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We assess the effects of aerobic exercise on the soleus and plantaris muscles in adult rats submitted to maternal protein restriction (MPR) during pregnancy and lactation. Male offspring born from dams fed with control (17%-control) or low protein diets (6%-restricted) were randomly assigned to untrained or aerobic exercise, and morphological, biochemical, molecular, and proteomic analyses were performed. The proteome analysis showed many proteins involved with muscle energy metabolism, with emphasis on the glycolysis (ALDOA, ENO1, PGAM2, and TPI1) and glycogen (PYGM) pathways. MPR decreased ALDOA, TPI1, ENO1, PGAM2, and PYGM expression and increased glycogen content in Soleus (SOL); Plantaris (PL) increased PYGM, ALDOA, GAPDH, PKM, and TPI1 protein expression. Aerobic exercise (AE) normalized the glycemic index in restricted animals and increased the expression of proteins PYGM, ALDOA, ENO1, PGAM2, and TPI1, also decreasing glycogen content in the SOL. In the PL, aerobic exercise increased PYGM, ALDOA, GAPDH, PKM, and TPI1 proteins without a change in muscle glycogen content. Our study demonstrates that MPR and AE promoted differential muscle-specific adaptations, and aerobic exercise can represent a way to attenuate early muscle morphophysiological and metabolic changes in offspring rats submitted to MPR.

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Developing tailor-made conductive filaments has emerged as a promising niche for producing affordable and high-performance 3D-printed electrochemical sensors. In this context, we propose a novel conductive filament based on graphite, nickel, and polylactic acid (G/Ni/PLA) for the fabrication of non-enzymatic electrochemical sensors aimed at glucose (GLU) determination, a key biomarker in diabetes diagnosis. The materials were thoroughly characterized using morphological, structural, elemental, and electrochemical techniques, which confirmed the effective incorporation of G and Ni into the thermoplastic matrix. Special emphasis was placed on the electrochemical conversion of Ni2⁺ in an alkaline medium (0.1 mol L⁻1 NaOH) into redox-active species (Ni(OH)2 and NiOOH), which mediate the electrocatalytic oxidation of GLU. Additionally, the influence of varying nickel contents (7.5 %, 10 %, and 12.5 % wt.) on the electrochemical response towards GLU was systematically investigated, with the best performance observed at the highest nickel loading. The innovative 3D-printed G/Ni/PLA sensor was integrated with a batch injection analysis (BIA) system for rapid and sensitive amperometric detection of GLU in artificial biological fluids. The sensor demonstrated a wide linear range (50-1500 µmol L⁻1), a low detection limit (2.6 µmol L⁻1), excellent repeatability (RSD < 9.0 %), and high selectivity, even in the presence of potential interferents such as urea, uric acid, and ascorbic acid. Furthermore, the method was successfully applied to analyze synthetic saliva (a non-invasive sample matrix) and blood plasma under normal and abnormal GLU levels, achieving satisfactory recovery rates ranging from 93 % to 100 %. Therefore, the proposed analytical approach is simple, selective, precise, and accurate, making it highly suitable for non-enzymatic GLU sensing in clinical samples, contributing to the effective diagnosis of diabetes.

