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  1. Article ; Online: Reaction to the birth of a child with cleft lip or cleft palate in Zimbabwe.

    Mzezewa, S / Muchemwa, F C

    Tropical doctor

    2010  Volume 40, Issue 3, Page(s) 138–140

    Abstract: Cleft lip and palate (CLP) is often a distressful abnormality for both mother and child. In our setting, CLP is generally associated with witchcraft or ancestral spirits. The mother is often accused of infidelity during pregnancy. We wanted to determine ... ...

    Abstract Cleft lip and palate (CLP) is often a distressful abnormality for both mother and child. In our setting, CLP is generally associated with witchcraft or ancestral spirits. The mother is often accused of infidelity during pregnancy. We wanted to determine the feelings of parents and the wider public towards CLP babies, to establish what parents believed were the causes of CLP and to establish the postpartum marital status. One hundred and twenty-four parents were prospectively included in the study. They were interviewed using a structured questionnaire. One hundred and fifteen mothers and four fathers said they loved their babies. Thirty-eight parents attributed CLP to witchcraft. Nineteen percent of the mothers were divorced. The responses to our questionnaire show that although CLP babies are loved by their parents, the condition is associated with stigma and superstition.
    MeSH term(s) Adult ; Child, Preschool ; Cleft Lip/ethnology ; Cleft Lip/etiology ; Cleft Lip/psychology ; Cleft Palate/ethnology ; Cleft Palate/etiology ; Cleft Palate/psychology ; Culture ; Family ; Female ; Health Knowledge, Attitudes, Practice ; Humans ; Infant ; Infant, Newborn ; Interviews as Topic ; Male ; Marital Status ; Parents/psychology ; Perception ; Pregnancy ; Prospective Studies ; Social Support ; Superstitions ; Young Adult ; Zimbabwe
    Language English
    Publishing date 2010-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 193169-6
    ISSN 1758-1133 ; 0049-4755
    ISSN (online) 1758-1133
    ISSN 0049-4755
    DOI 10.1258/td.2010.090329
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1056: Show issues Location:
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  2. Article ; Online: PDGFB quantification is a useful tool in the diagnosis of dermatofibrosarcoma protuberans: a study of 10 cases.

    Muchemwa, F C / Wakasugi, S / Honda, Y / Ihn, H

    Clinical and experimental dermatology

    2010  Volume 35, Issue 3, Page(s) 295–299

    Abstract: Background: Genetic aberrations involving the platelet-derived growth factor-beta (PDGFB) gene and the collagen type 1 alpha1 (COL1A1) gene have been implicated in the pathogenesis of dermatofibrosarcoma protuberans (DFSP), a slow-growing and locally ... ...

    Abstract Background: Genetic aberrations involving the platelet-derived growth factor-beta (PDGFB) gene and the collagen type 1 alpha1 (COL1A1) gene have been implicated in the pathogenesis of dermatofibrosarcoma protuberans (DFSP), a slow-growing and locally infiltrative dermal tumour.
    Aim: To investigate the genetic rearrangements in 10 patients who presented with a clinical diagnosis of DFSP.
    Methods: Total RNA was obtained from frozen sections and sections embedded in paraffin wax, and used for direct sequencing of the cDNA produced from reverse transcription (RT) PCR. The expression of PDFGB mRNA in each of these cases was also examined.
    Results: Of the 10 samples examined, 9 had the COL1A1/PDGFB fusion transcript by DNA sequencing. The sequenced products showed that there was a fusion between the end of exons 6, 8, 29 (two cases), 38, 25 or 47 (three cases) and the start of exon 2 of the PDGFB gene. Quantitative RT-PCR identified all samples as having significantly higher expression of the PDGFB gene compared with normal skin or dermatofibroma.
    Conclusions: Detection of the COL1A1/PDGFB fusion transcript may be important for the diagnosis of DFSP. Furthermore, relative PDGFB gene quantification by real-time PCR may also provide a good diagnostic tool when other methods fail to give conclusive results.
    MeSH term(s) Adult ; Biomarkers, Tumor/genetics ; Child ; Chromosome Mapping ; Collagen Type I/genetics ; Dermatofibrosarcoma/genetics ; Dermatofibrosarcoma/pathology ; Female ; Humans ; Male ; Middle Aged ; Oncogene Proteins, Fusion/genetics ; Platelet-Derived Growth Factor/genetics ; Reverse Transcriptase Polymerase Chain Reaction/methods ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Statistics as Topic
    Chemical Substances Biomarkers, Tumor ; COLIA1-PDGFB fusion protein, human ; Collagen Type I ; Oncogene Proteins, Fusion ; Platelet-Derived Growth Factor
    Language English
    Publishing date 2010-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 195504-4
    ISSN 1365-2230 ; 0307-6938
    ISSN (online) 1365-2230
    ISSN 0307-6938
    DOI 10.1111/j.1365-2230.2009.03474.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Heat shock protein 105 is overexpressed in squamous cell carcinoma and extramammary Paget disease but not in basal cell carcinoma.

