The prophage of SP beta c2dcitK1, A defective specialized transducing phage of Bacillus subtilis.

The defective specialized transducing phage SP beta c2dcitK1 carries two known bacterial genes, kauA and citK, as well as SP beta hage markers including the heat-sensitive repressor allele, c2. Some phage genes (including essential ones) are missing. When SP beta c2dcitK1 transduces SP beta-sensitive cells of Bacillus subtilis, the defective prophage is inserted into sites in the homologous bacterial DNA of the attSP beta-kauA-citK region of the recipient chromosome. During the growth of these transductants, occasional excisions occur that result in the loss of the phage genes and of the heterogenotic state. These excisions increase greatly in frequency during growth at repressor-inactivating temperatures. The kinds of insertions and excisions seen suggest that a Campbell-type (CAMPBELL 1962) circular phage genome may occur transiently. If the transductants are superinfected by SP beta c2 or by the clear-plaque mutant SP beta c1, the resulting double lysogen can be heat induced to release high-frequency-of-transduction (HFT) lysates for kauA and citK.

Primary pulmonary hypertension and cirrhosis: are they related?

The relationship of primary pulmonary hypertension to longstanding portal hypertension secondary to hepatic cirrhosis was examined. An unselected series of 17,901 autopsied patients older than 1 yr of age showed that primary pulmonary hypertension occurred with a prevalence of 0.13% in all patients, but with a prevalence of 0.73% among patients with cirrhosis (p less than 0.001). A clinical series of 2,459 patients with biopsy-proved hepatic cirrhosis showed a prevalence of primary pulmonary hypertension of 0.61%, also significant (p less than 0.001) when compared with the prevalence among all patients older than 1 yr of age at autopsy. These data appear to exclude a coincidental association of cirrhosis with the development of the vascular lesions of primary pulmonary hypertension.