bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ductus venosus blood flow assessment at 11 to 14 weeks of gestation and fetal outcome
Authors: Toyama J. M. , Brizot M. L. , Liao A. W. , Lopes L. M. , Nomura R. M. Y. , Saldanha F. A. T. , Zugaib M. 
Published: March 2004

AbstractObjectiveTo evaluate the association between abnormal ductus venosus (DV) at 11–14 weeks' gestation and chromosomal abnormalities, structural defects and fetal outcome.MethodsDV flow‐velocity waveform (DV‐FVW) and nuchal translucency thickness (NT) were prospectively evaluated in 1217 singleton pregnancies.ResultsThe DV‐FVW was abnormal in 84 fetuses, NT was above the 95th centile in 160 fetuses and both markers were observed in 41 fetuses. Chromosomal defects were diagnosed in 22 fetuses. The sensitivity, specificity and positive and negative predictive values for an abnormal karyotype were 86.4%, 86.9%, 11.9% and 99.7%, respectively, for an increased NT. These values were 68.2%, 96.9%, 31.3% and 99.3%, respectively, for DV‐FVW abnormalities and 68.2%, 97.6%, 36.6% and 99.3%, respectively, when both markers were found simultaneously. Regarding structural defects, these values were 43.8%, 92.9%, 8.3% and 99.1% for an abnormal NT, 25.0%, 92.6%, 4.8% and 98.8% for DV‐FVW abnormalities and 25.0%, 97.9%, 15.4% and 98.9% for both together. Considering those cases of unexplained fetal demise, the values were 44.4%, 85.9%, 5.0% and 98.9% for NT abnormalities, 22.2%, 92.6%, 4.8% and 98.6% for an abnormal DV‐FVW and 22.2%, 98%, 15.4% and 98.7% for both. In cases with increased NT, the percentage of live births with normal karyotype and no major fetal structural defects decreased from 93.8% in normal DV‐FVW fetuses to 77.3% in abnormal ones.ConclusionDV assessment at 11–14 weeks' gestation is useful in screening for fetal chromosomal abnormalities and may help to reduce the false‐positive rate when combined with NT measurement. Abnormal DV‐FVW is also associated with an increase in adverse perinatal outcome in fetuses with enlarged NT. However, the value of DV‐FVW assessment in cases with normal NT is unclear. Copyright © 2004 ISUOG. Published by John Wiley & Sons, Ltd.
EPA External Research Grants Program faces steep budget cuts
Authors: Showstack Randy 
Published: March 2004

The Bush administration—s proposed budget cuts to the Environmental Protection Agency's research grants program, Science to Achieve Results (STAR),came under criticism at a hearing of the Science Subcommittee on Environment, Technology and Standards of the U.S. House of Representatives. The hearing was held 11 March.Subcommittee members and several witnesses said that a proposed $36 million cut to the STAR'S fiscal year 2005 budget—compared to the FY2004 proposed budget—is too steep. They said the proposed $65‐million budget—which would be a cut of more than 30% from the previous fiscal year—would harm the program, as well as the agency's ability to receive outside research advice on a range of cutting‐edge environmental issues. Funding for STAR graduate fellowships also would be cut by $3.1 million, compared to the enacted level for FY2004.
Immunoglobulin V‐Lambda Transcription Profiling of Systemic Lupus Erythematosus Patients Reveals Biased Usage of Genes Located Near the Jλ–Cλ Segments
Authors: Trevisan G. L. , Tamia‐Ferreira M. C. , Junta C. M. , Passos G. A. S. 
Published: March 2004

