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[PMID]: 25188519
[Au] Autor:Guo W; Liu R; Bhardwaj G; Yang JC; Changou C; Ma AH; Mazloom A; Chintapalli S; Xiao K; Xiao W; Kumaresan P; Sanchez E; Yeh CT; Evans CP; Patterson R; Lam KS; Kung HJ
[Ad] Address:Department of Biochemistry and Molecular Medicine, University of California Davis, Sacramento, CA 95817, USA....
[Ti] Title:Targeting Btk/Etk of prostate cancer cells by a novel dual inhibitor.
[So] Source:Cell Death Dis;5:e1409, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Btk and Etk/BMX are Tec-family non-receptor tyrosine kinases. Btk has previously been reported to be expressed primarily in B cells and has an important role in immune responses and B-cell malignancies. Etk has been shown previously to provide a strong survival and metastasis signal in human prostate cancer cells, and to confer androgen independence and drug resistance. While the role of Etk in prostate carcinogenesis is well established, the functions of Btk in prostate cancer have never been investigated, likely due to the perception that Btk is a hematopoietic, but not epithelial, kinase. Herein, we found that Btk is overexpressed in prostate cancer tissues and prostate cancer cells. The level of Btk in prostate cancer tissues correlates with cancer grades. Knockdown of Btk expression selectively inhibits the growth of prostate cancer cells, but not that of the normal prostate epithelial cells, which express very little Btk. Dual inhibition of Btk and Etk has an additive inhibitory effect on prostate cancer cell growth. To explore Btk and Etk as targets for prostate cancer, we developed a small molecule dual inhibitor of Btk and Etk, CTN06. Treatment of PC3 and other prostate cancer cells, but not immortalized prostate epithelial cells with CTN06 resulted in effective cell killing, accompanied by the attenuation of Btk/Etk signals. The killing effect of CTN06 is more potent than that of commonly used inhibitors against Src, Raf/VEGFR and EGFR. CTN06 induces apoptosis as well as autophagy in human prostate cancer cells, and is a chemo-sensitizer for docetaxel (DTX), a standard of care for metastatic prostate cancer patients. CTN06 also impeded the migration of human prostate cancer cells based on a 'wound healing' assay. The anti-cancer effect of CTN06 was further validated in vivo in a PC3 xenograft mouse model.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.343

  2 / 3987596 MEDLINE  
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[PMID]: 25188518
[Au] Autor:Lalevée S; Lapaire O; Bühler M
[Ad] Address:Laboratory for Prenatal Medicine, Department of Biomedicine, University Hospital Basel, Basel CH-4031, Switzerland.
[Ti] Title:miR455 is linked to hypoxia signaling and is deregulated in preeclampsia.
[So] Source:Cell Death Dis;5:e1408, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Preeclampsia is a severe pregnancy-related disorder and a leading cause of maternal and fetal mortality worldwide. Early identification of patients with an increased risk for preeclampsia is thus one of the most important goals in obstetrics. Here we identify two related human microRNAs as potential biomarkers to detect at-risk pregnancies. We demonstrate that miR455-3P and miR455-5P are significantly downregulated in placentas from preeclampsia patients, whereas other placenta-specific microRNAs remain unaffected. microRNA target prediction and validation revealed a potential link of miR455-3P to hypoxia signaling. Together with our observation that expression levels of miR455-3P and miR455-5P are upregulated during trophoblast differentiation, our results suggest a model in which miR455-3P represses a hypoxia response that might otherwise prevent cytotrophoblasts from syncytiotrophoblast differentiation. In summary, our work reveals aberrant hypoxia signaling in preeclampsia that can be explained by deregulated expression of miR455. As miR455 has been found in circulating blood, the development of noninvasive prenatal tests enabling early diagnosis of preeclampsia may be possible.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.368

