Search

UNESCO’nun 2019 yilini “Uluslararasi Kimyasal Elementlerin Periyodik Cizelgesi Yili” olarak ilan etmesiyle, dunyanin cesitli universiteleri periyodik cetveli konu alan cok sayida etkinlige ev sahipligi yapti. Prof. Dr. Emre Dolen, Istanbul Universite Edebiyat Fakultesi Bilim Tarihi Bolumu etkinlikleri cercevesinde verdigi “Periyodik Cizelgenin 150 Yillik Oykusu” baslikli konferans, bunlardan biriydi. Konferans, 21 Kasim 2019’da Edebiyat Fakultesi Genel Kurul Odasinda 13.30-15.30 arasinda gerceklesti. Konferansa, Bilim Tarihi Bolumu ogrencileri, ogretim uyeleri ve Istanbul Universitesi Kimya Fakultesi Kimya Muhendisligi Bolumu mezunlarindan (1975 girisliler) bir grup katildi.

Parkinson’s disease (PD) is a complex, chronic, and progressive neurodegenerative disease that is characterized by irreversible dopaminergic neuronal loss in the substantia nigra. Alpha-synuclein is normally a synaptic protein that plays a key role in PD due to pathological accumulation as oligomers or fibrils. Clustered alpha-synuclein binds to the Toll-like receptors and activates the microglia, which initiates a process that continues with pro-inflammatory cytokine production and secretion. Pro-inflammatory cytokine overproduction and secretion induce cell death and accelerate PD progression. Microglia are found in a resting state in physiological conditions. Microglia became activated by stimulating Toll-like receptors on it under pathological conditions, such as alpha-synuclein aggregation, environmental toxins, or oxidative stress. The interaction between Toll-like receptors and its downstream pathway triggers an activation series, leads to nuclear factor-kappa B activation, initiates the inflammasome formation, and increases cytokine levels. This consecutive inflammatory process leads to dopaminergic cell damage and cell death. Microglia become overactive in response to chronic inflammation, which is observed in PD and causes excessive cytotoxic factor production, such as reactive oxidase, nitric oxide, and tumor necrosis factor-alpha. This inflammatory process contributes to the exacerbation of pathology by triggering neuronal damage or death. Current treatments, such as dopaminergic agonists, anticholinergics, or monoamine oxidase inhibitors alleviate PD symptoms, but they can not stop the disease progression. Finding a radical treatment option or stopping the progression is essential when considering that PD is the second most reported neurodegenerative disorder. Many cytokines are released during inflammation, and they can start the phagocytic process, which caused the degradation of infected cells along with healthy ones. Therefore, targeting the pathological mechanisms, such as microglial activation, mitochondrial dysfunction, and oxidative stress, that should be involved in the treatment program is important. Neuroinflammation is one of the key factors involved in PD pathogenesis as well as alpha-synuclein accumulation, synaptic dysfunction, or dopaminergic neuronal loss, especially in the substantia nigra. Therefore, evaluating the therapeutic efficiency of the mechanisms is important, such as microglial activation and nuclear factor-kappa B pathway or inflammasome formation inhibition, and cytokine release interruption against neuroinflammation may create new treatment possibilities for PD. This study examined the pathological relation between PD and neuroinflammation, and targeting neuroinflammation as an opportunity for PD treatments, such as Toll-like receptor antagonists, NOD-like receptor family pyrin domain containing-3 inflammasome inhibitors, cytokine inhibitors, peroxisome proliferator-activated receptor-γ agonists, reactive oxygen species inhibitors, and nonsteroidal anti-inflammatory drugs.

Objective: Our aim was to investigate the relation between unilateral hippocampal and/or nigral alpha-synucleinopathy and cognitive dysfunction, anxiety and anhedonia. Materials and Methods: Female Sprague-Dawley rats were stereotactically injected adeno-associated viruses carrying alpha-synuclein (α-syn) into unilateral dentate gyrus (DG), substantia nigra (SN) or both SN + DG. The animals were tested for motor functions and memory, spatial learning, anxiety and hedony. Levels of α-syn and synaptophysin were evaluated by Western blot (WB) analysis. Results: In apomorphine-induced rotation test, a mild motor dysfunction was found in SN-α-syn group compared to control. DG- α-syn group showed memory impairment in novel object recognition test. All the α-syn injected groups spent more time to find the platform compared to controls in Morris water maze but this difference did not reach statistical significance. DG-α-syn group consumed more sucrose solution in sucrose consumption test and spent more time on the open arm in elevated plus maze, while the opposite was observed in SN-α-syn group compared to controls. We showed α-syn protein expression in the injected areas of all α-syn groups by WB and immunohistochemical staining. In WB analysis, both hippocampal and striatal synaptophysin expression levels were lower in the α-syn groups compared to controls. Conclusion: Parkinson’s disease (PD) is characterized by both motor and non-motor symptoms (NMS). However, an animal model recapitulating NMS with the background of dopaminergic denervation is still lacking. This model may help to investigate hippocampal α-syn pathology correlated especially with cognitive dysfunction and other NMS of PD.

Cancer is a disease arising from DNA alterations that dysregulate gene structure and function. These deregulated genes can also play a role in tumor invasion and metastasis or resistance to treatment. In this study, we determined the gene expression during transcription of PTGS2 (Prostaglandin-endoperoxide synthase 2), MAGE-A3 (Melanoma-associated antigen 3), CALR (Calreticulin), KRT19 (Cytokeratin 19), and TMPRSS4 (Transmembrane protease, serine 4) in HCT116 colon cancer cell line and PC3 prostate cancer cell line. After RNA isolation and cDNA conversion, DNA amplification was performed with Real-Time PCR. We determined the altered transcriptional expression level of those genes. In HCT116 colon cancer cell line, expression of the TMPRSS4 gene, MAGEA3 gene and KRT19 gene was found as increased and expression of the CALR gene and the PTGS2 gene was found as decreased. Especially a 93.70-fold increase in expression of the KRT19 gene was found in HCT116 colon cancer cell line. In PC3 prostate cancer cell lines, TMPRS4 gene expression and MAGEA3 gene expression were found as increased. But there was 50 fold decrease in PTGS2 gene expression.