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- Bravo, L, et al.
(författare)
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- 2021
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swepub:Mat__t
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- Tabiri, S, et al.
(författare)
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- 2021
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swepub:Mat__t
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- Han, W, et al.
(författare)
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Trends in live births in the past 20 years in Zhengzhou, China
- 2011
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Ingår i: ACTA OBSTETRICIA ET GYNECOLOGICA SCANDINAVICA. - 0001-6349. ; 90:4, s. 332-337
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Tidskriftsartikel (refereegranskat)abstract
- Abstract: Objective. To evaluate changing trends in neonatal births and deaths in a provincial women's and children's hospital over the past 20 years. Design: Retrospective longitudinal study. Setting. Henan Provincial Women's and Children's Hospital, China. Population. Live births in Henan Provincial Women's and Children's Hospital from January 1987 to December 2006. Methods: Data was stratified by sex, birth weight, delivery type, maternal age, gestational age, and single or multiple births. The incidence of low Apgar scores and neonatal death was calculated for each fiscal year. Main outcome measures: Trends in the fundamental status of hospital-born live births and risk factors for neonatal death. Results. 26 760 hospital live births were included. The ratio of males to females was 1.16:1. The mean gestational age decreased from 39.5 +/- 1.4 weeks to 38.4 +/- 2.5 weeks (p<0.001) and multiple births increased from 1.5 to 7.3% (p<0.001). The proportion of preterm births increased from 4.7 to 18.9% (p<0.001), maternal age increased from 25.9 +/- 3.7 years to 29.0 +/- 4.4 years (p<0.001), and cesarean deliveries increased from 23.7 to 65.5% (p<0.001). The incidence of low Apgar scores decreased from 12.9 to 1.1% (p<0.001). The incidence of neonatal death was 8.5/1 000 live births, with preterm births and low Apgar scores accounting for 72.8 and 16.2% of all neonatal deaths, respectively. Conclusion. Preterm births, multiple births, and cesarean deliveries increased dramatically. Preterm birth is the leading cause of neonatal death.
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- Liu, AQ, et al.
(författare)
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Leukotriene B4 activates T cells that inhibit B-cell proliferation in EBV-infected cord blood-derived mononuclear cell cultures
- 2008
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Ingår i: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 111:5, s. 2693-2703
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Tidskriftsartikel (refereegranskat)abstract
- Epstein-Barr virus (EBV)–specific cellular memory is not transferred from mother to child. Therefore, EBV-induced B-cell proliferation in in vitro–infected cord blood mononuclear cell cultures is not inhibited. However, by addition of immunomodulators, polysaccharide K (PSK) or truncated thioredoxin (Trx80) that activate monocytes, EBV-specific T-cell response could be generated in such cultures. Presently, we demonstrate that leukotriene B4 (LTB4) is involved in the effect of the immunomodulators. LTB4 was detected in the medium, and T-cell activation was compromised by addition of leukotriene biosynthesis inhibitors. Moreover, we found that LTB4 added to infected cultures, which did not receive the immunomodulators, induced functional activation of the T cells. LTB4 activated the monocytes and acted directly on the T cells. In consequence, addition of LTB4 inhibited the EBV-induced proliferation of B lymphocytes. Specific cytotoxicity could be generated by restimulation of the T cells. The experiments showed successive stages of T-cell activation in acquisition of their immunologic effector function. This is orchestrated by complex cellular interactions, and autocrine loops mediated by soluble factors—here interferon (IFN)-γ, interleukin (IL)-15, IL-12, and LTB4. Importantly, the results indicate that endogenous LTB4 can induce T-cell activation that inhibits the EBV-induced proliferation of B lymphocytes.
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- Liu, AQ, et al.
