The morphological changes of the mandibular condyle in patients with temporomandibular joint disorder were studied. The subjects were 420 patients (103 males and 317 females, 8 to 80 years of age, mean age 39.8 years) who were clinically diagnosed as temporomandibular joint disorder. MR imaging was performed with a GE-Signa 1.5 Tesla MR imaging system using the body coil as a transmitter and 3-inch bilateral surface coils. The patients were examined by a multiplanar gradient echo technique in a closed-loop cine fashion on both sagittal and coronal planes. The results obtained were as follows: 1) Morphological changes of the mandibular condyle were detected in 47.0% of the patients. The predominant morphological changes were then formation of osteophyte and marginal proliferation (65.8%). 2)The incidence of morphological changes in the mandubular condyle did not show any significant difference between male and female, and tended to be higher in patients over 40 years of age, and the incidence in patients under 20 years of age was lower, compared to that in patients from 20 to 39 years of age. 3)The incidence of morphological changes in patients with anterior disk displacement without reduction was higher than in those with anterior disk displacement with reduction (P<0.001). The incidence of morphological changes in patients with rotational disk displacement was higher than in those with medial disk displacement (P<0.001). 4)The anterior translation of mandibular condyle was influenced more by anterior disk displacement rather than by morphological changes. From these results, it is suggested that simultaneous bilateral condyle pseudodynamic MR imaging was useful in the diagnosis of internal derangement, evaluation of morphological changes and assessment of motional abnormality of the condyle.

A soluble mitogenic factor was partially purified from the culture supernatant of Streptococcus anginosus by DEAE-Sephadex column chromatography, followed by Sephadex G-100 column chromatography. In Sephadex G-100, three protein fractions were separated. Fraction 1 (F1) from Sephadex G-100 contained mitogenic activity for human peripheral blood mononuclear cells. The specific activity of F1 was increased to 4.4 times that of the of culture supernatant. The mitogenic activity of F1 rose at from 0.1μg/ml to 1μg/ml, but the activity fell at a dose of 10μg/ml. These results suggest that the novel mitogenic factor from S. anginosus culture supernatant may cause inflammation.

Abdominal ganglion cells of an Aplysia contain a characteristic GABA-receptor, the activation of which induces a marked hyperpolarization due to a specific increase in the membrane permeability of Cl^-. The GABA-receptor of this type was named an H_cl-type. A two-minutes exposure to 10_^-3M lidocaine (LIDO) had little effect on resting membrane potential with a receptor of the _GABAH_cl-type but significantly depressed the response to 10^-3M GABA. The depressing effect of LIDO on this type of response was completely reversible after 15 miniutes of rinsing with normal Aplysia blood. The dose-inhibition curves, with relative responses to given doses (GABA) plotted against log (LIDO), showed no shift in either direction with increase in GABA. These findinigs suggest that LIDO depresses the GABA receptor in a noncompetitive manner.

Treatment with 10^-4M diazepam (DZ) also reversively depressed the same type of response to 10^-3M GABA. The dose-inhibition curves, in which relative responses to given doses of GABA were plotted against DZ, showed no shift in either direction, and this indicated that the mode of depression of the GABA-receptor was also noncompetitive.

Further, the interaction between LIDO and DZ on GABA-receptor was studied. 10^-6M DZ restores the response to 10^-3M GABA which was depressed by 10^-3M of LIDO when applied simultaneously. The 10^-3M GABA-induced response was reduced to 70% of the control by 10^-3M LIDO, but this was restored to 40% of the control by 10^-6M DZ, however when pretreated with l10^-6M DZ, the blocking effect of 10^-3M LIDO was decreased to only 10% of the control.

Two-hundred subjects with completed permanent dentition were divided into two groups: a normal dentition group and a crowded dentition group. The histories of dental treatment in these subjects were analyzed. The sizes of their dental arches, basal arches and individual teeth, before and after dental treatment, were compared between these two groups to clarify factors responsible for the formation of crowded dentitions. The following results were obtained: 1) Of the 200 subjects, 42.5% had undergone dental arch expansion, 11.5% had serial extraction of teeth, 9.5% had been treated with a space maintainer, and 36.5% no treatment. 2) Of all subjects. 67.5% had normal dentition in completed permanent dentition. 3) In males, the dental arch width and the basal arch width were smaller in crowded dentition than normal dentition in the upper jaw, while the total sum of the crown widths was greater in crowded dentition than normal dentition in the lower jaw. In females, the total sum of the crown widths was significantly greater in the crowded dentition group than in the normal dentition group. These results indicate that factors responsible for the formation of crowded dentition differ between males and females.

Compound action potentials (CAP) in response to orthodromic stimulation of the presynaptic nerve trunk were recorded extracellularly from the bullfrog sympathetic ganglion. Application of lidocaine, procaine, tetracaine, or dibucaine significantly depressed the amplitude of CAP. When evaluated from the dose-inhibition curves, those local anesthetics have the following order of blocking Potency: dibucaine ≧ tetracaine > procaine ≧ lidocaine. In addition, these local anesthetics were depressed the action potentials being conducted through the sympathetic nerve trunk at a higher concentration than that which blocked the synaptic transmission. The acetylcholine-induced depolarizing response intracellularly recorded from a sympathetic ganglion cell was markedly depressed by lidocaine at a concentration that blocked the synaptic transmission. The modes of inhibition of the synaptic transmission by lidocain and procaine were both noncompetitive, while that by d-tubocurarine was competitive. These results suggest that local anesthetics mainly block the allosteric site of a nicotinic ACh receptor at the postsynaptic membrane rather than inhibiting the release of transmitter at the presynaptic terminal, to effecting the blocking of synaptic transmission.