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Does the Farnsworth D15 test predict the ability to name colours?

BACKGROUND: The Farnsworth D15 test is designed to categorise colour vision deficiency as severe or moderate. The level of difficulty of the test was set so that those who passed it should be able to recognise surface colour codes, such as those used for electrical wiring. The test is widely used to provide advice to patients with abnormal colour vision and is often used for occupational selection when reliable recognition of surface colour codes is required. However, there has been only one previous study of the correlation between performance at the D15 test and the naming of surface colour codes and there has been no study of whether a person who passes the D15 can reliably name surface colours. METHODS: One hundred and two people aged 11 to 65 years with abnormal colour vision were recruited from consecutively presenting optometric patients and were asked to name the colours of fabric, paint and cotton thread samples. There were 10 colours in each class of material and the samples were presented in a large (five to 10 degree angular subtense) and small size (2.5 deg and a single thread). The errors made were compared to those made by an age-matched control group of equal size with normal colour vision. RESULTS: The correlations between the Farnsworth D15 colour confusion index and colour naming errors were 0.62 for the large stimuli and 0.73 for the small stimuli. Its sensitivity and specificity identifying those who made more errors than the worst performing colour normal person were 0.80 and 0.69 (large stimuli) and 0.75 and 0.71 (small stimuli). A Nagel anomaloscope range of less than 35 scale units provides essentially the same sensitivity and specificity. CONCLUSIONS: About 40 per cent of those with abnormal colour vision can name the main colours correctly under good visibility conditions. The D15 test is an imperfect predictor of those who can name surface colour codes correctly but it does provide useful information for general counselling. It is not suitable as a single test for occupational selection because it will pass 20 per cent who cannot name surface colours correctly and fail 30 per cent who can. In occupations in which recognition of surface colour codes is of critical importance, it may be best not to select people with abnormal colour vision because of the lack of a colour vision test that is a perfect predictor of the ability to recognise surface colours.

Adolescent↗

The electrophysiological correlates sustaining the retrieval of face-name associations: an ERP study.

An ERP study on 9 healthy participants was carried out to temporally constrain the neural network proposed by Campanella et al. (2001) in a PET study investigating the cerebral areas involved in the retrieval of face-name associations. Three learning sessions served to familiarize the participants with 24 face-name associations grouped in 12 male/female couples. During EEG recording, participants were confronted with four experimental conditions, requiring the retrieval of previously learned couples on the basis of the presentation of name-name (NN), face-face (FF), name-face (NF), or face-name (FN) pairs of stimuli. The main analysis of this experiment consisted in the subtraction of the nonmixed conditions (NN and FF) from the mixed conditions (NF and FN). It revealed two main ERP components: a negative wave peaking at left parieto-occipital sites around 285 ms and its positive counterpart recorded at left centro-frontal electrodes around 300 ms. Moreover, a dipole modeling using three dipoles whose localization corresponded to the three cerebral areas observed in the PET study (left inferior frontal gyrus, left medial frontal gyrus, left inferior parietal lobe) explained more than 90% of the variance of the results. The complementarity between anatomical and neurophysiological techniques allowed us to discuss the temporal course of these cerebral activities and to propose an interactive and original anatomo-temporal model of the retrieval of face-name associations.

Adult↗

Anti-nociceptive activity of nitric oxide synthase inhibitors in the mouse: dissociation between the effect of L-NAME and L-NMMA.

