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  • 1
    Electronic Resource
    Electronic Resource
    Hepatoid adenocarcinoma of the pancreas (1999)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Histopathology 35 (1999), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.1999.0728f.x
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  • 2
    Electronic Resource
    Electronic Resource
    Desmoplastic malignant melanoma of the uterine cervix: a rare primary malignancy in the uterus mimicking a sarcoma (1998)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Histopathology 33 (1998), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.1998.0415h.x
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  • 3
    Electronic Resource
    Electronic Resource
    Gastrointestinal hepatoid adenocarcinoma: venous permeation and mimicry of hepatocellular carcinoma, a report of four cases (1997)
    Oxford, UK : Blackwell Science Ltd
    Histopathology 31 (1997), S. 0 
    Details
    ISSN: 1365-2559
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Aims: Four cases of hepatoid adenocarcinoma, three in the stomach, and one in the sigmoid colon, are presented to emphasize venous permeation and mimicry of hepatocellular carcinoma by metastatic liver nodules. Methods and results: Tumour cells in all cases extensively invaded veins, and intravenous tumour thrombi in two cases were grossly observed as anastomosing, worm-like cords up to 10 mm in diameter in the lesser omentum and mesentery in continuity with the primary mucosal lesions. The cytological features and trabecular architecture of the metastatic liver nodules in these subjects mimicked primary hepatocellular carcinoma. In a third case the tumour contained grossly visible bile in a metastatic lung nodule, but there was no evidence of bile production in the primary gastric or metastatic liver lesions. In the fourth case, detailed histopathological study revealed a gastric origin of the hepatoid adenocarcinoma, rather than primary hepatocellular carcinoma metastatic to the stomach, the initial diagnosis. Conclusions: These cases are reported here to draw attention to this rare variant of gastrointestinal adenocarcinoma, its mimicry of hepatocellular carcinoma when metastatic to the liver and other sites, and its propensity for venous permeation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2559.1997.5740812.x
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  • 4
    Electronic Resource
    Electronic Resource
    Purification of glycosylphosphatidylinositol-anchoring aminopeptidase in from the plasma membrane of larval midgut epithelial cells of the silkworm, Bombyx mori
    Amsterdam : Elsevier
    International Journal of Biochemistry 26 (1994), S. 977-986 
    Details
    ISSN: 0020-711X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0020-711X(94)90068-X
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  • 5
    Electronic Resource
    Electronic Resource
    GENETIC DIFFERENCES BETWEEN TWO SUBSTRAINS OF NZB MICE (1985)
    Oxford, UK : Blackwell Publishing Ltd
    International journal of immunogenetics 12 (1985), S. 0 
    Details
    ISSN: 1744-313X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: We have compared the NZB/BINJ (/NJ) and NZB/BlPt (/Pt) mouse substrains with respect to a number of immunological and biochemical polymorphisms. In agreement with earlier findings by other workers, we detected histocompatibility antigen difference(s) between the two substrains. Serological analysis indicated that /NJ and /Pt expressed the same allotypes of H-2, Thy-1 and Lyt-1 antigens, while they differed for the Lyt-2 antigen. Amongst 15 biochemical polymorphisms, which we assayed, /NJ and /Pt differed for four, namely Pep-3, Mup-1, Gpd-1 and Hbb. In addition, the two NZB substrains differed for the Hc marker (haemolytic complement).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1744-313X.1985.tb00831.x
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  • 6
    Electronic Resource
    Electronic Resource
    Abortive alloantigen presentation by donor dendritic cells leads to donor-specific tolerance: a study with a preoperative CTLA4Ig inoculation (2000)
    Springer
    Urological research 28 (2000), S. 69-74 
    Details
    ISSN: 1434-0879
