TASK DEFINITION: In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.
PROBLEM: Our purpose was to determine the aerobic capacities (VO2max) of a group of black female adolescents (age = 11.4-15.8 years) randomly chosen from a single urban school. Of 91 girls selected, 64 performed an incremental treadmill running test to volitional exhaustion and achieved VO2max as determined from expired gas measures. Other measures included height (m), weight (kg), and calf and triceps skinfolds (for % fat estimates). Girls were also asked whether they had achieved menarche. VO2max averaged 37.3 +/- 6.2 ml.kg-1 x min-1 and was significantly correlated (r[62]) with height (-.32, p < .01), body mass index (-.63, p < .001), and % fat (-.65, p < .001) but not with age (-.16, p > .10). Postmenarchal girls were significantly taller and older than premenarchal girls. Contrary to previous studies, the girls' VO2max values were not related to biological age. Our subjects' aerobic capacity values averaged 14% less than those of nonblack U.S. female adolescents previously reported in the literature. This difference in VO2max was primarily a function of body weight. Study implications support the possibility that overweight in adult black women may originate prior to or during early adolescence. Future longitudinal studies should be designed to investigate the effects of aerobic fitness on cardiovascular risk factor reduction in black adolescent girls.

SOLUTION: Aerobic capacity in black adolescent girls.

PROBLEM: Caspase recruitment domain-containing membrane-associated guanylate kinase protein-1 (CARMA1) is a critical component of the NF-kappaB signaling cascade mediated by TCR engagement. In addition to activation of naive T cells, TCR signaling is important for the development of agonist-selected T-cell subsets such as Treg, NKT cells, and CD8-alpha alpha T cells. However, little is known about the role of CARMA1 in the development of these lineages. Here we show that CARMA1-deficient mice (CARMA1(-/-)) have altered populations of specific subsets of agonist-selected T cells. Specifically, CARMA1(-/-) mice have impaired natural and adaptive Treg development, whereas NKT cell numbers are normal compared with wild-type mice. Interestingly, CD8-alpha alpha T cells, which may also be able to develop through an extrathymic selection pathway, are enriched in the gut of CARMA1(-/-) mice, whereas memory-phenotype CD4(+) T cells (CD62L(low)/CD44(high)) are present at reduced numbers in the periphery. These results indicate that CARMA1 is essential for Treg development, but is not necessary for the development of other agonist-selected T-cell subsets. Overall, these data reveal an important but differential role for CARMA1-mediated TCR signaling in T-cell development.

SOLUTION: Differential requirement for CARMA1 in agonist-selected T-cell development.

PROBLEM: Bacterial lipopolysaccharide (LPS) triggers innate immune responses through Toll-like receptor (TLR) 4. We show here that the suppressor of cytokine-signaling-1 (SOCS1/JAB) is rapidly induced by LPS and negatively regulates LPS signaling. SOCS1(+/-) mice or SOCS1(-/-) mice with interferon-gamma (IFNgamma)-deficient background were more sensitive to LPS-induced lethal effects than were wild-type littermates. LPS-induced NO(2)(-) synthesis and TNFalpha production were augmented in SOCS1(-/-) macrophages. Furthermore, LPS tolerance, a protection mechanism against endotoxin shock, was also strikingly reduced in SOCS1(-/-) cells. LPS-induced I-kappaB and p38 phosphorylation was upregulated in SOCS1(-/-) macrophages, and forced expression of SOCS1 suppressed LPS-induced NF-kappaB activation. Thus, SOCS1 directly suppresses TLR4 signaling and modulates innate immunity.

SOLUTION:
SOCS1/JAB is a negative regulator of LPS-induced macrophage activation.