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AIMS: Type 2 diabetes (T2D) is a prevalent metabolic disease linked to obesity and metabolic syndrome (MS). The glucolipotoxic environment (GLT) impacts tissues causing low-grade inflammation, insulin resistance and the gradual loss of pancreatic ß-cell function, leading to hyperglycemia. We have previously shown that Compound A (CpdA), a plant-derived dissociative glucocorticoid receptor-modulator with inflammation-suppressive activity, displays protective effects on ß-cells in type 1 diabetes murine models. This study aimed to evaluate whether the administration of CpdA can attenuate GLT effects and improve pathophysiological parameters in a murine model of T2D/MS. MAIN METHODS: Eight-week-old male C57BL/6NCrl mice were fed either a standard chow diet or a high-fat/high-sucrose diet (HFHS) for 15 weeks. From week 5 of feeding, each group received i.p. injections of CpdA (2.5 µg/g) or vehicle three times a week. We also examined CpdA in vitro effect against GLT using the insulinoma cell line INS-1E and naïve isolated mouse islets. KEY FINDINGS: CpdA administration in HFHS fed mice improved glucose homeostasis and insulin sensitivity with no apparent side effects. CpdA treatment also preserved pancreatic islet architecture and insulin expression, while reducing hepatic steatosis and visceral adipose tissue inflammation induced by HFHS diet. In vitro assays in INS-1E cells and naïve isolated mouse islets demonstrated that CpdA counteracted GLT-induced inhibition of glucose-stimulated insulin secretion and supported the expression of key ß-cell identity genes under GLT conditions. SIGNIFICANCE: These findings highlight the potential protective effect of CpdA in preserving ß-cell functionality and peripheral tissue physiology in the context of T2D/MS.

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The metabolites gluconic acid, 5-ketogluconic acid, proline, and glutamic acid, produced by Pseudomonas reptilivora B-6bs, are industrially important, particularly in food and pharmaceutical sectors. However, producing these metabolites involves biotin supplementation to enhance yields, which is an expensive additive, and reducing its use can significantly lower production costs. Thus, This study aimed to enhance the production of gluconic acid, 5-ketogluconic acid, proline, and glutamic acid without biotin supplementation. To achieve this, a full factorial design was employed, varying agitation speed, glucose concentration, and temperature to determine the optimal conditions for metabolite production. Metabolite concentration was measured using spectrophotometric analysis and thin-layer chromatography (TLC), and the results were statistically analyzed using Minitab® 18. The findings demonstrate that Pseudomonas reptilivora B-6bs effectively produce gluconic acid (50.51 ± 0.035 g/L, YP/S: 0.917 g/g) and 5-ketogluconic acid (44.46 ± 0.23 g/L, YP/S: 0.947 g/g), along with proline (0.1727 ± 0.00085 g/L, YP/S: 0.00004 g/g) and glutamic acid (0.853 ± 0.142 g/L, YP/S: 0.013 g/g) without biotin supplementation. Optimal production was observed with a glucose concentration of 55 g/L. These findings provide a viable biotin-independent strategy for high-value metabolite production. This study contributes novel insights into cost-effective production processes, making it relevant to industrial applications.

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Diabetes mellitus is a metabolic syndrome that has grown globally to become a significant public health challenge. Hypothesizing that the plasma membrane protein, transient receptor potential ankyrin-1, is a pivotal target in insulin resistance, we investigated the mechanism of action of cinnamaldehyde (CIN), an electrophilic TRPA1 agonist, in skeletal muscle, a primary insulin target. Specifically, we evaluated the effect of CIN on insulin resistance, hepatic glycogen accumulation and muscle and adipose tissue glucose uptake. Furthermore, the in vitro role of CIN in glucose uptake and intracellular signaling was determined in insulin-resistant rats whose calcium influx was analyzed. Moreover, the serum lipid profile was assessed following short-term CIN treatment in rats, and lipid tolerance was analyzed. The effects of CIN on insulin resistance were mediated by TRPA1, with downstream signaling involving the activation of PI3-K, MAPK, PKC, as well as extracellular calcium and calcium release from intracellular stores. Additionally, cytoskeleton integrity was required for the complete action of CIN on glucose uptake in muscle. CIN also ameliorated the serum lipid profile and improved triglyceride tolerance following acute vivo exposure.

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Second-generation (2G) bioethanol production, derived from lignocellulosic biomass, has emerged as a sustainable alternative to fossil fuels by addressing growing energy demands and environmental concerns. Fungal sugar transporters (STs) play a critical role in this process, enabling the uptake of monosaccharides such as glucose and xylose, which are released during the enzymatic hydrolysis of biomass. This mini-review explores recent advances in the structural and functional characterization of STs in filamentous fungi and yeasts, highlighting their roles in processes such as cellulase induction, carbon catabolite repression, and sugar signaling pathways. The review also emphasizes the potential of genetic engineering to enhance the specificity and efficiency of these transporters, overcoming challenges such as substrate competition and limited pentose metabolism in industrial strains. By integrating the latest research findings, this work underscores the pivotal role of fungal STs in optimizing lignocellulosic bioethanol production and advancing the bioeconomy. Future prospects for engineering transport systems and their implications for industrial biotechnology are also discussed. KEY POINTS: STs present a conserved structure with different sugar affinities STs are involved in the signaling and transport of sugars derived from plant biomass Genetic engineering of STs can improve 2G bioethanol production.

