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We determined the prevalence of incidental extracardiac findings (IEF) at Magnetic Resonance Imaging (MRI) potentially related to anemia and hypoxia in age- and sex-matched populations (N = 318) with thalassemia major (TM) and thalassemia intermedia (TI) enrolled in the Myocardial Iron Overload in Thalassemia network. Overall, IEFs were detected in 33.3% and 25.8% of patients with TI and TM, respectively (P = 0.114). TI and TM patients had elevated but comparable prevalence of renal, splenic and liver cysts, and vertebral hemangiomas while TI patients had a significant higher frequency of extramedullary hematopoiesis (EMH) (15.1% vs 4.4%; P = 0.002). The prevalence of total IEFs increased with advancing age. TI non-transfusion-dependent patients had a significantly lower frequency of renal cysts than TI transfusion-dependent patients (8.8% vs 26.4%; P = 0.005). The prevalence of renal cysts in the thalassemic population was significantly higher than that in the general population (19.2% vs 1.9%; P < 0.0001). Our data on renal cysts indicate a significant higher prevalence of these IEFs compared to the general population, suggesting the role of the inappropriate activation of the hypoxia-inducible factor system linked to the chronic hypoxia. The significant prevalence of IEF in thalassemia patients undergoing MRI for iron quantification should prompt the discussion of the inclusion of IEF in the MRI report. [ABSTRACT FROM AUTHOR]

Objectives: To assess the transferability of the magnetic resonance imaging (MRI) multislice multiecho T2* technique for pancreatic iron overload assessment.Methods: Multiecho T2* sequences were installed on ten 1.5-T MRI scanners of the three main vendors. Five healthy subjects (n = 50) were scanned at each site. Five patients with thalassemia (n = 45) were scanned locally at each site and were rescanned at the reference site within 1 month. T2* images were analyzed using a previously validated software and the global pancreatic T2* value was calculated as the mean of T2* values over the head, body, and tail.Results: T2* values of healthy subjects were above 26 ms and showed inter-site homogeneity. The T2* values measured in the MRI sites were comparable to the correspondent values observed in the reference site (12.02 ± 10.20 ms vs 11.98 ± 10.47 ms; p = 0.808), and the correlation coefficient was 0.978 (p < 0.0001). Coefficients of variation (CoVs) ranged from 4.22 to 9.77%, and the CoV for all the T2* values independently from the sites was 8.55%. The intraclass correlation coefficient (ICC) for each MRI site was always excellent and the global ICC was 0.995, independently from the sites. The mean absolute difference in patients with pancreatic iron (n = 39) was -0.15 ± 1.38 ms.Conclusion: The gradient-echo T2* MRI technique is an accurate and reproducible means for the quantification of pancreatic iron and may be transferred among MRI scanners by different vendors in several centers.Key Points: • The gradient-echo T2* MRI technique is an accurate and reproducible means for the quantification of pancreatic iron. • The gradient-echo T2* MRI technique for the quantification of pancreatic iron may be transferred among MRI scanners by different vendors in several centers. • Pancreatic iron might serve as an early predictor of cardiac siderosis and is the strongest overall predictor of glucose dysregulation. [ABSTRACT FROM AUTHOR]

