RGB-D Indoor mapping using deep features

RGB-D indoor mapping has been an active research topic in the last decade with the advance of depth sensors. However, despite the great success of deep learning techniques on various problems, similar approaches for SLAM have not been much addressed yet. In this work, an RGB-D SLAM system using a deep learning approach for mapping indoor environments is proposed. A pre-trained CNN model with multiple random recursive structures is utilized to acquire deep features in an efficient way with no need for training. Deep features present strong representations from color frames and enable better data association. To increase computational efficiency, deep feature vectors are considered as points in a high dimensional space and indexed in a priority search k-means tree. The search precision is improved by employing an adaptive mechanism. For motion estimation, a sparse feature based approach is adopted by employing a robust keypoint detector and descriptor combination. The system is assessed on TUM RGB-D benchmark using the sequences recorded in medium and large sized environments. The experimental results demonstrate the accuracy and robustness of the proposed system over the state-of-the-art, especially in large sequences. © 2019 IEEE

Investigation of the effect of fetal microchimeric cell following brain injury

...Türkiye Bilimsel ve Teknolojik Araştırma Kurumu (TUBITAK

Effects of neurotrophic factors cdnf and manf on brain plasticity and repair after brain ischemia

Küçük protein yapıları ile nörotrofik faktörler, nöronların gelişimi sırasındaki rollerinin yanı sıra beyinde nöronların hayatta kalımı, nörogenez ve sinaptik bağlantıların korunmasında da mutlak rol oynamaktadırlar. Nörotrofik faktörlerin ifadelerindeki azalma veya bu faktörlerin yokluğu birçok nörodejeneratif hastalığın patobiyolojisinde rol oynamaktadırlar. Yapısal olarak birbirlerine benzerlikleri ile bilinen iki nörotrofik faktör olan Serebral Dopamin Nörotrofik Faktör (CDNF) ve Mezensefalik Astrosit-Kökenli Nörotrofik Faktör (MANF) literatürde daha önceden tanımlanmış olan nörotrofik faktörlerden farklı, benzersiz bir protein yapısına sahiptirler. Bu farklılığın, MANF ve CDNF'nin diğer nörotrofik faktörlerden farklı sinyal yolakları kullanmalarına ve bu nedenle daha önceden bilinen nörotrofik faktörlerden farklı etkilere sahip olmalarına yol açabileceği düşünülmektedir. Bu nedenle, yeni mekanizmaların bulunması, başta beyin felci olmak üzere nörodejeneratif hastalıkların tedavisinde yeni yaklaşımlar sunabilecek potansiyele sahiptir. Bu tezde MANF ve CDNF nörotrofik faktörlerinin hasar sonrası in vivo şartlarda nöronal hayatta kalım, aracılık eden sinyal iletim yolakları, doku modellemesi, nörogenez, gliogenez ve piramidal trakt plastisitesi üzerine olan restoratif etkilerinin araştırılması ve aynı zamanda fonksiyonel iyileşme üzerine olan etkileri ile karşılaştırılması amaçlanmıştır. Bu mekanizmaların çalışılması amacıyla, insanlarda inme vakalarının yaklaşık % 80'inden sorumlu olan iskemik beyin felci modeli olarak farede orta serebral arter tıkanması tekniği kullanılmıştır. İskemi sonrası hem CDNF hem de MANF tedavisinin apoptotik hücre sayısını azalttığı, yeni nöron oluşumunu arttırdığı, glial yara alanını düşürdüğü, motor koordinasyon ve el çekme/kavrama gücünü arttırarak fonksiyonel geri kazanımı sağladığı ve özellikle kontralateral striatumda gen ve protein seviyesinde yaptığı değişiklikler sayesinde aksonal uzamayı arttırarak plastisiteyi sağladığı görülmüştür. Elde edilen bulguların beyin felci gibi nörodejeneratif hastalıkların tedavisine yönelik yeni hedef moleküllerin bulunmasına katkı sağlaması beklenmektedir.Neurotrophic factors are small proteins that play essential roles in development of neurons and the maintenance of neuronal synaptic function. Decrease of absence of neurotrophic factor levels play important roles in pathobiology of several neurodegenerative disorder. Recently identified CDNF (Cerebral Dopamine Neurotrophic Factor) and MANF (Mesencephalic Astrocyte-Derived Neurotrophic Factor) have unique protein structures which are different than the other known neurotrophic factor families. This difference is considered to be the reason for MANF and CDNF to use distinct signaling pathways than other neurotrophic factors. To this end, elucidating the new mechanisms has the potential to offer new approaches in the treatment of neurodegenerative disorders including brain ischemia. In this project, restorative effects of MANF and CDNF on in vivo neuronal survival following an insult, mediating signaling pathways, tissue modelling, neurogenesis, gliogenesis and pyramidal tract plasticity were investigated and also compared with their effects on functional recovery. In order to study these mechanisms, Middle Cerebral Artery Occlusion, which is responsible for approximately 80 % of all stroke cases in humans was used. Both CDNF and MANF treatment decreased the number of apoptotic cells and glial scar, increased neurogenesis, motor coordination and grip strength, ameliorates functional recovery and regulates several protein and gen expression in the contralateral hemisphere finally axonal growth and plasticity after cerebral ischemia. With the use of this method and due to its similarity of this method with clinical stroke cases, it is expected this thesis to contribute to the identification of novel target molecules in several neurodegenerative disorders including stroke

