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H-type bovine spongiform encephalopathy (BSE) has been identified in aged cattle in Europe and North America. To determine the localization of disease-associated prion protein (PrPSc) in the peripheral nerve tissues of cattle affected with H-type BSE, we employed highly sensitive immunohistochemical and immunofluorescence techniques with the tyramide signal amplification (TSA) system. PrPSc deposition was detected in the inferior ganglia, sympathetic nerve trunk, vagus nerve, spinal nerves, cauda equina, and adrenal medulla, using this system. Notably, granular PrPSc deposits were present mainly in the Schwann cells and fibroblast-like cells and occasionally along certain nerve fibers at the surface of the axons. In the adrenal gland, PrPSc immunolabeling was observed within the sympathetic nerve fibers and nerve endings in the adrenal medulla. Although our results were limited to only 3 experimental cases, these results suggest that the TSA system, a highly sensitive immunohistochemical procedure, may help in elucidating the peripheral pathogenesis of H-type BSE. [ABSTRACT FROM AUTHOR]

The origin and transmission routes of atypical bovine spongiform encephalopathy (BSE) remain unclear. To assess whether the biological and biochemical characteristics of atypical L-type BSE detected in Japanese cattle (BSE/JP24) are conserved during serial passages within a single host, 3 calves were inoculated intracerebrally with a brain homogenate prepared from first-passaged BSE/JP24-affected cattle. Detailed immunohistochemical and neuropathologic analysis of the brains of second-passaged animals, which had developed the disease and survived for an average of 16 months after inoculation, revealed distribution of spongiform changes and disease-associated prion protein (PrPSc) throughout the brain. Although immunolabeled PrPSc obtained from brain tissue was characterized by the presence of PrP plaques and diffuse synaptic granular accumulations, no stellate-type deposits were detected. Western blot analysis suggested no obvious differences in PrPSc molecular mass or glycoform pattern in the brains of first- and second-passaged cattle. These findings suggest failures to identify differences in mean incubation period and biochemical and neuropathologic properties of the BSE/JP24 prion between the first and second passages in cattle. [ABSTRACT FROM PUBLISHER]

The article discusses a study which characterizes the biological and biochemical properties of H-type bovine spongiform encephalopathy (BSE) by experimenting on the transmission of BSE with bovinized transgenic mice. The researchers used immunohistochemistry, Western blot and paraffin-embedded tissue blot to determine the distribution of disease-oriented prion protein. Results showed the conservation of higher molecular weight of the glycoform pattern within several brain locations in mice.

Summary [ABSTRACT FROM AUTHOR]

We recently reported the intraspecies transmission of L-type atypical bovine spongiform encephalopathy (BSE). To clarify the peripheral pathogenesis of L-type BSE, we studied prion distribution in nerve and lymphoid tissues obtained from experimentally challenged cattle. As with classical BSE prions, L-type BSE prions accumulated in central and peripheral nerve tissues. [ABSTRACT FROM AUTHOR]

Aim: A chronic decrease in the activation and loading levels of skeletal muscles as occurs with hindlimb unloading (HU) results in a number of detrimental changes. Several proteolytic pathways are involved with an increase in myofibrillar protein degradation associated with HU. Exercise can be used to counter this increase in proteolytic activity and, thus, may be able to protect against some of the detrimental changes associated with chronic decreased use. The purpose of the present study was to determine the potential of a single bout of preconditioning endurance exercise in attenuating the effects of 2 weeks of HU on the mass, phenotype and force-related properties of the soleus muscle in adult rats. Methods: Male Wistar rats were subjected to HU for 2 weeks. One half of the rats performed a single bout of treadmill exercise for 25 min immediately prior to the 2 weeks of HU. Results: Soleus mass, maximum tetanic tension, myofibrillar protein content, fatigue resistance and percentage of type I (slow) myosin heavy chain were decreased in HU rats. In addition, markers for the cathepsin, calpain, caspase and ATP-ubiquitin-proteasome proteolytic pathways were increased. The preconditioning endurance exercise bout attenuated all of the detrimental changes associated with HU, and increased HSP72 mRNA expression and protein levels. Conclusion: These findings indicate that exercise preconditioning may be an effective countermeasure to the detrimental effects of chronic decreases in activation and loading levels on skeletal muscles and that an elevation in HSP72 may be one of the mechanisms associated with these responses. [ABSTRACT FROM AUTHOR]