    Muchemwa, F C / Nakatsura, T / Ihn, H / Kageshita, T

    The British journal of dermatology

    2006  Volume 155, Issue 3, Page(s) 582–585

    Abstract: Background: Heat shock protein (HSP) 105 is a 105-kDa protein, recently discovered by serological analysis of recombinant cDNA expression libraries prepared from tumour cells (SEREX), and is still undergoing intensive research. SEREX can define strongly ...

    Abstract Background: Heat shock protein (HSP) 105 is a 105-kDa protein, recently discovered by serological analysis of recombinant cDNA expression libraries prepared from tumour cells (SEREX), and is still undergoing intensive research. SEREX can define strongly immunogenic tumour antigens that elicit both cellular and humoral immunity. Previous studies have shown that HSP105 is a cancer testis antigen and is overexpressed in various internal malignancies. The expression of HSP105 has not been studied in skin cancers.
    Objectives: To assess the expression of HSP105 in skin cancers including extramammary Paget disease (EMPD), cutaneous squamous cell carcinoma (SCC) and basal cell carcinoma (BCC).
    Methods: Samples of EMPD (n = 25), SCC (n = 23, of which three were metastatic lesions) and BCC (n = 23) were collected from patients treated in our department between January 2002 and December 2004. Western blot and immunohistochemical staining methods were used to investigate the expression of HSP105.
    Results: Results of Western blot analysis showed overexpression of HSP105 in EMPD and SCC, and minimal expression in BCC. Immunohistochemistry results showed that 56% of EMPD, 60% of primary and 100% of metastatic SCC highly expressed HSP105 while only 13% of BCC lesions showed increased staining.
    Conclusions: EMPD and SCC overexpress HSP105 while BCC does not. Tumours overexpressing HSP105 present ideal candidates for vaccination by HSP105-derived peptides or DNA.
    MeSH term(s) Aged ; Aged, 80 and over ; Blotting, Western ; Carcinoma, Basal Cell/metabolism ; Carcinoma, Squamous Cell/metabolism ; Female ; HSP110 Heat-Shock Proteins/metabolism ; Humans ; Immunoenzyme Techniques ; Male ; Middle Aged ; Neoplasm Proteins/metabolism ; Paget Disease, Extramammary/metabolism ; Skin Neoplasms/metabolism
    Chemical Substances HSP110 Heat-Shock Proteins ; HSPH1 protein, human ; Neoplasm Proteins
    Language English
    Publishing date 2006-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80076-4
    ISSN 1365-2133 ; 0007-0963
    ISSN (online) 1365-2133
    ISSN 0007-0963
    DOI 10.1111/j.1365-2133.2006.07362.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Role of c-Jun N-terminal kinase isoforms in the cellular activity of melanoma cell lines.

    Kogushi-Nishi, H / Jinnin, M / Kobayashi, Y / Muchemwa, F C / Hirano, A / Makino, T / Fukushima, S / Masuguchi, S / Ishihara, T / Inoue, Y / Ihn, H

    Clinical and experimental dermatology

    2013  Volume 38, Issue 8, Page(s) 890–896

    Abstract: Background: The c-Jun N-terminal kinase (JNK) is thought to be involved in inflammation, proliferation and apoptosis.: Aim: To examine the role of JNK isoforms in metastasis, proliferation, migration and invasion of the malignant melanoma (MM) cell ... ...

