Software Phase Correction Technique for Passive Radar

A traditional radar actively transmits pulses and receive the corresponding echoes. By computing the time taken to receive the echoes the system is able to detect targets and estimate their ranges. However, mainly for military applications, an active radar has a major drawback: it can be detected by the enemy since it radiates electromagnetic pulses. As such, there is currently high research and development activity in the field of passive radar systems. In this alternative scenario, the radar does transmit any signal. Instead, it uses signals already present in the environment, such as TV, radio broadcasts and satellite digital video broadcast as transmitters of opportunity. By measuring the time difference between the signal received by the transmitter of opportunity and the signal echoed by the targets, the radar can detect targets and estimate their ranges. In scenarios which use very low power illuminators of opportunity, such as satellite DVB-S or GPS, relatively long integration times are required in order to obtain reasonable values of signal to noise ratio. This implies that, besides frequency correction, the coherency of local oscillators in the receivers need to be maintained during long time intervals, which can be very difficult. The paper presents a novel phase correction technique for passive radar which uses targets of opportunity, already present in the target area, as references to maintain the coherency of the oscillators for all the integration interval. The proposed methodology is quite simple and enables the use of low-cost hardware with independent oscillators for the reference and surveillance channels which can be geographically distributed. The obtained results illustrate the effectiveness and applicability of the method

Development of ligament tissue biodegradable devices: A review

This bibliographic review is focused on ligament tissue rehabilitation, its anatomy-physiology, and, mainly, on the dimensioning considerations of a composite material solution. The suture strength is problematic during the tissue recovering, implying reduction of mobility for several months. However, early postoperative active mobilization may enable a faster and more effective recovering of tissue biomechanical functions. As the risk of tendon rupture becomes a significant concern, a repair technique must be used to withstand the tensile forces generated by active mobilization. However, to avoid stress shielding effect on ligament tissue, an augmentation device must be designed on stiffness basis, that preferably will decrease. Absorbable biocomposite reinforcements have been used to allow early postoperative active mobilization and avoid the shortcomings of current repair solutions. Tensile strength decrease of the repair, during the initial inflammatory phase, is expected, derived from oedema and tendon degradation. In the fibroblastic phase, stiffness and strength will increase, which will stabilize during the remodeling phase. The reinforcement should be able to carry the dynamic load due to locomotion with a mechanical behavior similar to the undamaged natural tissue, during all rehabilitation process. Moreover, the degradation rate Must also be compatible with the ligament tissue recovering. The selection and combination of different biodegradable materials, in order to make the biocomposite reinforcement functionally compatible to the damaged sutured tissue, in terms of mechanical properties and degradation rate, is a major step on the design process. Modelling techniques allow pre-clinical evaluation of the reinforcement functional compatibility, and the optimization by comparison of different composite solutions in terms of biomechanical behavior

Role of microRNAs in the age-associated decline of pancreatic beta cell function in rat islets

This is a freely-available open access publication. Please cite the published version which is available via the DOI link in this record.AIMS/HYPOTHESIS: Ageing can lead to reduced insulin sensitivity and loss of pancreatic beta cell function, predisposing individuals to the development of diabetes. The aim of this study was to assess the contribution of microRNAs (miRNAs) to age-associated beta cell dysfunction. METHODS: The global mRNA and miRNA profiles of 3- and 12-month-old rat islets were collected by microarray. The functional impact of age-associated differences in miRNA expression was investigated by mimicking the observed changes in primary beta cells from young animals. RESULTS: Beta cells from 12-month-old rats retained normal insulin content and secretion, but failed to proliferate in response to mitotic stimuli. The islets of these animals displayed modifications at the level of several miRNAs, including upregulation of miR-34a, miR-124a and miR-383, and downregulation of miR-130b and miR-181a. Computational analysis of the transcriptomic modifications observed in the islets of 12-month-old rats revealed that the differentially expressed genes were enriched for miR-34a and miR-181a targets. Indeed, the induction of miR-34a and reduction of miR-181a in the islets of young animals mimicked the impaired beta cell proliferation observed in old animals. mRNA coding for alpha-type platelet-derived growth factor receptor, which is critical for compensatory beta cell mass expansion, is directly inhibited by miR34a and is likely to be at least partly responsible for the effects of this miRNA. CONCLUSIONS/INTERPRETATION: Changes in the level of specific miRNAs that occur during ageing affect the proliferative capacity of beta cells. This might reduce their ability to expand under conditions of increased insulin demand, favouring the development of type 2 diabetes.Swiss National Science FoundationFondation Francophone pour la Recherche sur le DiabèteWellcome Trust Senior Investigator AwardMRC Programme GrantRoyal Society Wolfson Research Merit AwardWellcome Trust project gran