AbstractTo evaluate the distribution of usage and to quantify the transcription levels of the immunoglobulin lambda variable (IGLV) genes in patients with systemic lupus erythematosus (SLE) and normal individuals (NIs), cDNA samples from peripheral blood lymphocytes were prepared and probed with IGLV‐specific oligonucleotides. Because recombinations involving V‐lambda pseudogenes are nonproductive, we analysed the IGLV productive repertoire, as cDNAs were copied from IGLV mRNA producing B lymphocytes. Increased expression of the IGLV8a gene in SLE led us to analyse the transcription levels of all IGLV genes.We developed an expression profiling approach to scan the entire V‐lambda locus on chromosome 22q11.2. The transcription profiling showed that usually the V‐lambda genes located near the Jλ–Cλ cluster were preferentially expressed in both groups, i.e. patients and NIs, with the expression levels of SLE patients being significantly higher.However, genes displaying peaks of expression independent of Jλ–Cλ cluster proximity were observed along the IGLV locus. Our data permit us to conclude that there are differences in V‐lambda gene expression between SLE patients and NIs, and a preferential usage of genes located near the Jλ–Cλ cluster. The data also demonstrate the occurrence of Vλ–Jλ–Cλ‐productive recombinations independent of gene localization along the locus.
Regulation of Pituitary Corticotropin Releasing Factor Type‐1 Receptor mRNA Binding Proteins by Modulation of the Hypothalamic‐Pituitary‐Adrenal Axis
Authors: Wu Z. , Ji H. , Hassan A. , Aguilera G. , Sandberg K. 
Published: March 2004

AbstractLong‐term adrenalectomy (ADX) is associated with marked down‐regulation of pituitary corticotropin releasing factor type‐1 receptors (CRF‐R1) but normal CRF‐R1 mRNA levels, suggesting that regulation of receptor levels occurs at post‐transcriptional sites. We have reported that adrenal cytosolic proteins, which bind to cis elements in the 5′ leader sequence (5′LS) of the rat angiotensin II type 1a receptor (AT1aR) mRNA, participate in the regulation of AT1aR density by inhibiting AT1aR mRNA translation. In this study, we examined anterior pituitary cytosolic proteins that form RNA protein complexes (RPC) with the 5′LS of the CRF‐R1 and the AT1aR. Competition studies and ultraviolet‐crosslinking analysis suggest that formation of CRF‐R1 and AT1aR 5′LS RPC require at least some proteins that are common to both receptor mRNAs. Pituitaries isolated from male Sprague‐Dawley rats six days after ADX showed significant (P < 0.05) increases of 2.9‐fold in CRF‐R1 5′LS RNA binding protein (BP) activity compared to pituitaries from sham‐operated rats; this effect of ADX was prevented by glucocorticoid replacement. By contrast, no differences in the number of pituitary AT1aR binding sites or pituitary AT1aR 5′LS BP activity were observed between sham and ADX rats, indicating that the effect of ADX on RPC formation was specific for CRF‐R1 mRNA. Addition of pituitary cytosolic extracts inhibited in vitro translation of CRF‐R1 mRNA by 79% under conditions that had no significant effects on the translation of a control mRNA. The data suggest that CRF‐R1 translation is regulated by modulation of the HPA axis through pituitary cytosolic proteins binding to the CRF‐R1 5′LS.
Regulation of Slo Potassium Channel Alternative Splicing in the Pituitary by Gonadal Testosterone
Authors: Mahmoud S. F. , McCobb D. P. 
Published: March 2004

Abstract Slo gene‐encoded BK potassium channels are prominent in both adrenomedullary and pituitary tissues. At one alternative splicing site, both tissues express variants with and without the optional ‘STREX’ exon. In adrenal chromaffin cells, this splicing choice, which has important ramifications for cell excitability, has been shown to be regulated by steroid hormones, including glucocorticoids and adrenal androgens. Moreover, striking sex differences are seen between male and female tree shrews. Here, we test the hypothesis that gonadal testosterone regulates splicing in these tissues. No significant sex differences were found in rats, in either adrenals or pituitaries. In the adrenal medulla, prepubertal castration in male rats increased the relative abundance of STREX transcripts slightly, but not significantly, as measured several weeks after puberty. However, castration substantially decreased STREX representation in the rat pituitary. Silastic implants of testosterone inserted at castration prevented this STREX decline. In postpubescent males, castration or T implants had less effect. Thus, we report (i) steroidal regulation of Slo splicing in the pituitary and (ii) participation of the male gonads in this regulation.
CARDIOVASCULAR EFFECTS OF THE ESSENTIAL OIL OF OCIMUM GRATISSIMUM LEAVES IN RATS: ROLE OF THE AUTONOMIC NERVOUS SYSTEM
Authors: Lahlou Saad , Interaminense Leylliane de Fátima Leal , Leal‐Cardoso José Henrique , Morais Selene Maia , Duarte Gloria Pinto 
Published: March 2004

