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Biomedicine & pharmacotherapy
Masson Pub. USA, Inc.
Biomedicine & pharmacotherapy

Masson Pub. USA, Inc.

0753-3322

Biomedicine & pharmacotherapy/Journal Biomedicine & pharmacotherapySCIISTP
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    Retraction notice to "Knockdown of ANRIL aggravates H2O2-induced injury in PC-12 cells by targeting microRNA-125a" [Biomed. Pharmacother. 92 (2017) 952-961]

    Ran LiFei YinYing-Ying GuoKun-Chi Zhao...
    1页
    查看更多>>摘要:This article has been retracted: please see Elsevier Policy on Article Withdrawal ({https://www。elsevier。com/about/our-business/policies /article-withdrawal))。 This article has been retracted at the request of the Editor-in-Chief。 Given the comments of Dr。 Elisabeth Bik regarding this article "This paper belongs to a set of over 400 papers (as per February 2020) that share very similar Western blots with tadpole-like shaped bands, the same background pattern, and striking similarities in title structures, paper layout, bar graph design, and - in a subset - flow cytometry panels", the journal requested the authors to provide the raw data。 However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article。

    Retraction notice to "Astragalus polysaccharide ameliorates lipopolysaccharide-induced cell injury in ATDC5 cells via miR-92a/KLF4 mediation" [Biomed. Pharmacother. 118 (2019) 109180]

    Lei FanMing LiFu-Yang CaoZhi-Wei Zeng...
    1页
    查看更多>>摘要:This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www。elsevier。com/about/our-business/policies /article-withdrawal)。 This article has been retracted at the request of the Editor-in-Chief。 Given the comments of Dr Elisabeth Bik regarding this article "。。。 the Western blot bands in all 400+ papers are all very regularly spaced and have a smooth appearance in the shape of a dumbbell or tadpole, without any of the usual smudges or stains。 All bands are placed on similar looking backgrounds, suggesting they were copy/pasted from other sources, or computer generated", the journal requested the authors to provide the raw data。 However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article。

    Retraction notice to "Sinomenine inhibits proliferation, migration, invasion and promotes apoptosis of prostate cancer cells by regulation of miR-23a" [Biomed. Pharmacother. 112 (2019) 108592]

    Feng XuQi LiZhiyu WangXiangming Cao...
    1页
    查看更多>>摘要:This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www。elsevier。com/about/our-business/policies /article-withdrawal)。 This article has been retracted at the request of the Editor-in-Chief。 Given the comments of Dr Elisabeth Bik regarding this article "In almost all papers, Western blot panels within the same figure, and across figures and papers, appear to share the same background, while the bands are regularly spaced, all have similar rounded edges without the usual smudges and specks, and with some bands showing a recognizable "jumping sardine" shape", the journal requested the authors to provide the raw data。 However, the authors were not able to fulfil this request and therefore the Editor-in-Chief decided to retract the article。

    Insights into the implementation of Fibronectin 1 in the cartilage tissue engineering

    Murad AladalWei YouRongxiang HuangZhiqin Deng...
    1页
    查看更多>>摘要:Recently, cartilage tissue engineering has become a cornerstone to treat cartilage degeneration and osteoarthritis (OA)。 Fibronectin1 (FN1) is described as multiple functional glycoproteins that play an essential role in chon-drogenic and osteogenic differentiation。 Few studies reported the potential of FN1 to enhance tissue engineering and reduce the death of chondrocytes in OA。 Further, FN1 possesses multiple binding domains including collagen, integrin, and heparin that can interact with heparan sulfate proteoglycans at the surface of chondrocyte leading to promote cell signaling and differentiation。 Recent studies suggested that FN1 can promote chondrocyte differentiation by upregulating TGF-β/PI3K/Akt pathways。 Further, FN1 can inhibit the apoptosis of chondrocytes by preventing the release of metalloproteinases through lowering the expression of p-PI3K/PI3K and p-AKT/AKT pathways。 However, the use of FN1 in cartilage repair studies using animal models or clinical trials was rarely reported。 Therefore, this article provides new insights into the importance of FN1 in cartilage tissue engineering to encourage more studies concerning FN1 in cartilage repair studies。 Further, we provided new suggestions for advanced applications of FN1 to treat OA and cartilage degeneration。

