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.

Context: The mechanism involved in AD is complex, which has prompted to develop compounds that could simultaneously interact with several potential targets. Here, we report a new synthesized compound SCR-1693 which is designed to target both AChE and calcium channels that are potential for AD therapy.', 'We investigated the effects of SCR-1693 on AChE and calcium channels, the effects of neuroprotection and anti-amnesia in icv-Aβ25-35-injected mice, and the potential mechanisms.', 'AChE activity assay, intracellular Ca(2+) content and calcium currents measurement, and Aβ25-35-induced cellular death determine were performed for validation of designed targets and neuroprotection of SCR-1693. Mice were orally administrated with SCR-1693 once daily after an Aβ25-35 injection. The Morris water maze and Y-maze test, and hippocampal protein detection were conducted on days 5-10, day 11, and day 8. The pyramidal neuron number, hippocampal AChE activity, and synaptic transmission were measured on day 12.', 'SCR-1693 acted as a selective, reversible, and noncompetitive inhibitor of AChE, and a nonselective voltage-gated calcium channel blocker. SCR-1693 also inhibited the increase of AChE activity in the mouse hippocampus. SCR-1693 was more effective than donepezil and memantine in preventing Aβ25-35-induced long-term and short-term memory impairment, maintaining the basal transmission of Schaffer collateral-CA1 synapses, and sustaining LTP in mouse hippocampus. SCR-1693 attenuated Aβ25-35-induced death of SH-SY5Y cell and the loss of hippocampal pyramidal neurons, and regulated Aβ25-35-induced signal cascade in neurons.
Answer: All these findings indicated that SCR-1693, as a double-target-direction agent, is a considerable candidate for AD therapy.
Does a novel acetylcholinesterase inhibitor and calcium channel blocker SCR-1693 improve Aβ25-35-impaired mouse cognitive function?

Context: Cells of the myeloid lineage comprise a very heterogeneous population with many phenotypes and functional activities including macrophages and dendritic cells. To investigate the status, differentiative potential and lineage commitment of monocytic cells in systemic lupus erythematosus (SLE) patients, this study isolated and cultured peripheral blood monocytes from patients and healthy donors.', 'Monocytes were isolated by gradient centrifugation and adherence to plastic dishes. The cells were then cultured for three days, partially supplemented with GM-CSF and interleukin 4 (IL4) to obtain dendritic cells. The differentiation status was monitored by the expression of surface markers using flow cytometry and cytokine secretion.', 'Monocytes from SLE patients expressed significantly lower numbers of the monocytic marker CD14 and HLA-DR while secreting significantly more tumour necrosis factor alpha (TNFalpha) than monocytes from healthy donors. The addition of GM-CSF and IL4 resulted in an inhibition of TNFalpha secretion, but was not sufficient to generate monocytederived dendritic cells.
Answer: Monocytes from SLE patients are severely altered in phenotype and function and have a limited differentiation flexibility towards the accessory type of monocytic cells.
Are monocytes from systemic lupus erythematous patients severely altered in phenotype and lineage flexibility?

Context: To investigate vessel density changes with increasing age in three areas of the brain and to correlate these changes with leukoaraiosis (LA) on the basis of magnetic resonance (MR) images and location in deep white matter (WM).', 'Internal review board approval or informed consent from next of kin was not required. Brains of 21 subjects (mean age, 72.5 years; 12 men, nine women) were evaluated at autopsy with MR imaging. The presence of LA was indicated by confluent or patchy areas of hyperintensity in deep WM. Microvascular density (percentage of vessel area divided by total area) in subjects with LA was measured with computerized morphometric analysis in LA lesions, healthy-appearing WM at MR imaging, and the cortex. These measurements were compared with each other and with measurements from corresponding areas in healthy subjects. Afferent vasculature was stained with alkaline phosphatase in celloidin sections. Hypotheses were tested with computation of a series of repeated-measures linear mixed models.', 'Autopsy brains from 12 subjects with LA (mean age, 72 years; six men, six women) and nine subjects without LA (mean age, 73 years; six men, three women) were studied. Afferent microvascular density +/- standard deviation in LA lesions in deep WM (2.56% +/- 1.56) was significantly lower than that in corresponding deep WM of healthy subjects (3.20% +/- 1.82) (P = .018). Subjects with LA demonstrated decreased afferent vascular density at early ages in all three areas of the brain when compared with healthy subjects of the same age.
Answer: Findings of decreased afferent vascular density in the area of LA and outside the lesion indicate that LA is a generalized cerebrovascular disease process rather than one confined to deep WM.

Does quantification of afferent vessels show reduced brain vascular density in subjects with leukoaraiosis?