Background: Hypertrophic cardiomyopathy (HCM), the most common genetic heart disease, is characterized by heterogeneous phenotypic expression. Body mass index has been associated with LV mass and heart failure symptoms in HCM. The aim of our study was to investigate whether regional (trunk, appendicular, epicardial) fat distribution and extent could be related to hypertrophy severity and pattern in HCM. Methods: Cardiovascular magnetic resonance was performed in 32 subjects with echocardiography-based diagnosis of HCM (22M/10F, 57.2±12.6 years) characterized by predominant hypertrophy at the interventricular septum (IVS). Regional fat distribution was assessed by dual-energy X-ray absorptiometry. Results: Gender differences were detected in maximum IVS thickness (M: 18.3±3.8 mm vs. F: 14.3±4 mm, p = 0.012), right ventricle (RV) systolic function (M: 61.3±6.7%; F: 67.5±6.3%, p = 0.048), indexed RV end-diastolic (M: 64.8±16.3 ml/m2; F: 50.7±15.5 ml/m2, p = 0.04) and end-systolic volumes (M: 24.3±8.3 ml/m2; F: 16.7±7.4 ml/m2, p = 0.04). After adjusting for age and gender, maximum IVS thickness was associated with truncal fat (Tr-FAT) (β = 0.43, p = 0.02), but not with either appendicular or epicardial fat. Epicardial fat resulted independently associated with NT-proBNP levels (β = 0.63, p = 0.04). Late Gadolinium Enhancement-positive subjects displayed greater maximum IVS thickness (p = 0.02), LV mass index (p = 0.015) and NT-proBNP levels (p = 0.04), but no associations with fat amount or distribution were observed. Conclusion: Truncal, but not appendicular or epicardial fat amount, seems to be related with maximum IVS thickness, the hallmark feature in our cohort of HCM patients. Further prospective researches are needed to assess a potential causative effect of central adiposity on HCM phenotype. [ABSTRACT FROM AUTHOR]

Accumulation of fat at ectopic sites has been gaining attention as pivotal contributor of insulin resistance, metabolic syndrome and related cardiovascular complications. Intermuscular adipose tissue (IMAT), located between skeletal muscle bundles and beneath muscle fascia, has been linked to physical inactivity, ageing and body mass index, but little is known about its relationship with the other AT compartments, in particular with increasing age. To address this issue, erector spinae IMAT, epicardial (EAT), intraabdominal (IAAT) and abdominal subcutaneous adipose tissue (SAT) were simultaneously measured by Magnetic Resonance Imaging (MRI) and related to waist circumference measurements and age in 32 sedentary subjects without cardiovascular disease (18 men; 14 women; mean age 48.5±14 years). Fasting glucose, triglycerides and HDL-cholesterol were also assessed. We observed that, after dividing individuals according to age (≤ or >50 years), IMAT and EAT depots were significantly more expanded in older subjects (63.2±8.3 years) than in the younger ones (38.4±5.2 years) (p<0.001). Overall, both IMAT and EAT showed stronger positive associations with increasing age (β = 0.63 and 0.67, respectively, p<0.001 for both) than with waist circumference (β = 0.55 and 0.49, respectively, p<0.01 for both) after adjusting for gender. In addition, the gender-adjusted associations of IMAT and EAT with waist circumference and IAAT were significant in individuals ≤50 years only (p<0.05 for all) and not in the older ones. In contrast, no age-related differences were seen in the relationships of IAAT and SAT with waist circumference. Finally, serum triglycerides levels turned out not to be independently related with ectopic IMAT and EAT. In conclusion, the expansion of IMAT and EAT in sedentary subjects is more strongly related to age than waist circumference, and a positive association of these ectopic depots with waist circumference and IAAT amount can be postulated in younger individuals only. [ABSTRACT FROM AUTHOR]

Introduction: Left ventricular thrombosis (LVT) is a possible complication of acute myocardial infarction. Aim of our study was to evaluate incidence and clinical characteristics of patients with LVT after ST elevation myocardial infarction (STEMI) using contrast- enhanced magnetic resonance (CMR). Methods and Results: In a prospective cohort of 36 consecutive patients with STEMI acutely reperfused with primary percutaneous coronary intervention, CMR was performed within one week. LVT was found in 7 patients (19%), and was located in left ventricle apex or adherent to antero-septum. Compared to the rest of population patients with LVT have lower ejection fraction (38 ± 7% versus 51 ± 6%, P = 0.009), larger left ventricle end systolic volume (95.8 ± 19 ml versus 68.9 ± 19 ml, P = 0.02), higher time to reperfusion (9.3 ± 7.2 versus 5 ± 3.6, P = 0.03) and left anterior descending artery was constantly involved (100% versus 41 %, P = 0.06). In 5 cases the LVT was also detected by echocardiography, however, in 2 cases it was missed. Conclusions: The incidence of LVT after STEMI is not negligible and was accurately detected by CMR. Localization of myocardial infarction, time to reperfusion, ejection fraction and left ventricle end systolic volume are the most important predictors of left ventricle thrombus formation. [ABSTRACT FROM AUTHOR]

