701 research outputs found

    Efficacy of lactoferrin oral administration in the treatment of anemia and anemia of inflammation in pregnant and non-pregnant women: an interventional study

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    The discovery of the ferroportin-hepcidin complex has led to a critical review on the treatment of anemia and anemia of inflammation (AI). Ferroportin, the only known mammalian iron exporter from cells to blood, is negatively regulated by hepcidin, a hormone peptide able to bind to ferroportin, leading to its degradation. Therefore, new efficient therapeutic interventions acting on hepcidin and ferroportin are imperative to manage anemia and AI. Bovine milk derivative lactoferrin (bLf), a glycoprotein able to chelate two ferric ions per molecule, is emerging as a natural anti-inflammatory substance able to modulate hepcidin and ferroportin synthesis through the down-regulation of interleukin-6 (IL-6). Here, an interventional study (ClinicalTrials.gov Identifier: NCT01221844) was conducted by orally administering 100 mg of 20-30% iron-saturated bLf (corresponding to 70-84 μg of elemental iron) twice a day. This treatment was compared with the Italian standard therapy, consisting in the oral administration of 329.7 mg of ferrous sulfate once a day (corresponding to 105 mg of elemental iron). Treatments were carried out on 29 anemic women with minor ß-thalassemia (20 pregnant and 9 non-pregnant), 149 women with hereditary thrombophilia (HT) (70 pregnant and 79 non-pregnant) affected by AI and 20 anemic pregnant women suffering from various pathologies. In anemic pregnant and non-pregnant women with minor ß-thalassemia, presenting undetectable hepcidin levels, differently from ferrous sulfate management, bLf decreased IL-6 (from 25 ± 8 to 6 ± 3 pg/ml) and increased total serum iron (TSI) (from 54 ± 17 to 80 ± 9 μg/dl). BLf was also more efficient than ferrous sulfate in AI treatment in HT pregnant and non-pregnant women by decreasing both serum IL-6 (from 89 ± 8 to 58 ± 6 pg/ml) and hepcidin (from 115 ± 23 to 65 ± 10 ng/ml), thus increasing hematological parameters, such as the number of red blood cells (RBCs), the concentration of hemoglobin, TSI and serum ferritin. BLf was also efficient in treating anemia in other pathological pregnancies. Taken together all the results, bLf, showing a greater benefit and efficacy than the standard ferrous sulfate management, can be considered as a promising compound in treating anemia and AI through its ability to down-regulate IL-6, thus restoring ferroportin-mediated iron export from cells to blood in a hepcidin-dependent or independent way

    Leggendo Blaga

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    A sei anni dalla morte di Lucían Blaga (9 maggio 1961), nel nr. 18 di "Gazeta Literará” del 4 maggio 1967 (XIV) compariva il testo inedito di una lírica, Grádate, che qui riproduciamo nella lingua origínale, tentandone, al tempo stesso, una traduzione in lingua italiana. * L ’editrice, Dorli Blaga, lo faceva procederé da una pagina di diario, punteggiata d’interruzioni e lacune, giustificate forse dal carattere prowisorio di queste note, che rappresentano solo degli appunti a soccorso della memoria, in vista di una ulteriore definitiva elaborazione.Facultad de Humanidades y Ciencias de la Educació

    Angiotensin II or epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats

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    AIM To study hepatic vasoconstriction and glucose release induced by angiotensin (Ang) II or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat (SHR). METHODS Isolated liver perfusion was performed following portal vein and vena cava cannulationAng. or epinephrine (Epi) was injected in bolus and portal pressure monitoredglucose release was measured in perfusate aliquots. RESULTS The portal hypertensive response (PHR) and the glucose release induced by Ang. of L-NAME were similar to normal rats (WIS). On the other hand, the PHR induced by Epi in L-NAME was higher whereas the glucose release was lower compared to WIS. Despite the similar glycogen content, glucose release induced by Ang. was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar. CONCLUSION Ang. and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems to be involved in the hepatic effects induced by Epi but not by Ang.the diminished glucose release induced by Ang. in SHR is not related to glycogen content.Fundacao de Amparo a Pesquisa do Estado de Sao PauloCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)Univ Fed Sao Paulo, Dept Biochem, Expt Hepatol Lab, BR-04023900 Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Biosci, Expt Hepatol Lab, BR-11015020 Santos, BrazilUniv Fed Sao Paulo, Dept Med, Expt Hepatol Lab, BR-04023900 Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Biochem, Expt Hepatol Lab, BR-04023900 Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Biosci, Expt Hepatol Lab, BR-11015020 Santos, BrazilUniv Fed Sao Paulo, Dept Med, Expt Hepatol Lab, BR-04023900 Sao Paulo, BrazilFAPESP: 2011/13974-8|CAPESWeb of Scienc

    False memories formation is increased in individuals with insomnia

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    Previous studies suggest that sleep can influence false memories formation. Specifically, acute sleep loss has been shown to promote false memories production by impairing memory retrieval at subsequent testing. Surprisingly, the relationship between sleep and false memories has only been investigated in healthy subjects but not in individuals with insomnia, whose sleep is objectively impaired compared to healthy subjects. Indeed, this population shows several cognitive impairments involving prefrontal functioning that could affect source monitoring processes and contribute to false memories generation. Moreover, it has been previously reported that subjects with insomnia differentially process sleep-related versus neutral stimuli. Therefore, the aim of the present study was to compare false memories production between individuals with insomnia symptoms and good sleepers, and to evaluate the possible influence of stimulus category (neutral versus sleep-related) in the two groups. The results show that false memories are globally increased in participants reporting insomnia symptoms compared to good sleepers. A reduction in source monitoring ability was also observed in the former group, suggesting that an impairment of this executive function could be especially involved in false memories formation. Moreover, our data seem to confirm that false memories production in individuals with insomnia symptoms appears significantly modulated by stimulus category
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