The anti-nociceptive effect of selective inhibitors of nitric oxide synthase has been assessed in a formalin-induced paw-licking model in mice. L-NG-Nitro arginine methyl ester (L-NAME) but not L-NG-monomethyl arginine (L-NMMA) exhibited anti-nociceptive activity in both the early and late phases of paw licking following intraperitoneal administration. The effect on the late phase response was more pronounced. L-NAME (0.1-100 micrograms) and L-NG-nitro arginine base (L-NOARG; 10 micrograms) but not D-NAME (10 micrograms) were also anti-nociceptive following intracerebroventricular administration. L-NAME (10 micrograms) administered by this route did not influence locomotor activity. L-NMMA was inactive at doses up to 40 micrograms by this route. At higher doses (75-200 micrograms) L-NMMA produced a similar and non-dose related reduction in early/late phase paw-licking time. D-NMMA (100 micrograms) was inactive. The greater anti-nociceptive effect of L-NAME in this model accords with recently published biochemical data indicating that L-NAME is several orders of magnitude more potent than L-NMMA as an inhibitor of brain nitric oxide synthase. These data support the use of L-NAME as a selective tool to investigate the central pharmacological effects of nitric oxide.

Amino Acid Oxidoreductases↗

Recognition of cigarette brand names and logos by primary schoolchildren in Ankara, Turkey.

OBJECTIVE: To assess the smoking behaviour of primary schoolchildren and their ability to recognise brand names and logos of widely advertised cigarettes, compared with other commercial products intended for children. DESIGN: Cross-sectional survey in classroom settings using a questionnaire designed to measure attitudes towards smoking and the recognition of brand names and logos for 16 food, beverage, cigarette, and toothpaste products. SETTING: Ankara, Turkey. SUBJECTS: 1093 children (54.6% boys, 44.4% girls) aged 7-13 years (mean = 10, SD = 1), from grades 2-5. The student sample was taken from three primary schools--one school in each of three residential districts representing high, middle, and low income populations. MAIN OUTCOME MEASURES: Prevalence of ever-smoking, recognition of brand names and logos. RESULTS: Prevalence of ever-smoking was 11.7% overall (13.9% among boys and 9.1% among girls; p < 0.05). Children aged eight years or less had a higher prevalence of ever-smoking (19.6%) than older children (p < 0.002). Ever-smoking prevalence did not differ significantly across the three school districts. Ever-smoking prevalence was higher among children with at least one parent who smoked (15.3%) than among those whose parents did not (4.8%) (p < 0.001). Brand recognition rates ranged from 58.1% for Chee-tos (a food product) to 95.2% for Samsun (a Turkish cigarette brand). Recognition rates for cigarette brand names and logos were 95.2% and 80.8%, respectively, for Samsun; 84.0% and 90.5%, respectively, for Camel; and 92.1% and 69.5%, respectively, for Marlboro. The Camel logo and the Samsun and Marlboro brand names were the most highly recognised of all product logos and brand names tested. CONCLUSIONS: The high recognition of cigarette brand names and logos is most likely the result of tobacco advertising and promotion. Our results indicate the need to implement comprehensive tobacco control measures in Turkey.

Adolescent↗

Chronic L-NAME hypertension in rats and autoregulation of juxtamedullary preglomerular vessels.

The impact of chronic NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension (20 mg.kg-1.day-1 po, for 25 days) on pressure responsiveness was assessed in vessels ranging from arcuate arteries (ArcA) to juxtaglomerular afferent arterioles (JAA), using videomicroscopy and blood-perfused juxtamedullary nephron (JMN) preparations. Respective tail-cuff pressures of control and L-NAME rats were 127 +/- 2 (n = 8) and 173 +/- 4 mmHg (n = 5). Corresponding vessels of both groups had similar calibers at 60 mmHg. Increasing blood perfusion pressure to 200 mmHg constricted control ArcA and JAA by 26 +/- 4% (n = 20) and 43 +/- 5% (n = 15), respectively. Instead, a respective 3 +/- 4% (n = 15) and 21 +/- 9% (n = 6) pressure-induced dilation occurred in L-NAME vessels, and 86 +/- 2% of glomeruli expressed alpha-smooth muscle actin. Responses to acetylcholine (1 microM) but not to nitroprusside (1 mM) were impaired by L-NAME. Maximal relaxation induced by Mn2+ (10 mM) revealed equal basal tone and similar passive viscoelastic properties in control and L-NAME vessels. No vascular hypertrophy was found in L-NAME vessels. Chronic L-NAME hypertension is therefore associated with a selective loss of vascular autoregulation in JMNs, which may contribute to glomerular injury.

