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.

[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).
[A]: Does recurrent recessive mutation in deoxyguanosine kinase cause idiopathic noncirrhotic portal hypertension?


[Q]: Context: A patient with a suspected cervical spine injury may be at risk for secondary neurologic injury when initially placed and repositioned to the center of the spine board.', 'We sought to determine which centering adjustment best limits cervical spine movement and minimizes the chance for secondary injury.', 'Using five lightly embalmed cadaveric specimens with a created global instability at C5-C6, motion sensors were anchored to the anterior surface of the vertebral bodies. Three repositioning methods were used to center the cadavers on the spine board: horizontal slide, diagonal slide, and V-adjustment. An electromagnetic tracking device measured angular (degrees) and translation (millimeters) motions at the C5-C6 level during each of the three centering adjustments. The dependent variables were angular motion (flexion-extension, axial rotation, lateral flexion) and translational displacement (anteroposterior, axial, and medial-lateral).', 'The nonuniform condition produced significantly less flexion-extension than the uniform condition (p\xa0=\xa00.048). The horizontal slide adjustment produced less cervical flexion-extension (p\xa0=\xa00.015), lateral bending (p\xa0=\xa00.003), and axial rotation (p\xa0=\xa00.034) than the V-adjustment. Similarly, translation was significantly less with the horizontal adjustment than with the V-adjustment; medial-lateral (p\xa0=\xa00.017), axial (p\xa0<\xa00.001), and anteroposterior (p\xa0=\xa00.006).
Answer: Of the three adjustments, our team found that horizontal slide was also easier to complete than the other methods. The horizontal slide best limited cervical spine motion and may be the most helpful for minimizing secondary injury based on the study findings.
[A]: Does horizontal Slide create Less Cervical Motion When Centering an Injured Patient on a Spine Board?


[Q]: Context: For many years, adipose tissue has been mainly considered as an inert reservoir for storing triglycerides. Since the discovery that adipocytes may secrete a variety of bioactive molecules (hormones, chemokines, and cytokines), an endocrine and paracrine role for white adipose tissue (WAT) in the regulation of energy balance and other physiological processes has been established, particularly with regard to brain and muscle. In contrast, little is known about the interactions of WAT with liver. Hence, we examined the effect of the secretory products of WAT on hepatocytes. Conditioned medium of human WAT explants induced significant steatosis in hepatocyte cell lines. Factor(s) responsible for the conditioned medium-induced steatosis were screened by a battery of blocking antibodies against different cytokines/chemokines shown to be secreted by WAT. In contrast to interleukin-8 and interleukin-6, the monocyte chemoattractant protein-1 was capable of inducing steatosis in hepatocytes in a time-dependent manner at concentrations similar to those found in conditioned medium. Incubation of conditioned medium with antimonocyte chemoattractant protein-1 antibodies prevented triglyceride accumulation. Investigation of the mechanism leading to the triglyceride accumulation showed that both a diminution of apolipoprotein B secretion and an increase in phosphoenolpyruvate carboxykinase messenger RNA may be involved.
Answer: The monocyte chemoattractant protein-1 secreted by adipose tissue may induce steatosis not only recruiting macrophages but also acting directly on hepatocytes.
[A]:
Does monocyte chemoattractant protein-1 secreted by adipose tissue induce direct lipid accumulation in hepatocytes?