common names as well as proper names, though at a lesser extent. Whereas there was no category effect between names of animate and inanimate stimuli, we observed a relative sparing of first letter knowledge selectively for animate categories, although less marked than with proper names. This case is discussed within the theoretical framework of two-stage models of name production. Knowledge of the initial letter of proper names supports the psychological reality of the "phonological address" as a preliminary stage of the production of this class of names. Moreover, the qualitative similarity between errors observed with proper names and with names of animate objects suggests that the production of names belonging to these classes may conform, at least in part, to analogous algorithms.
Anomia↗
Effect of imidapril on myocardial remodeling in L-NAME-induced hypertensive rats is associated with gene expression of NOS and ACE mRNA.
Chronically administered N(omega)nitro-L-arginine methyl ester (L-NAME) produces vascular structural changes and fibrosis of the left ventricle (LV). However, very few studies have evaluated whether the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors on these myocardial remodelings are associated with local gene expression of nitric oxide synthase (NOS) and ACE mRNA in the LV. Effects of long term treatment with imidapril, an ACE inhibitor, on gene expression of endothelial-cell NOS (eNOS) and ACE mRNA in the LV and its relation to myocardial remodeling in L-NAME-induced hypertensive rats were evaluated. Fifteen male Sprague-Dawley rats were given L-NAME (60 mg/ kg/day) in drinking water for 6 weeks to induce hypertension, and then treated with imidapril (L-NAME-I, n = 8, 1 mg/kg/day, subdepressor dose), or a vehicle (L-NAME-V, n = 7) for 4 weeks. Age-matched rats (C, n = 7) served as a control group. Blood pressure in L-NAME-V and L-NAME-I was similar and significantly higher than that in C. The level of eNOS mRNA in the LV was significantly decreased in L-NAME-V compared with C, and was significantly increased in L-NAME-I compared with C and L-NAME-V. The ACE mRNA and type I collagen mRNA expression levels were significantly increased in L-NAME-V compared with C, and significantly suppressed in L-NAME-I compared with L-NAME-V. L-NAME-V demonstrated a significant increase in wall-to-lumen ratio, perivascular fibrosis, and myocardial fibrosis. These changes in the microvasculature were improved significantly by imidapril. Myocardial remodeling in L-NAME-induced hypertensive rats was significantly ameliorated by a subdepressor dose of imidapril, which may be due to an increase in local eNOS mRNA expression and a decrease in angiotensin II in the LV.
Angiotensin-Converting Enzyme Inhibitors↗
Alteration of flow-induced dilatation in mesenteric resistance arteries of L-NAME treated rats and its partial association with induction of cyclo-oxygenase-2.
1. We investigated the response to pressure (myogenic tone) and flow of rat mesenteric resistance arteries cannulated in an arteriograph which allowed the measurement of intraluminal diameter for controlled pressures and flows. Rats were treated for 3 weeks with NG-nitro-L-arginine methyl ester (L-NAME, 50 mg kg-1 day-1) or L-NAME plus the angiotensin I converting enzyme inhibitor (ACEI) quinapril (10 mg kg-1 day-1). 2. Mean blood pressure increased significantly in chronic L-NAME-treated rats (155 +/- 4 mmHg, n = 8, vs control 121 +/- 6 mmHg, n = 10; P < 0.05). L-NAME-treated rats excreted significantly more dinor-6-keto prostaglandin F1 alpha (dinor-6-keto PGF1 alpha), the stable urinary metabolite of prostacyclin, than control rats. The ACEI prevented the rise in blood pressure and the rise in urinary dinor-6-keto PGF1 alpha due to L-NAME. 3. Isolated mesenteric resistance arteries, developed myogenic tone in response to stepwise increases in pressure (42 +/- 6 to 847 +/- 10 mN mm-1, from 25 to 150 mmHg, n = 9). Myogenic tone was not significantly affected by the chronic treatment with L-NAME or L-NAME + ACEI. 4. Flow (100 microliters min-1) significantly attenuated myogenic tone by 50 +/- 6% at 150 mmHg (n = 10). Flow-induced dilatation was significantly attenuated by chronic L-NAME to 22 +/- 6% at 150 mmHg (n = 10, p = 0.0001) and was not affected in the L-NAME + ACEI group. 5. Acute in vitro NG-nitro-L-arginine (L-NOARG, 10 microM) significantly decreased flow-induced dilation in control but not in L-NAME or L-NAME + ACEI rats. Both acute indomethacin (10 microM) and acute NS 398 (cyclo-oxygenase-2 (COX-2) inhibitor, 1 microM) did not change significantly flow-induced dilatation in controls but they both decreased flow-induced dilatation in the L-NAME and L-NAME + ACEI groups. Acute Hoe 140 (bradykinin receptor inhibitor, 1 microM) induced a significant contraction of the isolated mesenteric arteries which was the same in the 3 groups. 6. Immunofluorescence analysis of COX-2 showed that the enzyme was expressed in resistance mesenteric arteries in L-NAME and L-NAME + ACEI groups but not in control. COX-1 expression was identical in all 3 groups. 7. We conclude that chronic inhibition of nitric oxide synthesis is associated with a decreased flow-induced dilatation in resistance mesenteric arteries which was compensated by an overproduction of vasodilator prostaglandins resulting in part from COX-2 expression. The decrease in flow-induced dilatation was prevented by the ACEI, quinapril.
