bluuebunny/crossref_metadata_2025_split huggingface dataset:
<i>Helicobacter pylori</i> Infection Affects Eosinophilic Cationic Protein in the Gastric Juice of Patients with Idiopathic Chronic Urticaria
Authors: Ojetti V. , Armuzzi A. , De Luca A. , Nucera E. , Franceschi F. , Candelli M. , Zannoni G.F. , Danese S. , Di Caro S. , Vastola M. , Schiavino D. , Gasbarrini G. , Patriarca G. , Pola P. , Gasbarrini A. 
Published: April 2003

<i>Background:</i><i>Helicobacter pylori,</i> the main cause of gastritis and peptic ulcer, has been associated with idiopathic chronic urticaria (ICU), an immunological skin disorder of unknown origin. Eosinophilic cationic protein (ECP) is a cytotoxic molecule secreted by the activated eosinophils involved in the pathogenesis of ICU. We assessed serum/gastric juice ECP levels and gastric mucosal eosinophil infiltration in ICU patients infected or not with <i>H. pylori</i> and evaluated the modification after bacterium eradication. <i>Methods:</i> 33 patients with ICU and 25 dyspeptic controls underwent upper gastrointestinal endoscopy for histological evaluation and assessment of <i>H. pylori</i> infection. One-week triple therapy was given to <i>H. pylori</i>-positive patients. Serum and gastric juice ECP levels, eosinophil infiltration from gastric mucosal sections and urticaria symptoms were evaluated in all patients at enrolment and 8 weeks after eradication. <i>Results:</i> 19 of 33 (57%) ICU patients and 16 of 25 (64%) controls were found to be infected with <i>H. pylori</i>. Serum ECP was significantly higher in ICU patients compared to controls, regardless of infectious status. Gastric juice ECP and gastric eosinophil infiltration were significantly higher in infected ICU patients when compared both to uninfected ICU patients and controls. <i>H. pylori</i> eradication determined a significant decrease in gastric juice ECP and gastric eosinophil infiltration only in ICU patients. Moreover, a total or partial remission of urticaria symptoms was observed only in ICU patients in whom the bacterium was eradicated. <i>Conclusions:</i> Although <i>H. pylori</i> infection affects gastric juice ECP and eosinophil infiltration of ICU patients, the role of the bacterium in the pathogenesis of this skin disorder still remains uncertain.
Safety of Chronic Fetal Vascular Access in the Sheep Model
Authors: Paek Bettina W. , Lopoo John B. , Jennings Russell W. , Farmer Diana L. , Albanese Craig T. , Harrison Michael R. 
Published: April 2003

<i>Objective:</i> Long-term access to the fetal circulation has the potential to open up new perspectives in the treatment of numerous fetal anomalies. The purpose of this study was to investigate the safety of long-term catheterization of fetal placental vessels. <i>Methods:</i> A midline laparotomy was performed in 4 time-mated pregnant ewes at 125 days’ gestation (term 145 days). Placental vessels were exposed by a small uterine incision. A specially designed catheter was inserted into a placental vessel over a length of 3 cm, the distal end of the catheter was tunneled underneath the maternal skin and attached to a subcutaneous port implanted in the maternal flank. All pregnancies were allowed to go to term. <i>Results:</i> Ewes and fetuses tolerated the placement of the catheter and port without complications. The catheter remained patent in all cases. All lambs were delivered vaginally at term and did not require resuscitation after birth. No fetal anomalies or growth restriction were noted. <i>Conclusion:</i> The ovine placental vessel can be accessed long term without complication.
Validity of Sonographic Formulas for Estimating Fetal Weight below 1,250 g: A Series of 119 Cases
Authors: Jouannic Jean-Marie , Grangé Gilles , Goffinet François , Benachi Alexandra , Cabrol Dominique 
Published: April 2003

