Expression of 25 kDa heat shock protein by synovial type B cells of the mouse temporomandibular joint.

Earlier studies have demonstrated immunoreactivity for heat shock protein 25 (Hsp25) in type B synovial lining cells of the rat temporomandibular joint, and also the presence of characteristic cytoplasmic processes in these cells, but it is unclear whether or not the type B cells in other animals possess such elaborate cytoplasmic projections and as there is as yet no evidence for the synthesis of this protein by these cells. For these reasons, the expression of Hsp25 was investigated in the synovial membrane of the mouse temporomandibular joint by immunocytochemistry and by in situ hybridization using a specific cRNA probe. Intense immunoreaction for Hsp25 was found in the cytoplasm of certain synovial lining cells that were identified as type B by immunoelectron-microscopy. These Hsp25-positive cells had slender cytoplasmic processes, either projecting towards or covering the synovial surface. Morphological differences between cytoplasmic processes seemed to depend on the location of the type B cell bodies. In situ hybridization showed intense signals for Hsp25 mRNA in the synovial lining cells, suggesting that the type B cells produce, rather than resorb, Hsp25. These findings indicate that Hsp25 is a useful marker for the identification of the synovial type B cells in the temporomandibular joint. It is further hypothesized that Hsp25 in type B cells is involved in maintaining their specific profile and epithelial-like arrangement, and in protecting against mechanical stress.

The exact expression of glial fibrillary acidic protein (GFAP) in trigeminal ganglion and dental pulp.

The expression in various cell types of peripheral tissues of glial fibrillary acidic protein (GFAP), first discovered as an intermediate filament specific for astrocytes, remains controversial owing to numerous reports of a wide distribution for GFAP-immunoreactivity in various cells. The present study employed immunohistochemistry to investigate the precise expression of GFAP in the dental pulp and trigeminal ganglion of adult rats and wild-type mice as well as GFAP-knockout mice. The exhibition of GFAP-immunoreactivity in the trigeminal ganglion was further examined by a reverse transcription polymerase chain reaction (RT-PCR) technique, and in situ hybridization histochemistry using a specific cRNA probe prepared by us. The immunoreaction for GFAP was recognizable in the axons, Schwann cells, and the fibroblasts in the dental pulp of rats and wild-type littermate mice. However, mice with null mutations in the GFAP gene remained immunoreactive for GFAP in all these locations. Intense GFAP-immunoreactivity was found in a small number of satellite cells in the trigeminal ganglion in all animals examined in this study. RT-PCR analysis demonstrated bands for the GFAP gene corresponding to the length expected from the primer design in the samples of trigeminal ganglion and dental pulp. In situ hybridization histochemistry also showed intense signals for GFAP mRNA in some satellite cells of the trigeminal ganglion, but never in the neurons. These data suggest that the GFAP-immunoreactive molecules in the pulpal axons and fibroblasts react non-specifically with the polyclonal antibody and are probably a closely related type of intermediate filament.

Transient expression of heat shock protein (Hsp)25 in the dental pulp and enamel organ during odontogenesis in the rat incisor.

The expression of heat shock protein (Hsp) 25 during odontogenesis in the dental pulp and enamel organ of rat incisors was investigated by immunocytochemistry and confocal microscopy. In the process of dentin formation, immature odontoblasts first exhibited Hsp 25-immunoreactivity, and increased in immunointensity with the advance of their differentiation. In the dental pulp, in contrast, intense immunoreaction in the mesenchymal cells became weak or negative in parallel with the progress of cell differentiation. The immunoreaction for Hsp 25 in the enamel organ revealed a characteristic stage-related alteration during amelogenesis. In secretory ameloblasts, the immunoreaction for Hsp 25 was found throughout their cell bodies, intense reactivity being located near the proximal and distal terminal webs. At the maturation stage, ruffle-ended ameloblasts (RA) consistently showed Hsp 25-immunoreactivity throughout the cell bodies, whereas smooth-ended ameloblasts (SA) lacking a ruffled border were weak in immunoreaction at the distal cytoplasm. Other cellular elements of the enamel organ were negative. The subcellular localization of Hsp 25-immunoreactivity in this study appeared essentially identical to that of actin filaments as demonstrated by confocal microscopy using rhodamine-labeled phalloidin. These immunocytochemical data suggest that the Hsp 25 molecule is involved in reinforcement of the cell layer following cell movement during odontogenesis and in the formation and maintenance of the ruffled border of RA.