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BACKGROUND: The aims of this review were to identify and to analyze the clinical studies that used subcutaneous injections of dextrose for treating musculoskeletal pain, in order to establish an overview. METHODS: A systematic search was carried out in scientific databases including Web of Science, Cochrane Central Register of Controlled Trials, PUBMED and other sources, up until March 2024. We included clinical studies that used subcutaneous injections of dextrose in the treatment of individuals with musculoskeletal pain associated with tendinopathies, enthesopathy, osteoarthritis, ligament sprains, muscle strains or bursitis of various locations. RESULTS: Twenty studies that met the criteria were included in this review; of those, 13 were randomized clinical trials, one non-randomized comparative study and six were case series studies, comprising a total of 1226 patients. In all included studies, efficacy in pain reduction was reported in the groups treated with dextrose when comparing evaluations at baseline, short term and medium term. CONCLUSIONS: Subcutaneous injections of dextrose could be a beneficial treatment for reducing musculoskeletal pain; however, factors such as the high heterogeneity in the treatment schemes, uncertainty in the mechanisms of action and the level of evidence found, indicate that this technique is still under development.

Injections of sugar, a sweet solution against painWhat is this article about?People with problems in their joints, tendons or muscles are often in pain, and in many occasions their mobility is quite poor. Recently, medical personnel started using injections of watery sugar in these painful areas, and the results have been great. Instead of taking pain killers, or pay for expensive treatments (such as massages, application of heat, injections of steroids, etc.), liquid sugar is injected around the painful area and the pain eases or even goes away completely for many weeks. This information was found on the Internet, in medical studies.What were the results?Several people who have joint pain, tendon pain or muscle pain received a few injections of liquid sugar; then, little by little, they felt less and less pain. These people said that the pain was gone for weeks or even months after receiving the injections; they also loved the fact that they did not feel any negative effects.What do the results of the study mean?Because the injections of liquid sugar have a low cost and are easy to apply, they should be used more often in people who suffer pain in joints, tendons and/or muscles, and forget about more problematic treatments. More medical studies have to confirm this.

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OBJECTIVE: The efficacy of icodextrin versus glucose patients undergoing peritoneal dialysis remains unclear. The study was designed to compare the effects of once-daily long-dwell icodextrin versus glucose on markers of hypervolemia and survival among patients with kidney failure undergoing an unplanned initiation of automated peritoneal dialysis. METHODS: This was a randomized, non-blinded, and prospective controlled study. Prevalent and stable patients undergoing automated peritoneal dialysis with a recent peritoneal equilibration test showing a dialysate/plasma creatinine of >0.50 were randomized to receive either 7.5% icodextrin or 2.5% glucose solution. Patients were evaluated at baseline (one month after the start of peritoneal dialysis), 3 months, and 6 months after inclusion. The peritoneal dialysis solution was used for at least 3 months, with a follow-up period of 24 months. RESULTS: Thirty patients were enrolled. There were no baseline differences between the groups. During the study period, patients in the Icodextrin Group showed improvements in the phase angle and ultrafiltration, whereas there were no changes in the Glucose Group. Additionally, extracellular water was significantly lower in the Icodextrin Group at the end of the study than at baseline. No statistical differences between the two groups were observed in urine volume, ultrafiltration, extracellular water, phase angle, renal creatinine clearance, use of diuretics and antihypertensives, or blood pressure. During the 24-month follow-up, the number of events related to overall mortality was seven (Icodextrin Group, n=4; Glucose Group, n=3), with no difference between the groups for this outcome or technique survival. CONCLUSION: Icodextrin significantly improved ultrafiltration, extracellular water, and phase angle at the end of the study compared to baseline in patients on the urgent start of automated peritoneal dialysis. REGISTRY OF CLINICAL TRIALS: (www.ctri.nic.in) under the number RBR-97z4wh6.

