Homologies of Deoxyribonucleic Acids from Brucella ovis, Canine Abortion Organisms, and other Brucella Species

The bacterium that causes canine abortion has polynucleotide sequences similar, in deoxyribonucleic acid (DNA)-DNA homology studies, to those of Brucella suis and, by inference from previous data, those of B. abortus and B. melitensis as well as B. neotomae. Therefore, the organism causing canine abortion appears to be a member of the genus Brucella. DNA preparations from Serratia marcescens, Alcaligenes faecalis, and Bordetella bronchiseptica, 58, 62, and 66 mole% guanine plus cytosine, respectively, do not have detectable polynucleotide sequence homologies with B. suis DNA which is 56 mole% guanine plus cytosine. B. ovis DNA lacks some of the polynucleotide sequences present in B. suis DNA and appears to be a deletion mutant. However, a large proportion of B. ovis polynucleotides are similar to those of other Brucella species, which supports the inclusion of B. ovis in the genus.     

A Staining Procedure for Use in the Brucella Opsonocytophagic Test

The following staining procedure is recommended for use in the Brucella opsonocytophagic test in order to avoid confusing results obtained with stains of the Hasting or Wright type: Fix spreads for 5 minutes or longer in absolute methyl alcohol. Stain for 10 to 30 minutes in a solution of the following: 0.5 g. NaCl, 0.5 g. phenol, 0.5 g. methylene blue, 0.02 g. Na₂HPO₄+12H₂O, 50 cc. distilled water, 50 cc. methyl alcohol. Wash slides gently in water. Air dry. By this procedure, the bacteria and the nuclei of the leucocytes appear deep blue. The cytoplasm of the leucocytes appears faintly green with the cell outline distinctly visible. Cytoplasmic granules do not stain.     

Leber hereditary optic neuropathy: involvement of the mitochondrial ND1 gene and evidence for an intragenic suppressor mutation.

A large Queensland family has an extreme form of Leber hereditary optic neuropathy (LHON) in which several neurological abnormalities and an infantile encephalopathy are present in addition to the characteristic ophthalmological changes. Sequence analysis of the seven mitochondrial genes encoding subunits of respiratory chain complex I (NADH-ubiquinone oxidoreductase) reveals two novel features of the etiology of this mitochondrial genetic disease. The first conclusion from these studies is that the ophthalmological and neurological deficits in this family are produced by a mutation at nucleotide 4160 of the ND1 gene. This nucleotide alteration results in the substitution of proline for the highly conserved leucine residue at position 285 of the ND1 protein. Secondary-structure analysis predicts that the proline replacement disrupts a small alpha helix in a hydrophilic loop. All nine family members analyzed were homoplasmic for this mutation. The second major result from these studies is that the members of one branch of this family carry, at nucleotide 4136 of the same gene, a second mutation, also homoplasmic, which produces a cysteine-for-tyrosine replacement at position 277. The clinical and biochemical phenotypes of the family members indicate that this second nucleotide substitution may function as an intragenic suppressor mutation which ameliorates the neurological abnormalities and complex I deficiency.     

Internal carotid flow velocity with exercise before and after acclimatization to 4,300 m.