SUMMARY1. The cardiovascular effects of intravenous (i.v.) administration of the essential oil of Ocimum gratissimum (EOOG) were investigated in rats. In addition, the present study examined: (i) whether the autonomic nervous system is involved in the mediation of EOOG‐induced changes in mean aortic pressure (MAP) and heart rate (HR); and (ii) whether these changes could be attributed, at least in part, to the actions of eugenol, the major constituent of EOOG.2. In both pentobarbitone‐anaesthetized and conscious rats, i.v. bolus injections of EOOG (1–20 mg/kg) elicited immediate and dose‐dependent decreases in MAP and HR. These responses to EOOG were of the same order of magnitude irrespective of whether the animal was under general anaesthesia.3. Pretreatment of anaesthetized rats with bilateral vagotomy did not significantly modify the EOOG‐induced dose‐dependent hypotension, whereas it significantly reduced the bradycardia at the highest dose used.4. In conscious rats, i.v. injections of bolus doses (1–10 mg/kg) of eugenol also elicited immediate and dose‐dependent decreases in MAP and HR. Intravenous pretreatment of conscious rats with either methylatropine (1 mg/kg) or hexamethonium (30 mg/kg) significantly reduced the EOOG‐induced dose‐dependent bradycardia without affecting the hypotension.5. These data show, for the first time, that i.v. administration of EOOG to either anaesthetized or conscious rats induces an immediate and significant hypotension and bradycardia, which appear to be due, at least in part, to the actions of the major constituent of EOOG, eugenol. These cardiovascular effects appear to be mediated by different pathways because only EOOG‐induced hypotension appears to be independent of the presence of an operational autonomic nervous system. This may suggest that the hypotensive activity of EOOG results from its vasodilatory effects directly upon vascular smooth muscle.
NITRIC OXIDE INHIBITION ACCELERATES HYPERTENSION AND INDUCES PERIVASCULAR INFLAMMATION IN RATS
Authors: Hsieh Nan‐Kuang , Wang Jia‐Yi , Liu Jiang‐Chuan , Wang Shwun‐De , Chen Hsing I 
Published: March 2004

