Essen BioScience Presents Next Generation Live-Cell Analysis System at IMMUNOLOGY 2017 – SelectScience

Visit the Essen BioScience booth #442 at AAI IMMUNOLOGY 2017 to discover the new Next-Generation IncuCyte S3 Live-Cell Analysis System and the latest trends and applications in live-cell analysis.

Change can happen in an instant. Find out how the IncuCyte S3 System and IncuCyte reagents and consumables make it easier than ever to visualize cell behavior and quantify cell function in real time. Derive deeper and more physiologically relevant information about your cells, plus real-time kinetic data, without ever removing your cells from the incubator.

Also, stop by for a chance to win prizes! Spin the wheel of fortune or test your cell culture genius with our raffle quiz to win t-shirts, mugs, and more.

At the show, visit the Essen BioScience poster presentation, led by Dr. Dan Appledorn, Director of Biology, showing innovative new research from Essen BioScience highlighting the powerful insights gained from IncuCyte live-cell analysis. Or join our exhibitor workshop, also presented by Dr. Appledorn, to learn the benefits of incorporating real-time, automated cell imaging and analysis into your in vitro assay workflow for immunology research.

Title: 81.15 CD47 Antibody-Induced Engulfment of Human T Cell Leukemia Cells by Bone Marrow-Derived Macrophages

Presenter: Dan Appledorn, Ph.D., Director of Biology, Essen Bioscience

Session Date and Time: Saturday, May 13, 2017, 2:30 - 3:45 PM

Location: Exhibit/Poster Hall

Session: Technological Innovations I

Number: P1092

Title: Live Cell Assay Approaches for Immunology and Immuno-oncology: Cell Health, Chemotaxis, Immune Cell Killing, and More

Date/Time: Monday, May 15, 2017, 12:30 - 1:15 PM

Location: EXHIBITOR WORKSHOP ROOM 2

Presenter: Dan Appledorn, Ph.D., Director of Biology, Essen Bioscience

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Essen BioScience Presents Next Generation Live-Cell Analysis System at IMMUNOLOGY 2017 - SelectScience

Night Owl or Early Bird? The Reason Might Be Genetic – Fortune

George Marks Getty Images

Michael W. Young has been studying sleep disorders for more than 45 years. When he started his research, as a graduate student at the University of Texas in the early 1970s, the field was largely unformed.

We still dont know exactly why we sleep, but in the intervening decades weve learned a lot about the underlying mechanisms. For one, we now know about circadian rhythm, or the bodys internal clock, which dictates sleep-wake cycles. More specifically, were starting to pinpoint why this cycle often gets disrupted. By isolating the mutations responsible for changes in the circadian rhythm in flies and mice, researchers are beginning to identify corresponding genes in humans. Its a slow and imperfect processwere (reassuringly) far more complex than either speciesbut were gaining a better understanding of how our genes influence our sleep. For example, Young and a team of researchers recently published a paper in Cell that links delayed sleep phase disorder to a mutation in the CRY1 gene.

Whereas in the past, being a night owl or a morning lark was attributed to vague mix of genetics and personal preferences, the study gets specific. Those with either one or two copies of the variant CRY1 gene, it found, displayed a more than two-hour shift in night sleep times. Their circadian cycle was delayed, meaning they had a difficult time falling asleep before 2 a.m. or 3 a.m., and, if able, would sleep until 10 a.m. or later.

While its unclear the percentage of people with the mutationits likely far less than the percentage of people who identify as night owls, which suggests environmental factors are also at playthe study is a good reminder that sleep is complicated. Our understanding is evolving; theres still a lot we dont know.

What is clear: a lack of sleep predisposes us to a host of health issues, including diabetes, obesity and depression. Thats a problem, because many of us arent getting enough of it. Between 50 million and 70 million adults in the U.S. have a sleep disorder, according to The Centers for Disease Control and Prevention.

Below, Young outlines some factors believed to play a large role in determining when, and how well, we sleep, along with strategies for adopting a more normal sleep-wake cycleeven when our genetics seem to be hardwired against it.

