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Biomedical subjects

K H Johnson

Publications and source records attributed to K H Johnson.

At least 91 records · Page 5Linked to original sources
PubMed1986

Bovine amyloid protein AA: isolation and amino acid sequence analysis.

Amyloid-laden renal glomeruli were selectively isolated from a cow with a history of multiple organ inflammatory diseases which terminated in amyloid-induced glomerulopathy and severe proteinuria. Lyophilized amyloid fibrils obtained by water extraction procedures were dissolved in 6M guanidine hydrochloride and gel filtered on Sepharose CL6B and Sephacryl S-300 Superfine columns for slab gel electrophoresis, analytic isoelectric focusing, and amino acid sequence analyses. Electrophoresis of material from the major retarded peak of the elution profile revealed that bovine protein AA moves as one band with an apparent molecular mass of about 14,000 Daltons. Several distinct bands between approximately pH 4.0 and 5.0 were observed when this material was evaluated by analytic isoelectric focusing, thus having a pattern resembling that of human and dog protein AA. A blocked N-terminus was demonstrated when protein from the major retarded peak was subjected to amino acid sequencing, but cyanogen bromide cleavage followed by gel filtration produced 3 peptide fragments for amino acid sequence analysis. These peptides had a high degree of homology with positions 4-14, 18-24 and 25-49 of human protein AA. An apparent complete homology between bovine protein AA and protein AA from other species was apparent at positions 35-45, providing further evidence that this is a functionally significant part of the serum protein AA (SAA) molecule.

Amino Acid Sequence↗
PubMed1986

Effects of bacterial endotoxin on protecting copper-deficient rats from hyperoxia.

The administration of very low doses of bacterial endotoxin protects rats during exposure to hyperoxia and is associated with the induction of lung antioxidant enzyme activities. Copper-deficient rats have increased susceptibility to O2 toxicity, which may be related to their decreased lung superoxide dismutase activity (SOD) or decreased plasma ceruloplasmin concentrations. To determine whether endotoxin can protect against hyperoxia in this susceptible model, we exposed copper-deficient and control rats to a fractional inspiratory concentration of O2 greater than 0.95 for 96 h after pretreatment with 500 micrograms/kg of bacterial endotoxin or phosphate-buffered saline (PBS). Mortality in the copper-deficient and control rats given PBS and exposed to O2 for 96 h was 100%. Copper-deficient rats died significantly earlier during the exposure than controls. No mortality occurred in either group treated with endotoxin and hyperoxia despite the decreased activity of copper-dependent enzymes in the copper-deficient rats. Copper-deficient rats treated with endotoxin and exposed to hyperoxia did increase lung Cu-Zn-SOD activity, but activity remained below levels found in air-exposed controls. Mn-SOD activity was found to be induced above air-exposed controls in the copper-deficient rats treated with endotoxin and exposed to hyperoxia. Hyperoxic exposure resulted in a marked increase in plasma ceruloplasmin concentrations in the control rats, but no increases in ceruloplasmin occurred in the copper-deficient animals. Endotoxin protects copper-deficient rats from hyperoxia despite their decreased lung Cu-Zn-SOD activity, and decreased plasma ceruloplasmin.

Animals↗
PubMed1986

Feline mammary sarcoma composed of cells resembling myofibroblasts.

A recurrent mammary sarcoma from an 11-year-old, female domestic cat was studied by light and electron microscopy and immunohistochemistry. The tumor consisted of interlacing bands of spindle cells with elongated blunt-ended nuclei and variable amounts of stroma. Multinucleated tumor giant cells and mitoses were common. Ultrastructurally, tumor cells had abundant rough endoplasmic reticulum with dilated cisternae, a prominent Golgi complex, frequent mitochondria, bundles of intracytoplasmic filaments with focal densities, and discontinuous basal lamina-like material and cell junctions. These findings suggest that myofibroblast-like cells were the predominant type of tumor cell. Failure to demonstrate immunoreactivity for cytokeratins attested to the non-epithelial origin of these neoplastic cells. Uniform immunoreactivity with anti-vimentin antibodies and specific labelling of some tumor cells with antiserum to actin are compatible with an origin of this tumor from modified fibroblasts (i.e., myofibroblast-like cells). Tumors composed largely of myofibroblasts may be unique and warrant separate classification from other types of fibroblastic tumors in animals.

