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Coating seeds in taste-averting chemical defenses (e.g., capsaicin from Capsicum spp.) can reduce rodent seed predation, and thus might promote plant establishment and forest regeneration. However, the efficacy of such seed coatings remains unknown for many woody plant species, and seed coatings have not been evaluated across different habitats where forest managers might seek to promote forest regeneration. We used two complementary seed-removal experiments in closed-canopy forests (Michigan) and an old field undergoing reforestation (New York) to examine whether coating seeds of four native tree species (Acer rubrum, Fagus grandifolia, Pinus banksiana, and Pinus resinosa) with chili powder reduces seed removal by rodents. In all species and habitats, control seeds were removed more than seeds treated with capsaicin (94% more in the closed-canopy forest, 17% more in the old field). Seed coatings containing capsaicin may provide a generally effective tool to support native tree recruitment and promote restoration success. [ABSTRACT FROM AUTHOR]

Objectives: Although blood pressure is considered the major determinant of left ventricular hypertrophy in hypertension, genetic variability is increasingly being considered among the factors influencing this complication. β2-Adrenergic receptors (β2ARs) are up-regulated in hypertension and largely polymorphic within the human population. Recently, we have shown that the Glu27 β2AR variant is strongly associated with cardiac hypertrophy in hypertension. The objective of this study is to verify whether this polymorphism also affects hypertrophy regression in response to antihypertensive therapy.Methods: In a prospective follow-up study we screened 970 hypertensive patients of Caucasian descent for the Gly16Arg, Gln27Glu, and Thr164Ile β2AR polymorphisms and left ventricular echocardiographic hypertrophy and assigned selected patients to enalapril or atenolol to assess left ventricular hypertrophy regression after 2-year follow-up. Results were stratified according to treatment and the Glu27Gln polymorphism of the β2AR. In cells with stable overexpression of the Glu27 or Gln27 variant of β2AR, we also explored the implications of this polymorphism on hypertrophy-related intracellular signal transduction.Results: Among hypertensive patients, the Gly16 allele was found in 63% of patients and the Glu27 allele was found in 40.6%. Both polymorphisms were in linkage disequilibrium, as expected. Four hundred forty-one hypertrophic hypertensive patients completed the 2-year follow-up. At baseline, patients carrying at least 1 allele of the Glu27 variant presented with a larger cardiac size despite similar blood pressure levels (142.9 ± 22.5 g/m2 in Glu27 carriers versus 138.2 ± 18.4 g/m2 in Gln27 carriers, P < .02). Blood pressure normalization was achieved by both drugs. At follow-up, compared with the Gln27 patients, the Glu27 patients showed a larger reduction in hypertrophy when treated with enalapril (percent change in left ventricular mass, −6.3% ± 7.7% in Glu27 carriers versus −2.18% ± 7.9% in Gln27 carriers; P < .05) but not with atenolol therapy (−2.8% ± 8.9% in Glu27 carriers versus −2.4% ± 8.8% in Gln27 carriers, P = not significant). In in vitro studies the activation of p38 and extracellular signal-regulated kinase (ERK-) 1/2 (data not shown) and the activity of the atrial natriuretic factor (ANF) promoter after isoproterenol (INN, isoprenaline) stimulation were larger in Glu27 β2AR overexpressing cells than in Gln27 β2AR overexpressing cells (fold difference compared with unstimulated cells, 9.7 ± 2.9 for Glu27 β2AR versus 4.2 ± 0.3 for Gln27 β2AR; P < .05).Conclusions: The Glu27 variant of β2AR enhances hypertension-induced left ventricular hypertrophy. In these patients angiotensin-converting enzyme inhibitors are more efficient than β-blockers in reducing cardiac size.Clinical Pharmacology & Therapeutics (2006) 80, 633–645; doi: 10.1016/j.clpt.2006.09.006 [ABSTRACT FROM AUTHOR]

It is well established that gender strongly influences cardiovascular risk factors, playing a crucial role in cardiovascular prevention, clinical pathways, diagnostic approach and treatment. Beyond the sex, which is a biological factor, gender entails a socio-cultural condition that impacts access and quality of care due to structural and institutional barriers. However, despite its great importance, this issue has not been adequately covered. Indeed sex and gender differences scarcely impact the clinical approach, creating a lot of disparities in care and outcomes of patients. Therefore, it becomes essential to increase the awareness of the importance of sex and gender influences on cardiovascular diseases. Moreover, new strategies for reducing disparities should be developed. Importantly, these differences should be taken into account in guideline recommendations. In this regard, it is crucial to include a greater number of women in clinical trials, since they are currently underrepresented. Furthermore, more women should be involved as member of international boards in order to develop recommendations and guidelines with more attention to this important topic.The aim of this ANMCO position paper is to shed light on gender differences concerning many cardiovascular drugs in order to encourage a more personalized therapeutic approach.

