Mr Mahmoud Abdolhoseini
Mahmoud Abdolhoseini has started his PhD in Electrical Engineering at University of Newcastle, NSW, Australia since 2015. His research interest is image processing, system identification and their application in reconstruction, visualization and quantification of microscopy images. He is working on Glial cell microscopy images and collaborate with a neuroscience research group at Hunter Medical Research Institute (HMRI, NSW, Australia).
- Processing of Microscopy Image
- English (Fluent)
- Persian (excluding Dari) (Mother)
Fields of Research
|090699||Electrical and Electronic Engineering not elsewhere classified||100|
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (6 outputs)
Abdolhoseini M, Kluge MG, Walker FR, Johnson SJ, 'Segmentation of Heavily Clustered Nuclei from Histopathological Images', SCIENTIFIC REPORTS, 9 (2019) [C1]
Pietrogrande G, Zalewska K, Zhao Z, Abdolhoseini M, Chow WZ, Sanchez-Bezanilla S, et al., 'Low oxygen post conditioning prevents thalamic secondary neuronal loss caused by excitotoxicity after cortical stroke', Scientific Reports, 9 (2019) [C1]
© 2019, The Author(s). In the current study, we were interested in investigating whether Low oxygen post-conditioning (LOPC) was capable of limiting the severity of stroke-induce... [more]
© 2019, The Author(s). In the current study, we were interested in investigating whether Low oxygen post-conditioning (LOPC) was capable of limiting the severity of stroke-induced secondary neurodegeneration (SND). To investigate the effect of LOPC we exposed adult male C57/BL6 mice to photothrombotic occlusion (PTO) of the motor and somatosensory cortex. This is known to induce progressive neurodegeneration in the thalamus within two weeks of infarction. Two days after PTO induction mice were randomly assigned to one of four groups: (i) LOPC-15 day exposure group; (ii) a LOPC 15 day exposure followed by a 15 day exposure to normal atmosphere; (iii) normal atmosphere for 15 days and (iv) normal atmosphere for 30 days (n = 20/group). We observed that LOPC reduced the extent of neuronal loss, as indicated by assessment of both area of loss and NeuN + cell counts, within the thalamus. Additionally, we identified that LOPC reduced microglial activity and decreased activity within the excitotoxic signalling pathway of the NMDAR axis. Together, these findings suggest that LOPC limits neuronal death caused by excitotoxicity in sites of secondary damage and promotes neuronal survival. In conclusion, this work supports the potential of utilising LOPC to intervene in the sub-acute phase post-stroke to restrict the severity of SND.
Pietrogrande G, Mabotuwana N, Zhao Z, Abdolhoseini M, Johnson SJ, Nilsson M, Walker FR, 'Chronic stress induced disturbances in Laminin: A significant contributor to modulating microglial pro-inflammatory tone?', BRAIN BEHAVIOR AND IMMUNITY, 68 23-33 (2018) [C1]
Zalewska K, Pietrogrande G, Ong LK, Abdolhoseini M, Kluge M, Johnson SJ, et al., 'Sustained administration of corticosterone at stress-like levels after stroke suppressed glial reactivity at sites of thalamic secondary neurodegeneration', Brain, Behavior, and Immunity, 69 210-222 (2018) [C1]
© 2017 Elsevier Inc. Secondary neurodegeneration (SND) is an insidious and progressive condition involving the death of neurons in regions of the brain that were connected to but ... [more]
© 2017 Elsevier Inc. Secondary neurodegeneration (SND) is an insidious and progressive condition involving the death of neurons in regions of the brain that were connected to but undamaged by the initial stroke. Our group have published compelling evidence that exposure to psychological stress can significantly exacerbate the severity SND, a finding that has considerable clinical implications given that stroke-survivors often report experiencing high and unremitting levels of psychological stress. It may be possible to use one or more targeted pharmacological approaches to limit the negative effects of stress on the recovery process but in order to move forward with this approach the most critical stress signals have to be identified. Accordingly, in the current study we have directed our attention to examining the potential effects of corticosterone, delivered orally at stress-like levels. Our interest is to determine how similar the effects of corticosterone are to stress on repair and remodelling that is known to occur after stroke. The study involved 4 groups, sham and stroke, either administered corticosterone or normal drinking water. The functional impact was assessed using the cylinder task for paw asymmetry, grid walk for sensorimotor function, inverted grid for muscle strength and coordination and open field for anxiety-like behaviour. Biochemically and histologically, we considered disturbances in main cellular elements of the neurovascular unit, including microglia, astrocytes, neurons and blood vessels using both immunohistochemistry and western blotting. In short, we identified that corticosterone delivery after stroke results in significant suppression of key microglial and astroglial markers. No changes were observed on the vasculature and in neuronal specific markers. No changes were identified for sensorimotor function or anxiety-like behaviour. We did, however, observe a significant change in motor function as assessed using the inverted grid walk test. Collectively, these results suggest that pharmacologically targeting corticosterone levels in the future may be warranted but that such an approach is unlikely to limit all the negative effects associated with exposure to chronic stress.
