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Fruit ripening is a complex and highly coordinated developmental process involving the expression of many ripening-related genes under the control of a network of signalling pathways. The hormonal control of climacteric fruit ripening, especially ethylene perception and signalling transduction in tomato has been well characterized. Additionally, great strides have been made in understanding some of the major regulatory switches (transcription factors such as RIPENING-INHIBITOR and other transcriptional regulators such as COLOURLESS NON-RIPENING, TOMATO AGAMOUS-LIKE1 and ETHYLENE RESPONSE FACTORs), that are involved in tomato fruit ripening. In contrast, the regulatory network related to non-climacteric fruit ripening remains poorly understood. However, some of the most recent breakthrough research data have provided several lines of evidences for abscisic acid- and sucrose-mediated ripening of strawberry, a non-climacteric fruit model. In this review, we discuss the most recent research findings concerning the hormonal regulation of fleshy fruit ripening and their cross-talk and the future challenges taking tomato as a climacteric fruit model and strawberry as a non-climacteric fruit model. We also highlight the possible contribution of epigenetic changes including the role of plant microRNAs, which is opening new avenues and great possibilities in the fields of fruit-ripening research and postharvest biology.

Pollination of many flowers initiates a sequence of precisely regulated developmental events that include senescence of the perianth and development of the ovary. The plant hormone ethylene is known to play a key role in regulating the biochemical and anatomical changes that constitute the postpollination syndrome. For this reason, we have studied the pollination syndrome in Phalaenopsis orchids by examining the spatial and temporal location of ethylene biosynthesis within the orchid flower, and how this biosynthesis is regulated by factors that influence expression of genes that encode key enzymes in the ethylene biosynthetic pathway. In particular, we examined the role in the postpollination syndrome of the expression of the gene for 1-aminocyclopropanecarboxylate 1-(ACC) oxidase, which catalyzes the conversion of ACC to ethylene. In vivo incubation of tissues with the ethylene precursor ACC demonstrated that ACC oxidase activity increases after pollination in the stigma, contrary to the observation that activity is constitutive in petunia and carnation gynoecia. RNA blot hybridization of floral tissues indicates that the increase in ACC oxidase activity is due to de novo synthesis of mRNA and presumably protein, which is induced after pollination. Furthermore, the pattern of induction is consistent with a model of coordinate regulation of gene expression in which the pollination signal travels to other organs of the flower to induce their ethylene production. We have also used in situ hybridization to define further the temporal and spatial expression of ACC oxidase within the floral organs, showing that expression, and, by inference, the capability to oxidize ACC to ethylene, is induced in all living cells of the tissues examined after pollination. These findings contrast with work in petunia that suggests that ACC oxidase is localized to the stigmatic surface

Dark-grown pea seedlings (Pisum sativum L.) were irradiated for a short period each day with low intensity red light (662 nm), red light immediately followed by far red light (730 nm), or far red light alone. Other plants were transferred to a white light regime (14 hours light/10 hours dark). There was no change in the amount of RNA in the tissue on a fresh weight basis after the various treatments. However, compared with dark-grown seedlings, those plants irradiated with red light showed an increase in the net RNA content per stem apex. In addition there was a two- to three-fold increase in ribosomal RNA of the etioplasts relative to the total ribosomal RNA. These increases were comparable to those found in plants grown in the white light regime. The changes were much smaller if the dark-grown plants were irradiated either with red light followed by far red light, or with far red light alone. Thus continuous light is not essential for the production of ribosomal RNA in plastids, and the levels of ribosomal RNA found in chloroplasts can also be attained in etioplasts of pea leaves in the dark provided the leaf phytochrome is maintained in its active form.

