ABSTRACT In order to clarify teratogenic mechanisms of congenital absence of the digits in longitudinal deficiencies, ulnar deficiency, radial deficiency, central polydactyly, osseous syndactyly and cleft hand (central deficiency) were analyzed. Then, the same anomalies induced in rat fetuses with myleran were analyzed. In ulnar and radial deficiencies, the more severe was the degree of finger deficit, the more severe was the arrest of the forearm bone. The critical periods of these anomalies were earlier than those of other anomalies. Ulnar deficiencies were induced only in Gun:Wistar rats and radial deficiencies only in WKAH/Hkm rats. A genetic factor may influence the teratogenesis of ulnar and radial deficiencies. From histological analysis of tibia1 deficiency, it may be suggested that the cause of absence of digits in longitudinal deficiency is closely related to a deficit of mesenchymal cells. The analysis of skeletal changes of central polydactylies, osseous syndactylies and cleft hands suggested that there seemed to be the cleft hand formation process from osseous syndactylies and central polydactylies. These anomalies were often observed in both hands in various combinations. They could be induced by the same treatment at the same developmental stage in rats. The teratogenic mechanism of cleft hand seemed to be failure of induction of digital rays in the hand plate.
ABSTRACT Guinea pigs were given disulfiram (125 mgkg) orally once each morning of days 17-19 or 19-21 of pregnancy. Brain weight was reduced in the offspring whose mother was dosed during days 19-21 of pregnancy. Females of both experimental groups were found to have smaller brains compared with the expected brain weight of similar body weight female controls. Male offspring of both experimental groups did not display any obvious reduction in brain weight.
ABSTRACT Hyperthermia was induced in rats twice at an interval of eight hours on both days 13 and 14 of gestation by partial immersion in a water-bath. Deep rectal temperature was raised to 42.5<C for five minutes. Body weights of newborn rats were reduced, but by three weeks of age compensatory post-natal growth had eliminated the defect. In both newborn and 21-day-old rats, brain weight was significantly reduced compared with controls of similar body weight. No other anomalies were found.
ABSTRACT Clinical features and roentgenographic findings of 37 patients (65 hands) with congenital ankylosis of the digital joints, including symphalangism and other types of congenital ankylosis of the joints, were analyzed. Congenital ankylosis of the digital joints was divided into four types according to the clinical features as follows; Type A (typical symphalangism), 13 cases, Type B (symphalangism without associated anoma- lies), 6 cases, Type C (symphalangism associated with hypoplasia of the affected digit), 10 cases and Type D (symphalangism as a part of syndrome), 8 cases. Roentgenographic findings of the affected joints were divided into 4 types, such as normal type (Type I), narrow type (Type 2), flat type (Type 3) and bony ankylosis (Type 4). There seems to be 4 types of joint development in congenital ankylosis of the digital joints. In Types 1 and 2, the joint space of the affected joint and the secondary ossification center looks normal. The joint seems to develop normally in Type 1, but the condyle of the affected joint becomes flat in Type 2. In Type 3, the joint space is narrow in infancy, the secondary ossification center fuses with the proximally located phalanx and finally the affected joint develops bony ankylosis. In Type 4, there is osseous fusion of the affected joint at birth.