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Biomedical subjects

A B Johnson

Publications and source records attributed to A B Johnson.

At least 73 records · Page 4Linked to original sources
PubMed1982

Abomasal protein infusions for growing steers fed corn grain rations.

Casein was abomasally infused into five growing 226-kg steers consuming a urea-supplemented corn grain diet ad libitum. Infusate solutions in the 5 x 5 Latin square arrangement of treatments contained 0, 20, 40, 80 and 120 g casein made isocaloric and isonitrogenous by the addition of dextrose and urea. Feed intake averaged 5.4 kg dry matter daily and was not altered significantly by abomasal infusions. Apparent digestibility of N decreased from 71.7 to 66.8% as level of casein infusion increased. N retentions (NR) were 40.5, 35.5, 42.8, 35.1 and 32.7 g/d at the five levels of infusion, respectively. A second study was conducted to determine whether level of feed intake influenced the benefit seen from postruminal protein supplementation. Four steers (306 kg) ate ad libitum or were limit-fed (2.5 kg/d) a 1% urea-supplemented corn grain diet in a 4 x 4 Latin square design. These steers were abomasally infused with 120 g casein or an isocaloric, isonitrogenous dextrose-urea mixture. Daily ad libitum feed intake averaged 4.7 kg and was not altered significantly by infusion composition. NR tended to increase with casein infusion at both levels of intake, but, as a percentage, the increase tended to be greater with limit feeding (43 vs 20%). To determine whether supplemental abomasal urea might be beneficial, a third trial was conducted with four 313 kg steers consuming the same diet ad libitum in a crossover design. Infusates consisted of 120 g dextrose or 120 g dextrose plus 42.6 g urea/d. Daily feed intakes were 4.5 and 4.8 kg/d for the steers given the dextrose and the dextrose plus urea infusions, respectively. NR tended to increase with urea infusion (20.9 vs 29.7 g/d). Results suggest that energy, total N or other nutrients, but not postruminal amino acids, limited N balance of young growing steers fed a urea-supplemented, cracked corn diet and gaining weight at .9 kg daily.

Animals↗
PubMed1981

A marker for oligodendrocytes and its relation to myelinogenesis: an immunocytochemical study with experimental allergic encephalomyelitis serum and C.N.S. cultures.

To investigate a possible marker for oligodendrocytes and its relation to myelinogenesis, experimental allergic encephalomyelitis (EAE) serum has been used to study C.N.S. cultures from the time of explantation to maturity at 26 days in vitro (DIV). Cultures of foetal mouse spinal cord were exposed for 1 h to heated (complement-inactivated), rabbit anti-bovine white matter (WM-EAE) or control serum, fixed and processed by an immunoperoxidase technique for demonstrating bound immunoglobulin (Ig) by light and electron microscopy. From 5 to 26 DIV, cells morphologically identical to oligodendrocytes displayed binding of Ig to the plasmalemma of the cell body and its processes. At 5 DIV, immunoreactive oligodendrocytes had a large nucleus and nucleolus, prominent Golgi apparatus, and microtubules but no filaments. Occasionally a centriole was present, suggesting an early stage of differentiation. In myelinated cultures (from 11-12 DIV onwards), reaction product was present on the oligodendroglial outer plasmalemma apposed to myelin and along the outer loop. Sometimes it extended into the external mesaxon, outer layer of myelin, inner mesaxon and periaxonal space. No other structures were reactive, and oligodendroglia did not bind control Ig. These findings indicate that WM-EAE serum can be used as a marker for oligodendrocytes in cultures from 5 DIV onwards. The findings that oligodendrocytes acquire the antigen(s) prior to myelination and that the antigen(s) is localized on the plasmalemma of the inner and outer loops of actively myelinating oligodendroglial processes suggest that the antigen(s) may have a role in oligodendrocyte maturation and myelinogenesis. The antigen(s) involved is not yet established, but it is probably not myelin basic protein. This marker should prove useful in studies of C.N.S. development and the demyelinating diseases.

Animals↗
PubMed1981

Experimental allergic encephalomyelitis. Characterization of serum factors causing demyelination and swelling of myelin.

Serum factors in rabbits with white matter-induced experimental allergic encephalomyelitis (WM-EAE) were studied with respect to their role in demyelination in vitro in organotypic central nervous system (CNS) tissue cultures and in vivo in the myelinated retina of the rabbit eye. By absorption with staphylococcal protein A, IgG was quantitatively separated from the other serum proteins. No IgG was demonstrable in the absorbed IgG-depleted sera by Ouchterlony double diffusion, immunoelectrophoresis and SDS-polyacrylamide gel electrophoresis. Both the IgG-depleted WM-EAE sera and the IgG fractions had complement-dependent demyelinating activity on CNS cultures, and both contained immunoglobulin binding to myelin and oligodendroglia of the cultures, as demonstrated by an immunoperoxidase technique. However, only the purified IgG fractions in the absence of complement induced swelling of myelin and proliferation of oligodendroglial processes with redundant myelin in tissue cultures. The IgG-depleted complement-inactivated WM-EAE sera produced no morphological changes. In the rabbit eye model, antibody-dependent cell-mediated demyelination was observed only with the IgG fractions but not with the IgG-depleted EAE sera. No oligodendroglial proliferation occurred. These studies demonstrate for the first time that in CNS cultures, non-IgG immunoglobulins as well as IgG mediate complement-dependent demyelination and that these bind to myelin and oligodendrocytes, whereas only IgG causes myelin swelling and oligodendrocyte proliferation.