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Growth hormone (GH) has several metabolic effects, including a profound impact on glucose homeostasis. For example, GH oversecretion induces insulin resistance and increases the risk of developing diabetes mellitus. Here, we show that GH receptor (GHR) ablation in vesicular glutamate transporter 2 (VGLUT2)-expressing cells, which comprise a subgroup of glutamatergic neurons, led to a slight decrease in lean body mass without inducing changes in body adiposity. VGLUT2∆GHR mice exhibited reduced glycemia and improved glucose tolerance and insulin sensitivity. Among different glutamatergic neuronal populations, we found that GHR inactivation in Sim1-expressing cells recapitulated the phenotype observed in VGLUT2∆GHR mice. Furthermore, Sim1∆GHR mice exhibited reduced endogenous glucose production and improved hepatic insulin sensitivity without alterations in whole-body or muscle glucose uptake. Sim1∆GHR mice were protected against acute but not chronic diabetogenic effects of exogenous GH administration. Pharmacological activation of ATP-sensitive potassium channels in the brain normalized blood glucose levels in Sim1∆GHR mice. In conclusion, the absence of GHR signaling in VGLUT2/Sim1-expressing cells causes a persistent reduction in glycemia and improves hepatic insulin sensitivity. Central glucose-sensing mechanisms are likely involved in the reduced glycemia exhibited by Sim1∆GHR mice. The current findings uncover a mechanism involved in the effects of GHR signaling in regulating glucose homeostasis.

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This work reports on the assessment of a non-hydrolytic electrochemical sensor for glucose sensing that is developed using functionalized carbon nanotubes (fCNTs)/Co(OH)2. The morphology of the nanocomposite was investigated by scanning electron microscopy, which revealed that the CNTs interacted with Co(OH)2. This content formed a nanocomposite that improved the electrochemical characterizations of the electrode, including the electrochemical active surface area and capacitance, thus improving sensitivity to glucose. In the electrochemical characterization by cyclic voltammetry and chronoamperometry, the increase in catalytic activity by Co(OH)2 improved the stability and reproducibility of the glucose sensor without the use of enzymes, and its concentration range was between 50 and 700 µmol L-1. The sensor exhibited good linearity towards glucose with LOD value of 43.200 µmol L-1, which proved that the Co(OH)2-fCNTs composite is judicious for constructing cost effective and feasible sensor for glucose detection.

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BACKGROUND: During diabetes, prorenin is highly produced by the renal collecting ducts. The binding of prorenin to (pro)renin receptor (PRR) on the apical plasma membrane triggers intracellular profibrotic genes, including TGF-ß and CTGF. However, the underlying mechanisms contributing to the stimulation of these pathways remain unclear. Hence, we hypothesize that the glucose transporter-1 (GLUT1) favors the PRR-dependent stimulation of TGF-ß and CTGF in the distal nephron segments during high glucose (HG) conditions. METHODS: To test this hypothesis, primary cultured renal inner medullary collecting duct (IMCD) cells were treated with normal glucose (NG, 5 mM) or high glucose (HG, 25 mM) for 48 h in the presence or absence of the GLUT1-specific inhibitor BAY 876 (2 nM). Additionally, IMCD cells were treated with the PRR antagonist PRO20. The expression of TGF-ß and CTGF was quantified by immunoblot and qRT-PCR. RESULTS: HG increased GLUT1 mRNA and protein abundance, while BAY 876 inhibited these responses. HG treatment upregulated PRR, but the concomitant treatment with BAY 876 partially prevented this effect. TGF-ß and CTGF expressions were augmented in IMCD cells treated with HG. However, PRO20 prevented the increases in TGF-ß but not those of CTGF. GLUT1 inhibition partially prevented the increases in reactive oxygen species (ROS) during HG while PRO20 did not. ROS scavenging impaired CTGF upregulation during HG conditions. Additionally, long-term exposure to HG increases lipid peroxidation and reduced cell viability. CONCLUSIONS: The data indicate that glucose transportation via GLUT1 is implicated in the PRR-dependent upregulation of TGF-ß while CTGF is mediated mainly via a mechanism depending on ROS formation in renal medullary collecting duct cells.