Biliverdin reductase-A (BVR-A) is a pleiotropic enzyme and plays pivotal role in the antioxidant defense against free radicals as well as in cell homeostasis. Together with heme oxygenase, BVR-A forms a powerful system involved in the cell stress response during neurodegenerative disorders including Alzheimer's disease (AD), whereas due to the serine/threonine/tyrosine kinase activity the enzyme regulates glucose metabolism and cell proliferation. In this paper, we report results that demonstrate BVR-A undergoes post-translational oxidative and nitrosative modifications in the hippocampus, but not cerebellum, of subjects with AD and amnestic mild cognitive impairment (MCI). A significant increase of nitrated BVR-A was demonstrated only in AD and MCI hippocampi, whereas no significant modifications were found in cerebellar tissue. In addition, a significant reduction in protein carbonyl-derivatives of BVR-A was found in both AD and MCI hippocampi (15% and 18%, respectively). Biliverdin reductase-bound 4-hydroxynonenals were not modified in hippocampi and cerebella from AD and MCI subjects. These results supported the hypothesis of a prevalence of nitrosative stress-induced modifications on BVR-A structure, and this evidence was confirmed by a significant upregulation of inducible nitric oxide synthase in hippocampal tissue of subjects with AD and MCI that was not present in cerebellum. In conclusion, nitrosative stress-induced modifications on hippocampal BVR-A are an early event in the pathogenesis of AD since they appear also in MCI subjects and could contribute to the antioxidant and metabolic derangement characteristic of these neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

Biliverdin reductase-A (BVR-A) is a pleiotropic enzyme and plays pivotal role in the antioxidant defense against free radicals as well as in cell homeostasis. Together with heme oxygenase, BVR-A forms a powerful system involved in the cell stress response during neurodegenerative disorders including Alzheimer's disease (AD), whereas due to the serine/threonine/tyrosine kinase activity the enzyme regulates glucose metabolism and cell proliferation. In this paper, we report results that demonstrate BVR-A undergoes post-translational oxidative and nitrosative modifications in the hippocampus, but not cerebellum, of subjects with AD and amnestic mild cognitive impairment (MCI). A significant increase of nitrated BVR-A was demonstrated only in AD and MCI hippocampi, whereas no significant modifications were found in cerebellar tissue. In addition, a significant reduction in protein carbonyl-derivatives of BVR-A was found in both AD and MCI hippocampi (15% and 18%, respectively). Biliverdin reductase-bound 4-hydroxynonenals were not modified in hippocampi and cerebella from AD and MCI subjects. These results supported the hypothesis of a prevalence of nitrosative stress-induced modifications on BVR-A structure, and this evidence was confirmed by a significant upregulation of inducible nitric oxide synthase in hippocampal tissue of subjects with AD and MCI that was not present in cerebellum. In conclusion, nitrosative stress-induced modifications on hippocampal BVR-A are an early event in the pathogenesis of AD since they appear also in MCI subjects and could contribute to the antioxidant and metabolic derangement characteristic of these neurodegenerative disorders. [ABSTRACT FROM AUTHOR]

J. Neurochem. (2010) 113, 563–575. The importance of stress in modifying human behavior and lifestyle is no longer a matter of debate. Although mild stress enhances the immune response and prevents infections, prolonged stress seems to play pathogenic roles in depression and neurodegenerative disorders. The body has developed an adaptive stress response consisting of cardiovascular, metabolic, and psychological changes, which act in concert to eliminate stressors. One of the major components of this response is the hypothalamic–pituitary–adrenal axis, also known as the stress axis. Over the last 30 years, many studies have documented the integrated stress-axis regulation by neurotransmitters. They have also demonstrated that gaseous neuromodulators, such as NO, CO, and H2S, regulate the hypothalamic release of neuropeptides. The specific effects (stimulatory vs. inhibitory) of these gases on the stress axis varies, depending on the type of stress (neurogenic or immuno-inflammatory), its intensity (low or high), and the species studied (rodents or humans). This review examines the complex roles of NO, CO, and H2S in modulation of stress-axis activity, with particular emphasis on the regulatory effects they exert at the hypothalamic level. [ABSTRACT FROM AUTHOR]