Animals↗
PubMed1981

Demyelination in vitro. Absorption studies demonstrate that galactocerebroside is a major target.

Myelinated cultures of mouse spinal cord have been exposed to sera raised in rabbits against whole white matter (anti-WM), myelin basic protein (anti-MBP) and galactocerebroside (anti-GC), the major glycolipid of CNS myelin, to determine which factor in central nervous system (CNS) tissue in vitro is the target of serum demyelinating and myelin swelling antibodies. The sera were tested by radioimmunoassay for activity against MBP and against GC and were also specifically absorbed with MBP, GC and control antigens. Studies were also performed with and without active complement. The findings show that demyelination and myelin swelling in vitro are caused by antibodies against GC and not against MBP. Ultrastructurally, the effects of anti-WM and anti-GC sera with and without complement were indistinguishable. This study demonstrates that GC is a major target in antibody-mediated demyelination.

Absorption↗
PubMed1980

Granulofilamentous inclusions in a meningioma.

We have studied the histology, immunocytochemistry, and ultrastructure of a syncytial meningioma which contained the unusual feature of large eosinophilic intracytoplasmic inclusions. Electron microscopic examination revealed that these bodies were granular, osmiophilic masses, closely associated with cytoplasmic filaments of intermediate size. Desmosomal junctions with a somewhat abnormal morphology were also observed, and the possible relationship between the inclusions and the dense components of desmosomes is discussed. This tumor is also compared to other tumors of the central nervous system with hyaline and granulofilamentous inclusions.

Antigens, Neoplasm↗
PubMed1980

Breast carcinoma-associated antigen. An immunocytochemical study.

An antiserum raised against a high molecular weight fraction of a medullary carcinoma of the breast was used to study breast carcinomas by means of an indirect unlabeled antibody peroxidase-antiperoxidase (PAP) technic. Strong cytoplasmic staining was demonstrated in all of 30 breast cancers tested and in one of three intraductal papillomas. Weak cytoplasmic staining was detected in four of nine fibroadenomas, two malignant melanomas, and one of six carcinomas of the colon. No cytoplasmic staining was seen in 24 other specimens of breast tissue, including 12 specimens from patients who had fibrocystic disease and five fibroadenomas, or in 17 extramammary malignant tumors. The antiserum appears to identify a breast carcinopma-associated antigen.

Antigens, Neoplasm↗
PubMed1979

Effects of anti-white matter serum on myelin and lipid synthesis in brain prisms.

Tissue prisms prepared by choping whole mouse brain maintained respiratory capacity and ultrastructural integrity of 3 h in vitro. Normal rabbit serum (ca. 25%) caused no morphological change but inhibited the synthesis of galactolipids by the prisms. Heating the serum abolished the inhibition. Complement containing anti-white matter rabbit serum destroyed myelin and inhibited galactolipid synthesis to a greater degree than did normal serum. Structures other than myelin were unaffected by the antiserum. Incubation in the presence of heated anti-white matter serum eliminated the myelin destruction but resulted in specific morphological changes characterized by the doubling of the myelin lamellae at the intraperiod line. Immunoperoxidase studies suggest specific binding of immunoglobulin to components of myelin located at the intraperiod lone. These changes were similar to those found in organotypic cultures. Heated antiserum did not inhibit galactolipid synthesis but addition of complement (normal guinea pig serum) to the heated antiserum restored only that portion of the inhibition which exceeded that caused by normal serum. Heat labile factors in normal rabbit serum which inhibit myelin lipid synthesis in the prisms must be corrected for in studies in which the heating of serum is used to demonstrate that the effect is complement dependent. The prism system is simpler than that of organotypic cultures and may be useful in the study of myelinotoxic factors.

Animals↗
PubMed1979

Evidence that Alzheimer neurofibrillary tangles originate from neurotubules.

Antiserum against normal human neurotubules purified by in-vitro assembly precipitated both neurotubules and a polypeptide isolated from Alzheimer neurofibrillary tangles in Ouchterlony double-diffusion tests. The antiserum specifically labelled neurofibrillary tangles, in isolated neurons by immunofluorescence and in tissue sections by the peroxidase-antiperoxidase technique. These results indicate that neurofibrillary tangles in Alzheimer's disease probably originate from neurotubules.

Adult↗
PubMed1979

Alzheimer neurofibrillary tangles: antiserum and immunohistological staining.