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Bioethanol represents a clean and renewable alternative to fossil fuels, offering a significant reduction in environmental impact. Second-generation ethanol (2G) is produced using lignocellulosic biomass, which presents additional challenges due to the presence of hemicellulose. The pentose sugars within hemicellulose cannot be efficiently metabolized by conventional yeast strains like Saccharomyces cerevisiae. Consequently, the yeast Spathaspora passalidarum has emerged as a promising candidate for mixed fermentation processes, given its ability to utilize xylose. This study presents an in-depth metabolic, stoichiometric, and kinetic analysis of the fermentation performance of Sp. passalidarum NRRL Y-27907 in mixed glucose and xylose cultures. Emphasis was placed on examining variables from a novel perspective compared to existing literature. Specifically, the impacts of initial inoculum-substrate ratios, substrate composition, pH, temperature, and ethanol sensitivity were analyzed using a mathematical bioprocess approach. Sp. passalidarum NRRL Y-27907 exhibited sequential sugar consumption, with xylose being utilized only after glucose was exhausted. Ethanol yields in mixed cultures were comparable to those in individual-sugar cultures. The best fermentative performance was observed at 30 °C, with 25 g/L of xylose and an inoculum of 0.50 g/L. The strain exhibited significant robustness at pH 4.0 and was notably affected by initial ethanol concentrations up to 20 g/L. These findings provide crucial insights into the metabolic and fermentative behavior of Sp. passalidarum NRRL Y-27907, offering valuable information for the design of consolidated bioprocesses from lignocellulosic materials.

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Pharmacological preconditioning is an alternative to protect the heart against the consequences of damage from ischemia/reperfusion (I/R). It is based on the administration of specific drugs that imitate the effect of ischemic preconditioning (IPC). Peroxisomal proliferator-activated receptors (PPARs) can prevent apoptosis in pathologies such as I/R and heart failure. Therefore, our objective was to determine if the stimulation of PPARα with fenofibrate (feno) decreases the apoptotic process induced by hypoxia/reoxygenation (HR), high glucose (HG), and HR/HG. For that purpose, cardiomyocyte cultures were divided into the following groups: Group 1-control (Ctrl); Group 2-HR; Group 3-HR + 10 µM feno; Group 4-HG, (25 mM glucose); Group 5-HG + feno; Group 6-HR/HG, and Group 7-HR/HG + feno. Our results indicate that cell viability decreases in neonatal cardiomyocytes undergoing HR, HG, and their combination, while feno improved cell viability. Feno treatment decreased apoptosis compared with HG-, HR-, or HG/HR-vehicle-treated. Nuclear- and mitochondrial-apoptosis markers increased in neonatal cardiomyocytes from HR, HG, and HR/HG; while the cytotoxicity decreased in cells treated with feno. In addition, the expression of Bax, Bad, and caspase 9 decreased due to feno, while 14-3-3ɛ and Bcl2 were increased. Inner mitochondrial cytochrome C increased with feno in every condition, as well as mitochondrial activity. Feno treatment prevented injury in the ultrastructure and in the mitochondrial membranes. Thus, our results suggest that feno decreases apoptosis in neonatal cardiomyocytes, improving the ultrastructure of mitochondria in the pathological conditions studied.

