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Frontiers | Irisin Contributes to Neuroprotection by Promoting Mitochondrial Biogenesis After Experimental Subarachnoid Hemorrhage

1Department of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China 2Luzhou Key Laboratory of Neurological Diseases and Brain Function, The Affiliated Hospital of Southwest Medical University, Luzhou, China 3Academician (Expert) Workstation of Sichuan Province, The Affiliated Hospital of Southwest Medical University, Luzhou, China 4Sichuan Clinical Research Center for Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China Subarachnoid hemorrhage (SAH) is a devastating form of stroke, which poses a series of intractable challenges to clinical practice. Imbalance of mitochondrial homeostasis has been thought to be the crucial pathomechanism in early brain injury (EBI) cascade after SAH. Irisin, a protein related to metabolism and mitochondrial homeostasis, has been reported to play pivotal roles in post-stroke neuroprotection. However, whether this myokine can exert neuroprotection effects after SAH remains unknown. In t

Early Release - Anopheles stephensi Mosquitoes as Vectors of Plasmodium vivax and falciparum, Horn of Africa, 2019 - Volume 27, Number 2—February 2021 - Emerging Infectious Diseases journal

 , Temesgen Ashine 1, Hiwot Teka, Endashaw Esayas, Louisa A. Messenger, Wakweya Chali, Lisette Meerstein-Kessel, Thomas Walker, Sinknesh Wolde Behaksra, Kjerstin Lanke, Roel Heutink, Claire L. Jeffries, Daniel Abebe Mekonnen, Elifaged Hailemeskel, Surafel K. Tebeje, Temesgen Tafesse, Abrham Gashaw, Tizita Tsegaye, Tadele Emiru, Kigozi Simon, Eyuel Asemahegn Bogale, Gedeon Yohannes, Soriya Kedir, Girma Shumie, Senya Asfer Sabir, Peter Mumba, Dereje Dengela, Jan H. Kolaczinski, Anne Wilson, Thomas S. Churcher, Sheleme Chibsa, Matthew Murphy, Meshesha Balkew, Seth Irish, Chris Drakeley, Endalamaw Gadisa, and Teun Bousema Author affiliations: Armauer Hansen Research Institute, Addis Ababa, Ethiopia (F.G. Tadesse, T. Ashine, H. Teka, E. Esayas, W. Chali, S.W. Behaksra, D.A. Mekonnen, E. Hailemeskel, S.K. Tebeje, T. Tafesse, A. Gashaw, T. Tsegaye, T. Emiru, E.A. Bogale, G. Shumie, S.A. Sabir, E. Gadisa); Radboud University Medical Center, Nijmegen, the Netherlands (F.G

Frontiers | Quantification of Huntington s Disease Related Markers in the R6/2 Mouse Model

2Department of Health Studies, FH Joanneum University of Applied Sciences, Graz, Austria Huntington’s disease (HD) is caused by an expansion of CAG triplets in the huntingtin gene, leading to severe neuropathological changes that result in a devasting and lethal phenotype. Neurodegeneration in HD begins in the striatum and spreads to other brain regions such as cortex and hippocampus, causing motor and cognitive dysfunctions. To understand the signaling pathways involved in HD, animal models that mimic the human pathology are used. The R6/2 mouse as model of HD was already shown to present major neuropathological changes in the caudate putamen and other brain regions, but recently established biomarkers in HD patients were yet not analyzed in these mice. We therefore performed an in-depth analysis of R6/2 mice to establish new and highly translational readouts focusing on Ctip2 as biological marker for motor system-related neurons and translocator protein (TSPO) as a promising rea

Early Release - Role of Burkholderia pseudomallei–Specific IgG2 in Adults with Acute Melioidosis, Thailand - Volume 27, Number 2—February 2021 - Emerging Infectious Diseases journal

Melioidosis is a life-threatening infectious disease caused by the gram-negative bacillus Burkholderia pseudomallei. An effective vaccine is needed, but data on protective immune responses in human melioidosis are lacking. We used ELISA and an antibody-dependent cellular phagocytosis assay to identify the major features of protective antibodies in patients with acute melioidosis in Thailand. We found that high levels of B. pseudomallei–specific IgG2 are associated with protection against death in a multivariable logistic regression analysis adjusting for age, diabetes, renal disease, and neutrophil count. Serum from melioidosis survivors enhanced bacteria uptake into human monocytes expressing FcγRIIa-H/R131, an intermediate-affinity IgG2-receptor, compared with serum from nonsurvivors. We did not find this enhancement when using monocytes carrying the low IgG2–affinity FcγRIIa-R131 allele. The findings indicate the importance of IgG2 in protection against death in human me

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