Cerebral blood flow and O2 delivery during exercise are important for well-being at altitude but have not been studied. We expected flow to increase on arrival at altitude and then to fall as O2 saturation and hemoglobin increased, thereby maintaining cerebral O2 delivery. We used Doppler ultrasound to measure internal carotid artery flow velocity at sea level and on Pikes Peak, CO (4,300 m). In an initial study (1987, n = 7 men) done to determine the effect of brief (5-min) exercises of increasing intensity, we found at sea level that velocity [24.8 +/- 1.4 (SE) cm/s rest] increased by 15 +/- 7, 30 +/- 6, and 22 +/- 8% for cycle exercises at 33, 71, and 96% of maximal O2 uptake, respectively. During acute hypobaric hypoxia in a decompression chamber (inspired PO2 = 83 Torr), velocity (23.2 +/- 1.4 cm/s rest) increased by 33 +/- 6, 20 +/- 5, and 17 +/- 9% for exercises at 45, 72, and 98% of maximal O2 uptake, respectively. After 18 days on Pikes Peak (inspired PO2 = 87 Torr), velocity (26.6 +/- 1.5 cm/s rest) did not increase with exercise. A subsequent study (1988, n = 7 men) of the effect of prolonged exercise (45 min at approximately 100 W) found at sea level that velocity (24.8 +/- 1.7 cm/s rest) increased by 22 +/- 6, 13 +/- 5, 17 +/- 4, and 12 +/- 3% at 5, 15, 30, and 45 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Antiarrhythmic agents diminish thiourea-induced pulmonary vascular protein leak in rats

Drugs possessing membrane stabilizing activity might act to diminish the augmented microvascular permeability resulting from acute lung injury. To test this rats were pretreated with quinidine, procainamide, or lidocaine and then given the lung injury-inducing agent thiourea. Vascular permeability, assessed as the extravascular accumulation of radiolabeled protein, was increased more than threefold by thiourea. This increase was diminished by 29, 34, and 43% after pretreatment with procainamide, quinidine, and lidocaine, respectively. Lidocaine also returned the thiourea-induced increase in lung wet weight-to-dry weight ratios to control levels. This protection was not likely due to hemodynamic effects of these agents, since no differences were noted in cardiac output between pretreated rats and those receiving thiourea alone and a small increase in mean pulmonary arterial pressure in the lidocaine-pretreatment group was the only difference noted. O2 metabolites have been implicated in the pathogenesis of thiourea-induced lung injury. None of these agents scavenged O2- or H2O2 directly, but quinidine and procainamide diminished in vitro neutrophil O2- and H2O2 production, and lidocaine inhibited neutrophil H2O2 production. However, neutropenia (PMN less than 100/ml) induced with either vinblastine or cyclophosphamide (Cytoxan) failed to prevent thiourea-induced increases in pulmonary vascular protein leak. In conclusion, procainamide, quinidine, and lidocaine diminished lung injury in rats after thiourea. Although these agents diminish PMN O2 metabolite production in vitro their salutary role in thiourea-induced lung injury appears to be through an unknown mechanism that is independent of their effects on neutrophil O2 metabolite-dependent toxicity.     

Relatedness and kin-structured migration in a founding population: Plymouth Colony, 1620-1633

To test the common assumption of no genetic relationship in a founding population, we calculated average relatedness (r) for the emigrants to Plymouth Colony from Europe on seven voyages from 1620 to 1633. Of 355 individuals, 255 could be individually identified and 4 generations of genealogic depth accounted for. Mean r was 0.00399 (S.D. = 0.00395) and ranged from 0 for 76 individuals to 0.01574 for a single female. There was a strong sex difference in relatedness; 91 females had a mean r of 0.00557 (S.D. = 0.00428), and 161 males had a lower mean r of 0.00308 (S.D. = 0.00349) (t = 4.71, p less than 0.001). The major difference was in the lower proportion of females with no relations (n = 12, 13.2%) compared with males (n = 64, 39.8%) (t = 5.05; p less than 0.001). If relatedness is calculated only for those with relations, females still have a significantly higher mean r value (0.00641, S.D. = 0.00393) than males (0.00511, S.D. = 0.00312) (t = 2.38, p less than 0.05). Thus a higher proportion of females had relatives migrating to the colony, and relatedness is significantly higher among them. The majority of kin links (79.8%) were those within the nuclear family--parents, children or siblings. For the continuity of kin-structured migration, relatedness was highest among voyagers in the same boat load and lower between voyages, with no apparent time trend. The low relatedness value of the Plymouth migrants is a result of community history and recruitment practices for the new colony. For this European population average relatedness was approximately an order of magnitude below that of traditional groups, and the assumption of no genetic relationship is not unwarranted.