  3 / 3987596 MEDLINE  
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[PMID]: 25188517
[Au] Autor:Ma JX; Yan BX; Zhang J; Jiang BH; Guo Y; Riedel H; Mueller MD; Remick SC; Yu JJ
[Ad] Address:1] Department of Biochemistry, School of Medicine, Department of Basic Pharmaceutical Sciences, School of Pharmacy, and Mary Babb Randolph Cancer Center, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, West Virginia, USA [2] Department of Molecular Microbiology and Immun...
[Ti] Title:PSP94, an upstream signaling mediator of prostasin found highly elevated in ovarian cancer.
[So] Source:Cell Death Dis;5:e1407, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Ovarian cancer is a leading cause of cancer death as diagnosis is frequently delayed to an advanced stage. Effective biomarkers and screening strategies for early detection are urgently needed. In the current study, we identify PSP94 as a key upstream factor in mediating prostasin (a protein previously reported to be overexpressed in ovarian cancer) signaling that regulates prostasin expression and action in ovarian cancer cells. PSP94 is overexpressed in ovarian cancer cell lines and patients, and is significantly correlated with prostasin levels. Signaling pathway analysis demonstrated that both PSP94 and prostasin, as potential upstream regulators of the Lin28b/Let-7 pathway, regulate Lin28b and its downstream partner Let-7 in ovarian cancer cells. Expression of PSP94 and prostasin show a strong correlation with the expression levels of Lin28b/Let-7 in ovarian cancer patients. Thus, PSP94/prostasin axis appears to be linked to the Lin28b/Let-7 loop, a well-known signaling mechanism in oncogenesis in general that is also altered in ovarian cancer. The findings suggest that PSP94 and PSP94/prostasin axis are key factors and potential therapeutic targets or early biomarkers for ovarian cancer.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.374

  4 / 3987596 MEDLINE  
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[PMID]: 25188510
[Au] Autor:Hou JK; Huang Y; He W; Yan ZW; Fan L; Liu MH; Xiao WL; Sun HD; Chen GQ
[Ad] Address:Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), University of Chinese Academy of Sciences, Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai, China....
[Ti] Title:Adenanthin targets peroxiredoxin I/II to kill hepatocellular carcinoma cells.
[So] Source:Cell Death Dis;5:e1400, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Adenanthin, a natural diterpenoid isolated from the leaves of Isodon adenanthus, has recently been reported to induce leukemic cell differentiation by targeting peroxiredoxins (Prx) I and II. On the other hand, increasing lines of evidence propose that these Prx proteins would become potential targets to screen drugs for the prevention and treatment of solid tumors. Therefore, it is of significance to explore the potential activities of adenanthin on solid tumor cells. Here, we demonstrate that Prx I protein is essential for the survival of hepatocellular carcinoma (HCC) cells, and adenanthin can kill these malignant liver cells in vitro and xenografts. We also show that the cell death-inducing activity of adenanthin on HCC cells is mediated by the increased reactive oxygen species (ROS) levels. Furthermore, the silencing of Prx I or Prx II significantly enhances the cytotoxic activity of adenanthin on HCC, whereas the ectopic expression of Prx I and Prx II but not their mutants of adenanthin-bound cysteines can rescue adenanthin-induced cytotoxicity in Prxs-silenced HCC cells. Taken together, our results propose that adenanthin targets Prx I/II to kill HCC cells and its therapeutic significance warrants to be further explored in HCC patients.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1409
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.345

  5 / 3987596 MEDLINE  
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[PMID]: 25165882
[Au] Autor:Liu S; Wang J; Qin HM; Yan XM; Yang XS; Liu C; Yan Q
[Ad] Address:Liaoning Provincial Core Lab of Glycobiology and Glycoengineering, Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian, People's Republic of China....
[Ti] Title:LIF upregulates poFUT1 expression and promotes trophoblast cell migration and invasion at the fetal-maternal interface.
[So] Source:Cell Death Dis;5:e1396, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Trophoblast cell migration and invasion are crucial for the establishment of a successful pregnancy. Protein O-fucosyltransferases, such as poFUT1 and poFUT2, catalyze the O-fucosylation of proteins and have important roles in embryonic development. Leukemia inhibitory factor (LIF) is a critical cytokine in the regulation of embryonic development and implantation. However, the exact roles of poFUTs in embryo migration and invasion and the effects of LIF on the expression of poFUTs have not been studied in detail. In the current study, we showed that poFUT1 and LIF were highly expressed in human trophoblast cells and in the serum of women during the first trimester of a normal pregnancy. However, in patients with threatened abortion, poFUT1 and LIF levels were found to be reduced. There were no significant differences in the expression levels of poFUT2 between the two groups. The migration and invasion potential of trophoblasts in an explant culture and in an in vitro implantation model was decreased or increased upon altering poFUT1 expression levels by siRNA or cDNA transfection. Our results also revealed that LIF upregulated the expression of poFUT1. The upregulation of poFUT1 by LIF promoted trophoblast cell migration and invasion at the fetal-maternal interface by activating the PI3K/Akt signaling pathway. Taken together, these study findings suggest that poFUT1 may be used as a marker of embryo implantation.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.335