Long COVID is a clinical syndrome characterized by the persistence or development of symptoms due to COVID-19 at least 12 weeks after initial infection. More than 200 different symptoms have been ascribed to long COVID, the most common being fatigue, shortness of breath, and muscle weakness. Women have a three-fold higher risk of being diagnosed with long COVID, and the symptoms more often described are persistent weakness, chest pain, altered smell and taste, palpitations or muscle pain, as well as neurological, gastrointestinal and rheumatologic symptoms. Long COVID features are influenced by immune function, endothelial dysfunction and sex hormones. Moreover, it leads to systemic dysfunction, so various therapeutic strategies have been explored and still different trials are ongoing, mainly regarding anticoagulation and immuno-modulators. Nowadays the most quoted interventions are focused rehabilitation programs and pharmacological selected treatments in specifical cases. The aim of this review will be focusing the clinical and pathophysiological sex-related peculiarities to understand the different long COVID phenotypes and possibly address a better tailored approach and treatment.

Patients with severe aortic valve stenosis who are candidates for transcatheter aortic valve replacement represent a high-risk population for the presence of frequent comorbidities (reduced left ventricular ejection fraction, associated valve insufficiency, right ventricular dysfunction and/or pulmonary hypertension). Aortic valve stenosis can be associated with any other valve defects but among these mitral regurgitation is the most commonly associated valve disease. The simultaneous presence of severe mitral regurgitation in patients with aortic stenosis is a negative prognostic factor, resulting in increased mortality and a high diagnostic complexity, in particular in the accuracy of the evaluation of the two valve defects and therapeutic management which, at present, are not supported by strong scientific evidence.

We report the case of a 67-year-old female with a wide QRS complex tachycardia at 180 bpm. A diagnosis of class IC atrial flutter with aberrant ventricular conduction caused by flecainide therapy was formulated. Intravenous adenosine administration resulted in adequate slowing of the ventricular rate and normalization of QRS complexes. Restoration of sinus rhythm was achieved with intravenous amiodarone. The response to adenosine confirmed the diagnosis of supraventricular tachycardia with aberrant conduction, but the transition from arrhythmia onset to restoration of sinus rhythm showed interesting peculiarities.

Objectives: Although blood pressure is considered the major determinant of left ventricular hypertrophy in hypertension, genetic variability is increasingly being considered among the factors influencing this complication. beta(2)-Adrenergic receptors (beta(2)ARs) are up-regulated in hypertension and largely polymorphic within the human population. Recently, we have shown that the Glu27 beta(2)AR variant is strongly associated with cardiac hypertrophy in hypertension. The objective of this study is to verify whether this polymorphism also affects hypertrophy regression in response to antihypertensive therapy., Methods: In a prospective follow-up study we screened 970 hypertensive patients of Caucasian descent for the Gly16Arg, Gln27Glu, and Thr164Ile beta(2)AR polymorphisms and left ventricular echocardiographic hypertrophy and assigned selected patients to enalapril or atenolol to assess left ventricular hypertrophy regression after 2-year follow-up. Results were stratified according to treatment and the Glu27Gln polymorphism of the beta(2)AR. In cells with stable overexpression of the Glu27 or Gln27 variant of beta(2)AR, we also explored the implications of this polymorphism on hypertrophy-related intracellular signal transduction., Results: Among hypertensive patients, the Gly16 allele was found in 63% of patients and the Glu27 allele was found in 40.6%. Both polymorphisms were in linkage disequilibrium, as expected. Four hundred forty-one hypertrophic hypertensive patients completed the 2-year follow-up. At baseline, patients carrying at least 1 allele of the Glu27 variant presented with a larger cardiac size despite similar blood pressure levels (142.9 +/- 22.5 g/m(2) in Glu27 carriers versus 138.2 +/- 18.4 g/m(2) in Gln27 carriers, P < .02). Blood pressure normalization was achieved by both drugs. At follow-up, compared with the Gln27 patients, the Glu27 patients showed a larger reduction in hypertrophy when treated with enalapril (percent change in left ventricular mass, -6.3% +/- 7.7% in Glu27 carriers versus -2.18% +/- 7.9% in Gln27 carriers; P < .05) but not with atenolol therapy (-2.8% +/- 8.9% in Glu27 carriers versus -2.4% +/- 8.8% in Gln27 carriers, P = not significant). In in vitro studies the activation of p38 and extracellular signal-regulated kinase (ERK-) 1/2 (data not shown) and the activity of the atrial natriuretic factor (ANF) promoter after isoproterenol (INN, isoprenaline) stimulation were larger in Glu27 beta(2)AR overexpressing cells than in Gln27 beta(2)AR overexpressing cells (fold difference compared with unstimulated cells, 9.7 +/- 2.9 for Glu27 beta(2)AR versus 4.2 +/- 0.3 for Gln27 beta(2)AR; P < .05)., Conclusions: The Glu27 variant of beta(2)AR enhances hypertension-induced left ventricular hypertrophy. In these patients angiotensin-converting enzyme inhibitors are more efficient than beta-blockers in reducing cardiac size.