We evolved on a planet governed by cyclical fluctuations in light and temperature. Over the course of millions of years, our circadian rhythms developed to anticipate these changes, says Young. Our internal clocks work on a cellular level; appetite, metabolism, and sleep, along with other bodily functions, are designed to align with daily and yearly shifts in brightness and heat.

A standard circadian rhythm, then, essentially tracks the sun. Enzymes are released in the morning to stimulate metabolism, in anticipation of breakfast. Meanwhile, in the evening, your body temperature falls, and melatonin levels rise in anticipation of sleep. The energy moving through your body is quite rhythmic, says Young. Messing with this cellular schedulestaring at a bright light right before bed, for examplecan throw these synchronized clocks out of whack.

As mentioned above, a disrupted cycle is often due to environmental factors, and can be cured with better sleep hygiene. But thanks to researchers like Young, we know thats not always the casenot every individuals circadian rhythm neatly aligns with external temperature and light cues. In the Cell study, one of the participants habitual bedtime was at 3 a.m. or 4 a.m., with a desired wakeup time between 10 a.m. and noon. She tested positive for the CRY1 gene mutation, an indication that her internal clock was delayed in comparison with the normal population.

You can imagine what that does to someone with a normal work schedule, says Young. Theyre exhausted all the time.

So what if youre a night owl living in a world designed for early mornings? Youngs first suggestion is to figure out whether genetics are actually to blame (a CRY1 mutation can be determined by a spit test, as can other gene mutations linked to sleep disorders). Likely, part of the problem is tied to external, controllable factors, such as going to bed too late, or lying in the dark, staring at the glow from your smartphone. Or perhaps delayed sleep is a contained phase (college students have a tendency sleep in later than the adults they will grow up to become.)

But for individuals who have a lifelong problem...something that persists and is seemingly hardwired into their biology making adjustments is more difficultbut not impossible, says Young. One of the participants in the study, a lifelong night owl, tested positive for the CRY1 mutation; she also had a job that required her to wake up around 5 a.m. By sticking to a strict schedulesetting an alarm and waking up at 5 a.m., even on weekendsshe was able to partially rewire her sleep-wake cycle. But as with individuals who are genetically predisposed to weight gain, maintaining a meaningful shift required constant vigilance. If she lets her guard down, and sleeps in at a weekend, it produces all kind of problems, says Young.

As with a diet, where meals and calories are tightly controlled, Young recommends late-sleepers adopt a schedule in which a variety of factors, including meals, bedtime, wake up time, and exposure to light, are regulated.

The analogy to dieting is useful as circadian rhythm is deeply involved in metabolic control, says Young. While recreating a similar result in humans isnt feasible, Young believes, as with sleep, our eating patterns evolved to align with cyclical fluctuations in the environment. Our ancestors meals were constricted by external factors, including daylight. Today, of course, thats no longer the case. We can switch on the light at any time and make a sandwich, says Young, A great amount of people eat around the clock, says Young, which he believes could be a factor in Americas growing obesity crisis.

We know that obesity has become a problem in the last century, he says. Over that same period, our genes havent changed. Yes, the amount of caloriesparticularly via saturated-fats, refined grains, and sugarhas trended steadily upwards. But Young isnt convinced that this, alone, is enough to explain the spike in our average BMI. Instead, changes in behavior, particularly the American tendency to snack consistently, including right before bed and, frequently, during the night, are also contributors.

Too often, in both sleep and appetite, our schedules are erratic. Modern life has enabled our internal clocks to fall out of whack with the earths cycle. Above everything else, Young recommends sticking to a schedule. We were built to be rhythmic.