  6 / 3987596 MEDLINE  
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[PMID]: 25144719
[Au] Autor:Nugues AL; El Bouazzati H; Hétuin D; Berthon C; Loyens A; Bertrand E; Jouy N; Idziorek T; Quesnel B
[Ad] Address:Inserm, U837, Institut pour la Recherche sur le Cancer de Lille, place de Verdun, Lille F-59045, France....
[Ti] Title:RIP3 is downregulated in human myeloid leukemia cells and modulates apoptosis and caspase-mediated p65/RelA cleavage.
[So] Source:Cell Death Dis;5:e1384, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The receptor-interacting protein kinase 3 (RIP3) associates with RIP1 in a necrosome complex that can induce necroptosis, apoptosis, or cell proliferation. We analyzed the expression of RIP1 and RIP3 in CD34+ leukemia cells from a cohort of patients with acute myeloid leukemia (AML) and CD34+ cells from healthy donors. RIP3 expression was significantly reduced in most AML samples, whereas the expression of RIP1 did not differ significantly. When re-expressed in the mouse DA1-3b leukemia cell line, RIP3 induced apoptosis and necroptosis in the presence of caspase inhibitors. Transfection of RIP3 in the WEHI-3b leukemia cell line or in the mouse embryonic fibroblasts also resulted in increased cell death. Surprisingly, re-expression of a RIP3 mutant with an inactive kinase domain (RIP3-kinase dead (RIP3-KD)) induced significantly more and earlier apoptosis than wild-type RIP3 (RIP3-WT), indicating that the RIP3 kinase domain is an essential regulator of apoptosis/necroptosis in leukemia cells. The induced in vivo expression of RIP3-KD but not RIP3-WT prolonged the survival of mice injected with leukemia cells. The expression of RIP3-KD induced p65/RelA nuclear factor-κB (NF-κB) subunit caspase-dependent cleavage, and a non-cleavable p65/RelA D361E mutant rescued these cells from apoptosis. p65/RelA cleavage appears to be at least partially mediated by caspase-6. These data indicate that RIP3 silencing in leukemia cells results in suppression of the complex regulation of the apoptosis/necroptosis switch and NF-κB activity.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.347

  7 / 3987596 MEDLINE  
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[PMID]: 25144716
[Au] Autor:Silvestri I; Testa F; Zappasodi R; Cairo CW; Zhang Y; Lupo B; Galli R; Di Nicola M; Venerando B; Tringali C
[Ad] Address:Department of Medical Biotechnology and Translational Medicine, University of Milan, Segrate (Milan), Italy....
[Ti] Title:Sialidase NEU4 is involved in glioblastoma stem cell survival.
[So] Source:Cell Death Dis;5:e1381, 2014.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The human sialidase, NEU4, has emerged as a possible regulator of neuronal differentiation and its overexpression has been demonstrated to promote the acquisition of a stem cell-like phenotype in neuroblastoma cells. In this paper, we demonstrated that glioblastoma stem cells (GSCs) isolated from glioblastoma multiforme (GBM) cell lines and patients' specimens as neurospheres are specifically marked by the upregulation of NEU4; in contrast, the expression of NEU4 is very low in non-neurosphere-differentiated GBM cells. We showed that NEU4 silencing by miRNA or a chemical inhibitor of its catalytic activity triggered key events in GSCs, including (a) the activation of the glycogen synthase kinase 3ß, with the consequent inhibition of Sonic Hedgehog and Wnt/ß-catenin signalling pathways; (b) the decrease of the stem cell-like gene expression and marker signatures, evidenced by the reduction of NANOG, OCT-4, SOX-2, CD133 expression, ganglioside GD3 synthesis, and an altered protein glycosylation profile; and (c) a significant decrease in GSCs survival. Consistent with this finding, increased NEU4 activity and expression induced in the more differentiated GBM cells by the NEU4 agonist thymoquinone increased the expression of OCT-4 and GLI-1. Thus, NEU4 expression and activity appeared to help to determine the molecular signature of GSCs and to be closely connected with their survival properties. Given the pivotal role played by GSCs in GBM lethality, our results strongly suggest that NEU4 inhibition could significantly improve current therapies against this tumour.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/cddis.2014.349

