The frequency of the D allele of an insertion/deletion (II D) Invest. 1994Invest. .94:1085Invest. -1089

No abstract

ACE genotyping may be helpful in determining the diagnostic significance of mildly elevated serum ACE activity in patients with the II and ID genotypes.

Plasma angiotensinogen is elevated in essential hypertensives and shows a strong correlation with blood pressure. Patients with hypertension often display insulin resistance and we have found previously an association of a Rsal RFLP in intron 9 of the insulin receptor gene (INSR) with hypertension. Since insulin resistance is accompanied by hyperinsulinaemia and insulin can stimulate angiotensinogen production, we hypothesized that hypertension‐associated genotypes of INSR may be associated with elevation in plasma angiotensinogen. We used PCR to detect a Nsil RFLP in exon 8 of INSR and examined its relationship with plasma angiotensinogen, as well as hypertension, in 134 Caucasian hypertensives with two hypertensive parents and in 126 normotensives. Plasma angiotensinogen tracked weakly with the major allele of the Nsil RFLP in hypertensives (p=0.08). Moreover, the frequency of this allele was higher in lean hypertensives than in lean normotensives (p<0.05) and in normolipidaemic hypertensives than normolipidaemic normotensives (p<0.02). The present study thus suggests that there could be a relationship of plasma angiotensinogen with INSR genotype, and of each with hypertension.

Infection with poliovirus effectively inhibited the translation of Vero cell messengers (carrying type 1 or type 2 caps at the 5' end) and of influenza virus messengers (type 1 caps) in co-infections. In contrast, Kunjin virus RNA (type 1 caps) and Semliki Forest virus RNA (a togavirus, with type 0 caps) continued to be translated in the presence of co-infecting poliovirus. Translation of Kunjin virus RNA was also unaffected during co-infections with either influenza virus or Semliki Forest virus. Guanidine treatment effectively blocked poliovirus replication only, but the inhibitory effect on translation of cell messengers and influenza virus messengers was still observed, indicating that this effect was not caused by competition in translation with poliovirus messengers. It was therefore concluded that the observed inhibition was most likely caused by cleavage of the p220 subunit of the cap binding protein (CBP) complex of the cell normally required for translation of capped messengers, as reported by others. However, Kunjin virus RNA could be efficiently translated apparently in the absence of a functional CBP complex, except when its secondary structure was stabilized by hypertonic salt in the culture medium.