Background. The oral adsorbent, AST-120 Kureha Chemical, has been shown to attenuate the progression of chronic renal failure in rats and humans. Spontaneous hypercholesterolemic male rats, (SHC rats; SHCRs) have been introduced for experimentation because they develop progressive hyperlipidemia and glomerulosclerosis on a cholesterol-free standard diet by their 30th week of life. Methods. The effects of AST-120 were studied in SHCRs. Twenty 10-week-old SHCRs were divided into two groups: a control group ( n = 10), and an AST-120 group ( n = 10). The experiment was begun at the 12th week and completed at the 34th week of life. Results. At the end of the experiment, we found that the serum levels of total cholesterol were 40% lower in the AST-120 rats than in the control rats ( P < 0.01). The creatinine clearance in the AST group was 40% higher than that in the controls ( P < 0.05). At the age of 20 weeks, postheparin lipoprotein lipase in the AST-120 SHCRs and in Sprague-Dawley rats with normal serum lipid levels was comparable, but was clearly lower in the control SHCRs. Finally, in a pathological investigation that determined a sclerosis index for all kidneys, this was significantly lower in the AST group than in the control animals ( P < 0.01). Conclusions. The reduction of serum lipid levels following the administration of the AST-120 oral adsorbent is associated with amelioration of renal functional and structural changes in SHCRs. [ABSTRACT FROM AUTHOR]

The YIGSR (Tyr-Ile-Gly-Ser-Arg) laminin β1 chain sequence has an inhibitory effect on tumour growth and the metastasis of melanoma and fibrosarcoma cells. In the present study, we investigated whether the multimeric YIGSR peptide (Ac-Y16) has an anti-proliferative effect and/or prevents the metastasis of human pre-B acute lymphoblastic leukaemia cells (NALM6) in severe combined immune deficient (SCID) mice. In in vitro studies, Ac-Y16 significantly inhibited leukaemic cell colony formation and the invasion of NALM6 cells in a Matrigel-based assay. The tumour growth and leukaemic infiltration in peripheral tissues were also analysed in SCID mice 9 weeks after NALM6, Matrigel and Ac-Y16 were subcutaneously co-injected. The weight of the subcutaneous tumours was significantly suppressed by Ac-Y16 in a dose-dependent manner. Flow cytometry analysis showed that the leukaemic infiltration was significantly inhibited in all organs with 1.5-2.0 mg of Ac-Y16. Leukaemic infiltrations in the brain were inhibited with 0.5 mg of Ac-Y16, and those in brain and bone marrow were also inhibited with 1.0 mg of Ac-Y16. With Ac-S16, a control-scrambled peptide, the only significant inhibition of the leukaemic infiltration was observed in bone marrow at a much higher dose. These data suggest that the multimeric YIGSR peptide can inhibit the tumour growth and metastasis of leukaemic cells and may be useful as a potential therapeutic reagent for leukaemic infiltrations. [ABSTRACT FROM AUTHOR]

Three cases of amyloidosis cutis nodularis atrophicans (ACNA) were investigated histologically and immunohistochemically to determine the nature and origin of the deposited amyloid. A pulmonary lesion from a case of nodular pulmonary amyloidosis, and cutaneous lesions from three cases of primary systemic amyloidosis, two cases of secondary systemic amyloidosis and three cases of secondary cutaneous amyloidosis following basal cell epithelioma were also examined for comparison. Histology showed infiltration of numerous plasma cells adjacent to amyloid deposits in ACNA and nodular pulmonary amyloidosis, but not in systemic amyloidosis. Immunohistochemically, the cytoplasm of the plasma cells was stained with anti-immunoglobulin light chain or anti-Bence-Jones protein antisera or both, and amyloid material stained with anti-AL antiserum in ACNA and nodular pulmonary amyloidosis. These results suggest that, in ACNA, the plasma cells may produce and secrete immunoglobulin light chains or Bence-Jones protein or both, which undergo proteolysis to protein AL or amyloid fibril proteins which have the same immunoglobulin determinants as protein AL. The product is then deposited locally to form nodules in the dermis. [ABSTRACT FROM AUTHOR]