Animals↗
PubMed1985

AA-amyloidosis in dogs: partial amino acid sequence of protein AA and immunohistochemical cross-reactivity with human and cow AA-amyloid.

Protein AA was purified from the kidneys of dogs with spontaneous reactive amyloidosis. The protein had a blocked N-terminal. Sequence analysis of a peptide obtained after cyanogen bromide cleavage revealed an amino acid sequence corresponding to positions 24-42 of human AA. This region showed a strong homology to protein AA of other species. Antiserum to both human and dog protein AA reacted immunohistochemically with AA amyloid of human, dog and cow origin.

Amino Acid Sequence↗
PubMed1985

High dose intravenous glucose tolerance test and serum insulin and glucagon levels in diabetic and non-diabetic cats: relationships to insular amyloidosis.

The high dose intravenous glucose tolerance test and concurrent immunoreactive serum insulin and glucagon levels were measured and the results related to the presence or absence of pancreatic insular amyloid in 16 cats, seven of which were known to be diabetic. Control values for all parameters were established using seven additional clinicopathologically normal cats. Nine of the 16 cats had normal fasting blood glucose levels (less than 120 mg/dl) and impaired glucose tolerance. These cats had attenuated (3/9) or normal (6/9) 0 to 5 minute glucose-stimulated insulin secretion, rising 45 to 60 minute insulin secretion (7/9), low mean insulin/glucose ratio, and normal mean serum glucagon. Three of the nine cats with impaired glucose tolerance had insular amyloidosis. These three cats had significantly higher mean blood glucose levels during the glucose tolerance test than did cats with impaired glucose tolerance and no insular amyloid deposits. Also, these three cats accounted for three of the four longest glucose disappearance one-half times (T1/2S), three of the four lowest glucose disappearance coefficients, and three of the four lowest 0 to 5 minute insulin responses. The seven diabetic cats (fasting blood glucose levels greater than 120 mg/dl) had either low to low normal (6/7) or above normal (1/7) fasting insulin levels, no insulin response to intravenous glucose stimulation (6/7), and elevated mean serum glucagon levels. Insular amyloid was present in six of the seven diabetic cats. Three diabetic cats with marked insular amyloid deposits had glucose disappearance T1/2 and K (coefficient) values, serum insulin levels, serum glucagon levels, and insulin/glucose ratios which were not significantly different from the other three diabetic cats with slight to moderate insular amyloidosis. These results confirm a strong association between the occurrence, but not the extent of insular amyloidosis and diabetes mellitus in adult diabetic cats, although amyloid replacement of pancreatic islets does not appear to be the primary diabetogenic event. Rather, these results appear to be consistent with our hypothesis that insular amyloid deposition is a morphologic marker of primary B-cell dysfunction that is basic to the pathogenesis of the diabetic condition, and is reflected clinically by impaired glucose tolerance.

Amyloidosis↗
PubMed1985

Feline insular amyloid: immunohistochemical and immunochemical evidence that the amyloid is insulin-related.

Utilizing islet amyloid-laden pancreatic tissues from six diabetic cats, we demonstrated substantial immunoreactivity (peroxidase-antiperoxidase technique) of the islet amyloid with antiserum to a B chain-rich insulin fraction, but no reactivity with antisera to insulin, glucagon, or somatostatin. Islet amyloid was purified from two cats and a protein unique to the diabetic and islet amyloid-laden cats was separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Immunoreactivity of this protein with antiserum to the B chain-rich insulin fraction was also shown by immunoblotting. Attempts to obtain the amino acid composition of the purified unique protein (represented by a single 25,000 dalton band on gel electrophoresis) were not successful because the amount of protein was too small. These results provide important additional evidence that an insulin-related protein is involved in the formation of islet amyloid. Our study also shows that the diabetic cat provides several advantages for the continued study of the etiopathogenic relationship of islet amyloid and diabetes mellitus.

Amino Acids↗
PubMed1985

Pancreatic ganglioneuronal amyloid. Occurrence in diabetic cats with islet amyloidosis.

