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J F Cahill

Publications and source records attributed to J F Cahill.

10 recordsLinked to original sources
PubMed2001

Cholinergic and noncholinergic septal neurons modulate strategy selection in spatial learning.

Rats solving a simple spatial discrimination task in a plus maze initially employ a place-learning strategy, then switch to a motor response strategy. The hippocampus is required for the use of a place-learning strategy in this task. Rats with 192 IgG-saporin lesions of the medial septum/vertical limb of the diagonal band (MS/VDB), that selectively removed cholinergic neurons projecting to the hippocampus, were significantly facilitated in acquisition of the spatial discrimination, and switched from place to response strategies just as control rats did. Rats with ibotenic acid lesions of the MS/VDB, that produced cell loss in the MS/VDB but little damage to cholinergic neurons, were significantly impaired in acquiring the spatial discrimination and did not reliably employ either a place or response strategy at any point in training. This suggests that the MS/VDB modulates hippocampal involvement in place learning, but that cholinergic MS/VDB neurons are neither necessary nor sufficient for using a place strategy to solve a spatial discrimination.

Acetylcholine↗
PubMed1986

Interactions of a water extract of cotton bract with dog isolated airway smooth muscle.

The inhalation of cotton dust by cotton-mill workers causes byssinosis, a disease characterized by chest tightness and other symptoms indicative of bronchoconstriction. In the present study the dog isolated trachealis smooth muscle preparation was employed to examine the ability of a crude, water extract of cotton bracts (CBE) to (1) cause contractile responses mediated by receptors, (2) modify responses of the tissue to a number of excitatory and inhibitory agents, and (3) alter responsiveness of the preparations to electrical field stimulation mediated by intrinsic cholinergic, excitatory nerves and adrenergic, inhibitory nerves. CBE evoked contraction of the tissues by an action that did not involve muscarinic, histamine, or 5-hydroxytryptamine receptors. The maximum tissue responses to exogenous histamine, 5-hydroxytryptamine, and isoproterenol were enhanced significantly in the presence of CBE, while those to KCl and methacholine were unaffected. The sensitivities (EC50 values) of the tissues to these agents were not, however, altered by CBE. Contractions induced by cholinergic nerve stimulation were increased in the presence of CBE, via a mechanism that appears, at present, to result from a prejunctional facilitation of acetycholine release. Relaxations to adrenergic nerve stimulation were not affected by CBE. Results suggest that, in addition to its direct, contractile activity, CBE can alter indirectly the responsiveness of the tissue to a number of endogenous mediator substances. Intrinsic, cholinergic excitatory nerves may be a target for the acute action of CBE as well.

Animals↗
PubMed1986

Effects of a cotton bract extract on guinea pig isolated airway smooth muscle.

The effects of a water extract of cotton bracts (CBE) on guinea pig isolated trachealis smooth muscle was studied. The ability of CBE to evoke tension responses, to modify tissue reactivity to excitatory and inhibitory agents, and to modify electric field stimulation-induced neurogenic responses was evaluated. CBE caused contraction in low concentrations, which were not mediated by histamine H1-, muscarinic, or 5-hydroxytryptamine (5-HT) receptors, and caused relaxation in high concentrations. In the presence of CBE, the maximum contractile response to 5-HT and the sensitivity to KCl were reduced. The maximum relaxation responses and sensitivities to adenosine and ATP were increased by CBE. In contrast, contractile responses to histamine and methacholine and relaxation responses to isoproterenol were unaffected. Neurogenic cholinergic excitatory responses and neurogenic adrenergic responses did not appear to be affected by CBE. However, the relaxant effect of nonadrenergic inhibitory nerve stimulation was increased in the presence of CBE. These findings differ from previous ones observed in our laboratory for dog isolated trachealis smooth muscle preparations, which indicates that the effects of CBE in isolated airways is species-dependent. Virtually all of the contractile activity of CBE was dialyzable (molecular weight less than 14,000) and retained in ashed samples. Inorganic constituents may contribute to the spasmogenic activity of CBE.

