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.

[Q]: Context: The blasticidin S resistance gene (bsr) is a selectable marker used for gene transfer experiments. The bsr gene encodes for blasticidin S (BS) deaminase, which has a specific activity upon BS. Therefore, its expression is supposed to be harmless in cells. The work reported on herein consisted of experiments to verify a possible toxicity of bsr on mammalian cells, which include several cell lines and primary cultures.', 'Murine keratinocyte BALB/MK and human primary keratinocyte cells transduced with the retroviral vector LBmSN, which has an improved expression system of bsr, namely bsrm, died in five days after the transduction. Meanwhile the control vector LBSN, which expresses bsr, did not provoke cell death. The lethal activity of bsrm was observed only in human keratinocytes and BALB/MK cells among the cell types tested here. Death appears to be mediated by a factor, which is secreted by the BALB/MK transduced cells.\Question: Is over expression of the selectable marker blasticidin S deaminase gene toxic to human keratinocytes and murine BALB/MK cells?
[A]: By our study we demonstrated that the expression of bsrm gene is toxic to human keratinocytes and BALB/MK cells. It is likely over expression of BS deaminase gene is responsible for the death.


[Q]: Context: Secretory phospholipases A2 (sPLA2) initiate the biosynthesis of eicosanoids, are increased in the airways of people with severe asthma, and induce mucin hypersecretion. We used IL-13-transformed, highly enriched goblet cells and differentiated (ciliary cell-enriched) human bronchial epithelial cell culture to evaluate the relative contribution of ciliated and goblet cells to airway sPLA2 generation and response. We wished to determine the primary source(s) of sPLA2 and leukotrienes in human airway epithelial cells.', 'Human bronchial epithelial cells from subjects without lung disease were differentiated to a ciliated-enriched or goblet-enriched cell phenotype. Synthesis of sPLA2, cysteinyl leukotrienes (cysLTs), and airway mucin messenger RNA and protein was measured by real-time-polymerase chain reaction and an enzyme-linked immunosorbent assay, and the localization of mucin and sPLA2 to specific cells types was confirmed by confocal microscopy.', 'sPLA2 group IIa, V, and X messenger RNA expression was increased in ciliated-enriched cells (P < .001) but not in goblet-enriched cells. sPLA2 were secreted from the apical (air) side of ciliated-enriched cells but not goblet-enriched cells (P < .001). Immunostaining of sPLA2 V was strongly positive in ciliated-enriched cells but not in goblet-enriched cells. sPLA2 released cysLTs from goblet-enriched cells but not from ciliated-enriched cells, and this result was greatest with sPLA2 V (P < .05). sPLA2 V increased goblet-enriched cell mucin secretion, which was inhibited by inhibitors of lipoxygenase or cyclooxygenase (P < .02).\Question: Are secretory phospholipases A2 secreted from ciliated cells and increase mucin and eicosanoid secretion from goblet cells?
[A]: sPLA2 are secreted from ciliated cells and appear to induce mucin and cysLT secretion from goblet cells, strongly suggesting that airway goblet cells are proinflammatory effector cells.


[Q]: Context: Caudal block is a common technique for paediatric analgesia but with the disadvantage of short duration of action after single injection. Caudal dexmedetomidine and clonidine could offer significant analgesic benefits. We compared the analgesic effects and side-effects of dexmedetomidine and clonidine added to bupivacaine in paediatric patients undergoing lower abdominal surgeries.', 'Sixty patients (6 months to 6 yr) were evenly and randomly assigned into three groups in a double-blinded manner. After sevoflurane in oxygen anaesthesia, each patient received a single caudal dose of bupivacaine 0.25% (1 ml kg(-1)) combined with either dexmedetomidine 2 microg kg(-1) in normal saline 1 ml, clonidine 2 microg kg(-1) in normal saline 1 ml, or corresponding volume of normal saline according to group assignment. Haemodynamic variables, end-tidal sevoflurane, and emergence time were monitored. Postoperative analgesia, use of analgesics, and side-effects were assessed during the first 24 h.', 'Addition of dexmedetomidine or clonidine to caudal bupivacaine significantly promoted analgesia time [median (95% confidence interval, CI): 16 (14-18) and 12 (3-21) h, respectively] than the use of bupivacaine alone [median (95% CI): 5 (4-6) h] with P<0.001. However, there was no statistically significant difference between dexmedetomidine and clonidine as regards the analgesia time (P=0.796). No significant difference was observed in incidence of haemodynamic changes or side-effects.\Question: Does addition of clonidine or dexmedetomidine to bupivacaine prolong caudal analgesia in children?
[A]:
Addition of dexmedetomidine or clonidine to caudal bupivacaine significantly promoted analgesia in children undergoing lower abdominal surgeries with no significant advantage of dexmedetomidine over clonidine and without an increase in incidence of side-effects.