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Biomedical subjects

C Zurcher

Publications and source records attributed to C Zurcher.

89 records · Page 5Linked to original sources
PubMed1979

Type-C virus antigen detection in co-cultures of human leukaemic bone marrow and dog cells.

Bone marrow of leukaemic patients, non-leukaemic patients and normal individuals were co-cultivated with the canine cell line A7573. These co-cultures were screened for retrovirus antigens by means of the indirect cytoplasmic immunofluorescence assay (IFA). Rabbit antisera directed against the major structural protein (p30) of woolly monkey (simian) sarcoma leukaemia virus (grown in human lymphoid cells) and Rauscher murine leukaemia virus were used for testing. After 2 months in culture, 6 of 17 co-cultures containing cells from leukaemic patients showed positive staining in the IFA with the anti-simian virus serum. In control dog cells fluorescence was never observed. Five of the six positive cultures were derived from leukaemic children. One of 12 co-cultures of the non-leukaemic group and one of nine normal bone marrow co-cultures were positive with the simian virus antiserum. None of the 38 co-cultures stained positive in the IFA with Rauscher virus antiserum. Absorption of the simian virus antiserum with calf serum or mouse mammary tumour virus had no dramatic effect in the IFA on positive control cells or on cells of a positive co-culture. However, absorption with purified simian virus (grown in rat cells) completely abolished these fluorescence reactions. The results provide evidence that simian sarcoma-leukaemia virus related information was present in the original bone marrow samples and that co-cultivation with permissive mammalian cells enabled the detection of virus footprints.

Adult↗
PubMed1979

Idiopathic paraproteinemia. II. Transplantation of the paraprotein-producing clone from old to young C57BL/KaLwRij mice.

Transplantation experiments in the C57BL/KaLwRij mouse model of idiopathic paraproteinemia (IP) showed that an IP-producing clone can be further propagated in young, lethally irradiated mice and also equally as well in nonirradiated recipients by a bone marrow and/or spleen cell transfer. The latency period before the original paraprotein was detected in the sera of recipients varied in different experiments between 1 and 9 months after transplantation. With subsequent transplantations, the "take" frequency gradually decreased. Propagation of IP for three to four generations seems to be the final limit. In comparison to age-matched seems to be the final limit. In comparison to age-matched control groups, no substantial influence of the transplanted IP on the survival of the recipients was observed. In contrast, transplantation of cells from mice with a B cell lymphoma or a myeloma led to continuous propagation of the malignancy, with a high "take" frequency, progressive development of the paraproteinemia, and a shortened survival time of the recipients. These findings indicate that IP represents in its final stage in the aging C57BL mice an intrinsic cellular defect within the affected B cell clone, which is, however, different from that found in B cell malignancies.

Aging↗
PubMed1978

Type-C oncovirus isolate from human leukemic bone marrow: further in vitro and in vivo characterization.

Rabbit corneal cells transformed by a putative human type-C helper virus pseudotype of the mouse sarcoma virus produce large amounts of transforming and non-transforming viruses. The virions are antigenically related to the woolly monkey (simian) sarcoma-leukemia type-C oncovirus. Typical sarcoma virus lesions developed in newborn rats injected with virus-producing rabbit cells. Cells producing only the putative type-C helper viruses as a result of exposure to a high dilution of transforming virus stock induce lymphosarcomas after inoculation into newborn rats.

Animals↗
PubMed1978

Tumor-induced changes in T cell mitogen responses in rats: suppression of spleen and blood lymphocyte responses and enhancement of thymocyte responses.

Concanavalin A (Con A) and phytohemagglutinin (PHA) responses of spleen and blood lymphocytes from tumor-bearing (TB) rats were found to be markedly depressed in 4 different models employing tumors of spontaneous origin. Removal of phagocytic cells from both spleen and blood lymphocyte suspensions led to a complete restoration of the responses, indicating that the decreased responses were not due to intrinsic defects in the lymphocytes. The reduction was shown to be due to the inhibitory effect of an increase in the percentage of phagocytic cells. In addition, TB induced an atrophy of the thymus and a decrease in the number of thymic lymphocytes, mainly due to severe lymphocyte depletion in the cortex. The cells that remained in the thymus exhibited increased responsiveness to PHA and Con A as compared to thymus cells from normal rats. Similar results were found in hydrocortisone acetate-treated rats, suggesting that TB leads to a decrease in nonresponsive, cortical corticosteroid-sensitive thymocytes.

Animals↗
PubMed1977

Detection of human C-type "helper" viruses in human leukemic bone marrow with murine sarcoma virus-transformed human and rat non-producer cells.

Bone-marrow cells from two leukemic children were co-cultivated with the leukemic children A 7573. In early passages, C-type oncornaviruses were released as detected by extracellular reverse transcriptase assay. Co-cultivation of the infected canine cells with the non-producing cell lines R-970-5 (human) or K-NRK (rat) both transformed by Kirsten mouse sarcoma virus (MSV) yielded a new pseudotype of MSV that could transform rat embryo, rabbit SIRC and human kidney cells but not mouse embryo cells. The focur formation could be inhibited by an antiserum to the simian sarcoma virus but not by a serum directed against murine leukemia virus. A cell line derived from a focus of transformed cells became a highe virus is related to the simian sarcoma virus. It is concluded that the leukemic bone-marrow cells produce a C-type oncornavirus that can serve as a helper virus to the defective MSV.

