TASK DEFINITION: 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.
PROBLEM: Context: Stomatal guard cells monitor and respond to environmental and endogenous signals such that the stomatal aperture is continually optimised for water use efficiency. A key signalling molecule produced in guard cells in response to plant hormones, light, carbon dioxide and pathogen-derived signals is hydrogen peroxide (H(2)O(2)). The mechanisms by which H(2)O(2) integrates multiple signals via specific signalling pathways leading to stomatal closure is not known.', 'Here, we identify a pathway by which H(2)O(2), derived from endogenous and environmental stimuli, is sensed and transduced to effect stomatal closure. Histidine kinases (HK) are part of two-component signal transduction systems that act to integrate environmental stimuli into a cellular response via a phosphotransfer relay mechanism. There is little known about the function of the HK AHK5 in Arabidopsis thaliana. Here we report that in addition to the predicted cytoplasmic localisation of this protein, AHK5 also appears to co-localise to the plasma membrane. Although AHK5 is expressed at low levels in guard cells, we identify a unique role for AHK5 in stomatal signalling. Arabidopsis mutants lacking AHK5 show reduced stomatal closure in response to H(2)O(2), which is reversed by complementation with the wild type gene. Over-expression of AHK5 results in constitutively less stomatal closure. Abiotic stimuli that generate endogenous H(2)O(2), such as darkness, nitric oxide and the phytohormone ethylene, also show reduced stomatal closure in the ahk5 mutants. However, ABA caused closure, dark adaptation induced H(2)O(2) production and H(2)O(2) induced NO synthesis in mutants. Treatment with the bacterial pathogen associated molecular pattern (PAMP) flagellin, but not elf peptide, also exhibited reduced stomatal closure and H(2)O(2) generation in ahk5 mutants.
Answer: Our findings identify an integral signalling function for AHK5 that acts to integrate multiple signals via H(2)O(2) homeostasis and is independent of ABA signalling in guard cells.

SOLUTION: Does the histidine kinase AHK5 integrate endogenous and environmental signals in Arabidopsis guard cells?

PROBLEM: Context: Facial dog bite injuries pose a significant public health problem.', 'Seventy-five consecutive patients (45 males, 30 females) treated solely by plastic surgery service for facial dog bite injuries at a Level I trauma center in the Denver Metro area between 2006 and 2012 were retrospectively reviewed. The following information were recorded: breed, relationship of patient to dog, location and number of wounds, the duration between injury and surgical repair and dog bite incident, type of repair, and antibiotic prophylaxis. Primary end points measured were wound infection, the need for revision surgery, and patient satisfaction.', 'Ninety-eight wounds in the head and neck region were repaired (46 children; mean age, 6.8 years) and (29 adults; mean age, 47.3 years). Twelve different breeds were identified. There was no significant association between the type of dog breed and the number of bite injuries. The duration between injury and repair ranged from 4 hours to 72 hours (mean [SD], 13.7 [10.9] hours). The majority of bite wounds (76 of 98) involved the cheek, lip, nose, and chin region. Direct repair was the most common surgical approach (60 of 98 wounds) (p < 0.05). There was no statistically significant association between wounds needing reconstruction versus direct repair according to dog breed (p = 0.25). Ten wounds required grafting. Twenty-five wounds were managed by one-stage or two-stage flaps. Only three patients (3.06 %) underwent replantation/revascularization of amputated partial lip (n = 2) and of cheek (n = 1). There was one postoperative infection. Data from five-point Likert scale were available for fifty-two patients. Forty patients were satisfied (5) with the outcome, while five patients were somewhat satisfied (4), and seven were neutral.
Answer: Availability of the plastic surgery service at a Level I trauma center is vital for the optimal treatment of facial dog bite injuries. Direct repair and reconstruction of facial dog bite injuries at the earliest opportunity resulted in good outcomes as evidenced by the satisfaction survey data and low complication rate.

SOLUTION: Do retrospective analysis of facial dog bite injuries at a Level I trauma center in the Denver metro area?

PROBLEM: Context: Our previous studies suggested that brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) axis inhibited cardiomyocyte apoptosis in myocardial infarction (MI). However, the relationship between BDNF and microRNA (miRNA) in cardiomyocytes are unclear. The present study was performed to investigate the role of miR-195 and the interplay between BDNF and miR-195 in ischemic cardiomyocyte apoptosis.', 'Male Wistar rats were subjected to coronary artery ligation, and primary neonatal rat ventricular myocytes were treated with hypoxia or hydrogen peroxide (H2O2). BDNF level in rat ventricles was measured by enzyme linked immunosorbent assay (ELISA). miR-195 mimic, inhibitor or negative control was transfected into the cardiomyocytes. Cell viability and apoptosis were detected by MTT assay and TdT-mediated dUTP nick end labeling (TUNEL) staining, respectively. Cardiac function and apoptosis were detected in MI rats intravenously injected with antagomiR-195. Luciferase assay, Western blot and Real-time RT-PCR were employed to clarify the interplay between miR-195 and BDNF.', 'miR-195 level was dynamically regulated in response to MI and significantly increased in ischemic regions 24 h post-MI as well as in hypoxic or H2O2-treated cardiomyocytes. Meanwhile, BDNF protein level was rapidly increased in MI rats and H2O2-treated cardiomyocytes. Apoptosis in both hypoxic and H2O2-treated cardiomyocytes were markedly reduced and cell viability was increased by miR-195 inhibitor. Moreover, inhibition of miR-195 significantly improved cardiac function of MI rats. Bcl-2 but not BDNF was validated as the direct target of miR-195. Furthermore, BDNF abolished the pro-apoptotic role of miR-195, which was reversed by its scavenger TrkB-Fc.
Answer: Up-regulation of miR-195 in ischemic cardiomyocytes promotes ischemic apoptosis by targeting Bcl-2. BDNF mitigated the pro-apoptotic effect of miR-195 in rat cardiomyocytes. These findings may provide better understanding of the pro-apoptotic role of miR-195 in MI and suggest that BDNF/miR-195/Bcl-2 axis may be beneficial for limiting myocardial ischemic injury.

SOLUTION:
Does bDNF-mediates Down-regulation of MicroRNA-195 inhibit Ischemic Cardiac Apoptosis in Rats?