bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interleukin-1β but not IL-1α binds to fibrinogen and fibrin and has enhanced activity in the bound form
Authors: Sahni Abha , Guo Min , Sahni Sanjeev K. , Francis Charles W. 
Published: March 2004

AbstractFibrin is formed at sites of injury or inflammation and provides the temporary matrix to support vascular cell responses that are also mediated by cytokines including interleukin-1 (IL-1). We have shown previously that fibroblast growth factor 2 (FGF-2) binds with high affinity to fibrin(ogen). Because IL-1 has a structure similar to FGF-2, we have investigated the possible binding of IL-1 to fibrin(ogen). Experiments using IL-1 immobilized on Sepharose beads and soluble iodine 125 (125I)-labeled fibrinogen demonstrated no specific interaction of IL-1α with fibrinogen, but IL-1β showed saturable and specific binding. Scatchard analysis indicated a single binding site with an apparent Kd = 1.5 nM and a maximum molar binding ratio of IL-1β to fibrinogen of 1.8:1. Binding of 125I-IL-1β to Sepharose-immobilized fibrinogen also demonstrated a single binding site with an apparent Kd of 3.5 nM. IL-1β also bound specifically to fibrin monomer and polymerized fibrin with apparent Kds of 3.4 nM and 2.3 nM, respectively. IL-1β displaced FGF-2 for binding to fibrin, indicating an interaction with the same or a closely related site. Compared with free form, fibrinogen-bound IL-1β stimulated increased activation of endothelial cell nuclear factor κB (NF-κB), monocyte chemoattractant protein-1 (MCP-1) secretion, and nitric oxide (NO) synthesis. We conclude that IL-1β binds with high affinity to fibrin(ogen) and demonstrates increased activity in the bound form. (Blood. 2004; 104:409-414)
Estrogen Receptor β-Mediated Inhibition of Male Germ Cell Line Development in Mice by Endogenous Estrogens during Perinatal Life
Authors: Delbès Géraldine , Levacher Christine , Pairault Catherine , Racine Chrystèle , Duquenne Clotilde , Krust Andrée , Habert René 
Published: March 2004

AbstractEpidemiological, clinical, and experimental studies have suggested that excessive exposure to estrogens during fetal/neonatal life can lead to reproductive disorders and sperm abnormalities in adulthood. However, it is unknown whether endogenous concentrations of estrogens affect the establishment of the male fetal germ cell lineage. We addressed this question by studying the testicular development of mice in which the estrogen receptor (ER) β or the ERα gene was inactivated. The homozygous inactivation of ERβ (ERβ−/−) increased the number of gonocytes by 50% in 2- and 6-d-old neonates. The numbers of Sertoli and Leydig cells and the level of testicular testosterone production were unaffected, suggesting that estrogens act directly on the gonocytes. The increase in the number of gonocytes did not occur during fetal life but instead occurred just after birth, when gonocytes resumed mitosis and apoptosis. It seems to result from a decrease in the apoptosis rate evaluated by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method and cleaved caspase-3 immunohistochemical detection. Last, mice heterozygous for the ERβ gene inactivation behaved similarly to their ERβ−/− littermates in terms of the number of gonocytes, apoptosis, and mitosis, suggesting that these cells are highly sensitive to the binding of estrogens to ERβ. ERα inactivation had no effect on the number of neonatal gonocytes and Sertoli cells. In conclusion, this study provides the first demonstration that endogenous estrogens can physiologically inhibit germ cell growth in the male. This finding may have important implications concerning the potential action of environmental estrogens.
Direct and Indirect Effects of Aldosterone on Cyclooxygenase-2 and Interleukin-6 Expression in Rat Cardiac Cells in Culture and after Myocardial Infarction
Authors: Rebsamen Michela C. , Perrier Emeline , Gerber-Wicht Christine , Benitah Jean-Pierre , Lang Ursula 
Published: March 2004

