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Ative stress with lipid peroxidation, as occur in AD. The finding that chronic HFD feeding did not significantly alter tau or AbPP expression also supports our previous conclusion that HFD feeding contributes to, but is not sufficient to cause AD-type neurodegeneration [45,46]. The combined effect of early, limited NDEA exposure plus chronic HFD feeding significantly reduced insulin and ChAT mRNA
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Slapping was still regarded as the commonest type and choking or burning was considered the least common. The lifetime prevalence of moderate physical violence was greater than that of severe physical violence (21 vs. 17.9 ). In contrast, the past year prevalence of severe physical violence was higher than moderate physical violence (8.9 , vs. 6.2 ). Details of lifetime and past year physical IPV
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Ry. Early limited exposure to NDEA had no significant effect on any of the indices measured relative to control. Chronic HFD feeding significantly increased the mean levels of pGSK-3b, GFAP, and N-Tyr relative to all other groups (P
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Allele primers, amplifies a 434 bp DNA fragment from SRA-deficient ZK1, ZK2 and ZK6 cells. With primers for MARCO wild-type allele, amplifies a 500 bp DNA fragment from WT mice; with primers for MARCO mutant allele, amplifies a 850 bp DNA fragment from ZK cells. ZK1, ZK2 and ZK6 clones exhibited both MARCO and SRA-I/II-deficient. PCR products, ca.10 l/each was resolved on a 1.5 agarose gel by gel
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Cell lines from primary alveolar macrophages from MS-/- mice. Results: We used in vitro infection of the primary AMs with the J2 retrovirus carrying the v-raf and v-myc oncogenes. Following initial isolation in media supplemented with murine macrophage colony-stimulating factor (M-CSF), we subcloned three AM cell lines, designated ZK-1, ZK-2 and ZK-6. These cell lines grow well in RPMI-1640-10 FB