Bouffee de Petoncle de Mer

Is my French good? No. But this new recipe is. I was inspired to create this French title for my newest recipe, simply because it is so unbelievably delicious. It took time to get it right, but finally it is my great pleasure to share it with all of you. Your partner, spouse, guests will not believe that you made it; that’s how good it is, and easy, now that I’ve experimented with Jules, my best and favorite tester. The name of my recipe translates to: Puff of Sea Scallop, which is how it tastes. (if you like sea scallops).



1 pound very fresh sea scallops, rinsed and dried

1 pinch sea salt

1 pinch black pepper

2 teaspoons clam juice

6 fresh garlic cloves, sliced

One 2 inch piece of ginger, peeled then grated

6 scallions, thinly sliced (use the white part only)

Juice of 1/2 fresh lime

1 Tablespoon coconut flour

1/2 teaspoon baking soda

1/2 teaspoon baking powder

2 eggs but use the whites only, slightly beaten in a small cup

Extra virgin olive oil for cooking (or coconut oil or peanut oil)


You have to have a food processor for this recipe and a large skillet.


I bought the (real) sea shells for cooking, from Amazon. Even though you don’t have to use them, as you can see from the photos, serving in these shells, really adds to the presentation and the enjoyment. I highly recommend that you buy them. They’re not at all expensive.


Surprisingly, there’re not many ingredients in this wonderful recipe and all are easy to come by. I got the sea scallops from Whole Foods, the coconut flour from and all the rest from FreshDirect. ©Joyce Hays, Target Health Inc.



1. Get all your slicing, egg-separating, chopping, grating, done first.

2. Get out your food processor, a large skillet and the all-natural sea shells, for serving.

3. Make any number of sauces or toppings you want to use for the scallop puffs. I used an easy scallion cream sauce, a cashew cheese topping, mango chutney and pomegranate arils


Slicing scallions and grating the raw ginger. ©Joyce Hays, Target Health Inc.


In the photo above, all seasoning, garlic, scallions, grated ginger, clam juice, lime juice and egg whites have been added to the food processor. ©Joyce Hays, Target Health Inc.


In this photo, all of the previous ingredients have now been pulsed well. ©Joyce Hays, Target Health Inc.


4. All the ingredients are going to end up in your food processor, so it hardly matters, which goes in first, except, do this: add all of the dry ingredients last.


All the scallops were added and pulsed until all ingredients have been well combined. ©Joyce Hays, Target Health Inc.


Scallop Puff recipe ©Joyce Hays, Target Health Inc.


5. As you see above, add the dry ingredients to the food processor, last. Then, pulse until all ingredients have been completely and thoroughly combined. It’s important to do this right.

6. Next, with a narrow spatula, scrape all of the contents from your food processor, into a medium bowl. Get it all out, so it all goes into the Scallop Puffs


Scrape everything from the food processor, into a medium bowl. ©Joyce Hays, Target Health Inc.


7. Put oil in your large skillet and plan to cook no more than 3 or 4 Scallop Puffs at a time. Use a medium high flame and heat before cooking.

8. Rub some flour together, on your hands, then with a Tablespoon, scoop out of the bowl, some of the mixture, and with your other hand, form an oval shape while mixture is still in the Tablespoon, and plop it into the hot skillet, using fingers to get all of the mixture out of the Tablespoon. As you will see in the photos, there is no need to have each Puff look exactly the same. My concept was puffy clouds, none of which are ever the same.


All the Scallop Puffs will be slightly different shapes. ©Joyce Hays, Target Health Inc.


9. Cook 1 to 2 minutes on each side. Even though the flavor will be exquisite and delicate, you don’t have to be delicate while cooking, except to be sure they don’t burn. After flipping over the first time, you may see that this side needs to be cooked a little longer. Simply wait until the other side has cooked and browned, then flip back and cook a little longer, if needed. Both sides should be a golden brown, as you see in the photos.


