In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

[Q]: Context: Cord blood (CB) hematopoietic stem cell transplantation has often been limited by the scarcity of stem cells. Therefore, the number of CB hematopoietic stem/progenitor cells (HSPCs) should be increased while maintaining the stem cell characteristics.', 'We designed an ex vivo culture system using endothelial progenitor cells (EPCs) as stroma to determine the capacity of expanding CB-HSPCs in a defined medium, the effect on engraftment of the expanded cells in a mouse model and the underlying mechanism.', "After 7 days of culture, compared with those cultured with cytokines alone (3.25 ± 0.59), CD34+ cells under contact and non-contact co-culture with EPCs were expanded by 5.38 ± 0.61 (P = 0.003) and 4.06 ± 0.43 (P = 0.025)-fold, respectively. Direct cell-to-cell contact co-culture with EPCs resulted in more primitive CD34+ CD38- cells than stroma-free culture (156.17 ± 21.32 versus 79.12 ± 19.77-fold; P = 0.010). Comparable engraftment of day 7 co-cultured HSPCs with respect to HSPCs at day 0 in nonobese diabetic-severe combined immunodeficiency disease (NOD/SCID) mice was measured as a percentage of chimerism (13.3% ± 11.0% versus 16.0% ± 14.3%; P = 0.750). EPCs highly expressed interleukin 6 (IL6) and angiopoietin 1 (ANGPT1), the hematopoietic- related cytokines. A higher transcriptional level of WNT5A genes in EPCs and co-cultured HSPCs suggests that the activation of Wnt signaling pathway may play a role in HSPCs' expansion ex vivo.\Question: Do endothelial progenitor cells promote efficient ex vivo expansion of cord blood-derived hematopoietic stem/progenitor cells?
[A]: These data demonstrated that EPCs improve the CD34+ population but do not compromise the repopulating efficacy of the amplified HSPCs, possibly via cytokine secretion and Wnt signaling pathway activation.


[Q]: Context: Intrathecal adenosine is antinociceptive under conditions of central sensitization, but not in response to acute stimuli in normals. The reasons for this selective circumstance of action remain unclear, but some evidence links adenosine's antinociceptive effects to release of norepinephrine by terminals in the spinal cord. The purpose of this study was to test whether spinal adenosine induces norepinephrine release selectively in settings of hypersensitivity.", 'Rats randomly assigned to spinal nerve ligation, sham operation, or no operation were anesthetized. A microdialysis fiber was implanted in the spinal cord dorsal horn at the L5-L6 level and perfused with artificial cerebrospinal fluid. After washout and a baseline sample period, adenosine at various concentrations was infused through the fiber for 150 min, and samples were collected every 15 min.', "In ligated, but not in sham or normal animals, adenosine perfusion increased norepinephrine in spinal cord microdialysates in a concentration-dependent manner. The effects of adenosine plateaued after 75 min and remained stable until the end of the experiment. Intravenous injection of selective adenosine A1 and A2 receptor antagonists revealed that adenosine's effect on spinal norepinephrine release was A1 receptor mediated.\Question: Does intraspinal adenosine induce spinal cord norepinephrine release in spinal nerve-ligated rats but not in normal or sham controls?
[A]: This is the first study to provide direct evidence that adenosine is able to release norepinephrine in spinal cord dorsal horns in living animals. However, this effect was only seen in animals after spinal nerve ligation. These data are consistent with behavioral studies demonstrating that adenosine's antinociceptive effects in rats after spinal nerve ligation is totally dependent on intact spinal noradrenergic terminals and can be blocked by spinal alpha 2-adrenergic receptor antagonists.


[Q]: Context: For years, Uniform Resource Locator (URL) decay or "link rot" has been a growing concern in the field of biomedical sciences. This paper addresses this issue by examining the status of the URLs published in MEDLINE abstracts, establishing current availability and estimating URL decay in these records from 1994 to 2006. We also reviewed the information provided by the URL to determine if the context that the author cited in writing the paper is the same information presently available in the URL. Lastly, with all the documented recommended methods to preserve URL links, we determined which among them have gained acceptance among authors and publishers.', 'MEDLINE records from 1994 to 2006 from the National Library of Medicine in Extensible Mark-up Language (XML) format were processed yielding 10,208 URL addresses. These were accessed once daily at random times for 30 days. Titles and abstracts were also searched for the presence of archival tools such as WebCite, Persistent URL (PURL) and Digital Object Identifier (DOI).', 'Results showed that the average URL length ranged from 13 to 425 characters with a mean length of 35 characters [Standard Deviation (SD) = 13.51; 95% confidence interval (CI) 13.25 to 13.77]. The most common top-level domains were ".org" and ".edu", each with 34%. About 81% of the URL pool was available 90% to 100% of the time, but only 78% of these contained the actual information mentioned in the MEDLINE record. "Dead" URLs constituted 16% of the total. Finally, a survey of archival tool usage showed that since its introduction in 1998, only 519 of all abstracts reviewed had incorporated DOI addresses in their MEDLINE abstracts.\Question: Do an update on Uniform Resource Locator ( URL ) decay in MEDLINE abstracts and measures for its mitigation?
[A]:
URL persistence parallels previous studies which showed approximately 81% general availability during the 1-month study period. As peer-reviewed literature remains to be the main source of information in biomedicine, we need to ensure the accuracy and preservation of these links.