Protective effect of prostaglandins D2, E1 and I2 against cerebral hypoxia/anoxia in mice

The protective effect of prostaglandins (PGs) against cerebral hypoxia/anoxia was investigated with a variety of experimental models in relation to their CNS depressant effects in mice. Furthermore, the effect of PGs on the changes of cerebral energy metabolites and cyclic nucleotide was examined in hypoxic mice. Mice were given s.c. doses of PGs 30 min before tests. Among the PGs tested, treatment with PGD2, PGE1 and PGI2 Na showed a consistent and dose-dependent protection against cerebral anoxia induced by all models studied: histotoxic anoxia by KCN, hypobaric hypoxia, normobaric hypoxia and decapitation-induced gasping. However, PGA1, PGA2, PGB1, PGB2, PGE2, PGF1 alpha, PGF2 alpha and 6-keto-PGF1 alpha at a dose of 3 mg/kg were without effect against normobaric hypoxia and gasping duration. The three PGs, i.e. PGD2, PGE1 and PGI2 which showed anti-hypoxic effects decreased locomotor activity and potentiated hexobarbital-induced sleep. On the other hand, PGE2, PGA1, PGA2 and PGB2 also caused a decrease in locomotor activity. Similarly, PGE2 and PGA1 caused a potentiation of hexobarbital-induced sleep, but interestingly they did not cause clear-cut increase in cerebral resistance to hypoxia, in contrast with the former three PGs. Thus general depression of CNS function appears not to be responsible for the PGD2-, PGE1- and PGI2-induced increase in cerebral resistance to hypoxia. The levels of Cr-P and ATP were significantly reduced and those of ADP and AMP were markedly elevated in hypoxic brain, resulting in a decrease in a calculated energy charge potential. The lactate level and lactate/pyruvate ratio increased and the glucose level decreased markedly.(ABSTRACT TRUNCATED AT 250 WORDS)     

骨髓移植诱导免疫耐受家兔全耳同种移植

目的　为了减轻免疫诱导过程中对受体的侵袭 ,进一步探讨以家兔为动物模型 ,通过异体骨髓移植诱导同种皮肤移植免疫耐受。方法　通过骨髓腔内直接注射异体骨髓细胞 ,进行骨髓移植。结果　皮片的平均存活时间是 (88.0± 6 .0 )天 (P <0 .0 0 1 )。为了探讨其普遍性 ,我们用此诱导方法 ,还进行了同种全耳移植。平均存活时间是 (1 4 6 .0± 1 5 .1 )天 ,并有 1只移植耳存活时间已超过 1年 ,未见任何排斥反应。结论　本研究证明了以家兔为动物模型 ,在不使用免疫抑制剂的情况下 ,通过骨髓腔内直接注射异体骨髓细胞 ,进行骨髓移植的方法 ,不仅在皮肤移植上可以诱导长期稳定的特异性免疫耐受 ,而且在实质性器官耳的同种移植上取得了良好的效果     

Uterus didelphys with unilateral imperforate vagina and ipsilateral renal agenesis

Uterus didelphys with unilateral imperforate vagina is rare. Interestingly, in all reported cases in which the urinary tract was investigated renal agenesis was found on the side of the obstructed hemivagina. We report 2 cases of this unusual and interesting condition, and review the embryogenesis of müllerian duct abnormalities associated with renal agenesis, as well as the clinical findings, diagnosis and management. We stress the importance of prompt and accurate diagnosis, and treatment as a means to avoid unnecessary surgical procedures.     

Complement-mediated lysis of K562 human leukemic cells by antibodies to phosphotyrosine and identification of cell surface proteins phosphorylated on tyrosine

Intact K562 human leukemic cells showed bright membrane immunofluorescence after staining with monoclonal antibody to O-phosphotyrosine (PTyr). Up to 60% of the cells were lysed with mouse, rabbit, or human antibodies to PTyr by a complement-mediated mechanism. A new method has been developed for identifying proteins that have PTyr residues on the outside of cell membrane, and at least two species of PTyr-containing proteins with the molecular weights of 45,000 and 36,000 were identified as the most probable candidates of the antigens responsible for the membrane fluorescence and cell lysis.     

Inferior vena caval stent filter

New inferior vena caval filters for percutaneous placement were made by attaching filter wires similar to those in the bird's nest inferior vena caval filter onto expandable metallic stents. These stents formed a base on which to anchor the filter to the wall of the inferior vena cava. The stent filter can be introduced through a 12- to 13-French catheter sheath system. The system was successfully tested in 13 dogs.     

Mitogenic activity and receptor reactivity of hybrid molecules containing portions of the insulin-like growth factor I (IGF-I), IGF-II, and insulin molecules

Insulin and the insulin-like growth factors IGF-I and IGF-II are thought to exert their mitogenic effects in cultured chick embryo fibroblasts and human skin fibroblasts via IGF receptors rather than via insulin receptors. These effects appear to be mediated by the type I subtype of IGF receptor, which is structurally similar to the insulin receptor and exhibits significant cross-reactivity with insulin. As a first step in our long-range goal of defining those features of the IGF-I and IGF-II molecules that confer enhanced mitogenic activity and reactivity with these mitogenic type I IGF receptors, we have prepared two hybrid insulin-IGF molecules and examined their mitogenic and binding activities: (1) A27-insulin, containing an elongated 27-residue A-chain (in which the 6-residue D-domain of IGF-II was added to the carboxy-terminus of the 21-residue A-chain of insulin) combined with the B-chain of insulin; and (2) A insulin-B IGF-1, containing the A-chain of insulin and the synthetic 30-residue B-domain of IGF-I. Both hybrid molecules stimulated DNA synthesis and inhibited 125I-IGF-I binding to type I IGF receptors in both chick embryo and human fibroblast cultures. A27-insulin had considerably greater mitogenic potency and binding potency than A insulin-B IGF-I. Neither hybrid molecule was more potent in these assays than insulin, indicating that the presence of D IGF-II or B IGF-I by itself was not sufficient to increase the mitogenic potency of insulin in fibroblasts. By contrast, A insulin-B IGF-I showed enhanced reactivity with an antiserum to IGF-I. A27-insulin retained significant insulin-like metabolic activity despite the presence of the D-domain of IGF-II.     

Hydrops Fetalis Caused by Fetal Kasabach-Merritt Syndrome

There have been only 2 previous reports of nonimmunologic hydrops fetalis (NIHF) caused by fetal Kasabach-Merritt syndrome, both of which were pathological studies. This is the first clinical case report of NIHF due to fetal Kasabach-Merritt syndrome that was prenatally diagnosed by sonography, computerized tomography, and percutaneous umbilical blood sampling.