Sunday, August 9, 2020

GLYNDEBOURNE OPEN HOUSE

 


The Fairy Queen

Watch Purcell's The Fairy Queen online for free from Sunday 23 August

ONE CHARMING NIGHT…

Taking us from rowdiest, raunchiest comedy to bewitching beauty and pathos, Purcell’s The Fairy Queen is a theatrical fantasy unlike any other. Shakespeare’s A Midsummer Night’s Dream finds itself at the centre of a sequence of musical apparitions and conjurings – fairies romp and play, animals dance and mortals are manipulated by the gods. Through it all, love and desire weave their irresistible spell.

 Purcell’s score brings everything from English choral writing to Italian laments and French dances together in a rich musical tapestry. There’s comedy from lusty shepherds and tenderness from separated lovers – a musical story that winds around Shakespeare’s play and characters to create an exhilarating fusion of theatre, music and dance.

 Jonathan Kent’s ‘delectable’ production opens up a 17th-century cabinet of curiosities to reveal the contemporary magic within, working with conductor William Christie and a cast including Lucy Crowe, Carolyn Sampson and Ed Lyon to find the anarchic energy at the heart of this unusual work.

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Hamlet

About the opera

BEFORE YOU SET OUT FOR REVENGE, MAKE SURE YOU DIG TWO GRAVES.

Tormented by his father’s death, Hamlet plots revenge. But it’s a long way from anger to murder, and soon the Prince finds himself losing his grip on sanity, strength, love and even life itself.

 Rapturously received at its 2017 premiere, Brett Dean and Matthew Jocelyn’s Hamlet is an award-winning reimagining of Shakespeare’s most famous play. Placing his audience at the heart of the drama, immersing them in sound and even physical sensation, Dean invites us all into Hamlet’s consciousness, to inhabit the mind of one of the cleverest, wittiest, most troubled heroes in all literature. 

Transforming the Glyndebourne auditorium into a ‘theatre of sound’, Dean’s richly lyrical score finds the music of Shakespeare’s language, amplifying it to create an evocative, disturbing soundscape. This is Hamlet, but not as you’ve ever heard it before.

 Neil Armfield directs an all-star cast led by Allan Clayton and Barbara Hannigan. Vladimir Jurowski conducts.

 

Hamlet was captured live at Festival 2017. It is available on DVD from our shop.

 

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Handel Giulio Cesare

BOLLYWOOD MEETS BAROQUE IN DAVID MCVICAR’S LEGENDARY STAGING

When Egypt’s seductive queen meets Rome’s powerful ruler, the stakes are high, both for politics and passion. Horrified by the brutal murder of his rival by Cleopatra’s brother Tolomeo, Cesare joins forces with Cleopatra to depose her unscrupulous sibling. But is their alliance one of love, lust or just mutual ambition?

A true Glyndebourne classic, David McVicar’s production brings all-singing, all-dancing energy to one of Handel’s greatest scores. Sumptuous designs that nod to Britain’s colonial history transform a tale of political intrigue into a dazzling spectacle, sweeping the audience up in its tangled web of power, revenge and romance.

 The resourceful, complicated Cleopatra and smooth statesman Cesare are two of Handel’s most fascinating creations – characters whose music, by turns heart-breaking and ecstatic, includes so many of the composer’s finest arias.

 William Christie conducts a cast led by Sarah Connolly’s Cesare and Danielle de Niese as Cleopatra.

 

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09 Jul 2020

New titles announced for Glyndebourne Open House

Glyndebourne has announced the next two opera titles in its virtual festival, Glyndebourne Open House - Britten’s Billy Budd and Rossini’s The Barber of Seville.

The Barber of Seville at Glyndebourne

Above: Janis Kelly as Berta, Taylor Stayton as Count Almaviva, Danielle de Niese as Rosina, Taylor Stayton as Figaro

Photo credit: Bill Cooper/Glyndebourne

 

Glyndebourne Open House throws open our doors to everyone, everywhere: join us at 5.00pm each Sunday and enjoy world-class opera in your living room for free.

In true Festival style, we hope you’ll use this as an opportunity to make memories - dust off your finery, clink a glass with friends and family and be united with opera lovers from across the globe. We can’t conjure the smell of the Glyndebourne roses or a view of the lake, but we can still create an experience to share.

Coming up this Sunday 12th July is Michael Grandage’s production of Billy Buddfollowed on 19th July by Annabel Arden’s staging of The Barber of SevilleThese two operas will be available to watch on Glyndebourne's website and YouTube channel.

Visit glyndebourne.com/OpenHouse

Glyndebourne Open House listings

12 JULY - BILLY BUDD

From 5pm on 12 July and on demand for one week. Watch on the Glyndebourne website or YouTube channel.

