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  • Alteration in chromogranin A, obestatin and total ghrelin levels of saliva and serum in epilepsy cases. 20172008

    This study was designed to measure the levels of chromogranin A (CgA), ghrelin and obestatin in serum and saliva (including CgA expression in healthy tissue) in epileptic patients to determine any significant differences between these patients and healthy controls. Samples were obtained from a total of 91 subjects: 10 newly-diagnosed primary generalized epilepsy (PGE) patients who had started treatment with valproic acid and phenytoin for seizure control; 18 PGE patients who were previously and currently receiving treatment with valproic acid and phenytoin for seizure control; 37 patients with partial epilepsy (PE) (simple, n=17 or complex, n=20) who had been and were still being treated with carbazebime for seizures; and 26 healthy controls. CgA immunoreactivity in healthy salivary gland was analyzed by immunohistochemistry and ELISA. The levels of CgA, total ghrelin and obestatin in serum and saliva were measured by ELISA. The results revealed that normal salivary gland produces its own CgA. Before treatment, CgA levels in saliva and serum were significantly greater in patients newly-diagnosed with PGE than controls. Ghrelin and CgA concentrations were also greater in PGE patients previously or currently treated with drugs, and in patients with simple or complex partial epilepsy (PE) previously or currently treated with drugs, than in healthy normal controls. In conclusion, salivary concentrations of CgA, ghrelin and obestatin were similar to their serum levels, so saliva might be a desirable alternative to serum for measuring these hormones because it is easy and painless to collect.
    Document Type:
    Reference
    Product Catalog Number:
    EZGRT-89K
    Product Catalog Name:
    Human Ghrelin (total) ELISA

  • Immunohistochemical evaluation of surfactant proteins and lymphocyte phenotypes in the lungs of cattle with natural tuberculosis. 20800246

    The aim of the present study was to evaluate the immunohistochemical expression of pulmonary surfactant proteins (SP-A, SP-B, SP-C) and lymphocytic phenotypes in the lungs of 12 cattle with natural tuberculosis. Grossly, the disease-affected cattle revealed numerous granulomas in the lung lobes. Histopathological examination found multiple lung granulomas with typical cellular elements. Type II pneumocytes with adenomatous proliferation around the granulomas were strongly immunopositive for SP-A and SP-B compared to normal type II cells. Clara cells showed also cytoplasmic immunopositivity for these surfactant proteins. Positive immunolabelling for proSP-C was detected exclusively in the normal and proliferative type II pneumocytes, and the reaction was marked in the perinuclear area of the cells. CD3(+) T and CD79αcy(+) B lymphocytes were predominantly localized in the fibrotic capsule margin of advanced granulomas, in greater numbers than in the early granulomas. In conclusion, the study found that type II pneumocytes proliferated highly and surrounded the tuberculous granulomas in the lungs, that hyperplastic type II pneumocytes synthesized and secreted larger amounts of surfactant proteins than the normal type II cells, and that SP-A might have played an important role in host defence against the mycobacterial agents. Additionally, the presence of high numbers of CD3(+) T cells throughout the granulomas confirmed the dominance of a cellular immune response in cattle tuberculosis.
    Document Type:
    Reference
    Product Catalog Number:
    AB3424
    Product Catalog Name:
    Anti-Surfactant Protein A Antibody

  • Persistent phosphorylation at specific H3 serine residues involved in chemical carcinogen-induced cell transformation. 27996159

    Identification of aberrant histone H3 phosphorylation during chemical carcinogenesis will lead to a better understanding of the substantial roles of histone modifications in cancer development. To explore whether aberrant H3 phosphorylation contributes to chemical carcinogenesis, we examined the dynamic changes of H3 phosphorylation at various residues in chemical carcinogen-induced transformed human cells and human cancers. We found that histone H3 phosphorylation at Ser10 (p-H3S10) and Ser28 (p-H3S28) was upregulated by 1.5-4.8 folds and 2.1-4.3 folds, respectively in aflatoxin B1 -transformed hepatocytes L02 cells (L02RT-AFB1 ), benzo(a)pyrene-transformed HBE cells (HBERT-BaP), and coke oven emissions-transformed HBE cells (HBERT-COE). The ectopic expression of histone H3 mutant (H3S10A or H3S28A) in L02 cells led to the suppression of an anchorage-independent cell growth as well as tumor formation in immunodeficient mice. In addition, an enhanced p-H3S10 was found in 70.6% (24/34) of hepatocellular carcinoma (HCC), and 70.0% (21/30) of primary lung cancer, respectively. Notably, we found that expression of H3 carrying a mutant H3S10A or H3S28A conferred to cells the ability to maintain a denser chromatin and resistance to induction of DNA damage and carcinogen-induced cell transformation. Particularly, we showed that introduction of a mutant H3S10A abolished the bindings of p-H3S10 to the promoter of DNA repair genes, PARP1 and MLH1 upon AFB1 treatment. Furthermore, we revealed that PP2A was responsible for dephosphorylation of p-H3S10. Taken together, these results reveal a key role of persistent H3S10 or H3S28 phosphorylation in chemical carcinogenesis through regulating gene transcription of DNA damage response (DDR) genes.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Detection of Ki67 antigen by a new sheep polyclonal antiserum. 8568003