Actins↗

L-NAME enhances pulmonary vasoconstriction without inhibiting EDRF-dependent vasodilation.

The purpose of the present study was to determine the influence of NG-nitro-L-arginine methyl ester (L-NAME) on pulmonary vascular responses to endothelium-dependent relaxing factor- (EDRF) dependent and EDRF-independent substances in the pulmonary vascular bed of the anesthetized cat. Because pulmonary blood flow and left atrial pressure were kept constant, changes in lobar arterial pressure directly reflect changes in pulmonary vascular resistance. When pulmonary vasomotor tone was actively increased by intralobar infusion of U-46619, intralobar bolus injections of acetylcholine, bradykinin, serotonin, and 5-carboxyamidotryptamine (a serotonin1A receptor agonist) decreased lobar arterial pressure in a dose-related manner. The pulmonary vasodilator response to serotonin, but not to 5-carboxyamidotryptamine, acetylcholine, and bradykinin, was significantly decreased by L-NAME (100 mg/kg i.v.). Administration of ritanserin (0.5 mg/kg i.v.), but not L-arginine (1 g/kg i.v. with 60 mg.kg-1 x min-1 i.v. infusion), reversed the inhibitory effects of L-NAME on the pulmonary vasodilator response to serotonin and abolished the enhanced pulmonary vasoconstrictor response to (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminoproprane hydrochloride (a serotonin2 receptor agonist) after L-NAME administration. In conclusion, the present experiments suggest that L-NAME inhibits the pulmonary vasodilator response to serotonin by increasing the sensitivity of serotonin2 receptor-mediated vasoconstriction and not by inhibiting EDRF formation. Because the pulmonary vasodilator responses to bolus administration of acetylcholine and bradykinin were not inhibited by L-NAME, these data suggest that L-NAME does not appear to be an adequate probe to study the role of endogenous EDRF in the adult feline pulmonary vascular bed in vivo.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

L-NAME does not affect exercise-induced pulmonary hypertension in thoroughbred horses.

The present study was carried out to examine the effects of nitric oxide synthase inhibition with Nomega-nitro-L-arginine methyl ester (L-NAME) on the right atrial as well as on the pulmonary arterial, capillary, and venous blood pressures of horses during rest and exercise performed at maximal heart rate (HRmax). Experiments were carried out on seven healthy, sound, exercise-trained Thoroughbred horses. Using catheter-tip manometers, with signals referenced at the point of the shoulder, we determined phasic and mean right atrial and pulmonary vascular pressures in two sets of experiments [control (no medications) and L-NAME (20 mg/kg iv given 10 min before exercise studies)]. The studies were carried out in random order 7 days apart. Measurements were made at rest and during treadmill exercise performed on a 5% uphill grade at 6, 8, and 14.2 m/s. Exercise on a 5% uphill grade at 14.2 m/s elicited HRmax and could not be sustained for >90 s. In quietly standing horses, L-NAME administration caused a significant rise in right atrial, as well as pulmonary arterial, capillary, and venous pressures. This indicates that nitric oxide synthase inhibition modifies the basal pulmonary vasomotor tone. In both treatments, exercise caused progressive significant increments in right atrial and pulmonary vascular pressures, but the values recorded in the L-NAME study were not different from those in the control study. The extent of exercise-induced tachycardia was significantly decreased in the L-NAME study at 6 and 8 m/s but not at 14.2 m/s. Thus, L-NAME administration may not modify the equine pulmonary vascular tone during exercise at HRmax. However, as indicated by a significant reduction in heart rate, L-NAME seems to modify the sympathoneurohumoral response to submaximal exercise.