<i>Objective:</i> The aim of this study was to determine the accuracy of sonographic methods for estimating fetal weight <1,250 g on the basis of ten published formulas falling into two principal categories: general formulas applied to all fetuses, and formulas specifically developed for very-low-weight fetuses. <i>Methods:</i> Recent biometric data (obtained less than 7 days before birth) on 119 fetuses weighing <1,250 g were used retrospectively. Estimated fetal weights derived from ten published formulas were compared to actual weights. For each equation, the errors in predicting fetal weight were used to calculate mean percentage error and standard deviation of the mean error. The t test was used to determine whether the mean errors were significatively different from zero. The F test was used to determine if there were significant differences in the standard deviation of the mean errors. <i>Results:</i> The mean birth weight of infants was 956 ± (SD) 183 g at a gestational age of 29 ± (SD) 2.3 weeks. The best three formulas were the Hadlock, Sabbagha and Mielke which generated a mean error of –0.25, 2.81 and 0.29 not statistically different from zero with standard deviations of 13.02, 9.14 and 11.96, which were not statistically different. <i>Conclusion:</i> In our population of very-low-birth-weight infants, the use of specific formulas targeted to those fetuses does not provide a more accurate estimation of fetal weight.
Characteristics of Heparin-Induced Platelet Aggregates in Chronic Hemodialysis with Long-Term Heparin Use
Authors: Matsuo Takefumi , Matsuo Miyako , Kario Kazuomi , Suzuki Shunji 
Published: April 2003

This study investigated the usefulness of a new platelet aggregometer with a laser-scattering method for detection of heparin-induced small platelet aggregates in chronic hemodialysis patients. Using this device, small platelet aggregates (particle size 9–25 µm) were detectable, but these aggregates could not be detected using a conventional light transmittance aggregometer. The laser-scattering intensity of the small aggregates was increased with an increasing dosage of heparin as agonist. These aggregates were disaggregated by heparin neutralization with protamine sulfate. Induction of small platelet aggregates by heparin was inhibited by preincubation with nafamostat mesilate, a synthetic protease inhibitor, and cilostazol, a platelet phosphodiesterase inhibitor, but not by the therapeutic doses of aspirin or argatroban, a selective thrombin inhibitor. The dialysis patients with long-term heparin use could be divided into two groups: responders to heparin, who formed small aggregates with a scattering intensity over 0.51 × 10<sup>5</sup> V after addition of 0.5 IU/ml of heparin obtained from normal platelet-rich plasma without inductor, and nonresponders, who showed an intensity under 0.51 × 10<sup>5</sup> V. The rate of heparin responders among dialysis patients was significantly higher than the rate among normal subjects. Heparin-induced small aggregates were detected in 13 (36.1%) of 36 normal subjects with no history of heparin infusion and in 37 (62.7%) of 59 dialysis patients who received heparin anticoagulation during each dialysis session. Dialysis patients with coronary heart disease did not have a significantly higher rate of heparin responders than patients without complications. There was no significant difference in the positivity rate between cases complicated by diabetes and those without diabetes. In patients who had more than 2 episodes of thrombotic occlusions of an arteriovenous fistula, the rate of responders and the enhancement of scattering intensity of small aggregates by heparin were significantly increased compared with these in patients without occlusions during the preceding 2 years. Moreover, dialysis patients with a positive heparin response showed a marked increase in scattering intensity of small aggregates after heparin infusion in each dialysis session. Determination of the response to heparin prior to heparin use in dialysis patients with repeated thromboembolic complication may be useful in choosing anticoagulant regimens.
Different Levels of Hypertension Induce Opposite Diuretic Behaviors from the Nonclipped Kidney in the Rat Two-Kidney, One-Clip Model
Authors: Al-Qattan K.K. 
Published: April 2003

This study was carried out on conscious two-kidney, one-clip (2K1C) rats to establish whether different levels of hypertension induced opposite diuretic behaviors from the nonclipped kidney. Mildly hypertensive rats and severely hypertensive rats were produced by, respectively, constricting their right renal arteries with 0.3-mm and 0.15-mm clips. On the 11th day of the study, the systolic blood pressure (SBP) of the 0.3-mm clip rats was 150 ± 2 mm Hg, the water intake was 24 ± 1 ml, and the urine output was 7 ± 1 ml. The SBP of the 0.15-mm clip rats was 231 ± 10 mm Hg, the water intake was 46 ± 4 ml, and the urine output was 27 ± 6 ml. The data from the two groups are significantly different. On the 19th day half of the mildly hypertensive (0.3-mm clip) rats that received cilazapril from day 15 had, with respect to their water-treated counterparts, a SBP of 140 ± 8 as compared with 159 ± 7 mm Hg, the water intake was 37 ± 5 as compared with 26 ± 4 ml, and the urine output was 18 ± 4 as compared with 12 ± 1 ml. In contrast, half of the severely hypertensive (0.15-mm clip) rats that received cilazapril had, with respect to their water-treated counterparts, a SBP of 143 ± 4 as compared with 227 ± 10 mm Hg, the water intake was 30 ± 2 as compared with 51 ± 9 ml, and the urine output was 8 ± 2 as compared with 29 ± 4 ml. All changes induced by cilazapril are significant in both groups. The data of this study suggest that different levels of hypertension in the rat 2K1C model induce opposite water elimination modes from the nonclipped kidney. This conclusion is supported by the different shift in the water intake and urine output among the cilazapril-treated rats of the two groups. This contrast in the response to cilazapril seems to be dependent on the magnitude of the resulting hypotension. Thus, it seems that in this model, when the hypertension is mild, the antidiuretic effect of angiotension II on the nonclipped kidney is exhibited, whereas, when the hypertension is severe, the diuretic influence of the blood pressure is evident. Irrespective of these different characteristics of the submodels of 2K1C, angiotensin I converting enzyme inhibitors, such as cilazapril, are effective in normalizing the blood pressure.
Renal Hemodynamic Effects of Captopril and Doxazosin during Slight Physical Activity in Hypertensive Patients with Type-1 Diabetes mellitus
Authors: Svarstad Einar , Gerdts Eva , Omvik Per , Ofstad Jarle , Iversen Bjarne M. 
Published: April 2003

