Semantic segmentation of landcover for cropland mapping and area estimation using Machine Learning techniques

ABSTRACTThe paper has focussed on the global landcover for the identification of cropland areas. Population growth and rapid industrialization are somehow disturbing the agricultural lands and eventually the food production needed for human survival. Appropriate agricultural land monitoring requires proper management of land resources. The paper has proposed a method for cropland mapping by semantic segmentation of landcover to identify the cropland boundaries and estimate the cropland areas using machine learning techniques. The process has initially applied various filters to identify the features responsible for detecting the land boundaries through the edge detection process. The images are masked or annotated to produce the ground truth for the label identification of croplands, rivers, buildings, and backgrounds. The selected features are transferred to a machine learning model for the semantic segmentation process. The methodology has applied Random Forest, which has compared to two other techniques, Support Vector Machine and Multilayer perceptron, for the semantic segmentation process. Our dataset is composed of satellite images collected from the QGIS application. The paper has derived the conclusion that Random forest has given the best result for segmenting the image into different regions with 99% training accuracy and 90% test accuracy. The results are cross-validated by computing the Mean IoU and kappa coefficient that shows 93% and 69% score value respectively for Random Forest, found maximum among all. The paper has also calculated the area covered under the different segmented regions. Overall, Random Forest has produced promising results for semantic segmentation of landcover for cropland mapping

Molecular Dynamics Analysis of Apolipoprotein-D - Lipid Hydroperoxide Interactions: Mechanism for Selective Oxidation of Met-93

Background: Recent studies suggest reduction of radical-propagating fatty acid hydroperoxides to inert hydroxides by interaction with apolipoprotein-D (apoD) Met93 may represent an antioxidant function for apoD. The nature and structural consequences of this selective interaction are unknown. Methodology/Principal Findings: Herein we used molecular dynamics (MD) analysis to address these issues. Longtimescale simulations of apoD suggest lipid molecules are bound flexibly, with the molecules free to explore multiple conformations in a binding site at the entrance to the classical lipocalin ligand-binding pocket. Models of 5s- 12s- and 15s hydroperoxyeicosatetraenoic acids were created and the lipids found to wrap around Met93 thus providing a plausible mechanism by which eicosatetraenoic acids bearing hydroperoxides on different carbon atoms can interact with Met93 to yield Met93 sulfoxide (Met93SO). Simulations of glycosylated apoD indicated that a second solvent exposed Met at position 49 was shielded by a triantennerary N-glycan attached to Asn45 thereby precluding lipid interactions. MD simulations of apoD showed B-factors of the loop containing Met93SO were higher in the oxidized protein, indicating increased flexibility that is predicted to destabilize the protein and promote self-association. Conclusions/Significance: These studies provide novel insights into the mechanisms that may contribute to the antioxidant function of apoD and the structural consequences that result if Met93SO is not redox-cycled back to its native state

Elucidation of apolipoprotein D lipid antioxidant mechanism and its relevance to Alzheimers disease

Apolipoprotein D (apoD) is a widely expressed, multifunctional apolipoprotein known for its lipid antioxidant properties in the brain. It is upregulated under oxidative stress conditions including aging and in neurodegenerative diseases. The mechanism of lipid antioxidant function of apoD and reasons for its upregulation in neurodegenerative diseases is unknown. Hence the aim of this thesis was to study the lipid antioxidant mechanism of apoD and its relevance to the most common form of neurodegenerative disease, Alzheimer's disease (AD). To study the mechanism of lipid antioxidant function of apoD, the interaction of recombinant apoD and its methionine mutants (methionine substituted with alanine) with hydroperoxyeicosatetraenoic acids (HpETE) were analysed using HPLC and amino acid analysis techniques. The Met93 residue of apoD was required for the reduction of HpETE to its hydroxyeicosatetraenoic acid derivative (HETE), and this reaction was concomitant with the formation of methionine sulfoxide (MetSO). Western blot analysis revealed that the oxidation of apoD Met residues causes apoD aggregation. This was supported by in-silico simulations which indicated that the oxidation of Met93 is accompanied by destabilisation of a surface-exposed hydrophobic domain that is predicted to increase the propensity for apoD to self-associate. Furthermore, the link between lipid peroxidation, apoD expression and aggregation of apoD was analysed with disease progression in AD brain using High performance liquid chromatography (HPLC), Gas chromatographyMass spectrometry (GC-MS) and Western blot analysis. Lipid conjugated dienes and F2- isoprostanes, measured as markers of lipid peroxidation, were increased in later stages of the disease. The expression of apoD also increased with disease progression and formation of apoD dimers were detected in the insoluble protein fraction of the hippocampus in late stage AD patients. Moreover, the formation of apoD dimers is closely correlated to lipid conjugated diene levels in AD hippocampus. In summary, the Met93 residue of apoD is required for the lipid antioxidant function of apoD. Furthermore, oxidation of methionine residues, particularly Met93, results in self-association of apoD and production of a stable dimer that is observed in vitro and in post-mortem brain derived from late stage AD cases. The increase in apoD expression with disease progression, similar to other antioxidants, suggests that apoD has the potential to reduce lipid peroxidation in AD brain. However, its self-association in late disease stages may prevent it from acting as a lipid antioxidant

Selective reduction of hydroperoxyeicosatetraenoic acids to their hydroxy derivatives by apolipoprotein D: implications for lipid antioxidant activity and Alzheimer\u27s disease

