TASK DEFINITION: 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.
PROBLEM: Context: Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice.', 'We found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p\xa0<\xa00.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p\xa0<\xa00.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver.\Question: Does astaxanthin ameliorate prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring?

SOLUTION: Taken together, these results suggest that prenatal maternal LPS-exposure leads to behavioral deficits in the adults, while astaxanthin ameliorates the behavioral deficits presumably via its antioxidant property.

PROBLEM: Context: Primary pneumonic plague is a rare but often fatal form of Yersinia pestis infection that results from direct inhalation of bacteria and is potentially transmissible from person to person. We describe a case of primary pneumonic plague in a wildlife biologist who was found deceased in his residence 1 week after conducting a necropsy on a mountain lion.', "To determine cause of death, a postmortem examination was conducted, and friends and colleagues were interviewed. Physical evidence was reviewed, including specimens from the mountain lion and the biologist's medical chart, camera, and computer. Human and animal tissues were submitted for testing. Persons in close contact (within 2 meters) to the biologist after he had developed symptoms were identified and offered chemoprophylaxis.", 'The biologist conducted the necropsy in his garage without the use of personal protective equipment. Three days later, he developed fever and hemoptysis and died approximately 6 days after exposure. Gross examination showed consolidation and hemorrhagic fluid in the lungs; no buboes were noted. Plague was diagnosed presumptively by polymerase chain reaction and confirmed by culture. Tissues from the mountain lion tested positive for Y. pestis, and isolates from the biologist and mountain lion were indistinguishable by pulsed-field gel electrophoresis. Among 49 contacts who received chemoprophylaxis, none developed symptoms consistent with plague.\Question: Do primary pneumonic plague contracted from a mountain lion carcass?

SOLUTION: The biologist likely acquired pneumonic plague through inhalation of aerosols generated during postmortem examination of an infected mountain lion. Enhanced awareness of zoonotic diseases and appropriate use of personal protective equipment are needed for biologists and others who handle wildlife.

PROBLEM: Context: To evaluate magnesium deficiency during and after acute myocardial infarction (AMI) and the role of intravenous magnesium therapy given in the early postinfarction period.', 'One hundred patients with AMI were randomly assigned to 2 equal groups and monitored over a 4-week period. The placebo group received intravenous dextrose solution and the trial group was given 15 g intravenous magnesium (62 mmol) over a 48-hour period. Serum magnesium levels were measured on days 1, 2, 4, and 6 after admission by calorimetry with methyl thymol blue.', 'The groups were comparable in prevalence of risk factors for coronary artery disease and other acute parameters of AMI. The serum magnesium levels of a group of 50 controls were higher (1.61 +/- 0. 21 vs 1.23 +/- 0.27mEq/L) than in patients with AMI (P <.001). There was an increase in serum magnesium levels in the trial group on day 2 (1.73 +/- 0.27 vs 1.29 +/- 0.28 mEq/L; P <.001) as well as on day 4 (1.62 +/- 0.25 vs 1.38 +/- 0.36 mEq/L; P <.001). The trial group also showed significantly lower incidence of arrhythmias (8% vs 34%) and death (4% vs 20%). The mortality rate from pump failure was reduced in the trial group (4% vs 14%).\Question: Is benefits of magnesium in acute myocardial infarction : timing crucial?

SOLUTION:
The serum magnesium levels in patients with AMI were lower compared with controls. The administration of intravenous magnesium to patients in the immediate postinfarction period is cardioprotective and decreases the incidence of arrhythmia, pump dysfunction, and death. Thus intravenous magnesium is a safe, effective, and inexpensive modality of treatment in AMI.