Biomedical subjects
R Rajan
Publications and source records attributed to R Rajan.
Performance of power assisted respirators during simulated asbestos removal.
Protection factors were measured on full face mask power assisted respirators when worn by experienced asbestos removal operatives under simulated asbestos removal work conditions. The sulfur hexafluoride test method as defined in European Standards was employed to determine the leakage into the respirators. Protection factors were measured on a total of 21 test volunteers. The test method allowed protection factors to be related to wearer activities and practices. Poor fitting techniques and simulated reduction in the respirator's performance resulted in a reduction in the protection factor. Visual inspection of the RPE usually worn by the volunteers identified inadequate maintenance. This study re-emphasises that careful selection, facepiece fit testing and correct use and maintenance of RPE are essential to ensure optimum protection to the wearer.
Correlations to predict droplet size in ultrasonic atomisation.
In conventional two fluid nozzles, the high velocity air imparts its energy to the liquid and disrupts the liquid sheet into droplets. If the energy for liquid sheet fragmentation can be supplied by the use of ultrasonic energy, finer droplets with high sphericity and uniform size distribution can be achieved. The other advantage of ultrasound induced atomisation process is the lower momentum associated with ejected droplets compared to the momentum carried by the droplets formed using conventional nozzles. This has advantage in coating and granulation processes. An ultrasonic probe sonicator was designed with a facility for liquid feed arrangement and was used to atomise the liquid into droplets. An ingenious method of droplet measurement was attempted by capturing the droplets on a filter paper (size variation with regard to wicking was uniform in all cases) and these are subjected to image analysis to obtain the droplet sizes. This procedure was evaluated by high-speed photography of droplets ejected at one particular experimental condition and these were image analysed. The correlations proposed in the literature to predict droplet sizes using ultrasound do not take into account all the relevant parameters. In this work, a truly universal correlation is proposed which accounts for the effects of physico-chemical properties of the liquid (flow rate, viscosity, density and surface tension), and ultrasonic properties like amplitude, frequency and the area of vibrating surface. The significant contribution of this work is to define dimensionless numbers incorporating ultrasonic parameters, taking cue from the conventional numbers that define the significance of different forces involved in droplet formation. The universal correlations proposed are robust and can be used for designing ultrasonic atomisers for different applications. Among the correlations proposed here, those ones that are based on the dimensionless numbers and Davies approach predict droplet sizes within acceptable limits of deviation. Also, an empirical correlation from experimental data has been proposed in this work.
Cortical reorganization in patients with high frequency cochlear hearing loss.
Animal research has shown that tonotopic representation in the auditory cortex is not statically fixed in the adult organism but can be altered after deafferentation. The present study examines the plasticity of the human auditory cortex in patients with high frequency cochlear hearing loss by means of magnetoencephalographic measurements. The data show that the cortical map can reorganize such that cortical neurons deprived of their usual most sensitive afferent input now respond to tone frequencies adjacent to the frequency range of the partial hearing loss. The results suggest that deafferentation due to cochlear damage in adults may lead to functional reorganization of auditory cortical structures.
Clinical and sensorimotor gating effects of ketamine in normals.
The clinical similarities between PCP psychosis and schizophrenia have contributed importantly to the development of the glutamate hypothesis of schizophrenia. Sensory gating, as measured by prepulse inhibition of the acoustic startle reflex (PPI), is impaired in patients with schizophrenia. In animals, the noncompetitive NMDA antagonists PCP and ketamine disrupt PPI in a way that resembles the defect seen in schizophrenia. The purpose of this work is to investigate the modulation of sensory gating in humans by subanaesthetic doses of ketamine. 16 healthy male subjects received a 60-min infusion of ketamine (0.5 mg/kg) or normal saline on two separate days in a randomized double-blind crossover design. Clinical ratings and PPI were done during the infusion on both days. Ketamine produced robust clinical effects. Dissociative symptoms as measured by the CADSS increased from 0 +/- 0.0 to 29.3 +/- 14.3; negative symptoms (Affect Rating Scale) increased from 17.2 +/- 0.8 to 24.8 +/- 3.1; and total BPRS scores increased from 18.3 +/- 0.8 to 26.4 +/- 5.1. ANOVAs for these ratings were all significant at the p <.000 level, although BPRS increases were not in the range seen in decompensated schizophrenic patients. The amplitudes of the startle responses to pulse-alone stimuli were not significantly different on ketamine and placebo days. Ketamine did not cause disruption in PPI as expected. On the contrary, in the first block of the PPI session ketamine significantly enhanced PPI (ANOVA; F=6.15, p =.026). These results indicate that the clinical effects of ketamine are not coupled with schizophrenic-like disruption of PPI in normal controls.
