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Biomedical subjects

G C Johnson

Publications and source records attributed to G C Johnson.

At least 55 records · Page 3Linked to original sources

Loss of absorptive capacity for sodium and chloride in the colon causes diarrhoea in Potomac horse fever.

Ehrlichia risticii, an obligate intracellular bacterium in the family Rickettsiaceae, causes Potomac horse fever which is often associated with severe watery diarrhoea. The mechanism of the diarrhoea is unknown. The aim of this study was to determine whether sodium and chloride transport, morphology and cyclic adenosine 3', 5'-monophosphate (cyclic AMP) content of colonic mucosa was altered in E risticii-infected horses. Mucosa-submucosa sheets from the large and small colon of nine infected and seven to nine uninfected horses were set up in Ussing chambers for measurement of short-circuit current and transepithelial 22Na and 36Cl fluxes. Uninfected tissues absorbed both sodium and chloride whereas absorption of sodium and chloride was abolished in infected tissues. Bethanechol and histamine evoked a concentration-dependent increase in short-circuit current in both groups, but the responses were attenuated at all concentrations in infected horses. Slight focal degeneration of colonic epithelial cells and loss of microvilli from glandular epithelial cells occurred in infected horses. There was a significant increase in cyclic AMP content in colonic mucosa of infected animals. The results suggest that E risticii infection induces focal microscopic degeneration of epithelial cells and an increase in intracellular cyclic AMP in colonic mucosa. These alterations are associated with malabsorption of sodium and chloride and could cause diarrhoea.

Animals↗

Electroconvulsive therapy and the chronic use of pseudocholinesterase-inhibitor (echothiophate iodide) eye drops for glaucoma. A case report.

A case is presented in which a patient who required treatment with electroconvulsive therapy had a history of being treated with pseudocholinesterase-inhibitor eye drops (echothiophate iodide) for glaucoma. As treatment with this antiglaucoma agent contraindicated the use of succinylcholine for a minimum of 10-14 days, the short-acting nondepolarizing agent atracurium was employed instead. The anesthetic management of this patient is described as a guide for clinicians facing similar clinical situations.

Aged↗

Thoracolumbar vertebral osteochondroma in a young dog.

Osteosarcoma was diagnosed in a 7-month-old female German Shepherd Dog with hind limb paresis. Radiography revealed a circumscribed calcified mass in the dorsal vertebral lamina at T13-L1 resulting in extradural compression of the spinal cord. Surgical excision of the mass resulted in gradual return to normal neurologic function. Four weeks after surgery, the dog became severely atactic after rolling onto its back. A chip fracture of T13 was identified, and the dog was euthanatized at the owners' request.

Animals↗

Inflammatory central nervous system disease in lupus-prone MRL/lpr mice: comparative histologic and immunohistochemical findings.

The brains of pathogen-free autoimmune MRL/lpr, NZBWF1 and NZB mice were examined for central nervous system (CNS) inflammation in premoribund 8-week-old animals and at ages when active systemic lupus erythematosus (SLE) was present. CNS inflammation was observed only in MRL/lpr mice. Immunohistochemical studies of brains from young MRL/lpr mice found that infiltrates were composed primarily of CD4+ cells. Older MRL/lpr mice (22 and 26 weeks of age) had CD4+ cells predominantly, but CD8+ and B220+ cells were also present. Perivascular leakage of IgG was a prominent and unexpected finding in the MRL/lpr model. Congenic MRL/+ mice with late-onset autoimmunity had no inflammatory cells in brain tissue, and there was no perivascular staining with IgG or albumin. Our findings suggest that MRL/lpr mice are a useful model for studies of lupus-associated CNS inflammatory disease, and perivascular leakage may be a primary mechanism for entry of IgG into the brain.

Animals↗

Calcium and acidosis in renal hypoxia.

