Auditory-nerve fibers (ANFs) in the cat have been subdivided according to spontaneous rate (SR), with high-SR fibers showing the lowest thresholds. Cochlear terminals of the three SR groups differ in caliber and synaptic position around the inner hair cell (Liberman [1982b] Science 216:1239-1241); central terminals differ in degree of branching and in which subregions of the cochlear nucleus (CN) are targeted (Liberman [1991] J. Comp. Neurol. 313:240-258). The present study investigates whether these SR-based differences in ANF connections are unique to the cat. Thirty ANFs from 15 guinea pigs were intracellularly labeled after measuring characteristic frequency, threshold, and SR. Labeled cochlear projections showed significant SR-based differences in axonal caliber, with low- and medium-SR fibers 20-40% thinner than those of high-SR fibers for both peripheral and central (modiolar) axons. Spatial segregation in the inner hair cell area could not be assessed; however, the peripheral axons in the osseous spiral lamina showed the same SR-based organization reported for the cat (Kawase and Liberman [1992] J. Comp. Neurol. 319:312-318). Labeled central projections also showed significant SR-based differences. Low- and medium-SR fibers: 1) were more highly branched, 2) sent significantly more terminals to the small-cell cap region of the CN, and 3) produced endbulb terminals (on spherical cells) that were significantly more complex than high-SR fibers. All of these SR-based trends for both central and peripheral projections are analogous to those reported in the cat, and, thus, may represent a fundamental organizational principle of the mammalian ear.
SUMMARY Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 ± 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a, a') derived from P-V and normalized P-V relations, respectively, for enddiastolic myocardial elastic stiffness (Es or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (Ks or KE) of the circumferential stress-strain relation.Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 ± 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV, dP/dV/V, E. and EE and a tendency for increase in the chamber stiffness constants (a, a') and myocardial stiffness constants (Ks, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid-and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.INCREASED LEFT VENTRICULAR diastolic stiffness has been cited as a cause of elevated left ventricular diastolic pressure, pulmonary venous hypertension and associated symptoms of dyspnea, reduced exercise tolerance and syncope in patients with valvular aortic stenosis.1,2,3 However, quantitation of diastolic stiffness in this common clinical disorder, using both pressure-volume analysis of the ventricular chamber and stress-strain analysis of the myocardial wall, has not been accomplished, pri
We report on five patients with high signals in the labyrinth on unenhanced magnetic resonance imaging who developed sudden hearing loss and vertigo. Weissman et al. (1992) suggested the possibility that such high signals were caused by hemorrhage. We assessed these patients using audiograms, caloric tests, and auditory brainstem responses to investigate the possibility of inner ear hemorrhage. Most of the patients were found to have severe and irreversible impairment of both cochlear and vestibular function. These findings were consistent with the hypothesis that their symptoms were caused by inner ear hemorrhage.
Although IgG4-related disease is characterized by extensive infiltration of IgG4-positive plasma cells and lymphocytes of various organs, the details of this systemic disease are still unclear. We screened serum total IgG levels in the patients with Hashimoto thyroiditis (HT) to illustrate the prevalence of IgG4-related thyroiditis in HT. Twenty-four of 94 patients with HT (25.5%) had elevated serum IgG levels and their serum IgG4 was measured. Five of the 24 cases had more than 135 mg/dL of IgG4, which is the serum criterion of IgG4-related disease. One was a female patient who was initially treated as Graves' disease and rapidly developed a firm goiter and hypothyroidism. The biopsy of her thyroid gland revealed that follicular cells were atrophic with squamous metaplasia, replaced with fibrosis, which was compatible with the fibrous variant of HT. Immunohistochemical examination revealed diffuse infiltration of IgG4-positive plasma cells, and the serum IgG4 level was 179 mg/dL. The levels of IgG and IgG4 were positively correlated with the titers of anti-thyroglobulin antibody or anti-thyroid peroxidase antibody. In conclusion, at least a small portion of patients with HT with high titers of anti-thyroid antibodies may overlap the IgG4-related thyroiditis.
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