Application of machine learning techniques to derive sea water turbidity from Sentinel-2 imagery

Earth Observation (EO) from satellites has the potential to provide comprehensive, rapid and inexpensive information about water bodies, integrating in situ measurements. Traditional methods to retrieve optically active water quality parameters from satellite data are based on semiempirical models relying on few bands, which often revealed to be site and season specific. The use of machine learning (ML) for remotely sensed water quality estimation has spread in recent years thanks to the advances in algorithm development and computing power. These models allow to exploit the wealth of spectral information through more flexible relationships and are less affected by atmospheric and other background factors. The present study explores the use of Sentinel-2 MultiSpectral Instrument (MSI) Level-1C Top of Atmosphere spectral radiance to derive water turbidity, through application of machine learning techniques. A dataset of 222 combination of turbidity measurements, collected in the North Tyrrhenian Sea – Italy from 2015 to 2021, and values of the 13 spectral bands in the pixel corresponding to the sample location was used. Two regression techniques were tested and compared: a Stepwise Linear Regression (SLR) and a Polynomial Kernel Regression. The two models show accurate and similar performance (R2 = 0.736, RMSE = 2.03 NTU, MAE = 1.39 NTU for the SLR and R2 = 0.725, RMSE = 2.07 NTU, MAE = 1.40 NTU for the Kernel). A band importance analysis revealed the contribution of the different spectral bands and the main role of the red-edge range. The work shows that it is possible to reach a good accuracy in turbidity estimation from MSI TOA reflectance using ML models, fed by the whole spectrum of available bands, although the possible generation of errors related to atmospheric effect in turbidity estimates was not evaluated. Comparison between turbidity estimates obtained from the models with turbidity data from Copernicus CMEMS dataset named ‘Mediterranean Sea, Bio-Geo-Chemical, L3, daily observation’ produced consistent results. Finally, turbidity maps from satellite imagery were produced for the study area, showing the ability of the models to catch extreme events

Chronotropic Incompentence and Functional Capacity in CHF

SUMMARY Aim: To assess the effect of chronotropic incompetence on functional capacity in chronic heart failure (CHF) patients, as evaluated as NYHA and peak oxygen consumption (pVO2), focusing on the presence and dose of β-blocker treatment. Methods: Nine hundred and sixty-seven consecutive CHF patients were evaluated, 328 of whom were discarded because they failed to meet the study criteria. Of the 639 analyzed, 90 were not treated with β-blockers whereas the other 549 were. The latter were further subdivided in high (n = 184) and low (n = 365) β-blockers daily dose group in accordance with an arbitrary cut-off of 25 mg for carvedilol and of 5 mg for bisoprolol. Failure to achieve 80% of the percentage of maximum age predicted peak heart rate (%Max PHR) or of HR reserve (%HRR) constituted chronotropic incompetence. Results: No differences were found in NYHA or pVO2 between patients with and without β-blockers and, similarly, between high and low β-blocker dose groups. Twenty and sixty-nine percent of not β-blocked patients showed chronotropic incompetence according to %Max PHR and %HRR, respectively, whereas this prevalence rose to 61% and 84% in those on β-blocker therapy. Patients taking β-blockers without chronotropic incompetence, as inferable from both %Max PHR and %HRR, showed higher NYHA and pVO2 regardless of drug dose, whereas, in not β-blocked patients, only %HRR revealed a difference in functional capacity. At multivariable analysis, HR increase during exercise (ΔHR) was the variable most strongly associated to pVO2 (β: 0.572; SE: 0.008; P < 0.0001) and NYHA class (β: −0.499; SE: 0.001; P < 0.0001). Conclusions: ΔHR is a powerful predictor of CHF severity regardless of the presence of β-blocker therapy and of β-blocker daily dose

The Role of Copper (II) on Kininogen Binding to Tropomyosin in the Presence of a Histidine–Proline-Rich Peptide

The antiangiogenic activity of the H/P domain of histidine&ndash;proline-rich glycoprotein is mediated by its binding with tropomyosin, a protein exposed on endothelial cell-surface during the angiogenic switch, in presence of zinc ions. Although it is known that copper ion serum concentration is significantly increased in cancer patients, its role in the interaction of H/P domain with tropomyosin, has not yet been studied. In this paper, by using ELISA assay, we determined the modulating effect of TetraHPRG peptide, a sequence of 20 aa belonging to H/P domain, on the binding of Kininogen (HKa) with tropomyosin, both in absence and presence of copper and zinc ions. A potentiometric study was carried out to characterize the binding mode adopted by metal ions with TetraHPRG, showing the formation of complex species involving imidazole amide nitrogen atoms in metal binding. Moreover, circular dichroism showed a conformational modification of ternary systems formed by TetraHPRG, HKa and copper or zinc. Interestingly, slight pH variation influenced the HKa-TetraHPRG-tropomyosin binding. All these results indicate that both metal ions are crucial in the interaction between TetraHPRG, tropomyosin and HKa

