Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Names”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed1999

Effects of L-NAME and 7-NI on NOS catalytic activity and behavioral outcome after traumatic brain injury in the rat.

Traumatic brain injury (TBI) produces transient increases in constitutive nitric oxide synthase (cNOS) activity and prolonged behavioral abnormalities. This study investigated the effects of nitro-L-arginine-methyl ester (L-NAME) and 3-bromo-7-nitroindazole (7-NI) treatment on cNOS catalytic activity and sensorimotor behavioral outcome after TBI. Rats underwent moderate (1.8-2.2 atm) parasagittal fluid percussion brain injury (FPI). At 5 min after FPI, cNOS activity was significantly increased within the damaged cerebral cortex of vehicle-treated rats compared to the noninjured contralateral cortex (206.7 +/- 150.5 % of contralateral, p < 0.01). Pretreatment with L-NAME and 7-NI significantly reduced injury-induced cNOS activation (47.7 +/- 42.6 %, p < 0.05, and 96.16 +/- 12.76, p < 0.05, respectively). Pretreatment with L-NAME and 7-NI also inhibited cNOS activity within the contralateral noninjured cerebral cortex compared to vehicle-treated rats (L-NAME 43.7 +/- 12.47%, p < 0.05; 7-NI 36.8 +/- 7.47%, p < 0.05). Furthermore, pretreatment with 7-NI, but not L-NAME, significantly reduced forelimb placing sensorimotor deficits (3.14 +/- 1.07, p < 0.05) at 1 day after TBI compared to vehicle-treated rats (5.38 +/- 0.42). These data indicate that inhibition of injury-induced elevations in neuronal NOS activity has a beneficial effect on neurological outcome after parasagittal FPI brain injury.

Animals↗
PubMed1982

Evidence for lexicographic processing in a patient with preserved written over oral single word naming.

A number of studies have shown superior written over oral performance in fluent aphasia. One reasonable explanation for this result is that writing in these cases takes place through a different set of output mechanisms than oral naming. Specifically, conversion of lexical information directly into graphemic code can occur for writing whereas output requires access to underlying phonology. If phonological processing is impaired, it is possible that written performance can still be sustained via lexicographic retrieval of information. A case study is described supporting this account of incongruous written over oral naming. Written naming for single words was markedly superior to spoken naming. Performance in rhyme matching tasks disclosed impaired retrieval of the underlying sound component of words and nonlexical phonological processing was severely impaired in writing to dictation. This suggests that written naming was mediated entirely by nonphological processes. In addition, recovery of function indicated considerable independence of phonological processing between reading and writing. While grapheme-phoneme conversion improved substantially six months post-onset, phoneme-grapheme transcoding remained severely impaired. This suggests that different neural mechanisms mediate access to phonology for reading and writing systems.

Aged↗
PubMed2003

Modulation of neural activity during object naming: effects of time and practice.

Repeated exposure to objects improves our ability to identify and name them, even after a long delay. Previous brain imaging studies have demonstrated that this experience-related facilitation of object naming is associated with neural changes in distinct brain regions. We used event-related functional magnetic resonance imaging (fMRI) to examine the modulation of neural activity in the object naming system as a function of experience and time. Pictures of common objects were presented repeatedly for naming at different time intervals (1 h, 6 h and 3 days) before scanning, or at 30 s intervals during scanning. The results revealed that as objects became more familiar with experience, activity in occipitotemporal and left inferior frontal regions decreased while activity in the left insula and basal ganglia increased. In posterior regions, reductions in activity as a result of multiple repetitions did not interact with time, whereas in left inferior frontal cortex larger decreases were observed when repetitions were spaced out over time. This differential modulation of activity in distinct brain regions provides support for the idea that long-lasting object priming is mediated by two neural mechanisms. The first mechanism may involve changes in object-specific representations in occipitotemporal cortices, the second may be a form of procedural learning involving a reorganization in brain circuitry that leads to more efficient name retrieval.

