Charity by Sara Kreindler OFS Tuesday 21 –Saturday 25 October A Pembroke musical about financial crises? The irony got out of its seat and gave me a good slap round the face when I entered the theatre. Sara Kreindler, a loquacious Canadian studying at Pembroke, has written both the book and score for this show. Her talents composing are never thrown into question throughout the piece, but a plausible narrative unity is lacking here. The curtain opens on the meeting of a foreign aid charity. Its members are trying hopelessly to organise the most important event of the year, the Charity Ball. Conflict soon arises, as the committee splits into two, hurling abuse at each other through the camp medium of song. But ultimately, this is a story about that ol’ chestnut Love. More specifically, of Anita (Reina Hardy) and Ben (Richard Power). These two insecure, inexperienced souls refuse to admit their powerful attraction to one another, rendered paralysed by their shared fear of rejection. Anita worries that her strength and intelligence will alienate any man (how out-of-character for a girl to think that), whilst Ben contracts verbal dysentery when speaking to the opposite sex. Power plays Ben with an endearing humility and diffidence. Although his character is shy and unforthcoming, Power has a tremendous presence on stage, combining the naivety and ingenuousness of Jack Lemmon with the zeal and tenacity of a confident leading man. His voice is as strong as his acting, making him the highlight of this production. The relationship of Suzy and Trevor is explored, too. This is where my initial delight at the show turned to an uneasy dislike. Alice Shepherd, in the role of Suzy, lacked the necessary qualities to convince us of her character’s dissatisfaction with the sweet, but unexciting, Trevor. Suzy does not want her lover to be so thoughtful and caring. I began to cringe as Suzy launched into her lamenting “Why can’t you be wrong for me?” number; I’ve heard girls complain about guys being too sweet enough times without hearing it committed to music. Stop bloody complaining! Ahem. A bit about the staging. The OFS is set up in traverse, to accentuate the polarisation of the charity board: radicals against moderates, men against women. This opposition is achieved well, where many of the songs, whether politically- or ardently-driven, feature a tête-à-tête between man and woman. Christine Chung plays the femme fatale, Mavis, with seductive intensity that inveigles poor Trevor into her arms. And in ‘Farewell’, the intertwining of Anita and Ben’s vocals strongly suggests a gradual intimacy between the two. The music itself, however, is somewhat repetitious from song to song, with little stylistic variation. Vocally, the male leads outshone their female counterparts, most significantly, in their enunciation. Kreindler is very lyrically skilled, and the songs have a verbal playful quality. But on leaving the theatre, I was not sure what I had learnt from the show. Was the political element really necessary to drive the amorous plotline forward? Does charity really help us to change ourselves fundamentally? I was not convinced.ARCHIVE: 1st Week MT2003
Source:https://www.kanazawa-u.ac.jp/ Immunofluorescence for Oatp2a1 in mice glial (left) and endothelial cells (right) in the brain. Immunoreactivity of Oatp2a1 (red color) was detected in F4/80-positive cells (e.g. microglia, green color) and in endothelial cells stained with CD34 (green color). White arrow indicates merge of fluorescence. Aug 31 2018Researchers from Kanazawa University report in Journal of Neuroscience performed a microdialysis study on mice to determine mechanisms underlying the inflammatory response in the brain associated with fever that might be used to develop new strategies for treatment. The appearance of fever is associated with the release in the hypothalamus of a lipid compound called prostaglandin E2 (PGE2), which has an important role in the regulation of body temperature. However, how PGE2 is supplied to or maintain in the brain, and the role of membrane transporters (in particular of the prostaglandin transporter OATP2A1, encoded by the gene SLCO2A1) in this process still needs to be elucidated.To shed light on this question, Takeo Nakanishi at Kanazawa University, Japan, and colleagues performed a microdialysis study on mice, published in the Journal of Neuroscience. The researchers used mice with normal Slco2a1, with total Slco2a1 deficiency or with monocyte-/macrophage-specific Slco2a1 deficiency. They first injected the mice with physiological saline, observing the same body temperature for mice with and without SLCO2A1, indicating that the presence of OATP2A1 does not affect the basal body temperature. They then administered to the mice a pyrogen, lipopolysaccharide, that normally causes a fever. Indeed, mice with Slco2a1 developed a fever after 2h, whereas the pyrogenic effect of lipopolysaccharide was not observed in mice with total SLCO2A1 deficiency. They further demonstrate the body temperature of mice with monocyte-/macrophage-specific Slco2a1 deficiency was partially attenuated. Intriguingly, an inhibitor of OATP2A1 injected to the brain of rats with normal Slco2a1 inhibited the febrile response — in this case only an initial rise in body temperature was observed.Related StoriesResearch team to create new technology for tackling concussionMercy Medical Center adds O-arm imaging system to improve spinal surgery resultsWearing a hearing aid may mitigate dementia riskThe study reveals that the onset of fever is associated with increased PGE2 concentration in the hypothalamus interstitial fluid, but not in the cerebrospinal fluid, thus OATP2A1 seems to work by maintaining high levels of PGE2 in the hypothalamus, either by stimulating its secretion from glial cells in the hypothalamus and from brain capillary endothelial cells or by facilitating its transport through the blood-brain barrier. OATP2A1 seems to be involved in the secretion of PGE2 from macrophages, but OATP2A1 in cells other than macrophages may also contribute to the febrile response.This newly gained insight of the mechanisms underlying the inflammatory response in the brain associated with fever might be used to develop new strategies for treatment, pointing to OATP2A1 as a useful therapeutic target.