Flipped too soon, so will cook second side until golden brown, then flip back and finish the first side. Important NOT to overcook, but get them the golden brown, that you see above. ©Joyce Hays, Target Health Inc.


10. Have the shells ready (or a serving platter), so that when cooked, put each Scallop Puff into its own shell and serve immediately with a sauce, with topping or plain which is just fine.


The Scallop Puffs are ready to serve. The fragrance is wonderful; you will NOT believe what a treat you’re in for. ©Joyce Hays, Target Health Inc.


The photos that follow, show a partial example of how the Scallop Puffs have been served, before sharing this new original recipe with you.


With scallion cream sauce. ©Joyce Hays, Target Health Inc.


After one bite and with scallion cream sauce. ©Joyce Hays, Target Health Inc.


Scallop Puff with Cashew Cheese Topping. ©Joyce Hays, Target Health Inc.


Nearly all eaten. Scallop Puff with Cashew Cheese Topping. ©Joyce Hays, Target Health Inc.


Scallop Puffs served plain with saffron rice and saut?ed broccoli. ©Joyce Hays, Target Health Inc.


Scallop Puffs served with saffron rice and mango chutney. Btw, the mango chutney is a fantastic combo with these Scallop Puffs. ©Joyce Hays, Target Health Inc.


Scallop Puff served with scallion cream and pomegranate arils. The seafood forks I used are one of my favorite stainless patterns, called: “Gone Fishing“ by the Japanese flatware company, Yamazaki. ©Joyce Hays, Target Health Inc.


Luscious Scallop Puff, half eaten with scallion cream sauce and pomegranate arils. ©Joyce Hays, Target Health Inc.


Scallop Puff extremely yummy with this scallion cream sauce and pomegranate arils. ©Joyce Hays, Target Health Inc.


The gourmet Scallop Puffs are as delicious as anything you could get at a good restaurant, probably as an appetizer and I am very proud of this. As for wine pairing, we prefer chilled white wine, or Proseco, or champagne or Blanc de Blancs. If you insist on a red, we would say, a very light-bodied red; however, the only red we’ve found that works well with seafood or fish is Hall’s cabernet sauvignon. ©Joyce Hays, Target Health Inc.


Weather here in Manhattan is now winter-y, we’ve added cozy plump puffy winter comforters for sleeping. Theater here continues to be stimulating and fun. We saw the comedy (which has extended the limited run, because it’s so popular) The Portuguese Kid, with Jason Alexander. This fine production is a fun-romp that’s light and playful. The acting is excellent, the constantly changing sets are terrific, the lighting design is perfect. If you liked the film, Moonstruck, you will love this play; they are like first cousins.


Hope you had a great week everyone!


From Our Table to Yours

Bon Appetit!


November 9, 2017

Yale University

A research team has uncovered how a very low calorie diet can rapidly reverse type 2 diabetes in animal models. If confirmed in people, the insight provides potential new drug targets for treating this common chronic disease, said the researchers.


A very low calorie diet can rapidly reverse type 2 diabetes in animal models, report scientists.
Credit: © Denis Pepin / Fotolia



In a new study, a Yale-led research team uncovers how a very low calorie diet can rapidly reverse type 2 diabetes in animal models. If confirmed in people, the insight provides potential new drug targets for treating this common chronic disease, said the researchers.

The study is published in Cell Metabolism.

One in three Americans will develop type 2 diabetes by 2050, according to recent projections by the Center for Disease Control and Prevention. Reports indicate that the disease goes into remission in many patients who undergo bariatric weight-loss surgery, which significantly restricts caloric intake prior to clinically significant weight loss. The Yale-led team’s study focused on understanding the mechanisms by which caloric restriction rapidly reverses type 2 diabetes.