ApoD (apolipoprotein D) is up-regulated in AD (Alzheimer\u27s disease) and upon oxidative stress. ApoD inhibits brain lipid peroxidation in vivo, but the mechanism is unknown. Specific methionine residues may inhibit lipid peroxidation by reducing radical-propagating L-OOHs (lipid hydroperoxides) to non-reactive hydroxides via a reaction that generates MetSO (methionine sulfoxide). Since apoD has three conserved methionine residues (Met49, Met93 and Met157), we generated recombinant proteins with either one or all methionine residues replaced by alanine and assessed their capacity to reduce HpETEs (hydroperoxyeicosatetraenoic acids) to their HETE (hydroxyeicosatetraenoic acid) derivatives. ApoD, apoDM49-A and apoDM157-A all catalysed the reduction of HpETEs to their corresponding HETEs. Amino acid analysis of HpETE-treated apoD revealed a loss of one third of the methionine residues accompanied by the formation of MetSO. Additional studies using apoD(M93-A) indicated that Met93 was required for HpETE reduction. We also assessed the impact that apoD MetSO formation has on protein aggregation by Western blotting of HpETE-treated apoD and human brain samples. ApoD methionine oxidation was associated with formation of apoD aggregates that were also detected in the hippocampus of AD patients. In conclusion, conversion of HpETE into HETE is mediated by apoD Met93, a process that may contribute to apoD antioxidant function

The @journal of the European Pentecostal Theological Association

Transgenic mice that express familial Alzheimer's disease mutant forms of the human amyloid precursor protein (hAPP) have proved to be invaluable in determining the impact that the neurotoxic amyloid-β peptide has in vivo. In addition to the propensity to accumulate cerebral amyloid plaques, a crucial characteristic of hAPP mouse models is their cognitive impairments. To date the most widely used test for analyzing cognitive impairment in hAPP mice is the Morris water maze (MWM) which, due to the fact that mice are not "natural" swimmers, may not always be the ideal paradigm to investigate cognitive behaviours. Furthermore, not all cognitive impairments have been replicated across research laboratories. In the current study, we characterised the cognitive abilities of the J20 transgenic mouse line (expressing the Swedish 670/671 KM->NL and Indiana (717 V->F hAPP mutations) and non-transgenic mice. Mice were assessed in the cheeseboard task (i.e., a 'dry version' of the MWM) and a variety of other cognitive paradigms to test fear conditioning, object recognition and short-term memory to broaden the understanding of the cognitive deficits in J20 mice. hAPP transgenic mice perform normally in tasks for fear conditioning, short-term object recognition and short-term memory of context familiarity. However, they were profoundly impaired in their spatial reference memory capabilities in the cheeseboard task. The cheeseboard task has potential to replace the MWM task in situations where the MWM is not suitable for particular mouse models

Interaction energy for MD simulation of apoD with arachidonate.

<p>Interaction energy of the four runs shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0034057#pone-0034057-g004" target="_blank">Figure 4</a> are plotted as a function of time. The conformations in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0034057#pone-0034057-g004" target="_blank">Figure 4</a> simulation 4 used for modeling of HpETE are indicated by a bar.</p

Increased apolipoprotein D dimer formation in Alzheimer\u27s disease hippocampus is associated with lipid conjugated diene levels

Previous studies indicate that apolipoprotein D (apoD) may have a lipid antioxidant function in the brain. We have shown that apoD can reduce free radical-generating lipid hydroperoxides to inert lipid hydroxides in a reaction that involves conversion of surface exposed apoD methione-93 (Met93) residue to Met93-sulfoxide (Met93-SO). One consequence of this reaction is the formation of a stable dimerized form of apoD. As cerebral lipid peroxidation is associated with Alzheimer\u27s disease (AD), in the present study we aimed to assess the possible presence of apoD dimers in postmortem hippocampal and cerebellar tissues derived from a cohort of pathologically defined cases ranging from control to late stage AD. Both soluble and insoluble (requiring guanidine HCl extraction) fractions of tissue homogenates were analyzed for apoD and its dimerized form. We also assessed amyloid-β levels by ELISA and levels of lipid peroxidation by lipid conjugated diene and F2-isoprostane analysis. Our studies reveal a significant association between soluble apoD levels and AD Braak stage whereas apoD dimer formation appears to increase predominantly in the advanced stages of disease. The formation of apoD dimers is closely correlated to lipid conjugated diene levels and occurs in the hippocampus but not in the cerebellum. These results are consistent with the hypothesis that apoD acts as a lipid antioxidant in the brain

CD spectra of recombinant apoD.

<p>Far-UV CD spectra of apoD and apoD-Met₉₃SO and the Met to Ala mutants indicated. Spectra were obtained in PBS, pH 7.4 at 22°C.</p

MD simulation of apoD with progesterone.

<p>(<i>A</i>) Orthogonal views of apoD in ribbon form with ligand-binding residues shown (cyan carbon atoms). The conformation of progesterone, sampled at 1 ns intervals, is shown (black carbon atoms). Methionine residues are represented as van der Waals spheres. (<i>B</i>) Interaction energy is plotted as a function of time.</p

MD simulation of apoD with arachidonate.

<p>Orthogonal views of apoD in ribbon form with ligand-binding residues shown (cyan carbon atoms). The conformation of arachidonate, sampled at 1 ns intervals, is shown for simulations 1 to 4 (black carbon atoms). Methionine residues are represented as van der Waals spheres.</p