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Night Owl or Early Bird? The Reason Might Be Genetic - Fortune

The remarkable promise of cell-free biology – The Economist

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'VsIBTU.DYy7g;JYU"k)SD:CCC[5 d-*C(+Y{:5Ss3RxLw^[K2|JSc>,~,?,CY>g1t@l[_6bI/a-r/1n+O<~f6zEi3w8!}T']I8 ? EqI}e}sz+$/c5RQ2@;+]pY.S(*cy]T'R IQeq_sqrQ8'AIrN9+6wejUM>&iTqUu!O!Us`Ng#CpZlHr#^lvbr=_8dE5gF6Oaj;pt,q)KF6-(36aU0U6#nyyi8`MOdWv~%^x2a TRPg+"dH_L2,H#/"+"lvUa_yB!sPy,BHfFo;J>!8/H ?RqlEOL' y? -t2"/Ld3"(GTs&zLn%mTTlt^iz0dPi|gn'yBqzMF*G.QPDmD&VbQz*Tt3 ]w"XbrVH@C 5BX;%N u.7uV`Ht%'^QYkfVv(lG6]w:Sv.J`~[ ma%I=p]@@G`KC1Ws p}nOSLVz%nPWZ&8@aluF ^$W=.s= LGp k2Yvv#jEkjjA/AQIG(;Z_SvBREjAGk! E!9Wa^FJLv.f$p)6z4/Fz5I[DyR+r4~~HkB}2

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The remarkable promise of cell-free biology - The Economist

USCA students earn research awards at Discover USC – Aiken Standard

Several USC Aiken students shared their research recently in Columbia as part of Discover USC, and many brought home honors.

More than 1,000 presenters shared their scholarly efforts as part of the event. Pacers made a total of 44 presentations and received 16 awards: four first place, eight second place and four honorable mentions.

USC Aiken students represented our campus very well, said Dr. Bill Pirkle, who leads USCAs sponsored research program.

Discover USC showcases research, scholarship, leadership and creative projects by undergraduate and graduate students, postdoctoral scholars and medical scholars representing the entire USC System, from the Upstate to the Lowcountry.

Rebecca Beaudry, biology. Mentor, Dr. William Jackson, biology/geology. Development of a bicistronic vector system to test anti-HIV 1 siRNAs that target the accessory protein VIF. Biology and Biomedical Sciences Poster Session F.

Christian Fay, biology. Mentor, Dr. William Jackson, biology/geology. siRNA mediated downregulation of HIV-Tat in anti-Tat siRNA protected Lymphocyte populations. Biology and Biomedical Sciences Poster Session G.

as-050617-ne-training-track-2, psychology, Magellan Scholar. Mentor, Dr. Keri Weed, psychology. The Influence of Perceived Control over Task Difficulty on Coping with Math Anxiety. Psychology and Neurosciences Poster Session E.

Davont Jenkins, communication. Mentor, Dr. William Harpine, communication. The Effects of Speaker Credibility in Race Relations: A Study of Two Speeches. Social Sciences Oral Session H.

Erin McLaughlin, biology, Magellan Scholar, Honors Program graduate. Mentor, Dr. William Jackson, biology/geology. Expression of Vif-resistant ApoBEC3G from a HIV-1-dependent lentiviral vector. Biology and Biomedical Sciences Poster Session H.

Natalie Arthur, biology. Mentor, Dr. William Jackson, biology/geology. Generating a HIV-1-dependent chimeric vector to deliver a pro-apoptotic gene. Biology and Biomedical Sciences Poster Session H.

Jazmine Benjamin, biology. Mentor, Dr. Nathan Hancock, biology/geology. Determining the Sequences Involved in mPing Transposition. STEM Oral Session C.

Tiana Chandler, biology, Honors Program graduate. Mentor, Dr. Nathan Hancock, biology/geology. Development of an mPing-based Activation Tag for Zebrafish Mutagenesis. STEM Oral Session E.

Harli Eggenberger, exercise and sports science, Magellan Scholar, and Brooke Clark, communication, Magellan Scholar, Honors Program graduate. Mentor, Dr. Brian Parr, exercise and sports science. Candy and Soda for Breakfast: Developing visual communication tools to promote healthy eating. Public Health Poster Session D.

Lianna Epstein, exercise and sports science. Mentor, Dr. Andrew Hatchett, exercise and sports science. A comparison of energy expenditure between motorized and non-motorized treadmills. Public Health Poster Session H.

Kenneth Glenn, biology, Magellan Scholar. Mentor, Dr. April DeLaurier, biology/geology. Generating mef2ca and mef2cb transgenic zebrafish lines using BAC-mediated recombination. STEM Oral Session Session A.