A 50,000-dalton polypeptide has been purified from fractions enriched with neurofibrillary tangles of paired helical filaments from human autopsy specimens of Alzheimer disease and senile dementia of the Alzheimer type. An antiserum to this polypeptide was raised in a rabbit. This antiserum formed an immunoprecipitation line with the purified antigen and with human neurotubules in ouchterlony double-diffusion plates. The reactivity of the anti-paired helical filament protein serum with neurofibrillary tangles was studied by immunofluorescence on cryostat sections of hippocampus from Alzheimer autopsy tissue and by the peroxidase-antiperoxidase technique on paraffin sections of an Alzheimer brain biopsy. The tangles were stained with the antiserum in both systems. Preimmune rabbit serum and unrelated hyperimmune sera, used as controls, did not stain the tangles. These results show that the 50,000-dalton polypeptide purified from the neurofibrillary tangle-enriched fractions is a constituent of Alzheimer neurofibrillary tangles and, perhaps, of the paired helical filaments of which the tangles are composed.

Alzheimer Disease↗
PubMed1979

Luteinizing hormone-releasing hormone (LH-RH) neurons in cultures of fetal rat hypothalamus.

Hypothalamic fragments from 21-day-old fetal rats were cultured in Maximow double-coverslip assemblies for 1 to 2 months. Neurons containing LH-RH were demonstrated immunohistochemically using an antiserum to LH-RH (Dermody; 1:500--1:4,000). LH-RH was demonstrable only in neuronal perikarya (8--13 micrometer) and in small (less than 1 micrometer) round structures nearby, primarily in explants of the median eminence-arcuate nucleus region. Reactive neurons were not found in explants of the preoptic area and could not be demonstrated in fetal hypothalami at the time of explantation. The presence of mature-looking LH-RH containing neurons in these cultures suggests that this tissue culture system can be used for the study of hypothalamic development.

Animals↗
PubMed1979

Immunocytochemical localization of hepatic legandin and Z protein utilizing frozen sections for light and electron microscopy.

Ligandin (glutathione-s-transferase) and Z protein are soluble hepatocellular proteins that are involved in the transfer of organic ions, including bilirubin and some hormones and carcinogens from the plasma to the liver. The intracellular distribution of ligandin and Z protein was studied by applying the peroxidase-antiperoxidase procedure of L. A. Sternberger (Immunocytochemistry, Prentice Hall Inc., 1974) to paraffin sections and free-floating 10-micrometers frozen sections that were processed for both light and electron microscopy. Ligandin and Z protein were localized to the cytosol of hepatocytes in association with smooth endoplasmic reticulum (SER), but no reaction product was present between cisternae of rough endoplasmic reticulum. Penetration of reagents was enhanced in 10-micrometers frozen sections and the preservation of subcellular structures was equivalent to thicker, unfrozen sections.

Animals↗
PubMed1977

Commercial horseradish peroxidase degrades myelin encephalitogenic protein during coupling for immunohistochemical studies.

Conjugates of myelin encephalitogenic basic protein (EP) and commercial horseradish peroxidase (HRP) have been used for immunohistochemical demonstrations of anti-EP antibody in animals with experimental allergic encephalomyelitis. We performed gel electrophoresis studies on EP-HRP conjugates prepared with glutaraldehyde and on mixtures of EP and HRP incubated without glutaraldehyde. The results show that under conditions of one-and two-step coupling HRP causes rapid loss of the native EP band, apparently due to EP degradation. The EP-HRP mixtures are not encephalitogenic in rabbits, or encephalitogenic activity is lost during processing. The immunohistochemical reactivity of conjugates, however, signals some preservation of antibody-combining sites. The mechanism of the HRP effect on EP is unknown. The possibilities of a contaminating proteinase or direct peroxidatic attack are suggested. Until this action of HRP can be overcome, the effect of coupling procedures on the biological activities of EP will be difficult to assess, and EP-HRP conjugates cannot be expected to reveal sites that may bind encephalitogenic portions of the EP molecule.

Animals↗
PubMed1976

Mucolipidosis IV. Clinical, ultrastructural, histochemical, and chemical studies of a case, including a brain biopsy.

A 7-year-old Ashkenazi Jewish boy with normal early development started to regress at 8 months of age and made no further developmental progress. Corneal clouding was noted at age 10 months. Corneal and conjunctival biopsy at 14 months, cerebral biopsy at 24 months, and fibroblast cultures at 32 months showed lysosomal inclusions, suggesting the storage of lipid-like and mucopolysaccharide-like material. In the brain, dense fluorescent inclusions resembled those in ceroid-lipofuscinosis. Total ganglioside content of white matter was raised, but the pattern was normal. The level of nonlipid hexosamine in the brain was normal. The cornea and conjunctiva contained electronlucent vacuoles resembling those in the mucopolysaccharidoses. Cornea, brain, and lymphocytes contained concentric membranous lamellar structures reminiscent of those in the gangliosidoses. The clinical picture and ultrastructural findings support the impression that this case belongs to a new variant of the mucolipidoses, mucolipidosis IV.

Cerebral Cortex↗