Amyloid in pancreatic ganglia and nerves (ganglioneuronal amyloid) was demonstrated in 4 of 8 diabetic cats with islet amyloid deposits. Eighteen nondiabetic cats (including 4 with islet amyloid) did not have detectable amyloid in pancreatic nerves or ganglia. Ganglioneuronal amyloid had staining characteristics identical to those previously reported for islet amyloid, including 1) congophilia, 2) resistance to oxidation by KMnO4, 3) immunoreactivity (PAP technique) with antiserum to a B-chain-rich insulin fraction, and 4) no reactivity with antisera to insulin, glucagon, or somatostatin. Nonneuronal cells with insulin, glucagon, and somatostatin immunoreactivity were seen in many pancreatic ganglia and nerves; and in a few instances, B cells were found near ganglioneuronal amyloid deposits. The premise that these ganglioneuronal amyloid deposits (like islet amyloid) are insulin-related is supported by their immunoreactivity with antiserum to B-chain-rich insulin and the demonstration of B cells in pancreatic ganglia and nerves.

Amyloid↗
PubMed1985

Systemic amyloidosis: a review with emphasis on pathogenesis.

Our knowledge about the composition of the deposits in amyloidosis has increased considerably during the last decade. Three different protein groups have been shown to form fibrils in systemic amyloidosis, namely monoclonal immunoglobulin light chains in primary and myeloma-associated amyloidosis, protein AA in secondary amyloidosis and prealbumin in the familial and senile forms of systemic amyloidosis. This review deals with known and postulated pathogenetic mechanisms involved in the creation of fibrils from these proteins.

Aging↗
PubMed1984

Amyloidosis in a case of canine systemic lupus erythematosus.

Concurrent systemic lupus erythematosus (SLE) and amyloidosis (renal and splenic) are reported in a 7-year-old female miniature Schnauzer. Treatment of tissue sections with potassium permanganate and dilute sulphuric acid prior to staining with Congo red indicated that the amyloid in this case is composed of AA protein (i.e. reactive systemic amyloid or so-called secondary amyloid). The rare association of amyloidosis and SLE, in both man and the dog, and the association with granulomatous pneumonia and leukopenia in this case are discussed.

Amyloidosis↗
PubMed1984

Progesterone receptors in feline mammary adenocarcinomas.

Estradiol and progesterone receptors were measured in tumor cytosols from 3 intact and 4 neutered female cats with spontaneously occurring mammary adenocarcinomas. Serum from 2 of the intact cats which had been in estrus 4 and 4 to 6 weeks before tumor excision contained progesterone concentrations of 16.2 and 2.2 ng/ml, respectively; serum progesterone in the other cats was less than 2 ng/ml. Estradiol receptors were not detected in any cytosols. Progesterone receptors were detected in all of the cytosols, in concentrations ranging from 4.0 to 11.7 (mean = 7.2) fmol/mg of protein. Scatchard plot analysis of tumor cytosol from an 8th cat with mammary adenocarcinoma revealed presence of high affinity progesterone binding with a dissociation constant (Kd) of 3.47 nM. Tumor receptor content could not be correlated with stage of the estrous cycle nor with whether the cat was intact or neutered.

Adenocarcinoma↗
PubMed1983

Ultrastructure of feline mammary hypertrophy.

The ultrastructure of feline mammary hypertrophy was studied in a five-month-old female which had aborted recently, a ten-year-old female which was one month postestrus, and a four-year-old progestin-treated neutered male. Morphologic comparisons were made to normal mammary tissue from a one-year-old female cat. Hypertrophied mammary tissue had the same cell types and spatial relationships as did the normal gland. Major differences included a more highly developed duct system composed of metabolically active cells which often were arranged in multiple cell layers, and periductular stroma with increased fibroblasts and vascularization. Hypertrophied epithelial cells were characterized generally by smooth-contoured nuclear membranes, more evenly dispersed heterochromatin, prominent nucleoli, increased polyribosomes, and elongated mitochondria. Secretory activity was developed significantly only in the cat that had aborted recently. Modifications in myoepithelial cells included: more evenly dispersed nuclear heterochromatin, thicker bundles of cytoplasmic filaments, more straight plasma membranes along the basal lamina, and elongated hemidesmosomes. Multilayering of the basal lamina was accentuated. Stromal fibroblasts had nuclear heterochromatin distributed similarly to that of epithelial and myoepithelial cells, and increased rough endoplasmic reticulum. Myoepithelial cells did not contribute to the increased stromal cellularity. No significant ultrastructural differences were noted between mammary hypertrophy in young, old, and progestin-treated cats.

