Ellefson, Ralph D.

Two infants and one child died suddenly and unexpectedly while receiving central venous hyperalimentation. The catheter tip in each case was wedged against myocardium resulting in myocardial necrosis and pericardial effusion. The importance of avoiding intracardiac indwelling hyperalimentation catheters is stressed.

Fifty-eight strains of nonphotochromogenic mycobacteria representing nine different serotypes were studied, including 38 strains of Mycobacterium avium and 20 strains of Battey bacilli. The lipids were extracted from whole cells, saponified with potassium hydroxide, and esterified with diazomethane. The fatty-acid profiles determined by gas-liquid chromatography included saturated fatty acids ranging from C 8 to C 24 , plus some unsaturated analogues and a branched-chain acid. No consistent differences in the fatty-acid profiles were observed between strains of M. avium and Battey bacilli. Quantitative differences in the means (significant at P < 0.01) were observed in the relative amounts of 14:0, 16:1, 18:0, 18:1, and a branched-chain acid among strains of the same serotype. We were unable to differentiate the fatty-acid profiles of recently isolated strains or those maintained in culture for more than 2 years.

Comparison of the cellular fatty acids of 10 strains of Mycobacterium marinum and 35 strains of Mycobacterium kansasii revealed similarities within each species but differences between these two photochromogenic mycobacteria. A branched-chain fatty acid characteristic of M. kansasii was found in trace amounts in 2 of the 10 strains of M. marinum .

The cellular fatty acids of 35 strains of Mycobacterium kansasii isolated from clinical material were analyzed to establish properties by which we could identify and characterize these acid-fast microorganisms. The fatty acids were extracted from cells grown in liquid synthetic media, and they were analyzed as methyl esters by gas-liquid chromatography. The fatty acid profiles of all strains were similar. They differed from fatty acid profiles of other mycobacteria by their content of a saturated fatty acid with a methyl group at C2.

Abstract We have purified Lp(a) lipoproteins from sera of four subjects by ultracentrifugation, selective precipitation, and chromatofocusing. Each subject had two forms of serum Lp(a) that were separable by chromatofocusing. We purified apolipoprotein (a) [apo(a)] from the eight isolated Lp(a)s and obtained only one form of apo(a) from each subject. The four apo(a)s seen on sodium dodecyl sulfate-polyacrylamide gel electrophoresis had different apparent molecular masses, ranging from 275 to 440 kDa. Chemical deglycosylation of the smallest apo(a) yielded a 235 kDa protein, which may be a core protein structure common to all apo(a)s. We conclude that there are many forms of serum Lp(a) and apo(a). The heterogeneity of serum Lp(a) particles can be ascribed in part to differences in size of apo(a), but other factors must account for the existence within a single patient of different Lp(a)s that contain apparently identical apo(a). One must consider the heterogeneity of Lp(a) when designing assays for this lipoprotein.

In 36 normolipemic pigs randomized to a 4-week feeding with regular pig chow (n = 18, control group) or chow supplemented with cod liver oil (1 ml/kg per day) (n = 18, treated group), treatment with cod liver oil produced a significant decrease in serum cholesterol, low density lipoprotein cholesterol, and triglycerides. Deep carotid arterial wall injury (media exposed) by balloon angioplasty was associated with less 111In-labeled platelet deposition (24.6 +/- 4.8 x 10(6)/cm2 versus 62.5 +/- 17.0 x 10(6)/cm2, p less than 0.05; difference, -33.8 x 10(6)/cm2; 95% confidence interval [CI], -1.9 x 10(6)/cm2 to -73.9 x 10(6)/cm2) and injury-related vasoconstriction (21.3 +/- 2.2% versus 30.9 +/- 2.9%, p less than 0.05; difference, -9.6%; 95% CI, -2.2% to -17.0%) in the cod liver oil-treated group than in the control group; with mild injury (media not exposed), platelet deposition was low and unchanged (6.2 +/- 0.5 x 10(6)/cm2 versus 7.8 +/- 0.7 x 10(6)/cm2; difference, -1.6 x 10(6)/cm2; 95% CI, -1.1 x 10(6)/cm2 to +4.3 x 10(6)/cm2), but associated vasoconstriction was reduced respectively (16.3 +/- 2.0% versus 23.0 +/- 2.2%, p less than 0.05; difference, -6.7%; 95% CI, -0.6% to -12.8%). When arterial blood from cod liver oil-treated pigs superfused normal aortic media ex vivo, platelet deposition onto the normal aortic media was lower than when arterial blood from control pigs superfused the normal aortic media (43.7 +/- 8.8 x 10(6)/cm2 versus 66.8 +/- 13.0 x 10(6)/cm2, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Background Elevated lipoprotein(a) [Lp(a)] levels have been associated with the presence of atherosclerotic disease. However, the results of prospective studies of Lp(a) and cardiovascular disease have been contradictory. Methods and Results From 1968 through 1982, lipoprotein analysis was performed in 11 335 Olmsted County residents. Quantitative cholesterol and triglycerides were obtained along with semiquantitative Lp(a) levels based on electrophoretic pattern. Lp(a) bands were scored from 0 (absent) to 3 (increased). A cohort of 4967 men and 4968 women with no prior history of atherosclerotic disease who had baseline Lp(a) determinations were followed up for 14 years for development of coronary artery disease (CAD) and cerebrovascular disease (CVD). During 131 330 person-years of follow-up, there were 1848 CAD events and 841 CVD events. Age, diabetes, hypertension, cholesterol, and triglycerides were significantly and independently associated with an increased risk of CAD and CVD in men and women. There was a significant increase in the adjusted hazards ratio for CAD with increasing Lp(a) levels for men and women. For Lp(a) level 3, the hazard ratio was 1.9 (range, 1.3 to 2.9) in women and 1.6 (range, 1.0 to 2.5) in men. The adjusted hazard ratio for CVD showed an irregular association with Lp(a) levels in men and no association in women. Conclusions In this cohort of 9936 men and women initially free of cardiovascular disease who were followed up for 14 years, Lp(a) was a significant predictor of risk of future CAD. Lp(a) was a weak risk factor for CVD in men and was not a significant predictor of CVD risk in women.