Age, Obesity, and Sex Effects on Insulin Sensitivity and Skeletal Muscle Mitochondrial Function Helen Karakelides , Brian A. Irving , Kevin R. Short , Peter O'Brien and K. Sreekumaran Nair From the Division of Endocrinology, Endocrinology Research Unit, Mayo Clinic College of Medicine, Rochester, Minnesota. Corresponding author: K. Sreekumaran Nair, nair.sree{at}mayo.edu . Abstract OBJECTIVE Reductions in insulin sensitivity in conjunction with muscle mitochondrial dysfunction have been reported to occur in many conditions including aging. The objective was to determine whether insulin resistance and mitochondrial dysfunction are directly related to chronological age or are related to age-related changes in body composition. RESEARCH DESIGN AND METHODS Twelve young lean, 12 young obese, 12 elderly lean, and 12 elderly obese sedentary adults were studied. Insulin sensitivity was measured by a hyperinsulinemic-euglycemic clamp, and skeletal muscle mitochondrial ATP production rates (MAPRs) were measured in freshly isolated mitochondria obtained from vastus lateralis biopsy samples using the luciferase reaction. RESULTS Obese participants, independent of age, had reduced insulin sensitivity based on lower rates of glucose infusion during a hyperinsulinemic-euglycemic clamp. In contrast, age had no independent effect on insulin sensitivity. However, the elderly participants had lower muscle MAPRs than the young participants, independent of obesity. Elderly participants also had higher levels inflammatory cytokines and total adiponectin. In addition, higher muscle MAPRs were also noted in men than in women, whereas glucose infusion rates were higher in women. CONCLUSIONS The results demonstrate that age-related reductions in insulin sensitivity are likely due to an age-related increase in adiposity rather than a consequence of advanced chronological age. The results also indicate that an age-related decrease in muscle mitochondrial function is neither related to adiposity nor insulin sensitivity. Of interest, a higher mitochondrial ATP production capacity was noted in the men, whereas the women were more insulin sensitive, demonstrating further dissociation between insulin sensitivity and muscle mitochondrial function. Footnotes The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Received April 22, 2009. Accepted October 6, 2009. © 2010 American Diabetes Association

Chronic inflammation is postulated to be involved in the development of end-stage renal disease in diabetes, but which specific circulating inflammatory proteins contribute to this risk remain unknown. To study this, we examined 194 circulating inflammatory proteins in subjects from three independent cohorts with type 1 and type 2 diabetes. In each cohort, we identified an extremely robust kidney risk inflammatory signature (KRIS), consisting of 17 proteins enriched in tumor necrosis factor-receptor superfamily members, that was associated with a 10-year risk of end-stage renal disease. All these proteins had a systemic, non-kidney source. Our prospective study findings provide strong evidence that KRIS proteins contribute to the inflammatory process underlying end-stage renal disease development in both types of diabetes. These proteins point to new therapeutic targets and new prognostic tests to identify subjects at risk of end-stage renal disease, as well as biomarkers to measure responses to treatment of diabetic kidney disease.A robust signature of circulating inflammatory proteins is causally associated with 10-year risk of progression to end-stage renal disease in diabetic patients

High-resolution MRI and histopathological study of the brains of patients who had died from Covid-19 showed punctate hyperintensities and punctate or linear hypointensities, which represented various forms of pauci-inflammatory microvasculopathy. No evidence of active viral infection was found.

Insulin is as a major postprandial hormone with profound effects on carbohydrate, fat, and protein metabolism. In the absence of exogenous insulin, patients with type 1 diabetes exhibit a variety of metabolic abnormalities including hyperglycemia, glycosurea, accelerated ketogenesis, and muscle wasting due to increased proteolysis. We analyzed plasma from type 1 diabetic (T1D) humans during insulin treatment (I+) and acute insulin deprivation (I-) and non-diabetic participants (ND) by 1H nuclear magnetic resonance spectroscopy and liquid chromatography-tandem mass spectrometry. The aim was to determine if this combination of analytical methods could provide information on metabolic pathways known to be altered by insulin deficiency. Multivariate statistics differentiated proton spectra from I- and I+ based on several derived plasma metabolites that were elevated during insulin deprivation (lactate, acetate, allantoin, ketones). Mass spectrometry revealed significant perturbations in levels of plasma amino acids and amino acid metabolites during insulin deprivation. Further analysis of metabolite levels measured by the two analytical techniques indicates several known metabolic pathways that are perturbed in T1D (I-) (protein synthesis and breakdown, gluconeogenesis, ketogenesis, amino acid oxidation, mitochondrial bioenergetics, and oxidative stress). This work demonstrates the promise of combining multiple analytical methods with advanced statistical methods in quantitative metabolomics research, which we have applied to the clinical situation of acute insulin deprivation in T1D to reflect the numerous metabolic pathways known to be affected by insulin deficiency.

