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1 ates with disease duration and the degree of spongiosis.
2 C) is depleted, in parallel with reversal of spongiosis.
3 ut not early, even in regions with prominent spongiosis.
4 eptor 2-mediated pruritus and MyD88-mediated spongiosis.
5 ive deposits, astrocytosis, myelin loss, and spongiosis.
6 d brainstem dissemination also induced acute spongiosis.
7                 There was superficial linear spongiosis affecting the frontal lobes in all three auto
8 ative scoring of neuronal loss, gliosis, and spongiosis and immunocytochemical and ultrastructural ch
9  psoriasiform acanthosis in association with spongiosis and infiltration of both the epidermis and de
10                                Minimal brain spongiosis and long incubation times are observed for th
11 endent manner, which is accompanied by focal spongiosis and occasional neuronal loss.
12 , CJD mice had the hallmark features of CJD, spongiosis and proteinase K-resistant PrP aggregates, in
13 d epidermal barrier, microbial colonization, spongiosis, and eosinophil infiltration, but also aspect
14     Histologically, scattered glial nodules, spongiosis, and mineralization were found in the basal g
15  (TCS) and S. hominis reduced RHE thickness, spongiosis, and NdS 18:0;2/24:0;0 levels.
16 on accompanied by progressive neuronal loss, spongiosis, and neurite degeneration in the cerebellum.
17 concentrated in regions of the brain rich in spongiosis, and the magnitude of responses was similar t
18 L-4 and IL-13, we found coal tar to diminish spongiosis, apoptosis, and CCL26 expression, all AD hall
19 mi-quantitative histopathological scoring of spongiosis, astrocytosis and prion protein deposition.
20                 Thus, in addition to causing spongiosis, FasL may play a direct role in triggering an
21  survival time, clinical tempo, or levels of spongiosis, gliosis, or PrPres in the brain.
22 keratinocytes and triggers the appearance of spongiosis in eczematous dermatitis.
23 eratinocytes is the main cause of eczema and spongiosis in patients with the common inflammatory skin
24                                     Although spongiosis is generally thought to be secondary to edema
25 ost closely resembled AD hallmarks including spongiosis, more severe keratinocyte differentiation def
26 lysis showed marked epidermal acanthosis and spongiosis, neovascularization, and elevated number of i
27 of circumscribed neuronal loss, gliosis, and spongiosis of limbic neocortical areas and frontal, temp
28 ICD showed exocytosis and similar degrees of spongiosis on RCM.
29     This occurs with minimal evidence of CNS spongiosis or apoptosis of neurons.
30 n cortical magnetization transfer ratios and spongiosis (P = 0.02), but not prion protein deposition
31 levant signaling pathways that contribute to spongiosis, proliferation, generation of proinflammatory
32 eft frontal SI correlated with the degree of spongiosis (r = 0.64, P = .047).
33 hese studies revealed that acute MLV-induced spongiosis results from two separable activities of Env.
34                          Second, Env induces spongiosis through a toxin activity that is MLV-receptor
35 um in its central portion, exhibiting marked spongiosis, vascular proliferation, and a chronic inflam
36                                              Spongiosis was present in the middle cerebellar peduncle