Inspired by Herman Melville’s novella, Benjamin Britten’s Billy Budd is a heart-breaking psychological study of good and evil and the many human shades of grey that lie between. Harnessing the power of a large orchestra and all-male chorus, the opera creates a vast and powerful voice for the sailors of the HMS Indomitable.

At the heart of this claustrophobic community is Billy Budd, a new recruit whose innocence, goodness and beauty attract the unwelcome attention of Master-at-arms Claggart. Conflicted and tormented by the emotions the boy stirs in him, Claggart vows to destroy him. False accusations lead to violence, tragedy and ultimately death.

Britten’s score blends lyricism and moments of startling beauty with evocative sea-shanties and sweeping orchestral textures to create one of his most moving operas.

Glyndebourne’s first ever production is directed by veteran British theatre director Michael Grandage, who makes his operatic debut with this award-winning production starring Jacques Imbrailo in the title role. Mark Elder conducts.

19 JULY - THE BARBER OF SEVILLE

From 5pm on 19 July and on demand for one weekWatch on the Glyndebourne website or YouTube channel.

The beautiful Rosina is kept all but prisoner by her guardian Dr Bartolo, who secretly hopes to marry his wealthy ward. But when Count Almaviva falls in love with Rosina from afar he enlists the help of cunning barber Figaro to help him outwit Bartolo. A comic battle of wills ensues, but will love or greed be triumphant?

Verdi thought it the greatest operatic comedy - a perfect marriage of wit, energy and exhilarating musical invention. Rossini’s score fizzes with virtuosic brilliance, combining bravura solo arias, set to some of the composer’s best-loved melodies, with breath-taking, intricate ensembles.

Embracing the opera’s Commedia dell’arte origins, Annabel Arden’s lively production is suffused with Spanish colour and warmth, with just a hint of the surreal. Enrique Mazzola conducts an all-star cast including Danielle de Niese, Alessandro Corbelli and Björn Bürger.

Saturday, August 8, 2020

To Hell and Back Review: Brain on Fire: My Month of Madness

Suppose you thought that you were losing your identity—changing almost overnight and doing things you could not explain? This inexplicable scenario helps launch Brain on Fire: My Month of Madness, in which Susannah Cahalan chronicles her experience with the rare disorder anti-NMDA-receptor encephalitis. The onset of this newly identified entity results from the production of antibodies against the N-methyl-D-aspartate (NMDA). The NMDA receptor regulates synaptic plasticity in the brain and is critical for learning and memory. The syndrome evolves over days to weeks and presents as a psychosis similar to that seen in schizophrenia. Cahalan, who suffered from seizures and other neurologic symptoms, creates a medical detective story from a patient’s perspective as she captivatingly describes her descent into madness. The result is entertaining reading that gets us to think about the biological origins of our own personalities.

Cahalan presents her experience as a remembrance three years after the onset of her disorder. At the book’s beginning, she is a young reporter struggling to find story ideas that will resonate with her editors at the New York Post. Over several weeks, she gradually finds her personality changing as she begins suffering from paranoia and hallucinations and withdraws from her friends and colleagues. She describes her thoughts (as she perceives them at the time) and confusion about the origin of her symptoms. Associated with her uncertainty is the realization that the medical community has no explanation for her rapid change.

Eventually, Cahalan develops the neurological features that lead to a correct diagnosis by a medical team at the NYU Langone Medical Center. After weeks of downward spiraling, the team puts all the facts together and arrives at the answer: anti-NMDA-receptor encephalitis, a multistage, autoimmune disease that varies wildly in its presentation. Cahalan slowly recovers after undergoing immunomodulatory therapies (steroids, IVIG treatment, and plasmapheresis) in the hospital for a month, plus six months of outpatient follow-up.

For a neuroscientific audience, Cahalan’s story stimulates readers to think about the essence of the brain and the personality on several levels. First is the way that she portrays the early events of her encephalitis. She is never sure whether her bizarre behavior is being driven by a disease or is the result of reactions to stress or other events. These reactions include irrational fears of jealously, emotional lability, and even illusions that she can sense other people’s thoughts. Almost all of her friends attribute these behaviors to the demands of her job or to psychological issues, but she later realizes that they are subtle early symptoms of anti-NMDA-receptor encephalitis. To a neuroscientist, Cahalan’s attempt to decipher her symptoms represents the core of the discussion about where the neurological features of disease end and those of psychiatry begin. It also shows the overlap between these disciplines. In addition, with treatment, the changes in Cahalan’s personality reverse not immediately but over long periods of time. This is consistent with the idea of a resilient, structural basis of memory and personality that is attacked by anti-NMDA-receptor encephalitis but is then slowly rebuilt. One issue, which Cahalan describes, is that anti-NMDA-receptor encephalitis is associated with a significant amnesia for the period of acute illness. Cahalan was able to trigger exquisite firsthand details about the experience by revisiting her family’s notes, diaries, and recollections, and she points out that it is difficult to tell where her personal memory ends and others’ memories begin. This paradox gives readers fascinating insight into the way that people constantly construct their own perceptions.

