Enzymatic preparations obtained from young plants and cell cultures of capulin were screened for hydroxynitrile lyase activity. The three week old plants, grown under sterile conditions, were used to establish a solid cell culture. Crude preparations obtained from this plant material were evaluated for the transformation of benzaldehyde to the corresponding cyanohydrin (mandelonitrile). The results show that the crude material from roots, stalks, and leaves of young plants and calli of roots, stalks, internodes and petioles biocatalyzed the addition of hydrogen cyanide (HCN) to benzaldehyde with a modest to excellent enantioselectivity.
Acetonitriles ; metabolism ; Aldehyde-Lyases ; metabolism ; Benzaldehydes ; metabolism ; Biocatalysis ; Cells, Cultured ; Hydrogen Cyanide ; metabolism ; Nitriles ; metabolism ; Prunus ; cytology ; enzymology

We aimed to characterize the participation of rapid non-genomic and delayed non-genomic/genomic or genomic mechanisms in vasoactive effects to triiodothyronine (T3), emphasizing functional analysis of the involvement of these mechanisms in the genesis of nitric oxide (NO) of endothelial or muscular origin. Influences of in vitro and in vivo T3 treatments on contractile and relaxant responsiveness of isolated rat aortas were studied. In vivo T3-treatment was 500 μg·kg–1·d–1, subcutaneous injection, for 1 (T31d) and 3 (T33d) days. In experiments with endothelium- intact aortic rings contracted with phenylephrine, increasing concentrations of T3 did not alter contractility. Likewise, in vitro T3 did not modify relaxant responses induced by acetylcholine or sodium nitroprusside (SNP) nor contractile responses elicited by phenylephrine or angiotensin II in endothelium-intact aortas. Concentration- response curves (CRCs) to acetylcholine and SNP in endothelium-intact aortic rings from T31d and T33d rats were unmodified. T33d, but not T31d, treatment diminished CRCs to phenylephrine in endothelium-intact aortic rings. CRCs to phenylephrine remained significantly depressed in both endothelium-denuded and endothelium- intact, nitric oxide synthase inhibitor-treated, aortas of T33d rats. In endotheliumdenuded aortas of T33d rats, CRCs to angiotensin II, and high K+ contractures, were decreased. Thus, in vitro T3 neither modified phenylephrine-induced active tonus nor CRCs to relaxant and contractile agonists in endothelium-intact aortas, discarding rapid non-genomic actions of this hormone in smooth muscle and endothelial cells. Otherwise, T33d-treatment inhibited aortic smooth muscle capacity to contract, but not to relax, in an endothelium- and NO-independent manner. This effect may be mediated by delayed non-genomic/genomic or genomic mechanisms.

We aimed to characterize the participation of rapid non-genomic and delayed non-genomic/genomic or genomic mechanisms in vasoactive effects to triiodothyronine (T3), emphasizing functional analysis of the involvement of these mechanisms in the genesis of nitric oxide (NO) of endothelial or muscular origin. Influences of in vitro and in vivo T3 treatments on contractile and relaxant responsiveness of isolated rat aortas were studied. In vivo T3-treatment was 500 μg·kg–1·d–1, subcutaneous injection, for 1 (T31d) and 3 (T33d) days. In experiments with endothelium- intact aortic rings contracted with phenylephrine, increasing concentrations of T3 did not alter contractility. Likewise, in vitro T3 did not modify relaxant responses induced by acetylcholine or sodium nitroprusside (SNP) nor contractile responses elicited by phenylephrine or angiotensin II in endothelium-intact aortas. Concentration- response curves (CRCs) to acetylcholine and SNP in endothelium-intact aortic rings from T31d and T33d rats were unmodified. T33d, but not T31d, treatment diminished CRCs to phenylephrine in endothelium-intact aortic rings. CRCs to phenylephrine remained significantly depressed in both endothelium-denuded and endothelium- intact, nitric oxide synthase inhibitor-treated, aortas of T33d rats. In endotheliumdenuded aortas of T33d rats, CRCs to angiotensin II, and high K+ contractures, were decreased. Thus, in vitro T3 neither modified phenylephrine-induced active tonus nor CRCs to relaxant and contractile agonists in endothelium-intact aortas, discarding rapid non-genomic actions of this hormone in smooth muscle and endothelial cells. Otherwise, T33d-treatment inhibited aortic smooth muscle capacity to contract, but not to relax, in an endothelium- and NO-independent manner. This effect may be mediated by delayed non-genomic/genomic or genomic mechanisms.

