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Hyperkinetic Movement Disorders
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Morales-Briceno Hugo, Victor S.C. Fung, Annu Aggarwal, Philip Thompson
Myoclonus, ataxia with relatively preserved cognition: Common causes: Unverricht–Lundborg disease (Baltic myoclonus).Myoclonic epilepsy with ragged red fibers (MERRF).Postanoxic myoclonus.Spinocerebellar degenerations.Uncommon causes: CD.MSA.GM2 gangliosidosis.NCL.DRPLA.North Sea progressive myoclonus epilepsy (GOSR2 mutations).Action myoclonus renal failure syndrome.MEAK syndrome (KCNC1 mutations).SCA14 (PRKCG mutations).POLG mutations.PRICKLE1 mutations.ASAH1 mutations.KCTD7 mutations.LMNB2 mutations.SLC25A46 mutations.
A comparison expression analysis of CXCR4, CXCL9 and Caspase-9 in dermal vascular endothelial cells between keloids and normal skin on chemotaxis and apoptosis
Published in Journal of Plastic Surgery and Hand Surgery, 2022
Xinhang Dong, Mingzi Zhang, Yuanjing Chen, Chengcheng Li, Youbin Wang, Xiaolei Jin
To some extent, keloids are an inflammatory disease involving the reticular dermis layer, and injuries of the reticular dermis and abnormal wound healing are major causes of the disease. Studies have shown that pro-inflammatory cytokines such as TNF-α (tumor necrosis factor-α), IL-1α (interleukin-1α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in keloid tissue are highly expressed, which could promote chronic inflammation and cause invasive growth of keloids [17]. As it is shown in the KEGG pathway analysis from Enrichr, inflammatory mediator regulation of TRP channels is significantly enriched in the KEGG pathway, including up-regulated DEGs of PRKCG, PRKCE, TRPV4, TRPV2, CALML4, ADCY1 and PRKACB. In this process, a large number of blood vessels are formed, while the functions are not complete. Moreover, due to the increase of blood vessel permeability and the induction of chemokines, a great number of inflammatory factors accumulate in the extracellular matrix, which is consistent with the high inflammation status shown by the HE staining results.
Genistein affects gonadotrophin-releasing hormone secretion in GT1-7 cells via modulating kisspeptin receptor and key regulators
Published in Systems Biology in Reproductive Medicine, 2022
Jingyuan Xiong, Ye Tian, Aru Ling, Zhenmi Liu, Li Zhao, Guo Cheng
In qRT-PCR analysis, relative mRNA levels of Sirt1 were upregulated with increasing concentrations of genistein, while relative mRNA levels of Prkcg and Mkrn3 decreased in a concentration dependent manner. When GT1-7 cells were treated with 20 μM genistein for 48 h, the relative mRNA level of Sirt1 was 1.44-fold higher than the control (Figure 5A), and the relative mRNA levels of Prkcg and Mkrn3 were 2.0-fold and 1.56-fold lower than the control, respectively (Figure 5B-C). These results showed that genistein treatment could significantly alter Sirt1, Prkcg and Mkrn3 mRNA levels compared to the control, demonstrating that genistein was able to influence multiple intrinsic regulators of GnRH secretion in GT1-7 cells.
The selective BDNF overexpression in neurons protects neuroglial networks against OGD and glutamate-induced excitotoxicity
Published in International Journal of Neuroscience, 2020
S. G. Gaidin, M. V. Turovskaya, M. S. Gavrish, A. A. Babaev, V. N. Mal’tseva, E. V. Blinova, E. A. Turovsky
GABA(B) receptors are tightly coupled with BDNF release [81,82]. For instance, the enhancement of BDNF release into extracellular space is observed under the activation of GABA(B) receptors. Besides, it is shown that this pathway includes PLC activation, diacylglycerol accumulation, activation of PKC and L-type voltage-gated calcium channels [82]. We have demonstrated that expression of the GABA(B) receptor subunit significantly increased which can be explained by the necessity of release of excessive BDNF concentrations from transduced neurons. Besides, the decrease of expression of PKCa and PKCg isoforms was observed in our experiments. It is known that the activity of protein kinases from cytosolic fraction of hippocampal neurons can be decreased under excessive activation of GABA(B) receptors [83]. Thus, increased Gabbr1 expression in cell cultures with BDNF overexpression can be considered as a positive modulator of BDNF release, contributing to network inhibition.