Meredith Hawcroft, English, Magellan Scholar, Honors Program graduate. Mentor, Dr. Todd Hagstette, English. The Battle of Bachelorhood and Domesticity in William Gilmore Simms Castle Dismal. Social Sciences and Humanities Poster Session.

Lisete Payero, biology, Magellan Scholar. Mentor, Dr. Nathan Hancock, biology/geology. Determining the role of homologous recombination in replicative transposition of mPing. Biology and Biomedical Sciences Poster Session E.

Johnny Carroll, biology. Mentor, Dr. William Jackson, biology/geology. T-Bid expression in ptBidTNG(INS2)R to induce Apoptosis in a HIV infected Cell. Biology and Biomedical Sciences Poster Session F.

Emma Nettles, psychology, Magellan Scholar. Mentor, Dr. Adam Pazda, psychology. Perspective Taking and Self-Other Overlap: How Self-Compassion Mitigates the Negative Effect of Blame on Helping Behavior. Psychology and Neuroscience Poster Session E.

Sara Puckett, psychology, and Matthew Haslinger, psychology. Mentors, Drs. Elaine Clanton Harpine, education; Adam Pazda, psychology; and William Harpine, Communication. Teaching Phonemic Awareness Improved Reading, Spelling, and Comprehension. Social Sciences Poster Session I.

Lauren Spires, biology. Mentor, Dr. William Jackson, biology/geology. Developing a HIV-1 Dependent Lentiviral Vector that Expresses an Innate Human Anti-Retroviral Gene. Biology and Biomedical Sciences Poster Session F.

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USCA students earn research awards at Discover USC - Aiken Standard

Advanced prostate cancer treatment failure due to cell reprogramming – Science Daily

Columbia University Medical Center (CUMC) researchers have discovered a molecular mechanism that reprograms tumor cells in patients with advanced prostate cancer, reducing their response to anti-androgen therapy. The findings, based on a study in mice, could help to determine which patients should avoid anti-androgen therapy and identify new treatments for people with advanced prostate cancer.

The study was published online April14th in the journal Cancer Discovery.

Since androgens (male hormones) are known to drive prostate cancer, patients with recurrent or advanced disease are typically treated with anti-androgen medications. However, most patients fail treatment and develop an aggressive form of prostate cancer known as castration-resistant prostate cancer, or CRPC.

"It's been a mystery why some patients do not respond to anti-androgens, and why a subset of these patients actually get worse after treatment," said study co-leader Cory Abate-Shen, PhD, the Michael and Stella Chernow Professor of Urological Oncology and professor of urology, medicine, systems biology, and pathology and cell biology at CUMC. "Our findings show that in many of these patients, the tumor cells are reprogrammed so that they are no longer dependent on androgens."

To learn about the molecular mechanisms that drive resistance to anti-androgens, Drs. Abate-Shen and Michael Shen co-led a team to develop a strain of mice that lack two tumor-suppressor genes, Trp53 and Pten. These genes are both mutated in about 25 percent of patients with advanced prostate cancer. Mice that were treated with the anti-androgen drug abiraterone failed to respond and had accelerated tumor growth -- similar to some humans with advanced prostate cancer who do not respond to anti-androgen therapy.

"We found a number of genes that were overexpressed in mice with CRPC and also conserved in patients with the disease. Among the most interesting of these was SOX11, which regulates the development of the nervous system," said study co-leader Michael M. Shen, PhD, professor of medical sciences at CUMC.

Most localized, slow-growing prostate cancers are largely composed of epithelial cells, which are rich in androgen receptors that increase their susceptibility to anti-androgen therapy. In contrast, aggressive prostate cancers, particularly those that fail treatment, often contain many neuroendocrine-like cells, which lack androgen receptors and are therefore less responsive to anti-androgen therapy.

"This raised the question, where are the neuroendocrine-like cells in prostate tumors coming from?" said Dr. Abate-Shen. "While previous research hinted that epithelial tumor cells may be reprogrammed to become neuroendocrine-like cells, our study provides the first direct evidence that this reprogramming is actually occurring and that it is mediated, at least in part, by SOX11."

