Biomedical subjects
Publications and source records attributed to Y L Lai.
A sinus tract adjacent to teeth is usually considered to be of endodontic origin and root canal therapy is the primary treatment to achieve healing. A case of a sinus tract is presented in which a suspected endodontic-periodontic lesion was successfully treated by periodontal therapy alone. The sinus tract healed and the radiograph showed bony repair.
On the basis of the previous findings that alpha-difluoromethylornithine (DFMO, an inhibitor of ornithine decarboxylase, which is the rate-limiting enzyme in polyamine biosynthesis) treatment prevents monocrotaline-(MCT) induced pulmonary hypertension and that ventilatory dysfunction precedes pulmonary hypertension in MCT-treated rats, we hypothesize that MCT-induced changes in airway/lung function are polyamine dependent. To evaluate this hypothesis, in phase 1, 48 young Sprague-Dawley rats were evenly divided into four groups: control, DFMO, MCT, and DFMO + MCT. Each DFMO rat received DFMO in its drinking water (2%) for 11 days, with additional injections (400 mg/kg sc) on the 5th day. Each MCT rat received a single injection of MCT (60 mg/kg sc) 1 wk before the functional study. Each DFMO + MCT rat received the same DFMO and MCT treatments as above, and MCT was administered on the 5th day of the DFMO treatment. In the MCT group, there were marked rightward shifts in pressure-volume and maximal flow-static recoil (MFSR) curves and significant decreases in dynamic and quasi-static compliance, the maximal expiratory flow, slope of the MFSR curve, and the carbon monoxide diffusing capacity, as well as a significant increase in alveolar wall thickness. However, in rats treated with DFMO + MCT, most of MCT-induced changes were significantly attenuated. To evaluate whether MCT causes bronchoconstriction, a bronchodilator, terbutaline (0.2 mg/kg i.v.), was administered to control (n = 7) and MCT (n = 11) rats in phase 2. Terbutaline significantly reversed MCT-induced decreases in maximal expiratory flow and slope of the MFSR curve, whereas it did not alter these parameters in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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Pressure-volume (PV) and conductance-volume (GV) curves were obtained in trained dogs awake and then anesthetized with thiopental sodium, in the prone left lateral decubitus, and supine positions. By paired analyses, induction of anesthesia had no significant effect on lung volumes, static PV curves of the lung or chest wall, or static compliance of the lung or chest wall. In addition, change of posture had little effect on these variables in either the awake or the anesthetized state. Frequently, however, individual dogs showed changes in lung PV curves after induction of anesthesia or change of posture. These PV curve shifts were not accompanied by predictable changes in GV relations. Therefore, we concluded that such changes in the lung PV curve reflect either local artifacts or local deformation of the respiratory system.
Lung volumes and respiratory pressures were measured in anesthetized male hamsters weighing an average 117 g. In 16 supine animals functional residual capacity (FRC) determined by body plethysmograph was 1.12 +/- 0.23 (SD) ml (about 20% total lung capacity, TLC) slightly and significantly larger than the FRC measured by saline displacement, 1.01 +/- 0.15 ml. Similar results were found in six prone animals. Paralysis did not significantly alter supine FRC. Contrary to published reports, pleural pressure (Ppl) estimated from esophageal pressure was negative at FRC. The fact that lung volume decreased by 0.2 ml (about 4% TLC) when the chest was opened at FRC provided additional evidence of negative Ppl at FRC. No consistent changes in the lung pressure-volume curve were found after the chest was opened. Deflation chest wall compliance just above FRC was about twice lung compliance. The vital capacity and reserve volumes in this study agreed with values reported in the literature. However, absolute lung volumes (TLC, FRC, and residual volume) were lower by about 1.4 ml, possibly because of earlier overestimates of box FRC.
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Functional residual capacity (FRC) and pressure-volume (PV) curves of the lung, chest wall, and total respiratory system were studied in 15 anesthetized rats, weighing 307 +/- 10 (SE) g. Pleural pressure was estimated from the esophageal pressure measured with a water-filled catheter. The FRC determined by body plethysmograph was slightly and significantly larger than FRC determined from saline displacement of excised lungs. The difference may be accounted for by O2 uptake by lung tissue, escape of CO2 through the pleura, and abdominal gas. Paralysis in the prone position did not affect FRC, and abdominal gas content contributed only slightly to the FRC measured by body plethysmograph. Values of various pulmonary parameters (mean +/- SE) were as follows: residual volume, 1.26 +/- 0.13 ml; FRC, 2.51 +/- 0.20 ml; total lung capacity, 12.23 +/- 0.55 ml; compliance of the lung, 0.90 +/- 0.06 ml/cmH2O; chest wall compliance, 1.50 +/- 0.11 ml/cmH2O; and respiratory system compliance, 0.57 +/- 0.03 ml/cmH2O. The lung PV curve did not show a consistent change after the chest was opened.