Adult↗
PubMed2005

Odor naming methodology: correct identification with multiple-choice versus repeatable identification in a free task.

Since there is rarely a social labeling consensus in the identification of odors, it would be better to assess whether participants identify an odor by the same name upon repeated presentation rather than by the name designated as 'correct' by the experimenter (veridical label) in identification tasks. To examine the relevance of this proposition, participants were asked to identify familiar odors both in a free and a multiple-choice task. The free task was replicated in order to determine the percentage of repeatable identification. Results showed that the difference between the percentage of correct identification in the multiple-choice task and the percentage of repeatable identification in the free task was small, and that participants often used a repeatable name which differed from the veridical label. Thus, it was suggested that allowing participants to give their own name to an odor when it is not present on a pre-developed list, and measuring whether participants repeat the same name in independent measurements, might improve the relevance of multiple-choice tasks.

Adolescent↗
PubMed1991

Recognizing and naming tunes: memory impairment in the elderly.

Subjects over the age of 50 listened to theme tunes of remote, recent, and frequent television programs. If they recognized the tune, they were asked for the name of the program and for as much information about the program as possible. From the responses to a subsequent questionnaire, it was possible to divide the data according to whether or not the subjects watched the programs. There was no effect of age on the recognition and naming of programs subjects never watched. For programs they watched (a true test of memory), older subjects recognized fewer tunes as familiar and were less able than younger subjects to name the programs with familiar tunes. Neither the amount of exposure nor the delay since exposure had a significant influence on the recognition and naming impairments with age. Older subjects reported less information about programs they watched than younger subjects. In multiple regression analyses, age was a better predictor of performance than measures of current cognitive ability. The results are compared with the effects of age on the recognition and naming of famous faces (Maylor, 1990a). It is argued that the studies together support the view that the information processing rate decreases with age; therefore the elderly are poor at speeded tasks, the most dramatic effects appearing for later components of sequential processes.

Acoustic Stimulation↗
PubMed2002

Named reporting and mandatory partner notification in New York State: the effect on consent for perinatal HIV testing.

The impact of the implementation of named reporting and mandatory partner notification on the percentage of patients not accepting prenatal human immunodeficiency virus (HIV) testing or deferring prenatal care has been examined in only a preliminary fashion. This retrospective, population-based cohort study of 5,007 patients admitted to a tertiary care labor-and-delivery unit in Central New York State between December 15, 1999, and March 14, 2001, is the first study to address the impact of named reporting and mandatory partner notification on prenatal HIV testing and prenatal care seeking. The percentage of patients who did not undergo prenatal HIV testing was significantly increased after the institution of named reporting and mandatory partner notification: 118/4,030 preimplementation, 59/966 postimplementation, with relative risk (RR) = 2.09 (1.54 < RR < 2.83). This remained significant after logistic regression controlled for confounding variables, with odds ratio (OR) = 1.5 (1.07 < OR < 2.10). The percentage of patients who did not receive prenatal care was significantly increased after the institution of named reporting and mandatory partner notification: 14/4,030 preimplementation, 18/966 postimplementation, with RR = 5.36 (2.68 < RR < 10.75). This remained significant after logistic regression controlled for confounding variables. OR = 3.77 (1.84 < OR < 7.72). There is a strong indication that the institution of named reporting and mandatory partner notification has significantly impacted the willingness of pregnant women to undergo HIV testing and prenatal care. Further analysis of the impact in perinatal populations is needed before the continued implementation of this controversial public policy initiative.

AIDS Serodiagnosis↗
PubMed1999

Nasal administration of the nitric oxide synthase inhibitor L-NAME induces daytime somnolence.