Acute Disease↗
PubMed1977

A naturally occurring epizootic caused by Sendai virus in breeding and aging rodent colonies. I. Infection in the mouse.

An acute Sendai virus epizootic occurred simultaneously in a breeding colony, in experimental and stock animal rooms, and in a colony of aging mice. During the 2-month period that the infection was at its maximum, death rates were approximately doubled. In some strains, the preweanling death rate reached 100%. RFM and BALB/c mice were most susceptible and NZB mice least susceptible. The mortality during the period of Sendai virus infection was increased for most strains and age groups except for the oldest female RFM and NZB mice. Death rates during the epizootic were lowest in young adult mice (greater than 10 weeks of age) and highest in the very young mice (less than 10 weeks of age) and in the oldest male and the moderately aged female mice. Although a substantial number of older mice died during the epizootic, examination of the age-specific death rates indicated that the increase in deaths remained relatively constant for all ages over 10 weeks. This showed that the older mice were not more susceptible to Sendai virus infection. As a sequela of the epizootic, focal chronic pneumonia was found in 10-40% of the mice coming to necropsy even 1 year later.

Age Factors↗
PubMed1977

A naturally occurring epizootic caused by Sendai virus in breeding and aging rodent colonies. II. Infection in the rat.

Sendai virus infected a hysterectomy derived, barrier maintained breeding colony and a conventional aging rat colony. The virus produced seroconversion in the colonies followed by a 7-month period of decreasing titers. Clinical signs were absent during the months when titers were highest, and there was no increase in mortality, but multifocal interstitial pneumonia with perivascular and peribronchial cuffing by lymphocytes and plasma cells was present in rat lungs examined histologically. Such lesions were absent before the period of seroconversion. During the months of declining titers, the interstitial and perivascular lesions decreased in frequency and severity. The peribronchial lesions did not decrease, however, and were still present in many rats 7 months after the acute infection. Attempts to isolate the virus from weanling rats were unsuccessful.

Age Factors↗
PubMed1975

Attempts to transform murine hemopoietic cells by Rauscher leukemia virus.

Primary Rauscher leukemia virus (RLV)-induced myeloid leukemias can produce many small clones in agar in the absence of a factor needed for the proliferation of normal myeloid cells. It seems that leukemic cells can more efficiently utilize the small amount of colony-stimulating factor (CSF) that is produced by them. At optimal stimulation by exogenous CSF, leukemic cells exhibit a poorer rate of proliferation than normal bone marrow cells. Hemopoietic cells can replicate the virus after infection in vitro. In some experiments, infection of normal bone marrow cells leads to the production of some cells with the same growth pattern as cells from primary leukemias.

Animals↗
PubMed1975

Engraftment of allogeneic dog bone marrow.

Resistance to allogeneic bone-marrow grafts (AR) was found to occur in many species, including the dog. The i.v. administration of silica particles suppressed AR in vivo in this species. Genetic studies provide suggestive evidence for the existence of a previously unrecognized system or systems in the canine major histocompatibility complex controlling AR.

Animals↗
PubMedDate not supplied

Inflammatory demyelinating neuropathy in C57BL/KaLwRij mice.

Neuropathies associated with monoclonal gammopathy (MG) in humans have been extensively studied in the past few years, but experimental models have proved difficult to create. C57BL mice are prone to develop benign MG and it has been reported that some of these mice with benign IgG MG present an inflammatory demyelinating neuropathy (IDN). In order to verify such findings, the serum and the sciatic nerve of the first group of 28 C57BL/KaLwRij mice were examined: none of 10 mice with normal serum showed ultrastructural abnormalities in the sciatic nerve, while lesions of IDN were present in three out of 10 mice with benign IgG MD, in two out of seven with benign IgM MG, and in a mouse with Waldenström-like lymphoma. The second group of animals was studied in the same way; it was composed of seven C57BL mice with transplanted multiple myeloma, and six C57BL mice with Morbus Waldenström-like lymphoma. In none of these animals, which were younger than those of the first group, was any lesion of IDN observed.

Animals↗
PubMedDate not supplied

Ultrastructure of epidermis of mice with chronic proliferative dermatitis.

C57BL/Ka mice with chronic proliferative dermatitis (cpdm/cpdm) develop chronic persistent skin lesions characterized by epidermal hyperplasia, infiltration by granulocytes and macrophages, and vascular dilatation. Similar lesions are present in other orthokeratotic epithelia in affected mice, in particular the esophagus and forestomach. Here, we report on further characterization of epidermal hyperplasia and the granulocytes. Keratinocytes of lesional skin, but not of normal skin, show round and electron-dense mitochondrial inclusions that are present in all layers of the epidermis. Similar inclusions are also present in the esophagus and forestomach of affected mice. There appears to be a direct relation between the presence of intramitochondrial inclusions and epidermal hyperplasia in the mouse. Furthermore, the presence of keratinocyte-derived apoptotic bodies in the epidermis, esophagus, and forestomach was frequently observed in the lesions, which is consistent with previous light microscopic observations of single cell death of keratinocytes. The granulocytes present in the skin, esophagus, and forestomach were mainly eosinophils. There were widespread gaps observed in the lamina densa in the epidermis that were mostly directly associated with dermal or epidermal eosinophils. This type of gap is also observed in psoriasiform diseases in humans. This electron microscopic study demonstrated that this mouse model should be useful to screen potential therapeutic strategies for psoriasiform and other inflammatory skin disorders.

Animals↗