Plasticity of excitation and inhibition in the receptive field of primary auditory cortical neurons after limited receptor organ damage.
Permanent receptor organ damage can cause plasticity of topographic cortical maps of that receptor surface while temporary receptor organ damage, and conditions mimicking such damage, can unmask new excitatory inputs in central sensory neurons receiving input from that receptor surface. Cortical plasticity is associated with an anatomically or pharmacologically defined decrease in inhibition in cortex. It is therefore widely proposed that a reduction incentral inhibition underlies cortical neural plasticity. Here I demonstrate that small receptor organ damage results, in primary auditory cortical (A1) neurons, in loss of one component of functionally defined afferent inhibition but unmasking of another component of afferent inhibition along with new excitatory responses. Overall, there did not appear to be any change in the strength of afferent inhibition or in the strength of excitation. Thus, auditory receptor organ damage can unmask new excitatory inputs as well as inhibitory inputs from within the receptive field of the neurons.
Unilateral hearing losses alter loud sound-induced temporary threshold shifts and efferent effects in the normal-hearing ear.
In animals with bilaterally normal hearing, olivocochlear pathways can protect the cochlea from the temporary shifts in hearing sensitivity (temporary threshold shifts; TTSs) caused by short-duration intense loud sounds. The crossed olivocochlear pathway provides protection during binaural loud sound, and uncrossed pathways protect when monaural or binaural loud sounds occur in noise backgrounds. Here I demonstrate that when there is a chronic unilateral hearing loss, effects of loud sounds, and efferent effects on loud sound, in the normal-hearing ear differ markedly from normal. Three categories of test animals with unilateral hearing loss were tested for effects at the normal-hearing ear. In all categories a monaural loud tone to the normal-hearing ear produced lower-than-normal TTSs, apparently because of a tonic re-setting of that ear's susceptibility to loud sound. Second, in the two test categories in which the hearing-loss ear was only partly damaged, binaural loud sound exacerbated TTSs in the normal-hearing ear because it caused threshold shifts that were a combination of "pure" TTSs and uncrossed efferent suppression of cochlear sensitivity. (In normal cats, this binaural tone results in crossed olivocochlear protection that reduces TTS.) Binaural loud sound did not produce such uncrossed efferent effects in the test category in which the nontest ear had suffered total hearing loss, suggesting that this uncrossed efferent effect required binaural input to the CNS. It is noteworthy that, in the absence of this uncrossed efferent suppression, the pure loud sound-alone induced TTSs after binaural exposure were low. Thus in the absence of any efferent effect, the normal-hearing cochlea had a reduced susceptibility to loud tone-induced damage. Finally, the results suggest that, with respect to cochlear actions at high sound levels, uncrossed and crossed efferent pathways may exert different effects at the one type of receptor cell.
Noise priming and the effects of different cochlear centrifugal pathways on loud-sound-induced hearing loss.