In preliminary studies, human subjects complained of drowsiness after aerosolization of NG-nitro-L-arginine methyl ester (L-NAME) into the nasal passages. We compared the effects of a nasal aerosol of L-NAME (0.5 M, 4 ml) to those of saline on sleep onset latency and exhaled nasal nitric oxide (NO). L-NAME decreased sleep onset latency and exhaled nasal NO. Vasoconstriction and local effects of L-NAME on NO synthesis are unlikely to explain this effect since oxymetazoline, a vasoconstrictor, decreased exhaled NO but had no effect on sleep onset latency. We conclude that aerosolization of L-NAME to the nasal passages induces daytime sleepiness.

Administration, Intranasal↗
PubMed2003

Word length modulates neural activity in auditory cortex during covert object naming.

Several lines of evidence show that posterior portions of left auditory cortex participate in aspects of speech production. A current hypothesis is that these regions play a specific role in processing phonological codes. We used event-related fMRI to test this hypothesis. Subjects covertly named objects that had names varying in length from one to four syllables. Behavioral data, both in previous work and in the present study, show an increase in naming reaction time as words get longer, reflecting the increase in phonological load. If left posterior auditory areas participate in phonological aspects of production, word length should modulate neural activity in this region. Object naming activated the left planum temporale in each subject, confirming previous findings of auditory cortex involvement in speech production. The timecourse of activation in this region showed a length effect, consistent with its hypothesized role in phonological processing. Similar effects were also observed in premotor cortex, but not in occipital-temporal cortex, which presumably supports visual processing of the pictures to be named.

Auditory Cortex↗
PubMed2000

Polymorphonuclear leukocytes (PMNs) functions in SHR, L-NAME- and DOCA/salt-induced hypertensive rats.

OBJECTIVES: To clarify ex-vivo polymorphonuclear leukocytes (PMNs) functions, we examined superoxide anion (O2-) production and adhesion to a plastic plate of isolated PMNs obtained from spontaneously hypertensive rats (SHR/lzm), NG-nitro-L-arginine methyl ester (L-NAME)- and deoxycorticosterone acetate (DOCA)/salt-induced hypertensive rats. DESIGN: Sixteen week-old male SHR/Izm and Wistar-Kyoto rats (WKY/Izm) were used as a model of hypertension and its control, respectively. L-NAME-hypertension was induced by oral administration of 100 mg/kg per day of L-NAME twice daily for 4 weeks using 4-week-old male Wistar rats. DOCA/salt-hypertension was induced by once daily subcutaneous injection of 1 mg DOCA with 1% NaCl drinking water for 2 weeks using 8-week-old male Wistar rats with heminephrectomy. METHODS: Heparinized whole blood was obtained from abdominal aorta. PMNs were isolated by density gradient following dextran sedimentation. A production of superoxide anion (O2-) by PMNs stimulated with phorbol ester myristate acetate (PMA, 100 ng/ml) was determined by a superoxide dismutase (SOD)-inhibitable cytochrome-C reduction method. Adhesion of PMNs was evaluated by their protein content on a plastic plate measured by Lowry method. RESULTS: SHR/Izm showed a significant enhancement of O2- production by isolated PMNs compared with WKY/Izm. Rats treated with L-NAME showed a lower O2- production by PMNs compared to control animals. In DOCA/salt hypertensive rats, O2- production was not different from that in the control rats. Adherent function of isolated PMNs did not differ significantly among these hypertensive animal models. CONCLUSIONS: These results suggest that O2- production by circulatory PMNs is augmented in SHR, but not in L-NAME and DOCA/salt hypertensive rats. This enhanced function, which is also observed in human essential hypertension, might contribute to the development of cardiovascular damage in genetically determined hypertension.

Animals↗
PubMed2001

Influence of irbesartan and enalapril on changes of renal function associated with the established phase of l-NAME hypertension.

