2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

ACC/AHA
: American College of Cardiology/American Heart Association
ACCF/AHA
: American College of Cardiology Foundation/American Heart Association
ACE
: angiotensin-converting enzyme
ACEI
: angiotensin-converting enzyme inhibitor
ACS
: acute coronary syndrome
AF
: atrial fibrillation

/pdf/2016-esc-guidelines-for-the-diagnosis-and-treatment-of-acute-z18hg30pp1.pdf

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

/pdf/2016-esc-guidelines-for-the-diagnosis-and-treatment-of-acute-53v7yllhiz.pdf

Rapid progress in deciphering the biological mechanism of Alzheimer's disease (AD) has arisen from the application of molecular and cell biology to this complex disorder of the limbic and association cortices. In turn, new insights into fundamental aspects of protein biology have resulted from research on the disease. This beneficial interplay between basic and applied cell biology is well illustrated by advances in understanding the genotype-to-phenotype relationships of familial Alzheimer's disease. All four genes definitively linked to inherited forms of the disease to date have been shown to increase the production and/or deposition of amyloid β-protein in the brain. In particular, evidence that the presenilin proteins, mutations in which cause the most aggressive form of inherited AD, lead to altered intramembranous cleavage of the β-amyloid precursor protein by the protease called γ-secretase has spurred progress toward novel therapeutics. The finding that presenilin itself may be the long-sought γ-...

Alzheimer's Disease: Genes, Proteins, and Therapy

NOREPINEPHRINE is found in appreciable amounts in mammalian brain tissue. VOGT (1954) showed that this amine was unequally distributed in various regions of the cat brain, the highest concentrations being found in the hypothalamus. Similar findings were reported for other animal species (BERTLER and ROSENGREN, 1959a; MCGEER, MCGEER and WADA, 1963) and man (SANO, GAMO, KAKIMOTO, TANAGUCHI, TAKE~ADA and NISHINUMA, 1959). Dopamine is also present in the brain in comparable amounts to norepinephrine (MONTAGU, 1957 ; CARLSSON, LINDQVIST, MAGNUSSON and WALDECK, 1958) but with a different regional distribution, the highest concentrations being in the corpus striatum of both animals and man (BERTLER and ROSENGREN, 1959a; SANO et al., 1959; EHRINGER and HORNYKIEWICZ, 1960; BERTLER, 1961). The anatomical distribution of these two catecholamines in the brain was confirmed by the use of fluorescent histochemical techniques which allow a precise description of the cellular localization of the amines in brain tissue (CARLSSON, FALK and HILLARP, 1962; DAHLSTROM and FUXE, 1964; FUXE, 1965). These techniques revealed that norepinephrine and dopamine are specifically localized in complex systems of neurons in the brain, a finding which lends support to the hypothesis that both amines may be neurotransmitters in the central nervous system. The metabolism of catecholamines in the rat brain was studied by introducing small amounts of radioactive norepinephrine or dopamine directly into the lateral ventricle (MILHAUD and GLOWINSKI, 1962, 1963; GLOWINSKI, KOPIN and AXELROD, 1965; GLOWINSKI, IVERSEN and AXELROD, 1966). By this approach the blood-brain barrier to catecholamines can be circumvented, penetration of the radioactive catecholamines into the brain being allowed. The disposition of PHInorepinephrine in the whole brain indicates that [3H]norepinephrine introduced into the lateral ventricle of the brain mixes with the endogenous amine and can be used as a tracer to study the biochemical behaviour of norepinephrine in the brain (GLOWINSKI and AXELROD, 1966). PHIDopamine, which is also taken up and retained in the brain, is rapidly metabolized and converted to norepinephrine (GLOWINSKI et a!., 1966). The unequal regional distribution of the endogeneous catecholamines in the brain led us to undertake a study of the disposition of radioactive norepinephrine and dopamine in various brain regions after intraventricular injection. The regional

Regional studies of catecholamines in the rat brain. I. The disposition of [3H]norepinephrine, [3H]dopamine and [3H]dopa in various regions of the brain.

Differential pathways for interleukin-1β production activated by chromogranin A and amyloid β in microglia

4-methoxyphenylethylamine and 3,4-dimethoxyphenylethylamine in human urine

Proteolysis of non-phosphorylated and phosphorylated tau by thrombin.

THE ROLE of gamma aminobutyric acid (GABA) is not definitely established although its exclusive localization to the central nervous system in mammals has suggested that it has a key function in brain. The GABA shunt has long been considered an important source of cerebral oxidative metabolism.1 GABA itself has a depressant action on nerve transmission.2 Therefore, it may be a vital intermediate in an energy cycle or a neurotransmitter or both. The possibility that disturbances in GABA metabolism may be involved in certain human neurological disorders is suggested by two lines of evidence. First, GABA and its synthesizing enzyme, glutamic acid decarboxylase (GAD), are unequally distributed in brain. The high levels of GABA and GAD in extrapyramidal structuress-6 have drawn attention to the possibility that extrapyramidal disorders may be associated with deranged GABA metabolism. Second, the convulsant action of certain hydrazides which depress GAD activity has raised the question of whether some forms of epilepsy may involve faulty GABA metabolism.7 GAD is an enzyme which has a considerable degree of postmortem stability. Reasonably reliable results on GAD can therefore be obtained on human tissue. Reliable values for glutamic acid and GABA cannot be obtained as readily because the enzyme continues to function postmortem, converting the glutamic acid to GABA. This paper reports further details on the distribution of GAD in human brain. Normal and neurological cases are considered with particular reference to specific areas of the cortex and the basal ganglia. Data from coroner’s cases are compared with data from pa-

Patrick L. McGeer

Papers

Differential pathways for interleukin-1β production activated by chromogranin A and amyloid β in microglia

4-methoxyphenylethylamine and 3,4-dimethoxyphenylethylamine in human urine

Proteolysis of non-phosphorylated and phosphorylated tau by thrombin.

Glutamic acid decarboxylase in Parkinson's disease and epilepsy

Toxicity of human THP-1 monocytic cells towards neuron-like cells is reduced by non-steroidal anti-inflammatory drugs (NSAIDs).