Priming/conditioning the cochlea with moderately loud sound can reduce damage caused by subsequent loud sound. This study examined immediate effects of short-term priming with monaural broadband noise on temporary threshold shifts (TTSs) in hearing caused by a subsequent loud high-frequency tone and the role of centrifugal olivocochlear pathways. Priming caused delay-dependent changes in tone-induced TTSs, particularly or only at frequencies higher than the peak tone-affected frequency, through two general effects: a short-lasting increase in cochlear susceptibility to loud sound and longer-lasting complex end effects of centrifugal pathways. The results indicated the following points. Priming noise had "pure" cochlear effects, outlasting its presentation and declining with delay, that exacerbated tone-induced TTSs at frequencies higher than the peak tone-affected frequency. The centrifugal uncrossed medial olivocochlear system (UMOCS) could prevent this noise exacerbation and as this noise effect declined, could even reduce tone-induced TTSs below those to the unprimed tone. For longer delays, when priming noise no longer had any exacerbative "pure" cochlear effects on TTSs, UMOCS exacerbated TTSs above those to the unprimed tone. The crossed medial olivocochlear system (CMOCS) appeared to show a gradual "build-up" of effects postpriming. A parallel study showed it exercised no end effect on TTSs when noise and tone were concurrent. With priming, CMOCS effects were observed. For the shortest priming delay, the CMOCS blocked a UMOCS effect preventing noise exacerbation of tone-induced TTSs. For longer delays, CMOCS end effects, when present, reduced tone-induced TTSs below those to the unprimed tone. The CMOCS may oscillate between producing these effects and exerting no end-effect. With increasing delay CMOCS protection occurred in a greater proportion of animals. Finally, with a delay of 600 s between primer and loud tone, all these systems appeared to have reset to normal so that TTSs were similar to those in the unprimed condition. Thus the effects of short-term priming are not simple and do not suggest that centrifugal pathways act automatically as a protective system during such priming.
Cochlear outer-hair-cell efferents and complex-sound-induced hearing loss: protective and opposing effects.
Centrifugal crossed and uncrossed medial olivocochlear systems (CMOCS and UMOCS) terminate on cochlear outer hair cells (OHCs) and exercise effects through a nicotinic cholinergic receptor. Hence their cochlear effects have not been differentiated. Recent work on protection from loud-sound-induced temporary threshold shifts (TTSs) in hearing sensitivity suggest the two OHC efferent systems may act differently. This was tested, using traumatic complex sound, to determine if such sound could activate both MOCS components and then reveal whether they exerted different effects on TTSs to such stimuli. Traumatic noise bands activated crossed and uncrossed MOCS efferents. Two different CMOCS effects were observed. For frequencies in the noise (within-band frequencies), it protected hearing sensitivity as expected. Novel findings were that at frequencies higher than the noise band range (high-side frequencies), it acted to worsen hearing sensitivity and that this was opposed by a UMOCS effect generally targeted to these frequency regions. It is proposed that the two crossed MOCS actions are extensions of a contrast-enhancement action for low-level noise bands. It is also proposed that the UMOCS plays a state-restoration role to prevent an undesired CMOCS side-effect of exacerbation of high-side TTSs to high-level noise bands.
Centrifugal pathways protect hearing sensitivity at the cochlea in noisy environments that exacerbate the damage induced by loud sound.
Loud sounds damage the cochlea, the auditory receptor organ, reducing hearing sensitivity. Previous studies demonstrate that the centrifugal olivocochlear pathways can moderately reduce these temporary threshold shifts (TTSs), protecting the cochlea. This effect involves only the olivocochlear pathway component known as the crossed medial olivocochlear system pathway, originating from the contralateral brainstem and terminating on outer hair cells in the cochlea. Here I demonstrate that even moderate noise backgrounds can significantly exacerbate the cochlear TTSs induced by loud tones, but this is prevented because in such conditions there is additional activation of uncrossed olivocochlear pathways, enhancing protection of cochlear hearing sensitivity. Activation of the uncrossed pathways differs from that of the crossed pathway in that it is achieved only in noise backgrounds but can then be obtained under monaural conditions of loud tone and background noise. In contrast, activation of the crossed pathway is achieved only by binaural loud tones and is not further enhanced by background noise. Thus, conjoint activation of both crossed and uncrossed efferent pathways can occur in noise backgrounds to powerfully protect the cochlea under conditions similar to those encountered naturally by humans.
The clinical burden of prostate cancer in Canada: forecasts from the Montreal Prostate Cancer Model.