Abstract
Aldosterone contributes to cardiac failure, which is associated with induction of inflammatory mediators. Moreover, aldosterone was shown to induce a vascular inflammatory phenotype in the rat heart. Using Western blotting and/or real-time RT-PCR, we examined the effect of aldosterone on the expression of the proinflammatory molecules, cyclooxygenase-2 (COX-2), and IL-6 in neonatal rat ventricular cardiac myocytes and fibroblasts as well as in adult cardiomyocytes after myocardial infarction. In cardiomyocytes, aldosterone induced COX-2 but not IL-6 expression. After 4–18 h of stimulation with 1 μm aldosterone, a significant increase in COX-2 protein expression was observed, preceded by an increase of COX-2 mRNA levels. After 18 h treatment, 100 nm and 1 μm aldosterone increased COX-2 protein amount by 2- and 4-fold, respectively. Consistently, aldosterone increased by 2.5-fold prostaglandin E2 secretion in cardiomyocytes. In cardiac fibroblasts, aldosterone increased neither COX-2 nor IL-6 mRNA expression. Interestingly, prostaglandin E2 (100 nm) strongly induced both proinflammatory molecules in fibroblasts and cardiomyocytes. Our results indicate that aldosterone directly induces COX-2 expression in cardiomyocytes and suggest that the subsequent increase in prostaglandin secretion may act in an autocrine and/or paracrine manner inducing in turn COX-2 and IL-6 expression. In vivo, myocardial infarction strongly increased both COX-2 and IL-6 expression in ventricular cardiomyocytes. Administration of the aldosterone antagonist RU28318 completely prevented COX-2 induction by infarction and partially inhibited the increase in IL-6 mRNA. These data suggest that after myocardial infarction, mineralocorticoid receptor activity is responsible for COX-2 induction and indirectly participates in IL-6 expression in cardiomyocytes.
Loss-of-Function Mutation of the Galanin Gene Is Associated with Perturbed Islet Function in Mice
Authors: Ahrén Bo , Pacini Giovanni , Wynick David , Wierup Nils , Sundler Frank 
Published: March 2004

AbstractThe neuropeptide galanin is expressed in sympathetic nerve terminals that surround islet cells and inhibits insulin secretion. To explore its role for islet function, we studied mice with a loss-of-function mutation in the galanin gene [galanin knockout (KO) mice]. Intravenous 2-deoxy-glucose, which activates both the sympathetic and parasympathetic branches of the autonomic nervous system, caused an initial (1–5 min) inhibition of insulin secretion that was impaired in galanin KO mice (P = 0.027), followed by a subsequent stimulation of insulin secretion that was augmented in galanin KO mice (P &lt; 0.01). Similar effects were seen after chemical sympathectomy by 6-hydroxydopamine. In contrast, galanin KO mice had a reduced insulin response to glucose, both in vivo (P &lt; 0.001) and in isolated islets (P &lt; 0.001), and to arginine, both in vivo (P = 0.012) and in vitro (P = 0.018). During an iv glucose tolerance test, galanin KO mice had impaired glucose disposal (P = 0.005) due to a reduced insulin response (P &lt; 0.001) and a reduced insulin-independent glucose elimination (glucose effectiveness; P = 0.040). Insulin sensitivity, as judged by a euglycemic, hyperinsulinemic clamp technique, was slightly increased in galanin KO mice (P = 0.032). We conclude that 1) galanin may contribute to sympathetic influences inhibiting insulin secretion in mice, and 2) galanin KO mice have a reduced glucose-induced insulin secretion.
Minireview: Gut Peptides Regulating Satiety
Authors: Druce Maralyn R. , Small Caroline J. , Bloom Stephen R. 
Published: March 2004

Abstract
The gastrointestinal tract and the pancreas release hormones regulating satiety and body weight. Ghrelin stimulates appetite, and glucagon-like peptide-1, oxyntomodulin, peptide YY, cholecystokinin, and pancreatic polypeptide inhibit appetite. These gut hormones act to markedly alter food intake in humans and rodents. Obesity is the current major cause of premature death in the United Kingdom, killing almost 1000 people per week. Worldwide, its prevalence is accelerating. There is currently no effective answer to the pandemic of obesity, but replacement of the low levels of peptide YY observed in the obese may represent an effective antiobesity therapy.
Physical and Functional Interaction of Growth Hormone and Insulin-Like Growth Factor-I Signaling Elements
Authors: Huang Yao , Kim Sung-Oh , Yang Ning , Jiang Jing , Frank Stuart J. 
Published: March 2004