Adenosine↗
PubMed1985

Effects of a two-year inhalation exposure of rats to coal dust and/or diesel exhaust on tension responses of isolated airway smooth muscle.

This study was performed to determine whether chronic inhalation exposure of rats to levels of coal dust (CD) and/or diesel exhaust (DE) similar to those experienced by underground miners affects the pharmacologic characteristics of the animal's airway smooth muscle. Animals were exposed for 2 yr to CD alone (2 mg/m3 of respirable particulates), DE alone (2 mg/m3 of respirable particulates), or CD and DE (CD + DE) in combination (1 mg/m3 CD plus 1 mg/m3 DE). Concentration-response relationships for tension changes induced with acetylcholine, 5-hydroxytryptamine, potassium chloride, and isoproterenol were assessed in vitro on isolated preparations of rat airway smooth muscle (trachealis). Compared with control animals, the maximal contractile responses to acetylcholine of tissues from CD-, DE-, and CD + DE-exposed animals were significantly increased; the effects of CD and DE exposure were additive. The CD + DE exposure, but not the individual treatments, resulted in a significant increase in the maximal relaxation response elicited by isoproterenol; this interaction may have resulted from the addition of, or the synergism between, the nonsignificant effects of CD and DE alone. No treatment altered the sensitivity (EC50 values) of the muscles to the agonists used. The results indicate that chronic exposure to CD, DE, and CD + DE produces differential modifications in the behavior of rat airway smooth muscle. These findings may have some bearing on humans exposed to these substances.

Administration, Intranasal↗
PubMed1981

An unusual cause of neonatal respiratory distress. RDS in a neonate with a neuro-enteric cyst.

A 2.5 kg male infant developed respiratory distress in the neonatal period. A diagnosis of idiopathic hyaline membrane disease was made and he was treated accordingly. At 24 hours of age he required intubation, and the immediate and dramatic improvement in his condition suggested that the original diagnosis was incorrect. Closer examination of the chest X-ray revealed an intrathoracic cyst and abnormal vertebrae. The cyst was removed surgically, and histological examination showed it to be a neuro-endodermal cyst.

Humans↗
PubMed1977

Terminally repeated sequences in the avian sarcoma virus RNA genome.

The initiation of DNA synthesis in vitro by RNA-directed DNA polymerase (deoxynucleosidetriphosphate: DNA deoxynucleotidyltransferase, EC 2.7.7.7) of avian oncornaviruses requires a tRNAtrp primer molecule located close to the 5' end of the viral RNA genome. DNA transcripts, 100 nucleotides in length, initiated on the tRNAtrp primer molecule contain nucleotide sequences complementary to a large (25 nucleotides) RNase T1 oligonucleotide, T-13, located at the 5' terminus of the avian sarcoma virus RNA genome. tRNAtrp-initiated DNA transcripts with a length of about 70 nucleotides contain substantially fewer nucleotide sequences complementary to this 5'-terminal oligonucleotide, suggesting that the tRNAtrp primer associated with the avian sarcoma virus RNA is located approximately 100 nucleotides from the 5' end of the RNA. In addition, we present evidence to demonstrate that DNA transcribed from avian sarcoma virus RNA sequences located at the 3' end, immediately adjacent to the poly(A), contains nucleotide sequences that are complementary to the 5'-terminal T1 oligonucleotide T-13. These data indicate that the 5' end of the viral genome contains nucleotide sequences that are repeated at the 3' end of the genome. We conclude that the avian oncornavirus RNA genome is terminally redundant.

Avian Sarcoma Viruses↗
PubMed1971

Role of Biological Mimicry in the Pathogenesis of Rat Arthritis Induced by Mycoplasma arthritidis.