Delayed expression of calbindin D28k during regeneration of the periodontal Ruffini endings of the rat incisor following injury to the inferior alveolar nerve.

Expression of calbindin D28k (CB)-like immunoreactivity (-LI) was compared with that of protein gene product 9.5 (PGP 9.5), a general neuronal marker, in the periodontal ligament of the rat lower incisor following resection of the inferior alveolar nerve (IAN). In normal animals, the periodontal nerve fibers showing PGP 9.5-LI formed either Ruffini endings with expanded arborization or thin free nerve endings in the alveolar half of the ligament. Thick CB-like immunoreactive (-IR) nerve fibers terminated in a dendritic fashion in the same region, but thin CB-IR nerve fibers were rarely detected. During the 3 days following resection of the IAN, most of the PGP 9.5-IR and all CB-IR nerve fibers disappeared. Regenerated PGP 9.5-IR nerve fibers appeared around 7 days after resection, in contrast to the very small number of regenerated CB-IR nerve fibers. Around 21-28 days following resection, the number and terminal morphology of regenerated PGP 9.5-IR nerve fibers were comparable to those observed in normal animals, but the number of regenerated CB-IR nerve fibers was still smaller. The terminal morphologies of these regenerated CB-IR nerve fibers showed less expansion compared with normal animals at these post-injured periods. The number of regenerated CB-IR nerve fibers increased gradually to return to normal by 56 days following injury. The delayed expression of CB in the regenerated periodontal Ruffini endings suggests that the functional recovery of periodontal Ruffini endings occurred after the regeneration of periodontal Ruffini endings had been completed.

Immunocytochemical demonstration of laminin in the synovial lining layer of the rat temporomandibular joint.

This immunocytochemical study describes the distribution of laminin in the synovial lining of the rat temporomandibular joint. Laminin immunostaining was present around some synovial lining cells and blood vessels. Ultrastructurally, immunoreactive products for laminin were deposited around cells with a well-developed rough endoplasmic reticulum and secretory granules, suggesting that they were type B synovial lining cells. The localization of laminin immunoreactivity was not uniform around the cell membrane, the most intense immunoreaction being present on the basal aspect membrane as is seen in the basement membrane of epithelia. In contrast, macrophage-like synovial lining type A cells did not show laminin immunoreactivity. This different immunostaining pattern suggests that laminin acts as an adhesion molecule for the type B cells in their epithelial-like arrangement.

Concomitant use of prostaglandin E1 and prednisolone; inhibition of superoxide anion production by polymorphonuclear leucocytes.

We investigated the effect of prostaglandin E1 (PGE1) or prednisolone on superoxide anion production by polymorphonuclear leucocytes (PMN) stimulated by opsonized zymosan (OZ). The production of superoxide anion by PMN was significantly suppressed by treatment with either PGE1 or prednisolone. Concomitant use of PGE1 and prednisolone suppressed it significantly more than PGE1 or prednisolone alone. Both PGE1 and prednisolone suppressed the Ca2+ influx into PMN, which was a crucial event for production of superoxide anion in stimulation by OZ. The effect of concomitant use of PGE1 and prednisolone in vivo was confirmed in rat peritonitis. The additional use of PGE1 with prednisolone may provide a strategy to reduce the amount of prednisolone required in treatments.

Clinical effectiveness of lansoprazole in patients with gastric ulcers: evaluation of quality of ulcer healing based on endoscopic ultrasonographic findings.

The effects of lansoprazole (30 mg/day) in 18 patients with gastric ulcers and the quality of ulcer healing were studied using endoscopy (including dye endoscopy) and endoscopic ultrasonography (EUS). The results showed an 8-week endoscopic healing rate of 94.4% and an S2-stage shift rate of 11.1%. In dye endoscopic findings of 11 S1-stage patients, S1b healing with regenerated mucosa close to S2 was seen in 63.6%. In a study of EUS findings, E0 with few relapses and high quality of healing accounted for 44.4%. When E0 rates were compared with the scarring images seen in endoscopic findings, the rates were 100% for S2, 66.7% for S1b, and 33.3% for S1a. These results indicate that a high degree of ulcer healing was achieved with lansoprazole, as good contraction of the ulcer tissue and early maturation of regenerated epithelium were observed.