AbstractGH and IGF-I are critical regulators of growth and metabolism. GH interacts with the GH receptor (GHR), a cytokine superfamily receptor, to activate the cytoplasmic tyrosine kinase, Janus kinase 2 (JAK2), and initiate intracellular signaling cascades. IGF-I, produced in part in response to GH, binds to the heterotetrameric IGF-I receptor (IGF-IR), which is an intrinsic tyrosine kinase growth factor receptor that triggers proliferation, antiapoptosis, and other biological actions. Previous in vitro and overexpression studies have suggested that JAKs may interact with IGF-IR and that IGF-I stimulation may activate JAKs. In this study, we explore interactions between GHR-JAK2 and IGF-IR signaling pathway elements utilizing the GH and IGF-I-responsive 3T3-F442A and 3T3-L1 preadipocyte cell lines, which endogenously express both the GHR and IGF-IR. We find that GH induces formation of a complex that includes GHR, JAK2, and IGF-IR in these preadipocytes. The assembly of this complex in intact cells is rapid, GH concentration dependent, and can be prevented by a GH antagonist, G120K. However, it is not inhibited by the kinase inhibitor, staurosporine, which markedly inhibits GHR tyrosine phosphorylation. Moreover, complex formation does not appear dependent on GH-induced activation of the ERK or phosphatidylinositol 3-kinase signaling pathways or on the tyrosine phosphorylation of GHR, JAK2, or IGF-IR. These results suggest that GH-induced formation of the GHR-JAK2-IGF-IR complex is governed instead by GH-dependent conformational change(s) in the GHR and/or JAK2. We further demonstrate that GH and IGF-I can synergize in acute aspects of signaling and that IGF-I enhances GH-induced assembly of conformationally active GHRs. These findings suggest the existence of previously unappreciated relationships between these two hormones.
Photomagnetic Co–Fe Prussian Blue Thin Films Fabricated by the Modified Langmuir–Blodgett Technique
Authors: Yamamoto Takashi , Umemura Yasushi , Sato Osamu , Einaga Yasuaki 
Published: March 2004

Abstract
Co–Fe Prussian blue thin films have been prepared by means of a modified Langmuir–Blodgett technique, in which the hybrid monolayer composed of amphiphiles and clay platelets plays a template role for the formation Co–Fe Prussian blue thin films. Photoinduced magnetization was observed in the thin films as observed in the bulk Co–Fe Prussian blue. To the best of our knowledge, this is the first example of successful formation of Co–Fe Prussian blue thin films, which possess the ordered structure and, in addition, exhibit photoinduced magnetization.
Weight Gain Mitigation with Topiramate in Mood Disorders
Authors: Woods Tonja M , Eichner Samantha F , Franks Andrea S 
Published: March 2004

OBJECTIVE To review the evidence of weight loss with use of topiramate in patients with mood disorders. DATA SOURCES Literature search included MEDLINE (1966—December 2003), International Pharmaceutical Abstracts (1970–December 2003), and EMBASE (1980—December 2003). Search terms included topiramate, weight loss, adverse effect, mood disorders, bipolar disorder. DATA SYNTHESIS Weight gain is a common adverse effect of many agents used to treat mood disorders. Topiramate has been evaluated in the management of some mood disorders, and weight loss may be a beneficial side effect in these patients. Case reports, letters to the editor, prospective investigations, and retrospective observational studies were reviewed to identify evidence of weight loss with topiramate use in patients with mood disorders. CONCLUSIONS Current evidence suggests an association between topiramate and weight loss. Based on the limited data, controlled studies need to be conducted to define the role of topiramate in patients with mood disorders who would also benefit from weight reduction.
Parecoxib for Parenteral Analgesia in Postsurgical Patients
Authors: Amabile Celene M , Spencer Anne P 
Published: March 2004

OBJECTIVE To review the pharmacology, pharmacokinetics, clinical efficacy and safety studies, adverse effects, drug interactions, and dosage and administration of parecoxib sodium, a selective cyclooxygenase-2 (COX-2) inhibitor. DATA SOURCES Information was obtained from MEDLINE searches of the English-language literature (1996—May 2003). Search terms included parecoxib, parecoxib sodium, SC-69124A, and selective cyclooxygenase-2 inhibitor. STUDY SELECTION AND DATA EXTRACTION We reviewed available literature, which included abstracts, clinical trials, and data on file with the manufacturer. DATA SYNTHESIS Parecoxib sodium is a novel selective COX-2 inhibitor under development for parenteral administration. It has produced efficacious analgesia following dental, gynecologic, and orthopedic surgery. The adverse effect profile has been compared with that of ketorolac; no statistically significant differences were identified. There are no documented drug interactions when parecoxib is coadministered with midazolam, propofol, or unfractionated heparin. CONCLUSIONS Parecoxib sodium is in the final stages of Phase III trials and has a favorable safety and efficacy profile. Its place in moderate to severe postsurgical pain management will be further defined when more pharmacoeconomic and postmarketing safety data are available. Theoretical benefits are its lower potential for gastrointestinal adverse effects compared with ketorolac and lower opioid requirements after surgery.
Fenoldopam Versus Nitroprusside for the Treatment of Hypertensive Emergency
Authors: Devlin John W , Seta Maria L , Kanji Salmaan , Somerville Allison L 
Published: March 2004

