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Buckle S 《Bioethics》1988,2(3):226-253
Buckle's article is one of three discussing the potentiality of the human embryo in this issue of Bioethics devoted to the subject of embryo research. (See also Michael Lockwood's "Warnock v. Powell (and Harradine): when does potentiality count?" and Richard M. Hare's "When does potentiality count? A comment on Lockwood.") In his essay, Buckle analyzes some of the distinct ways of arguing about potential, and the different senses of potential on which these arguments rely. He also examines some of the criticisms of the argument from the potential and replies to them, and shows why the argument's protagonists and critics are often at cross-purposes.  相似文献   
96.
Summary Canine cardiac sarcoplasmic reticulum is phosphorylated by adenosine 3,5-monophosphate (cAMP)-dependent and by calcium · calmodulin-dependent protein kinases on a 27 000 proteolipid, called phospholamban. Both types of phosphorylation are associated with an increase in the initial rates of Ca2+ transport by SR vesicles which reflects an increased turnover of elementary steps of the calcium ATPase reaction sequence. The stimulatory effects of the protein kinases on the calcium pump may be reversed by an endogenous protein phosphatase, which can dephosphorylate both the CAMP-dependent and the calcium · calmodulin-dependent sites on phospholamban. Thus, the calcium pump in cardiac sarcoplasmic reticulum appears to be under reversible regulation mediated by protein kinases and protein phosphatases.  相似文献   
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Summary Suppression of Lutheran blood group expression is usually associated with an autosomal dominant suppressor gene In(Lu) which results in the rare Lu(a-b-) phenotype. X-linked recessive suppression can also occur under the control of the XS locus with normal (XS1) and suppressor (XS2) alleles. The only known kindred with XS2 segregating was examined for polymorphic DNA markers with known regional localisations on the X chromosome. Two point linkage analysis suggested linkage of XS to DXS14 (p58.1) with =0.00, =1.96. DXS14 is situated near the centromere at Xp11. Recombinants with DXS84 (distal to DXS14 on Xp) and recombinants with DXYS1 (pDP34) (on the proximal part of Xq) suggests a localisation for XS near the centromere, between DXS84 and DXYS1 (Xp21.2-Xq21.1). Linkage to a marker on the X chromosome confirms the original assignment of XS to the X chromosome, which was based on pedigree inspection from this family.  相似文献   
98.
Summary The relationship between immune function and chemically induced hepatocarcinogenesis was studied employing an in vivo murine model. Neonatal B6C3F1 mice were given a single carcinogenic dose of diethylnitrosamine (DEN) and the time-response kinetics for the early (foci of alteration) and late (adenomas/carcinomas) phases of hepatocellular carcinogenesis were compared to changes in hematopoiesis and immune functions associated with immune surveillance and natural resistance. Increases in hematopoiesis occurred just prior to or concurrent with the appearance of hepatocellular carcinomas, while increased macrophage and natural killer cell cytotoxicity and suppression of cell-mediated immunity occurred following tumor appearance and progressed with increasing tumor burden. Neither immunological nor hematopoietic changes were associated with early phases of hepatocarcinogenesis, as monitored by the appearance of altered hepatocellular foci. Although changes in hematopoiesis may represent an early indicator for hepatocarcinogenesis in the mouse tumor model, the data suggest that altered immune surveillance and natural resistance are not factors in the development of chemically induced hepatocellular tumors, and the changes in immune function are probably secondary to tumor development.  相似文献   
99.
Summary The autosomal dominant form of polycystic kidney disease (ADPKD) has been linked to the -globin gene locus on 16p. Linkage studies between the autosomal recessive type (ARPKD) and the 3 HVR of the -globin gene cluster showed that the ARPKD and ADPKD are not allelic.  相似文献   
100.
Summary An inherited genetic disorder causes XY embryos of the horse to develop as mares. On the basis of our study of 38 such mares, we have identified four grades or classes of XY sex reversal according to this scheme: class I, nearly normal female, of which some are fertile; class II, female with gonadal dysgenesis, normal mullerian development; calss III, intersex mare with gonadal dysgenesis, abnormal mullerian development, enlarged clitoris; class IV, virilized intersex characterized by high levels of testosterone. In general, class I and calss II mares were typed H-Y antigen-negative whereas class III and class IV mares were typed H-Y antigen-positive.  相似文献   
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