Academic literature on the topic 'Resine angiotensine'

Hypertrophic cardiomyopathy (HCM) is characterized by the presence of increased left ventricular (LV) wall thickness that is not explained by loading conditions. The LV diastolic function is impaired in the majority of patients, and resting or provocable LV outflow tract obstruction is often present. The management of HCM is directed towards minimizing symptoms, improving LV diastolic function, and reducing LV outflow tract obstrucion. Beta-blockers reduce myocardial oxygen demand and improve LV filling via their negative chronotropic and inotropic effects. Moreover, they decrease LV outflow tract obstruction. The calcium channel blockers verapamil and diltiazem can be used when beta-blockers are contraindicated or ineffective. Diuretics improve dyspnoea in patients with increased pulmonary capillary pressure, and their use is mandatory if signs of fluid retention are present. The role of non-pharmacological treatment (surgery, electrical and mechanical device implantation) is important in specific groups of patients. Dilated cardiomyopathy is defined by the presence of LV dilatation and systolic dysfunction in the absence of abnormal loading conditions or coronary artery disease. Treatment of symptomatic patients should follow the therapeutic algorithm proposed by European Society of Cardiology guidelines on heart failure. First-line treatment includes diuretics, angiotensin-converting enzyme (ACE) inhibition (or angiotensin receptor blockade), beta-blockade, and aldosterone antagonism. The complex neprilysin inhibitor sacubitril/valsartan is recommended to replace ACE inhibitors in patients who remain symptomatic despite optimal treatment. The If channel inhibitor ivabradine should be considered for patients in sinus rhythm and with a resting heart rate of >70 bpm. ICD implantation with cardiac resynchronization function, LV assist devices, and heart transplantation are indicated in selected patients.

Hypertrophic cardiomyopathy (HCM) is characterized by the presence of increased left ventricular (LV) wall thickness that is not explained by loading conditions. The LV diastolic function is impaired in the majority of patients, and resting or provocable LV outflow tract obstruction is often present. The management of HCM is directed towards minimizing symptoms, improving LV diastolic function, and reducing LV outflow tract obstruction. Beta-blockers reduce myocardial oxygen demand and improve LV filling via their negative chronotropic and inotropic effects. Moreover, they decrease LV outflow tract obstruction. The calcium channel blockers verapamil and diltiazem can be used when beta-blockers are contraindicated or ineffective. Diuretics improve dyspnoea in patients with increased pulmonary capillary pressure, and their use is mandatory if signs of fluid retention are present. The role of non-pharmacological treatment (surgery, electrical and mechanical device implantation) is important in specific groups of patients. Dilated cardiomyopathy is defined by the presence of LV dilatation and systolic dysfunction in the absence of abnormal loading conditions or coronary artery disease. Treatment of symptomatic patients should follow the therapeutic algorithm proposed by European Society of Cardiology guidelines on heart failure. First-line treatment includes diuretics, angiotensin-converting enzyme (ACE) inhibition (or angiotensin receptor blockade), beta-blockade, and aldosterone antagonism. The complex neprilysin inhibitor sacubitril/valsartan is recommended to replace ACE inhibitors in patients who remain symptomatic despite optimal treatment. The If channel inhibitor ivabradine should be considered for patients in sinus rhythm and with a resting heart rate of >70 bpm. ICD implantation with cardiac resynchronization function, LV assist devices, and heart transplantation are indicated in selected patients.

