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Biomedical subjects

M Shoji

Publications and source records attributed to M Shoji.

At least 289 records · Page 16Linked to original sources
PubMed1989

[Assessment of dentofacial growth changes using quadrilateral analysis].

This study was investigated to demonstrate the normal standards of the quadrilateral analysis and thereafter to clarify the mode of growth change by assessment of skeletal, dental and soft tissue proportion by the means of quadrilateral analysis. The materials used in this study consisted of cephalograms of 30 girls with normal occlusion. Cephalograms were taken longitudinally from first year grade of elementary school to third year grade of middle high school. For the group of each year grade, mean facial diagram, mean values of conventional cephalometric analysis and those of quadrilateral analysis were made, and compared and discussed for each other. The results were as follows: 1) The mandible grows forward with the decrease of gonial angle and forward rotation of mandibular plane. 2) In quadrilateral analysis, both jaws grow proportionally to the 6 year grade of elementary school, and after then mandible grows more forward than maxilla. 3) Though occlusal plane tended to rotate counterclockwisely to the palatal plane, it fell at right angle with A'B'. 4) Upper centrals tended to incline labially to the cranial base from first year grade to 6 year grade of elementary school and after that stage it remained stable. Lower centrals varied to third year grade of elementary school, but after that stage it remained stable. 5) Distances of upper and lower incisors to A'B' showed comparatively constant increase after the full eruption of permanent incisors. 6) Distance of nose tip to A'B' increased the most in the soft tissue landmarks. Subnasale soft pogonion line was considered to be effective base line of soft tissue profile because the angle with A'B' was stable along the growth and the distances of that to upper and lower lips were stable.

Adolescent↗
PubMed1989

[An immunocytochemical study of alpha 1-antichymotrypsin in the senescent cerebral amyloid].

An immunocytochemical study of alpha 1-antichymotrypsin (alpha 1ACT) was performed in order to demonstrate its localization and the relationship between alpha 1ACT and senescent cerebral amyloid. We examined 5 brains with dementia of the Alzheimer type (SDAT), a peripheral nerves of familial amyloidotic polyneuropathy (variant transthyretin type, FAP) and dorsal root ganglions of a primary amyloidosis with peripheral neuropathy (AL type, PA). Avidin-biotin-peroxidase complex method and double immunoenzymatic staining method (peroxidase-antiperoxidase method combined with avidin-biotin-alkaline phosphatase complex method) were used. Anti-beta protein serum was used as the marker of cerebral amyloid. About 98% of senile plaques had alpha 1ACT like-immunoreactivity (alpha 1ACTI). All types of plaques showed the immunoreactivity: Core and peripheral of typical plaques, primitive plaques, core plaques and amorphous cerebral amyloid deposits. Although, a part of a senile plaque showed beta protein like-immunoreactivity alone and the other part had alpha 1ACT, many remainder part of a senile plaque had both immunoreactivity. Of the other pathological changes of SDAT, eosinophilic tangles and cerebrovascular amyloid were positive, in contrast, intracellular tangles, granulovacuolar degeneration and Hirano body were negative. The amyloid from FAP had weak alpha 1ACTI and diffusely stained. alpha 1ACTI was seen in the peripheral margin of the amyloid from PA. These results indicate that alpha 1ACT is closely associated with senile plaques formation.

Aged↗
PubMed1989

Electron micrograph of diffuse plaques. Initial stage of senile plaque formation in the Alzheimer brain.

The ultrastructure of diffuse plaques (devoid of both amyloid core and swollen neurites) in the frontal cortex of an Alzheimer brain was examined, using paired routine electron microscopic ultrathin sections and adjacent 0.4-micron-thick semithin sections. The semithin sections, treated with formic acid and beta protein immunostain, showed abundant diffuse plaques. In the adjacent ultrathin section, diffuse plaques usually showed some scattered bundles of amyloid fibrils between focally blurred membranes of cell process. The diffuse plaques were nearly undetectable without the semithin beta protein immunostained preparations, because the neuropils within these plaques appeared almost normal morphologically. Capillaries, which rarely appeared in the center of the diffuse plaques, demonstrated no amyloid fibrils in their walls. These findings suggest that in the initial stages of senile plaque formation amyloid fibrils are formed sporadically between cell processes, but not around the capillaries.

Aged↗
PubMed1989

Immunocytochemical study of alpha 1-antichymotrypsin in the senescent cerebral amyloid.

