Human T Lymphocytes Require Lipid as Either Lipoprotein or Nonesterified Fatty Acid for In Vitro Activation

Serum, which is required for activation of T cells in vitro, was fractionated to isolate and identify major supportive components. The serum activity concentrated exclusively with the lipoprotein fractions LDL and HDL. Furthermore, oleic and linoleic acids were equally active supplements, suggesting that resting T cells may require exogenous lipid because they are incapable of synthesizing fatty acid. A survey of fatty acids disclosed that all were capable of some degree of support. Titration delineated the narrow concentration range of lipid supplements successful in supporting T cell proliferation and demonstrated that concentrations must be rigidly controlled to optimize cell proliferation.     

The platelet interactivity phenotype of Streptococcus sanguis influences the course of experimental endocarditis.

A strain of Streptococcus sanguis that induced rabbit platelets to aggregate in vitro (Agg+ phenotype) was hypothesized to be a more virulent pathogen than an Agg- strain in experimental endocarditis in rabbits. A left ventricular catheter was implanted, and then an Agg+ or Agg- strain was inoculated intravenously. Vegetations formed on the aortic semilunar valves but were unaffected by the duration of implantation of the catheter. Vegetations enlarged by accumulating platelets and their mass increased directly with the duration of endocarditis. Inoculation of the Agg+ strain consistently caused endocarditis with significantly larger vegetations, a more severe clinical course (including febrile episodes, hematological changes, and signs of myocardial ischemia), more gross lesions in major organs, and greater mortality than inoculation with the Agg- strain, saline, or the Agg+ strain pretreated with monospecific rabbit immunoglobulin G or Fab fragments against its platelet aggregation-associated protein (PAAP; class II). In experimental endocarditis, PAAP expressed by Agg+ S. sanguis appeared to be an important virulence factor.     

Endocardial fibroelastosis with coronary artery thromboembolus and myocardial infarction

We report a case of an 18-month-old male, born to a woman with third trimester febrile illness, who had a history of congestive heart failure and respiratory distress, cardiomegaly, and electrocardiographic (ECG) findings suggestive of cardiomyopathy and myocarditis. After gradual improvement in heart size and function with pharmacologic therapy, he developed a terminal episode of respiratory distress and cardiogenic shock, with ECG findings of an anterolateral infarct. At autopsy it was found that endocardial fibroelastosis with mural thrombi in the left ventricle had been complicated by thromboembolism to the left anterior descending coronary artery, resulting in transmural infarction of the anteroseptal region of the left ventricle. Myocardial infarction is a potential but unusual thromboembolic complication of endocardial fibroelastosis. A high index of suspicion for coronary artery thromboemboli should be maintained in pediatric patients with cardiomyopathy and suspected myocardial infarction.     

A novel human leucocyte antigen-DRB1 genotyping method based on multiplex primer extension reactions

We have developed and validated a semi-automated fluorescent method of genotyping human leucocyte antigen (HLA)-DRB1 alleles, HLA-DRB1*01-16, by multiplex primer extension reactions. This method is based on the extension of a primer that anneals immediately adjacent to the single-nucleotide polymorphism with fluorescent dideoxynucleotide triphosphates (minisequencing), followed by analysis on an ABI Prism 3700 capillary electrophoresis instrument. The validity of the method was confirmed by genotyping 261 individuals using both this method and polymerase chain reaction with sequence-specific primer (PCR-SSP) or sequencing and by demonstrating Mendelian inheritance of HLA-DRB1 alleles in families. Our method provides a rapid means of performing high-throughput HLA-DRB1 genotyping using only two PCR reactions followed by four multiplex primer extension reactions and PCR-SSP for some allele groups. In this article, we describe the method and discuss its advantages and limitations.     

Degree of Immunity Induced by Killed Vaccines to Experimental Salmonellosis in Mice

Killed vaccines, deoxycholate-extracted or heated, were shown to induce an effective degree of immunity which protected against death (100%), prevented extensive multiplication, and left the mice with low residual salmonella populations in spleen and liver after intravenous (iv) or intraperitoneal (ip) challenge with virulent Salmonella typhimurium. Protection was most effective against the ip challenge route and less effective against the iv route. A study of the kinetics of the population of bacteria in the spleens and livers of immunized animals showed that after ip challenge there was an initial reduction of 99% at 6 hr after challenge, maintenance of levels of less than 10(3) bacteria per organ, and a final population of 10(2) to 10(3) per organ at 21 days. With iv challenge, after an initial reduction of 90% at 6 hr, growth ensued to levels above 10(6) bacteria per organ until 8 days, followed by a steady decline yielding residual populations of 10(3) to 10(4) in some cases. Organ hypertrophy correlated with bacterial population. Morbidity was prevented (as measured by gain in body weight) by immunization against ip challenge but not against iv challenge. Killed vaccines protected by their ability to induce an immune state which reduced the initial challenge population, prevented extensive multiplication, yet allowed "cellular immunity" to develop due to response to the living challenge infection itself. The consequence was a low-level carrier state similar to that induced by recovery from sublethal virulent infection.     

Cystic fibrosis: Synthesis of ciliary inhibitor by amniotic cells

The presence of a ciliary inhibitor in media of cultured amniotic cells obtained from a fetus heterozygous for cystic fibrosis has been observed by the oyster gill cilia assay. The chromatographic fraction containing the inhibitor corresponded to eluted fractions chromatographed from cystic fibrosis fibroblast media and serum. An analogous chromatographic fraction from media of cultured amniotic cells from two proportedly normal fetuses did not inhibit cilia. The chromatographic fraction from media of cultured amniotic cells of a fetus at high risk for cystic fibrosis did not inhibit ciliary activity. Serum was collected from this baby seven weeks after birth and also did not inhibit ciliary action, indicating a homozygous normal genotype. These observations may lead to the development of an antenatal test for cystic fibrosis.     

Antetorsion of the femur neck. A variable of the trochanter minor?

The antetorsion angle (beta) of the femoral neck and the "retrotorsion" angle (alpha) of the lesser trochanter were measured in 52 female and 34 male femora taken from 46 human cadavers (age at death 80.3 +/- 8.67 years). In addition, the diameter of the femoral head (d) and the length of the femur (l) were measured. As expected, the antetorsion angle varied over a wide range (beta = 10.5 degrees +/- 9.22 degrees). Measurements on right and left demonstrated an asymmetry: beta right = 8.2 degrees +/- 9.14 degrees; beta left = 12.6 degrees +/- 8.99 degrees. The measurements for retrotorsion of the lesser trochanter also varied in a similar way: alpha total = 31.5 degrees +/- 11.8 degrees; alpha right = 35 degrees +/- 10.7 degrees; alpha left = -28 degrees +/- 11.9 degrees. If alpha and beta are combined to couples, a strong regression is visible (r = 0.7657): beta = 29.5 degrees +/- 0.6 . alpha. Thus, the antetorsion angle depends on the retrotorsion angle or vice versa. The measurements of d and l show marked symmetry: d total = 47.4 +/- 3.6 mm; d right = 47.6 +/- 3.6 mm; d left = 47.2 +/- 3.5 mm; l total = 442.7 +/- 24.6 mm; l right = 441.3 +/- 24.4 mm; l left = 444.0 +/- 24.8 mm. Thus, d and l also vary in dependence on each other (r = 0.578). As the length of the femur is determined by body height, there must be a correlation between the diameter of the femoral head and height; that is to say, a short patient will have a small femoral head.