    Molecular biological mechanism of action in cancer therapies: Juglone and its derivatives, the future of development

    Yu Ting TangYang LiPeng ChuXiao Dong Ma...
    1页
    查看更多>>摘要:Juglone (5 - hydroxy -1,4- naphthalene diketone) is a kind of natural naphthoquinone, present in the roots, leaves, nut-hulls, bark and wood of walnut trees。 Recent studies have found that Juglone has special significance in the treatment of cancer, which plays a significant role in the resistance of cancer cell proliferation, induction of cancer cell apoptosis, induction of autophagy, anti-angiogenesis and inhibition of cancer cell migration and invasion, etc。 Additionally, its derivatives also play a tumor suppressive effect。 In conclusion, Juglone and its derivatives have been identified as effective anticancer drugs。 This paper reviews action mechanisms of Juglone and its derivatives in cancer treatment。

    Contribution of cyclooxygenase-1-dependent prostacyclin synthesis to bradykinin-induced dermal extravasation

    Michael KrybusMarc SieradzkiEhsan FahimiSara Metry...
    1页
    查看更多>>摘要:Background: Non-allergic angioedema is a potentially life-threatening condition caused by accumulation of bradykinin and subsequent activation of bradykinin type 2 receptors (B2)。 Since COX activity plays a pivotal role in B2 signaling, the aim of this study was to determine which prostaglandins are the key mediators and which COX, COX-1 or COX-2, is predominantly involved。 Methods: We used Miles assays to assess the effects of inhibitors of COX, 5-lipoxygenase, epoxyeicosatrienoic acid generation, cytosolic phospholipase A_2α and a variety of prostaglandin receptor antagonists on bradykinin-induced dermal extravasation in C57BL/6 and COX-1-deficient mice (COX-1~-/-)。 In addition, the prostacyclin metabolite 6-keto-PGF_1α was quantified by ELISA in subcutaneous tissue from C57BL/6 and human dermal microvascular endothelial cells。 In the latter, 6-keto-PGF_1α was also quantified and identified by LC-MS/MS。 Results: Unspecific COX inhibition by ibuprofen and diclofenac significantly reduced B2-mediated dermal extravasation in C57BL/6 but not COX-1~-/-。 Likewise, inhibition of cytosolic phospholipase A_2α showed similar effects。 Furthermore, extravasation in COX-1~-/- was generally lower than in C57BL/6。 Of the prostaglandin antagonists used, only the prostacyclin receptor antagonist RO1138452 showed a significant reduction of dermal extravasation。 Moreover, 6-keto-PGF_1α concentrations were increased after bradykinin treatment in subcutaneous tissue from C57BL/6 as well as in human dermal microvascular endothelial cells and this increase was abolished by diclofenac。 Conclusion: Our findings suggest that COX-1-dependent prostacyclin production is critically involved in dermal extravasation after activation of B2 in small dermal blood vessels。 Targeting prostacyclin production and/or signaling appears to be a suitable option for acute treatment of non-allergic angioedema。

    The contribution of sterile inflammation to the fatty liver disease and the potential therapies

    Mohamed E. Shaker
    1页
    查看更多>>摘要:Hepatic inflammation is prevalent in several metabolic liver diseases。 Recent scientific advances about the pathogenesis of metabolic liver diseases showed an emerging role of several damage-associated molecular patterns (DAMPs), including DNA, high-mobility group box 1 (HMGB1), ATP and uric acid。 For these DAMPs to induce inflammation, they should stimulate pattern recognition receptors (PRRs), which are located in the hepatic immune cells like resident Kupffer cells, infiltrated neutrophils, monocytes or dendritic cells。 As a consequence, proinflammatory cytokines like interleukins (ILs)-1β and 18 alongside tumor necrosis factor (TNF)-α are overproduced and released, leading to pronounced hepatic inflammation and cellular death。 This review highlights the contribution of these DAMPs and PRRs in the settings of alcoholic and nonalcoholic steatohepatitis。 The review also summarizes the therapeutic usefulness of targeting NLR family pyrin domain containing 3 (NLRP3)-inflammasome, Toll-like receptors (TLRs) 4 and 9, IL-1 receptor (IL-1R), caspase 1, uric acid and GMP-AMP synthase/stimulator of interferon genes (cGAS/STING) in these hepatic inflammatory disorders。