We immunocytochemically examined the brains of patients with dementia of the Alzheimer type (DAT), to clarify the relation between alpha 1-antichymotrypsin and cerebral amyloid. Antiserum to synthetic beta protein (1-28 residue) was used to stain the senile plaque amyloid and cerebrovascular amyloid. Cryostat sections and paraffin embedded sections pretreated with formic acid were prepared for staining beta protein-like immunoreactivity. Fine, amorphous cerebral amyloid deposits were also positive. alpha 1-antichymotrypsin-like immunoreactivity was also found in senile plaques and cerebrovascular amyloid. Primitive plaque, typical plaque, core plaque and amorphous cerebral amyloid deposits had alpha 1-antichymotrypsin-like immunoreactivity. Eosinophilic extracellular tangles were also positive. Hirano bodies were weakly stained. Intracellular tangles and granulovacuolar degeneration were negative. Double immunoenzymatic staining revealed that alpha 1-antichymotrypsin-like immunoreactivity was very closely related to beta protein-positive senile plaques. About 99% of all plaques had both alpha 1-antichymotrypsin- and beta protein-like immunoreactivities. These results indicate that alpha 1-antichymotrypsin is one of the components of the senile plaque amyloid.

Alzheimer Disease↗
PubMed1989

Serum concentration of alpha 1-antichymotrypsin is elevated in patients with senile dementia of the Alzheimer type.

Levels of the serum protease inhibitors (alpha 1-antichymotrypsin, alpha 1-antitrypsin, and inter-alpha-trypsin inhibitor) were measured in patients with senile dementia of the Alzheimer type (SDAT) to determine whether these levels might be useful as diagnostic markers of SDAT. The levels of alpha 1-antichymotrypsin were found to have no relationship to either age or sex. The SDAT group showed levels of alpha 1-antichymotrypsin significantly higher than those of any of the following groups: normal control group (p less than 0.001), vascular dementia group (p less than 0.01), mixed type dementia group (p less than 0.05), and 3 other groups (Parkinson's disease, spinocerebellar degeneration, cerebrovascular disease) (p less than 0.001). The serum concentration of alpha 1-antichymotrypsin seemed to increase slightly in advanced stages of the disease. The serum levels of both alpha 1-antitrypsin and inter-alpha-trypsin inhibitor differed insignificantly in comparison of the SDAT group and normal control group. Of the 3 serum protease inhibitors measured, only alpha 1-antichymotrypsin was found to increase significantly in SDAT. These findings suggest that the measurement of serum concentration of alpha 1-antichymotrypsin may prove useful as a diagnostic marker of SDAT.

Adult↗
PubMed1989

Immunogold electron microscopic study of cerebrovascular and senile plaque amyloid using anti-beta protein antibody.

Both light and immunogold electron microscopy revealed that beta protein is closely associated with cerebrovascular and senile plaque amyloid. Diffuse (very primitive) plaques of the cerebral cortex and cerebellum in subjects with senile dementia of the Alzheimer type (SDAT) were seen as ill-defined areas of the fine fibrillar materials labeled by beta protein immunostain and silver impregnation. Electron and immunogold electron microscopic investigation revealed that cerebral diffuse plaques consist of accumulations of small bundles of amyloid fibrils scattered among the normal-looking neurites including a few altered neurites. The cell process membranes just adjacent to amyloid fibrils were frequently missing. Cerebellar diffuse plaques had structures similar to cerebral diffuse plaques, with two qualifications. First, the former had more altered neurites, and second, enlarged neurites contained mainly dense bodies and abnormally dense mitochondria lacking filamentous materials. In conclusion, cerebral diffuse plaques, which are the main plaques in SDAT, consist chiefly of amyloid fibrils interspersed among a majority of normal-looking neurites and a minority of altered neurites. This suggests the importance of amyloid deposition in the genesis of senile plaques.

Alzheimer Disease↗
PubMed1988

Effects of thioether phospholipid BM 41.440 on protein kinase C and phorbol ester-induced differentiation of human leukemia HL60 and KG-1 cells.

