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.
One example: Alterations of the architecture of cerebral white matter in the developing human brain can affect cortical development and result in functional disabilities. A line scan diffusion-weighted magnetic resonance imaging (MRI) sequence with diffusion tensor analysis was applied to measure the apparent diffusion coefficient, to calculate relative anisotropy, and to delineate three-dimensional fiber architecture in cerebral white matter in preterm (n = 17) and full-term infants (n = 7). To assess effects of prematurity on cerebral white matter development, early gestation preterm infants (n = 10) were studied a second time at term. In the central white matter the mean apparent diffusion coefficient at 28 wk was high, 1.8 microm2/ms, and decreased toward term to 1.2 microm2/ms. In the posterior limb of the internal capsule, the mean apparent diffusion coefficients at both times were similar (1.2 versus 1.1 microm2/ms). Relative anisotropy was higher the closer birth was to term with greater absolute values in the internal capsule than in the central white matter. Preterm infants at term showed higher mean diffusion coefficients in the central white matter (1.4 +/- 0.24 versus 1.15 +/- 0.09 microm2/ms, p = 0.016) and lower relative anisotropy in both areas compared with full-term infants (white matter, 10.9 +/- 0.6 versus 22.9 +/- 3.0%, p = 0.001; internal capsule, 24.0 +/- 4.44 versus 33.1 +/- 0.6% p = 0.006). Nonmyelinated fibers in the corpus callosum were visible by diffusion tensor MRI as early as 28 wk; full-term and preterm infants at term showed marked differences in white matter fiber organization. The data indicate that quantitative assessment of water diffusion by diffusion tensor MRI provides insight into microstructural development in cerebral white matter in living infants.
Solution is here: Microstructural development of human newborn cerebral white matter assessed in vivo by diffusion tensor magnetic resonance imaging.
Explanation: This title is appropriate for the given abstract because the focus of this abstract is cerebral white matter assesment.

Now, solve this: &NA; Despite the importance of programmed cell death1 (PD1) in inhibiting T cell effector activity, the mechanisms regulating its expression remain poorly defined. We found that the chromatin organizer special ATrich sequencebinding protein1 (Satb1) restrains PD1 expression induced upon T cell activation by recruiting a nucleosome remodeling deacetylase (NuRD) complex to Pdcd1 regulatory regions. Satb1 deficienct T cells exhibited a 40fold increase in PD1 expression. Tumorderived transforming growth factor &bgr; (Tgf&bgr;) decreased Satb1 expression through binding of Smad proteins to the Satb1 promoter. Smad proteins also competed with the Satb1NuRD complex for binding to Pdcd1 enhancers, releasing Pdcd1 expression from Satb1mediated repression, Satb1deficient tumorreactive T cells lost effector activity more rapidly than wildtype lymphocytes at tumor beds expressing PD1 ligand (CD274), and these differences were abrogated by sustained CD274 blockade. Our findings suggest that Satb1 functions to prevent premature T cell exhaustion by regulating Pdcd1 expression upon T cell activation. Dysregulation of this pathway in tumorinfiltrating T cells results in diminished antitumor immunity. Graphical Abstract Figure. No caption available. HighlightsT cell activation increased the expression of Satb1 in mature CD8+ and CD4+ T cellsRecruitment of the NuRD repression complex by Satb1 inhibits expression of Pdcd1In tumors, TGF&bgr; inhibits Satb1 expression in T cells, increasing Pdcd1 expressionSatb1/ T cells express high amounts of PD1 and have decreased antitumor activity &NA; Stephen et al. show that the chromatin organizer Satb1 controls expression levels of PD1 upon T cell activation through the recruitment of a deacetylase complex to regulatory regions of the Pdcd1 gene. Tumorderived TGF&bgr; dysregulates this pathway, unleashing PD1 expression in tumorinfiltrating T cells and decreasing antitumor immunity.
Solution:
SATB1 Expression Governs Epigenetic Repression of PD1 in TumorReactive T Cells