  8 / 3987596 MEDLINE  
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[PMID]: 24708482
[Au] Autor:Zaias N; Escovar SX; Rebell G
[Ad] Address:Dermatology division, Greater Miami Skin and Laser, Mount Sinai Medical Center, Miami Beach, FL, USA.
[Ti] Title:Opportunistic toenail onychomycosis. The fungal colonization of an available nail unit space by non-dermatophytes is produced by the trauma of the closed shoe by an asymmetric gait or other trauma. A plausible theory.
[So] Source:J Eur Acad Dermatol Venereol;28(8):1002-6, 2014 Aug.
[Is] ISSN:1468-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Opportunistic onychomycosis is defined, when a non-dermatophyte mould is cultured from an abnormal nail unit in the absence of a dermatophyte. The presumption is that the mould has caused the abnormal clinical appearance of the nail unit, yet there are no data available to substantiate this claim. Reports have only identified the mould being recovered from the nail unit niche. A review of the published dermatologic literature describing toenail opportunistic onychomycosis by non-dermatophyte fungi has shown toenails with onycholysis, nail bed (NB) keratosis and nail plate surface abnormalities. The appearance of these clinical changes is indistinguishable from the diagnosis of the Asymmetric Gait Nail Unit Signs (AGNUS). AGNUS is produced by the friction of the closed shoe in patients with an asymmetric gait, resulting primarily from the ubiquitous uneven flat feet. Most commonly, species of Acremonium (Cephalosporium), Aspergillus, Fusarium, Scopulariopsis and rarely species of many different fungi genera are capable of surviving and reproducing in a keratinous environment and change the clinical appearance of the involved nail unit. AGNUS toenails predispose to the colonization by the non-dermatophyte opportunistic fungi but not by dermatophyte fungi.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/jdv.12458

  9 / 3987596 MEDLINE  
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[PMID]: 24661336
[Au] Autor:Heilskov S; Rytter MJ; Vestergaard C; Briend A; Babirekere E; Deleuran MS
[Ad] Address:Department of Dermatology, Aarhus University Hospital, Aarhus, Denmark; Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
[Ti] Title:Dermatosis in children with oedematous malnutrition (Kwashiorkor): a review of the literature.
[So] Source:J Eur Acad Dermatol Venereol;28(8):995-1001, 2014 Aug.
[Is] ISSN:1468-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Children with oedematous malnutrition, known as kwashiorkor, may develop a characteristic skin lesion, named 'Dermatosis of Kwashiorkor' (DoK). Only a few studies have been concerned with this condition, and the reason for the development of DoK remains unexplained. This study review the existing studies concerning DoK, including its clinical manifestations, histopathology, suggested pathophysiology, current treatment and prognosis for children of the age of 6 months to 5 years. Standardized clinical studies are needed to further understand the implications of DoK. Such studies would suffer from the lack of consistency concerning the terminology and scoring of the lesions in DoK. We therefore stress the need for a standardized scoring of the degree of DoK. This would facilitate valid and comparable studies and the development of better treatment for this vulnerable group of patients.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/jdv.12452

  10 / 3987596 MEDLINE  
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[PMID]: 24372877
[Au] Autor:Massone C; Maak D; Hofmann-Wellenhof R; Soyer HP; Frühauf J
[Ad] Address:Department of Dermatology, Medical University of Graz, Graz, Austria.
[Ti] Title:Teledermatology for skin cancer prevention: an experience on 690 Austrian patients.
[So] Source:J Eur Acad Dermatol Venereol;28(8):1103-8, 2014 Aug.
[Is] ISSN:1468-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Recent studies investigated the value of teledermatology (TD) as a valid tool for a dermatologist-directed triage systems. OBJECTIVE: To investigate the feasibility of a store-and-forward TD triage system in a large number of patients. METHODS: Previously trained general practitioners selected suspicious skin tumours in the setting of a general preventive medicine screening programme and transmitted their dermoscopic images via virtual private network for decision-making. Within 48 h, two teleconsultants highly experienced in dermoscopy first assessed image quality, then made a diagnosis and answered if lesions were to follow-up, to excise or to be re-evaluated at face-to-face (FTF). RESULTS: A total of 955 lesions were telediagnosed [743 (78%) benign melanocytic, six (0.6%) malignant melanocytic, 186 (19%) benign non-melanocytic and 20 (2%) malignant non-melanocytic]. Excision was recommended for 111 (12%) lesions, 10 lesions (1%) were referred to FTF examination. Follow-up was recommended for 707 (74%) lesions. The vast majority of the lesions (82%) were screened as benign and an intervention was requested in only 18% of cases. Eighty-two patients (12% of the total) were lost at follow-up. The diagnostic accuracy was of 94% with sensitivity of 100% and specificity of 95.8%. CONCLUSIONS: We confirm that TD is suitable to triage skin cancers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/jdv.12351


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