No abstract available.
Adrenergic beta-3 Receptor Agonists/therapeutic use ; Humans ; Muscarinic Antagonists/therapeutic use ; Precision Medicine/methods/*trends ; Urinary Bladder, Overactive/*therapy

Adrenergic beta-Agonists ; therapeutic use ; Aged ; Androstadienes ; therapeutic use ; Cholinergic Antagonists ; therapeutic use ; Fluticasone ; Humans ; Male ; Middle Aged ; Scopolamine Derivatives ; therapeutic use ; Silicosis ; drug therapy ; Tiotropium Bromide

OBJECTIVEPostural tachycardia syndrome (POTS) is one of the major causes of orthostatic intolerance in children. We systematically reviewed the pathogenesis and the progress of individualized treatment for POTS in children.

DATA SOURCESThe data analyzed in this review are mainly from articles included in PubMed and EMBASE.

STUDY SELECTIONThe original articles and critical reviews about POTS were selected for this review.

RESULTSStudies have shown that POTS might be related to several factors including hypovolemia, high catecholamine status, abnormal local vascular tension, and decreased skeletal muscle pump activity. In addition to exercise training, the first-line treatments mainly include oral rehydration salts, beta-adrenoreceptor blockers, and alpha-adrenoreceptor agonists. However, reports about the effectiveness of various treatments are diverse. By analyzing the patient's physiological indexes and biomarkers before the treatment, the efficacy of medication could be well predicted.

CONCLUSIONSThe pathogenesis of POTS is multifactorial, including hypovolemia, abnormal catecholamine state, and vascular dysfunction. Biomarker-directed individualized treatment is an important strategy for the management of POTS children.

Adrenergic alpha-Agonists ; therapeutic use ; Adrenergic beta-Antagonists ; therapeutic use ; Catecholamines ; metabolism ; Humans ; Postural Orthostatic Tachycardia Syndrome ; drug therapy ; metabolism ; pathology ; therapy

Adrenal Cortex Hormones ; therapeutic use ; Adrenergic beta-Agonists ; therapeutic use ; Anti-Asthmatic Agents ; therapeutic use ; Asthma ; drug therapy ; Humans ; Medication Adherence

The studies on gene polymorphisms in biological pathways of the drugs for the treatment of asthma refer to the studies in which pharmacogenetic methods, such as genome-wide association studies, candidate gene studies, genome sequencing, admixture mapping analysis, and linkage disequilibrium, are used to identify, determine, and repeatedly validate the effect of one or more single nucleotide polymorphisms on the efficacy of drugs. This can provide therapeutic strategies with optimal benefits, least side effects, and lowest costs to patients with asthma, and thus realize individualized medicine. The common drugs for asthma are β2 receptor agonists, glucocorticoids, and leukotriene modifiers. This article reviews the research achievements in polymorphisms in biological pathways of the common drugs for asthma, hoping to provide guidance for pharmacogenetic studies on asthma in future and realize individualized medicine for patients with asthma soon.
Adrenergic beta-2 Receptor Agonists ; therapeutic use ; Asthma ; drug therapy ; genetics ; Glucocorticoids ; therapeutic use ; Leukotrienes ; genetics ; therapeutic use ; Metabolic Networks and Pathways ; Pharmacogenetics ; Polymorphism, Single Nucleotide ; Precision Medicine

OBJECTIVETo observe the effects of combined beta(1) adrenergic receptor (AR) antagonist with beta(2)AR agonist therapy on cardiac function and cardiomyocyte apoptosis in heart failure rats.

METHODSHeart failure was induced by isoproterenol and rats were randomly divided into metoprolol group (50 mg/kg twice daily/gavage, n = 11), combined treatment group (fenoterol 125 microg/kg and metoprolol 50 mg/kg twice daily/gavage, n = 11) and placebo group (saline, n = 10), another normal 9 male Wistar rats served as control group. After 8 weeks' treatment, cardiac function, apoptosis index (AI), Caspase-3 activity, expression levels of bcl-2 and bax protein, organ weight/body weight and collagen volume fraction (CVF) were evaluated.