BACKGROUND While sodium nitroprusside remains first-line therapy for hypertensive emergency (HEM), fenoldopam is increasingly being used because of its benign safety profile and potential renal protective effects. OBJECTIVE To compare the efficacy, safety, and cost of sodium nitroprusside versus fenoldopam for the treatment of HEM. METHODS This study was a retrospective analysis of consecutive patients with HEM admitted to a university-affiliated, level 1 trauma center from 1999 to 2001 and treated with either nitroprusside (n = 21) or fenoldopam (n = 22) for >30 minutes. Time to reach mean arterial pressure (MAP) goal, change in MAP over time, time to initiation of oral antihypertensive therapy, change in renal function, incidence of cyanide toxicity, and cost of therapy were compared between groups. RESULTS Demographic parameters were similar between groups, except renal failure, which was more prevalent in the fenoldopam group (10% vs 46%; p = 0.009). Neither the mean ± SD pretreatment MAP (nitroprusside 168 ± 19; fenoldopam 163 ± 19; p = 0.45), time to reach MAP goal (3.6 [0.4–30] vs 4 [1–22] h; p = 0.51), nor infusion duration (18 [0.7–113] vs 18 [3–74] h; p = 0.45) differed between the patient groups. Time to initiation of oral antihypertensive therapy was similar between nitroprusside- (4.5 h [0.5–22] and fenoldopam- (6.5 h [1–100] treated patients; p = 0.65). Additional intravenous antihypertensives were administered to 16 patients in each group (p = 0.80). Change in creatinine clearance and incidence of tachycardia did not differ between groups. No symptoms of cyanide toxicity were detected. Cost of drug therapy was greater with fenoldopam ($597.60, $199.20–6675.20); than nitroprusside ($2.66, $1.68–3.48; p < 0.001). CONCLUSIONS Treatment of HEM with fenoldopam appears to result in patient outcomes equivalent to those with nitroprusside but at a substantially higher cost. Further study is required to delineate the exact role of fenoldopam for treatment of HEM.
Thiazolidinedione-Induced Congestive Heart Failure
Authors: Cheng Alice YY , Fantus I George 
Published: March 2004

OBJECTIVE To report 2 cases of thiazolidinedione (TZD)-associated congestive heart failure (CHF). As of March 13, 2004, one of the cases may represent the first description of TZD-associated cardiomyopathy in humans. CASE SUMMARIES A 57-year-old obese white man with type 2 diabetes was treated with pioglitazone 30 mg/day and insulin. He had no prior history of CHF and had an excellent exercise tolerance. Over the first 4 weeks of pioglitazone therapy, the patient experienced significant weight gain and subsequently developed CHF and pulmonary edema. A 50-year-old obese white man with type 2 diabetes presented with cardiogenic shock. Rosiglitazone 4 mg once daily had been initiated 6 weeks prior to presentation. He had no prior history of cardiac disease, and investigations did not reveal a cause for the cardiogenic shock. Rosiglitazone therapy was discontinued on admission. He improved and was discharged 21 days later. DISCUSSION TZDs are oral agents used for the treatment of type 2 diabetes. TZD-associated CHF and pulmonary edema have been reported in patients with a prior history of CHF. These 2 cases highlight that this adverse event can occur even in the absence of any preexisting history of clinical heart failure or cardiac disease. The second case may represent the first description of TZD-associated cardiomyopathy in humans. In both cases, an objective causality assessment using the Naranjo probability scale revealed that the adverse drug reaction between cardiomyopathy and rosiglitazone in this patient was probable. CONCLUSIONS TZD should be considered as a cause in the differential diagnosis of CHF and pulmonary edema in patients without a prior history of clinical CHF or cardiac disease. Healthcare professionals should be aware of the possible association between TZDs and cardiomyopathy.
Holo-Transcobalamin Concentration and Transcobalamin Saturation Reflect Recent Vitamin B12 Absorption Better than Does Serum Vitamin B12
Authors: Bor Mustafa Vakur , Nexø Ebba , Hvas Anne-Mette 
Published: March 2004

