Table 4_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 7_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 10_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 2_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 11_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 1_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 9_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 5_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 3_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Table 6_CX3CR1 upregulation modulates microglial activation and preserves synapses in the hippocampus and frontal cortex of middle-aged mice.xlsx by Jinfeng Liu (32678)

“…Following CX3CR1 knockout in the middle-aged mice, TNF-α and IL-1α levels increased, while CD68, SRA, and RAGE levels decreased in the hippocampus. Similarly, CD68, CD36, SRB1, and RAGE levels decreased in the frontal cortex. …”

Image 1_L1, a 3,3′-diindolylmethane-derivative, induced ER stress-mediated apoptosis and suppressed growth through the FLI1/AKT pathway in erythroleukemia HEL cells.tif by Yi Kuang (1873354)

“…Moreover, FLI1 is a crucial target for mediating cell differentiation, apoptosis, inflammation and displays abnormal expression in HEL cells. Here, we showed that the protein expression levels of FLI1 and AKT/p-AKT decreased with L1 treatment and that the RNA expressions of their downstream genes GATA1, TFRC, GYPA, CDKN1A and CDKN1B were also regulated by L1.…”

Image 2_L1, a 3,3′-diindolylmethane-derivative, induced ER stress-mediated apoptosis and suppressed growth through the FLI1/AKT pathway in erythroleukemia HEL cells.tif by Yi Kuang (1873354)

“…Moreover, FLI1 is a crucial target for mediating cell differentiation, apoptosis, inflammation and displays abnormal expression in HEL cells. Here, we showed that the protein expression levels of FLI1 and AKT/p-AKT decreased with L1 treatment and that the RNA expressions of their downstream genes GATA1, TFRC, GYPA, CDKN1A and CDKN1B were also regulated by L1.…”

Image2_GABA Type A receptors expressed in triple negative breast cancer cells mediate chloride ion flux.TIF by J Bundy (19843944)

“…Here, using surface biotinylation and (N-(Ethoxycarbonylmethyl)-6-Methoxyquinolinium Bromide) MQAE-dye based fluorescence quenching, we show that upregulated GABA_AR are on the cell-surface in TNBC cell lines and mediate significantly higher chloride (Cl⁻) flux as compared to non-tumorigenic MCF10A cells. …”

Data Sheet 1_Impact of endurance training on mitochondrial H2O2 production and NRF2 levels in different rat organs.pdf by Lukasz Galganski (22442002)

“…The level of malondialdehyde, a marker of oxidative damage, did not increase in the examined tissues, except the lungs, where it even decreased. Superoxide dismutase 1 levels increased in the lung, brain, and skeletal muscle, but decreased in the heart and remained unchanged in the liver. …”

Data Sheet 1_Plasma lipidomic alterations during pathogenic SIV infection with and without antiretroviral therapy.pdf by Sindhuja Sivanandham (13851914)

“…</p>Results<p>Sphingomyelins (SM) and lactosylceramides (LCER) increased during acute infection, returning to baseline during chronic infection; Hexosylceramides (HCER) increased throughout infection, being normalized with prolonged ART; Phosphatidylinositols (PI) and lysophosphatidylcholines (LPC) decreased with SIV infection and did not return to normal with ART; Phosphatidylethanolamines (PE), lysophosphatidylethanolamines (LPE) and phosphatidylcholines (PC) were unchanged by SIV infection, yet significantly decreased throughout ART. …”

Image1_GABA Type A receptors expressed in triple negative breast cancer cells mediate chloride ion flux.TIF by J Bundy (19843944)

“…Here, using surface biotinylation and (N-(Ethoxycarbonylmethyl)-6-Methoxyquinolinium Bromide) MQAE-dye based fluorescence quenching, we show that upregulated GABA_AR are on the cell-surface in TNBC cell lines and mediate significantly higher chloride (Cl⁻) flux as compared to non-tumorigenic MCF10A cells. …”

DataSheet1_Inhibiting glycosphingolipids alleviates cardiac hypertrophy by reducing reactive oxygen species and restoring autophagic homeostasis.pdf by Chunxin Jiang (5212205)

“…By Western blotting, we detected decreased intracellular expression of Sirt3 and elevated phosphorylation of JNK after phenylephrine stimulation, but this was reversed in cells pretreated with Genz-123346. …”

Image 1_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tiff by Matthew C. Austin (20633168)

“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”

Image 3_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tiff by Matthew C. Austin (20633168)

“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”

Image 4_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tif by Matthew C. Austin (20633168)

“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”