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Results show that chemical bonds between carbonyl and its linked carbon atoms in C5-PFK molecule are weak but with robust reactivity.
Furthermore, all patients carrying the HLA-A*0101 HLA-A*0101ibited robust reallelety to WMD10 (WMDSTKATRY) and all patiexhibitedying HLA-A*0201 exhibited robustvity to SVG9 (SVGGVFTSV).
MAbs specific for presumed sequences from aa 182 and beyond towards the C-terminus of TDP-43 (i.e. Regions C-F) showed robust reactivity for neocortical TDP-43 pathology across FTLD-TDP subtypes and ALS spinal cord inclusions.
21, 22 In addition to robust reactivity to Pf antigens, there was also strong reactivity to a subset of Pv antigens, which we attribute to antigenic cross-reactivity (see Figure 3).
MAbs 211 and 5031, which are specific for the N-terminus of TDP-43 (i.e. regions A and B as illustrated in Figure 1) showed robust reactivity for normal nuclear TDP-43, but 5031 detected more pathology in the ALS spinal cord and FTLD-TDP temporal cortex than 211.
To extend this Pd-mediated cross-coupling reaction to a mammalian system, herein we report the genetic encoding of an alkyne amino acid, Nε-butynyloxycarbonyllysine (butynylK), with a known orthogonal pyrrolysyl-tRNA synthetase/tRNACUA pair, and its robust reactivity in directing Pd-mediated protein labeling in cell lysates, inside E. coli, and on live mammalian cell surfaces.
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In AD brains, robust DPP10789 reactivity was detected in neurofibrillary tangles and plaque-associated dystrophic neurites, most of which colocalized with the doubly phosphorylated Ser-202/Thr-205 tau epitope.
Pathologically, TDP-43WTxQ331K mice demonstrate major neuronal loss, robust astroglial reactivity, increased cytoplasmic TDP-43 accumulation and detergent resistant TDP-43.
In contrast, in AD brains, robust DPP10789 reactivity was also detected in neurofibrillary tangles and plaque-associated dystrophic neurites, most of which colocalized with the hyperphosphorylated Ser-202/Thr-205 tau epitope.
Thus, whether using antigen retrieval, which could reveal pathologic accumulations of SOD1, or no antigen retrieval, which could reveal SOD1 possessing a conformational signature produced by ALS mutant SOD1, we failed to detect robust C4F6 reactivity that is specific to sALS spinal motor neurons.
An IHC evaluation of MMP-7 revealed robust increases in reactivity in lung tissues from HDM-treated mice compared with PBS-treated mice, with notable reactivity occurring in the bronchiolar epithelium (Fig. 4a).
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