The researchers also demonstrated that SOX11 acts in a similar fashion in human prostate cancer cells.

"By giving anti-androgens to patients with CRPC, we are eliminating the cancer cells that need androgen to survive and enriching the tumor with the remaining neuroendocrine-like cells. The net effect is to create an even more aggressive tumor," said Dr. Shen.

The researchers also identified several "master regulators" -- genes that control SOX11 and other genes involved in prostate cancer reprogramming -- that might be targeted for new prostate cancer treatments.

"Based on our findings, genetic testing to identify SOX11 and the master regulators may be considered before embarking on anti-androgen therapy for patients with advanced prostate cancer," said Dr. Shen.

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Advanced prostate cancer treatment failure due to cell reprogramming - Science Daily

Platelets suppress T cell immunity against cancer – Medical Xpress – Medical Xpress

May 5, 2017 Stylized illustration of a platelet and T cell. Plus and negative signs are used to symbolically indicate the positive (clotting) and negative (downregulating T cell immunity) effects of platelets. Credit: Emma Vought of the Medical University of South Carolina.

Blood platelets help disguise cancer from the immune system by suppressing T cells, report scientists at the Medical University of South Carolina (MUSC) in the May 5, 2017 issue of Science Immunology. In extensive preclinical tests, a promising T cell therapy more successfully boosted immunity against melanoma when common antiplatelet drugs such as aspirin were added.

Zihai Li, M.D., Ph.D., senior author on the article, is chair of the MUSC Department of Microbiology and Immunology, the program leader for the Cancer Immunology Research Program at MUSC Hollings Cancer Center, and the SmartState Sally Abney Rose Chair in Stem Cell Biology & Therapy. Li studies how tumors hide themselves from the immune system.

Li's team found that platelets release a molecule that suppresses the activity of cancer-fighting T cells. That molecule, unsurprisingly, was TGF-beta, which has been recognized for decades for its role in cancer growth.

Yet this study is the first of its kind. Most TGF-beta is inactive. Li and his group found that the surface of platelets has a protein called GARP, a molecular hook that is uniquely able to trap and activate TGF-beta. Platelets, which are small cell fragments that circulate throughout the blood and are normally involved in clotting, become the major source of activated TGF-beta that invading tumor cells use to suppress T cells. In other words, platelets help give tumors their invisibility cloak from the immune system.

Scientists have known for several years that certain cancers suppress T cells to avoid the immune system. That is why adoptive T cell therapy is one of the most promising advances in modern cancer treatment. It is a type of immunotherapy that awakens the immune system by retraining a patient's T cells to recognize their cancer. T cells are isolated from a patient's blood and retrained, or "primed," to recognize tumor cells. They are then injected back into the patient's bloodstream where they can now hunt and fight cancer.

There was some evidence that platelets might make cancer worse. For example, patients who have excessive clotting related to their cancer almost always have a worse prognosis, according to Li.

"Over the years, it has become appreciated that platelets are doing more than just clotting," says Li.

The first clue that cancer-fighting T cells might be suppressed by the body's own clotting system came when the researchers gave melanoma to mice with genetically defective platelets. Melanoma tumors grew much more slowly and primed T cells were much more active than in mice with normal platelets.

Next, the team isolated platelets and T cells from blood drawn from humans and mice. In both cases, platelets with activated clotting activity suppressed T cell response. It then used mass spectrometry to thoroughly identify the molecules released by activated platelets that most suppressed T cell activity. The molecule with the most T cell suppression was TGF-beta.

Li and his team then studied how platelets activate TGF-beta. In genetically modified mice without GARP, the molecular hook on the surface of platelets, adoptive T cell therapy was more successful at controlling melanoma. This meant that platelets without the ability to grab and activate TGF-beta were not able to suppress cancer-fighting T cells. Similar experiments confirmed this result in mice with colon carcinoma.

Finally, mice with normal platelets that were given melanoma and then adoptive T cell therapy survived longer and relapsed less when aspirin and clopidogrel, two antiplatelet drugs, were added. The researchers noted that antiplatelet drugs by themselves were not successful in combating melanoma in their experiments.