The synthetic thioether phospholipid BM 41.440 (1-S-hexadecyl-2-methoxymethyl-rac-glycero-3-phosphocholine) was found to inhibit protein kinase C (PKC) activity competitively with respect to phosphatidylserine, with an apparent Ki value of about 6.4 microM. The agent also inhibited the enzyme activated by diolein or 12-O-tetradecanoylphorbol-13-acetate (TPA), without affecting binding of [3H]phorbol-12,13-dibutyrate to the enzyme. Myosin light chain kinase and cAMP-dependent protein kinase were not inhibited by BM 41.440, indicating a specificity of the action of the agent. BM 41.440 partly blocked the TPA-induced depletion of soluble PKC in HL60 and KG-1 cells (responsive to the differentiating effect of TPA) but not in K562 cells (resistant to the TPA effect). The thioether inhibited the phosphatidylserine/Ca2+-dependent phosphorylation of several common proteins in the solubilized homogenates of HL60 and KG-1 cells, and that of apparently distinct proteins in the preparation of K562 cells. The TPA-induced differentiation of HL60 and KG-1 cells was inhibited by BM 41.440 at a concentration inhibitory to PKC, but differentiation of HL60 cells promoted by dimethyl sulfoxide, retinoic acid, and 1,25-dihydroxyvitamin D3, on the other hand, was not affected. The present data suggested that PKC inhibition might partly account for the antineoplastic effect of BM 41.440, and that the agent could be useful in studying involvements of the PKC system in cellular processes.

Cell Differentiation↗
PubMed1988

Surgical therapy in two patients with pedunculated hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) occurring as an appendage from the main hepatic parenchyma is a rare entity, of which two cases are herein described. Because proper surgical management of this tumor (pedunculated HCC) is unclear, the world's literature was reviewed to determine optimal therapy. Thirty-four cases were documented, including the two cases reported herein. Diagnosis was usually obscure, despite modern invasive and noninvasive methods, and laparotomy or autopsy were required for specific identification of tumor type. Sixteen resections were reported among 18 explorations. One patient had transarterial embolization. Fifteen received medical therapy only. Surgically treated patients usually died of metastatic disease, whereas most medically treated patients died of gastrointestinal or tumor hemorrhage. Pedunculated HCC may be more amenable to curative resection than ordinary HCC due to its unique localization and growth pattern.

Aged↗
PubMed1988

Diffuse type of senile plaques in the brains of Alzheimer-type dementia.

We studied the nature of diffuse type of senile plaques (SP) in the brains of six autopsied subjects with Alzheimer-type dementia (ATD). The densities of SP in the entorhinal cortex were evaluated using serial sections stained by four different methods. Compared with beta protein immunostaining (100% as a reference), the modified Bielschowsky stain (103%) and the periodic acid-methenamine silver (PAM) stain (109%) labeled similar numbers of SP, whereas the Bodian stain labeled only a minor proportion (42%) of these. The vast majority of Bodian-negative plaques were diffuse plaques, which were seen as ill-defined areas of fine fibrillar material after beta protein immunostain with formic acid pretreatment, modified Bielschowsky stain, and PAM stain. They were not stained by Congo red or periodic acid-Schiff stains. Double staining using Bodian and beta protein methods demonstrated that diffuse plaques were free of swollen neurites. Argyrophilia of the diffuse plaques shown by the modified Bielschowsky and PAM stains, became undetectable when sections were pretreated with formic acid. Such treatment made the diffuse plaques immunoreactive to beta protein antiserum, suggesting that diffuse plaques consisted mainly of amyloid, but not neuritic components. The diffuse plaques were distributed in various cortical areas and in the amygdala, and comprised a considerable population of the SP in the ATD brains.

Aged↗
PubMed1988

A variety of cerebral amyloid deposits in the brains of the Alzheimer-type dementia demonstrated by beta protein immunostaining.

We studied cerebral amyloid deposits in the hippocampal area immunohistochemically, using antiserum to synthetic beta peptide (1-28) in 66 patients with or without dementia and aged 17 to 91 years old. Senile plaques (SP) and amyloid angiopathy (AA) were detected in 36 (55%) and 19 (29%) patients, respectively. Also, cerebral amyloid deposits from the brains of seven patients with dementia and five patients without were studied in serial sections stained with Bodian, modified Bielschowsky, Congo red, and beta protein immunostain. In the patients with Alzheimer-type dementia (ATD) diffuse plaques, typical of this group, were stained with beta protein antiserum but not with Bodian stain, because the plaques were devoid of abnormally swollen neuritic processes. The diffuse plaques often contained one or more neuronal cell bodies. As well as primitive and classic plaques and AA, the beta protein immunostain demonstrated small deposits among the SP, small stellate deposits of layer 1, subpial fibrillar deposits, and focal cribriform deposits of parasubiculum, which may be new types of amyloid deposits. Amyloid plaques within the subcortical white matter were only found in ATD brains. In the non-demented patients various kinds of SP, including diffuse and compact ones, were immunostained. They tended to be small and few. beta protein immunostain with formic acid pretreatment is a useful method for the identification of a variety of senile cerebral amyloid deposits.

