Integrated usage of historical geospatial data and modern satellite images reveal long-term land use/cover changes in Bursa/Turkey, 1858-2020.

Land surface of the Earth has been changing as a result of human induced activities and natural processes. Accurate representation of landscape characteristics and precise determination of spatio-temporal changes provide valuable inputs for environmental models, landscape and urban planning, and historical land cover change analysis. This study aims to determine historical land use and land cover (LULC) changes using multi-modal geospatial data, which are the cadastral maps produced in 1858, monochrome aerial photographs obtained in 1955, and multi-spectral WorldView-3 satellite images of 2020. We investigated two pilot regions, Aksu and Kestel towns in Bursa/Turkey, to analyze the long-term LULC changes quantitatively and to understand the driving forces that caused the changes. We propose methods to facilitate the preparation of historical datasets for the LULC change detection and present an object-oriented joint classification scheme for multi-source datasets to accurately map the spatio-temporal changes. Our approach minimized the amount of manual digitizing required for the boundary delineation of LULC classes from historical geospatial data. Also, our quantitative analysis of LULC maps indicates diverging developments for the selected locations in the long period of 162 years. We observed rural depopulation and gradual afforestation in Aksu; whereas, agricultural land abandonment and deforestation in Kestel.

Phosphorylation of PI3K/Akt at Thr308, but not phosphorylation of MAPK kinase, mediates lithium-induced neuroprotection against cerebral ischemia in mice.

Lithium, in addition to its effect on acute and long-term bipolar disorder, is involved in neuroprotection after ischemic stroke. Yet, its mechanism of action is still poorly understood, which was only limited to its modulatory effect on GSK pathway. Therefore, we initially analyzed the dose-dependent effects of lithium on neurological deficits, infarct volume, brain edema and blood-brain barrier integrity, along with neuronal injury and survival in mice subjected to focal cerebral ischemia. Thereafter, we investigated the involvement of the PI3K/Akt and MEK signal transduction pathways and their components. Our observations revealed that 2 mmol/kg lithium significantly improved post-ischemic brain tissue survival. Although, 2 mmol/kg lithium had no negative effect on brain microcirculation, 5 and 20 mmol/kg lithium reduced brain perfusion. Furthermore, supratherapeutic dose of lithium in 20 mmol/kg lead to animal death. In addition, improvement of brain perfusion with L-arginine, did not change the effect of 5 mmol/kg lithium on brain injury. Additionally, post-stroke blood-brain barrier leakage, hemodynamic impairment and apoptosis have been reversed by lithium treatment. Interestingly, lithium-induced neuroprotection was associated with increased phosphorylation of Akt at Thr308 and suppressed GSK-3ß phosphorylation at Ser9 residue. Lithium upregulated Erk-2 and downregulated JNK-2 phosphorylation. To distinguish whether neuroprotective effects of lithium are modulated by PI3K/Akt or MEK, we sequentially blocked these pathways and demonstrated that the neuroprotective activity of lithium persisted during MEK/ERK inhibition, whereas PI3K/Akt inhibition abolished neuroprotection. Collectively, we demonstrated lithium exerts its post-stroke neuroprotective activity via the PI3K/Akt pathway, specifically via Akt phosphorylation at Thr308, but not via MEK/ERK.

Identification of Earthquake Induced Damage Areas Using Fourier Transform and SPOT HRVIR Pan Images.