The effects of lowering extracellular calcium concentration on hypoxic injury in the thick ascending limb of Henle (TAL) were studied in the isolated perfused rat kidney. At standard conditions of pH 7.4 and total perfusate calcium 1.9 mM, widespread TAL necrosis results from the combined effects of low medullary O2 delivery and the demands of solute transport activity. Reducing calcium to 0.5 or 0.1 mM, effectively prevented TAL membrane fragmentation. This cytoprotection was not accompanied by improved O2 delivery or by any consistent effects on renal physiology (glomerular filtration rate, sodium reabsorption, free water clearance or O2 consumption) that might have suggested that the mechanism was reduced O2 demand. In addition, the medullary ATP depletion which characteristically precedes TAL necrosis was not reversed. Finally, reduced perfusate calcium also markedly decreased TAL damage in an alternative model of hypoxia-like injury caused by a respiratory uncoupler. In aggregate, these findings indicate that reducing extracellular calcium does not prevent hypoxia itself, but rather disrupts the mechanism of its effects on cell integrity. The relationship of H+ and Ca2+ in the pathogenesis of hypoxic TAL injury was also studied. Lowering media pH to 7.0 reduced TAL damage but this cytoprotection was overcome by increasing media calcium concentration. Furthermore, with more severe acidosis (media pH 6.5 or 6.0), progressively greater perfusate calcium concentrations were required to reproduce severe TAL damage. These results indicate that extracellular calcium promotes the development of hypoxic TAL necrosis and that the cytoprotective effect of acidosis in hypoxia may be to counteract the calcium-dependent mechanism of injury.

Acidosis↗

Phosphorylated variant of bovine prolactin.

Bovine pituitary explants and cell cultures were incubated with [32P]orthophosphate. Extracts were prepared from the explants and analyzed by sodium dodecyl sulfate-containing acrylamide gel electrophoresis and autoradiography revealing a phosphoprotein that co-migrated with authentic bovine prolactin. Clonal antibodies to bovine prolactin were produced, purified and used to prepare affinity columns. Extracts of [32P]orthophosphate-labeled explants and cells or media were applied to prolactin affinity columns and a radiolabeled protein was eluted with a pH 2.8 wash. The eluted protein was identified as prolactin by co-migration with standard on gel electrophoresis and by amino acid analysis. Treatment of immunoaffinity-purified pituitary prolactin with alkaline phosphatase reduced the phosphate associated with prolactin in a time-dependent manner, indicating a covalent phosphate linkage. Autoradiography of gels revealed prolactin from explants, cells and their associated media to be a phosphoprotein. A phosphorylated variant of bovine prolactin is synthesized and secreted in both explant and cell cultures.

Animals↗

Extramedullary plasmacytoma and immunoglobulin-associated amyloidosis in a cat.

Extramedullary plasmacytoma with immunoglobulin-associated amyloidosis was diagnosed in a 10-year-old cat. The primary tumor was a large, circumferential mass of the right tarsal region. Metastasis developed in the regional lymph nodes, spleen, and liver. Permanganate-resistant amyloid deposits were associated with plasma cells in the primary and metastatic tumors. Treatment with prednisone and melphalan had little effect on the progression of the disease, and the cat died four weeks later.

Amyloidosis↗

Neuroradiographic diagnosis and surgical repair of tethered cord syndrome in an English bulldog with spina bifida and myeloschisis.

A 3-month-old English Bulldog had excretory incontinence and sensory deficits in the distribution of pudendal nerves. Noncontrast radiography, myelography, and computed tomography revealed spina bifida beginning at L7, an expanded subarachnoid space caudal to L7, and a taut, thick filum terminale. Microsurgical exploration of the lumbosacral spine confirmed the presence of a tethered cord, and the filum terminale was transected. The spinal cord immediately migrated cranially about 1 cm. Although some sensory improvement was evident during a 2-week postoperative period, the dog was euthanatized. Postmortem examination confirmed spina bifida and atrophy of sacral nerve roots and perineal muscles, thoracic hemivertebrae, and hydrocephalus.

Animals↗

Adenine nucleotides, transport activity and hypoxic necrosis in the thick ascending limb of Henle.

