In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".

[EX Q]: Abstract: The cell-cycle regulating gene, p16INK4A, encoding an inhibitor of cyclin-dependent kinases 4 and 6, is considered to play an important role in cellular aging and in premature senescence. Although there is an age-dependent increase of p16INK4A expression in human fibroblast senescence in vitro, no data are available regarding the age dependency of p16INK4A in vivo. To determine whether p16INK4A expression in human skin correlates with donor age, p16INK4A expression was analyzed by immunohistochemistry as well as the expression of the p16INK4A repressor BMI1. Samples from the age groups 0-20, 21-70, and 71-95 years were selected from a bank of healthy human skin. We show that the number of p16INK4A positive cells is significantly higher in elderly individuals compared to the younger age groups. The number of p16INK4A positive cells was found to be increased in both epidermis and dermis, compartments with strictly different proliferative activities. BMI1 gene expression was significantly down-regulated with increasing donor age, whereas no striking age differences were observed for Ki67. In immunofluorescence co-expression studies, Ki67-positive cells were negative for p16INK4A and BMI1-expressing cells also stained negatively for Ki67. In conclusion, we provide for the first time evidence that p16INK4A expression directly correlates with chronological aging of human skin in vivo. p16INK4A therefore is a biomarker for human aging in vivo. The data reported here suggest a model for changes in regulatory gene expression that drive aging in human skin.. Title: p16INK4A is a robust in vivo biomarker of cellular aging in human skin.
[EX A]: yes

[EX Q]: Abstract: Tuberculosis remains one of the world's leading infectious causes of death. Approximately 80% of all disease is due to postprimary (secondary) tuberculosis in the lung. Unfortunately, tissues of developing lesions are seldom available and there are no recognized models of postprimary tuberculosis. In the preantibiotic era when tissues were more abundant, several investigators described early postprimary tuberculosis as a lipid pneumonia quite different from the caseating granulomas commonly described today. We used histopathologic, immunohistochemical and acid fast stains to examine tissues from several people with untreated primary and postprimary tuberculosis and compared the findings with those of mice with reactivation tuberculosis. The results confirmed that developing postprimary tuberculosis begins as a lipid pneumonia accompanied by bronchial obstruction in which infection is restricted to foamy alveolar macrophages. Cavities result from a combination of caseation of tuberculous pneumonia and microvascular occlusion characteristic of delayed type hypersensitivity (DTH). Reactivation tuberculosis in the mouse begins as a similar tuberculous lipid pneumonia with bronchial obstruction and evidence for participation of DTH. Developing necrosis in both species is associated with localization of organisms within lipid droplets. These results suggest that reactivation tuberculosis in mice is a valuable model of developing human postprimary tuberculosis.. Title: Cohesins and condensins orchestrate the 4D dynamics of yeast chromosomes during the cell cycle
[EX A]: no

[EX Q]: Abstract: We report a comprehensive analysis of gene expression differences between sexes in multiple somatic tissues of 334 mice derived from an intercross between inbred mouse strains C57BL/6J and C3H/HeJ. The analysis of a large number of individuals provided the power to detect relatively small differences in expression between sexes, and the use of an intercross allowed analysis of the genetic control of sexually dimorphic gene expression. Microarray analysis of 23,574 transcripts revealed that the extent of sexual dimorphism in gene expression was much greater than previously recognized. Thus, thousands of genes showed sexual dimorphism in liver, adipose, and muscle, and hundreds of genes were sexually dimorphic in brain. These genes exhibited highly tissue-specific patterns of expression and were enriched for distinct pathways represented in the Gene Ontology database. They also showed evidence of chromosomal enrichment, not only on the sex chromosomes, but also on several autosomes. Genetic analyses provided evidence of the global regulation of subsets of the sexually dimorphic genes, as the transcript levels of a large number of these genes were controlled by several expression quantitative trait loci (eQTL) hotspots that exhibited tissue-specific control. Moreover, many tissue-specific transcription factor binding sites were found to be enriched in the sexually dimorphic genes.. Title: Tissue-specific expression and regulation of sexually dimorphic genes in mice.
[EX A]:
yes