AbstractBackground: We evaluated whether measurement of vitamin B12-saturated transcobalamin (holo-TC) concentrations or TC saturation (holo-TC:total TC) reflects active vitamin B12 absorption in healthy individuals and patients after vitamin B12 intake.Methods: We obtained blood samples from 31 healthy individuals (age range, 25–57 years) before (days −1 and 0) and after (days 1, 2, and 6) oral administration of three 9-μg doses of vitamin B12. The blood samples from seven patients (age range, 22–39 years) suspected to have decreased vitamin B12 absorption were obtained before and 1 day after the vitamin B12 intake. The blood samples were analyzed for vitamin B12, total TC, and holo-TC. The TC saturation was calculated.Results: Intraindividual variation was &lt;13% for all measured values, as calculated from samples removed on day −1 and 0. In healthy individuals (n = 31) after intake of vitamin B12, the maximum median (range) increase (as percentages and absolute values) was in TC saturation [52 (−2% to 128)% and 0.04 (0–0.23) as a fraction], closely followed by holo-TC concentrations [39 (0–108)% and 34 (0–149) pmol/L]. All but one healthy individual had an increase of ≥15% in these markers. Serum vitamin B12 showed a smaller increase [14 (−8 to 51)% and 36 (−27 to 290) pmol/L]. After vitamin B12 intake, three patients with Crohn disease had the lowest increases in holo-TC concentration (3, 7, and 14 pmol/L) and in TC saturation (0.004, 0.01, and 0.01) among patients and 30 healthy individuals.Conclusion: Holo-TC concentrations and TC saturation reflect normal vitamin B12 absorption better than does serum vitamin B12.
Blind separation of delayed instantaneous mixtures: a cross‐correlation based approach
Authors: Z. Ikram Muhammad 
Published: March 2004

AbstractA cross‐correlation based method is proposed for blind separation of statistically uncorrelated i.i.d. signals. In contrast to much of the existing work in the area, the proposed method allows the separation of more sources than sensors and the sensors are not restricted to have non‐Gaussian distributions. The mixed signals are modelled as a sum of attenuated and delayed source signals. As compared to the delayless mixture model commonly employed in the literature, incorporating delays in the model may offer better fit to practical applications, such as source separation in an anechoic environment. We estimate the delay and attenuation parameters from the peak locations and strengths of the cross‐correlation function, respectively. Using these parameters, we then discuss the use of four methods for the recovery of source signals. These methods are compared and their usage is proposed under different operating conditions. Copyright © 2004 John Wiley & Sons, Ltd.
Blind separation of convolutive mixtures of cyclostationary signals
Authors: Wang Wenwu , Jafari Maria G. , Sanei Saeid , Chambers Jonathon A. 
Published: March 2004

AbstractAn adaptive blind source separation algorithm for the separation of convolutive mixtures of cyclostationary signals is proposed. The algorithm is derived by applying natural gradient iterative learning to a novel cost function which is defined according to the wide sense cyclostationarity of signals and can be deemed as a new member of the family of natural gradient algorithms for convolutive mixtures. A method based on estimating the cycle frequencies required for practical implementation of the proposed algorithm is presented. The efficiency of the algorithm is supported by simulations, which show that the proposed algorithm has improved performance for the separation of convolved cyclostationary signals in terms of convergence speed and waveform similarity measurement, as compared to the conventional natural gradient algorithm for convolutive mixtures. Copyright © 2004 John Wiley & Sons, Ltd.
Severe hemolytic anemia due to cold agglutinin complicating untreated chronic hepatitis C: Efficacy and safety of anti‐CD20 (rituximab) treatment
Authors: Etienne Anne , Gayet Stéphane , Vidal Florian , Poullin Pascale , Brunet Corinne , Harlé Jean‐Robert , Kaplanski Gilles 
Published: March 2004

AbstractAutoimmune hemolytic anemia (AIHA) is rare and difficult to treat during chronic hepatitis C. We report herein the case of a hepatitis C patient with severe and resistant AIHA who experienced a good and sustained response with anti‐CD20 monoclonal antibody treatment. Am. J. Hematol. 75:243–245, 2004. © 2004 Wiley‐Liss, Inc.
Direct demonstration of iron in a term placenta in two cases of β‐thalassemia
Authors: Artico M. , Ballati G. , Bosco S. , Cantarelli D. , Nagar G. , Grosso A. , Leali F.M. Tranquilli , Cavallotti C. 
Published: March 2004

AbstractThe aim of this study was to quantify iron in the placentas at the end of pregnancy in two patients suffering from β‐thalassemia and compare the data to that recorded from the placentas of healthy women. Iron was quantified in placental specimens taken after the delivery. The specimens were subjected to chemical treatments in order to remove extracellular iron and leave the intracellular iron intact. After coloration, each specimen was subjected to quantitative analysis of images in order to identify and quantify iron. Our results demonstrated that in β‐thalassemia there is an accumulation of iron in the outer basal cytoplasm of the epithelial cells of placental cotyledons. Am. J. Hematol. 75:241–242, 2004. © 2004 Wiley‐Liss, Inc.