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Biomedical subjects

C K Chai

Publications and source records attributed to C K Chai.

At least 19 recordsLinked to original sources
PubMed1985

The inheritance of spontaneous amyloidosis development in mice: a model for hereditary threshold metabolic disorders.

To study the inheritance of spontaneous amyloidosis development in mice, we crossed the LLC strain (with a high incidence) with the A/J strain (with a low incidence) and with the HLC strain (with a zero incidence of amyloidosis). We produced the F1 and a backcross generation to each parental strain in each cross. Examination of the spleen, liver, and kidneys of each mouse for the presence of amyloid was made between age 15 and 18 months. The data fit neither a dominant nor a recessive single gene hypothesis for the development of amyloidosis. In consideration of amyloidosis as a hereditary threshold character, we developed an additive gene model. Subsequently, a test for fitness of the observed percentages to the expected percentages in the backcross generations was made according to this model. The observed percentages of amyloidosis in the spleens, livers, and individual mice agreed with the expected percentages in the LLC X A/J crosses but not in the LLC X HLC crosses. Therefore, we conclude that for the development of amyloidosis, a difference exists at one locus between LLC and A/J and at more than one locus between LLC and HLC. The probability of development of amyloidosis in an individual depends on the effects of the genes at these loci. For hereditary metabolic disorders that cannot be explained by either a single dominant or recessive gene hypothesis, this genetic model may be useful to test whether the development of the disease is due to additive effects of genes.

Amyloidosis↗
PubMed1984

Amyloidosis development in LLC mice.

Using electron microscopy and the protein A-gold labelling technique we studied amyloidosis in the LLC mice, an inbred strain developing amyloidosis spontaneously. We found that the reticular cells lining around the sinuses in the red pulp of the spleen were converted to amyloid. Evidence suggests that the amyloid originates in the cells themselves. The process of amyloid formation is discussed.

Amyloidosis↗
PubMed1978

Spontaneous amyloidosis in LLC mice.

Practically all low leukocyte count (LLC) mice over 1 year of age develop renal amyloidosis. Renal amyloid is deposited in the glomeruli and in the interstitium between the convoluted as well as collecting tubules, with consequent development of cysts and necrosis. LLC mice die of chronic renal failure. Electron microscopic studies reveal amyloid fibrils in the mesangium, a thickening of the basement membranes, and fusion of the foot processes in the glomeruli. Massive amounts of amyloid fibrils are also present in the interstitium, where intracellular fibrils in the fibroblasts as well as in the tubular epithelium cells are found. Vesicles, which are probably formed from membrane disruption, and amorphous materials are seen along the basement membranes. LLC mouse amyloidosis is discussed with regard to its potential as a model for studies on amyloidosis as well as the etiology and origin of amyloid fibrils.

Amyloid↗
PubMed1976

Reticular cell hyperplasia and amyloidosis in a line of mice with low leukocyte counts.

Two pathologic conditions, reticular cell hyperplasia and amyloidosis, were studied in a strain of mice selectively bred for low leukocyte counts (LLC). At the age of 3 to 6 months, 70% of the mice developed reticular cell hyperplasia in the inguinea lymph nodes, and at 11 to 18 months, about 100% of them developed amyloidosis in the spleen and in the kidney, liver, and adrenal glands. Immunofluorescence was revealed in the glomeruli, interstitium of the tubules, and the amyloid skeleton of the papilla when the kidney sections were incubated with fluorescein-labeled antimouse immunoglobulins. Both intracellular and extracellular amyloid fibrils were found in the liver, spleen, and kidney sections by electron microscopy. Distended rough endoplasmic reticulum (RER) cisternae and hypertrophy of RER with or without the simultaneous presence of amyloid fibrils in the reticular cells of the spleen and Kupffer cells of the liver were observed. In this light, we believe that the pathologic conditions are manifestations of immunologic events that are characteristic of the LLC mice with immune deficiency or abnormality in the immune system. We conclude that the origin of amyloid protein is at the RER. We discuss processes of amyloid fibril formation and some genetic aspects of amyloid development.

Adrenal Glands↗
PubMed1975

Class differences in the antibody response of HLC and LLC mice to sheep red blood cells.

The immune response to sheep red blood cells (SRBC) has been studied in two mouse lines selectively bred for a difference in leukocyte levels. Low leukocyte count (LLC) mice responded to multiple injections of 4 x 10(7) SRBC with a predominant IgM response whereas high leukocyte count (HLC) mice produced IgG almost exclusively, even after a single injection of SRBC. F1 mice responded like the LLC parent and backcross data implied genetic control at multiple loci. No correlation was found between the class of antibody produced in response to SRBC and the leukocyte count in backcross mice. Large numbers of plaque-forming cells (PFC) were detected in the spleens of HLC mice relative to the number detected in LLC spleens after primary and secondary immunizations with SRBC.

Animals↗