    Keywords: Key words Kidney transplantation ; Dendritic cell ; Antigen presentation ; CTLA4Ig ; Donor-specific tolerance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Donor dendritic cells (DCs) within allografts initiate the induction of an allospecific T cell response, while an abortive alloantigen presentation by DCs may induce allospecific unresponsiveness. We thus investigated the tolerogenic effect of donor DCs that were made incompetent in alloantigen presentation by treatment of CTLA4Ig. When we treated rats with donor DCs (2 × 106/rat i.v.) on the preoperative day, nine rejected allografts in an accelerated manner (5.0 ± 2.2 vs. 8.2 ± 1.6 days in the control group). Preoperative inoculation of DCs pulsed with CTLA4Ig, a procedure which suppresses an allogeneic mixed lymphocyte reaction (MLR), also provoked an accelerated rejection (5.6 ± 1.7 days). When DCs and CTLA4Ig (500 μg/rat i.p. on days −9, −7 and −5) were concomitantly inoculated, allograft survival was significantly prolonged (〉38.7 ± 40.0 days); a preoperative CTLA4Ig inoculation alone failed to do so (7.5 ± 1.2 days). Long-term graft survivors tolerated skin grafts from the donor but not from those from a third party. These results indicate that abortive alloantigen presentation by donor DCs, upon which an accessory signal pathway is suppressed by CTLA4Ig, leads to prolonged graft survival and donor-specific tolerance.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002400050013
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  • 7
    Electronic Resource
    Electronic Resource
    The role of prostatic specific antigen in monitoring prostatic cancer and its prognostic importance (1990)
    Springer
    Urological research 18 (1990), S. 331-336 
    Details
    ISSN: 1434-0879
    Keywords: Prostatic specific antigen ; Tumor marker ; Prognostic factor ; Prostatic cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serum prostatic specific antigen (PA) and prostatic acid phosphatase (PAP) levels were measured in 113 untreated patients with prostatic cancer and in 137 patients with benign prostatic hypertrophy (BPH). Of the 113 cancer patients, 81% and 69%, respectively, were detectable by means of PA or PAP assay alone. PA was a more sensitive indicator, than PAP in all stages, especially localized disease (stages A, B and C). Using the BPH group as a negative control, specificities of PA and PAP were 81% and 94% respectively, In another group of 68 patients with BPH whose blood samples were taken immediately after prostatic manipulation, both PA and PAP levels were elevated significantly. In 87 of the 113 cancer patients the two markers were serially determined, and 22 patients presented disease progression. Concerning the sensitivity within 6 months before progression, PA appears to be more reliable than PAP in early detection of disease progression. According to Kaplan-Meier projections, the patients with normal pretreatment PA levels had significantly longer intervals to progression than did those with moderate to marked PA elevation (more than 100 ng/ml) (P〈0.05). This study shows that PA is more reliable than PAP for detection and monitoring of prostatic cancer. Pretreatment PA levels appear to be of a high prognostic value for time to progression, irrespective of stage and treatment regimen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00300782
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  • 8
    Electronic Resource
    Electronic Resource
    A rat model of HTLV-I infection: development of chronic progressive myeloneuropathy in seropositive WKAH rats and related apoptosis (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 483-490 
    Details
    ISSN: 1432-0533
    Keywords: Key words HTLV-I ; HTLV-I-associated ; myelopathy/tropical spastic paraparesis ; Rat model ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In seropositive HTLV-I carrier rats of the WKAH strain inoculated with 2 × 107 MT-2 cells at 3–6 months of age, chronic progressive myeloneuropathy, tentatively designated as HTLV-I-associated myelopathy (HAM) rat disease, occurred when the rats were 19–23 months old. Clinical and pathological findings were basically identical to those of seronegative HAM rats of the same strain neonatally inoculated with MT-2 cells. It appears that a high dose of MT-2 cells (108 cells) is more effective for the induction and acceleration of HAM rat disease. Seronegative and seropositive carriers of other strains (F344, ACI, and LEW), WKAH rats inoculated with HUT-78 (a human T cell line without HTLV-I infection), and untreated WKAH rats at comparable ages did not develop HAM rat disease, thereby indicating that development of this disease is caused by HTLV-I infection and is under strict genetic restriction of the host strain. Chronological examination of HAM rat disease induced by 107 MT-2 inoculation into newborn rats showed that the spinal cord lesion began to develop by 12 months of age. T cells were absent in the affected spinal cord throughout the disease process. There was morphological evidence of apoptotic death of oligodendrocytes in the affected spinal cord. Apoptosis was also confirmed by the specific nick end labeling of the nuclear fragmentation in situ, and the apoptotic oligodendrocytes confined to the demyelinating foci, and the number of apoptotic cells positively correlated with severity of the spinal cord lesion. The collective evidence suggests that the major pathogenetic pathway of HAM rat disease appears to be closely related to apoptotic death of the oligodendrocytes, directly or indirectly associated with HTLV-I infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571502