Adolescent↗
PubMed1988

Synthesis and hypolipidemic activity of 2-substituted isobutyric acid derivatives.

A series of 2-substituted isobutyric acid derivatives have been synthesized and evaluated as hypolipidemic agents. Compounds 11 and 20 were found to decrease the level of plasma total cholesterol in experimental hyperlipidemic rats to a greater extent than clofibrate (CF) and to increase the level of plasma high-density lipoprotein cholesterol to the same extent as gemfibrozil (GF). Increase in liver weight caused by these compounds were less than those with CF and GF.

Animals↗
PubMed1988

Effect of vasopressin on atrial natriuretic peptide release and renal function in dogs.

To assess the effect of arginine vasopressin (AVP) and 1-deamino-8-D-AVP (DDAVP) on atrial natriuretic peptide (ANP) release, renal water and electrolyte excretion, and cardiovascular function, AVP and DDAVP were administered at a dose of 10 ng.kg-1.min-1 iv for 30 min into anesthetized dogs receiving saline infusion at a rate of 1 ml.kg-1.min-1 (n = 12). In the control study, saline was infused alone (n = 6). AVP potentiated the plasma ANP response to an increase in plasma volume produced by saline infusion, increased mean arterial blood pressure (MAP), and exaggerated the natriuresis and kaliuresis. DDAVP did not potentiate the increase in plasma ANP but enhanced the natriuresis without any rise in MAP. Saline alone increased plasma ANP as well as sodium and potassium excretion with no changes in MAP. Inulin and p-aminohippuric acid clearances did not change during these studies. The results suggest that in hydrated dogs, AVP may increase ANP release and arterial blood pressure via the vasopressor activity of AVP and potentiate the natriuresis and kaliuresis, but the increased ANP may play little role in the natriuresis.

Animals↗
PubMed1988

Effects of hemorrhage on vasopressin and Met-Enk releases in blood and cerebrospinal fluid in dogs.

To assess whether hemorrhagic shock causes simultaneous release of methionine enkephalin-like substance (MELS) and arginine vasopressin (AVP) both in cerebrospinal fluid (CSF) and circulating blood, continuous bleeding at a rate of 1 ml.kg-1.min-1 was undertaken for 40 min in anesthetized dogs (n = 6) and mean arterial pressure and heart rate were measured. In a time control study (n = 6), hemorrhage was omitted. Plasma AVP and MELS concentrations did not differ from CSF AVP and MELS in the control period in either the hemorrhage or the control groups. In the hemorrhage group, plasma AVP increased at 20 min and thereafter during the hemorrhagic shock, and plasma MELS increased at 30 and 40 min. No changes in AVP and MELS in the CSF occurred during hemorrhage, except a rise in AVP at 40 min. In the control group, AVP and MELS in the plasma and CSF did not change during the study, except for a rise in CSF AVP at 40 min. MELS was found in three forms: its large-molecular-weight form, methionine enkephalin, and metabolite; but the large-molecular-weight form was only observed in the CSF. These results showed that hemorrhage increases circulating MELS and AVP, but not MELS and AVP in the CSF, except for a slight rise in AVP during severe hypotension.

Animals↗
PubMed1988

[Pharmacological studies of "reiousan" which contains bezoar and ginseng].

Pharmacological properties of "Reiousan", a crude drug preparation consisting of bezoar and ginseng, were studied. The hypotensive effect on spontaneously hypertensive rat, inhibition of platelet aggregation, acetic acid-induced writhing, stress ulcer, CCl4 and d-galactosamine-induced hepatic injury, and facilitation of recovery from neuroparalysis and muscular fatigue, protective effect on anoxic brain damages, antipyretic effect, and facilitation of learning in aged mice were observed after administration of "Reiousan". It was suggested that bezoar and ginseng act synergistically in causing the hypotensive effect, acetic acid-induced writhing and drug-induced hepatic injury, and protection from anoxic brain damages and muscular fatigue.

Animals↗