Animals↗

Influence of L-NAME on pulmonary O2 uptake kinetics during heavy-intensity cycle exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak Vo(2) with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and Vo(2) kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME conditions (L) for baseline Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) response in phase II was significantly smaller (mean +/- SE: C: 25.1 +/- 3.0 s; L: 21.8 +/- 3.3 s; P < 0.05), and the amplitude of the Vo(2) slow component was significantly greater (C: 240 +/- 47 ml/min; L: 363 +/- 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) kinetics after L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial Vo(2) by nitric oxide. The cause of the larger Vo(2) slow-component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.

Adult↗

Cardiopulmonary effects of chronic administration of the NO synthase inhibitor L-NAME in the chick embryo.

BACKGROUND: Experimental observations in mammalian models suggest that endothelial nitric oxide (NO) synthase (NOS) content and activity are decreased in persistent pulmonary hypertension of the newborn. OBJECTIVES: To test the hypothesis that disruption of NO signaling in the developing chick embryo lung may contribute to pulmonary hypertension. METHODS: We analyzed pulmonary arterial reactivity and structure and heart morphology of 19-day chick embryos (incubation time 21 days) that received a daily injection of the NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME, 20 mug per gram egg) or vehicle from day 12 until day 18. RESULTS: Exposure to L-NAME did not affect embryonic survival or body mass of the embryos. The contractile responses to KCl, endothelin-1, the thromboxane A2 mimetic U46619, noradrenaline, and electrical-field stimulation were not affected by exposure to L-NAME. In contrast, in ovo L-NAME exposure reduced the sensitivity of pulmonary arteries to acetylcholine (pD2: 6.53 +/- 0.14 vs. 6.96 +/- 0.13; p < 0.05) and this effect was reversed by the NOS substrate L-arginine. Relaxations induced by sodium nitroprusside or forskolin were not altered by chronic L-NAME. Pulmonary vessel density was not different, but the percentage medial wall area of small pulmonary arteries (external diameter 10-50 microm) was slightly but significantly increased in the embryos exposed to L-NAME. In addition, hearts of L-NAME-exposed embryos showed an increase in right and left ventricular wall area. CONCLUSIONS: Chronic inhibition of NOS produced, in the chick embryo, impairment of endothelium-dependent relaxation, structural remodeling of the pulmonary vascular bed and biventricular cardiac enlargement.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

Renoprotective effects of felodipine and/or enalapril in spontaneously hypertensive rats with and without L-NAME.

To determine the renoprotective effects of a calcium antagonist (felodipine) and an angiotensin-converting enzyme (ACE) inhibitor (enalapril), alone or in combination, 10 groups of 19-week-old spontaneously hypertensive rats (SHR) (with or without N(G)-nitro-L-arginine methyl ester [L-NAME]) were studied using renal micropuncture techniques. Group 1 (control), group 2 (felodipine, 30 mg x kg(-1) x d[-1]), group 3 (enalapril, 30 mg x kg(-1) x d[-1]), and group 4 (felodipine plus enalapril, 15 mg x kg(-1) x d(-1) each agent) were studied after 3 weeks of treatment without L-NAME. L-NAME (50 mg/L) cotreatment was administered in drinking water to groups 6 through 10 using the same doses of each agent as in groups 1 through 4: group 5 (only L-NAME), group 6 (felodipine), group 7 (enalapril), and group 8 (felodipine plus enalapril). Groups 9 and 10 received L-NAME initially for 3 weeks followed by felodipine or felodipine plus enalapril, respectively, for the subsequent 3 weeks. All three treatments resulted in reductions in mean arterial pressure and total peripheral vascular resistance (P<.001) that were associated with important structural and functional renal microcirculatory improvements. Thus, the pathological nephrosclerosis (subcapsular and juxtamedullary) glomerular and arteriolar injury scores were improved (P<.05 at least) in association with normalization of afferent and efferent arteriolar resistances, and single-nephron glomerular filtration rate, plasma flow, and blood flow were significantly improved, as well as the ultrafiltration coefficient (compared with group 5, L-NAME). Thus, the calcium antagonist felodipine, alone or in combination with an ACE inhibitor, not only prevented but also reversed L-NAME-exacerbated hypertensive nephrosclerosis in SHR.