OBJECTIVES: The incidence of prostate cancer is increasing, as is the number of diagnostic and therapeutic interventions to manage this disease. We developed a Markov state-transition model--the Montreal Prostate Cancer Model--for improved forecasting of the health care requirements and outcomes associated with prostate cancer. We then validated the model by comparing its forecasted outcomes with published observations for various cohorts of men. METHODS: We combined aggregate data on the age-specific incidence of prostate cancer, the distribution of diagnosed tumours according to patient age, clinical stage and tumour grade, initial treatment, treatment complications, and progression rates to metastatic disease and death. Five treatments were considered: prostatectomy, radiation therapy, hormonal therapies, combination therapies and watchful waiting. The resulting model was used to calculate age-, stage-, grade- and treatment-specific clinical outcomes such as expected age at prostate cancer diagnosis and death, and metastasis-free, disease-specific and overall survival. RESULTS: We compared the model's forecasts with available cohort data from the Surveillance, Epidemiology and End Results (SEER) Program, based on over 59,000 cases of localized prostate cancer. Among the SEER cases, the 10-year disease-specific survival rates following prostatectomy for tumour grades 1, 2 and 3 were 98%, 91% and 76% respectively, as compared with the model's estimates of 96%, 92% and 84%. We also compared the model's forecasts with the grade-specific survival among patients from the Connecticut Tumor Registry (CTR). The 10-year disease-specific survival among the CTR cases for grades 1, 2 and 3 were 91%, 76% and 54%, as compared with the model's estimates of 91%, 73% and 37%. INTERPRETATION: The Montreal Prostate Cancer Model can be used to support health policy decision-making for the management of prostate cancer. The model can also be used to forecast clinical outcomes for individual men who have prostate cancer or are at risk of the disease.
The economic burden of prostate cancer in Canada: forecasts from the Montreal Prostate Cancer Model.
BACKGROUND: We developed an economic model of prostate cancer management from diagnosis until death. We have used the Montreal Prostate Cancer Model to estimate the total economic burden of the disease in a cohort of Canadian men. METHODS: Using this Markov state-transition simulation model, we estimated the probability of prostate cancer, annual prostate cancer progression rates and associated direct medical costs according to patient age, tumour stage and grade, and treatment modalities in a 1997 cohort of Canadian men. The estimated lifetime costs of prostate cancer included the costs of clinical staging, initial treatments and complications, follow-up cancer therapies, routine outpatient care, and palliative care following metastatic disease. RESULTS: The clinical burden of prostate cancer forecasted using the model was similar to the projections of the National Cancer Institute. In the 1997 cohort of 5.8 million Canadian men between 40 and 80 years old, prostate cancer would be diagnosed in an estimated 701,491 men (12.1%) over their lifetime. Direct medical costs would total $9.76 billion, or $3.89 billion when discounted 5% annually. INTERPRETATION: The Montreal Prostate Cancer Model indicates that the economic burden of prostate cancer to Canada's health care system will be substantial. Further analyses are needed to identify the most efficient means of treating this disease.
Impaired prepulse inhibition of acoustic startle in schizophrenia.
BACKGROUND: Schizophrenics show deficits in sensorimotor gating, as measured by prepulse inhibition of acoustic startle (PPI). The goal of this investigation is to further characterize PPI and habituation deficits in schizophrenia, and to examine whether differing subgroups of schizophrenics would show comparable PPI deficits. METHODS: PPI was measured in 24 male schizophrenic subjects (9 acutely decompensated inpatients and 15 stable outpatients) and in 20 age-matched normal control subjects. Schizophrenic subjects were rated for positive and negative symptoms at the time of testing. RESULTS: Schizophrenic subjects showed deficits in prepulse inhibition and habituation as compared to normal subjects. Similar latency facilitation was produced by the prepulse in both groups. Acutely decompensated inpatients and stable outpatients did not differ in percent PPI. PPI did not correlate with severity of positive or negative symptoms. CONCLUSIONS: These results suggest that schizophrenic subjects have impaired central inhibitory mechanisms as measured by PPI, and support the hypothesis that periods of relative clinical remission are not accompanied by normalization of sensorimotor gating.
Injury-induced reorganization in adult auditory cortex and its perceptual consequences.