(författare)
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Proprotein convertase subtilisin kexin 9 is associated with disease activity and is implicated in immune activation in systemic lupus erythematosus
- 2020
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Ingår i: Lupus. - : SAGE Publications. - 1477-0962 .- 0961-2033. ; 29:8, s. 825-835
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Tidskriftsartikel (refereegranskat)abstract
- Low-density lipoprotein (LDL) levels are increased by proprotein convertase subtilisin kexin 9 (PCSK9) which targets the LDL receptor. We recently reported that PCSK9 ameliorates dendritic cell (DC) activation by oxidized LDL (OxLDL), which is abundant in atherosclerotic plaques and is also associated with cardiovascular disease (CVD) in systemic lupus erythematosus (SLE). Here, we investigated the role of PCSK9 in SLE. Methods PCSK9 levels were determined by ELISA among SLE patients ( N = 109) and age- and sex-matched population-based controls ( N = 91). Common carotid intima–media thickness (IMT) and plaque occurrence were determined by B-mode ultrasound. Plaques were graded by echogenicity. Human peripheral blood monocytes from SLE patients or controls were differentiated into DCs. The effects of PCSK9 and its inhibition by silencing were studied. Results PCSK9 levels were non-significantly higher among SLE-patients compared to controls but significantly associated with SLE disease activity, as determined by the Systemic Lupus Activity Measure ( p = 0.020) or the SLE Disease Activity Index ( p = 0.0178). There was no association between PCSK9 levels and atherosclerosis as determined by IMT, prevalence of plaques or echolucent (potentially vulnerable) plaques. PCSK9 levels were significantly associated with CVD among SLE patients but not after adjusting for age. OxLDL induced PCSK9 in DCs and DC maturation with increased expression of CD86 and HLA-DR. The effects were significantly stronger in DCs from SLE patients than from controls. Silencing of PCSK9 abolished OxLDL-induced DC maturation. Conclusions PCSK9 is associated with disease activity in SLE. One underlying cause could be OxLDL promoting DC activation which depends on PCSK9. OxLDL induces PCSK9 – an effect which is higher among SLE patients. PCSK9 could play an unexpected immunological role in SLE.
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| 20. |
- Liu, AQ, et al.
(författare)
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PSK and Trx80 inhibit B-cell growth in EBV-infected cord blood mononuclear cells through T cells activated by the monocyte products IL-15 and IL-12
- 2005
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Ingår i: Blood. - : American Society of Hematology. - 0006-4971 .- 1528-0020. ; 105:4, s. 1606-1613
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Tidskriftsartikel (refereegranskat)abstract
- Epstein-Barr virus (EBV)–specific immunologic memory is not transferred from mother to child. In vitro infection of cord blood cells can therefore readily lead to the outgrowth of transformed B lymphocytes. We found that the immunomodulator polysaccharide K (PSK) or the mitogenic cytokine truncated thioredoxin (Trx80) inhibited the EBV-induced B-cell proliferation. Using signaling lymphocytic activation molecule (SLAM)–associated protein (SAP) induction as a sign for T- and natural killer (NK) cell activation, we could follow it without any need for cell separation because neither macrophages nor B lymphocytes express SAP. The results suggest the following scenario: EBV infected and activated B lymphocytes. Upon interacting with these cells, T cells became posed for responding to cytokines produced by monocytes. Both PSK and Trx80, which is a secreted C-terminally truncated thioredoxin, activated the monocytes, which then produced cytokines in the presence of the primed T cells. PSK induced interleukin-15 (IL-15), while Trx80 induced IL-12 production. Both cytokines activated the T cells for function. Phosphatidylinositol 3–(PI 3)–kinase and reactive oxygen species (ROSs) were involved in the PSK-induced activation of monocytes. Restimulation of the cultures with EBV-transformed B cells generated specific cytotoxic activity.
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- Runarsson, G, et al.
(författare)
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Leukotriene B-4 plays a pivotal role in CD40-dependent activation of chronic B lymphocytic leukemia cells
- 2005
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Ingår i: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 105:3, s. 1274-1279
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Tidskriftsartikel (refereegranskat)abstract
- Blosynthesis of leukotrienes (LTs) occurs in human myeloid cells and B lymphocytes. However, the function of leukotrienes in B lymphocytes is unclear. Here, we report that B-cell chronic lymphocytic leukemia (B-CLL) cells produce leukotriene B-4, and that specific leukotriene biosynthesis inhibitors counteracted CD40-dependent activation of B-CLL cells. Studies on the expression of the high-affinity receptor for LTB4 (BLT1) by flow cytometry analysis showed that the receptor was expressed, to a varying degree, in all investigated B-CLL clones. At a concentration of 100 nM, the drugs BWA4C (a specific 5-lipoxygenase inhibitor) and MK-886 (a specific 5-lipoxygenase activating protein inhibitor) markedly inhibited CD40-induced DNA synthesis (45% and 38%, respectively) and CD40-induced expression of CD23, CD54, and CD150. Addition of exogenous LTB4 (150 nM) almost completely reversed the effect of the inhibitors on DNA synthesis and antigen expression. Taken together, the results of the present study suggest that leukotriene biosynthesis inhibitors may have a therapeutic role in B-CLL.
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