This study could inform future treatment of melanoma and other cancers and offers a sound reason to test antiplatelet drugs in clinical trials of adoptive T cell therapy. In patients with melanoma or other cancers, adoptive T cell therapy may be successful if highly available platelet-blocking drugs such as aspirin are added to the treatment. However, the current standard of care for melanoma is not adoptive T cell therapy, but so-called checkpoint inhibitors.

Li and his group want to know if combination therapy with antiplatelet drugs could improve existing cancer treatment. They are waiting for approval to begin a clinical trial that will test certain checkpoint inhibitors in combination with aspirin and clopidogrel for the treatment of patients with advanced cancers. Li's trial will complement clinical trials that are already testing adoptive T cell therapy as a single treatment for cancer.

"I'm very excited about this," says Li. "We can test simple, over-the-counter antiplatelet agents to really improve immunity and make a difference in how to treat people with cancer."

Explore further: Aspirin slows growth of colon, pancreatic tumor cells

More information: "Platelets subvert T cell immunity against cancer via GARP-TGF axis," Science Immunology (2017). immunology.sciencemag.org/lookup/doi/10.1126/sciimmunol.aai7911

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If you scanned the body for relatively higher TGF concentrations, could you use that information to find active cancers?

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Platelets suppress T cell immunity against cancer - Medical Xpress - Medical Xpress

Grey’s Anatomy Recap: Stephanie Steps Up and Meredith Moves On – Cosmopolitan.com

All I could think about during last night's episode of Grey's Anatomy is how it will feel to watch the series if the Affordable Care Act is fully repealed. To be very clear: I know there are far worse consequences of the bill than its impact on TGIT programming. Thousands will sicken and die. I could easily be one of them. All I'm trying to do is illuminate the lens through which I was watching the episode. And to be even clearer: The repeal isn't set in stone yet. Keep calling, keep writing, get louder.

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To be fair, Grey's has always shied away from delving too deeply into the financial lives of its patients (they've been all too eager to dig into the financial health of the hospital though). We don't see patients frantically paging through bills once they've been discharged or calling their insurance companies to get procedures cleared. But it bears mentioning that the show's two most memorable episodes about financial hardship for patients both aired during the Bush administration: Joe the bartender's inability to pay for his expensive brain surgery and Ryan, the young boy who "trick or treated" for doctors and nurses to staff a pro bono surgery to give him ears. (Sidebar: That little boy grew into Dylan Minnette, who played Clay in 13 Reasons Why. What is time!?!?)

As the Affordable Care Act was rolled out, Grey's wove subtle references to it into its storytelling. At least one character talked about Obamacare specifically, and others mentioned finally being able to afford health care, or getting ongoing health issues checked out now that they were insured. So if Grey's wants to continue acknowledging America's health-care landscape next season, what would that even look like? Arizona performing a fetal surgery only to have to immediately stop because the baby's reached its lifetime limit already? Owen turning patients away from the emergency room? Doctors playing fast and loose with diagnoses so as to not document pre-existing conditions on patients' charts? SHOULD BE PRETTY FUN TO WATCH.

Anyway, it's not a great reflection on last night's episode that I had plenty of time in which to obsess over how the series might reflect our political climate a year from now, but here we are. I cannot get past my case of "She doesn't even go here!" when it comes to Eliza, and I'm frustrated that she continues to be used as a plot device rather than a person. She kisses Arizona! She meddles with residents! Who is she? GREAT QUESTION, NO ONE KNOWS.

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It's especially frustrating when she decides that Ben doesn't take enough risks as a surgeon. This is a dude who literally did a C-section on a kitchen table and who was ballsy enough to take point in a room full of squabbling surgeons, like, three episodes ago, so I'm not sure what more he's supposed to be doing. One-handed surgery? Blindfolded, perhaps? He's always been confident, so this feels more like the writers trying to back-door justify why he hasn't necessarily had much to do this season.