OBJECTIVE: Reversibility of the systemic and renal alterations induced by N(omega)-nitro-L-arginine-methyl ester(L-NAME) was assessed by treatment with irbesartan and enalapril (30 and 10 mg/kg per 24 h, respectively) alone or in combination. DESIGN: L-NAME (20 mg/kg per 24 h) was given to rats for 6 weeks and treatments were administered during the last 2 weeks. Glomerular filtration rate and renal plasma flow [GFR and RPF per g of kidney weight (KW)] were determined using the clearance technique. RESULTS: Arterial pressure was similarly reduced by treatments. GFR was lower in L-NAME-treated rats than in controls (552 +/- 52 versus 1106 +/- 78 microl/min per g KW), whereas RPF was reduced to a larger extent, thus resulting in an increase in filtration fraction. GFR was normalized by irbesartan but not enalapril or the combination (1042 +/- 50, 790 +/- 79 and 725 +/- 38 microl/min per g KW, respectively). RPF returned to normal and filtration fraction fell markedly with the combination. All treatments reduced the lesions of preglomerular vessels and reversed L-NAME-induced albuminuria and cardiovascular hypertrophy. At a dose of 3 mg/kg per 24 h, irbesartan only reduced the lesions of the afferent arteriole. CONCLUSIONS: Through its effects on AT1 receptors, angiotensin II may play an important role in the maintenance of L-NAME hypertension and associated alterations. The lower GFR and filtration fraction observed with enalapril in the presence of irbesartan suggests the intervention of non-angiotensin II-mediated mechanism, and at the postglomerular level, in the effect of angiotensin-converting enzyme (ACE) inhibitors.

Angiotensin Receptor Antagonists↗
PubMed2003

Role of angiotensin II in L-NAME-induced systemic and renal hemodynamic effects in hydrochlorothiazide-pretreated hypertensive subjects.

BACKGROUND: Experimental evidence suggests that in conditions associated with an activated renin-angiotensin system, unopposed activity of angiotensin II underlies the marked renal vasoconstrictor response to nitric oxide synthase inhibition. In the present study, we investigated whether this holds true in hypertensive subjects pretreated with hydrochlorothiazide (HCT). METHODS: Systemic N(G)-nitro-L-arginine methyl ester (L-NAME) infusions (12.5 microg/kg per min for 40 min) were given to eight hypertensive subjects (age 53 +/- 6 years) during placebo, and during pretreatment with HCT (25 mg once daily) or HCT and losartan (LOS) (50 mg twice daily), both for 9 days. The glomerular filtration rate (GFR) and renal plasma flow were estimated from the clearances of radiolabeled thalamate and hippuran. Renal blood flow (RBF) was calculated as renal plasma flow/1 - hematocrit and the renal vascular resistance (RVR) as mean arterial pressure (MAP) divided by RBF. RESULTS: Compared with placebo, plasma renin increased (P < 0.001) from 15 +/- 4 mU/l during placebo to 26 +/- 7 mU/l during HCT and to 133 +/- 51 mU/l during HCT + LOS. MAP (110 +/- 3 mmHg) decreased to 102 +/- 4 mmHg during HCT and to 98 +/- 5 mmHg during HCT + LOS. RBF (579 +/- 36 ml/min), GFR (97 +/- 6 ml/min) and filtration fraction (29 +/- 2%) did not change, whereas RVR (200 +/- 15 RU) decreased to 183 +/- 13 RU during HCT and to 165 +/- 14 RU during HCT + LOS (P < 0.05). In response to L-NAME, MAP and RVR increased maximally by 10 +/- 3 and 67 +/- 9%, whereas RBF and GFR decreased maximally by 42 +/- 6 and 18 +/- 4%. Compared with these responses, the responses of MAP, RBF and RVR were not affected by pretreatment of HCT or HCT + LOS, but the L-NAME-induced decrease in GFR (26 +/- 5% during HCT and 29 +/- 5% during HCT and LOS) was enhanced (P < 0.01). CONCLUSIONS: In hypertensive subjects with an activated renin-angiotensin system, unopposed activity of angiotensin II is not involved in L-NAME-induced pressor and renal vasoconstrictor response, whereas the L-NAME-induced decrease in GFR is enhanced, indicating greater dependency of GFR on nitric oxide-mediated vasodilator tone during sodium depletion.