Insulin is as a major postprandial hormone with profound effects on carbohydrate, fat, and protein metabolism. In the absence of exogenous insulin, patients with type 1 diabetes exhibit a variety of metabolic abnormalities including hyperglycemia, glycosurea, accelerated ketogenesis, and muscle wasting due to increased proteolysis. We analyzed plasma from type 1 diabetic (T1D) humans during insulin treatment (I+) and acute insulin deprivation (I-) and non-diabetic participants (ND) by (1)H nuclear magnetic resonance spectroscopy and liquid chromatography-tandem mass spectrometry. The aim was to determine if this combination of analytical methods could provide information on metabolic pathways known to be altered by insulin deficiency. Multivariate statistics differentiated proton spectra from I- and I+ based on several derived plasma metabolites that were elevated during insulin deprivation (lactate, acetate, allantoin, ketones). Mass spectrometry revealed significant perturbations in levels of plasma amino acids and amino acid metabolites during insulin deprivation. Further analysis of metabolite levels measured by the two analytical techniques indicates several known metabolic pathways that are perturbed in T1D (I-) (protein synthesis and breakdown, gluconeogenesis, ketogenesis, amino acid oxidation, mitochondrial bioenergetics, and oxidative stress). This work demonstrates the promise of combining multiple analytical methods with advanced statistical methods in quantitative metabolomics research, which we have applied to the clinical situation of acute insulin deprivation in T1D to reflect the numerous metabolic pathways known to be affected by insulin deficiency.

There is limited evidence about how vocational rehabilitation (VR) for people with multiple sclerosis (MS) can be delivered through the United Kingdom's (UK) National Health Service (NHS) and how it works. To understand the mechanisms and context for implementing a VR intervention for people with MS in the NHS and develop an explanatory programme theory. A realist evaluation, including a review of evidence followed by semi-structured interviews. A realist review about VR for people with MS in the NHS was conducted on six electronic databases (PubMed, MEDLINE, PsychINFO, Web of Science, CINAHL, and EMBASE) with secondary purposive searches. Included studies were assessed for relevance and rigour. Semi-structured interviews with people with MS, employers, and healthcare professionals, were conducted remotely. Data were extracted, analysed, and synthesised to refine the programme theory and produce a logic model. Data from 13 studies, and 19 interviews (10 people with MS, five employers, and four healthcare professionals) contributed to producing the programme theory. The resulting programme theory explains the implementation of VR in the NHS for MS populations, uncovering the complex interplay between the healthcare and employment sectors to influence health and employment outcomes. VR programmes that offer timely support, tailored to the needs of the person with MS, and that support and empower the employee beyond the healthcare context are most likely associated with improved employment outcomes, for example, job retention. Embedding VR support within the NHS requires substantial cultural and organisational change (e.g., increased staff numbers, training, and awareness about the benefits of work). This study emphasises the need to routinely identify people with MS at risk of job loss and follow a collaborative approach to address employment issues. This realist evaluation provides insight on how to improve the quality of care available to people with MS.

Parkinson’s Disease (PD) is the second most common neurodegenerative disease behind Alzheimer’s Disease, currently affecting more than 10 million people worldwide and 1.5 times more males than females. The progression of PD results in the loss of function due to neurodegeneration and neuroinflammation. The etiology of PD is multifactorial, including both genetic and environmental origins. Here we explored changes in RNA editing, specifically editing through the actions of the Adenosine Deaminases Acting on RNA (ADARs), in the progression of PD. Analysis of ADAR editing of skeletal muscle transcriptomes from PD patients and controls, including those that engaged in a rehabilitative exercise training program revealed significant differences in ADAR editing patterns based on age, disease status, and following rehabilitative exercise. Further, deleterious editing events in protein coding regions were identified in multiple genes with known associations to PD pathogenesis. Our findings of differential ADAR editing complement findings of changes in transcriptional networks identified by a recent study and offer insights into dynamic ADAR editing changes associated with PD pathogenesis.