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Biomedical subjects

R Rajan

Publications and source records attributed to R Rajan.

134 records · Page 8Linked to original sources

Effect of pregnancy plasma and monoclonal antibodies to HLA and DR antigens on leukocyte migration.

We studied the effect of pregnancy plasma and monoclonal antibodies to the histocompatibility antigens HLA and DR on migration of normal leukocytes from capillaries. It was observed that plasma from women in the first trimester of pregnancy significantly enhanced leukocyte migration at a concentration of 10% (mean area of migration = 50.7 +/- 9.2 cm2), as compared with plasma from nonpregnant women (22.8 +/- 7.0 cm2; p less than 0.05). This effect was less during the second trimester (39.5 +/- 3.5 cm2; p less than 0.05) and no enhancement was noted with plasma obtained from the third trimester of pregnancy. Similar results were obtained with a 20% concentration of plasma also. On the other hand, the monoclonal anti-HLA and anti-DR antibodies had an inhibitory effect on migration of leukocytes. These results are discussed in relation to the immunoregulatory role of pregnancy plasma in the nonrejection of the fetal allograft.

Antibodies, Monoclonal↗

Neuronal responses across cortical field A1 in plasticity induced by peripheral auditory organ damage.

The adult auditory cortex is capable of a plastic reorganization of its tonotopic map after damage to restricted parts of the cochlear sensory epithelium. We examine the precise conditions of cochlear damage required to demonstrate such plasticity in the primary auditory cortex (A1) of the cat and the changes observed in neuronal responses in the A1 which has reorganized in plasticity of the tonotopic map. From these data we attempt to predict the conditions required for similar plasticity to occur in humans after cochlear damage.

Animals↗

Injury- and use-related plasticity in adult auditory cortex.

After restricted cochlear lesions in adult animals the frequency selectivity of neurons in the cortical region deprived of its normal input by the lesion is changed such that the region is occupied by expanded representations of adjacent (perilesion) frequencies. These changes reflect a dynamic process of reorganization (plasticity) and are not explicable as passive consequences of the lesion. Analogous plasticity of cortical frequency selectivity and organization is seen following behavioural training that enhances the significance of particular acoustic stimuli. The occurrence of injury- and use-related auditory cortical plasticity gives rise to a number of questions relating to the mechanisms involved, the perceptual consequences and functional significance of such plastic changes, and their implications for the central processing of input from prosthetic devices. Evidence relating to these issues is briefly summarized in this review, and the directions of future research are considered.

Auditory Cortex↗

Crossed and uncrossed olivocochlear pathways exacerbate temporary shifts in hearing sensitivity after narrow band sound trauma in normal ears of animals with unilateral hearing impairment.

Olivocochlear (OC) pathways have been shown to reduce the temporary threshold shifts (TTSs) caused by traumatic sounds. More recently they have been shown to exacerbate TTSs under certain conditions. One condition is the normal-hearing ear of animals with a chronic unilateral hearing loss. Testing with pure tone trauma showed that then (a) the normal-hearing ear had a lower-than-normal 'intrinsic' susceptibility to intense tones, (b) binaural trauma exacerbated TTSs in the normal-hearing ear through the activity of uncrossed OC (UOC) pathways, and (c) there was no effect on TTSs of the crossed OC (COC) pathway to the normal-hearing ear. The present study is an examination in such animals of effects with noise band trauma. The effects here confirm the previous finding that under such conditions the normal-hearing ear has a lower-than-normal susceptibility to loud sound, and binaural loud sounds exacerbate TTSs in the normal-hearing ear. They extend the previous study by demonstrating that with this traumatic sound, both COC and UOC pathways exacerbate TTSs. These effects contrast against the effects seen in animals with bilaterally normal hearing for the same noise band. Given the commonality of unilateral hearing losses in the normal human population, these data have implications for the functional effects of the OC pathways on loud sound-induced hearing damage.

Animals↗

Stability of efferent-mediated protection against acoustic overexposure with long maintenance under barbiturate anaesthesia.

When anaesthetized animals are maintained over a long period, crossed-cochlear suppressive and enhancement-in-noise effects mediated by the olivocochlear bundle (OCB), as well as some OCB neuronal responses, show time-dependent variations. The present study determined if there were any such changes in OCB-mediated crossed-cochlear protection against compound action potential (CAP) threshold losses caused by a standard loud sound exposure at 11 kHz, presented under conditions either not evoking OCB-mediated protection (i.e. monaural exposure) or evoking protection (binaural exposure). Maintaining animals for periods up to approximately 30 h from initial anaesthetization resulted in non-significant changes in pre-exposure CAP thresholds. There were also only small changes over select frequency ranges in threshold losses caused by the monaural or binaural loud sound, after a single exposure as well as when the testing of OCB function was extended to examine effects after dual successive exposures, the latter result being determined by application of a previously described additivity model. The features of OCB-mediated protection also showed good stability over the long maintenance. These results are discussed as providing further circumstantial evidence that protection is mediated by a different OCB subcomponent to that/those responsible for other OCB-mediated crossed-cochlear effects. In general, the results show that the barbiturate anaesthetic used here does not significantly modulate the crossed-cochlear OCB effect of protection, even though it has been shown elsewhere to significantly depress other crossed-cochlear OCB effects.

Anesthesia, General↗