A devastating earthquake with a magnitude of Mw 7.4 occurred on the North Anatolian Fault Zone (NAFZ) of Turkey on August 17, 1999 at 00:01:39 UTC (3:01 a.m. local time). The aim of this study is to propose a new approach to automatically identify earthquake induced damage areas which can provide valuable information to support emergency response and recovery assessment procedures. This research was conducted in the Adapazari inner city, covering a 3 × 3 km area, where 11,373 buildings collapsed as a result of the earthquake. SPOT high resolution visible infrared (HRVIR) Pan images obtained before (25 June 1999) and after (4 October 1999) the earthquake were used in the study. Five steps were employed to conduct the research and these are: (i) geometric and radiometric correction of satellite images, (ii) Fast Fourier Transform (FFT) of pre- and post-earthquake images and filtering the images in frequency domain, (iii) generating difference image using Inverse Fast Fourier Transform (IFFT) pre- and post- earthquake images, (iv) application of level slicing to difference image to identify the earthquake-induced damages, (v) accuracy assessment of the method using ground truth obtained from a 1/5,000 scale damage map. The total accuracy obtained in the research is 80.19 %, illustrating that the proposed method can be successfully used to automatically identify earthquake-induced damage areas.

Time-of-Day Dependent Neuronal Injury After Ischemic Stroke: Implication of Circadian Clock Transcriptional Factor Bmal1 and Survival Kinase AKT.

Occurrence of stroke cases displays a time-of-day variation in human. However, the mechanism linking circadian rhythm to the internal response mechanisms against pathophysiological events after ischemic stroke remained largely unknown. To this end, temporal changes in the susceptibility to ischemia/reperfusion (I/R) injury were investigated in mice in which the ischemic stroke induced at four different Zeitgeber time points with 6-h intervals (ZT0, ZT6, ZT12, and ZT18). Besides infarct volume and brain swelling, neuronal survival, apoptosis, ischemia, and circadian rhythm related proteins were examined using immunohistochemistry, Western blot, planar surface immune assay, and liquid chromatography-mass spectrometry tools. Here, we present evidence that midnight (ZT18; 24:00) I/R injury in mice resulted in significantly improved infarct volume, brain swelling, neurological deficit score, neuronal survival, and decreased apoptotic cell death compared with ischemia induced at other time points, which were associated with increased expressions of circadian proteins Bmal1, PerI, and Clock proteins and survival kinases AKT and Erk-1/2. Moreover, ribosomal protein S6, mTOR, and Bad were also significantly increased, while the levels of PRAS40, negative regulator of AKT and mTOR, and phosphorylated p53 were decreased at this time point compared to ZT0 (06:00). Furthermore, detailed proteomic analysis revealed significantly decreased CSKP, HBB-1/2, and HBA levels, while increased GNAZ, NEGR1, IMPCT, and PDE1B at midnight as compared with early morning. Our results indicate that nighttime I/R injury results in less severe neuronal damage, with increased neuronal survival, increased levels of survival kinases and circadian clock proteins, and also alters the circadian-related proteins.

Evidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice.

Conflicting data in the literature about the function of P2X7R in survival following ischemia necessitates the conductance of in-depth studies. To investigate the impacts of activation vs inhibition of the receptor on neuronal survival as well as the downstream signaling cascades, in addition to optic nerve transection (ONT), 30min and 90min of middle cerebral artery occlusion (MCAo) models were performed in mice. Intracellular calcium levels were assessed in primary cortical neuron cultures. Here, we show that P2X7R antagonist Brilliant Blue G (BBG) decreased DNA fragmentation, infarct volume, brain swelling, neurological deficit scores and activation of microglial cells after focal cerebral ischemia. BBG also significantly increased the number of surviving retinal ganglion cells (RGCs) after ONT and the number of surviving neurons following MCAo. Importantly, receptor agonist BzATP resulted in increased activation of microglial cells and induced phosphorylation of ERK, AKT and JNK. These results indicated that inhibition of P2X7R with BBG promoted neuronal survival, not through the activation of survival kinase pathways, but possibly by improved intracellular Ca2+ overload and decreased the levels of Caspase 1, IL-1ß and Bax proteins. On the other hand, BzATP-mediated increased number of activated microglia and increased survival kinase levels in addition to increased caspase-1 and IL-1ß levels indicate the complex nature of the P2X7 receptor-mediated signaling in neuronal injury.