Religious conversion among high security hospital patients: a qualitative analysis of patients’ accounts and experiences on changing faith

Research has shown the importance of religion in recovery from mental illness. Previous studies have investigated why individuals change faith during custody in prison, but there has been no research to date on religious conversion in forensic-psychiatric hospitals. The aim of this study was to understand the experience of religious conversion among patients detained in a UK secure hospital. Thirteen patients who had converted their religion were interviewed and the resultant data were analysed using thematic analysis. Three superordinate themes (‘reasons for changing faith’, ‘benefits of having a new faith’ and ‘difficulties with practising a faith’), incorporating eight subordinate themes, emerged. Understanding patients’ reasons for religious conversion is important for the treatment and support not merely of these individuals, but more broadly with patients in forensic psychiatric care

Sulfentrazone efficiency on Ipomoea hederifolia and Ipomoea quamoclit as influenced by rain and sugarcane straw

The aim of this study was to assess the capacity of sulfentrazone applied in pre-emergence in controlling Ipomoea hederifolia and Ipomoea quamoclit as a function of the time interval between herbicide application and the occurrence of rain, and the presence of sugarcane straw on the soil surface. Two greenhouse experiments and one field experiment were conducted. For the greenhouse experiments, the study included three doses of sulfentrazone applied by spraying 0, 0.6, and 0.9 kg ha-1, two amounts of straw on the soil (0 and 10 t ha-1), and five time intervals between the application of herbicide and rain simulation (0, 20, 40, 60, and 90 days). In the field experiment, five herbicide treatments (sulfentrazone at 0.6 and 0.9 kg ha-1, sulfentrazone + hexazinone at 0.6 + 0.25 kg ha-1, amicarbazone at 1.4 kg ha-1, and imazapic at 0.147 kg ha-1) and two controls with no herbicide were studied. Management conditions with or without sugarcane straw on the soil were also assessed. From the greenhouse experiments, sulfentrazone application at 0.6 kg ha-1 was found to provide for the efficient control of I. hederifolia and I. quamoclit in a dry environment, with up to 90 days between herbicide application and rain simulation. After herbicide application, 20 mm of simulated rain was enough to leach sulfentrazone from the straw to the soil, as the biological effects observed in I. hederifolia and I. quamoclit remained unaffected. Under field conditions, either with or without sugarcane straw left on the soil, sulfentrazone alone (0.6 or 0.9 kg ha-1) or sulfentrazone combined with hexazinone (0.6 + 0.25 kg ha-1) was effective in the control of I. hederifolia and I. quamoclit, exhibiting similar or better control than amicarbazone (1.4 kg ha-1) and imazapic (0.147 kg ha-1).Objetivou-se neste trabalho avaliar o controle em pré-emergência de Ipomoea hederifolia e Ipomoea quamoclit pelo herbicida sulfentrazone em função do intervalo de tempo entre a aplicação e a ocorrência de chuva e da manutenção ou não de palha de cana-de-açúcar na superfície do solo. Três experimentos foram desenvolvidos: dois em casa de vegetação e um em campo. Nos experimentos em casa de vegetação, foram estudadas três doses de sulfentrazone (0, 0,6 e 0,9 kg ha-1) pulverizado em duas quantidades de palha na superfície do solo (0 e 10 t ha-1) e cinco intervalos de tempo entre a sua aplicação e a simulação de chuva (0, 20, 40, 60 e 90 dias). No experimento em campo, foram avaliados cinco tratamentos de herbicida (sulfentrazone a 0,6 e 0,9 kg ha-1; sulfentrazone + hexazinone a 0,6 + 0,25 kg ha-1; amicarbazone a 1,4 kg ha-1; e imazapic a 0,147 kg ha-1) e duas testemunhas sem aplicação. A manutenção ou não da palha de cana sobre o solo também foi estudada. Em casa de vegetação, a aplicação de 0,6 kg ha-1 de sulfentrazone foi suficiente para o controle adequado de I. hederifolia e I. quamoclit num ambiente seco com até 90 dias sem chuva após a aplicação. Os 20 mm de chuva simulados após a aplicação do herbicida foram suficientes para remover o sulfentrazone da palha para o solo, pois o efeito biológico de controle de I. hederifolia e I. quamoclit não foi alterado. Em campo, sem ou com a permanência de palha de cana sobre o solo, o sulfentrazone isolado (0,6 e 0,9 kg ha-1) ou em mistura com hexazinone (0,6 + 0,25 kg ha-1) foi eficaz para I. hederifolia e I. quamoclit, com resposta similar ou melhor que a do amicarbazone (1,4 kg ha-1) e imazapic (0,147 kg ha-1)

Dysregulated Phenylalanine Catabolism Plays a Key Role in the Trajectory of Cardiac Aging