Kluge MG, Abdolhoseini M, Zalewska K, Ong LK, Johnson SJ, Nilsson M, Walker FR, 'Spatiotemporal analysis of impaired microglia process movement at sites of secondary neurodegeneration post-stroke', Journal of Cerebral Blood Flow and Metabolism, (2018)
© The Author(s) 2018. It has recently been identified that after motor cortex stroke, the ability of microglia processes to respond to local damage cues is lost from the thalamus,... [more]
© The Author(s) 2018. It has recently been identified that after motor cortex stroke, the ability of microglia processes to respond to local damage cues is lost from the thalamus, a major site of secondary neurodegeneration (SND). In this study, we combine a photothrombotic stroke model in mice, acute slice and fluorescent imaging to analyse the loss of microglia process responsiveness. The peri-infarct territories and thalamic areas of SND were investigated at time-points 3, 7, 14, 28 and 56 days after stroke. We confirmed the highly specific nature of non-responsive microglia processes to sites of SND. Non-responsiveness was at no time observed at the peri-infarct but started in the thalamus seven days post-stroke and persisted for 56 days. Loss of directed process extension is not a reflection of general functional paralysis as phagocytic function continued to increase over time. Additionally, we identified that somal P2Y12 was present on non-responsive microglia in the first two weeks after stroke but not at later time points. Finally, both classical microglia activation and loss of process extension are highly correlated with neuronal damage. Our findings highlight the importance of microglia, specifically microglia dynamic functions, to the progression of SND post-stroke, and their potential relevance as modulators or therapeutic targets during stroke recovery.
Kluge MG, Kracht L, Abdolhoseini M, Ong LK, Johnson SJ, Nilsson M, Walker FR, 'Impaired microglia process dynamics post-stroke are specific to sites of secondary neurodegeneration', GLIA, 65 1885-1899 (2017) [C1]
© 2017 Wiley Periodicals, Inc. Stroke induces tissue death both at the site of infarction and at secondary sites connected to the primary infarction. This latter process has been ... [more]
© 2017 Wiley Periodicals, Inc. Stroke induces tissue death both at the site of infarction and at secondary sites connected to the primary infarction. This latter process has been referred to as secondary neurodegeneration (SND). Using predominantly fixed tissue analyses, microglia have been implicated in regulating the initial response at both damage sites post-stroke. In this study, we used acute slice based multiphoton imaging, to investigate microglia dynamic process movement in mice 14 days after a photothrombotic stroke. We evaluated the baseline motility and process responses to locally induced laser damage in both the peri-infarct (PI) territory and the ipsilateral thalamus, a major site of post-stroke SND. Our findings show that microglia process extension toward laser damage within the thalamus is lost, yet remains robustly intact within the PI territory. However, microglia at both sites displayed an activated morphology and elevated levels of commonly used activation markers (CD68, CD11b), indicating that the standardly used fixed tissue metrics of microglial ¿activity¿ are not necessarily predictive of microglia function. Analysis of the purinergic P2Y12 receptor, a key regulator of microglia process extension, revealed an increased somal localization on nonresponsive microglia in the thalamus. To our knowledge, this is the first study to identify a non-responsive microglia phenotype specific to areas of SND post-stroke, which cannot be identified by the classical assessment of microglia activation but rather the localization of P2Y12 to the soma.
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Conference (1 outputs)
Johnson SJ, Abdolhoseini M, Walker F, 'Automated Tracing of Microglia Using Multilevel Thresholding and Minimum Spanning Trees', http://ieeexplore.ieee.org/xpl/mostRecentIssue.jsp?punumber=7580725, Florida USA (2016) [E1]