Complement fixation (CF), immunofluorescence, and agar gel double-diffusion tests were used to demonstrate an antigenic relationship between rat tissues and Mycoplasma arthritidis. Rabbit antisera against six strains of M. arthritidis exhibited positive reactions in the CF test with an ethyl alcohol-saline extract of rat muscle, whereas only 6 of 18 antisera against other Mycoplasma species were positive. With the use of gel diffusion techniques, absorption of various M. arthritidis antigens with antiserum against rat muscle removed at least one precipitin band when the absorbed mycoplasma antigens were reacted against homologous antisera. Rabbit antiserum against M. arthritidis was conjugated with fluorescein isothiocyanate and reacted against frozen sections of muscle tissues of various animals. As controls, unlabeled normal rabbit serum and rabbit anti-M. arthritidis serum were included to determine the specificity of the reaction. Rat, hamster, and mouse skeletal muscle exhibited specific fluorescence, whereas chicken, beef, frog, and turtle muscles exhibited no specific fluorescence. Mice injected at birth with rat lymphocytes were found to be more susceptible to subsequent infection by M. arthritidis than were normal mice or mice injected at birth with mouse lymphocytes. These results indicate the occurrence of a heterogenetic antigen(s) common to M. arthritidis and rat tissues. Preliminary evidence suggests that this heterogenetic antigen(s) may enable the mycoplasmas to become established in their host.

Journal Article↗
PubMed1971

Chronic proliferative arthritis of mice induced by Mycoplasma arthritidis. I. Induction of disease and histopathological characteristics.

Mice injected intravenously with Mycoplasma arthritidis developed a chronic arthritis which persisted through at least 269 days. Rats similarly treated developed an acute short-term infection. The mouse disease was characterized by periods of remission and exacerbation and was proliferative in nature, gradually spreading to adjacent joints. M. arthritidis strain 158 P10 was found to be less arthritogenic for mice than for rats, but further passage of this strain in mice substantially increased its virulence. Unlike rats, mice appeared to be susceptible to a "toxin" of M. arthritidis and they developed a necrotic spreading abscess after subcutaneous administration of the organisms. Histopathological studies revealed that mice varied greatly in the degree of joint inflammation, destruction, and repair. The disease was characterized by (i) an initial acute phase with infiltration of the articular and periarticular tissues with polymorphonuclear leukocytes and a mild hyperplasia of the synovial membrane; (ii) a mixed acute-chronic phase in which new areas of acute inflammation developed alongside areas of chronic lesions; (iii) a chronic phase followed which was characterized by massive synovial proliferation with mononuclear cell infiltration, irregularity in the articulating cartilage, pannus formation, and "punched out" defects in cortical bone near cartilagenous osseous junctures. The clinical course and histopathological characteristics of the chronic phase of mouse arthritis induced by M. arthritidis closely resembled those of rheumatoid arthritis of man.

Abscess↗
PubMed1969

Immunological responses of the rat to Mycoplasma arthritidis.

Arthritis was produced in rats by the intravenous injection of Mycoplasma arthritidis. Metabolic inhibiting antibody and indirect hemagglutinating antibody could not be detected in the sera of arthritic or convalescent animals. Nonmurine species of mycoplasma were capable of inducing metabolic inhibiting antibody in the rat. A hypothesis based upon the possible occurrence of heterogenetic antigens common to M. arthritidis and rat tissue was brought forward to explain these findings. Complement-fixing antibody to M. arthritidis was detected 3 to 4 days after injection and subsequently rose to high levels, depending upon the severity of arthritis and number of organisms injected. Animals that had recovered from intravenous or subcutaneous inoculation with M. arthritidis were resistant to subsequent infections by the organism. Immunity could be passively transferred by the intravenous injection of convalescent serum. Adsorption of the convalescent serum with antigen greatly reduced the complement fixation titer but did not significantly alter the protective properties of the serum. The presence of complement-fixing antibody could not be related to the development of immunity. An avirulent strain of M. arthritidis and a strain previously classified as M. hominis type 2 were capable of inducing resistance to subsequent injection by virulent M. arthritidis.

Animals↗