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  1. Article: Association between the effect of controlled fluid resuscitation on massive hemorrhage and expression of human neutrophil lipocalin.

    Yu, Jie-Yang / Peng, Jia-Hua / Hui, Li / Huang, Hui-Quan / Tan, Ming-Hua / Jian, Guo

    Experimental and therapeutic medicine

    2018  Volume 16, Issue 4, Page(s) 3534–3538

    Abstract: The present study was designed to investigate the association between the effect of controlled fluid resuscitation on massive hemorrhage and expression of human neutrophil lipocalin (HNL). A total of 112 patients confirmed with traumatic hemorrhage were ... ...

    Abstract The present study was designed to investigate the association between the effect of controlled fluid resuscitation on massive hemorrhage and expression of human neutrophil lipocalin (HNL). A total of 112 patients confirmed with traumatic hemorrhage were enrolled as study subjects and were randomly divided into the control group (n=56) and observation group (n=56). The control group was treated with rapid fluid resuscitation, and the observation group was treated with controlled fluid resuscitation. The success rate of resuscitation, incidence rate of complications, and HNL levels were compared both before and after resuscitation at multiple time intervals. The success rate of resuscitation showed a significant improvement while the incidence rate of complications were decreased. The HNL levels in both groups revealed increase after resuscitation at 3-10 h, thereby, they showed decline following peak point. However, the peak reduction in the observation group appeared earlier, while the HNL levels at 24 and 72 h were significantly lower than those in the control group. The study concluded that the effect of controlled fluid resuscitation on massive hemorrhage was superior to that of rapid fluid resuscitation. Moreover, controlled fluid resuscitation was also able to decrease the level of HNL as well as inflammatory response.
    Language English
    Publishing date 2018-08-09
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2683844-8
    ISSN 1792-1015 ; 1792-0981
    ISSN (online) 1792-1015
    ISSN 1792-0981
    DOI 10.3892/etm.2018.6591
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Ping-Chong-Jiang-Ni Formula Induces Apoptosis and Inhibits Proliferation of Human Ectopic Endometrial Stromal Cells in Endometriosis via the Activation of JNK Signaling Pathway.

    Liang, Rui-Ning / Li, Pei-Shuang / Zou, Yang / Liu, Yu-Ling / Jiang, Zhen / Liu, Zhen / Fan, Pei / Xu, Ling / Peng, Jia-Hua / Sun, Xue-Yan

    Evidence-based complementary and alternative medicine : eCAM

    2017  Volume 2017, Page(s) 6489427

    Abstract: Endometriosis is a common gynecological condition in childbearing age women and its therapy in modern medicine achieves usually temporary cure. Ping-Chong-Jiang-Ni formula (PCJNF), a Chinese herbal medicine (CHM), was shown to be clinically effective on ... ...

    Abstract Endometriosis is a common gynecological condition in childbearing age women and its therapy in modern medicine achieves usually temporary cure. Ping-Chong-Jiang-Ni formula (PCJNF), a Chinese herbal medicine (CHM), was shown to be clinically effective on endometriosis. Meanwhile, c-Jun N-terminal kinase (JNK) signaling pathway was involved in the therapeutic process of CHM on endometriosis. Here, we explored the effect of PCJNF on the ectopic endometrial stromal cells (EESCs) from endometriosis and test whether JNK signaling was involved. After being treated with PCJNF-containing serum obtained from Sprague Dawley rat, cell proliferation, migration, invasion, and apoptosis were evaluated in EESCs, and the total and phosphorylated JNK, ERK, and p38 proteins were detected. Our results showed that PCJNF could suppress cell proliferation, migration, and invasion and induce apoptosis in EESCs. The suppressed proliferation and increased apoptosis were dependent on JNK activation. Additionally, PCJNF caused cell cycle arrest at G2/M phase and this effect was mediated by JNK signaling, while the decreased cell migration and invasion treated by PCJNF were independent of JNK signaling. In summary, our results provided the first evidence that PCJNF could suppress cell proliferation, migration, and invasion, while increasing apoptosis in EESCs, and the suppressed proliferation and enhanced apoptosis were mediated by JNK signaling.
    Language English
    Publishing date 2017-06-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2171158-6
    ISSN 1741-4288 ; 1741-427X
    ISSN (online) 1741-4288
    ISSN 1741-427X
    DOI 10.1155/2017/6489427
    Database MEDical Literature Analysis and Retrieval System OnLINE

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