Iatrogenic pelvic pseudoaneurysm with concomitant arteriovenous fistula has been described as a rare and challenging complication, which may occur during transurethral resection of the prostate. We provide the first report of this complication after holmium laser enucleation of the prostate for the treatment of benign prostatic hyperplasia. The attempt to control the bleeding by conversion to open surgery and placement of haemostatic stitches into the prostatic fossa failed. Angiography with superselective arterial embolization proved to be a modern, quick, safe, and efficient treatment of this uncommon complication. [ABSTRACT FROM AUTHOR]

Bilirubin-IX-α (BR) is an endogenous molecule with a strong antioxidant feature due to its ability to scavenge free radicals. In this paper, we demonstrated that BR, at concentrations close to those found within the cell (0.1–2.5 μM), acted as a denitrosylating agent and increased the release of nitric oxide from S-nitrosoglutathione (GSNO) and S-nitrosocysteine (SNOC) (2.5 μM). The complexation of BR with saturating concentrations of human serum albumin (HSA, 2.5 μM) did not further increase nitric oxide release from GSNO and SNOC. At concentrations similar to those reached in plasma (5–20 μM), BR denitrosylated S-nitroso-HSA (2.5 μM), the main circulating S-nitrosothiol, and this effect was potentiated by the complexation of BR with saturating HSA (20 μM). Furthermore, the product(s) of the reaction between nitric oxide and BR were identified. Ultraviolet and mass spectrometry analysis revealed that nitric oxide binds to BR forming a N-nitroso derivative (BR–nitric oxide) with extinction coefficients of 1.393 mM−1cm−1 and 2.254 mM−1cm−1 in methanol and NaOH, respectively. The formation of BR–nitric oxide did not occur only in a reconstituted system, but was confirmed in rat fibroblasts exposed to pro-oxidant stimuli. These results provided novel insights on the antioxidant characteristic of BR through its interaction with nitric oxide, a gaseous neurotransmitter with a well-known dual effect, namely neuroprotective under physiological conditions or neurotoxic if produced in excess, and proposed BR–nitric oxide as a new biomarker of oxidative/nitrosative stress. [ABSTRACT FROM AUTHOR]

KCNQ2 and KCNQ3 subunits encode for the muscarinic-regulated current (IKM), a sub-threshold voltage-dependent K+ current regulating neuronal excitability. In this study, we have investigated the involvement of IKM in dopamine (DA) release from rat striatal synaptosomes evoked by elevated extracellular K+ concentrations ([K+]e) and by muscarinic receptor activation. [3H]dopamine ([3H]DA) release triggered by 9 mmol/L [K+]e was inhibited by the IKM activator retigabine (0.01–30 μmol/L; Emax = 54.80 ± 3.85%; IC50 = 0.50 ± 0.36 μmol/L). The IKM blockers tetraethylammonium (0.1–3 mmol/L) and XE-991 (0.1–30 μmol/L) enhanced K+-evoked [3H]DA release and prevented retigabine-induced inhibition of depolarization-evoked [3H]DA release. Retigabine-induced inhibition of K+-evoked [3H]DA release was also abolished by synaptosomal entrapment of blocking anti-KCNQ2 polyclonal antibodies, an effect prevented by antibody pre-absorption with the KCNQ2 immunizing peptide. Furthermore, the cholinergic agonist oxotremorine (OXO) (1–300 μmol/L) potentiated 9 mmol/L [K+]e-evoked [3H]DA release ( Emax = 155 ± 9.50%; EC50 = 25 ± 1.80 μmol/L). OXO (100 μmol/L)-induced [3H]DA release enhancement was competitively inhibited by pirenzepine (1–10 nmol/L) and abolished by the M3-preferring antagonist 4-diphenylacetoxy N-methylpiperidine methiodide (1 μmol/L), but was unaffected by the M1-selective antagonist MT-7 (10–100 nmol/L) or by Pertussis toxin (1.5–3 μg/mL), which uncouples M2- and M4-mediated responses. Finally, OXO-induced potentiation of depolarization-induced [3H]DA release was not additive to that produced by XE-991 (10 μmol/L), was unaffected by retigabine (10 μmol/L), and was abolished by synaptosomal entrapment of anti-KCNQ2 antibodies. Collectively, these findings indicate that, in rat striatal nerve endings, IKM channels containing KCNQ2 subunits regulate depolarization-induced DA release and that IKM suppression is involved in the reinforcement of depolarization-induced DA release triggered by the activation of pre-synaptic muscarinic heteroreceptors. [ABSTRACT FROM AUTHOR]