Thick ascending limb of Henle (TAL) necrosis in the isolated perfused kidney is an important model of renal hypoxia, but physiologic and metabolic correlation with this morphologic damage has been inadequate. More precise estimation of TAL adenine nucleotides in this model was obtained in the present study by high pressure liquid chromatography analysis of biopsy samples from the inner stripe of the outer medulla during perfusion. The inner stripe, which is the zone where TAL are concentrated, showed ATP depletion and low adenylate energy charge (AEC) early in perfusion prior to the appearance of TAL necrosis. Free water clearance (CH2O) was used as an estimate of TAL transport activity; the CH2O observed during 90 minute perfusions was found to be predictive of the extent of TAL necrosis in each experiment. The results support the idea that there is significant medullary hypoxia in the isolated perfused kidney and that TAL solute transport is a determinant of injury in this model. In further studies, the effects of ouabain (10(-3) M), furosemide (10(-4) M) or acidosis (pH 7.0 rather than the usual pH 7.4) on TAL transport activity and adenine nucleotide levels were compared. All three maneuvers have been shown previously to reduce TAL injury in the isolated perfused kidney. Addition of ouabain or furosemide reduced CH2O and TAL necrosis in parallel while acidosis had no effect on CH2O during perfusion. Both ouabain and furosemide attenuated ATP depletion and resulted in higher AEC while acidosis had no effect on these indices of cellular hypoxia. Therefore, the mechanism of cytoprotection by acidosis appears distinct from that of ouabain or furosemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

The health fraud battle. Education is the best defense.

Despite the regulatory and educational efforts of the Food and Drug Administration and other agencies and organizations, large numbers of American consumers continue to be fooled by unsubstantiated "miracle cure" claims made by manufacturers of fraudulent medical products. Physicians who are familiar with the language of health fraud advertising and product labels may be able to help patients avoid unnecessary expense, false hope, and physical and emotional harm.

Advertising↗

Leucogyrophana pinastri, a wood decay fungus as a probable cause of an extrinsic allergic alveolitis syndrome.

Two patients were suspected of having extrinsic allergic alveolitis due to exposure to an agent in their home environment. On inspection of their houses, fungal decay was evident in the floorboards, and fungal spores were found deposited on many surfaces. The decay fungus was later identified as Leucogyrophana pinastri. Using an extract of the fruiting bodies and mycelium of this fungus, precipitating antibodies were identified in the sera of both patients. Based on the known exposure by the two patients to these small spores, the absence of a likely alternative allergen, the similarity between these two cases, and the positive precipitin test results, L. pinastri was considered to be the most likely cause of extrinsic allergic alveolitis in our cases.

Adolescent↗

Ultrastructure of junctional epidermolysis bullosa in Belgian foals.

Ultrastructural examination of a mechanobullous disease of probable hereditary nature in Belgian foals, confirmed light microscopic findings that separation of the dermo-epidermal junction occurred through the lamina lucida of the basement membrane, leaving the intact lamina densa adherent to the dermis and the plasmalemma of the basal epithelial cells intact. The location of the cleft and the presence of small hemidesmosomes in adjacent intact skin are additional characteristics which make this condition similar to junctional epidermolysis bullosa of man.

Animals↗

Production of immunoglobulin G and increased antiviral antibody in cerebrospinal fluid of dogs with delayed-onset canine distemper viral encephalitis.

Sera and cerebrospinal fluid (CSF) from four dogs with delayed-onset canine distemper viral (CDV) encephalitis (old dog encephalitis) were compared with samples from dogs with acute CDV and from recently vaccinated controls. Dogs with old dog encephalitis (ODE) had elevated CSF IgG concentrations (122 micrograms/ml) compared to controls (13 micrograms/ml) without elevated CSF albumin; their CSF IgG index was significantly greater. CSF proteins banding in the alkaline region of isoelectric focusing gels were immunochemically identified as IgG. Detectable viral neutralizing antibody was present in ODE CSF, and formed a larger proportion of IgG in CSF than in serum. Serum samples containing 2 mg IgG bound to all viral polypeptides of both R252 and Onderstepoort CDV isolates by immunoblot analysis. CSF samples of ODE patients bound viral antigens when diluted to contain as little as 5-40 micrograms IgG, while patient serum could be diluted to 40-200 micrograms IgG content compared to serum IgG of 100 micrograms/ml in vaccinated controls. Serial CSF dilutions consistently bound to H and NP polypeptides at the highest dilutions, similar to the binding of serums from recently vaccinated dogs. Thus, dogs with delayed-onset CDV encephalitis have elevated concentrations of CSF IgG, much of which is virus-specific, with an antigen binding pattern similar to that of sera of recently immunized dogs.

Acute Disease↗