Angiotensin II↗
PubMed2004

Systemic hemodynamics in non-anesthetized L-NAME- and DOCA-salt-treated mice.

OBJECTIVE: Long-term cardiac output measurements in non-anesthetized mice are now possible. We used this technology to study two different hypertensive models in mice. DESIGN: We combined telemetric blood pressure and heart rate recordings with Doppler flow probe cardiac output measurements in mice during treatment with Nomega-nitro-L-arginine methyl ester (L-NAME) and deoxycorticosterone acetate (DOCA)-salt. METHOD: The mice received a flowprobe around the ascending aorta and, 10-18 days later, blood pressure telemetry. After recovery, baseline values were recorded and the mice were given L-NAME (5 mg/10 ml tap water), L-NAME followed by valsartan (50 mg/kg per day per gavage), or DOCA-salt (50 mg DOCA-pellet, 0.9% saline to drink, uninephrectomy). Mean arterial pressure, heart rate, stroke volume and cardiac output were recorded daily and total peripheral resistance was calculated. RESULTS: L-NAME resulted in an abrupt increase in mean arterial pressure caused solely by an increase in total peripheral resistance. Cardiac output was decreased. Valsartan treatment decreased blood pressure and total peripheral resistance, while cardiac output was restored to normotensive values. DOCA-salt required 3 days before hypertension developed. Contrary to the volume expansion, increased cardiac output, autoregulation hypothesis, the blood pressure increase was only associated with increased total peripheral resistance, while cardiac output was not changed. CONCLUSION: Both L-NAME and DOCA-salt increased blood pressure by increasing total peripheral resistance. Comprehensive hemodynamics can be done in non-anesthetized, free-moving mice. The methods provide new perspectives for studying mouse models in the long-term.

Animals↗
PubMed2003

Ouabain changes arterial blood pressure and vascular reactivity to phenylephrine in L-NAME-induced hypertension.

Ouabain is an endogenous compound that has been associated with the genesis and maintenance of hypertension. This compound inhibits the Na+ pump activity, which leads to an accumulation of intracellular Na and ultimately might increase vascular tone. In nanomolar concentrations, it enhances vasopressor responses to phenylephrine in some vascular beds from normotensive and hypertensive rats. However, it is not known whether this action of ouabain is a common mechanism for all models of hypertension. The aim of this work was to determine whether ouabain can alter pressor responses to phenylephrine in rats with Nomega-nitro-l-arginine methyl ester (L-NAME)-induced hypertension. In anesthetized rats, ouabain (0.18 microg/kg, i.v.) increased arterial blood pressure in L-NAME-treated rats but not in controls. Ganglionic blockade by hexamethonium (5 mg/kg, i.v.) prevented the increase in arterial blood pressure produced by ouabain in L-NAME-treated rats. Additional studies using isolated perfused tail artery preparations were performed to investigate which factors are involved in the action of ouabain in L-NAME-treated rats. The effects of 10 nM ouabain on the vasoconstrictor actions of phenylephrine were determined on preparations with intact or damaged endothelium or in the presence of tetraethylammonium (a K+-channel blocker). Ouabain reduced pressor actions of phenylephrine in preparations with an intact endothelium. However, after endothelial damage or infusing tetraethylammonium, the response to phenylephrine was increased after ouabain. In tails from L-NAME-treated rats, the functional activity of the Na, K+-ATPase was reduced, and 10 nM ouabain did not produce any further reduction. In conclusion, in this model of hypertension, a low dose of ouabain (0.18 microg/kg) increased arterial blood pressure in vivo probably as a result of increased sympathetic tone. However, this effect was not accompanied by an enhanced action of phenylephrine on the tail vascular bed with an intact endothelium. The results suggest that this was due to the release of an endothelium-derived K+-channel opener.

Animals↗
PubMed2002

The effects of simultaneous administration of alpha(2) -adrenergic agents with L-NAME or L-arginine on the development and expression of morphine dependence in mice.

