絞り込み

16645

広告

新たに3人肺炎か 乗客ら受け入れの医療センター 愛知 岡崎

新型コロナウイルスの集団感染が確認されたクルーズ船の乗客らを受け入れている、愛知県岡崎市の「藤田医科大学岡崎医療センター」では、新たに19日夜到着した乗客らのう...

  1. 新型肺炎 クルーズ船乗客ら500人がきょ...
  2. 新型肺炎 クルーズ船、2人死亡 乗客初、...
  3. 新型肺炎 基本的対処、政府策定へ (毎日...
  4. 新型肺炎 「一般参加抜き」 名古屋ウィメ...

ニュース一覧

スターを付ける スターを付ける     (6view , 1users)

Full Text Sources

Medical

Miscellaneous

Other Literature Sources

Apolipoprotein-E (ApoE) has been implicated in Alzheimer's disease, atherosclerosis, and other unresolvable inflammatory conditions but a common mechanism of action remains elusive. We found in ApoE-deficient mice that oxidized lipids activated the classical complement cascade (CCC), resulting in leukocyte infiltration of the choroid plexus (ChP). All human ApoE isoforms attenuated CCC activity via high-affinity binding to the activated CCC-initiating C1q protein (K~140-580 pM) in vitro, and C1q-ApoE complexes emerged as markers for ongoing complement activity of diseased ChPs, Aβ plaques, and atherosclerosis in vivo. C1q-ApoE complexes in human ChPs, Aβ plaques, and arteries correlated with cognitive decline and atherosclerosis, respectively. Treatment with small interfering RNA (siRNA) against C5, which is formed by all complement pathways, attenuated murine ChP inflammation, Aβ-associated microglia accumulation, and atherosclerosis. Thus, ApoE is a direct checkpoint inhibitor of unresolvable inflammation, and reducing C5 attenuates disease burden.
PMID: 30692699 [PubMed - as supplied by publisher]
印刷用ページを開く Endnote用テキストダウンロード