Calmodulin (CaM) is the major Ca2+ receptor in eukaryotic cells (Means and Rasmussen, 1988). This paper begins an investigation into the structural requirements for neurotoxic peptide binding to CaM. In resting cells, CaM is deficient in Ca2+ (the protein has the potential for binding four Ca2+ ions with high affinity, pKd > 6 (Means and Rasmussen, 1988)). Following nerve cell excitation, intracellular levels of Ca2+ increase dramatically, from about 0.1 μM to about 10 μM, allowing CaM to become fully-loaded with Ca2+ . Ca2+ - loaded CaM has the ability to activate a number of neural enzymes, including cyclic nucleotide phosphodiesterase, adenylate cyclase, Ca2+ - CaM kinase and calcineurin (Kennedy, 1989). A tight-binding neurotoxic peptide would be expected to competitively inhibit activation of these enzymes. The high level of intercellular coordination required by higher organisms is attained, in part, by the complex interplay of the nervous and endocrine systems. Two important second messengers are involved in information transfer processes associated with the normal operation of these two systems: cyclic AMP (cAMP) and Ca2+ . Cyclic AMP is involved in trans-membrane information flow following the interaction of cell surface receptors with certain hormones (e.g., glucagon, epinephrine and ACTH), while Ca2+ is the principal information carrier in the nerve cell following stimulation of the system by membrane depolarization. CaM plays a pivotal role in second messenger function in both the nervous and endocrine systems. In the nervous system, calmodulin is the principal target for Ca2+. In the endocrine system, CaM (complexed with Ca2+) is responsible for activating the enzymes responsible for both cAMP synthesis (i.e., adenylate cyclase) and degradation (i.e., cyclic nucleotide phosphodiesterase). Additional linkage between the nervous and endocrine systems is evident from the fact that both systems are responsive to some of the same peptide messengers. For example, insulin, glucagon, angiotensin, and somatostatin have been found in the brain, and may function as neurotransmitters (Malencik and Anderson, 1982) perhaps through CaM mediation.

Peptides play key structural and functional roles in biochemistry, pharmacology, and neurobiology, and are important probes for research in enzymology, immunology, and molecular biology. The amino acid building blocks can be among the 20 genetically encoded L-residues, or else unusual ones, and the sequences can be linear, cyclic, or branched. It follows that rapid, efficient, and reliable methodology for the chemical synthesis of these molecules is of utmost interest. A number of synthetic peptides are significant commercial or pharmaceutical products, ranging from the sweet dipeptide L-Asp-L-Phe-OMe (aspartame) to clinically used hormones such as oxytocin, adrenocorticotropic hormone, calcitonin, and gonadotropin releasing hormone (GnRH) super-agonists. Synthesis can lead to potent and selective new drugs by judicious substitutions that change functional groups and/or conformations of the parent peptide. These include introduction of N- or C-alkyl substituents, unnatural or D-amino acids, side-chain modifications including sulfate or phosphate groups or carbohydrate moieties, and constraints such as disulfide bridges between half-cystines or side-chain lactams between Lys and Asp or Glu. Commercially important products that evolved from such studies include protease inhibitors, such as captopril and other angiotensin converting enzyme (ACE) inhibitors, peptidomimetic HIV protease inhibitors, and the somatostatin analog lanreotide. Most of the biologically or medicinally important peptides which are the targets for useful structure-function studies by chemical synthesis comprise under 50 amino acid residues, but occasionally a synthetic approach can lead to important conclusions about small proteins (full or domains) in the 100-200 residue size range. Methods for synthesizing peptides are divided conveniently into two categories: solution (classical) and solid-phase pep tide synthesis (SPPS). The classical methods have evolved since the beginning of the twentieth century, and they are described amply in several reviews and books (Wünsch, 1974; Finn and Hofmann, 1976; Bodanszky and Bodanszky, 1984; Goodman et al, 2001). The solid-phase alternative was conceived and elaborated by R. B. Merrifield beginning in 1959, and has also been covered comprehensively (Erickson and Merrifield, 1976; Birr, 1978; Barany and Merrifield, 1979; Stewart and Young, 1984; Merrifield, 1986; Barany et al., 1987, 1988; Kent, 1988; Atherton and Sheppard, 1989; Fields and Noble, 1990; Barany and Albericio, 1991; Fields et al., 1992; Gutte, 1995; Fields, 1997; Lloyd-Williams et al., 1997; Chan and White, 2000; Kates and Albericio, 2000).

La granulomatoses oro-faciale (GOF) est une entité rare regroupant toutes les pathologies caractérisées par une inflammation granulomateuse non caséeuse de la région oro-faciale. Le diagnostic est histologique. L’étiologie n’est pas connue. L’oedème labial d’abord intermittent, pouvant s’installer de manière permanente, est un symptôme classique de la GOF. D’autres signes cliniques, extra-oraux, peuvent être associées lorsque la GOF s’inscrit dans le cadre d’une pathologie systémique : maladie de Crohn, Sarcoïdose, maladie de Wegener. Nous présentons le cas d’un patient pour qui l’exploration