Mitochondrial targeting adaptation of the hominoid-specific glutamate dehydrogenase driven by positive Darwinian selection

Many new gene copies emerged by gene duplication in hominoids, but little is known with respect to their functional evolution. Glutamate dehydrogenase (GLUD) is an enzyme central to the glutamate and energy metabolism of the cell. In addition to the single, GLUD-encoding gene present in all mammals (GLUD1), humans and apes acquired a second GLUD gene (GLUD2) through retroduplication of GLUD1, which codes for an enzyme with unique, potentially brain-adapted properties. Here we show that whereas the GLUD1 parental protein localizes to mitochondria and the cytoplasm, GLUD2 is specifically targeted to mitochondria. Using evolutionary analysis and resurrected ancestral protein variants, we demonstrate that the enhanced mitochondrial targeting specificity of GLUD2 is due to a single positively selected glutamic acid-to-lysine substitution, which was fixed in the N-terminal mitochondrial targeting sequence (MTS) of GLUD2 soon after the duplication event in the hominoid ancestor ~18–25 million years ago. This MTS substitution arose in parallel with two crucial adaptive amino acid changes in the enzyme and likely contributed to the functional adaptation of GLUD2 to the glutamate metabolism of the hominoid brain and other tissues. We suggest that rapid, selectively driven subcellular adaptation, as exemplified by GLUD2, represents a common route underlying the emergence of new gene functions

Genetic Modulation of the Erythrocyte Phenotype Associated with Retinopathy of Prematurity—A Multicenter Portuguese Cohort Study

The development of retinopathy of prematurity (ROP) may be influenced by anemia or a low fetal/adult hemoglobin ratio. We aimed to analyze the association between DNA methyltransferase 3 β (DNMT3B) (rs2424913), methylenetetrahydrofolate reductase (MTHFR) (rs1801133), and lysine-specific histone demethylase 1A (KDM1A) (rs7548692) polymorphisms, erythrocyte parameters during the first week of life, and ROP. In total, 396 infants (gestational age < 32 weeks or birth weight < 1500 g) were evaluated clinically and hematologically. Genotyping was performed using a MicroChip DNA on a platform employing iPlex MassARRAY®. Multivariate regression was performed after determining risk factors for ROP using univariate regression. In the group of infants who developed ROP red blood cell distribution width (RDW), erythroblasts, and mean corpuscular volume (MCV) were higher, while mean hemoglobin and mean corpuscular hemoglobin concentration (MCHC) were lower; higher RDW was associated with KDM1A (AA), MTHFR (CC and CC + TT), KDM1A (AA) + MTHFR (CC), and KDM1A (AA) + DNMT3B (allele C); KDM1A (AA) + MTHFR (CC) were associated with higher RDW, erythroblasts, MCV, and mean corpuscular hemoglobin (MCH); higher MCV and MCH were also associated with KDM1A (AA) + MTHFR (CC) + DNMT3B (allele C). We concluded that the polymorphisms studied may influence susceptibility to ROP by modulating erythropoiesis and gene expression of the fetal/adult hemoglobin ratio.info:eu-repo/semantics/publishedVersio

Retinopathy of Prematurity in Eight Portuguese Neonatal Intensive Care Units: Incidence, Risk Factors, and Progression—A Prospective Multicenter Study