The Inorganic Perspective of VEGF: Interactions of Cu2 + with Peptides Encompassing a Recognition Domain of the VEGF Receptor

The vascular endothelial growth factor A (VEGF-A) is a potent angiogenic factor, its activity may be influenced by the presence of copper(II) ions. To mimic the interaction between copper(II) and VEGF (Vascular Endotelial Growth Factor), the N- and C-terminally blocked peptide fragments VEGF73-101 and VEGF84-101, owing to VEGF165 protein, have been synthesized. These protein domains represent a specific recognition site with the VEGF receptor (VEGFR). Copper(II) complexes with VEGF73-101 and VEGF84-101 were investigated by means of potentiometry and UV-Vis, ESI-MS, CD, EPR spectroscopic methods. Both peptides have three histidine residues and display a binding high affinity for copper(II) ions. The proliferative activity of the peptides in the absence and presence of copper(II) ions as well as of VEGF-165 protein was also tested on HUVEC cells (Human Umbilical Vein Endothelial Cells). The VEGF73-101 showed a dose-dependent anti-proliferative activity, while the shorter peptide VEGF84-101 did not affect HUVEC proliferation, both in the presence and in the absence of VEGF

Small Hexokinase 1 Peptide against Toxic SOD1 G93A Mitochondrial Accumulation in ALS Rescues the ATP-Related Respiration

Mutations in Cu/Zn Superoxide Dismutase (SOD1) gene represent one of the most common causes of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder that specifically affects motor neurons (MNs). The dismutase-active SOD1 G93A mutant is responsible for the formation of toxic aggregates onto the mitochondrial surface, using the Voltage-Dependent Anion Channel 1 (VDAC1) as an anchor point to the organelle. VDAC1 is the master regulator of cellular bioenergetics and by binding to hexokinases (HKs) it controls apoptosis. In ALS, however, SOD1 G93A impairs VDAC1 activity and displaces HK1 from mitochondria, promoting organelle dysfunction, and cell death. Using an ALS cell model, we demonstrate that a small synthetic peptide derived from the HK1 sequence (NHK1) recovers the cell viability in a dose–response manner and the defective mitochondrial respiration profile relative to the ADP phosphorylation. This correlates with an unexpected increase of VDAC1 expression and a reduction of SOD1 mutant accumulation at the mitochondrial level. Overall, our findings provide important new insights into the development of therapeutic molecules to fight ALS and help to better define the link between altered mitochondrial metabolism and MNs death in the disease

Relationship between surfactant proteins and RAGE levels and general, clinical, pulmonary function and cardiopulmonary exercise data in the heart failure population.

<p>SPs, RAGE, Peak VO₂, VE/VCO₂ slope and BNP levels are transformed into natural logarithm. BMI: body mass index. For all abbreviations see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0115030#pone-0115030-t001" target="_blank">table 1</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0115030#pone-0115030-t002" target="_blank">table 2</a>.</p><p>Relationship between surfactant proteins and RAGE levels and general, clinical, pulmonary function and cardiopulmonary exercise data in the heart failure population.</p

Comorbidities in chronic heart failure: An update from Italian Society of Cardiology (SIC) Working Group on Heart Failure

The increasing number of patients with heart failure HF and comorbidities is due to aging population and increase of life expectancy of patients with cardiovascular disease. Encouraging results derived by recent trials may suggest some comorbidities as new targets for new drugs, highlighting the need for a better understanding of the comorbidities' effects in HF patients and the need of a multidisciplinary approach for the management of chronic HF with comorbidities. We report a brief review about main cardiovascular and non-cardiovascular comorbidities in HF patients in order to update physicians and researchers engaged in the HF research or in "fight against heart failure.

Representative image for immature surfactant protein type B (SPB) immunoblotting of plasma samples derived from the control group and HF patients grouped according New York Heart Association (NYHA) class.

<p>Representative image for immature surfactant protein type B (SPB) immunoblotting of plasma samples derived from the control group and HF patients grouped according New York Heart Association (NYHA) class.</p

The surfactant protein type B (SPB) gene, mRNA and protein.

<p>The human SPB is encoded by 11 exons on chromosome 2. The SPB RNA of approximately 2 kb encodes a preprotein of 381 amino acids. Processing of the precursor includes removal of a signal peptide of approximately 23 residues, and glycosilatyion at amino acids 129 to 131 and 311 to 313. These events occur within the endoplasmic reticulum. Sequential proteolytic cleavages by proteases ultimately yield the 8 kDa 79 amino acid active mature SPB, which is encoded in exons 6 and 7. These sequential cleavage occurs in the medial and trans/post Golgi, and finally in the multivescicular body. Mature SPB sequence contains 52% hydrophobic amino acids, 8 conserved positively-charges residues and 1 conserved negatively-charged residue. The primary structure also includes 7 cysteines, six of which are involved in the formation of the three intra-molecular disulphide bridges, while the seventh cysteine is involved in an intermolecular disulphide responsible for the dimerization of the protein.</p