    Abstract Background: The c-Jun N-terminal kinase (JNK) is thought to be involved in inflammation, proliferation and apoptosis.
    Aim: To examine the role of JNK isoforms in metastasis, proliferation, migration and invasion of the malignant melanoma (MM) cell lines SK-MEL-28, SK-MEL-3 and WM164, using a kinase-specific inhibitor or isoform-specific small interfering (si)RNAs.
    Results: SK-MEL-3, a cell line established from metastatic MM, showed slightly increased phosphorylation of both JNK1 and JNK2, whereas WM164, a cell line derived from primary MM, showed significant phosphorylation of JNK1. A JNK inhibitor, SP600125, inhibited cell proliferation of SK-MEL-3 but not SK-MEL-28 or WM164. Transfection of JNK1-specific siRNA reduced the migratory activity of WM164 cells, while silencing of either JNK1 or JNK2 strongly suppressed the invasive activity of SK-MEL-3.
    Conclusions: Our study suggests that JNK isoforms have different roles in MM. Metastasis of MM may be regulated by JNK2, while invasion is regulated by both JNK1 and JNK2. JNK1 and JNK2 respectively mediate cell migration and cell proliferation. Further understanding of the specific roles of JNK isoforms in the pathogenesis of MM may lead to the development of therapies targeting specific isoforms.
    MeSH term(s) Anthracenes/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Humans ; Immunoblotting ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Melanoma/enzymology ; Melanoma/pathology ; Mitogen-Activated Protein Kinase 8/physiology ; Mitogen-Activated Protein Kinase 9/physiology ; Neoplasm Invasiveness ; Protein Isoforms/physiology ; Skin Neoplasms/enzymology ; Skin Neoplasms/pathology
    Chemical Substances Anthracenes ; Protein Isoforms ; pyrazolanthrone (1TW30Y2766) ; Mitogen-Activated Protein Kinase 9 (EC 2.7.1.24) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24)
    Language English
    Publishing date 2013-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 195504-4
    ISSN 1365-2230 ; 0307-6938
    ISSN (online) 1365-2230
    ISSN 0307-6938
    DOI 10.1111/ced.12102
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1278: Show issues Location:
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  5. Article: Constitutive activation of the phosphatidyl inositol 3 kinase signalling pathway in acral lentiginous melanoma.

    Muchemwa, F C / Ma, D / Inoue, Y / Curtin, J A / Bastian, B C / Ihn, H / Kageshita, T

    The British journal of dermatology

    2008  Volume 158, Issue 2, Page(s) 411–413

    MeSH term(s) Enzyme Activation/genetics ; Female ; Genes, ras/genetics ; Humans ; Male ; Melanoma/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins B-raf/genetics ; Skin Neoplasms/metabolism
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2008-02
    Publishing country England
    Document type Letter
    ZDB-ID 80076-4
    ISSN 1365-2133 ; 0007-0963
    ISSN (online) 1365-2133
    ISSN 0007-0963
    DOI 10.1111/j.1365-2133.2007.08292.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui VI Zs.23: Show issues Location:
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  6. Article ; Online: Basic fibroblast growth factor stimulates the proliferation of human dermal fibroblasts via the ERK1/2 and JNK pathways.

    Makino, T / Jinnin, M / Muchemwa, F C / Fukushima, S / Kogushi-Nishi, H / Moriya, C / Igata, T / Fujisawa, A / Johno, T / Ihn, H

    The British journal of dermatology

    2010  Volume 162, Issue 4, Page(s) 717–723

    Abstract: Background: Basic fibroblast growth factor (bFGF, FGF-2) has been described as a multipotent cytokine that regulates cell growth as well as differentiation, matrix composition, chemotaxis, cell adhesion and migration in numerous cell types. It is known ... ...

    Abstract Background: Basic fibroblast growth factor (bFGF, FGF-2) has been described as a multipotent cytokine that regulates cell growth as well as differentiation, matrix composition, chemotaxis, cell adhesion and migration in numerous cell types. It is known that bFGF stimulates proliferation of cultured fibroblasts. However, the detailed mechanism of fibroblast proliferation induced by bFGF in vitro still remains to be elucidated. Objectives We investigated the precise effects of bFGF on fibroblast proliferation and the signalling pathways responsible for bFGF-induced proliferation in cultured human dermal fibroblasts (HDFs).
    Methods: HDFs were cultured with bFGF in the presence or absence of specific inhibitors against MAPK signalling pathways including ERK, JNK and p38. The number of cells was counted and immunoblotting findings were examined for the activation of ERK1/2 and JNK. Furthermore, the inhibitory effects of ERK1, ERK2 and JNK1 were proven by the transfection of siRNA.
    Results: bFGF increased the number of HDFs in a dose- and time-dependent manner. The bFGF-induced proliferation was suppressed by the MEK inhibitors PD98059 and U0126, and the JNK inhibitor SP600125. bFGF increased the phosphorylation levels of ERK1/2 and JNK1. Treatment with ERK1, ERK2 or JNK1 siRNA significantly inhibited bFGF-induced proliferation.
    Conclusions: This study indicates that ERK1/2 and JNK pathways play an important role in the bFGF-mediated effect in HDFs. This study also suggests that controlling ERK1/2 and/or JNK signalling may therefore be a new therapeutic approach for the treatment of chronic and untreatable skin ulcers.
    MeSH term(s) Cell Proliferation/drug effects ; Cells, Cultured ; Fibroblast Growth Factor 2/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; MAP Kinase Signaling System/drug effects ; Signal Transduction/drug effects ; Skin/cytology
    Chemical Substances Fibroblast Growth Factor 2 (103107-01-3) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2010-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80076-4
    ISSN 1365-2133 ; 0007-0963
    ISSN (online) 1365-2133
    ISSN 0007-0963
    DOI 10.1111/j.1365-2133.2009.09581.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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