Plasma Olink Proteomics Identifies CCL20 as a Novel Predictive and Diagnostic Inflammatory Marker for Preeclampsia.

Inflammation is generally thought to be involved in the occurrence and development of preeclampsia (PE), but its specific effect on PE remains unclear. In the present study, the expression levels of 92 inflammation-related proteins were measured in the late pregnancy maternal plasma from patients with PE ( = 15) and normal pregnant controls ( = 15) using the Olink inflammation panel based on the highly sensitive and specific proximity extension assay technology. A total of 28 inflammation-related markers differed between the PE and control groups.

Effects of dexmedetomidine on stress hormones in patients undergoing cardiac valve replacement: a randomized controlled trial.

Background: Stress response always occurs in cardiac valve replacement patients undergoing cardiopulmonary bypass (CPB).

Methods: 60 patients undergoing cardiac valve replacement were recruited and randomized into control and Dex groups. Dex group received 1.

OCH-mediated shift of Th1 and Th2 cytokines by NKT cells in mice with aplastic anemia.

The immune-mediated destruction of bone marrow (BM) is the major cause of aplastic anemia (AA) in most patients. It has been shown that an imbalance of Th1 and Th2 cells is involved in immune-mediated destruction of BM in patients with AA. In the present study, we determined the role of NKT cells in regulating the balance of Th1 and Th2 cytokines.

OCH ameliorates bone marrow failure in mice via downregulation of T-bet expression.

The aim of this study is to evaluate the immune mechanism of OCH in the treatment of AA (also named bone marrow failure, BMF) induced in mice. OCH at a dose of 400 μg/kg was injected intraperitoneally (I.P.

Long term cultured HL-60 cells are intrinsically resistant to Ara-C through high CDA activity.

Cytarabine (araC) is a highly active antimetabolite against hematological malignancy while the agent shows limited activity for some patients despite maintenance or continued therapy with ara-C-containing regiments. In this study, we focused to elucidate the mechanism of intrinsic resistance to araC. The concentration of intracellular ara-CTP and incorporated ara-CTP were monitored in human leukemia cell line-HL-60 for different passages in parental with its variant HL-60R.

Experimental bone marrow failure in mice ameliorated by OCH via tippling the balance of released cytokines from Th1 to Th2.

Background: OCH was reported to stimulate natural killer T (NKT) cells to produce predominantly T helper type 2 (Th2) cytokines. The present study was attempted to evaluate potential protection of OCH on acquired bone marrow failure syndromes (BMFS) in mice model.

Methods: BMFS in mice model was established by exposure to sublethal irradiation followed by infusion with 5 × 10(6) B6 lymph nodes cells.