Angiotensin-converting enzyme inhibitors are renoprotective in diabetes mellitus through their intrarenal hemodynamic effects. Alpha-1 blockade has variable pre- and postglomerular vasodilatory effects dependent upon the stimulation of the sympathetic nervous system. We tested the hypothesis that the two different classes of drugs have similar renal hemodynamic effects when the patients are examined in an upright position where the sympathetic nervous system is activated. Mean blood pressure (MAP), glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were examined in 28 hypertensive type-1 diabetic patients with variable degree of nephropathy treated for a mean period of 7.6 ± 0.4 months with captopril (n = 13) or doxazosin (n = 15). Average treatment doses were 112 ± 7 mg/day in the captopril group and 8 ± 1 mg/day in the doxazosin group. Sitting MAP decreased from 118 ± 3 to 106 ± 4 mm Hg after captopril (p < 0.05), and from 117 ± 4 to 110 ± 3 mm Hg after doxazosin (p = 0.07). GFR and ERPF were unchanged in both groups. The filtration fraction (FF) decreased from 0.27 ± 0.02 to 0.25 ± 0.02 after captopril (p < 0.05) and from 0.26 ± 0.01 to 0.25 ± 0.01 after doxazosin (p = 0.08). Calculation of 95% confidence intervals of the difference between the post-treatment values as well as the difference between pre- and post-treatment values of MAP, GFR, ERPF and FF of the two drugs indicates no difference in renal hemodynamic response between the drugs. In conclusion, captopril and doxazosin have similar renal hemodynamic responses when the patients are examined in a situation where the sympathetic nervous system is stimulated, and this suggests that doxazosin has a renoprotective effect beyond the blood pressure-lowering effect.
Factor Analysis, Including Antihypertensive Medication, of the Outcome of Pregnancy in Pregnancy-Associated Hypertension
Authors: Hussein Magdi M. , Mooij Jaap M.V. , Roujouleh Haysam 
Published: April 2003

<i>Aim:</i> To study the influence of different maternal factors, inlcuding antihypertensive medication, on the outcome of pregnancy in primi- and multiparas with pregnancy-associated hypertension. <i>Methods:</i> A retrospective, multiple-variate analysis was undertaken of the influence of several maternal factors, including antihypertensive medication, on fetal death and Apgar scores and the correlation between the medication and the number of caesarean sections in 127 episodes of pregnancy-associated hypertension was studied for the whole group as well as for primi- and multiparas separately. Of the multiparas, 40.8% had a history of preeclampsia, 19.7% of chronic hypertension and 9.2% of diabetes mellitus. Antihypertensive treatment aimed at achieving a blood pressure of 140/90 mm Hg. Forty-one patients (32.3%) received intravenous hydralazine, 25 (19.7%) received nifedipine per os and 44 (34.6%) received labetalol per os. <i>Results: </i> The maximum systolic and diastolic blood pressure in the patients given intravenous hydralazine, nifedipine per os or labetalol per os did not differ, whereas in the multiparas, the number of patients who reached the target blood pressure while using labetalol was higher than with the two other medications, especially in comparison with intravenous hydralazine. For the primiparas, the time of delivery was the only factor with a significant impact on the Apgar scores. In the multiparas, there was an additional negative influence of the use of intravenous hydralazine. This was not seen in the patients using nifedipine and labetalol. <i>Conclusion: </i>The results suggest that in multiparas, intravenous hydralazine is possibly associated with more fetal distress when compared to primiparas.
Calcium/Calmodulin-Dependent Protein Kinase II Involvement in Release of Gonadotropin-Releasing Hormone
Authors: Waters Wendy W. , Chen Pat L. , McArthur Newell H. , Moreno Pete A. , Harms Paul G. 
Published: April 2003

