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.

The role of the immune system in neurodegenerative disorders.

High stability of mRNAs postmortem and protocols for their assessment by RT-PCR.

Oligodendroglial microtubular masses: an abnormality observed in some human neurodegenerative diseases.

THE concept of inhibitory processes occurring in the nervous system of various organisms is part of classical neurophysiology, but the idea of inhibitory neurons with axons whose endings release a specific inhibitory transmitter substance is relatively new (ECCLES, 1957). Evidence for the presence of inhibitory cells in the central nervous system of mammals is now abundant but, as yet, no inhibitory transmitter has been chemically identified. CURTIS and WATKINS (19604 have, however, suggested some criteria that such a substance should fulfil. An inhibitory transmitter might be contained in Factor I, a crude preparation from mammalian brain described originally by FLOREY (1954) and FLOREY and MCLENNAN (1955u, b), and which has been shown by MCLENNAN (1960) t o meet some of the criteria set up by CURTIS and WATKINS (1960~1, b). Identification of inhibitory transmitter substances is an important objective of current neurophysiological research, and suitable bioassay procedures are essential for such work. One convenient and widely used preparation is the slowly-adapting stretch receptor neuron of the crayfish. Inhibition of the discharge of this neuron was used by BAZEMORE, LLIOTT and FLOREY (1957) to identify GABA as an active component of Factor I preparations. This and subsequent work (ELLIOTT, 1958) led to the suggestion that GABA might account for most or all of the activity of Factor I-containing brain extracts. However, it was shown later that not all of the actions of Factor I are duplicated by GABA (MCLENNAN, 1957~). Moreover, a number of other amino acids, some of which occur in mammalian brain, have also been shown to have inhibitory effects on the crayfish stretch receptor neuron (BAZEMORE, ELLIOTT and FLOREY, 1957; EDWARDS and KUFFLER, 1959). The effects of GABA have since been investigated on many biological systems (ROBERTS, 1960), and the concept is developing that this amino acid functions, a t least in the central nervous system of mammals, not as a specific inhibitory transmitter substance, but as a neuronal depressant (CURTIS, PHILLIS and WATKINS, 1959). It now appears that the crayfish stretch receptor neuron is not a specific bioassay system; such lack of specificity may be of advantage in indicating the inhibitory characteristics of compounds not previously suspected of possessing such properties. In the study now reported, a series of compounds has been tested for inhibitory

The inhibitory action of 3‐hydroxytyramine, gamma‐aminobutyric acid (gaba) and some other compounds towards the crayfish stretch receptor neuron*

— The distribution of tryptophan hydroxylase in the cat brain was investigated and found to parallel roughly the distribution of serotonin. The most active areas are the caudate nucleus, septal area, anterior perforating substance, hypothalamus, amygdala and various areas of the midbrain.

Patrick L. McGeer

Papers

The role of the immune system in neurodegenerative disorders.

High stability of mRNAs postmortem and protocols for their assessment by RT-PCR.

Oligodendroglial microtubular masses: an abnormality observed in some human neurodegenerative diseases.

The inhibitory action of 3‐hydroxytyramine, gamma‐aminobutyric acid (gaba) and some other compounds towards the crayfish stretch receptor neuron*

The distribution of tryptophan hydroxylase in cat brain