Eliza's meddling doesn't stop there. ("Meddling" is probably unfair, because she literally is just doing her job, but she's doing a very, very, very, very, very confusing/irritating version of it.) She places herself squarely in the middle of a case of Alex and Stephanie's as they try to care for a young boy with a brain tumor whose parents are declining medical help for religious reasons. Alex is back to being his "Karev, Defender of Tiny Humans" self in a pretty awesome way, but Eliza gets right into the thick of it, telling him that he of all people should be "following the letter of the law" right now. Dude, ONLY MEREDITH CAN TALK TO ALEX THAT WAY. Or possibly Bailey. Alex and Stephanie play fast and loose to treat the child without his parents' consent. They save his life, but Stephanie loses her surgical privileges after chucking an iPad at the father's head. It is incredibly satisfying to watch.

In the middle of all of that business, Eliza tells Arizona that she has "naked plans" for her later, which is maybe the least sexy way I've ever heard a person invite someone to hook up. I'm all for Arizona getting hers! Just don't call it that. Arizona has a patient and can't make their sex date, so she and Eliza flirt and sexy tease each other in an elevator. Sorry, Eliza, but you have to earn elevator sexcapades. They do wind up having sex at the end of the episode and it's fine, whatever, sure, but it's just another moment that cements Eliza's status as a plot device, not a person.

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Also, Maggie attempts a heart surgery that's basically impossible (and ultimately fails) to help her cope with her feelings about Meredith and Riggs? Or something?

This week, the early stage of Meredith's relationship with Riggs continues to be almost unbearably drawn out, but I was too worried about losing my health insurance and maybe dying to be too annoyed by it. Congratulations, everyone! We did it! Meredith starts putting pieces of her relationship with Derek aside to make room, literally and figuratively, for Riggs. She takes down the diagram of a spinal tumor that Derek once drew on her walls; she puts the Post-it note vows in a drawer.

It's an important moment in Meredith's healing process, and giving the tumor drawing to Amelia might mend the resentment she has toward Meredith for not calling her to Derek's deathbed to say good-bye. (Amelia hasn't brought it up in a while, but you know it's still been festering.) But goddamnit, it still hurts to see her tuck away reminders of her past with Derek. As time has gone on, I don't miss Derek as, essentially, Meredith's manic pixie dream boy. But the tumor picture and the Post-it vows show how fun it was to watch them when they were when truly a couple, working alongside one another. I miss that. Riggs and Meredith finally leave the hospital hand-in-hand at the end of the episode, so I'll say what I have been saying in at least six recaps this season: I guess they're finally going to really go for it now!

Also, Deluca tries to profess his love for Jo and I'd love to tell you more about that, but the second it started happening, I fell into a deep, deep sleep. WAKE ME UP WHEN SHE HAS A CONVERSATION WITH ALEX.

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Grey's Anatomy Recap: Stephanie Steps Up and Meredith Moves On - Cosmopolitan.com

Stanford art students get lesson on the evolution of anatomy illustration – Stanford Medical Center Report

Speaking to the current group ofstudents, Bourn told them that VesaliusFabrica was more than an anatomy textbook; it changed the way medicine was taught. In 1537, Vesalius graduated with what was then a classical European medical education. In anatomy courses, his professors would read straight from the works of the ancient Greek physician Galen, who was born in 129, while an assistant dissected a cadaver to illustrate the structures discussed in the text. Galens teachings were considered the gold standard for more than 1,000 years, and they were above reproach.

Then Vesalius moved to Padua University to teach surgery. And after he began dissecting his own cadavers, he made a shocking discovery: Some of Galens facts were inaccurate because, for religious reasons, hed never dissected a human body only pigs, oxen, dogs and monkeys.

So, at age 23, Vesalius meticulously began separating fact from fiction in Galens anatomical works. For example, he discovered that the human jaw is one bone, not two, and the breastbone has three segments, not seven. This information wasnt well-received by the medical establishment; to overcome resistance, Vesalius held public dissections, built skeletal models and published Fabrica, with its 600 anatomical charts and illustrations. (To keep up with Vesalius demand for cadavers, students and Padua city officials often had to repurpose bodies from cemeteries and the hangmans noose.)