Brain on Fire is also very effective as an illustration of the diagnostic odyssey of an individual with an unknown disease. Cahalan’s signs seem so clear as she presents them three years later, now that the number of individuals reported with anti-NMDA-receptor encephalitis has risen from several hundred to many thousands and the disorder is no longer a research curiosity. Cahalan was diagnosed and treated only after weeks of progression, after finally being admitted to a specialized neurology service in a tertiary care center—and even at that center, the tale is presented as if only one specialist was familiar with the condition. Viewed from that perspective, Cahalan could be considered lucky even to have received the correct diagnosis. The author does not condemn physicians unaware of the diagnosis, as she recognizes the difficulty in staying abreast of new developments in medicine. The book is dedicated to undiagnosed patients, a group that goes far beyond anti-NMDA-receptor encephalitis. Even in the age of whole-genome sequencing, the medical community lacks much information about even common diseases, much less rare ones. Good news is that the NIH Undiagnosed Diseases Program is currently undergoing revision and expansion, in recognition of the number of disorders that remain unknown and might become recognizable.

In some ways, Cahalan oversimplifies the medical and scientific communities. For example, she essentially attributes her diagnosis and the original discovery of anti-NMDA-receptor encephalitis to single individuals. This presentation fails to recognize the manner in which medical care is delivered by interactive teams and the collaborative way that science moves forward. But the perspective presented provides insight on how people outside the medical and scientific communities view their work, and suggests that there is a need for broader education on the collaborative nature of the scientific and medical fields, particularly as the available time for such collaboration decreases.

Another misperception reflects the increasing incidence of anti-NMDA-receptor encephalitis. As Cahalan notes in her discussions with neurological experts, it is easy to speculate that this disorder might be responsible for many episodes of demonic possession or mental illness throughout history. However, this speculation does not match present medical observations, as untreated anti-NMDA-receptor encephalitis is an almost uniformly debilitating disease; scientists have identified few spontaneous survivors who did not have ICU-level care in the acute period. Thus, it seems unlikely that this specific disorder caused such reversible events throughout history, though an as-yet-unappreciated variant conceivably could have done so.

After reading Cahalan’s riveting account, neuroscientists may wonder about the specific molecules that influence memory and personality, while physicians may contemplate where the next new disease will arise. 


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704309/


Brain on Fire: My Month of Madness [Excerpt]

In a new memoir a young journalist traces her recovery from an autoimmune disorder that masqueraded as psychosis

In 2009 Susannah Cahalan was a healthy 24-year-old reporter at the New York Post, one of the country's oldest newspapers, when she suddenly developed a range of worrying symptoms. Her left hand went numb, paranoid thoughts obsessed her mind, and migraines and stomachaches beset her body. Initially diagnosed with mononucleosis, Cahalan continued to grow worse, eventually suffering a series of near-fatal seizures, psychosis, and a gradual loss of brain function. She ended up at New York University's Langone Medical Center, where a team of doctors, led by neurologist Souhel Najjar, diagnosed her with a disease that had been discovered only two years earlier: NMDA-receptor autoimmune encephalitis. In this excerpt Cahalan tells the story of how University of Pennsylvania neuro-oncologist Josep Dalmau first identified the disorder.

Excerpt from BRAIN ON FIRE, by Susannah Cahalan. Copyright © 2012 by Susannah Cahalan. Reprinted by permission of Simon & Schuster, Inc., N.Y.

Four years earlier, in 2005, Dr. Dalmau had been the senior author on a paper in the neuroscience journal Annals of Neurology that focused on four young women who had developed prominent psychiatric symptoms and encephalitis. All had white blood cells in their cerebrospinal fluid, confusion, memory problems, hallucinations, delusions, and difficulty breathing, and they all had tumors called teratomas in their ovaries. But the most remarkable finding was that all four patients had similar antibodies that appeared to be reacting against specific areas of the brain, mainly the hippocampus. Something about the combination of the tumor and the antibodies was making these women very sick.

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Dr. Dalmau had noticed a pattern in these four women; now he had to learn more about the antibody itself. He and his research team began to work night and day on an elaborate immunohistrochemistry experiment involving frozen sections of rat brains, which had been sliced into paper-thin pieces and then exposed to the cerebrospinal fluid of those four sick women. The hope was that the antibodies from the cerebrospinal fluid would bind directly to some receptors in the rat brain and reveal a characteristic design. It took eight months of tinkering before a pattern finally emerged.