Animals↗

Cortical regions associated with perceiving, naming, and knowing about colors.

Positron emission tomography (PET) was used to investigate whether retrieving information about a specific object attribute requires reactivation of brain areas that mediate perception of that attribute. During separate PET scans, subjects passively viewed colored and equiluminant gray-scale Mondrians, named colored and achromatic objects, named the color of colored objects, and generated color names associated with achromatic objects. Color perception was associated with activations in the lingual and fusiform gyri of the occipital lobes, consistent with previous neuroimaging and human lesion studies. Retrieving information about object color (generating color names for achromatic objects relative to naming achromatic objects) activated the left inferior temporal, left frontal, and left posterior parietal cortices, replicating previous findings from this laboratory. When subjects generated color names for achromatic objects relative to the low-level baseline of viewing gray-scale Mondrians, additional activations in the left fusiform/lateral occipital region were detected. However, these activations were lateral to the occipital regions associated with color perception and identical to occipital regions activated when subjects simply named achromatic objects relative to the same low-level baseline. This suggests that the occipital activations associated with retrieving color information were due to the perception of object form rather than to the top-down influence of brain areas that mediate color perception. Taken together, these results indicate that retrieving previously acquired information about an object's typical color does not require reactivation of brain regions that subserve color perception.

Adult↗

Selective predictive value of rapid automatized naming in poor readers.

This study considers the differential predictive value of rapid naming tests for various aspects of later reading, where the differential is between nondisabled and poor readers. Two large-N longitudinal samples of students who have been evaluated from third through eighth grades are studied: (a) a randomly accessed, normally distributed group including students with varying degrees of reading ability (N = 154), and (b) a group of poor readers whose single-word reading in third grade is at or below the population 10th percentile (N = 64). Outcomes in fifth and eighth grade were measured in both groups. Single-word reading in both grades was strongly predicted from third-grade rapid naming only within the poor readers, even when IQ, socioeconomic status, and third-grade single-word reading were statistically controlled. Although rapid naming had predictive value within the large, normally distributed group, its predictive power was entirely absent in the average-reading nondisabled students who were between the 10th and 90th percentiles (n = 122). The fact that rapid naming has predictive power only for poor readers but not for average readers is interpreted as suggesting that impaired readers are qualitatively different from the normal-reading population and are not simply the "tail" of a normal distribution of reading ability. It also seems that it is the automaticity of retrieval, not the knowledge of names itself (as in confrontational naming tasks), that gives the predictive power in rapid naming. These data are considered in light of the one- and two-factor theories of the underlying processes involved in reading disability or dyslexia.

Anomia↗

Life span effects of lexical factors on oral naming.

This study investigated how lexical access in naming tasks (picture naming, naming to open-ended sentences, and naming to category exemplars) might be influenced by different lexical factors during adolescence and adulthood. Participants included 1075 individuals, ranging in age from 12 to 83 years. Lexical factors examined included word frequency and familiarity, age of acquisition, neighborhood density, and phonotactic probability. As expected, each of these factors influenced lexical access, and there was a general trend towards less accurate naming with age. More interestingly, word frequency and neighborhood density both showed larger effects for adolescents than for adults, but then showed constant effects on lexical access throughout adulthood. Phonotactic probability showed constant effects across the lifespan. Effects of word familiarity and age of acquisition interacted with age in adulthood; lexical access of older adults was more greatly affected by a word's familiarity and age of acquisition than was the lexical access of younger adults. These lexical factors impact on adult naming so that words that were learned later in life and which are judged to be less familiar are more difficult to retrieve then their counterparts (words learned earlier and judged to be more familiar) as individuals age. This suggests that age of acquisition and familiarity may play a protective role in adult naming. In contrast, word frequency and form-based properties of words appear to have similar effects throughout adulthood. Implications of these findings for theories of aging and for models of lexical access are discussed.

Adolescent↗

Assessing attitudes toward new names for chronic fatigue syndrome.

