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 Input:
Abstract: We isolated a mutant allele of dnaX, encoding the tau and gamma subunits of the DNA polymerase III holoenzyme, that causes extreme cell filamentation but does not affect either cell growth or DNA replication. This phenotype results from a defect in daughter chromosome decatenation during rapid growth. In these cells, ParC, one subunit of topoisomerase IV, no longer associated with the replication factory, as occurs in wild-type cells, and was instead distributed uniformly on the nucleoid; the distribution of ParE, the other subunit of topoisomerase IV, was unaffected. In addition, the majority of topoisomerase IV activity in synchronized cell populations was restricted to late in the cell cycle, when replication was essentially complete. These observations suggest that topoisomerase IV activity in vivo might be dependent on release of ParC from the replication factory.. Title: Temporal regulation of topoisomerase IV activity in E. coli.

Ex Output:
yes

Ex Input:
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 Output:
no

Ex Input:
Abstract: INTRODUCTION Endothelial activation leading to vascular barrier breakdown plays an essential role in the pathophysiology of multiple-organ dysfunction syndrome (MODS) in sepsis. Increasing evidence suggests that the function of the vessel-protective factor Angiopoietin-1 (Ang-1), a ligand of the endothelial-specific Tie2 receptor, is inhibited by its antagonist Angiopoietin-2 (Ang-2) during sepsis. In order to reverse the effects of the sepsis-induced suppression of Ang-1 and elevation of Ang-2 we aimed to investigate whether an intravenous injection of recombinant human (rh) Ang-1 protects against MODS in murine sepsis.
METHODS Polymicrobiological abdominal sepsis was induced by cecal ligation and puncture (CLP). Mice were treated with either 1 g of intravenous rhAng-1 or control buffer immediately after CLP induction and every 8h thereafter. Sham-operated animals served as time-matched controls.
RESULTS Compared to buffer-treated controls, rhAng-1 treated septic mice showed significant improvements in several hematologic and biochemical indicators of MODS. Moreover, rhAng-1 stabilized endothelial barrier function, as evidenced by inhibition of protein leakage from lung capillaries into the alveolar compartment. Histological analysis revealed that rhAng-1 treatment attenuated leukocyte infiltration in lungs and kidneys of septic mice, probably due to reduced endothelial adhesion molecule expression in rhAng-1 treated mice. Finally, the protective effects of rhAng-1 treatment were reflected by an improved survival time in a lethal CLP model.
CONCLUSIONS In a clinically relevant murine sepsis model, intravenous rhAng-1 treatment alone is sufficient to significantly improve a variety of sepsis-associated organ dysfunctions and survival time, most likely by preserving endothelial barrier function. Further studies are needed to pave the road for clinical application of this therapy concept.. Title: Acute administration of recombinant Angiopoietin-1 ameliorates multiple-organ dysfunction syndrome and improves survival in murine sepsis.

Ex Output:
yes