1 The involvement of adenosine triphosphate (ATP) and carbon monoxide (CO) in the non-nitrergic ncinpeptidergic component of high-frequency electrical field stimulation (EFS)-induced nonadrenergic noncholinergic (NANC) relaxation of lotigitudinal muscle strips from the rat gastric fundus was investigated. 2 Under NANC conditions (1 μM atropine + 5 μM guanethidine). N6-nitro-L-arginine methyl ester (L-NAME. 1 mM) slightly reduced the amplitude, but did not affect the area under the curve (ALIC) of EFS (13 Hz. 2min)-induced relaxation of 9.1 l-dideoxy-9α,11α-methanoepoxy prosiaglandin F2α (U46619. 0.1 μM)-precontracted strips. With L-NAME (1 mM) plus α-chymotrypsin (1 U ml-2). The amplitude and the AUC of relaxation were reduced to approximately two-third and one-third of controls, respectively. 3 Pyridoxal-phosphate-6-azophcnyl-2',4'-disulphonic acid (100 μM). apamin (0.3 μM). desensitization to ATP, suramin (100 μM). zinc protoporphirin IX (300 μM) or ferrous haemoglobin (100 μm) did not inhibit the component of relaxation resistant to L-NAME plus α-chymotrypsin, 4 L-NAME (1 μM) plus anti-vasoactive intestinal peptide (VIP) serum (1:100) reduced the amplitude and the AUC of relaxation to a similar extent as L-NAME (1 mM) plus α-chymotrypsin (1 U ml-1). Adding apamin (0.1 μM) to L-NAME (1 mM) plus anti-VIP serum ( 1 : 100) further reduced the amplitude and the AUC of relaxation. 5 These findings suggest that the non-nitrergic nonpeplidergic component of NANC relaxation of the rat gastric fundus induced by high-frequency stimulation is mediated by a neurotransniitter that acts through apamin-sonsitive mechanisms, that is neither ATP nor CO. [ABSTRACT FROM AUTHOR]

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The costs associated with the development of new drugs have increased dramatically in recent years, and fewer truly innovative drugs are making their way to the market. The reversal of this trend has therefore become an urgent priority for the pharmaceutical industry. What are the factors that contribute to these costs, and to what extent can they be effectively controlled? Does the solution lie in new technologies? How is the industry dealing with these problems? And what are the ethical implications of these trends? [ABSTRACT FROM AUTHOR]

