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Moreover, immunofluorescence microscopy analysis revealed induction of type IV collagen by Ring1b- or Suz12-knockdown (Fig. 1I).
Fluorescence microscopy analysis revealed that the Nef:MHC-I interaction co-localized with mCherry-Rab5, suggesting that the complex is present in early endosomes (Fig. 3a; Pearson's = 0.612).
The electron microscopy analysis revealed that filamentation (pseudohyphae) was associated with ring and rough colonies.
Transmission electron microscopy analysis revealed that the obtained nanofibers are polycrystalline in nature.
Scanning electron microscopy analysis revealed that bacterial foulants were significant contributors to membrane fouling.
Scanning transmission electron microscopy analysis revealed that the PolyQKd-32 fibrils have 50% higher mass-per-length than PolyQKd-33.
Electron microscopy analysis revealed evidence of an environment-assisted failure with extensive secondary cracking near the main fracture-surface.
Notably, scanning electron microscopy analysis revealed that in nocodazole-treated cultures, the invading cell was still capable of forming cavity in the entotic cell (Fig. 6d), but the outer cell didn't form a flattened membrane protrusion.
Confocal scanning laser microscopy analysis revealed that elements bioleached from anorthosite created surface coats on the BC nanofibril web.
Scanning electron microscopy analysis revealed that void nucleation occurs by ferrite grain-boundary decohesion in the neighborhood of martensite grains.
X-ray diffraction and transmission electron microscopy analysis revealed the retention of nanoscale structure and localized grain refinement.
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