Interaction of melatonin and Bmal1 in the regulation of PI3K/AKT pathway components and cellular survival

The circadian rhythm is driven by a master clock within the suprachiasmatic nucleus which regulates the rhythmic secretion of melatonin. Bmal1 coordinates the rhythmic expression of transcriptome and regulates biological activities, involved in cell metabolism and aging. However, the role of Bmal1 in cellular- survival, signaling, its interaction with intracellular proteins, and how melatonin regulates its expression is largely unclear. Here we observed that melatonin increases the expression of Bmal1 and both melatonin and Bmal1 increase cellular survival after oxygen glucose deprivation (OGD) while the inhibition of Bmal1 resulted in the decreased cellular survival without affecting neuroprotective effects of melatonin. By using a planar surface immunoassay for PI3K/AKT signaling pathway components, we revealed that both melatonin and Bmal1 increased phosphorylation of AKT, ERK-1/2, PDK1, mTOR, PTEN, GSK-3 alpha beta, and p70S6K. In contrast, inhibition of Bmal1 resulted in decreased phosphorylation of these proteins, which the effect of melatonin on these signaling molecules was not affected by the absence of Bmal1 . Besides, the inhibition of PI3K/AKT decreased Bmal1 expression and the effect of melatonin on Bmal1 after both OGD in vitro and focal cerebral ischemia in vivo. Our data demonstrate that melatonin controls the expression of Bmal1 via PI3K/AKT signaling, and Bmal1 plays critical roles in cellular survival via activation of survival kinases

Inhibition but not activation of neuronal P2X7 receptors plays roles in brain injury after optic nerve transaction and focal cerebral ischemia

Journal of Neurology...European Federation of Neurological Societie

Inhibition but not activation of neuronal P2X7 receptors plays roles in brain injury after optic nerve transaction and focal cerebral ischemia

Joint Congress of European Neurology -- MAY 31-JUN 03, 2014 -- Istanbul, TURKEYWOS: 000337563600219European Journal of Neurology…European Federation of Neurological Societie

The phosphatidylinositol-3 kinase/Akt pathway mediates melatonin's neuroprotective activity after focal cerebral ischemia

Joint Congress of European Neurology -- MAY 31-JUN 03, 2014 -- Istanbul, TURKEYWOS: 000337563601023European Journal of Neurology…European Federation of Neurological Societie

The phosphatidylinositol-3 kinase/Akt pathway mediates melatonin's neuroprotective activity after focal cerebral ischemia

