Background Depressed patients perform poorly on tests of autobiographical memory specificity (AMS); this may have negative consequences for other important cognitive abilities, delays recovery from mood episodes, and, in recovered patients, may mediate vulnerability to future episodes. Although the cognitive mechanisms underlying AMS deficits are beginning to be understood, the neurobiological mechanisms remain unclear. Serotonin is implicated in both depression and long-term memory; therefore, temporary lowering of brain serotonin function via acute tryptophan depletion (ATD) offers a means of studying the role of serotonin in autobiographical memory specificity. Materials and methods In this study, 24 previously depressed women underwent low-dose ATD or sham depletion and completed tests of initial and delayed memory, recollection- and familiarity-based recognition, and AMS. Results ATD did not differentially affect state mood. Compared with sham depletion, ATD impaired immediate recall on the Auditory Verbal Learning Test. Although ATD did not differentially impair recollection- and familiaritybased recognition, it did slow recognition of positive words. ATD also reduced autobiographical memory specificity in response to negative cue words. Discussion The results confirm previous findings that lowdose ATD can reinstate depression-congruent biases in cognition without causing depressive mood in vulnerable populations. The ATD-induced reduction in memory specificity suggests that serotonergic dysfunction may mediate depressive deficits in autobiographical memory; the interaction of cognitive and neurobiological vulnerability mechanisms is discussed
Serotonergic involvement has been implicated in preferential consumption of treat foods. We tested the effect of acute tryptophan depletion (ATD) on food consumption by overweight and lean adults with and without a history of recurrent major depressive disorder (MDD). ATD and taste-matched placebo challenges were administered double-blind in counter-balanced order. Participants were classified as lean (n=36) or overweight (n=19) on the basis of body mass index (BMI). Total calorie, carbohydrate, protein, and sweet food consumption were assessed via a test meal 8-h following ATD. Four food items of comparable palatability were offered as a part of the test: two sweet (one arbohydrate-rich, and one protein-rich) and two non-sweet (one carbohydrate-rich, and one protein-rich). As compared to the placebo challenge, ATD significantly increased sweet calorie intake among overweight participants and increased their propensity to consume sweet food first before any other type of food. Lean participants’ sweet calorie intake and food preference were unaffected by ATD. Findings suggest serotonergic involvement in the sweet food consumption by overweight individuals.
The purpose of the present study was to evaluate the effects of losartan and the combination of losartan and L-arginine on endothelial function and hemodynamic variables in patients with heart failure (HF). Endothelium-dependent vasodilation is impaired in patients with HF. It was hypothesized that the administration of losartan and the combination of losartan and L-arginine might increase nitric oxide production and have a beneficial additive effect on endothelial function and hemodynamic variables in patients with HF. Nine patients with HF (ejection fraction <35%) were given losartan 50 mg orally on 2 consecutive days. On the second day, 1 hour after losartan 50 mg administration, L-arginine 20 g was given by intravenous infusion. Endothelial function in the form of endotheliumdependent brachial artery flow-mediated vasodilation (FMV) was measured by ultrasound.
Hemodynamic variables were estimated using Doppler echocardiography at baseline and at 2 and 4 hours after losartan alone and after combination therapy. Urinary levels of nitrite (NO2) or nitrate (NO3) were measured. Four hours after losartan administration, significant reductions in systemic vascular resistance and estimated end-systolic elastase were observed. On the second day, 1 hour after L-arginine infusion, an additive hemodynamic effect was observed, with significant increases in the cardiac index and stroke volume and significant reductions in systemic vascular resistance and calculated left ventricular enddiastolic pressure. A trend toward improved FMV was observed with losartan alone, but without statistical significance. Combination therapy significantly improved ostintervention FMV compared with baseline. The increase in urinary nitric oxide excretion after losartan treatment and combination therapy was significantly correlated with improved hemodynamic variables and improved FMV. In conclusion, losartan induces significant afterload reduction, reduced contractility, and increased nitric oxide urinary excretion. The
combination of L-arginine and losartan seems to have superior effects on hemodynamic variables and endothelium-dependent vasodilation compared with losartan alone.