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  • 9
    Electronic Resource
    Electronic Resource
    A rat model of HTLV-I infection: development of chronic progressive myeloneuropathy in seropositive WKAH rats and related apoptosis (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 483-490 
    Details
    ISSN: 1432-0533
    Keywords: HTLV-I ; HTLV-I-associated ; myelopathy/tropical spastic paraparesis ; Rat model ; Apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In seropositive HTLV-I carrier rats of the WKAH strain inoculated with 2×107 MT-2 cells at 3–6 months of age, chronic progressive myeloneuropathy, tentatively designated as HTLV-I-associated myelopathy (HAM) rat disease, occurred when the rats were 19–23 months old. Clinical and pathological findings were basically identical to those of seronegative HAM rats of the same strain neonatally inoculated with MT-2 cells. It appears that a high dose of MT-2 cells (108 cells) is more effective for the induction and acceleration of HAM rat disease. Seronegative and seropositive carriers of other strains (F344, ACI, and LEW), WKAH rats inoculated with HUT-78 (a human T cell line without HTLV-I infection), and untreated WKAH rats at comparable ages did not develop HAM rat disease, thereby indicating that development of this disease is caused by HTLV-I infection and is under strict genetic restriction of the host strain. Chronological examination of HAM rat disease induced by 107 MT-2 inoculation into newborn rats showed that the spinal cord lesion began to develop by 12 months of age. T cells were absent in the affected spinal cord throughout the disease process. There was morphological evidence of apoptotic death of oligodendrocytes in the affected spinal cord. Apoptosis was also confirmed by the specific nick end labeling of the nuclear fragmentation in situ, and the apoptotic oligodendrocytes confined to the demyelinating foci, and the number of apoptotic cells positively correlated with severity of the spinal cord lesion. The collective evidence suggests that the major pathogenetic pathway of HAM rat disease appears to be closely related to apoptotic death of the oligodendrocytes, directly or indirectly associated with HTLV-I infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571502
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  • 10
    Electronic Resource
    Electronic Resource
    A rat model of human T lymphocyte virus type I (HTLV-I) infection: in situ detection of HTLV-I provirus DNA in microglia/macrophages in affected spinal cords of rats with HTLV-I-induced chronic progressive myeloneuropathy (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 107-112 
    Details
    ISSN: 1432-0533
    Keywords: Key words HTLV-I ; HTLV-I-associated myelopathy/ ; tropical spastic paraparesis ; Microglia/macrophage ; Rat model ; In situ hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To investigate the pathogenetic role of human T lymphocyte virus type I (HTLV-I) in central nervous system disease, a rat model for HTLV-I-associated myelopathy/tropical spastic paraparesis, designated as HAM rat disease, has been established. Wistar-King-Aptekman-Hokudai strain rats with induced HTLV-I infection develop a chronic progressive myeloneuropathy with paraparesis of hind limbs after an incubation period of 15 months. In the affected spinal cord in these rats, white matter degeneration, demyelination and vacuolar change with microglia/macrophage infiltration are present as are the provirus DNA and the virus mRNA. To identify infected cells in the affected lesions, we carried out in situ hybridization of amplified fragments of the provirus DNA by polymerase chain reaction on thin sections, plus immunohistochemistry on the same sections. The provirus DNA was localized in some microglia/macrophages in the spinal cord lesion. In addition, the HTLV-I provirus was clearly evident not only in ED-1-negative lymphoid cells but also in ED-1-positive macrophages from lymph nodes. These observations suggest that cells of microglia/macrophage lineage may be one of dominant viral reservoirs in the spinal cords and lymph nodes in HAM rat disease. These infected microglia/macrophages may relate to cause the myeloneuropathy through neurotoxic cytokine synthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050962
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