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.
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Question: Context: Observational and clinical studies suggest different responses upon sex hormone replacement therapy in ischaemic heart disease. Few studies, however, have examined the impact of oestrogen receptor-dependent mechanisms on the extent of injury after myocardial infarction (MI). Therefore, we set out to evaluate the effect of oestrogen (E2) replacement on infarct size and remodelling, and the respective role of the oestrogen receptors (ER)alpha and -beta in this process, using ERalpha- and ERbeta-deficient mice.', 'Wild type (WT) (ERalpha(+/+) and ERbeta(+/+)), ERalpha-deficient (ERalpha(-/-)) and ERbeta-deficient (ERbeta(-/-)) mice were ovariectomized and subsequently supplemented with E2 or placebo using subcutaneous 60-day release pellets. MI was induced by left coronary artery ligation. Two weeks following MI, haemodynamic function was assessed and infarct size was determined.', 'There was no significant difference in infarct size between E2- or placebo-treated WT (ERalpha(+/+) and ERbeta(+/+)) mice. Surprisingly, E2 treatment did result in smaller infarct sizes in ERalpha(-/-) mice, but increased the infarct size in ERbeta(-/-) mice. Increase of the left ventricular mass post-MI was significantly larger in the E2-treated ERalpha(-/-) animals compared with placebo-treated animals. E2 treatment also significantly increased post-MI mortality in ERalpha(+/+), ERbeta(+/+) and ERalpha(-/-) animals, but not in ERbeta(-/-) mice.
Answer: Although E2 modulates the infarct size in ERalpha(-/-), it also appears to be responsible for the higher mortality following MI. ERbeta appears to be the receptor involved in the modulating effects of E2 in the infarcted heart.

Answer: Does oestrogen modulate cardiac ischaemic remodelling through oestrogen receptor-specific mechanisms?


Question: Context: In atherogenesis, dendritic cells, beside presenting antigens, may be sources of tumour necrosis factor (TNF)alpha and nitric oxide (NO), together with mast cells and smooth muscle cells.', 'We have looked at the expression of TNFalpha and inducible NO synthase (iNOs) by these cells by affinity cytochemistry in autoptical specimens from normal carotid arteries and not ruptured, hemorrhagic or calcified atheromata.', 'Round to dendritic, major histocompatibility complex class II molecules (MHC-II+) cells and avidin-labeled mast cells were rare in normal arteries and significantly more numerous in atheromata. Many MHC-II+ cells expressed S-100 antigen; while a few were positive for phalloidin; appreciable fractions of these cells were immunoreactive for TNFalpha and iNOs, both in control specimens and atheromata. The fraction of mast cells labeled for iNOs was significantly lower in atheromata than in controls. Phalloidin positive cells were the most abundant cell type in the normal intima and atheromata; the fractions of these cells labeled for TNFalpha and iNOs were significantly higher in atheromata than in controls. Very few of these cells were also labeled for MHC-II. Computerized image analysis confirmed that the amounts of iNOs and TNFalpha were higher in atheromata than in controls. The increase in TNFalpha in atheromata was also confirmed by western blot.
Answer: Dendritic cells and mast cells can participate to the generation of TNFalpha and NO in the normal arterial wall and in atheromata, but myointimal cells are candidates as major sources of these molecules.

Answer: Are smooth muscle cells , dendritic cells and mast cells sources of TNFalpha and nitric oxide in human carotid artery atherosclerosis?


Question: Context: Increasing evidence suggests that posttraumatic stress disorder (PTSD) is associated with small hippocampal size. The authors compared trauma-exposed subjects with PTSD and trauma-exposed subjects without PTSD to clarify whether small hippocampal size is related to PTSD or to mere trauma exposure.', 'Three-dimensional structural magnetic resonance imaging was used to assess hippocampal volumes in 30 men who had recently been exposed to a severe burn trauma and 15 matched healthy comparison subjects.', 'Relative to the comparison subjects, the trauma-exposed subjects with PTSD (N=15) as well as the trauma-exposed subjects without PTSD (N=15) had significantly smaller volumes of the right hippocampus (subjects with PTSD: -12%; subjects without PTSD: -13%). Larger total areas of burned body surface were significantly related to smaller left hippocampal volumes. Use of analgesic/sedative treatment with the N-methyl-d-aspartic acid (NMDA) antagonist ketamine was significantly related to larger right hippocampal volumes and to stronger PTSD symptoms.
Answer: PTSD is not a necessary condition for small hippocampal size in trauma-exposed individuals. Rather, the results provide evidence that smaller hippocampal size in trauma-exposed individuals is a result of traumatic stress. The posttraumatic application of NMDA antagonists may protect against hippocampal damage induced by traumatic stressors but increases the patient's risk of developing PTSD symptoms.

Answer:
Do hippocampal volume in adult burn patients with and without posttraumatic stress disorder?