High-performance physical activity and postexercise recovery lead to significant changes in amino acid and protein metabolism in skeletal muscle. Central to these changes is an increase in the metabolism of the BCAA leucine. During exercise, muscle protein synthesis decreases together with a net increase in protein degradation and stimulation of BCAA oxidation. The decrease in protein synthesis is associated with inhibition of translation initiation factors 4E and 4G and ribosomal protein S6 under regulatory controls of intracellular insulin signaling and leucine concentrations. BCAA oxidation increases through activation of the branched-chain a-keto acid dehydrogenase (BCKDH). BCKDH activity increases with exercise, reducing plasma and intracellular leucine concentrations. After exercise, recovery of muscle protein synthesis requires dietary protein or BCAA to increase tissue levels of leucine in order to release the inhibition of the initiation factor 4 complex through activation of the protein kinase mammalian target of rapamycin (mTOR). Leucine’s effect on mTOR is synergistic with insulin via the phosphoinositol 3-kinase signaling pathway. Together, insulin and leucine allow skeletal muscle to coordinate protein synthesis with physiological state and dietary intake.
Purpose of review
Glycine, a non-essential amino acid, has been found to protect against oxidative stress in several pathological situations, and it is required for the biosynthesis of structural proteins such as elastin. As hypertension is a disease in which free radicals and large vessel elasticity are involved, this article will examine the possible mechanisms by which glycine may protect against high blood pressure.
The addition of glycine to the diet reduces high blood pressure in a rat model of the metabolic syndrome. Also, glycine supplemented to the low protein diet of rat dams during pregnancy has a beneficial effect on blood pressure in their offspring. The mechanism by which glycine decreases high blood pressure can be attributed to its participation in the reduction of the generation of free radicals, increasing the availability of nitric oxide. In addition, as glycine is required for a number of critical metabolic pathways, such as the synthesis of the structural proteins collagen and elastin, the perturbation of these leads to impaired elastin formation in the aorta. This involves changes in the aorta’s elastic properties, which would contribute to the development of ypertension.
The use of glycine to lower high blood pressure could have a significant clinical impact in patients with the metabolic syndrome and with limited resources. On the other hand, more studies are needed to explore the beneficial effect of glycine in other models of hypertension and to investigate possible side-effects of treatment with glycine.
Terça, 23 de Agosto: 20:00 as 23:00.
Via internet: http://www.atmancapacitacao.com.br
Repassar informações sobre a bioquímica de nutrientes e como os seus níveis interferem na homeostase do organismo, reflexos na clínica do paciente e o seu uso como apoio terapêutico.
A aula será projetada via internet, os alunos receberão a apostila com os slides três dias antes por e-mail ou para baixar em site, das 20:00h as 22:00h exposição do palestrante e das 22:00h as 23:00h respostas as duvidas pelo chat. Os alunos poderão assistir novamente a aula em vídeo via internet. Sempre as terças.
Henry Okigami, farmacêutico, especialista em homeopatia, fitoterapia, administração de serviços de saúde, farmácia hospitalar.
– A aula será dividida por tópicos e em cada tópico será abordado o caminho bioquímico, as consequências de alterações nestes caminhos bioquímicos, sua relação com a fisiopatologia, seu uso associado ao tratamento e trabalhos clínicos mostrando o uso e benefícios. Quando for o caso, será abordado sobre fitoterápicos que aumentam a atividade do suplemento ou potencializam o seu efeito no tratamento, bem como também a terapia medicamentosa. Exemplo: quando da aula sobre ferro, será comentado seu papel bioquímico, papel na fisiopatologia, suplementos de ferro, benefícios riscos, sobrecarga de ferro, etc.
As aulas terão custo de R$ 50,00 (cinquenta reais) por módulo de 3 horas, caso o aluno queira pagar antecipadamente ou antecipar pagamentos, terão descontos.
Nativa da Ásia tropical e Austrália, é cultivada como alimento e também pelas qualidades curativas (acredita-se que alivia inflamações). No Brasil a produção é associada aos imigrantes japoneses. As flores também são comestíveis, assim como as folhas mais novas, as sementes e o rizoma, vulgarmente chamado de raíz de lótus. As folhas maiores são usadas para embalar alimentos. Quando fatiados revelam vários orifícios que parecem desenhos. Quando crua, a raíz é crocante, lembrando um pedaço de cana de açúcar sem as fibras. O sabor é neutro e adocicado, levemente floral. Na culinária japonesa ela é preparada frita, refogada em saladas, bolinhos e recheadas.
É bom para pessoas de todas as idades, pois é rica em vitaminas B2 e B6 e minerais como potássio e fósforo, além de ser pobre em gorduras e consumir crua, porque é boa fonte de vitamina C.
É ruim para quem precisa de uma dieta de alto teor de proteína, pois é pobre nesse nutriente; e hipertensos devem evitar consumir a conserva industrial, que pode contar alto teor de sódio.