Involvement of calcium/calmodulin-dependent protein kinase II (CaM kinase II) in regulation of GnRH release was tested by determining the effect of CaM kinase II antagonists (KN-62 or KN-93) on GnRH release from rat or cattle infundibular (stalk median eminence) explants. Preincubation of male rat infundibular explants for 30 min with KN-62 (0.5, 1, 5 or 10 µ<i>M</i>) 1.5 h prior to the addition of 59.3 m<i>M</i> (high) K<sup>+</sup> resulted in a dose-dependent suppression of GnRH release. A longer pretreatment period (2 h) of rat infundibular explants with KN-62 (1 or 10 µ<i>M</i>) appeared to enhance the suppressive effect of the CaM kinase II antagonist. Exposure (2 h) of rat infundibular explants to 10 µ<i>M</i>, but not 0.1 µ<i>M</i> KN-93, resulted in a complete inhibition of high K<sup>+</sup>-induced GnRH release. Exposure of steer infundibular explant halves to KN-62 (50 or 100 µ<i>M</i>) or KN-93 (50 µ<i>M</i>) inhibited high K<sup>+</sup>-induced GnRH release. Likewise, treatment of heifer infundibular explant halves with KN-93 (50 µ<i>M</i>) abolished high K<sup>+</sup>-induced GnRH release. The period of exposure required for KN-62 to elicit its effect was relatively short since exposure of KN-62 (100 µ<i>M</i>) for only 91–150 min of incubation was sufficient to block high K<sup>+</sup>-induced GnRH release from steer infundibular explant halves. In conclusion, these results: (1) support the hypothesis that CaM kinase II is involved in GnRH release from the rat and cattle infundibulum, (2) demonstrate that the effect of CaM kinase II on GnRH release from cattle infundibula is independent of reproductive state, (3) confirm previous reports supporting Ca<sup>2+</sup> and CaM involvement in GnRH release from rat and cattle infundibula and (4) establish that infundibular explants incubated in vitro are useful for studying selected mechanisms regulating hypothalamic neurohormone release from neuron terminals.
Is GnRH Reduced at the Midcycle Surge in the Human?
Authors: Martin Kathryn A. , Welt Corrine K. , Taylor Ann E. , Smith Julie A. , Crowley Jr. William  F. , Hall Janet E. 
Published: April 2003

Recent studies indicate that the midcycle gonadotropin surge in the human occurs without an increase in hypothalamic gonadotropin-releasing hormone (GnRH) pulse frequency. In addition, previous studies employing a GnRH antagonist to provide a semiquantitative estimate of endogenous GnRH secretion suggest that the overall amount of GnRH secreted is decreased at the time of the surge. To investigate the hypothesis that a normal gonadotropin surge can be generated in the human with a decreased amount of GnRH at the midcycle, 7 GnRH-deficient subjects underwent two cycles of a physiologic regimen of intravenous pulsatile GnRH therapy. In the control cycle, 75 ng/kg/bolus of GnRH, a dose known to be sufficient for folliculogenesis, was administered throughout the cycle, using physiological frequencies. In a second cycle, the bolus dose of GnRH was decreased by one-half log order to 25 ng/kg just prior to the luteinizing hormone surge and returned to 75 ng/kg after documented ovulation. All cycles were ovulatory. The peak luteinizing hormone level (77.4±9.7 vs. 67.5±17.6 IU/l) did not differ between the control and decreased GnRH cycles. There was no difference in the peak serum estradiol level (475.8±144.1 vs. 493.2±93.0 pg/ml), follicular phase length (15.0±1.3 vs. 14.8±0.6 days), or progesterone level (22.4±5.1 vs. 34.8±5.7 ng/ml) on day 6 of the luteal phase in the control and decreased GnRH cycles, respectively. Three pregnancies were achieved in each of the control and reduced GnRH cycles. We conclude that a decreased overall amount of GnRH generates a normal midcycle gonadotropin surge and has no significant impact on luteal phase adequacy or fertility. These results provide further evidence that a decrease in endogenous hypothalamic GnRH secretion may occur at the midcycle in normal women. This study also provides evidence that the GnRH requirements for normal follicular and luteal phase dynamics may well be greater than those required for generation of a normal midcycle gonadotropin surge and ovulation in women.
Effect of Serotonin Inhibition on Glucocorticoid and Mineralocorticoid Expression in Various Brain Structures
Authors: Semont Alexandra , Fache Marie-Pierre , Ouafik L’Houcine , Hery Micheline , Faudon Maxime , Hery Francis 
Published: April 2003