SUMMARY1. Inflammatory changes in peripheral arteries have been reported in animal models of hypertension. Whether they occur in cerebral arteries (CA) with hypertension induced by deprivation of endogenous nitric oxide (NO) remains unknown.2. In the present study, we compared the arteriolar injury score (AIS) and perivascular inflammation in CA between hypertensive and normotensive rats following NO deprivation with the NO synthase inhibitor Nω‐nitro‐l‐arginine methyl ester (l‐NAME). Five‐week‐old male spontaneously hypertensive rats (SHR) and Wistar ‐Kyoto (WKY) rats were fed with l‐NAME (1 mg/mL) for 4 weeks.3. Nitric oxide deprivation resulted in time‐dependent elevations in tail‐cuff pressure (representing systolic blood pressure (SBP)) in both SHR and WKY rats. The magnitude of increase in SBP was larger in SHR (+81.0 ± 3.2 vs+25.0 ± 2.2 mmHg; P < 0.01). Arteriolar hyalinosis and AIS in various segments of the CA were assessed with periodic acid‐Schiff staining and inflammatory cells were immunostained with the antibody against macrophage/monocyte marker (ED1). The ED1+ cells appeared in the middle CA of l‐NAME‐treated SHR as early as 2 weeks after treatment. These cells were not observed in l‐NAME‐treated WKY rats and untreated SHR. More ED1+ cells were found in l‐NAME‐treated SHR than l‐NAME‐treated WKY rats after 4 weeks treatment.4. The AIS and number of ED1+ cells around the perivascular area of the internal carotid artery were significantly higher in l‐NAME‐treated compared with untreated rats (AIS: 137 ± 28 vs 46 ± 10 for WKY rats, respectively; 169 ± 18 vs 53 ± 6 for SHR, respectively (P < 0.01); ED1+ cells: 7.9 ± 0.6 vs 1.3 ± 0.9 for WKY rats, respectively; 13.6 ± 2.7 vs 2.1 ± 0.9 for SHR, respectively (P < 0.01)), although SBP was higher in untreated SHR than in l‐NAME‐treated WKY rats (170 ± 4 vs 137 ± 4 mmHg, respectively; P < 0.05).5. These findings suggest that ED1+ cells appeared in the middle CA of l‐NAME‐SHR as early as 2 weeks after treatment. Chronic inhibition of NO accelerates hypertension and induces perivascular inflammation.
Indomethacin decreases particulate guanylyl cyclase activity in rat kidney
Authors: Lee JongUn , Kim Soo Wan , Jung Tack‐Kyoon , Oh YoonWha , Park Choon Soon , Ma Seong Kwon , Kim Nam Ho , Choi Ki Chul 
Published: March 2004

SUMMARY1. Effects of non‐steroidal anti‐inflammatory drugs on the local atrial natriuretic peptide (ANP) and nitric oxide (NO) systems in the kidney were investigated.2. Male Sprague‐Dawley rats were treated with indomethacin (5 mg/kg, every 12 h, i.p.) for 2 days. The expression of ANP and natriuretic peptide receptor‐A (NPR‐A) mRNA was determined in the kidney, as was that of endothelial NO synthase (NOS) proteins. Particulate and soluble guanylyl cyclase activities were determined separately.3. Following treatment with indomethacin, urinary sodium excretion decreased significantly. Although the renal expression of ANP was not changed significantly, that of NPR‐A decreased significantly. The expression of NOS increased significantly. Particulate guanylyl cyclase activity was decreased, whereas the activity of soluble guanylyl cyclase was increased. The catalytic activity of Na+/K+‐ATPase was increased, with no significant changes in its expression. The expression of the type 3 Na/H exchanger and Na–K−2CL cotransporters increased significantly.4. The indomethacin‐induced decrease in urinary sodium excretion may be attributed, at least in part, to decreased activity of the local ANP/cGMP system. The increased activity of the NO/cGMP system may be a compensatory response to the diminished activity of the prostaglandin system.
RESTING METABOLIC RATE AND POST‐PRANDIAL THERMOGENESIS BY LEVEL OF AEROBIC POWER IN OLDER ATHLETES
Authors: Sullo Alessio , Cardinale Pasquale , Brizzi Guglielmo , Fabbri Bruno , Maffulli Nicola 
Published: March 2004

SUMMARY1. The aim of the present study was to evaluate the resting metabolic rate (RMR) and thermogenic effect of a meal (TEM) in older athletes.2. Eighteen older male volunteers were divided into three groups according to their aerobic power related to fat‐free mass (FFM) as follows: (i) group I, high aerobic power (Vo2max > 70 mL/kg FFM per min); (ii) group II, moderate aerobic power (Vo2max = 55–70 mL/kg FFM per min); and (iii) group III, low aerobic power (Vo2max < 55 mL/kg FFM per min).3. The RMR values, covariated for FFM using analysis of covariance (ancova), were higher in group I (mean (±SEM) 1.09 ± 0.04 kcal/min) than in groups II and III (0.99 ± 0.05 and 0.91 ± 0.03 kcal/min, respectively). Group I had a tendency for higher mean TEM values compared with the other groups, but the differences were not statistically significant for absolute or percentage values.4. Master endurance athletes with high aerobic power exhibit a higher RMR than master endurance athletes of similar age and body composition but with lower aerobic power.
EFFECT OF HIGH‐SALT DIET OR CHRONIC CAPTOPRIL TREATMENT ON EXERCISE CAPACITY IN NORMOTENSIVE RATS
Authors: Minami Naoyoshi , Mori Nobuyoshi , Nagasaka Makoto , Harada Taku , Kurosawa Hajime , Kanazawa Masayuki , Kohzuki Masahiro 
Published: March 2004