RESULTS(1) Left ventricular end diastolic dimension, left ventricular end systolic dimension and E/A ratio were significantly increased and fractional shortening, ejection fraction significantly reduced post isoproterenol (all P < 0.05 vs. control) and these changes were significantly attenuated by metoprolol alone (all P < 0.05 vs. placebo) and further attenuated by the metoprolol and fenoterol combination therapy (all P < 0.05 vs. placebo and metoprolol). (2) Left ventricular weight to body weight ratio, lung weight to body weight ratio and CVF were also significantly reduced in metoprolol and combined treatment group than those in placebo group (all P < 0.01). (3) Compared with placebo group, AI and Caspase-3 activity were significantly lower in metoprolol group (all P < 0.01 vs. placebo) and further reduced in combined treatment group (all P < 0.01 vs. metoprolol). (4) The expression level of bax protein was significantly lower in metoprolol group while bcl-2/bax significantly higher than those in placebo group. These changes were more significant in combined treatment group (all P < 0.01 vs. metoprolol).

CONCLUSIONSbeta(1)AR antagonist in combination with beta(2)AR agonist further improved the cardiac function and prevented cardiac remodeling compared with using beta(1)AR antagonist alone in heart failure rats. Downregulated bax and upregulated bcl-2/bax expressions might contribute to the observed beneficial therapy effects by reducing cardiomyocyte apoptosis in these animals.

Adrenergic beta-1 Receptor Antagonists ; Adrenergic beta-2 Receptor Agonists ; Adrenergic beta-Agonists ; pharmacology ; therapeutic use ; Adrenergic beta-Antagonists ; pharmacology ; therapeutic use ; Animals ; Apoptosis ; drug effects ; Drug Therapy, Combination ; Heart Failure ; drug therapy ; Male ; Myocytes, Cardiac ; cytology ; Rats ; Rats, Wistar ; Ventricular Remodeling

Adolescent ; Adrenergic beta-Agonists ; therapeutic use ; Albuterol ; analogs & derivatives ; therapeutic use ; Asthma ; drug therapy ; physiopathology ; Child ; Child, Preschool ; Female ; Forced Expiratory Volume ; drug effects ; Humans ; Male ; Salmeterol Xinafoate

Adrenal Cortex Hormones ; administration & dosage ; Adrenergic beta-Agonists ; therapeutic use ; Bronchodilator Agents ; therapeutic use ; Humans ; Pulmonary Disease, Chronic Obstructive ; drug therapy

Adolescent ; Adrenergic beta-Agonists ; therapeutic use ; Adult ; Asthma ; drug therapy ; Bronchodilator Agents ; therapeutic use ; Butylamines ; therapeutic use ; Ethanolamines ; therapeutic use ; Female ; Heart Rate ; drug effects ; Hemodynamics ; drug effects ; Humans ; Injections, Subcutaneous ; Male ; Regional Blood Flow ; drug effects ; Resorcinols ; therapeutic use

After the approval and introduction of mirabegron, tadalafil, and botulinum toxin A for treatment of lower urinary tract symptoms/overactive bladder, focus of interest has been on their place in therapy versus the previous gold standard, antimuscarinics. However, since these agents also have limitations there has been increasing interest in what is coming next - what is in the pipeline? Despite progress in our knowledge of different factors involved in both peripheral and central modulation of lower urinary tract dysfunction, there are few innovations in the pipe-line. Most developments concern modifications of existing principles (antimuscarinics, beta3-receptor agonists, botulinum toxin A). However, there are several new and old targets/drugs of potential interest for further development, such as the purinergic and cannabinoid systems and the different members of the transient receptor potential channel family. However, even if there seems to be good rationale for further development of these principles, further exploration of their involvement in lower urinary tract function/dysfunction is necessary.
Adrenergic beta-3 Receptor Agonists/therapeutic use ; Botulinum Toxins, Type A/therapeutic use ; Drug Therapy, Combination ; Humans ; Molecular Targeted Therapy/methods/trends ; Muscarinic Antagonists/therapeutic use ; Neuromuscular Agents/therapeutic use ; Urinary Bladder, Overactive/*drug therapy