Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

[EX Q]: Context: Therapeutic angiogenesis is a promising strategy for treating ischemia. Our previous work showed that endogenous endothelial tissue factor (TF) expression induces intracrine signaling and switches-on angiogenesis in microvascular endothelial cells (mECs). We have hypothesized that activated mECs could exert a further paracrine regulation through the release of TF-rich microvascular endothelial microparticles (mEMPs) and induce neovascularization of ischemic tissues.', 'Here, we describe for the first time that activated mECs are able to induce reparative neovascularization in ischemic zones by releasing TF-rich microparticles. We show in vitro and in vivo that mEMPs released by both wild-type and TF-upregulated-mECs induce angiogenesis and collateral vessel formation, whereas TF-poor mEMPs derived from TF-silenced mECs are not able to trigger angiogenesis. Isolated TF-bearing mEMPs delivered to nonperfused adductor muscles in a murine hindlimb ischemia model enhance collateral flow and capillary formation evidenced by MRI. TF-bearing mEMPs increase angiogenesis operating via paracrine regulation of neighboring endothelial cells, signaling through the 1-integrin pathway Rac1-ERK1/2-ETS1 and triggering CCL2 (chemokine [C-C motif] ligand 2) production to form new and competent mature neovessels.
Answer: These findings demonstrate that TF-rich mEMPs released by microvascular endothelial cells can overcome the consequences of arterial occlusion and tissue ischemia by promoting postischemic neovascularization and tissue reperfusion.
[EX A]: Do angiogenic microvascular endothelial cells release microparticles rich in tissue factor that promotes postischemic collateral vessel formation?

[EX Q]: Context: Despite advances in the diagnosis and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive. Insight may be gained from study of early-onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may account for disease. We performed exome sequencing of eight subjects from six kindreds with onset of portal hypertension of indeterminate etiology during infancy or childhood. Three subjects from two consanguineous families shared the identical rare homozygous p.N46S mutation in DGUOK, a deoxyguanosine kinase required for mitochondrial DNA replication; haplotype sharing demonstrated that the mutation in the two families was inherited from a remote common ancestor. All three affected subjects had stable portal hypertension with noncirrhotic liver disease for 6-16 years of follow-up. This mutation impairs adenosine triphosphate binding and reduces catalytic activity. Loss-of-function mutations in DGUOK have previously been implicated in cirrhosis and liver failure but not in isolated portal hypertension. Interestingly, treatment of patients with human immunodeficiency viral infection with the nucleoside analogue didanosine is known to cause portal hypertension in a subset of patients and lowers deoxyguanosine kinase levels in vitro; the current findings implicate these effects on deoxyguanosine kinase in the causal mechanism.
Answer: Our findings provide new insight into the mechanisms mediating inherited and acquired noncirrhotic portal hypertension, expand the phenotypic spectrum of DGUOK deficiency, and provide a new genetic test for a specific cause of idiopathic noncirrhotic portal hypertension. (Hepatology 2016;63:1977-1986).
[EX A]: Does recurrent recessive mutation in deoxyguanosine kinase cause idiopathic noncirrhotic portal hypertension?

[EX Q]: Context: The purpose of this study was to determine whether oxygen treatment could attenuate the alterations in cerebral energy metabolism found in the brain following hypoxia-ischemia.', 'Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2 hrs of hypoxia (8% oxygen at 37 degrees C). The concentrations of high-energy phosphate compounds and glycolytic intermediates and the activity of Na+/K+-adenosine triphosphatase were measured at 4-72 hrs of recovery. Brain weight was used to determine the severity of the brain injury at 2 wks after insult.', 'Experimental setting.', 'Rat pups.', 'Pups were treated with 100% oxygen 1 hr after the insult at 2.5 atmospheres absolute (hyperbaric oxygen) or at normobaric pressure for a duration of 2 hrs.', 'During the initial period of recovery from hypoxia-ischemia, values of adenosine triphosphate and phosphocreatine remained at levels below normal, whereas the levels of glucose and other glycolytic intermediates were elevated. Hyperbaric oxygen and normobaric oxygen both attenuated brain injury, restored the levels of adenosine triphosphate and phosphocreatine, decreased the levels of the glycolytic intermediates, and increased the utilization of energy.
Answer: These results suggest that oxygen treatment during the initial period of recovery from a hypoxia-ischemic insult is able to attenuate energy deficits in the brain, which ultimately leads to a reduction in brain injury.
[EX A]:
Does oxygen treatment restore energy status following experimental neonatal hypoxia-ischemia?