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COVID-19, caused by SARS-CoV-2, presents diverse symptoms, including neurological manifestations. This study investigated COVID-19's neurological sequelae, focusing on the central nervous system's involvement through cerebral glycolytic metabolism assessed via PET/CT. Twenty-two patients with mild long COVID cognitive symptoms and 20 healthy volunteers without cognitive, psychiatric, or neurological impairments and no history of COVID-19 infection underwent cerebral PET/CT scans using [18F]FDG to assess cerebral metabolism. The study meticulously evaluated the uptake of [18F]FDG in various brain regions, employing the CortexID Suite software for quantitative analysis. The analysis focused on identifying areas of hypometabolism and hypermetabolism, indicative of altered glucose metabolism possibly related to COVID-19's neurological impact. No statistically significant differences were found between the mild COVID and healthy groups. Although our sample was too small to generate a statistical difference between groups, future studies should explore some findings, such as hypometabolism in 15 regions and hypermetabolism in 11 regions in the mild COVID group. These changes, especially in areas linked to executive functions, sensory perception, and emotional regulation, suggest nuanced alterations in brain function. Our study did not find significant glycolytic metabolic changes in patients with mild long COVID. However, areas of glycolytic hypometabolism and hypermetabolism found in some patients showed biological plausibility with the cognitive and affective symptoms they presented. Future investigations with a larger sample size should be correlated with neuropsychological and neuropsychiatric examinations to confirm this relationship.

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Perinatal asphyxia (PA) is a clinical condition characterized by oxygen supply suspension before, during, or immediately after birth, and it is an important risk factor for neurodevelopmental damage. Its estimated 1/1000 live births incidence in developed countries rises to 5-10-fold in developing countries. Schizophrenia, cerebral palsy, mental retardation, epilepsy, blindness, and others are among the highly disabling chronic pathologies associated with PA. However, so far, there is no effective therapy to neutralize or reduce PA-induced harm. Selective regulators of estrogen activity in tissues and selective estrogen receptor modulators like raloxifene have shown neuroprotective activity in different pathological scenarios. Their effect on PA is yet unknown. The purpose of this paper is to examine whether raloxifene showed neuroprotection in an oxygen-glucose deprivation/reoxygenation astrocyte cell model. To study this issue, T98G cells in culture were treated with a glucose-free DMEM medium and incubated at 37 °C in a hypoxia chamber with 1% O2 for 3, 6, 12, and 24 h. Cultures were supplemented with raloxifene 10, and 100 nM during both glucose and oxygen deprivation and reoxygenation periods. Raloxifene 100 nM and 10 nM improved cell survival-65.34% and 70.56%, respectively, compared with the control cell groups. Mitochondrial membrane potential was preserved by 58.9% 10 nM raloxifene and 81.57% 100 nM raloxifene cotreatment. Raloxifene co-treatment reduced superoxide production by 72.72% and peroxide production by 57%. Mitochondrial mass was preserved by 47.4%, 75.5%, and 89% in T98G cells exposed to 6-h oxygen-glucose deprivation followed by 3, 6, and 9 h of reoxygenation, respectively. Therefore, raloxifene improved cell survival and mitochondrial membrane potential and reduced lipid peroxidation and reactive oxygen species (ROS) production, suggesting a direct effect on mitochondria. In this study, raloxifene protected oxygen-glucose-deprived astrocyte cells, used to mimic hypoxic-ischemic brain injury. Two examiners performed the qualitative assessment in a double-blind fashion.

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BACKGROUND: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have demonstrated cardiovascular benefits in various settings. However, their impact after myocardial infarction (MI) in patients without prior heart failure remains unclear. Therefore, we conducted a meta-analysis comparing SGLT2i to placebo in post-MI patients. METHODS: We systematically searched Pubmed, Embase, and Cochrane Central for randomized controlled trials (RCTs) comparing SGLT2i to placebo in post-MI patients. We calculated the Risk Ratio (RR) for binary outcomes and 95% confidence intervals (CI). Statistical analysis was performed using Review Manager 5.4. A random-effects model was used for all outcomes. Heterogeneity was examined with I2 statistics. RESULTS: We included 3 RCTs comprising 11,065 patients in this meta-analysis, where 79.5% were male with a mean age of 61.9 years old. Two studies evaluated Empaglifozin and one Dapagliflozin. There was no statistically significant difference between groups in all-cause mortality (RR 1.05; 95% CI 0.78-1.41; p= 0.76; Figure 1A) and cardiovascular mortality (RR 1.04; 95% CI 0.84-1.29; p= 0.73; Figure 1B). There was a statistically significant reduction in the incidence of heart failure hospitalization in the SGLT2i group (RR 0.73; 95% CI 0.61-0.88; p< 0.01; Figure 1C). CONCLUSION: Our systematic review and meta-analysis found that SGLT2i significantly reduced the incidence of heart failure hospitalization in patients following MI, without significantly affecting all-cause or cardiovascular mortality.