Background/Aims: This study aims to investigate the association between Binge Eating Disorder and functional dyspepsia in a Mexican population, focusing on symptomatology and demographic characteristics. Methods: We conducted a cross-sectional study on 1016 subjects, evaluating binge eating disorder (BED) and functional dyspepsia based on the Rome IV criteria. Data collection included sociodemographic information, gastrointestinal symptom severity, and anxiety/depression screening using validated tools. A multivariate logistic regression analysis with the 2 test was conducted for comparison analysis. Results: The prevalence of dyspepsia in BED was 53.6% (95% CI, 46-56). Postprandial fullness (OR, 1.52; 95% CI, 1.06-2.17; P = 0.021) and overlap syndrome (OR, 1.80; 95% CI, 1.25-2.60; P = 0.002) were significantly associated with BED. Patients with BED also presented more severe postprandial distress syndrome (P = 0.027). Anxiety was prevalent in BED patients, while depression was more prominent in patients with BED and dyspepsia overlap. Conclusions BED patients have a high prevalence of dyspepsia with an association between postprandial fullness and this eating disorder. BED appears to be more prevalent in younger individuals and males. These findings underscore the importance of considering dyspepsia in the management of BED and highlight the need for further research on this association.

Background/Aims: This study aims to investigate the association between Binge Eating Disorder and functional dyspepsia in a Mexican population, focusing on symptomatology and demographic characteristics. Methods: We conducted a cross-sectional study on 1016 subjects, evaluating binge eating disorder (BED) and functional dyspepsia based on the Rome IV criteria. Data collection included sociodemographic information, gastrointestinal symptom severity, and anxiety/depression screening using validated tools. A multivariate logistic regression analysis with the 2 test was conducted for comparison analysis. Results: The prevalence of dyspepsia in BED was 53.6% (95% CI, 46-56). Postprandial fullness (OR, 1.52; 95% CI, 1.06-2.17; P = 0.021) and overlap syndrome (OR, 1.80; 95% CI, 1.25-2.60; P = 0.002) were significantly associated with BED. Patients with BED also presented more severe postprandial distress syndrome (P = 0.027). Anxiety was prevalent in BED patients, while depression was more prominent in patients with BED and dyspepsia overlap. Conclusions BED patients have a high prevalence of dyspepsia with an association between postprandial fullness and this eating disorder. BED appears to be more prevalent in younger individuals and males. These findings underscore the importance of considering dyspepsia in the management of BED and highlight the need for further research on this association.

Background/Aims: This study aims to investigate the association between Binge Eating Disorder and functional dyspepsia in a Mexican population, focusing on symptomatology and demographic characteristics. Methods: We conducted a cross-sectional study on 1016 subjects, evaluating binge eating disorder (BED) and functional dyspepsia based on the Rome IV criteria. Data collection included sociodemographic information, gastrointestinal symptom severity, and anxiety/depression screening using validated tools. A multivariate logistic regression analysis with the 2 test was conducted for comparison analysis. Results: The prevalence of dyspepsia in BED was 53.6% (95% CI, 46-56). Postprandial fullness (OR, 1.52; 95% CI, 1.06-2.17; P = 0.021) and overlap syndrome (OR, 1.80; 95% CI, 1.25-2.60; P = 0.002) were significantly associated with BED. Patients with BED also presented more severe postprandial distress syndrome (P = 0.027). Anxiety was prevalent in BED patients, while depression was more prominent in patients with BED and dyspepsia overlap. Conclusions BED patients have a high prevalence of dyspepsia with an association between postprandial fullness and this eating disorder. BED appears to be more prevalent in younger individuals and males. These findings underscore the importance of considering dyspepsia in the management of BED and highlight the need for further research on this association.