[An autopsy case of a patient with myasthenia gravis who showed various symptoms of collagen diseases and complicated with malignant thymoma].

A 37-year-old man suffered from photosensitivity and urinary casts with serological findings of positive anti-DNA antibody, LE cells and false positive VD reaction in September of 1979. He developed general fatigue, dyspnea and diplopia with ptosis of bilateral eyelids in November of 1979, which were improved by the anti-cholinesterase drugs. In January of 1980, he had an attack of unconsciousness and his chest X-ray film showed several tumorous shadows in the anterior mediastinum and middle and lower lung fields. Treating him with chemotherapy of VEMP, the pulmonary shadows disappeared. However, he developed severe muscle weakness with an elevated CPK (430 mU/ml) and a myogenic EMG pattern along with an increased anti-acetylcholine receptor antibody (243 n Mol/l), dysphagia and eyelid-ptosis. He died in September of 1985 and his autopsy disclosed a malignant thymoma of mixed type in the anterior mediastinum and an atrophy and fibrosis with infiltration of inflammatory cells in the striated muscles.

[Myocardial contrast echocardiography using artificial blood (Fluosol-DA): a comparison with left ventricular wall motion in the experimental ischemic heart].

In the present study, myocardial contrast echocardiographic enhancement was compared with left ventricular wall motion in an experimental ischemic heart according to the degree of narrowing of the coronary artery. Artificial blood (Fluosol-DA) was used as a contrast agent. In eight adult mongrel dogs, ischemic hearts with 0, 50, 70 to 90 and 100% narrowing of the coronary artery were produced by controlling a balloon catheter in a closed-chest system. Fluosol-DA was injected into the left main coronary artery and myocardial contrast echocardiograms were recorded. The short-axis images of the left ventricle were subdivided into octants using a "floating" reference system to analyze wall motion by an image analyzer (Cardias GP2000), and to evaluate density values in the echocardiogram by densitometry (MSR Vx-50). With 0 and 50% narrowing of the coronary artery, the entire circumferential myocardium was filled with marked contrast echoes, and no change was observed in left ventricular wall motion. In 70 to 90% narrowing, the perfusion area of the narrowed coronary artery was filled with mild contrast echoes compared to the other areas showing marked contrast echoes. But no change was observed in left ventricular wall motion. During total occlusion, the perfusion area of the occluded coronary artery was not filled with contrast echoes and a distinct difference was observed between this and the other areas. Marked abnormality of wall motion was also observed. The area with abnormal wall motion tended to be wider than the area of contrast enhancement defect. The ischemic area can therefore be more accurately confirmed by simultaneously observing the changes in contrast echocardiographic enhancement and in wall motion abnormalities.

[Left ventricular hypertrophy in hypertensive and athlete's hearts: echocardiographic and vectorcardiographic characteristics].

The difference in the patterns of left ventricular hypertrophy (LVH) between the athlete's heart (Judo player: Judo-Ath group) and the hypertensive heart (HT group) was studied using vectorcardiography and echocardiography. The both groups were classified into two types based on the pattern of a QRS loop vector in the horizontal plane, respectively. One type (type II) satisfied the vectorcardiographic criteria of LVH by Upshaw, and the other (type I) did not satisfy it. The subjects composed of 12 Ath-I, 18 Ath-II, 10 HT-I and 16 HT-II. In the Ath-I, the characteristic vectorcardiogram was demonstrated in the horizontal plane, where an increased amplitude of an initial QRS vector was in the right and anterior direction. A mean ratio of the thickness of the interventricular septum to left ventricular posterior wall (IVSTd/PWTd) was 1.20 (p less than 0.001) in their echocardiograms. In HT-I, on the other hand, a decreased amplitude of an initial anterior vector and an increased amplitude of a posterior vector were observed in the horizontal plane. IVSTd and PWTd did not increase in these patients. These results indicated that an increased amplitude of an initial QRS vector in Ath-I is a reflection of the increased IVSTd. In type II, both IVSTd and PWTd were symmetrically increased. Concerning a spatial maximum QRS magnitude and left ventricular mass (LV mass), there was a significant correlation between the two only in HT-II (r = 0.75, p less than 0.01). It was concluded that there was some vectorcardiographic and echocardiographic differences between the left ventricular hypertrophic patterns of the athlete's heart and the hypertensive heart.