Vesalius work raised anatomical illustration to a new level of accuracy and artistry. Because he lived in northern Italy during the Renaissance, he had access to some of the most talented artists of the times. Historians believe that he outsourced the illustrations in Fabrica to artists working in master painter Titians studio. The resulting woodcuts were both amazing works of art and disturbing, showing cadavers staged in dramatic poses with layers of skin peeling off to reveal muscle and bone, often drawn with bucolic Italian landscapes in the background. They looked more like storyboard sketches for a zombie apocalypse movie than scientific illustrations.

Artists are still referring to Fabrica today, primarily through restaging these now iconic poses in a contemporary context, said Wight, a new-media artist who is drawn to the intersection of biology, neurology and technology. The woodcuts in Fabrica "convey essential information about anatomy, yes, but they also convey complex attitudes about the human condition and their reflection in human culture.

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Stanford art students get lesson on the evolution of anatomy illustration - Stanford Medical Center Report

Grey’s Anatomy Star Will Head Cast of Bay Street’s Intimate Apparel … – Playbill.com

Bay Street Theater has announced complete casting for its upcoming production of two-time Pulitzer Prize winner Lynne Nottage's Intimate Apparel, which will be presented at the Sag Harbor venue July 430.

Directed by Bay Street Theater Artistic Director Scott Schwartz, the cast will be headed by Kelly McCrearyone of the stars of ABC's Grey's Anatomyas Esther Mills.

McCreary will be joined by Portia (Ruined, McReele, Our Lady of 121st Street) as Mrs. Dickson, Blake DeLong (Othello; Natasha, Pierre & the Great Comet of 1812) as Mr. Marks, Julia Motyka (Bay Street's Travesties, Richard III) as Mrs. Van Buren, Edward O'Blenis (Uncle Vanya, Tall Grass) as George, and Shayna Small (The Colored Museum) as Mayme.

In Intimate Apparel, according to Bay Street, there's a delicate line between love and desire. Esther Mills is a skilled African American seamstress and has her own successful business in 1905 making lingerie for both society ladies and ladies of the night. But she is lonely. As she searches for something more in her life, she unearths truths long hidden in the deepest recesses of her heart.

The creative team includes composer Michael Holland, set designer Jeff Cowie, lighting designer Mike Billings, costume designer Emilio Sosa, sound designer Jill B.C. DuBoff, props designer Andrew Diaz, production stage manager Gwen Gilliam, and dialect coach Stephen Gabis. Casting is by Stewart/Whitley.

Nottage is also the author of the Pulitzer Prize-winning Ruined and Sweat; the latter is a 2017 Tony nominee for Best Play.

For ticket information, call (631)725-9500 or visit BayStreet.org.

LOVE BROADWAY? CHECK OUT THE NEW ARRIVALS AT THE PLAYBILL STORE!

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Grey's Anatomy Star Will Head Cast of Bay Street's Intimate Apparel ... - Playbill.com

Riverdale Season 1, Episode 12 Recap: "Anatomy Of A Murder" – Refinery29

Dramatic revelations in penultimate episodes often prove to be pivotal in the life of a new series beyond mere plot mechanics. Its at this point that a show either proves to be worthy of admiration or falls apart under the weight of its own ambition. Riverdale has been one of the most engaging, blissfully bonkers, and visually rich new shows Ive seen in a long time. It knows exactly how to hit that elusive sweet spot that so many teen dramas aim for. But I was worried that the reveal of Jasons murderer wouldnt meet my expectations. Part of my apprehension stems from the nagging issues that have been weighing down recent episodes like Veronicas off-putting characterization and the complete sidelining of characters I previously enjoyed like Josie. But Anatomy of a Murder didnt just meet my expectations it exceeded them. Im left yearning for more high-intensity drama, witty comebacks, and family drama. This episode has everything. Incest, maple syrup intrigue, unhinged mothers, several showdowns, and Alice holding a gun, proving once again shes not one to be messed with. This isnt the kind of exhilarating and fun episode that quickly fades from memory. By exploring the fractures within these families its able to be emotionally impactful too.

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Riverdale Season 1, Episode 12 Recap: "Anatomy Of A Murder" - Refinery29