SUMMARY1. We investigated whether chronic suppression of the renin–angiotensin system, which is known to be associated with reductions in microvascular density and vasodilator responsiveness of skeletal muscle, could affect exercise capacity in normotensive rats.2. Rats were placed on normal rat chow, normal rat chow with captopril (100 mg/kg per day) or a high‐salt diet (HS; 4%) for 4 weeks. Following these interventions, rats with indwelling carotid artery catheters were submitted to stepwise increasing exercise on a motor treadmill at a speed of 10, 20 and 30 m/min for 4 min while blood lactate was measured.3. Blood lactate after exercise at a speed of 20 m/min was significantly higher and the duration during which rats were able to run at a speed of 30 m/min was significantly shorter in captopril‐treated rats and rats fed an HS diet compared with control rats.4. We conclude that chronic treatment with captopril or HS diet could reduce the exercise capacity in inactive normotensive rats, probably through chronic inhibition of the renin–angiotensin system.
A NOVEL WATER‐SOLUBLE VITAMIN E DERIVATIVE PREVENTS ACUTE LUNG INJURY BY BACTERIAL ENDOTOXIN
Authors: Uchiyama Kazuhiko , Takano Hirohisa , Yanagisawa Rie , Inoue Ken‐ichiro , Naito Yuji , Yoshida Norimasa , Yoshino Shin , Murase Hironobu , Ichinose Takamichi , Yoshikawa Toshikazu 
Published: March 2004

SUMMARY1. Various chemokines, such as keratinocyte chemoattractant (KC), macrophage inflammatory protein (MIP)‐1α and macrophage chemoattractant protein (MCP)‐1, are involved in the pathogenesis of acute lung injury induced by bacterial endotoxin (lipopolysaccharide; LPS). Oxidative stress is an important regulator of the expression of these chemokines, whereas vitamin E protects against LPS‐induced insults. In the present study, we determined the effects of 2‐(α‐d‐glucopyranosyl) methyl‐2,5,7,8‐tetramethylchroman‐6‐ol (TMG), a novel water‐soluble vitamin E derivative with excellent anti‐oxidant activity, on acute lung injury induced by intratracheal instillation of LPS (125 µg/kg) in mice.2. When TMG was administered intratracheally and intravenously (0.1, 1.0 or 10 mg/kg), it dose‐dependently decreased the infiltration of neutrophils into bronchoalveolar lavage fluid after LPS challenge.3. Histological examination showed that treatment with TMG ameliorated the LPS‐induced infiltration of neutrophils into the lungs. Furthermore, TMG attenuated the LPS‐induced increase in pulmonary expression of KC, MIP‐1α and MCP‐1 at both the transcriptional and translational levels.4. These results indicate that TMG is a possible treatment for acute lung injury, especially that caused by Gram‐negative bacteria. The therapeutic effect of TMG may be mediated, at least in part, by suppression of the local expression of chemokines, possibly through its strong anti‐oxidant activity.
EFFECTS OF TAURINE AND HOMOCYSTEINE ON CALCIUM HOMEOSTASIS AND HYDROGEN PEROXIDE AND SUPEROXIDE ANIONS IN RAT MYOCARDIAL MITOCHONDRIA
Authors: Chang Lin , Zhao Jing , Xu Jianxin , Jiang Wei , Tang Chao Shu , Qi Yong Fen 
Published: March 2004