Joint Congress of European Neurology -- MAY 31-JUN 03, 2014 -- Istanbul, TURKEYWOS: 000347674000755…European Federation of Neurological Societie

Effects of normobaric oxygen and melatonin on reperfusion injury: Role of cerebral microcirculation

WOS: 000363185200028PubMed ID: 26416428In order to protect the brain before an irreversible injury occurs, penumbral oxygenation is the primary goal of current acute ischemic stroke treatment. However, hyperoxia treatment remains controversial due to the risk of free radical generation and vasoconstriction. Melatonin is a highly potent free radical scavenger that protects against ischemic stroke. Considering its anti-oxidant activity, we hypothesized that melatonin may augment the survival-promoting action of normobaric oxygen (NBO) and prevent brain infarction. Herein, we exposed mice to 30 or 90 min of intraluminal middle cerebral artery occlusion (MCAo) and evaluated the effects of NBO (70% or 100% over 90 min), administered either alone or in combination with melatonin (4 mg/ kg, i.p.), on disseminate neuronal injury, neurological deficits, infarct volume, blood-brain barrier (BBB) permeability, cerebral blood flow (CBF) and cell signaling. Both NBO and particularly melatonin alone reduced neuronal injury, neurological deficits, infarct volume and BBB permeability, and increased post-ischemic CBF, evaluated by laser speckle imaging (LSI). They also improved CBF significantly in the ischemic-core and penumbra, which was associated with reduced IgG extravasation, DNA fragmentation, infarct volume, brain swelling and neurological scores. Levels of phosphorylated Akt, anti-apoptotic Bcl-xL, pro-apoptotic Bax and endothelial nitric oxide synthase (NOS) were re-regulated after combined oxygen and melatonin delivery, whereas neuronal and inducible NOS, which were increased by oxygen treatment, were not influenced by melatonin. Our present data suggest that melatonin and NBO are promising approaches for the treatment of acute-ischemic stroke, which encourage proof-of-concept studies in human stroke patients.TUBITAK (The Scientific and Technological Research Council of Turkey) [111S418, 114S402]; Turkish Academy of Sciences (TUBA); EMBO (European Molecular Biology Organization) installation grantThis work was supported by TUBITAK (The Scientific and Technological Research Council of Turkey/111S418; 114S402), Turkish Academy of Sciences (TUBA) and EMBO (European Molecular Biology Organization) installation grant

Targeting different pathophysiological events after traumatic brain injury in mice: Role of melatonin and memantine

WOS: 000369471900016PubMed ID: 26639427The tissue damage that emerges during traumatic brain injury (TBI) is a consequence of a variety of pathophysiological events, including free radical generation and over-activation of N-methyl-D-aspartate-type glutamate receptors (NMDAR). Considering the complex pathophysiology of TBI, we hypothesized that combination of neuroprotective compounds, targeting different events which appear during injury, may be a more promising approach for patients. In this context, both NMDAR antagonist memantine and free radical scavenger melatonin are safe in humans and promising agents for the treatment of TBI. Herein, we examined the effects of melatonin administered alone or in combination with memantine on the activation of signaling pathways, injury development and DNA fragmentation. Both compounds reduced brain injury moderately and the density of DNA fragmentation significantly. Notably, melatonin/memantine combination decreased brain injury and DNA fragmentation significantly, which was associated with reduced p38 and ERK-1/2 phosphorylation. As compared with melatonin and memantine groups, SAM/INK-1/2 phosphorylation was also reduced in melatonin/memantine combined animals. In addition, melatonin, memantine and their combination decreased iNOS activity significantly. Here, we provide evidence that melatonin/memantine combination protects brain from traumatic injury, which was associated with decreased DNA fragmentation, p38 phosphorylation and iNOS activity.EMBO (European Molecular Biology Organization); Turkish Academy of Sciences (TUBA)This work was supported by EMBO (European Molecular Biology Organization) installation grant and Turkish Academy of Sciences (TUBA)