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Morphological changes in retinas of aging Fischer 344 rats were characterized. The numbers of photoreceptor cells gradually decreased as rats aged. The outer nuclear layer was 12 cells thick at 3 months, but was reduced to less than 8 cells by 18 months. The decrease of photoreceptor cells was more pronounced in rats housed under a light intensity of 32-ft-c than in rats housed under a light intensity of 1 ft-c. Inner and outer segments of surviving photoreceptor cells were morphologically normal. A new form of retinal degeneration was discovered in aged Fischer rats characterized by selective degeneration of peripheral retina. Degeneration was characterized by severe loss of photoreceptor cells in the far peripheral retina. Microcystoids were found in about 25% ofthe affected retinas, and the loss of photoreceptor cells was followed by proliferation and vascularization of the retinal pigment epithelium and disorganization of retinal structures. The incidence and severity of peripheral retinal degeneration increased with aged and prolonged exposure to comparatively high-intensity light. All Fischer rats ((5/5) housed under light intensity of 32 ft-c developed severe peripheral retinal degeneration by 24 months. Peripheral retinal degeneration was an age-related change but appeared to be exaggerated by ambient light.
The disorder in Wag/Rij rats is a spontaneous, bilateral retinal deneration. It is characterized by an early onset, slowly progressive degeneration of the photoreceptor cells leading to destruction of the retina. Degeneration affects both rod cells and cone cells, and to a lesser degree the cells in the inner nuclear layer. The remarkable alterations in the retinal pigment epithelium during the course of the disease suggest a profound change in metabolism and function of the pigment epithelium and implicate a possibility of interaction between the pigment epithelium and the photoreceptors. Since degenerated cells have also been observed in the inner nuclear layers, there is a possibility that Muller's cells are involved in the retinal degeneration. Controlled experiments have demonstrated that the disease is not induced by light damaging effects of the retina, and initial breeding experiments suggest that the disease is inheritable, probably as an autosomal dominant trait. The retinal degeneration in Wag/Rij rats is a new, unique system and it is a potentially very useful animal model of retinitis pigmentosa.
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Esophageal elastance was measured in trained dogs placed in the prone, supine, and left lateral postures before and during sodium thiopental anesthesia. Esophageal elastance was measured from static pressure-volume curves and during spontaneous breathing at functional residual capacity. There was a significant decrease in esophageal elastance, estimated from the pressure-volume curves, during anesthesia in both prone and lateral positions but not in the supine posture. Changes in vagal tone produced by stimulation of the vagal nerves did not alter esophageal elastance. Therefore, underlying mechanisms for these changes in esophageal elastance are not fully understood. There was an increase in esophageal elastance when lung volumes increased from 55 to 80% total lung capacity. However, we did not find a significant change in esophageal elastance between awake and anesthetized conditions or between positions during spontaneous breathing at functional residual capacity.
A high incidence of keratoconjunctivitis was observed in a closed colony of inbred Lewis/Wistar rats. Clinical signs including blinking, ocular discharge, circumcorneal flush, corneal opacity, ulceration, pannus, hypopyon, and hyphema were observed at about three weeks of age. Acute disease subsided by six weeks of age, but some lesions progressed to low-grade chronic keratitis. Six per cent of affected rats developed megaloglobus, which usually appeared by three weeks of age. Lesions included focal or diffuse interstitial keratitis, corneal ulceration, anterior synechia, and inflammatory exudate in the anterior chamber. A high incidence of lenticular and retinal degeneration was associated with megaloglobus. Most affected rats also had harderian dacryoadenitis. Sialodacryoadenitis virus (SDA) was recovered from nasal washes, but not from affected eyes. Serological evidence indicated that SDA virus infection was widespread in the colony.
A spontaneous, hereditable, bilateral retinal degeneration affecting all adult animals in a closed, imbred colony of Wag/Rij rats has been discovered. The disorder is characterized by early onset and a slow progressive course. Early lesions are detected by one month in retinas which are otherwise fully developed. Destruction of the photoreceptor layer proceeds as more and more cells degenerate. Degeneration appears to begin in the photoreceptor cell body and only secondarily affects the outer segment. Futhermore, phagocytic activity of pigment epithelium remains intact until late in the disease. Endstage lesions include retinal disorganization, proliferation and vascularization of pigment epithelium, and migration of pigment epithilial cells into the retina. The temporal and structural characteristics of this retinopathy indicate it may serve as a useful model for study of retinitis pigmentosa in man.