6-Ketoprostaglandin F1 alpha↗
Endothelin-A blockade attenuates systemic and renal hemodynamic effects of L-NAME in humans.
Eight Na-repleted volunteers underwent 3 separate 90-minute infusions of either N(G)-nitro-L-arginine methyl ester (L-NAME) 3.0 mg. kg(-1). min(-1) or endothelin-A receptor (ET-A) blocker BQ-123 (BQ) 0.125 nmol. kg(-1). min(-1) or both. Mean arterial pressure (MAP), glomerular filtration rate (GFR), renal blood flow (RBF), renal vascular resistances (RVR), and sodium excretion rate (UNaV) were measured at baseline (b) and from 0 to 45 minutes (period 1) and 45 to 90 minutes (period 2) of infusion. BQ alone had no effect. GFR declined by 4.9% (P<0.001 versus b) in period 1, to 9.9% (P<0. 001) in period 2 with L-NAME, and by 3.3% (P<0.01) to 6.6% (P<0.001) with L-NAME plus BQ (P=NS between L-NAME and L-NAME plus BQ). UNaV fell equally with L-NAME or L-NAME plus BQ. MAP rose significantly in period 2 with L-NAME (6.9%; P<0.001) but not with coinfused BQ (2. 1%; P=NA versus b, P=0.005 versus L-NAME alone). RBF declined by 12. 2% (P<0.001) to 18.3% (P<0.001) with L-NAME and by 4.6% (P<0.005) to 8.2% (P<0.001) with L-NAME plus BQ. These changes were smaller with L-NAME plus BQ (P<0.05 in period 1 and P<0.02 in period 2). Blunted changes were also seen for RVR (P<0.005 in period 1 and P<0.001 in period 2 between L-NAME alone and L-NAME plus BQ). These findings show that systemic and renal vasoconstriction due to L-NAME are attenuated by BQ, which suggests that an interaction between endogenous nitric oxide production and ET-A activity participates in the maintenance of baseline systemic and renal vascular tone in humans.
Adult↗
Conversation and convention: enduring influences on name choice for common objects.
The name chosen for an object is influenced by both short-term history (e.g., speaker-addressee pacts) and long-term history (e.g., the language's naming pattern for the domain). But these influences must somehow be linked. We propose that names adopted through speaker-addressee collaboration have influences that carry beyond the original context. To test this hypothesis, we adapted the standard referential communication task. The first director of each matching session was a confederate who introduced one of two possible names for each object. The director role then rotated to naive participants. The participants later rated name preference for the introduced and alternative names for each object. They also rated object typicality or similarity to each named category. The name that was initially introduced influenced later name use and preference, even for participants who had not heard the name from the original director. Typicality and similarity showed lesser effects from the names originally introduced. Name associations built in one context appear to influence retrieval and use of names in other contexts, but they have reduced impact on nonlinguistic object knowledge. These results support the notion that stable conventions for object names within a linguistic community may arise from local interactions, and they demonstrate how different populations of speakers may come to have a shared understanding of objects' nonlinguistic properties but different naming patterns.
Choice Behavior↗
Retrieval failures in face naming.
Several authors have reported that the incidence of retrieval failures is higher for people's names than for object names. The first aim of the paper was to evaluate the role of one factor that might contribute to making face naming difficult. Face naming usually requires the retrieval of one specific label: the name of the seen individual. Object naming is less restricting. First, object names may have synonyms. Second, labels available from different levels of categorisation of an object may be appropriate to name that object (e.g. trousers, jeans, Levis). Such a degree of freedom does not exist in naming faces. The hypothesis that face naming is made difficult by the simple fact that people have only one name was tested by studying faces having the exceptional property of bearing two names: faces of actors playing nameable characters (e.g. Harrison Ford playing Indiana Jones). Consistent with the hypothesis, data from two experiments showed that when bypassing a block is possible by producing another name that is known for a face, the incidence of blocks falls dramatically. The other aim of the paper was to test the reversed frequency effect in person naming reported previously in several diary studies, in an experimental setting. A direct frequency effect rather than a reversed frequency effect was obtained in the present study.
Adolescent↗