ABSTRACT The teratogenicity of anti-testis antiserum was confirmed by an ex- periment using C57BL/6J mice. When the antiserum was administered intraperi- toneally to females on day 12.5 of pregnancy, reduction deformity of limbs and cleft palates were produced in the fetuses. Examinations of the internal organs and skeletons revealed no abnormality in the antiserum-treated mice. Immuno- histological analysis suggests the possibility that some antigen in the testis base- ment membrane may be involved.
ABSTRACT The hindleg rectus femoris muscles of normal (?I+) and dystrophic (dyldy) mice of the strain C57BL/6J-dy were examined morphometrically on their cross sectional microscopic images. The diameter of dystrophic muscles was similar to that of normal muscles at 11 and 14 days of postnatal age, and increased with age up to 26 days at a slower rate than that of normal muscles, and then stopped increasing. After 90 days of age, it tended to decrease slightly. The number of myofibers per muscle was always much smaller in dystrophic than in normal mus- cles during a period from 11 to 32 days, and remained almost unchanged in dystro- phic muscles during and after the period up to 120 days of age. The mean diameter of the largest fifty myofibers in dystrophic muscles steadily increased, and the dia- meter-frequency histogram of these myofibers shifted to the larger diameter, with age up to 70 days even after the diameter of muscles had stopped increasing. This paradoxical growth of a small population of the large or “hypertrophied” myo- fibers in growth-arrested muscles of dystrophic mice was discussed in relation not to an abnormal “hypertrophy” preceding degeneration but to a variation in growth capabilities of myofibers greatly shifted to incompetence.
ABSTRACT Embryopathy in yellow KK mice with non-insulin dependent diabetes mellitus was examined among the conceptuses of females mated at 7, 11, and 13 weeks of age. The numbers of corpora lutea and implants were comparable in all maternal age groups. Early embryonic deaths were frequently observed in all maternal age groups (37.7-46.4%), but no significant difference was found among the groups. The incidence of late embryonic deaths was significantly higher in 11- and 13-wk- old dams (25.6% and 28.8%) than in 7-wk-old dams (14.4%). Moreover, in 13-wk- old dams, but not in 7-wk-old dams, a positive correlation existed between maternal plasma glucose levels on day 18 of pregnancy and late embryonic deaths. Fetuses from 13-wk-old dams weighed less than those from 7-wk-old dams (0.73 g vs 0.86 g) Yellow KK mice mated at 13 weeks of age were treated with an oral-hypo- glycemic agent, 5- [4-( 1-methylcyclohexylmethoxy)benzyl] thiazolidine-2,4-dione (ciglitazone), as an 0.1% dietary admixture. Plasma glucose on day 18 of pregnancy was lower in all treated groups (159-170 mg/dl) than in the untreated control (345 mg/dl). A significant decrease of late embryonic deaths (12.7-15.6%) and a slight increase of fetal weights (0.79-0.81 g) were noted when compared with the un- treated controls (36.8% and 0.74 g).
ABSTRACT The trend of the delivery of health care services for developmentally disabled children, especially those with congenital anomalies, is described. The importance of how the organization of community health services and the role of medicine and medical facilities mesh together in Japan is emphasized.
ABSTRACT Advances in research (bio-medical, psychological, and social) can provided a better understanding of the causes and effects of mental retardation. And also, fundamental research (bio-medical, social, and neurobehavioral) into the causes of mental retardation is encouraged and facilitated. For the critical evalua- tion of neurobehavioral teratogenical effects, the Collaborative Studies for the Standardization of Behavioral Teratology Methods (CSSBTM) started in November 1983 in Japan. The Third CSSBTM in 1986 had in principle detailed evaluation on errors in the pultiple water T-maze. The Collaborative Behavioral Teratology Study was also conducted in USA, which had more extensive testing procedures rather than the CSSBTM. Apparently, advances in knowledge and techniques will increase our success in preventing the more severe conditions of mental retardation.
ABSTRACT Primordial germ cells (PGCs) in amniotes separate from the endoderm of the early embryo and finally migrate through the dorsal mesentery (DM), which is the last portion of the migratory pathway, into the gonadal anlage, while in birds and some reptiles, the cells temporarily circulate via the blood vascular system before undergoing this migration. To understand the role of extracellular matrix in the migration of PGCs, the distribution and localization of fibronectin (FN) were examined using direct immunoperoxidase staining in embryos of mice, chicks and man. In mouse embryos of 10.0 to 11.0 days of gestation, the DM was rich in FN, at which time the PGCs were at the peak of their migration. FN was localized at the sites of interaction between cytoplasmic processes of PGCs and the neighboring somatic cells. In man, a positive reaction to FN was found in the DM of 5-week old embryos, in which most of PGCs were migrating. In chick embryos at 2.5 days of incubation, the splanchnic mesoderm (SPM), into which the PGCs were passing from the blood vessels, was rich in FN. In 3.0-day-embryos, the DM, which was derived from the SPM, was rich in FN. FN was localized at the sites of interaction between pseudopodia of PGCs and the adjacent somatic cells. After the completion of PGC migration into the gonad, FN reaction was weakened or disappeared in every species examined. These results indicate that fibronectin plays a significant role in the interstitial migration of PGCs.
ABSTRACT Migration of newly-generated neuroblasts to their definitive loca- tions to form the laminated architecture of the brain is crucial in brain morpho- genesis. In order to understand the molecular mechanism operative in the neuro- blast migration, cell surface or pericellular glycoconjugates were isolated from the rat brains at various developmental stages. Hyaluronate (HA), chondroitin sulfate proteoglycans (CS-PGs), heparan sulfate proteoglycans (HS-PGs) and polysialosyl glycoproteins (N-CAMS) have been characterized so far. Our biochemical and immunohistochemical experiments indicate that HA and a CS-PG participate in construction of the hydrated extracellular milieu for the directional migration of neuroblasts. Dissociated fetal brain cells reaggregated and formed a tissue configuration, in aggregating culture for 48 h, similar to that observed in the original brain primor- dium. Therefore, one can consider that the in vitro process is regulated at least in part by the mechanism operative in brain morphogenesis in vivo. It was sug- gested that HS-PGs and N-CAMS were involved in the in vitro process of the tissue self-organization as cell membrane components. From these findings and others, we conclude that some developmental changes in the structure and the contents of these cell surface glycoconjugates of the brain are implicated in neuroblast migration in brain morphogenesis.
ABSTRACT Three major topics in vertebrate cardiogenesis were surveyed with special attention given to the cellular migration and the extracellular matrix (ECM). 1. Prior to primitive tubular heart formation, cardiogenic (lateral mesoderm) cells migrate on the endoderm to the definitive position ventral to the foregut. SEM observations of newt embryos revealed a subtle network of fine fibrils on the endodermal cell surface. These ECM fibrils were proved to be composed of fibronectin by immuno-SEM method using latex beads. 2. The epicardium does not differentiate in situ from so-called “epi-myo- cardium”, but is formed in such a way that tips of mesothelial cell clusters extend- ing from the septum transversum region attach to the dorsal side of the cardiac loop and spread gradually over the myocardium, eventually covering the entire heart. Using ruthenium red-containing fixative, precipitated ECM was found specifically on the myocardium. 3. Cells of the cushion mesenchyme are known to be liberated from the endo- thelial cells and migrate into the cardiac jelly. There is growing evidence that ECM affects the cellular behavior in this process. Furthermore, neural crest cells were shown to contribute to mesenchyme formation in the outflow tract. Dis- turbed formation of the cushion tissue likely results in various malformations of the heart.