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La hiperglucemia inducida por corticoides es un aumento anormal de la glucosa en sangre debido al uso de glucocorticoides (GC). Su incidencia varía según la dosis, la forma de administración y factores individuales como la edad, el IMC y los antece-dentes familiares de diabetes. Según la ADA, entre el 10% de los pacientes hospita-lizados reciben corticoides, y el 56-86% de estos pueden desarrollar hiperglucemia inducida por corticoides, incluso sin diabetes previa. Los glucocorticoides afectan el metabolismo de carbohidratos al disminuir la absor-ción de glucosa debido a la resistencia a la insulina en el hígado, músculos y otros tejidos periféricos. Los efectos varían según el tipo y la dosis de los glucocorticoides; los de acción intermedia (prednisona) causan principalmente hiperglucemia pos-tprandial, mientras que los de acción prolongada (dexametasona) generan hiperglu-cemia persistente más allá de las 24 horas.En cuanto al tratamiento, los objetivos deben individualizarse según las comorbili-dades, esperanza de vida, adherencia al tratamiento y riesgo de hipoglucemia. Se recomienda un rango objetivo de glucosa de 140 a 180 mg/dL para la mayoría de los pacientes hospitalizados, con ajustes según la condición clínica del paciente, el tipo de glucocorticoide y la dosis recibida. En casos leves, se pueden usar hipogluce-miantes orales como metformina, sulfonilureas, inhibidores de DPP-4 o agonistas del receptor GLP-1. En hiperglucemias más significativas, la insulina es el tratamiento de elección.Esta revisión busca ofrecer una guía completa para el diagnóstico, manejo y trata-miento de estos pacientes, con el objetivo de reducir el riesgo de complicaciones a corto y largo plazo, tanto en el entorno hospitalario como ambulatorio.En conclusión, la identificación de pacientes en riesgo, el monitoreo adecuado de los niveles de glucosa y el ajuste oportuno del tratamiento son fundamentales para minimizar complicaciones y mejorar los resultados clínicos,

Corticosteroid-induced hyperglycemia is an abnormal increase in blood glucose due to the use of glucocorticoids (GCs). Its incidence varies depending on the dose, the method of adminis-tration, and individual factors such as age, BMI, and family history of diabetes. According to the ADA, 10 to 15% of hospitalized patients receive corticosteroids, and 56 to 86% of them may develop corticosteroid-induced hyperglycemia, even without prior diabetes. Glucocorticoids affect carbohydrate metabolism by decreasing glucose absorption due to insulin resistance in the liver, muscle, and other peripheral tissues. The effects vary depending on the type and dose of glucocorticoids; intermediate-acting ones (prednisone) mainly cause postpran-dial hyperglycemia, while long-acting ones (dexamethasone) generate persistent hyperglycemia beyond 24 hours.Regarding treatment, the objectives must be individualized according to comorbidities, life ex-pectancy, adherence to treatment and risk of hypoglycemia. A target glucose range of 140 to 180 mg/dL is recommended for most hospitalized patients, with adjustments based on the patient's clinical condition, type of glucocorticoid, and dose received. In mild cases, oral hypoglycemic agents such as metformin, sulfonylureas, DPP-4 inhibitors, or GLP-1 receptor agonists may be used. In more significant hyperglycemia, insulin is the treatment of choice.This review aims to provide a comprehensive guide for the diagnosis, management and treat-ment of these patients, with the aim of reducing the risk of short- and long-term complications, both in the inpatient and outpatient setting.In conclusion, the identification of patients at risk, adequate control of glucose levels and timely adjustment of treatment are essential to minimize complications and improve clinical outcomes.