Abortion, Veterinary↗
PubMed1982

Unusual vascular findings in transplanted kidneys.

Of 189 unsuccessful renal transplant cases, eight were selected for retrospective analysis because they had been classified histologically as "chronic rejection with marked vascular changes" even though they had been removed less than 60 days after transplantation. Review of these cases revealed that only one of the eight transplants had postoperative function and that this transplant had only marginal functions. All eight kidneys had intimal damage that was unlike the usual lesions of rejection. Five kidneys showed evidence of thrombosis with recanalization, and five had what appeared to be a double layer of the intima. The findings in eight cases suggest that severe intimal damage occurred within 60 days of implantation and may not represent the usual rejection processes; it may reflect, in part, damage to the intima prior to or during implantation.

Adult↗
PubMed1981

Feline insular amyloid: histochemical distinction from secondary systemic amyloid.

Amyloid in islets of Langerhans from 48 domestic cats, one human, one non-human primate, and one raccoon was compared with secondary systemic amyloid from three domestic cats, one dog, one human, and one cow to determine affinity for Congo red dye after treatment of paraffin-embedded tissue sections with potassium permanganate and dilute sulfuric acid. Insular amyloid from all six species was resistant to pretreatment with potassium permanganate, i.e., affinity for Congo red was retained, whereas secondary systemic amyloid from all species was sensitive to the potassium permanganate pretreatment. Other stains did not distinguish between insular and secondary systemic amyloid. The potassium permanganate-Congo red staining procedure thus can be used to differentiate insular from secondary systemic amyloid in the cat and other species. The results also indicate that insular amyloid and secondary systemic amyloid are of different chemical composition and pathogenesis.

Adrenal Glands↗
PubMed1981

Feline insular amyloid: incidence in adult cats with no clinicopathologic evidence of overt diabetes mellitus.

Pancreatic tissues from 93 adult domestic cats with no clinicopathologic evidence of overt diabetes mellitus were examined for islet amyloid. Amyloid deposits were found in the pancreatic islets of 44 cats. Approximately one-third of these deposits were not seen with HE, but subsequently were identified with Congo red stain. The proportion of islets with amyloid, the intra-islet location of amyloid, and the amount of amyloid in individual islets also were characterized. In this select population of adult cats, the presence or absence of islet amyloid was not linked significantly (p = greater than 0.05) to age, breed, sex or primary anatomic diagnosis. Results of this study indicate that: the incidence of islet amyloid in cats is higher than previously recognized; as in man, islet amyloid can occur in cats without concurrent overt diabetes mellitus; and islet amyloid should not be considered pathognomonic for diabetes mellitus.

Amyloid↗
PubMed1981

Feline insular amyloid: association with diabetes mellitus.

Of 31 domestic cats with diabetes mellitus, 20 (65%) had amyloid deposits in their pancreatic islets (i.e., insular amyloid). The incidence of insular amyloidosis (p = 0.34) was not significantly different between diabetic and age-matched, non-diabetic cats from our previous study. Diabetic cats, however, had a significantly higher mean percentage of islets with amyloid (p = less than .005) and a significantly higher mean percentage of islets with abundant amyloid deposits (p = less than .005) than did non-diabetic cats. These results suggest that insular amyloidosis and diabetes are causally related and are not simply concurrent diseases associated with aging. Although the specific relationship of insular amyloidosis to the pathogenesis of diabetes mellitus was not determined, a functional islet cell abnormality probably precedes the diabetic state and the deposition of insular amyloid.

Amyloidosis↗
PubMed1981

Stress identification for social workers in health care: a preventive approach to burn-out.

The primary goal of this paper is to present a paradigm for identifying specific stresses related to providing social services in health care settings that can then be the basis of a stress management program. The authors review the occupational stress literature, with special emphasis on two frameworks: James House' conceptual paradigm of the interactive perspective of stress and John Adams' typologies for the assessment of stress. The social work literature is also reviewed for the possible stressors specific to the social work profession. A new framework is presented and discussed that is ecological in nature and provides a basis for future social work stress research in health care.

Hospitals↗