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Biomedical subjects

J M Hall

Publications and source records attributed to J M Hall.

At least 199 records · Page 11Linked to original sources

Effect of pretreatment with local corticosteroids on antibody-forming cells in the eye and draining lymph nodes.

To study the effect of pretreatment of rabbits with locally administered steroids, unilateral subconjunctival injections of 10 mg. triamcinolone suspension were given 10 and 3 days before intracorneal injection of the same eye with bovine gamma globulin. We killed the rabbits 6, 9, 12, 15, and 21 days after the BGG injection, and determined the number of antibody-producing cells in the homolateral lymph nodes, corneas, and uveal tracts. Corticosteroids did not significantly affect the PFC response in the draining lymph nodes, but the number of plaque-forming cells in the corneas and uveal tracts was reduced. Steroid-treated eyes were less inflammed than control eyes. The possible mechanisms for the effect of steroids on the ocular immune response are discussed.

Adrenal Cortex Hormones↗

Changes in the antigenic composition of cultured bovine corneas.

Several immunologic tests were used to compare the soluble antigens of cultured and normal bovine corneas. Results of fluorescent-antibody tests on normal corneas confirmed our earlier observation that the epithelium contained little serum protein, and that stroma and epithelium shared an antigen not found in bovine serum. Immunoelectrophoresis, immunodiffusion, and fluorescent-antibody tests preformed on extracts prepared from normal and cultured corneas indicated that corneas absorbed serum proteins during the incubation period. We also noted that very little intact epithelium remained on corneas cultured in the presence of calf serum. The extract prepared from cultured corneas did not contain the strongly antigenic protein present in extracts of normal cornea or epithelium. The implications of these findings are discussed.

Animals↗

Plate hemolysin test for the rapid screening of toxoplasma antibodies.

A plate hemolysin test was developed to screen serum specimens for the presence of toxoplasma antibodies. When we tested 130 sera by both this test and the standard toxoplasma dye test, we found the plate hemolysin test to be a rapid, sensitive, and economical method for detecting toxoplasma antibodies. In all but one instance it paralleled the dye test. A comparison of the results of testing six sera by the hemolysin, hemagglutination, and dye-test techniques suggested that the hemolytic antibodies were more closely related to hemagglutinating antibodies than to dye-test antibodies. We could not store sheep erythrocytes sensitized with toxoplasma lysate for more than 3 days without altering the sensitivity of the test. Concanavalin A proved to be an effective coupling agent for binding toxoplasma antigens to red-cell membranes, a quality attributed to its affinity for specific polysaccharide-combining sites.

Animals↗

Nonspecific resistance to intraocular infection. I. Elicitation of resistance by Neisseria meningitidis.

Both eyes of rabbits whose right eyes had previously been injected with Neisseria meningitidis were injected with Diplococcus pneumoniae. The pneumococci failed to grow in the right eye of most rabbits challenged 2 and 4 days after the injection of the meningococci, but grew well in all left eyes. The "protective" effect was less pronounced in the rabbits challenged on days 6 and 9 and virtually absent when the interval between the two injections was 14 or 22 days. Pneumococci grew equally well in both eyes of rabbits that had received nitrogen mustard treatment prior to the intravitreal injection of meningococci, indicating a possible role for the polymorphonuclear leukocyte in the protective effect.

Agglutination Tests↗

Selective inhibition of angiotensin pressor responses in the pithed rat by tetraethylthiuram disulphide (disulfiram) and sodium diethyldithiocarbamate (DDC).

1. Pressor responses to sympathetic outflow stimulation, noradrenaline and angiotensin have been recorded in pithed rats.2. Disulfiram (50 mg/kg) and sodium diethyldithiocarbamate (DDC) (5-100 mg/kg) both caused an initial increase in the pressor response to all three procedures followed by a selective inhibition of the angiotensin responses.3. Penicillamine (1-100 mg/kg) and ascorbic acid (1-500 mg/kg) increased the pressor responses to all three procedures without any subsequent blocking action.4. Reserpine (5 mg/kg daily for 3 days) abolished responses to sympathetic outflow stimulation but did not impair angiotensin or noradrenaline responses.5. In reserpinized rats, the initial enhancement of angiotensin responses after disulfiram and sodium diethyldithiocarbamate was absent or reduced and the onset of the subsequent block was accelerated.6. Possible mechanisms for the angiotensin-blocking action of disulfiram and sodium diethyldithiocarbamate are discussed.

Angiotensin II↗

Cellular Response of the Rabbit Eye to Primary Intravitreal Injection of Neisseria meningitidis.

New Zealand White rabbits were injected intravitreally with approximately 2,500 viable or heat-killed meningococci. The rabbits were killed at intervals from 30 min to 14 days after injection. None of the rabbits produced detectable antibodies. Local antibody production by uveal tract, spleen, or preauricular lymph node cells was not demonstrated. Viable organisms were recovered from the vitreous at periods from 30 min to 48 hr after injection. Failure to recover viable organisms could be correlated with the appearance of large numbers of polymorphonuclear neutrophiles (PMN) throughout the vitreous. Animals injected with viable meningococci demonstrated a progressive inflammatory reaction characterized by an early accumulation of PMN in the vitreous, limbus, and conjunctiva. The cellular infiltrate gradually became mononuclear. By the 14th day postinjection only a few residual inflammatory cells remained at the limbus. This extensive cellular response was lacking in recipients of heat-killed organisms. The defense of the rabbit against intraocular introduction of meningococci therefore seems to be predominantly a cellular mechanism.

Journal Article↗