SUMMARY1. Taurine and homocysteine are metabolites of methionine. Hyperhomocysteinaemia is one of the risk factors for cardiovascular disease. Although taurine may be a cardiovascular cytoprotective substance, we hypothesized that it may antagonize the effects of homocysteine on myocardial mitochondrial function.2. We studied the effects of taurine and homocysteine on [45Ca] uptake, Ca2+‐ATPase activity and generation of hydrogen peroxide and superoxide anions in vitro in rat isolated myocardial mitochondria.3. Results showed that the inhibition of mitochondrial [45Ca] uptake by homocysteine (0.1, 0.5 and 1.0 mmol/L) was concentration dependent. Taurine (5, 10 and 20 mmol/L) promoted [45Ca] uptake in a concentration‐dependent manner, as well as concentration dependently reducing the homocysteine (0.5 mmol/L)‐induced inhibition of mitochondrial [45Ca] uptake.4. Homocysteine significantly inhibited mitochondrial Ca2+‐ATPase activity, whereas taurine had a diphasic action on this activity. Taurine, at 5 and 10 mmol/L, increased Ca2+‐ATPase activity (P < 0.01), but 20 mmol/L taurine inhibited Ca2+‐ATPase activity (P < 0.05). Taurine attenuated the inhibitory effect of homocysteine on Ca2+‐ATPase activity.5. Homocysteine stimulated the generation of hydrogen peroxide and superoxide anions. Taurine had no effect on the generation of the anions, but inhibited their homocysteine‐stimulated generation.6. These results indicate that taurine and homocysteine have opposite effects in myocardial mitochondria with regard to [45Ca] uptake, Ca2+‐ATPase activity and the generation of hydrogen peroxide and superoxide anions. Our results may show an important mechanism for the cardiovascular protective effects of taurine.
HAEMODYNAMIC AND TUBULAR RENAL DYSFUNCTION IN RATS WITH SUSTAINED ARTERIAL CALCINOSIS
Authors: Quaglia Nora B , Brandoni Anabel , Villar Silvina R , Torres Adriana M 
Published: March 2004

SUMMARY1. In humans, two of the principal characteristics of vascular ageing are arterial wall calcification and decreased arterial distensibility, which induce organ damage. To amplify arterial calcium accumulation in laboratory animals, it is necessary to use an overdose of vitamin D3.2. The aim of the present study was to assess the impact of arterial calcium overload on renal function.3. Adult male Wistar rats were randomly divided into two groups: control and treated rats. Treated rats were injected 10 days before the experiment with a single dose of vitamin D3 (300 000 IU/kg, i.m.).4. Treated rats showed a decrease in renal blood flow and glomerular filtration rate. Tubular parameters were not modified under basal conditions. In contrast, a statistically significant increase in the fractional excretion of Na, K, Ca and H2O were observed in treated rats after the acute increment of sodium distal delivery, suggesting that the reabsorptive capacity of the thick ascending limb may be altered in treated rats.5. Thus, Na+/K+‐ATPase activity was evaluated in homogenates from renal cortex and medulla. Rats with arterial calcinosis presented a diminished activity of Na+/K+‐ATPase in medulla homogenates.6. An increment in the abundance of the Na–K–2Cl cotransporter (NKCC2) was observed in renal medulla homogenates from treated rats. It is suggested that this may compensate for the inefficiency of Na+/K+‐ATPase under basal conditions but, in the presence of acute distal sodium overload, the increment in NKCC2 abundance may not be sufficient to compensate for the decrease in Na+/K+‐ATPase activity.7. In summary, in our experimental model of arterial calcinosis, renal function is impaired, presenting a vascular compromise and altered function of the medullar thick ascending limb that becomes evident in the presence of acute high distal sodium delivery.