739 research outputs found
MEPACRINE PREVENTS PLATELET ACTIVATION BY H2O2
No full textThe effect of H2O2 is dependent on arachidonic acid metabolism because aspirin prevents H2O2-mediated platelet activation. Furthermore this activation seems to be dependent on arachidonic acid mobilization from platelet phospholipids by phospholipase A2 since mepacrine is able to block H2O2-mediated platelet activation
Monogenic epilepsies: Channelopathies, synaptopathies, mtorpathies, and otheropathies
No full textEpilepsy has been historically defined as the recurrence of two or more seizures, together with typical electroencephalogram (EEG) changes, and significant comorbidities, including cardiac and autonomic changes, injuries, intellectual disability, permanent brain damage, and higher mortality risk. Epilepsy may be the consequence of several causes, including genetic anomalies, structural brain malformations, hypoxic- ischemic encephalopathy, brain tumors, drugs, and all contributing factors to the imbalance between excitatory and inhibitory neurons and modulatory interneurons which in turn provoke abnormal, simultaneous electric discharge(s) involving part, or all the brain. In the pregenetic, pregenomic era, in most cases, the exact cause of such neuronal/interneuronal disequilibrium remained unknown and the term "idiopathic epilepsy"was used to define all the epilepsies without cause. At the same time, some specific epileptic syndromes were indicated by the eponym of the first physician who originally described the condition (e.g., the West syndrome, Dravet syndrome, Ohtahara syndrome, and Lennox-Gastaut syndrome) or by some characteristic clinical features (e.g., nocturnal frontal lobe epilepsy, absence epilepsy, and epilepsy and mental retardation limited to females). In many of these occurrences, the distinct epileptic syndrome was defined mainly by its most relevant clinical feature (e.g., seizure semiology), associated comorbidities, and EEGs patterns. Since the identification of the first epilepsy-associated gene (i.e., CHRNA4 gene: cholinergic receptor neuronal nicotinic α polypeptide 4), one of the genes responsible for autosomal dominant nocturnal frontal lobe epilepsy (currently known as sleep-related hypermotor epilepsy) in 1995, the field of epilepsy and the history of epilepsy gene discoveries have gone through at least three different stages as follows: (1) an early stage of relentless gene discovery inmonogenic familial epilepsy syndromes; (2) a relatively quiescent and disappointing period characterized by largely negative genome-wide association candidate gene studies; and (3) a genome-wide era in which large-scale molecular genetic studies have led to the identification of several novel epilepsy genes, especially in sporadic forms of epilepsy. As of 2021, more than 150 epilepsy-associated genes or loci are listed in the Online Mendelian Inheritance in Man database
Ongoing prothrombotic state in patients with antiphospholipid antibodies: A role for increased lipid peroxidation
No full textWe measured the urinary excretion of Isoprostane F2alpha-III and Isoprostane-F2alpha-VI, two markers of in vivo lipid peroxidation, and the circulating levels of the prothrombin fragment F1+2, a marker of thrombin generation, in 18 antiphospholipid antibodies-positive patients, in 18 antiphospholipid antibodies-negative patients with systemic lupus erythematosus, and in 20 healthy subjects. Furthermore, 12 patients positive for antiphospholipid antibodies were treated with (n = 7) or without (n = 5) antioxidant vitamins (vitamin E at 900 IU/d and vitamin C at 2, 000 mg/d) for 4 weeks. Compared with antiphospholipid antibodies-negative patients, antiphospholipid antibodies-positive patients had higher urinary values of Isoprostane-F2alpha-III (P =. 0001), Isoprostane-F2alpha-VI (P =.006), and plasma levels of the prothrombin fragment F1+2 (P =.0001). In antiphospholipid-positive patients, F1+2 significantly correlated with Isoprostane-F2alpha-III (Rho =.56, P =.017) and Isoprostane-F2alpha-VI (Rho =.61, P =.008). After 4 weeks of supplementation with antioxidant vitamins, we found a significant decrease in F1+2 levels (P <.005) concomitantly with a significant reduction of both Isoprostane-F2alpha-III (P =.007) and Isoprostane-F2alpha-VI (P <.005). No change of these variables was observed in patients not receiving antioxidant treatment. This study suggests that lipid peroxidation might contribute to the activation of clotting system in patients positive for antiphospholipid antibodies
Clinical Course of N-Methyl-D-Aspartate Receptor Encephalitis and the Effectiveness of Cyclophosphamide Treatment
No full textWe describe the cases of two unrelated girls, aged 5 and 7, respectively, affected by N-methyl-D-aspartate receptor (NMDAr) encephalitis. The clinical records of both patients were reviewed retrospectively including family and personal history, clinical findings, laboratory, and neuroradiological examinations, electroencephalogram, and treatment performed during admissions to the unit. In both patients, the clinical course was slow and progressive. Both showed anti-NMDAr antibodies in serum and cerebrospinal fluid. Treatment with intravenous immunoglobulin and methylprednisolone was not efficacious in the long term, with several relapses occurring in both patients. Second-line treatment with cyclophosphamide (1 g/m2 once a month) resulted in improvement of symptoms and disappearance of clinical signs that were sustained at 24 months follow-up. Side effects included neutropenia in one patient
Portal levels of the isoprostane F-2 alpha-III, a marker of lipid peroxidation, do not correlate with increased portal pressure in cirrhotic patients
