198 research outputs found

    Heat-induced Proteome Changes in Tomato Leaves

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    Three tomato (Solanum lycopersicum) cultivars [Walter LA3465 (heat-tolerant), Edkawi LA 2711 (unknown heat tolerance, salt-tolerant), and LA1310 (cherry tomato)] were compared for changes in leaf proteomes after heat treatment. Seedlings with four fully expanded leaves were subjected to heat treatment of 39/25 °C at a 16:8 h light–dark cycle for 7 days. Leaves were collected at 1200 hr, 4 h after the light cycle started. For ‘Walter’ LA3465, heat-suppressed proteins were geranylgeranyl reductase, ferredoxin-NADP (+) reductase, Rubisco activase, transketolase, phosphoglycerate kinase precursor, fructose–bisphosphate aldolase, glyoxisomal malate dehydrogenase, catalase, S-adenosyl-L-homocysteine hydrolase, and methionine synthase. Two enzymes were induced, cytosolic NADP-malic enzyme and superoxide dismutase. For ‘Edkawi’ LA2711, nine enzymes were suppressed: ferredoxin-NADP (+) reductase, Rubisco activase, S-adenosylmethionine synthetase, methioine synthase, glyoxisomal malate dehydrogenase, enolase, flavonol synthase, M1 family peptidase, and dihydrolipoamide dehydrogenase. Heat-induced proteins were cyclophilin, fructose-1,6-bisphosphate aldolase, transketolase, phosphoglycolate phosphatase, ATPase, photosystem II oxygen-evolving complex 23, and NAD-dependent epimerase/dehydratase. For cherry tomato LA1310, heat-suppressed proteins were aminotransferase, S-adenosyl-L-homocysteine hydrolase, L-ascorbate peroxidase, lactoylglutathione lyase, and Rubisco activase. Heat-induced enzymes were glyoxisomal malate dehydrogenase, phosphoribulokinasee, and ATP synthase. This research resulted in the identification of proteins that were induced/repressed in all tomato cultivars evaluated (e.g., Rubisco activase, methionine synthase, adenosyl-L-homocysteine hydrolase, and others) and those differentially expressed (e.g., transketolase)

    Heart Rate Profiles During Exercise and Incident Parkinson's Disease

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    Objective: To determine whether established heart rate parameters of exercise, related to cardiac autonomic function, are associated with incident Parkinson's disease, independent of both clinical and autonomic prodromal features. Methods: A study of UK Biobank participants who performed a standardized bicycle exercise test (2009–2013), followed until November 2022, and analyzed in January 2024, was carried out. Heart rate increase from rest to exercise, and heart rate decrease from peak exercise to recovery were associated with incident Parkinson's disease. Multivariable adjustment was performed both for clinical characteristics and for prodromal non‐cardiac autonomic features. Results: A total of 69,288 eligible participants (men 48%, mean age 56.8 years [SD 8.2 years]) were followed for 12.5 years: among the 319 (0.5%) who developed Parkinson's disease, recognized prodromal markers (constipation, bladder dysfunction) were more common at baseline. The median lag time to diagnosis was 9.3 years (interquartile range 4.4). Both heart rate increase (37.5 [SD 11.5] vs 40.8 [SD 12.4] b.p.m., p < 0.001) and recovery (23.4 [SD 8.8] vs. 27.8 [SD 10.3] b.p.m., p < 0.001) were significantly lower in incident cases compared with controls. Heart rate recovery was independently associated with incident Parkinson's disease, whereas heart rate increase was not. Specifically, a blunted heart rate lowering during recovery was associated with a 30% higher risk of incident Parkinson's disease (HR 1.3; 95% CI 1.1–1.4; p < 0.001 per 10 beats less recovery). Interpretation: Collectively, this suggests that cardiac autonomic involvement precedes clinically manifest Parkinson's disease, and that heart rate recovery might serve as a quantitative prodromal marker. ANN NEUROL 202

    Oxidative Modifications of Rat Liver Cell Components During Fasciola hepatica Infection