Restricted cochlear lesions in adult animals result in a reorganization of auditory cortex such that the cortical region deprived of its normal input by the lesion is occupied by expanded representations of adjacent cochlear loci, and thus of the frequencies represented at those loci. Analogous injury-induced reorganization is seen in somatosensory, visual and motor cortices of adult animals after restricted peripheral lesions. The occurrence of such reorganization in a wide range of species (including simian primates), and across different sensory systems and forms of peripheral lesion, suggests that it would also occur in humans with similar lesions. Direct evidence in support of this suggestion is provided by a small body of functional imaging evidence in the somatosensory and auditory systems. Although such reorganization does not seem to have a compensatory function, such a profound change in the pattern of cortical activation produced by stimuli exciting peri-lesion parts of the receptor epithelium would be expected to have perceptual consequences. However, there is only limited psychophysical evidence for perceptual effects that might be attributable to injury-induced cortical reorganization, and very little direct evidence for the correlation between the perceptual phenomena and the occurrence of reorganization.
Clinico-pathological correlation between allergic rhinitis and bronchial asthma.
A prospective study was carried out on 52 patients with allergic rhinitis, during March 1993-January 1995. This was to analyse the occurrence of bronchial asthma among them and to correlate the symptoms, signs and pathological findings of allergic rhinitis with that of bronchial asthma in those patients with both the disorders. The therapeutic benefits with regard to the symptoms of bronchial asthma in these patients were assessed after treatment of their nasal allergy for a period of at least four months. A definite aetio-clinico-pathological correlation could be established between allergic rhinitis and bronchial asthma and it could be concluded from the study that prompt attention to nasal symptoms in cases with co-existent bronchial asthma helps to a large extent in curbing the symptoms of the latter.
A para-testicular primitive neuroectodermal tumor in an adult: a case report and literature review.
OBJECTIVE: The authors describe the salient clinical, radiologic and histopathologic features of an extremely rare para-testicular primitive neuroectodermal tumor in a 25 year-old man. INTERVENTION: Excisional biopsy of the tumor en bloc was performed. Adjuvant VAdriaC-based chemotherapy (Vincristine, Doxorubicin, and Cyclophosphamide) was given post-operatively. MAIN OUTCOME MEASURES: Histopathologic examination and immunohistochemical studies were performed on formaldehyde-fixed, paraffin-embedded tumor tissue. RESULTS: Histologic examination showed an undifferentiated small cell tumor. The tumor cells stained positively with MIC-2, a marker specific for primitive neuroectodermal tumors. The patient is 12 months post surgery and has completed adjuvant chemotherapy with no evidence of recurrent disease. CONCLUSIONS: This highly unusual, peripheral primitive neuroectodermal tumor should be considered in the differential diagnosis of undifferentiated small cell neoplasms of the genitourinary system in adults, from the kidney to the testicle. We present a patient with a PNET treated based on a Ewing's family of tumors protocol.
Laparoscopy in the modern perspective.
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Absence of plasticity of the frequency map in dorsal cochlear nucleus of adult cats after unilateral partial cochlear lesions.
In adult animals, lesions to parts of the auditory receptor organ, the cochlea, can produce plasticity of the topographic (cochleotopic) frequency map in primary auditory cortex and a restricted or patchy plasticity in the auditory midbrain. This effect is similar to the plasticity of topographic maps of the sensory surface seen in visual and somatosensory cortices after restricted damage to the appropriate receptor surface in these sensory systems. There is dispute about the extent to which subcortical effects contribute to cortical plasticity. Here, we have examined whether topographic map plasticity similar to that seen in the auditory cortex and the midbrain is observed in the adult auditory brainstem. When partial cochlear lesions were produced in the same manner as those that were produced in the cortex and midbrain studies, we found no plasticity of the frequency map in the dorsal cochlear nucleus (DCN). Small regions of the DCN that were deprived of their normal, most sensitive frequency (characteristic frequency; CF) input by the cochlear lesion appeared to have acquired new CFs at frequencies at or near the edge of the cochlear lesion. However, examination of thresholds at the new CFs established that the changes simply reflected the residue of prelesion input to those sites: The patterns of CF thresholds were very well predicted by simple calculations of the patterns that were expected from such residual input. The results of this study suggest that the DCN does not exhibit the type of plasticity that has been found in the auditory cortex and midbrain; therefore, it does not account for the changes in responsiveness observed in the higher level structures under similar experimental conditions.