KCNQ subunits encode for the M current (I[subKM]), a neuron-specific voltage-dependent K[sup+] current with a well established role in the control of neuronal excitability. In this study, by means of a combined biochemical, pharmacological, and electrophysiological approach, the role of presynaptic I[subKM] in the release of previously taken up tritiated norepineprine (NE), GABA, and D-aspartate (D-ASP) from hippocampal nerve terminals (synaptosomes) has been evaluated. Retigabine (RT) (0.01-30 µM), a specific activator of I[subKM], inhibited [³H]NE, [³H]D-ASP, and [³H]GABA release evoked by 9 mM extracellular K[sup+] ([K[sup+][sube]). RT-induced inhibition of [³H]NE release was prevented by synaptosomal entrapment of polyclonal antibodies directed against KCNQ2 subunits, an effect that was abolished by antibody preabsorption with the KCNQ2 immunizing peptide; antibodies against KCNQ3 subunits were ineffective. Flupirtine (FP), a structural analog of RT, also inhibited 9 mM [K[sup+][sube] RT-induced [³H]NE release, although its maximal inhibition was lower than that of RT. Electrophysiological studies in KCNQ2-transfected Chinese hamster ovary cells revealed that RT and FP (10 µM) caused a -19 and -9 mV hyperpolarizing shift, respectively, in the voltage dependence of activation of KCNQ2 K[sup+] channels. In the same cells, the cognition enhancer 10,10-bis (4-pyridinylmethyl)-9(10H)-anthracenone (XE-991) (10 µM) blocked KCNQ2 channels and prevented their activation by RT (1-10 µM). Finally, both XE-991 (10-100 µM) and tetraethylammonium ions (100 µM) abolished the inhibitory effect of RT (1 µM) on [³H]NE release. These findings provide novel evidence for a major regulatory role of KCNQ2 K[sup+] channel subunits in neurotransmitter release from rat hippocampal nerve endings. [ABSTRACT FROM AUTHOR]

Hemangiomas are slowly growing benign vascular tumours which rarely involve the kidney. They usually occur in the mucosa or subepithelial tissue of the pelvis, in the pyramid of the kidney and in the cortex. We report a case of cavernous hemangioma presenting as a solid, paradoxically avascular mass of the right renal hilum.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Our objective was to analyze fast-field-echo dynamic subtracted (FFE/DS) MRI data in prostate cancer, in order to recognize enhancement patterns of tumoral tissue in comparison with non-tumoral peripheral prostatic tissue. Eleven consecutive patients with prostate cancer were proposed for radical prostatectomy. Before surgery, all patients underwent endorectal coil MRI examination. In addition to standard sequences, a dynamic study was performed by FFE/DS to evaluate tumoral behavior after Gd-DTPA rapid infusion. Analysis of the imaging was made by the means of the time/signal intensity curve obtained during early contrast medium enhancement, sampling both the abnormal enhancing focal area and the opposite lobe at the level of the main prostatic tissue. A focal area of increased enhancement was observed in the site of the tumor in all cases. The time/intensity curve sampled on this area and compared with the opposite lobe demonstrated a high confidence interval of the difference of the data: mean tumor maximal intensity 1331 (SD 187) vs normal 470 (SD 139) and mean tumor rise time 103 s (SD 30) vs normal 250 (SD 38; p<0.01). In tumoral tissue, the enhancement percentage of signal intensity (SI%=pre-contrast minus post-contrast/pre-contrast x100) was 316.7%. At FFE/DS, there is a typical behavior of the time/intensity curve of contrast enhancement in prostatic cancer that might be employed in diagnosis of the disease. [ABSTRACT FROM AUTHOR]