No full textBackground: Isoprostane F-2 alpha-III(iPF(2 alpha)-III), a recently described member of a family of prostaglandin F-2 alpha isomers and a biologically active end-product of lipid peroxidation, has been reported to increase portal pressure in cirrhotic rats, We found that its urinary levels were elevated in cirrhotic patients. Methods: To investigate whether portal levels of iPF(2 alpha)-III were elevated in cirrhotic patients and whether there was a relationship between these levels and the portal pressure in the same patients, peripheral and portal plasma from cirrhotic patients (n=18) undergoing elective transjugular intrahepatic portosystemic shunt and appropriate controls (n=18) were assayed for iPF(2 alpha)-III levels by using a gas chromatography/mass spectrometry assay. Portal pressure was measured in all cirrhotic patients. Results: Cirrhotic patients had higher peripheral plasma levels of iPF(2 alpha)-III [78 (27-150) pg/mL] than controls [18(10-30)pg/mL] (P< 0.001). Portal IPF2 alpha-III levels were higher than plasma peripheral levels [129(50-375) pg/mL; P< 0.0001]. No correlation was found between peripheral and portal levels of iPF(2 alpha)-III (Rho=0.17, P=0.5), Portal levels of iPF(2 alpha)-III and portal pressure did not correlate (Rho=0.17, P= 0.49), Conclusions: This study shows that peripheral and portal levels of iPF(2 alpha)-III, marker of in vivo lipid peroxidation, are elevated in liver cirrhosis, There is no correlation between iPF(2 alpha)-III portal levels and the portal pressure observed in these patients. These findings suggest that this biologically active isoprostane does not directly contribute to the portal hypertension observed in hepatic cirrhosis
Augmented Information Discovery using NFC Technology within a Platform for Disaster Monitoring
No full textCatastrophic and accidental natural events (e.g., earthquakes, sudden floods, fires, etc.) and deficiencies in appropriate management activities require proper plans for disaster management and real-time definition of safe paths and escape routes. Emergencies can affect the structural health status of structures and infrastructures and, consequently, the safety in highly populated areas (e.g., urban contexts, occasional assembly points for crowds, theme parks, etc.) is compromised. Consequently, the use of a decision platform for the management of structures and infrastructures, which is able to gather real-time data from sensors and provide alerts and augmented information about safe paths, paves the way to the adoption of a proactive form of risk management. In this work, objectives were confined into the validation of a Near-Field Communication (NFC) system. Data coming from user smartphones using the NFC technology and sensor data deriving from the decision platform were used as input in a Machine Learning (ML) algorithm. Results show that the ML algorithm mentioned above is able to refine the safe path recognition strategy defined from the platform. In addition, the bidirectional and touch less NFC technology allows the delivery of alerts and disaster plan dissemination, also in the case of connectivity shutdown
Propofol for sedation in the intensive care unit: Comparitive evaluation of 1 and 2 formulations
No full textInhibition of cyclooxygenase-independent platelet aggregation by low vitamin E concentration.
No full textPlatelet aggregation induced by threshold concentrations of agonists such as collagen, PAF or epinephrine was inhibited in vitro by 100 microM aspirin but was restored by stimulating platelets with high concentrations of collagen, PAF or by a combination of epinephrine and PAF. Incubating aspirin-treated platelets with 50-100 microM vitamin E or vitamin E acetate inhibited platelet aggregation by high concentrations of collagen and PAF and by the combination of epinephrine and PAF; platelet thromboxane A2 formation was less than 10% in samples incubated with 100 microM aspirin. Apyrase, added to aspirin-treated platelet, did not influence platelet aggregation induced by epinephrine and PAF. The present study suggests that concentrations of vitamin E as low as 50-100 microM inhibit cyclooxygenase-independent platelet aggregation when combined with an inhibitor of the arachidonate pathway
Vitamin E reduces monocyte tissue factor expression in cirrhotic patients
No full textClotting activation may occur in liver cirrhosis, but the pathophysiological mechanism has not been fully elucidated. Because a previous study demonstrated that lipid peroxidation is increased in cirrhosis, we analyzed whether there is a relationship between lipid peroxidation and clotting activation. Thirty cirrhotic patients (19 men and 11 women; age, 34 to 79 years) and 30 controls matched for sex and age were investigated. In all subjects, monocyte expression of tissue factor (TF) antigen and activity; plasma levels of prothrombin fragment 1 + 2 (F1 + 2), a marker of thrombin generation; and urinary excretion of Isoprostane-F-2 alpha-III, a marker of lipid peroxidation, were measured. Furthermore, the above-reported variables were re-evaluated after 30 days of treatment with standard therapy (n = 5) or standard therapy plus 300 mg vitamin E twice daily (n = 9). In addition, we analyzed in vitro if vitamin E (50 mu mol/L) influenced monocyte TF expression and F1 + 2 generation. Cirrhotic patients had higher values of isoprostane-F2 alpha-III (P < .0001), F1 + 2 (P < .0001), and monocyte TF antigen (P < .0001) and activity (P <.03) than controls. Isoprostane-F-2 alpha-III was significantly correlated with F1 + 2 (Rho = 0.85; P < .0001) and TF antigen (Rho = 0.95; P < .0001) and activity (Rho = 0.94; P < .0001). After vitamin E treatment, Isoprostane-F2 alphaIII (P = .008), F1 + 2 (P < .008), and monocyte TF antigen (P = .012) and activity (P = .008) significantly decreased; no changes of these variables were detected in patients not receiving vitamin E. In vitro, vitamin E significantly reduced the expression of monocyte TF antigen (-52%; P = .001) and activity (-55%; P = .003), as well as F1 + 2 generation (-51%; P = .025), This study shows that vitamin E reduces both lipid peroxidation and clotting activation and suggests that lipid peroxidation may be an important mediator of clotting activation in liver cirrhosis. (C) 1999 by The American Society of Hematology
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