Both alpha(2)-adrenoceptors and the L-arginine/nitric oxide (NO) pathway have been implicated in the modulation of morphine dependence. This study examined the effects of simultaneous administration of the alpha(2)-adrenoceptor agonist clonidine or the antagonist yohimbine together with the NO precursor L-arginine or the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on the induction and expression of morphine dependence as assessed by naloxone-precipitated withdrawal jumping and diarrhoea. Male NMRI mice weighing 20-30 g were used. In the induction phase, clonidine (0.01-0.1 mg/kg) intensified and yohimbine (0.5-2 mg/kg) attenuated the degree of morphine dependence. Yohimbine reversed the effect of clonidine. L-NAME (5 and 10 mg/kg) did not affect the development of morphine dependence, but significantly potentiated the effects of both subeffective (0.01 mg/kg) and effective (0.03 mg/kg) doses of clonidine. L-Arginine did not alter morphine dependence but inhibited the effect of clonidine. The effects of yohimbine in the induction phase were attenuated by L-NAME, but were not significantly affected by L-arginine. In the expression phase, clonidine attenuated and yohimbine intensified the signs of dependence. The effect of clonidine was inhibited by yohimbine. In the expression phase, L-NAME attenuated the withdrawal syndrome at 10 mg/kg and showed potentiation with clonidine in suppressing withdrawal signs. L-Arginine did not alter morphine dependence, but at 20 mg/kg inhibited and at 100 mg/kg potentiated the attenuating effect of clonidine on the expression of withdrawal syndrome. The effect of yohimbine on the expression phase was also attenuated by L-NAME, but was not significantly affected by L-arginine. In conclusion, alpha(2)-adrenergic and NO pathways seem to be functionally linked in the modulation of opioid dependence.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1998

Modulation of resuscitative effect of diaspirin cross-linked hemoglobin by L-NAME in rats.

Diaspirin Cross-linked Hemoglobin (DCLHb), a hemoglobin-based oxygen carrier, improves regional blood circulation and systemic hemodynamics in normal and hemorrhaged rats. The action of DCLHb is partly mediated by its scavenging effect on nitric oxide. This study was undertaken to determine the effect of DCLHb on nitric oxide mechanism in hemorrhagic conditions. We studied the modulation of cardiovascular effects of DCLHb by a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) in hemorrhaged rats. The base deficit, survival time, oxygen consumption, and blood circulation to the brain, heart, gastrointestinal tract, and kidneys were determined in 1) DCLHb (100 mg/kg, intravenously (i.v.), 2) L-NAME (2 mg/kg, i.v.), 3) L-NAME (2 mg/kg, i.v.) + DCLHb (100 mg/kg, i.v.), and 4) L-arginine (100 mg/kg/h, i.v.) + DCLHb (100 mg/kg, i.v.) treated rats. Hemorrhage was induced in urethane-anesthetized male rats by bleeding them at a rate of approximately .5 to 1 mL/min, until a mean arterial pressure of 35-40 mmHg was achieved. This blood pressure was maintained for 30 min. Sham-operated nonhemorrhaged rats survived for >300 min, whereas hemorrhaged rats survived for only 85+/-31 min. Hemorrhage significantly increased base deficit and decreased oxygen consumption. A significant decrease in heart rate, mean arterial pressure, cardiac output, stroke volume, and in blood flow to the gastrointestinal tract and kidneys was observed after hemorrhage. Resuscitation with DCLHb produced a significant increase in survival time, oxygen consumption, heart rate, mean arterial pressure, cardiac output, total peripheral resistance, and blood flow to the brain, heart, and kidneys. In contrast, resuscitation with L-NAME did not improve base deficit, survival time, oxygen consumption, systemic hemodynamics, or regional blood flow. L-arginine pretreatment did not affect DCLHb-induced resuscitation of hemorrhaged rats. Furthermore, L-NAME (pretreated or co-administered) attenuated the resuscitative effect of DCLHb. These data suggest that nitric oxide mechanism may not be the only mechanism involved in the resuscitative effect of DCLHb.