Background: Aging myocardium undergoes progressive cardiac hypertrophy and interstitial fibrosis with diastolic and systolic dysfunction. Recent metabolomics studies shed light on amino acids in aging. The present study aimed to dissect how aging leads to elevated plasma levels of the essential amino acid phenylalanine and how it may promote age-related cardiac dysfunction. Methods: We studied cardiac structure and function, together with phenylalanine catabolism in wild-type (WT) and p21 −/− mice (male; 2–24 months), with the latter known to be protected from cellular senescence. To explore phenylalanine’s effects on cellular senescence and ectopic phenylalanine catabolism, we treated cardiomyocytes (primary adult rat or human AC-16) with phenylalanine. To establish a role for phenylalanine in driving cardiac aging, WT male mice were treated twice a day with phenylalanine (200 mg/kg) for a month. We also treated aged WT mice with tetrahydrobiopterin (10 mg/kg), the essential cofactor for the phenylalanine-degrading enzyme PAH (phenylalanine hydroxylase), or restricted dietary phenylalanine intake. The impact of senescence on hepatic phenylalanine catabolism was explored in vitro in AML12 hepatocytes treated with Nutlin3a (a p53 activator), with or without p21-targeting small interfering RNA or tetrahydrobiopterin, with quantification of PAH and tyrosine levels. Results: Natural aging is associated with a progressive increase in plasma phenylalanine levels concomitant with cardiac dysfunction, whereas p21 deletion delayed these changes. Phenylalanine treatment induced premature cardiac deterioration in young WT mice, strikingly akin to that occurring with aging, while triggering cellular senescence, redox, and epigenetic changes. Pharmacological restoration of phenylalanine catabolism with tetrahydrobiopterin administration or dietary phenylalanine restriction abrogated the rise in plasma phenylalanine and reversed cardiac senescent alterations in aged WT mice. Observations from aged mice and human samples implicated age-related decline in hepatic phenylalanine catabolism as a key driver of elevated plasma phenylalanine levels and showed increased myocardial PAH-mediated phenylalanine catabolism, a novel signature of cardiac aging. Conclusions: Our findings establish a pathogenic role for increased phenylalanine levels in cardiac aging, linking plasma phenylalanine levels to cardiac senescence via dysregulated phenylalanine catabolism along a hepatic-cardiac axis. They highlight phenylalanine/PAH modulation as a potential therapeutic strategy for age-associated cardiac impairment. </jats:sec

Dysregulated Phenylalanine Catabolism Plays a Key Role in the Trajectory of Cardiac Aging

International audienceBackground: Aging myocardium undergoes progressive cardiac hypertrophy and interstitial fibrosis with diastolic and systolic dysfunction. Recent metabolomics studies shed light on amino acids in aging. The present study aimed to dissect how aging leads to elevated plasma levels of the essential amino acid phenylalanine and how it may promote age-related cardiac dysfunction. Methods: We studied cardiac structure and function, together with phenylalanine catabolism in wild-type (WT) and p21 −/− mice (male; 2–24 months), with the latter known to be protected from cellular senescence. To explore phenylalanine’s effects on cellular senescence and ectopic phenylalanine catabolism, we treated cardiomyocytes (primary adult rat or human AC-16) with phenylalanine. To establish a role for phenylalanine in driving cardiac aging, WT male mice were treated twice a day with phenylalanine (200 mg/kg) for a month. We also treated aged WT mice with tetrahydrobiopterin (10 mg/kg), the essential cofactor for the phenylalanine-degrading enzyme PAH (phenylalanine hydroxylase), or restricted dietary phenylalanine intake. The impact of senescence on hepatic phenylalanine catabolism was explored in vitro in AML12 hepatocytes treated with Nutlin3a (a p53 activator), with or without p21-targeting small interfering RNA or tetrahydrobiopterin, with quantification of PAH and tyrosine levels. Results: Natural aging is associated with a progressive increase in plasma phenylalanine levels concomitant with cardiac dysfunction, whereas p21 deletion delayed these changes. Phenylalanine treatment induced premature cardiac deterioration in young WT mice, strikingly akin to that occurring with aging, while triggering cellular senescence, redox, and epigenetic changes. Pharmacological restoration of phenylalanine catabolism with tetrahydrobiopterin administration or dietary phenylalanine restriction abrogated the rise in plasma phenylalanine and reversed cardiac senescent alterations in aged WT mice. Observations from aged mice and human samples implicated age-related decline in hepatic phenylalanine catabolism as a key driver of elevated plasma phenylalanine levels and showed increased myocardial PAH-mediated phenylalanine catabolism, a novel signature of cardiac aging. Conclusions: Our findings establish a pathogenic role for increased phenylalanine levels in cardiac aging, linking plasma phenylalanine levels to cardiac senescence via dysregulated phenylalanine catabolism along a hepatic-cardiac axis. They highlight phenylalanine/PAH modulation as a potential therapeutic strategy for age-associated cardiac impairment