miRNA-486–5p levels were stained by <i>in situ</i> hybridization.

<p><b>a</b> Hematoxylin and eosin (HE)-stained GC tissue. <b>b</b> miR-486–5p stained by <i>in situ</i> hybridization. <b>c</b> HE-stained neighboring normal tissue. <b>d</b> miR-486–5p stained by <i>in situ</i> hybridization; decreased miR-486–5p expression in GC compared with neighboring normal tissue. <b>e</b> HE-stained GC tissue. <b>f</b> miR-486–5p stained by <i>in situ</i> hybridization. <b>g</b> HE-stained neighboring normal tissue. <b>h</b> miR-486–5p stained by <i>in situ</i> hybridization; unchanged miR-486–5p expression in GC compared with neighboring normal tissue. <b>i</b> HE-stained GC. <b>j</b> miR-486–5p stained by <i>in situ</i> hybridization. <b>k</b> HE-stained neighboring normal tissue. <b>l</b> miR-486–5p stained by <i>in situ</i> hybridization; increased miR-486–5p expression in GC compared with neighboring normal tissue.</p

FGF9 expression was stained by immunohistochemistry and survival curves in patients with GC according to FGF9 levels.

<p><b>a</b> High expression of FGF9 stained in GC. <b>b</b> Low expression FGF9 stained in neighboring normal tissue. <b>c</b> Survival curves in patients with high expression of FGF9 in GC compared with patients with low expression of FGF9 (<i>P</i> = 0.001).</p

Univariate analysis of survival.

<p>Univariate analysis of survival.</p

miR-486-5p expression and clinicopathological features in patients with gastric adenocarcinoma.

<p>miR-486-5p expression and clinicopathological features in patients with gastric adenocarcinoma.</p

Characteristics of the study subjects.

<p>Characteristics of the study subjects.</p

Survival curves in patients with GC according to miRNA-486–5p levels.

<p><b>a</b> Overall survival curves in patients with GC according to miRNA-486–5p levels (<i>P</i> = 0.002). <b>b</b> Survival curves in stage-II GC according to miRNA-486–5p levels (<i>P</i> = 0.024). <b>c</b> Survival curves in stage-III GC according to miRNA-486–5p levels (<i>P</i> = 0.003).</p

Additional file 1: of Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2)

Figure S1. Oligomeric Aβ1–42 specifically binds to TREM2. Figure S2. Oligomeric Aβ1–42 specifically activates TREM2 reporter cells. Figure S3. The number of microglia clustered around Aβ is decreased in Trem2-KO mice. (PDF 1369 kb