    This report describes the characterisation of a polyclonal sheep antiserum against the Ki67 antigen. On western blots, this antiserum recognises a pair of bands of high molecular weight identical with those seen with another polyclonal Ki67 antiserum and the MIB 1 monoclonal antibody. The new antiserum showed nuclear staining of a proportion of cells in paraffin wax embedded tissue sections following antigen retrieval using a microwave oven or pressure cooker. This staining pattern was blocked by incubating the serum with the peptide used as immunogen. The proportion and distribution of immunostained nuclei was identical with that seen with the alternative reagents that recognise the Ki67 antigen. The new reagent stained the same proportion of cells when used over a wide range of dilutions. There was no cross-reactivity with unrelated antigens sometimes detected by the monoclonal antibodies.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Differential effects of arsenic on cutaneous and systemic immunity: focusing on CD4+ cell apoptosis in patients with arsenic-induced Bowen's disease. 19376847

    Bowen's disease (BD), a carcinoma in situ of the skin, has been identified as an early lesion in arsenic carcinogenesis. Patients with arsenic-induced Bowen's disease (As-BD) showed both cutaneous and systemic immune dysfunctions. We set out to evaluate the interactions between keratinocytes and lymphocytes in the context of As-BD carcinogenesis. Our results showed that As-BD lesions demonstrated a significant dermal CD4+ cell, an essential regulator of proper tumor immunity, undergoing apoptosis. In addition, it was found that the As-BD patients have lower percentage of peripheral CD4+ cells as compared with control subjects. However, the CD4+ cells from As-BD patients were less susceptible to arsenic-induced apoptosis, due to reduced tumor necrosis factor receptor 1 expression. Interestingly, arsenic was found to induce Fas expression on CD4+ cells and increase the soluble Fas ligand (sFasL) production from keratinocytes. This sFasL-containing keratinocyte supernatant was able to induce comparable CD4+ cell apoptosis for both patients and controls. Using immunofluorescent staining, increased FasL was observed in keratinocytes of As-BD lesions and Fas was expressed among infiltrating CD4+ cells. Our findings suggested that systemically, the percentage of CD4+ cells was decreased in the peripheral blood of As-BD patients. These residual CD4+ cells were less susceptible to arsenic-induced apoptosis. However, once infiltrated into the As-BD lesions, the selective CD4+ cell apoptosis might be mediated by FasL from keratinocytes. This additional tumor-anti-immune phenomenon present in the cutaneous environment provides a reasonable explanation for frequent occurrence of arsenic cancers in the skin.,
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Expression of simple epithelial keratins 8 and 18 in epidermal neoplasia. 1717607

    A systematic study of keratin expression in epidermal lesions (six actinic keratoses, 10 Bowen's disease, seven squamous cell carcinomas) has been undertaken by using a large panel of monospecific monoclonal antibodies to individual keratins. Expression of differentiation-specific keratins was frequently delayed or lost from dysplastic regions. Novel expression of the embryonic, or simple epithelial, keratins 8 and 18 was widely observed in intradermal areas of poorly differentiated squamous cell carcinomas. In addition, the most proliferative of in situ malignancies (Bowen's disease) also contained small numbers of cells expressing simple epithelial keratins. These observations suggest that the expression of simple epithelial keratins may be of functional importance in malignancy of keratinocytes and could be related to tumor invasion and/or to changes in epithelial-mesenchymal interactions.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Disease-independent skin recruitment and activation of plasmacytoid predendritic cells following imiquimod treatment. 16077073

    Imiquimod, an immune response modifier that is used topically to treat different types of skin cancer, induces the production of proinflammatory cytokines that stimulate an antitumor immune response. We assessed characteristics of the imiquimod-induced immune activation in epithelial and lymphoproliferative neoplasias of human skin. We focused on plasmacytoid predendritic cells (PDCs), the primary producer of interferon alpha (IFN-alpha) after imiquimod activation in vitro.We used Affymetrix oligonucleotide arrays to compare gene expression profiles from tumors from 16 patients, 10 with superficial basal cell carcinomas (sBCCs), five with cutaneous T-cell lymphomas (CTCLs), and one with Bowen's disease, before and after topical imiquimod treatment. We used quantitative immunohistochemistry with PDC-specific antibodies against BDCA-2 and CD123 to characterize the PDC population before and after imiquimod treatment in these specimens. Activation status of PDCs from four sBCC patients was assessed by intracellular IFN-alpha staining and flow cytometry.Expression of various IFN-alpha-inducible genes (e.g., CIG5, G1P2, OASL, IFIT1, STAT1, IFI35, OAS1, ISG20, MxA, and IRF7), the so-called IFN-alpha signature, was increased similarly in both sBCC and CTCL lesions after imiquimod treatment. PDCs were recruited and activated in both lesion types, and they produced IFN-alpha after imiquimod treatment in vivo (mean percentage of PDCs producing IFN-alpha = 14.5%, 95% confidence interval [CI] = 4.9% to 24%; range = 3.3%-27%, n = 4 lesions). Imiquimod induced similar immune activation patterns in all three diseases, and these patterns were associated with the number of PDCs recruited to the treatment site. Two imiquimod-treated sBCC patients who did not mount an inflammatory response to imiquimod and whose lesions lacked the IFN-alpha signature after treatment had fewer PDCs in treated lesions compared with other treated patients with such a response.Imiquimod induces immune activation patterns that relate to the number of the PDCs recruited to the treatment site, thus supporting the role of PDC in responsiveness to imiquimod in humans.
    Document Type:
    Reference
    Product Catalog Number:
    MABF938
    Product Catalog Name:
    Anti-MxA, clone M143 (CL143)
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