The role of peptide histidine isoleucine (PHI) as a neurotransmitter of the inhibitory motor neurones, the physiological role of PHI and vasoactive intestinal polypeptide (VIP) in the non-adrenergic non-cholinergic (NANC) relaxation and the relative amounts of VIP- and PHI-like immunoreactivity (LI) co-released by neuronal activation were investigated in the rat gastric fundus. Longitudinal muscle strips from the rat gastric fundus precontracted by the thromboxane receptor agonist U46619 (0.1 µM) were studied in organ baths under conditions of muscarinic receptor blockade by atropine (1 µM) and adrenergic neurone blockade by guanethidine (5 µM) ("NANC conditions"). Concentration-response curves were plotted for both amplitude and area under the curve (AUC) of the relaxant responses induced by VIP (0.3 nM–0.3 µM), PHI (0.3 nM–1 µM) and peptide histidine valine [PHV(1–42); 0.3 nM–1 µM]. All three peptides were more potent in the curve based on amplitude than in that based on the AUC of relaxation. In addition, VIP was 5.3 and 7 times more potent than PHI and PHV(1–42), respectively, in producing relaxation expressed as amplitude, and 2.7 and 2.8 times, respectively, in producing relaxation expressed as AUC. PHI and PHV(1–42) behaved as partial agonists with respect to VIP in producing relaxation expressed as AUC. Electrical field stimulation (EFS; 120 mA, 1 ms, 4–32 Hz, pulse trains of 2 min) evoked frequency-dependent relaxant responses. α-Chymotrypsin (1 u/ml or 3 u/ml), an anti-VIP serum (1:100 or 1:50) and an anti-PHI serum (1:25), slightly reduced the amplitude, but greatly inhibited the AUC of the NANC relaxation induced by EFS (13 Hz) [approximately 72%, 47% and 28% less than that seen in time controls or with normal rabbit serum (1:100 or 1:25), respectively]. EFS (8–32 Hz) caused significant, frequency-dependent increases in the outflow of VIP- and PHI-LI from the strips. The EFS-induced release of VIP-LI was approximately 20% of the PHI-LI release. These findings indicate that PHI is involved in EFS-induced NANC relaxation of the rat gastric fundus, the major physiological role of VIP and PHI is the maintenance of smooth muscle relaxation and VIP is co-released in equimolar amounts mainly with PHI. [ABSTRACT FROM AUTHOR]

Abstract Erythropoietin (EPO), a renal cytokine regulating haematopoiesis, is also produced by different cell types within the central nervous system, where it acts via the activation of specific receptors. Current evidence shows that EPO exerts neurotrophic and neuroprotective activities in different in vivo and in vitro models of brain damage. In the present study we investigated the effects of EPO on primary cultures of rat cortical microglia and astrocytes. We found that: (i) EPO exerted a marked stimulatory effect on microglial cell viability, assessed through the MTS assay, whereas astrocytes were almost unaffected; (ii) the cytokine increased microglial cell population size in a concentration-dependent manner; however, as microglia cultures undergo spontaneous apoptosis after separation from astrocytes, the apparent effect on cell proliferation could be attributed to EPO antagonism of normal apoptosis; (iii) subsequent flow cytometry analysis on microglial cells demonstrated both the trophic role of factor(s) released by astrocytes in mixed cultures, and the putative anti-apoptotic action of EPO; (iv) the latter was further confirmed through the assessment of gene expression of anti- and pro-apoptotic factors, which showed that EPO is able to shift the Bcl : Bax ratio towards a net anti-apoptotic effect; (v) EPO did not affect the pro-inflammatory function of microglial cells. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the mechanisms through which bacterial lipopolysaccharide (LPS) stimulates prostaglandin (PG) production in rat hypothalamic astroglial cells in vitro. The latter were treated with LPS alone or LPS plus antagonists of the interleukin-1 (IL-1) and nitric oxide (NO) pathways, and the subsequent changes in cyclooxygenase (COX) activity were monitored by measuring a COX end-product, prostaglandin E2 (PGE2), released into the incubation medium. LPS produced a concentration-dependent increase in PGE2 release from astroglia after 24 h incubation; experiments with selective antagonists showed that the increase in PGE 2 release induced by LPS may be, at least in part, mediated by IL-1 and NO. [ABSTRACT FROM PUBLISHER]

The article presents an abstract on a paper titled "Incremental Value of Cardiac Magnetic Resonance in the Characterization of Patients Referred for Left Ventricular Non Compaction Evaluation," presented at the 2011 Society for Cardiovascular Magnetic Resonance (CMR)/Euro CMR Joint Scientific Sessions held in France.

Presents a correction to the article "Involvement of peptide histidine isoleucine in non-adrenergic non-cholinergic relaxation of the rat gastric fundus induced by high-frequency neuronal firing," published in a previous issue of the journal "Naunyn-Schmiedeberg's Archives of Pharmacology."