The outer membrane protein (OMP) prepared from Escherichia coli was found to be a potent mitogen for murine B cells and to be capable of inducing polyclonal antibody formation as well as a proliferative response. Spleen cells from nude mica responded equally as well to OMP as those from their normal litter-mates, whereas nylon-wool-purified T cells or thymocytes failed to respond. The proliferative response was dependent on the presence of macrophages. The macrophage dependency of the polyclonal antibody response seemed to be less than that of the proliferation. OMP was mitogenic for lipopolysaccharide (LPS)-resistant C3H/HeJ spleen cells, further indicating that OMP is an unique B-cell mitogen distinct from LPS. OMP also enhanced the specific antibody response sixty-seven-fold to an optimal dose of sheep red blood cells (SRBC) in vitro, The kinetics of the response, however, was not altered from that of cultures without OMP, The anti-SRBC response of spleen cells from C3H/HeJ mice was also enhanced by the addition of OMP, suggesting that the adjuvant effects were not due to the LPS in the preparation Antibody responses in vitro to TI-I antigens, trinitrophenyl-LPS (Boivin) (TNP-LPSB) and TNP-Brucella abortus, were not enhanced in the presence of OMP. In contrast OMP enhanced the response to TI-2 antigens. TNP-LPSw (Westphal) and dinitrophenyt-Ficoll and T cells were shown to be required for these augmented antibody responses Enhancement was not seen in nude mouse spleen cell cultures but was seen when nylon-wool-purified T cells were added to the cultures. [ABSTRACT FROM AUTHOR]

The distribution of HSV-1 during the development of zosteriform skin lesions in SCID mice was analyzed by immunofluorescence and electron microscopy. The virus initially appeared within certain keratinocytes, sometimes surrounded by keratinocytes whose surfaces were also positive for the antigens, in the lower epidermal layers including the hair follicles, and then extended upward to the entire epidermis and downward to the sebaceous glands 1-2 days later, when no macroscopic skin lesion was seen. The affected epidermal cells subsequently degenerated and lost their viral antigens within a day, when the zosteriform lesion then became evident. This was followed by a degeneration of the dermis. The sebaceous glands eventually degenerated in 10 days, but some glands in the necrotic skin areas preferentially retained HSV-1. The horizontal spread of the virus in the epidermis beyond the first invaded dermatome occurred much later. In mice passively immunized with specific immune serum, viral antigens were observed even 20 days after the infection in sebaceous glands in necrotized areas. Therefore, HSV-1 appears to spread first via the extracellular fluid among the keratinocytes after being shed from nerve endings, and then produces a successive degeneration of the affected keratinocytes which may prevent any further extension of horizontal viral spread. The pilosebaceous apparatus is possibly acting as a site not only for the replication of HSV-1 with a delayed cytopathic effect, but also as an area that is temporarily sheltered from host defense mechanisms. [ABSTRACT FROM AUTHOR]

Herpes simplex virus type 1 (HSV-1) infection in mutant mice with severe combined immunodeficiency (SCID mice), i.e., mice in which the differentiation of both T and B lymphocytes is severely impaired, was studied. All control (infected and not treated with antibodies or with immune spleen cells) SCID mice were dead by 17 days after intracutaneous injection in the right midflank with 1 × 10 PFU of a virulent HSV-1 strain, Hayashida. Immunization with an avirulent strain of HSV-1 (SKa) did not protect them from death or prolong the survival time. Tissue virus titration of infected mice killed at various times after inoculation detected infectious virus in various organs, dorsal root ganglia, spinal cord, brain, kidney and adrenal gland in addition to the inoculation site of the skin in SCID mice, whereas virus could be detected only in the inoculation site and the nervous tissues in euthymic BALB/c mice, and in the adrenal gland from only one out of 17 nude mice. Human gamma globulin containing neutralizing antibody against HSV-1 prolonged the survival time but did not protect SCID mice from death. Transfer of spleen cells from immunized BALB/c mice protected the infected SCID mice from death. Treatment of spleen cells with anti-Thy 1.2 monoclonal antibody and complement abolished the protection. [ABSTRACT FROM AUTHOR]

Intravascular papillary endothelial hyperplasia (IPEH) was first described by Masson.[SUP1] It is characterized by the development of endothelial-lined papillary projections in a vascular lumen. In Japan the disease was first reported by Tanimura et al.[SUP2] in 1976, and since then over 30 cases have been described. In this report we describe a case of IPEH together with the review of these Japanese cases. [ABSTRACT FROM AUTHOR]

Two cases of localized multiple neurofibromas are reported. The patients had fairly large, closely grouped neurofibromas limited to a circumscribed part of the body, a very different clinical feature from segmental neurofibromatosis, but with otherwise had typical histopathological features. Possible aetiology is discussed. [ABSTRACT FROM AUTHOR]