Many studies have shown the existence of functional interactions between central neurotransmitter systems and the hypothalamo-pituitary adrenal axis. Mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) are regulated by multiple factors including glucocorticoids themselves. Neurotransmitters such as serotonin (5-hydroxytryptamine: 5-HT) can regulate brain corticosteroid receptors in a complex way. The present study examined the short-term (48 h) effects of parachlorophenylalanine (PCPA), a drug which specifically inhibits 5-HT synthesis, on corticosteroid receptor levels and on the expression of their respective messenger ribonucleic acids (mRNA) in the rat hippocampus, hypothalamus and brain stem. The study was performed in bilaterally adrenalectomized animals, in order to avoid potential drug-induced changes in plasma corticosterone levels, which could secondarily regulate MR and GR. Short-term inhibition of 5-HT synthesis by PCPA significantly increased the number of hippocampal MR-binding sites. PCPA treatment did not alter the number of GR-binding sites in the hippocampus, hypothalamus and brain stem. We observed no change in the affinities of GR and MR sites in all the structures studied. In PCPA-treated rats, restoration of control 5-HT levels by injection of its immediate precursor, 5-hydroxytryptophan (5-HTP) brings the number of hippocampal MR-binding sites back to control levels. It can therefore be concluded that the increase in number of MR-binding sites induced by acute PCPA treatment is dependent on the decrease in 5-HT levels. The increase in hippocampal MR binding sites was correlated with an induction of their messengers, suggesting that 5-HT modulates the synthesis of MR protein. Although PCPA did not modify the number of hippocampal GR-binding sites, a decrease in hippocampal GR mRNA expression was observed. This study shows that 5-HT inhibits hippocampal mineralocorticoid receptor synthesis and that this effect is not mediated by changes in corticosterone hormone secretion, and illustrates the existence of complex mechanisms for corticosteroid receptor regulation in the hippocampus.
A Comparative Study of the Effects of Nitric Oxide and Carbon Monoxide on the in vivo Release of Gonadotropin-Releasing Hormone and Neuropeptide Y from Rat Hypothalamus during the Estradiol-Induced Luteinizing Hormone Surge: Estimation by Push-Pull Perfusion
Authors: Kohsaka Akira , Watanobe Hajime , Kakizaki Yoshifumi , Suda Toshihiro 
Published: April 2003

Recent evidence suggests that nitric oxide (NO), a free radical gas, plays an important role in regulating the function of a variety of neuroendocrine systems. With respect to the hypothalamo-pituitary-gonadal axis, a stimulatory effect of NO on the release of gonadotropin-releasing hormone (GnRH) from rat hypothalamus has been demonstrated in vitro. However, no previous study has reported NO-stimulated secretion of GnRH from in vivo hypothalamus, and also the precise cellular site of action of NO within the GnRH neuronal system remains to be elucidated. In the present study, utilizing the push-pull perfusion technique of rat hypothalamus, we examined the effect of L-arginine (L-Arg), an NO donor, on the release of GnRH, neuropeptide Y and cyclic GMP (c-GMP), which is a pivotal second messenger molecule of the NO system. For comparison, we also examined the effect of carbon monoxide (CO), another putative gaseous neurotransmitter, using hematin, a CO donor. During the period of 11.00–18.00 h, we collected blood and hypothalamic perfusates from ovariectomized adult rats that had been implanted with an estradiol capsule 2 days before. During the entire period of observation, L-Arg (1.0 or 10 mM), hematin (10 or 100 µM) or artificial cerebrospinal fluid alone (as the control) was infused into the medial preoptic area (MPOA) where there are cell bodies of GnRH neurons, or the median eminence-arcuate nucleus complex (ME-ARC) where axon terminals of GnRH neurons are localized. Although 10 mM of L-Arg significantly stimulated GnRH and c-GMP, but not neuropeptide Y, levels in both the MPOA and ME-ARC, GnRH and c-GMP in the ME-ARC were already increased by 1.0 mM of L-Arg. By contrast, both concentrations of hematin were without effect at either site of the hypothalamus. This study is the first to demonstrate that NO is capable of stimulating GnRH release from rat hypothalamus in vivo. Our data also suggests that both cell bodies and axon terminals of GnRH neurons may be sites of action of NO. Our data do not support a previous study by other investigators that reported a stimulatory effect of CO on the GnRH release.