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    The aim of this paper was to assess the influence of Fasciola hepatica infection on oxidative modifications of rat liver cell components such as proteins and lipids. Wistar rats were infected per os with 30 metacercariae of F. hepatica. Activities and concentrations of liver damage markers were determined in the 4th, 7th, and 10th week postinfection (wpi). A decrease in antioxidant capacity of the host liver, manifested by a decrease in total antioxidant status (TAS), was observed. Diminution of antioxidant abilities resulted in enhanced oxidative modifications of lipids and proteins. F. hepatica infection enhanced lipid peroxidation, which was visible in the statistically significant increase in the level of different lipid peroxidation products such as conjugated dienes (CDs), lipid hydroperoxides (LOOHs), malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE). The level of protein modification markers in the rat liver was also significantly changed and the most intensified changes were observed at seventh week postinfection. Concentration of carbonyl groups and dityrosine was significantly increased, whereas the level of tryptophan and sulfhydryl and amino groups was decreased. Changes in the antioxidant abilities of the liver and in the lipid and protein structure of the cell components resulted in destruction of the function of the liver. F. hepatica infection was accompanied by raising serum activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as markers of liver damage. A significant decrease in lysosomal as well as in the total activity of cathepsin B during fasciolosis was also observed

    Rationale and design of the PRAETORIAN-COVID trial:A double-blind, placebo-controlled randomized clinical trial with valsartan for PRevention of Acute rEspiraTORy dIstress syndrome in hospitAlized patieNts with SARS-COV-2 Infection Disease

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    There is much debate on the use of angiotensin receptor blockers (ARBs) in severe acute respiratory syndrome–coronavirus-2 (SARS-CoV-2)–infected patients. Although it has been suggested that ARBs might lead to a higher susceptibility and severity of SARS-CoV-2 infection, experimental data suggest that ARBs may reduce acute lung injury via blocking angiotensin-II–mediated pulmonary permeability, inflammation, and fibrosis. However, despite these hypotheses, specific studies on ARBs in SARS-CoV-2 patients are lacking. Methods: The PRAETORIAN-COVID trial is a multicenter, double-blind, placebo-controlled 1:1 randomized clinical trial in adult hospitalized SARS-CoV-2–infected patients (n = 651). The primary aim is to investigate the effect of the ARB valsartan compared to placebo on the composite end point of admission to an intensive care unit, mechanical ventilation, or death within 14 days of randomization. The active-treatment arm will receive valsartan in a dosage titrated to blood pressure up to a maximum of 160 mg bid, and the placebo arm will receive matching placebo. Treatment duration will be 14 days, or until the occurrence of the primary end point or until hospital discharge, if either of these occurs within 14 days. The trial is registered at clinicaltrials.gov (NCT04335786, 2020). The PRAETORIAN-COVID trial is a double-blind, placebo-controlled 1:1 randomized trial to assess the effect of valsartan compared to placebo on the occurrence of ICU admission, mechanical ventilation, and death in hospitalized SARS-CoV-2–infected patients. The results of this study might impact the treatment of SARS-CoV-2 patients globally

    Association of Objectively Measured Sedentary Behavior With Arterial Stiffness: Findings From the Nijmegen Exercise Study

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    Sedentary behavior (SB) may affect arterial stiffness, preceding the development of cardiovascular disease. We investigated the association of objectively measured SB with arterial stiffness. We also investigated factors that affected this association. We recruited adult volunteers and measured SB with thigh-worn accelerometery for 24 hrs/day for eight consecutive days. Central (carotid-femoral pulse wave velocity, cfPWV, gold standard) and local carotid arterial stiffness (stiffness index Beta and pressure-strain elasticity EP) were measured with ultrasound. Linear regression was used and adjusted for demographics, cardiometabolic factors, and moderate-to-vigorous physical activity (MVPA) volume. Effect modification was studied with interaction terms. Participants (N = 664, 64 (standard deviation: 11, range: 23–89) years, 397 (59.8%) male) demonstrated 9.1 (1.6) hrs/day of SB, and arterial stiffness was 8.6 (3.0) m/s for cfPWV, 6.4 (2.9) for Beta, and 87 (43) kPa for EP. SB was not associated with cfPWV (β = 0.04 95% CI (−0.11, 0.18), p = 0.60). The association of SB with local arterial stiffness was modified by systolic blood pressure (SBP) and MVPA volume. Stratified analyses revealed positive associations of SB with Beta (β = 0.29 (0.05, 0.53), p = 0.016) and EP (β = 4.83 (1.39, 8.27), p = 0.006) in participants with SBP > 134 mmHg or > 103 min/day of MVPA (β = 0.23 (0.03, 0.42), p = 0.024 and β = 3.55 (0.82, 6.29), p = 0.011, respectively). We found no association of objectively measured SB with central arterial stiffness. However, SB was positively associated with local carotid stiffness in participants with higher SBP or MVPA levels. In certain subgroups, SB may affect carotid arterial stiffening, reinforcing the relation between SB and cardiovascular disease
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