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Quinoa (Chenopodium quinoa Will.) is an annual herbaceous Andean plant. In recent years there is a growing interest on it due to its high quality as food, its wide adaptation to agroecological conditions and resistance to different abiotic stresses. In this work, we evaluate the growth pattern of quinoa plants cv. ‘Titicaca’, subjected to different levels of salinity, focusing on leaf production and nutrient content. In this sense, the results have shown that a high concentration of salinity negatively affects the growth of quinoa plants. In fact, plants grown with 200 mM NaCl reduced the photosynthetic rate and levels of chlorophylls and carotenoids in comparison with the rest of the treatments. Likewise, it has been proven how the progressive increase in salinity has negative effects on transpiration, stomatal conductance and photosynthetic rate, with significant subsequent reductions in shoot biomass, leaf area and nutrient adquisition, but without a decline in leaf dry weight (DW) production. However, the treatment of 200 mM NaCl demonstrated the best results regarding the water-use efficiency, as well as the number of saline glands. According to our results, the quinoa plant cv. ‘Titicaca’ seems to be tolerant to moderate concentrations of salinity (50–100 mM NaCl). This study could serve as a reference on this little known and cultivated species in the Mediterranean region, since it could become an alternative crop in areas with moderate salinity problems.

Background: Subjective cognitive decline (SCD) is a risk factor for future cognitive impairment and dementia. It is uncertain whether the neurodegeneration of the cholinergic system is already present in SCD individuals. We aimed to review the current evidence about the association between SCD and biomarkers of degeneration in the cholinergic system., Method: Original articles were extracted from three databases: Pubmed, Web of Sciences, and Scopus, in January 2023. Two researchers screened the studies independently., Results: A total of 11 research articles were selected. SCD was mostly based on amnestic cognitive complaints. Cholinergic system biomarkers included neuroimaging markers of basal forebrain volume, functional connectivity, transcranial magnetic stimulation, or biofluid. The evidence showed associations between basal forebrain atrophy, poorer connectivity of the cholinergic system, and SCD CONCLUSIONS: Degenerative changes in the cholinergic system can be present in SCD. Subjective complaints may help when identifying individuals with brain changes that are associated with cognitive impairment. These findings may have important implications in targeting individuals that may benefit from cholinergic-target treatments at very early stages of neurodegenerative diseases., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

The Undecimated Wavelet Transform is commonly used for signal processing due to its advantages over other wavelet techniques, but it is limited for some applications because of its computational cost. One of the methods utilized for the implementation of the Undecimated Wavelet Transform is the one known as Cycle Spinning. This paper introduces an alternative Cycle Spinning implementation method that divides the computational cost by a factor close to 2. This work develops the mathematical background of the proposed method, shows the block diagrams for its implementation and validates the method by applying it to the denoising of ultrasonic signals. The evaluation of the denoising results shows that the new method produces similar denoising qualities than other Cycle Spinning implementations, with a reduced computational cost., Competing Interests: The author declares no conflict of interest.

Ultrasound diagnosis is a widely used medical tool. Among the various ultrasound techniques, ultrasonic imaging is particularly relevant. This paper presents an improvement to a two-dimensional (2D) ultrasonic system using measurements taken from perpendicular planes, where digital signal processing techniques are used to combine one-dimensional (1D) A-scans were acquired by individual transducers in arrays located in perpendicular planes. An algorithm used to combine measurements is improved based on the wavelet transform, which includes a denoising step during the 2D representation generation process. The inclusion of this new denoising stage generates higher quality 2D representations with a reduced level of speckling. The paper includes different 2D representations obtained from noisy A-scans and compares the improvements obtained by including the denoising stage.

Sorafenib is an oral multikinase inhibitor approved for the treatment of hepatocellular carcinoma (HCC). Its antitumor activity is attributed to inhibition of tyrosine kinase receptors (VEGFR, PDGFR, c-kit) and intracellular serine/threonine kinases (Raf), which alter gene expression to promote apoptosis and downregulate survival and angiogenesis pathways. The beneficial properties of sorafenib have also been related to a reduction in liver fibrosis trough regulation of TGF-βR-related STAT3 signaling. Sorafenib plays a role in the regulation of mitochondrial function, ATP, and autophagy, a process leading to either survival or apoptotic cell death depending on its intensity and duration, by altering several cellular pathways such as mTOR, AMPK, activating endoplasmic reticulum stress responses, and deregulating miRNAs that modulate autophagy. Sorafenib reduces S-nitrosation of cell death receptors and caspase-3, triggering a switch to caspase-3 from caspase-8. In this paper, we review the antitumor effects of sorafenib by interaction with cell survival and apoptosis pathways, metabolic reprogramming, and effect on oxidative and nitrosative stress, along with different mechanisms that might be involved in resistance to the drug.

Coenzyme Q10 deficiency is a clinically and genetically heterogeneous disorder, with manifestations that may range from fatal neonatal multisystem failure, to adult-onset encephalopathy. We report a patient who presented at birth with severe lactic acidosis, proteinuria, dicarboxylic aciduria, and hepatic insufficiency. She also had dilation of left ventricle on echocardiography. Her neurological condition rapidly worsened and despite aggressive care she died at 23 h of life. Muscle histology displayed lipid accumulation. Electron microscopy showed markedly swollen mitochondria with fragmented cristae. Respiratory-chain enzymatic assays showed a reduction of combined activities of complex I+III and II+III with normal activities of isolated complexes. The defect was confirmed in fibroblasts, where it could be rescued by supplementing the culture medium with 10 μM coenzyme Q10. Coenzyme Q10 levels were reduced (28% of controls) in these cells. We performed exome sequencing and focused the analysis on genes involved in coenzyme Q10 biosynthesis. The patient harbored a homozygous c.545T>G, p.(Met182Arg) alteration in COQ2, which was validated by functional complementation in yeast. In this case the biochemical and morphological features were essential to direct the genetic diagnosis. The parents had another pregnancy after the biochemical diagnosis was established, but before the identification of the genetic defect. Because of the potentially high recurrence risk, and given the importance of early CoQ10 supplementation, we decided to treat with CoQ10 the newborn child pending the results of the biochemical assays. Clinicians should consider a similar management in siblings of patients with CoQ10 deficiency without a genetic diagnosis.

Background: COQ4 encodes a protein that organises the multienzyme complex for the synthesis of coenzyme Q(10) (CoQ(10)). A 3.9 Mb deletion of chromosome 9q34.13 was identified in a 3-year-old boy with mental retardation, encephalomyopathy and dysmorphic features. Because the deletion encompassed COQ4, the patient was screened for CoQ(10) deficiency., Methods: A complete molecular and biochemical characterisation of the patient's fibroblasts and of a yeast model were performed., Results: The study found reduced COQ4 expression (48% of controls), CoQ(10) content and biosynthetic rate (44% and 43% of controls), and activities of respiratory chain complex II+III. Cells displayed a growth defect that was corrected by the addition of CoQ(10) to the culture medium. Knockdown of COQ4 in HeLa cells also resulted in a reduction of CoQ(10.) Diploid yeast haploinsufficient for COQ4 displayed similar CoQ deficiency. Haploinsufficency of other genes involved in CoQ(10) biosynthesis does not cause CoQ deficiency, underscoring the critical role of COQ4. Oral CoQ(10) supplementation resulted in a significant improvement of neuromuscular symptoms, which reappeared after supplementation was temporarily discontinued., Conclusion: Mutations of COQ4 should be searched for in patients with CoQ(10) deficiency and encephalomyopathy; patients with genomic rearrangements involving COQ4 should be screened for CoQ(10) deficiency, as they could benefit from supplementation.