Dr. Dalmau had prepared the rat brain slides all the same, placing a small amount of cerebrospinal fluid from each of the four patients on each. Twenty-four hours later…[f]our beautiful images, like cave drawings or abstract seashell patterns, revealed the antibodies' binding to the naked eye. "It was a moment of great excitement," Dr. Dalmau later recalled. "Everything had been negative. Now we became totally positive that all four not only had the same illness, but the same antibody."

He had clarified that the pattern of reactivity was more intense in the hippocampus of the rat brain, but this was only the beginning. A far more difficult question now arose: Which receptors were these antibodies targeting? Through a combination of trial and error, plus a few educated guesses about which receptors are most common in the hippocampus, Dr. Dalmau and his colleagues eventually identified the target. Using a kidney cell line bought from a commercial lab that came with no receptors on their surfaces at all, a kind of "blank slate," his lab introduced DNA sequences that direct the cells to make certain types of receptors, allowing the lab to control which receptors were available for binding. Dalmau chose to have them express only NMDA receptors, after figuring out that those were the most likely to have been present in high volume in the hippocampus. Sure enough, the antibodies in the cerebrospinal fluid of the four patients bound to the cells. There was his answer: the culprits were NMDA-receptor-seeking antibodies.

NMDA (N-methyl-D-aspartate acid) receptors are vital to learning, memory, and behavior, and they are a main staple of our brain chemistry. If these are incapacitated, mind and body fail. NMDA receptors are located all over the brain, but the majority are concentrated on neurons in the hippocampus, the brain's primary learning and memory center, and in the frontal lobes, the seat of higher functions and personality. These receptors receive instructions from chemicals called neurotransmitters. All neurotransmitters carry only one of two messages: they can either "excite" a cell, encouraging it to fire an electrical impulse, or "inhibit" a cell, which hinders it from firing. These simple conversations between neurons are at the root of everything we do, from sipping a glass of wine to writing a newspaper lead.

In those unfortunate patients with Dr. Dalmau's anti-NMDA-receptor encephalitis, the antibodies, normally a force for good in the body, had become treasonous persona non grata in the brain. These receptor-seeking antibodies planted their death kiss on the surface of a neuron, handicapping the neuron's receptors, making them unable to send and receive those important chemical signals. Though researchers are far from fully understanding how NMDA receptors (and their corresponding neurons) affect and alter behavior, it's clear that when they are compromised the outcome can be disastrous, even deadly.

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Still, a few experiments have offered up some clues as to their importance. Decrease NMDA receptors by, say, 40 percent, and you might get psychosis; decrease them by 70 percent, and you have catatonia. In "knockout mice" without NMDA receptors at all, even the most basic life functions are impossible: most die within ten hours of birth due to respiratory failure. Mice with a very small number of NMDA receptors don't learn to suckle, and they simply starve to death within a day or so. Those mice with at least 5 percent of their NMDA receptors intact survive, but exhibit abnormal behavior and strange social and sexual interactions. Mice with half their receptors in working order also live, but they show memory deficits and abnormal social relationships.

As a result of this additional research, in 2007, Dr. Dalmau and his colleagues presented another paper, now introducing his new class of NMDA-receptor-seeking diseases to the world. This second article identified twelve women with the same profile of neurological symptoms, which could now be called a syndrome. They all had teratomas, and almost all of them were young women. Within a year after publication, one hundred more patients had been diagnosed; not all of them had ovarian teratomas and not all of them were young women (some were men and many were children), enabling Dr. Dalmau to do an even more thorough study on the newly discovered, but nameless, disease.

"Why not name it the Dalmau disease?" people often asked him. But he didn't think "Dalmau disease" sounded right, and it was no longer customary to name a disease after its discoverer. "I didn't think that would be wise. It's not very humble." He shrugged.

By the time I was a patient at NYU, Dr. Dalmau had fine-tuned his approach, designing two tests that could swiftly and accurately diagnose the disease. As soon as he received my samples, he could test the spinal fluid. If he found that I had anti-NMDA-receptor autoimmune encephalitis, it would make me the 217th person worldwide to be diagnosed since 2007. It just begged the question: If it took so long for one of the best hospitals in the world to get to this step, how many other people were going untreated, diagnosed with a mental illness or condemned to a life in a nursing home or a psychiatric ward?

Friday, August 7, 2020

WSJ Everyday Math

 

EVERYDAY MATH

When a mathematician tries to sew a dress, the concept of positive and negative curvature can help—up to a point.

To understand everything from cancer risk to tax rates, we need to cultivate statistical literacy.

In principle, math should be able to tell us whether it will rain tomorrow—but in practice, things get complicated quickly.

When does C9F equal 3,231? When you’re using hexadecimal, one of the alternative number systems that make computers possible.

Arithmetic progressions, like the candles of Hanukkah or the gifts of ‘The Twelve Days of Christmas,’ can be powerful tools in number theory

The right equations can help solve congestion by treating cars on a road like fluid in a pipe

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