Human Granulin, GRN ELISA Kit (CKERS-GRN-244H)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
5plates
Species Reactivity
Human
Intended Use
The human GRN ELISA kit is for the quantitative determination of human GRN.
This ELISA kit contains the basic components required for the development of sandwich ELISAs. Each kit contains sufficient materials to run ELISAs on five 96-well plates.
Contents of Kit
1. Bring all reagents to room temperature before use.
2. Capture Antibody: 0.4 mg/mL of mouse anti-GRN monoclonal antibody.
3. Detection Antibody: Each vial contains 120 μg biotinylated rabbit anti-GRN polyclonal antibody. Reconstitute with sterile 1 mL distilled water. Dilute to a working concentration of 1.0 μg/mL in detection antibody dilution buffer before use.
4. Standard: Each vial contains 24 ng of recombinant GRN. Reconstitute power with sterile distilled water. A seven-point standard curve using 2-fold serial dilutions in sample dilution buffer, and a high standard of 1,000 pg/mL is recommended.
5. Streptavidin-HRP: 50μL of streptavidin conjugated to horse-radish-peroxidase. 1:2,000 Dilution in detection antibody dilution buffer before use.
Storage
Keep streptavidin-HRP at 4°C and protect it from prolonged exposure to light. Aliquot all other reagents and store at -20°C to -70°C in a manual defrost freezer.
Sensitivity
The minimum detectable dose of human GRN was determined to be approximately 15.6 pg/mL. This is defined as at least three times standard deviations above the mean optical density of 10 replicates of the zero standard.

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References


Outer rotor wound field flux switching machine for In-wheel direct drive application

IET ELECTRIC POWER APPLICATIONS

Authors: Ahmad, Naseer; Khan, Faisal; Ali, Hazrat; Ishaq, Samra; Sulaiman, Erwan

Nowadays the flux switching machines offer pivotal role in high speed applications. The flux sources (field excitation coil and armature winding or permanent magnet) are confined to the stator leaving rotor completely passive, and thus making the flux switching machine (FSM) more suitable for industrial applications. This paper emphasizes salient rotor pole and non-overlapping windings embedded in electrical machine design possess some pertinent features such as reduced copper losses, low-cost, and usage in high speed applications. The proposed design is analyzed for coil test analysis and flux linkage and torque. On the basis of the analysis performed, it is clear that 12-slot/13-pole has low cogging torque, high flux linkage, and maximum torque, compared with other topologies of outer rotor field excitation FSM. A deterministic optimization technique is adopted to enhance the performance of 12-slot/13-pole design. Further, finite element analysis (FEA) results are verified through Global Reluctance Network (GRN) methodology, which show close resemblance with error less than 1.2%. Hence, it validates the proposed design for outer rotor field excitation FSM direct drive application. The proposed design for hybrid electric vehicle torque characteristic is compared with existing interior permanent magnet synchronous machine (IPMSM) and 6-slot/7-pole wound field flux switching machine (WFFSM).

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

ACTA NEUROPATHOLOGICA

Authors: Pottier, Cyril; Ren, Yingxue; Perkerson, Ralph B., III; Baker, Matt; Jenkins, Gregory D.; van Blitterswijk, Marka; DeJesus-Hernandez, Mariely; van Rooij, Jeroen G. J.; Murray, Melissa E.; Christopher, Elizabeth; McDonnell, Shannon K.; Fogarty, Zachary; Batzler, Anthony; Tian, Shulan; Vicente, Cristina T.; Matchett, Billie; Karydas, Anna M.; Hsiung, Ging-Yuek Robin; Seelaar, Harro; Mol, Merel O.; Finger, Elizabeth C.; Graff, Caroline; Oijerstedt, Linn; Neumann, Manuela; Heutink, Peter; Synofzik, Matthis; Wilke, Carlo; Prudlo, Johannes; Rizzu, Patrizia; Simon-Sanchez, Javier; Edbauer, Dieter; Roeber, Sigrun; Diehl-Schmid, Janine; Evers, Bret M.; King, Andrew; Mesulam, M. Marsel; Weintraub, Sandra; Geula, Changiz; Bieniek, Kevin F.; Petrucelli, Leonard; Ahern, Geoffrey L.; Reiman, Eric M.; Woodruff, Bryan K.; Caselli, Richard J.; Huey, Edward D.; Farlow, Martin R.; Grafman, Jordan; Mead, Simon; Grinberg, Lea T.; Spina, Salvatore; Grossman, Murray; Irwin, David J.; Lee, Edward B.; Suh, EunRan; Snowden, Julie; Mann, David; Ertekin-Taner, Nilufer; Uitti, Ryan J.; Wszolek, Zbigniew K.; Josephs, Keith A.; Parisi, Joseph E.; Knopman, David S.; Petersen, Ronald C.; Hodges, John R.; Piguet, Olivier; Geier, Ethan G.; Yokoyama, Jennifer S.; Rissman, Robert A.; Rogaeva, Ekaterina; Keith, Julia; Zinman, Lorne; Tartaglia, Maria Carmela; Cairns, Nigel J.; Cruchaga, Carlos; Ghetti, Bernardino; Kofler, Julia; Lopez, Oscar L.; Beach, Thomas G.; Arzberger, Thomas; Herms, Jochen; Honig, Lawrence S.; Vonsattel, Jean Paul; Halliday, Glenda M.; Kwok, John B.; White, Charles L., III; Gearing, Marla; Glass, Jonathan; Rollinson, Sara; Pickering-Brown, Stuart; Rohrer, Jonathan D.; Trojanowski, John Q.; Van Deerlin, Vivianna; Bigio, Eileen H.; Troakes, Claire; Al-Sarraj, Safa; Asmann, Yan; Miller, Bruce L.; Graff-Radford, Neill R.; Boeve, Bradley F.; Seeley, William W.; Mackenzie, Ian R. A.; van Swieten, John C.; Dickson, Dennis W.; Biernacka, Joanna M.; Rademakers, Rosa

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole-genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25.5% and 13.9% of FTLD-TDP patients, respectively. Mutations in TBK1 (1.5%) and other known FTLD genes (1.4%) were rare, and the disease in 57.7% of FTLD-TDP patients was unexplained by the known FTLD genes. To unravel the contribution of common genetic factors to the FTLD-TDP etiology in these patients, we conducted a two-stage association study comprising the analysis of whole-genome sequencing data from 517 FTLD-TDP patients and 838 controls, followed by targeted genotyping of the most associated genomic loci in 119 additional FTLD-TDP patients and 1653 controls. We identified three genome-wide significant FTLD-TDP risk loci: one new locus at chromosome 7q36 within the DPP6 gene led by rs118113626 (p value = 4.82e - 08, OR = 2.12), and two known loci: UNC13A, led by rs1297319 (p value = 1.27e - 08, OR = 1.50) and HLA-DQA2 led by rs17219281 (p value = 3.22e - 08, OR = 1.98). While HLA represents a locus previously implicated in clinical FTLD and related neurodegenerative disorders, the association signal in our study is independent from previously reported associations. Through inspection of our whole-genome sequence data for genes with an excess of rare loss-of-function variants in FTLD-TDP patients (n >= 3) as compared to controls (n = 0), we further discovered a possible role for genes functioning within the TBK1-related immune pathway (e.g., DHX58, TRIM21, IRF7) in the genetic etiology of FTLD-TDP. Together, our study based on the largest cohort of unrelated FTLD-TDP patients assembled to date provides a comprehensive view of the genetic landscape of FTLD-TDP, nominates novel FTLD-TDP risk loci, and strongly implicates the immune pathway in FTLD-TDP pathogenesis.

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