instruction:
Given a passage, 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.
question:
The major immuno-modulating effects of Ganoderma lucidum include mitogenicity and activation of immune effector cells such as T cells, macrophages and natural killer cells resulting in the production of cytokines.', 'The purpose of this study was to evaluate the expression of CD40 and CD80 by G. lucidum-treated human peripheral blood mononuclear cells.', 'Monocytes were isolated and incubated at 37 C and 5% CO2 for 24 h and 48 h in the presence or absence of different concentrations of G. lucidum. Cells were then incubated with labelled monoclonal antibodies against CD14, CD40 and B7-1(CD80) molecules utilizing standard protocols, and analyzed by flow cytometry.', 'The results showed that incubation of monocytes with G. lucidum led to marked enhancement of CD40 and B7-1 expression in a dose- and time- dependent manner (p<0.001). G. lucidum was more effective in enhancing the expression of CD80 and CD40 molecules of cells obtained from females than male donors (p<0.001).
answer:
Does ganoderma lucidum induce the expression of CD40/CD86 on peripheral blood monocytes?

question:
Islet function is regulated by islet autonomic nerves. These nerves harbour not only the classical neurotransmitters, acetyl choline and noradrenaline, but also neuropeptides. This study examined whether the neuropeptides, pituitary adenylate cyclase activating polypeptide (PACAP) and gastrin releasing polypeptide (GRP) contribute to the regulation of insulin secretion in model experiments by using receptor gene deleted mice.', 'Anaesthetized mice with genetic deletion of one of the PACAP receptors (PAC1 receptors) or one of the GRP receptors (GRP receptor) or their wildtype counterparts were given glucose through a gastric gavage (150 mg) or intravenously (0.25, 0.50 or 1 g/kg). Blood samples were taken regularly during the following 120 min (after gastric glucose) or at 1 min (after intravenous glucose) for analysis of glucose and insulin.', 'The insulin response to gastric glucose was suppressed by 66% in PAC1 receptor gene deleted mice in association with impaired glucose elimination, whereas the insulin response to intravenous glucose was impaired by 36% only. The insulin response to glucose was suppressed in GRP receptor gene deleted mice by 24% together with impaired glucose elimination, whereas the insulin response to intravenous glucose was not significantly suppressed.
answer:
Is the insulin response to gastric glucose reduced in PAC1 and GRP receptor gene deleted mice?

question:
Antioxidant therapy has shown some promise in critical care medicine in which glutathione depletion and heart failure are often seen in critically ill patients. This study was designed to examine the impact of glutathione depletion and the free radical scavenger, metallothionein (MT), on cardiac function.', 'Friend virus B and MT transgenic mice were given the glutathione synthase inhibitor buthionine sulfoximine (buthionine sulfoximine [BSO], 30 mmol/L) in drinking water for 2 wks.', 'Echocardiographic and cardiomyocyte functions were evaluated, including myocardial geometry, fraction shortening, peak shortening, time-to-90% relengthening (TR90), maximal velocity of shortening/relengthening (+/-dL/dt), intracellular Ca2+ rise, sarcoplasmic reticulum Ca2+ release, and intracellular Ca2+ decay rate. Sacro (endo)plasmic reticulum Ca2+-ATPase function was evaluated by 45Ca uptake. Highly reactive oxygen species, caspase-3, and aconitase activity were detected by fluorescent probe and colorimetric assays.', 'BSO elicited lipid peroxidation, protein carbonyl formation, mitochondrial damage, and apoptosis. BSO also reduced wall thickness, enhanced end systolic diameter, depressed fraction shortening, peak shortening, +/-dL/dt, sarcoplasmic reticulum Ca2+ release, 45Ca uptake, and intracellular Ca2+ decay, leading to prolonged TR90. BSO-induced mitochondrial loss and myofilament aberration. MT transgene itself had little effect on myocardial mechanics and ultrastructure. However, it alleviated BSO-induced myocardial functional, morphologic, and carbonyl changes. Western blot analysis showed reduced expression of sacro (endo)plasmic reticulum Ca2+-ATPase2a, Bcl-2 and phosphorylated GSK-3beta, enhanced calreticulin, Bax, p53, myosin heavy chain-beta isozyme switch, and IkappaB phosphorylation in FVB-BSO mice, all of which with the exception of p53 were nullified by MT.
answer:
Does metallothionein alleviate glutathione depletion-induced oxidative cardiomyopathy in murine hearts?