A questionnaire was distributed at the American Association of Chronic Fatigue Syndrome's biannual convention in Washington in January 2001 as well as through various Internet Web sites and listserves during early February and March of 2001. The sample consisted of 432 respondents. Most respondents (86%) indicated they wanted a name change, although more patients than scientists were in favor of this change. It was also apparent that the patients and physicians were clearly split between adopting a name such as myalgic encephalopathy versus one such as neuro-endocrine immune disorder. Also, among those respondents who selected either of these two choices for a new name, less than 30% of them supported the other name. Although the majority of respondents feel the name should be changed at this time, this survey suggests there are different stakeholders involved in the name-change process, each with strong and sometimes disparate feelings about changing the name.

Fatigue Syndrome, Chronic↗

Effects of L-NAME and timolol on aqueous IL-1beta, IL-6, IL-8, TNF-alpha and NO levels after Nd:YAG laser iridotomy in rabbits.

PURPOSE: Pro-inflammatory cytokines are produced by tissues and play a vital role in the host inflammatory response and uveitis. Nitric oxide (NO) can be produced in large amounts as a response to experimentally-induced uveitis or cytokines. In this study, we measured the levels of pro-inflammatory cytokines such as interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha and free-radical in aqueous humor after Nd:YAG laser iridotomy in rabbits, and investigated whether timolol maleate an anti-glaucoma drug, or a NO synthase inhibitor, NG-nitro-L-arginine methyl esther (L-NAME) had an inhibitory effect on these molecules, since L-NAME is a known anti-inflammatory agent in rabbits. METHODS: Bilateral experimental Nd:YAG laser iridotomy (power 7.5 mJ, mode single burst, aiming beam 4) was performed on 18 rabbits under general plus topical anesthesia. Aqueous humor samples were taken by clear corneal paracentesis preoperatively, and 1 and 24 h postoperatively. Six rabbits (12 eyes) were given bilateral topical timolol maleate 0.5% (Timoptic) drop b.i.d. (group 1), six rabbits (12 eyes) received bilateral 0.1 ml subconjuntival injections of L-NAME (150 mg/kg) (group 2), and six rabbits (12 eyes) were treated with topical balanced salt solution (BSS) b.i.d. (control). RESULTS. Preoperative cytokine and NO levels were comparable in the three groups, with no significant differences. In addition, there was no significant difference in baseline cytokine levels between the right and left eyes. In all groups, pre- and postoperative mean IL-1beta levels were below the detection limit of the assay (<5.0 pg/ml). In the control group, postoperative mean IL-6, IL-8 and NO levels were significantly higher after Nd:YAG laser iridotomy than before (for each, p < 0.01). Timolol and L-NAME both inhibited the rise in IL-8 and TNF-alpha levels. Timolol also inhibited the rise in IL-6 but not NO. L-NAME had an inhibitory effect against NO, but not IL-6. CONCLUSIONS: L-NAME has an inhibitory effect on IL-8, TNF-alpha and NO, but not on IL-6. Timolol had inhibitory effects on IL-6, IL-8 and TNF-alpha, but not on NO. These preliminary experimental results might help in assssing the effect of Nd:YAG laser iridotomy in aqueous humor, and to understand the inhibitory effects of timolol and L-NAME against these molecules.

Adrenergic beta-Antagonists↗

N(omega) -nitro-L-arginine methyl ester (L-NAME) attenuates the acute inflammatory responses and brain injury during the early phase of experimental Escherichia coli meningitis in the newborn piglet.