Background/Objectives: Retinopathy of prematurity (ROP) is a retinal neovascular disease affecting preterm infants. Identifying risk factors for its development and progression is critical for effective screening and prevention. This study aimed to analyze the incidence of ROP and identify key risk factors for its development and progression. Methods: We conducted a prospective, observational cohort study on 455 neonates (gestational age [GA] < 32 weeks or birth weight < 1500 g) across eight Portuguese NICUs. Results: ROP incidence was 37.8%, with 4.6% requiring treatment. Multivariate analysis identified low GA and the number of red blood cell (RBC) transfusions as significant factors for ROP development and progression. After adjusting for these variables, platelet transfusions, high maximum fraction of inspired oxygen (FiO2) in the second week, and surfactant use remained significantly associated with ROP development, while early and late sepsis, maternal chronic hypertension, and delayed enteral nutrition were associated with progression to ROP requiring treatment. Conclusions: These findings underscore the importance of addressing low GAs and adult RBC transfusions in ROP risk management and suggest that maximum FiO2, platelet transfusions, and sepsis also play crucial roles. Larger studies are needed to validate these results and explore preventive interventions, particularly regarding the impact of multiple adult RBC transfusions on fetal hemoglobin percentages.info:eu-repo/semantics/publishedVersio

Combined low-carbohydrate diet and long-term exercise in hypoxia in type 2 diabetes: A randomized controlled trial protocol to assess glycemic control, cardiovascular risk factors and body composition

Background: Cardiovascular disease is the leading cause of mortality associated with diabetes, which is characterized by chronic hyperglycemia. Low-carbohydrate diet has gained popularity as an intervention in patients with type 2 diabetes mellitus, acting to improve glycemic profile and serum lipids. In its turn, exercise in hypoxia induces specific adaptations, mostly modulated via hypoxia-induced transcription factor signaling cascade, which increases with exposure to altitude, and promotes angiogenesis, glycogen supply, glucose tolerance, and raises GLUT-4 expression. Aim: Given that hyperglycemia decreases HIF-1 and it is better controlled when following a low-carbohydrate diet, this study aims to examine the hypothesis that a combination of both low-carbohydrate diet and chronic exercise in hypoxia in type 2 diabetes mellitus is associated with improved glycemic control and cardiovascular parameters, whose protocol is described. Methods: Patients with type 2 diabetes mellitus ( n=48) will be recruited and randomized into one of the three groups: (a) Control group: Control diet (low-fat and moderate-carbohydrate diet)+exercise in normoxia; (2) exercise in hypoxia group: Control diet+exercise in hypoxia; (3) intervention group: Low-carbohydrate diet (low-carbohydrate and high-fat diet)+exercise in hypoxia. Before and after 8 weeks of interventions, cardiopulmonary tests (Bruce protocol), body composition and blood pressure will be evaluated. Blood samples will be collected to measure hypoxia-induced transcription factor, C-reactive protein, glycemic and lipid profiles. Summary: This will be the first trial to examine the isolated and combined effect of chronic exercise in hypoxia and low-carbohydrate diet in type 2 diabetes mellitus. This trial will help to fill a significant research gap, guide future research and contribute to the combined nutrition and exercise approach to type 2 diabetes mellitus. </jats:p

Primary Tuberculosis of the Esophagus

Os autores reportam o caso de uma doente de 38 anos de idade com um quadro clínico de odinofagia, dor retroesternal e emagrecimento. Os exames complementares de diagnóstico revelaram a presença de uma lesão ulcerada no esófago, como forma de manifestação de tuberculose primária do esófago. A Tuberculose esofágica é uma doença pouco frequente, sendo responsável por 0,15% da mortalidade por tuberculose. A Tuberculose primária do esófago, sem envolvimento de outros órgãos, como o nosso caso clínico, é ainda mais raro. A maioria dos casos é tratada de forma eficaz com tuberculostáticos, sendo que o atraso no diagnóstico e início da terapêutica dita um mau prognóstico

Correction: Kindlovits et al. Eight Weeks of Intermittent Exercise in Hypoxia, with or without a Low-Carbohydrate Diet, Improves Bone Mass and Functional and Physiological Capacity in Older Adults with Type 2 Diabetes. Nutrients 2024, 16, 1624

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