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D-xylose, one of the most abundant sugars in lignocellulosic biomass, is not widely used to produce bioproducts with added value, in part due to the absence of industrial microorganisms able to metabolize it efficiently. Herbaspirillum seropedicae Z69 is a ß-proteobacterium able to accumulate poly-3-hydroxybutyrate, a biodegradable thermoplastic biopolymer, with contents higher than 50%. It metabolizes D-xylose by non-phosphorylative pathways. In the genome of Z69, we found the genes xylFGH (ABC D-xylose transporter), xylB, xylD, and xylC (superior non-phosphorylative pathway), and the transcriptional regulator xylR, forming the xyl cluster. We constructed the knock-out mutant Z69ΔxylR that has a reduced growth in D-xylose and in D-glucose, compared with Z69. In addition, we analyzed the expression of xyl genes by RT-qPCR and promoter fusion. These results suggest that XylR activates the expression of genes at the xyl cluster in the presence of D-xylose. On the other hand, XylR does not regulate the expression of xylA, mhpD (lower non-phosphorylative pathways) and araB (L-arabinose dehydrogenase) genes. The participation of D-glucose in the regulation mechanism of these genes must still be elucidated. These results contribute to the development of new strains adapted to consume lignocellulosic sugars for the production of value-added bioproducts.

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Conventionally, the optimization of glucose biosensors is achieved by varying the concentrations of the individual reagents used to immobilize the enzyme. In this work, the effect and interaction between glucose oxidase enzyme (GOx), ferrocene methanol (Fc), and multi-walled carbon nanotubes (MWCNTs) at different concentrations were investigated by a design of experiments (DoE). For this analysis, a factorial design with three factors and two levels each was used with the software RStudio for statistical analysis. The data were obtained by electrochemical experiments on the immobilization of GOx-Fc/MWCNT at different concentrations. The results showed that the factorial DoE method was confirmed by the non-normality of the residuals and the outliers of the experiment. When examining the effects of the variables, analyzing the half-normal distribution and the effects and contrasts for GOx-Fc/MWCNT, the factors that showed the greatest influence on the electrochemical response were GOx, MWCNT, Fc, and MWCNT:Fc, and there is a high correlation between the factors GOx, MWCNT, Fc, and MWCNT:Fc, as shown by the analysis of homoscedasticity and multicollinearity. With these statistical analyses and experimental designs, it was possible to find the optimal conditions for different factors: 10 mM mL-1 GOx, 2 mg mL-1 Fc, and 15 mg mL-1 MWCNT show a greater amperometric response in the glucose oxidation. This work contributes to advancing enzyme immobilization strategies for glucose biosensor applications. Systematic investigation of DoE leads to optimized immobilization for GOx, enables better performance as a glucose biosensor, and allows the prediction of some outcomes.

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The passion fruit peel (PFP) has a high cellulose and hemicellulose content, which can be used to produce fermentable sugars. In this context, this study aims to optimize the release of xylose and the production of xylitol from PFP. The optimized conditions were 0.71 M dilute sulfuric acid and a 21.84-minute treatment, yielding 19.03 g/L of xylose (PFP-1). Different PFP hydrolysates were evaluated to improve xylitol production by the yeast Kluyveromyces marxianus ATCC 36907: PFP-2 (PFP1 treated with Ca(OH)2), PFP-3 (PFP-1 treated with Ca(OH)2 and activated carbon), PFP-4 (PFP-3 with biological elimination of glucose with S. cerevisiae, and concentrated at different xylose concentrations). The applied methods resulted in higher xylitol production (14.97 g/L), when PFP hydrolysate was detoxified with Ca(OH)2, treated with activated charcoal for 1 h, biotreated for glucose removal, and concentrated to 40 g/L of xylose.