Effects of gradual expansign on arterial stenosis

The blood flow through an arterial stenosis can theoretically be increased by gradual expansion of the stenosis. This hypothesis was tested by comparing the flow through abruptly expanding and gradually expanding stenosed plastic conduits. The conduits were tested in non-pulsatile flow with water and bank blood and in pulsatile flow in dog's descending aorta. It was found that:

1. (a)
   The pressure drop in arterial stenoses is larger than that predicted by non-pulsatile theory.     

Some further comments on the DNA-protein coding problem: A correction and a note

An error appearing in the proof of Theorem 4 of a previous paper of the author’s (1959,Bull. Math. Biophysics,21, 289–97) is pointed out, and a new proof of the theorem is supplied. We also obtain a corollary from Theorem 3 ofloc. cit. which reveals the existence of a hitherto unrecognized class of codes.     

THE INTERSEXED PATIENT

There are at present two opposing points of view on problems of dealing with the intersexed patient (not the typical homosexual or transvestite) who has clearcut anatomical or biochemical qualities of the opposite sex. The first is that in the growing child or adult coming for treatment, the sex the patient should adopt is the summation of somatic sex. The other is that the sex role should be assigned according to the predominant psychological identification already present.A case history of a middle-aged pseudohermaphrodite, castrated in youth but raised from birth as a female and living thus in “homosexual” relations with women until examined and interviewed at UCLA Medical Center is presented to illustrate the psychological problems in sexual identity with which the patient had to cope.Psychiatric investigation revealed how confused the patient''s sex identity was until treatment by a team consisting of psychiatrist, psychologist and endocrinologist permitted the patient, even at so late a date, finally to establish what his gender is. The patient was able, despite early rearing as a female and a castrating operation, to swing to a more masculine identification. This was possible because of some uncertainty of sexual role from an early age.     

Identification of enteroviruses by hemagglutination-inhibition

Kern, Jerome (Pacific Research Section, Honolulu, Hawaii), and Leon Rosen. Identification of enteroviruses by hemagglutination-inhibition. J. Bacteriol. 91:1936-1942. 1966.-Approximately 40% of a group of 906 enterovirus isolates cytopathic for monkey cell cultures were found to possess hemagglutinins for human erythrocytes when tested at temperatures of 4 and 37 C and at pH 5.8 and 7.3. The hemagglutinating isolates could be classified by relatively simple techniques into 18 serotypes. Four of these serotypes, echovirus type 24 and coxsackievirus B types 1, 5, and 6, had not previously been known to include hemagglutinating strains. One serotype, Toluca-3, represented a previously unrecognized enterovirus, and two other serotypes may also represent previously unrecognized enteroviruses.     

Relative contribution of promoter and intragenic sequences in the hormonal regulation of rat beta-casein transgenes

In order to identify DNA sequences responsible for the regulation beta-casein gene expression, lines of transgenic mice bearing the entire rat beta-casein gene and two rat beta-casein promoter chloramphenicol acetyltransferase (CAT) fusion genes have been established. All three transgenes have been shown previously to be regulated in a tissue- and stage specific manner. To investigate the relative contribution of promoter and intragenic sequences in the hormonal regulation of the beta-casein gene, mammary explant cultures derived from these lines of mice have now been performed, and the effects of PRL and glucocorticoids on transgene as compared with endogenous beta-casein gene expression have been quantified. After the addition of PRL to cultures performed in the presence of insulin and glucocorticoids, a 25- to 40-fold induction of endogenous mouse beta-casein mRNA was observed after 48 hr. A comparable greater than 25-fold induction of transgene expression after PRL addition was observed in explant cultures derived from a line of mice expressing the entire rat beta-casein gene. In contrast, PRL addition elicited only a 1- to 4.5-fold increase in CAT activity in cultures derived from two lines of mice bearing casein-CAT fusion genes with either 524 or 2300 base pairs of 5'-flanking DNA. In the presence of insulin, glucocorticoid or PRL addition alone increased endogenous beta-casein gene expression 2- to 2.5-fold and 5- to 10-fold, respectively, but only a 1.2- to 2.5-fold induction of CAT activity was observed for each hormone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Function of the human immunodeficiency virus types 1 and 2 Rev proteins is dependent on their ability to interact with a structured region present in env gene mRNA.

The interaction of the human immunodeficiency virus type 1 (HIV-1) Rev protein with a structured region in env mRNA (the Rev-responsive element [RRE]) mediates the export of structural mRNAs from the nucleus to the cytoplasm. We demonstrated that unlike HIV-1 Rev, which functions with both the HIV-1 and HIV-2 RREs, HIV-2 Rev functions only with the HIV-2 RRE. Rev-RRE binding studies suggested that the lack of nonreciprocal complementation stems from the inability of HIV-2 Rev to interact with HIV-1 RRE RNA. Maintenance of RNA secondary structure, rather than the primary nucleotide sequence, appeared to be the major determinant for interaction of both HIV-1 and HIV-2 Rev with the HIV-2 RRE. Moreover, the binding domain of the HIV-2 RRE recognized by HIV-1 Rev was dissimilar to the binding domain of the HIV-1 RRE, in terms of both secondary structure and primary nucleotide sequence. Our results support the hypothesis that function of HIV Rev proteins and possibly the functionally similar Rex proteins encoded by the human T-cell leukemia viruses (HTLVs) HTLV-I and HTLV-II is controlled by the presence of RNA secondary structure generated within the RRE RNA.