Animals↗
PubMed2005

Potentiation of L-NAME-induced systemic and renal vasoconstrictor responses by alpha1-adrenoceptor antagonism.

BACKGROUND: Acute inhibition of nitric oxide synthase results in systemic and renal vasoconstriction, which might be attributable to unopposed activity of the sympathetic nervous (SNS) and the renin-angiotensin system (RAS). We studied the effects of N-nitro-L-arginine methyl ester (L-NAME) during alpha1-adrenoceptor blockade and concomitant angiotensin II type 1 (AT1)-receptor blockade in hypertensive individuals pretreated with hydrochlorothiazide (Hct; 25 mg once daily). METHODS: Thirteen individuals (47 +/- 9 years) were studied during administration of placebo, and after pretreatment with Hct + doxazosin (Dox; 8 mg twice daily for 9 days), with Hct + Dox + losartan (Los; 50 mg twice daily for 9 days), or (n = 5) with doxazosin or Dox + Los without hydrochlorothiazide. Mean arterial pressure (MAP) and cardiac output were derived from the finger blood pressure signal recorded by Finapres. Systemic vascular resistance (SVR) was calculated as MAP/cardiac output. Five renal clearance studies of 40 min were performed. Renal vascular resistance (RVR) was calculated as MAP divided by renal blood flow (RBF). L-NAME (12.5 microg/kg per min intravenously) was given during the third clearance period. RESULTS: MAP was 113 +/- 11 mmHg at baseline and decreased to 99 +/- 10 mmHg during the administration of Hct + Dox and to 92 +/- 10 mmHg during Hct + Dox + Los. This decrease in MAP was caused by a decrease in SVR (P = 0.0009). Pretreatment with Hct + Dox or Hct + Dox + Los had no effect on glomerular filtration rate or RBF. Infusion of L-NAME during the administration of Hct + Dox resulted in an augmented (P < 0.0001) increase in MAP (18%), SVR (61%) and RVR (70%) compared with those observed with placebo (8, 30 and 49%, respectively). This augmentation was abolished by losartan. CONCLUSION: L-NAME-induced systemic and renal vasoconstrictor responses are potentiated during alpha1-adrenoceptor blockade. This potentiation was abolished by AT1-receptor antagonism. In man, unopposed activity of the SNS or SNS and RAS is not involved in the systemic and renal vasoconstriction induced by L-NAME.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed2006

Proposal of Parvimonas gen. nov. and Quatrionicoccus gen. nov. as replacements for the illegitimate, prokaryotic, generic names Micromonas Murdoch and Shah 2000 and Quadricoccus Maszenan et al. 2002, respectively.

The prokaryotic, generic names Micromonas Murdoch and Shah 2000 and Quadricoccus Maszenan et al. 2002 are illegitimate* because they are later homonyms of the names Micromonas Manton and Parke 1960 (alga) and Quadricoccus Fott 1948 (alga). [Principle 2, Rule 51b(4) of the Bacteriological Code (1990 Revision)]. Such names have no claim to be correct names (Principle 6) and, therefore, replacement generic names must be proposed (Rule 54).

Bacteria↗
PubMed2002

Determinants of picture naming times in Icelandic.

Numerous studies have found that word frequency has a significant effect on the time it takes to name an object or read a word. Recently, claims have been made that this frequency effect is perhaps more correctly interpreted as an age of acquisition effect. This paper reports an experiment in which naming times in Icelandic for 175 stimuli from the Snodgrass and Vanderwart picture set were determined. A multiple regression analysis of naming times against a number of independent factors showed that objective age of acquisition was the strongest predictor of naming time, with familiarity and name agreement also showing a significant effect. The effect of word frequency was, however, not significant. Possible reasons for this are discussed.

Adolescent↗