We evaluated the anti-inflammatory and neuroprotective effect of nonselective NOS inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME), in experimental bacterial meningitis in the newborn piglet. Meningitis was induced by intracisternal injection of 10(8) colony forming units of Escherichia coli. L-NAME 10 mg kg(-1) was given intravenously 30 min before induction of meningitis. L-NAME significantly attenuated the increase in intracranial pressure and decrease in cerebrospinal fluid glucose concentration observed in the meningitis group. Systemic and cerebral perfusion pressure were even higher compared to the control and meningitis groups. However, the meningitis-induced increase in tumor necrosis factor-alpha level, leukocyte numbers and lactate level in the cerebrospinal fluid was not significantly attenuated with L-NAME administration. Reduced cerebral cortical cell membrane Na+, K+ -ATPase activity and increased lipid peroxidation products, indicative of meningitis-induced brain cell membrane dysfunction, were significantly improved with L-NAME treatment. Decreased brain glucose and ATP levels were also significantly improved with L-NAME treatment. These findings suggest that L-NAME was effective in attenuating the acute inflammatory responses and brain injury in neonatal bacterial meningitis.

Animals↗

L-NAME aggravates pulmonary oxygen toxicity in rats.

Exposure to high oxygen concentration leads to acute lung injury and death in rats after 72 h. The pathophysiology of this phenomenon relies on several mechanisms, including alteration of vascular reactivity, recruitment and activation of neutrophils and alveolar macrophages, production of cytokines and excess production of free radicals. In addition to its potent vasodilating effect, nitric oxide (NO) has also been reported to prevent free radical-mediated damage. We wanted to determine whether NG-nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, might modulate oxygen toxicity. In rats exposed to continuous high oxygen concentration, we studied the effect of administration of 50 mg.kg-1 of intraperitoneal L-NAME twice a day on the first day of oxygen exposure. L-NAME resulted in earlier death, since 57% of the animals exposed to oxygen and injected with L-NAME died within 60 h as compared to 22% of the animals exposed to oxygen and treated with saline (p < 0.01). Haematocrit and bronchoalveolar lavage fluid protein were also significantly increased in animals exposed to oxygen and receiving L-NAME. The lung water content was higher in the oxygen-exposed groups (p < 0.01) and slightly decreased by L-NAME (p < 0.05). Thiobarbituaric acid reactive substances (TBARS) were elevated in plasma (p < 0.01) and decreased in lung (p < 0.001) of oxygen-exposed animals, but no significant effect of L-NAME was observed. NG-nitro-L-arginine methyl ester had a deleterious effect in rats exposed to hyperoxia, which might suggest that endogenous nitric oxide has a protective role against hyperoxia-induced pulmonary lesions.

Animals↗

GENETAG: a tagged corpus for gene/protein named entity recognition.

BACKGROUND: Named entity recognition (NER) is an important first step for text mining the biomedical literature. Evaluating the performance of biomedical NER systems is impossible without a standardized test corpus. The annotation of such a corpus for gene/protein name NER is a difficult process due to the complexity of gene/protein names. We describe the construction and annotation of GENETAG, a corpus of 20K MEDLINE sentences for gene/protein NER. 15K GENETAG sentences were used for the BioCreAtIvE Task 1A Competition. RESULTS: To ensure heterogeneity of the corpus, MEDLINE sentences were first scored for term similarity to documents with known gene names, and 10K high- and 10K low-scoring sentences were chosen at random. The original 20K sentences were run through a gene/protein name tagger, and the results were modified manually to reflect a wide definition of gene/protein names subject to a specificity constraint, a rule that required the tagged entities to refer to specific entities. Each sentence in GENETAG was annotated with acceptable alternatives to the gene/protein names it contained, allowing for partial matching with semantic constraints. Semantic constraints are rules requiring the tagged entity to contain its true meaning in the sentence context. Application of these constraints results in a more meaningful measure of the performance of an NER system than unrestricted partial matching. CONCLUSION: The annotation of GENETAG required intricate manual judgments by annotators which hindered tagging consistency. The data were pre-segmented into words, to provide indices supporting comparison of system responses to the "gold standard". However, character-based indices would have been more robust than word-based indices. GENETAG Train, Test and Round1 data and ancillary programs are freely available at ftp://ftp.ncbi.nlm.nih.gov/pub/tanabe/GENETAG.tar.gz. A newer version of GENETAG-05, will be released later this year.

Animals↗