The research team investigated the effects of a very low calorie diet (VLCD), consisting of one-quarter the normal intake, on a rodent model of type 2 diabetes. Using a novel stable (naturally occurring) isotope approach, which they developed, the researchers tracked and calculated a number of metabolic processes that contribute to the increased glucose production by the liver. The method, known as PINTA, allowed the investigators to perform a comprehensive set of analyses of key metabolic fluxes within the liver that might contribute to insulin resistance and increased rates of glucose production by the liver — two key processes that cause increased blood-sugar concentrations in diabetes.

Using this approach the researchers pinpointed three major mechanisms responsible for the VLCD’s dramatic effect of rapidly lowering blood glucose concentrations in the diabetic animals. In the liver, the VLCD lowers glucose production by: 1) decreasing the conversion of lactate and amino acids into glucose; 2) decreasing the rate of liver glycogen conversion to glucose; and 3) decreasing fat content, which in turn improves the liver’s response to insulin. These positive effects of the VLCD were observed in just three days.

“Using this approach to comprehensively interrogate liver carbohydrate and fat metabolism, we showed that it is a combination of three mechanisms that is responsible for the rapid reversal of hyperglycemia following a very low calorie diet,” said senior author Gerald I. Shulman, M.D., the George R. Cowgill Professor of Medicine and Cellular and Molecular Physiology and an investigator at the Howard Hughes Medical Institute.

The next step for the researchers will be to confirm whether the findings can be replicated in type 2 diabetic patients undergoing either bariatric surgery or consuming very low calorie diets. His team has already begun applying the PINTA methodology in humans.

“These results, if confirmed in humans, will provide us with novel drug targets to more effectively treat patients with type 2 diabetes,” Shulman said.

Story Source:

Materials provided by Yale University. Original written by Ziba Kashef. Note: Content may be edited for style and length.

Journal Reference:

  1. Rachel J. Perry, Liang Peng, Gary W. Cline, Yongliang Wang, Aviva Rabin-Court, Joongyu D. Song, Dongyan Zhang, Xian-Man Zhang, Yuichi Nozaki, Sylvie Dufour, Kitt Falk Petersen, Gerald I. Shulman. Mechanisms by which a Very-Low-Calorie Diet Reverses Hyperglycemia in a Rat Model of Type 2 DiabetesCell Metabolism, November 2017 DOI: 10.1016/j.cmet.2017.10.004


Source: Yale University. “Study reveals how a very low calorie diet can reverse type 2 diabetes.” ScienceDaily. ScienceDaily, 9 November 2017. <>.

November 8, 2017

University of Cambridge

Sheep can be trained to recognise human faces from photographic portraits — and can even identify the picture of their handler without prior training — according to new research.


Sheep can distinguish individual human faces shown in photos.
Credit: Image courtesy of University of Cambridge



Sheep can be trained to recognise human faces from photographic portraits — and can even identify the picture of their handler without prior training — according to new research from scientists at the University of Cambridge.

The study, published today in the journal Royal Society: Open Science, is part a series of tests given to the sheep to monitor their cognitive abilities. Because of the relatively large size of their brains and their longevity, sheep are a good animal model for studying neurodegenerative disorders such as Huntington’s disease.

The ability to recognise faces is one of the most important human social skills. We recognise familiar faces easily, and can identify unfamiliar faces from repeatedly presented images. As with some other animals such as dogs and monkeys, sheep are social animals that can recognise other sheep as well as familiar humans. Little is known, however, about their overall ability to process faces.

Researchers from Cambridge’s Department of Physiology, Development and Neuroscience trained eight sheep to recognise the faces of four celebrities from photographic portraits displayed on computer screens.

Training involved the sheep making decisions as they moved around a specially-designed pen. At one end of the pen, they would see two photographs displayed on two computer screens and would receive a reward of food for choosing the photograph of the celebrity (by breaking an infrared beam near the screen); if they chose the wrong photograph, a buzzer would sound and they would receive no reward. Over time, they learn to associate a reward with the celebrity’s photograph.

After training, the sheep were shown two photograph — the celebrity’s face and another face. In this test, sheep correctly chose the learned celebrity face eight times out of ten.

In these initial tests, the sheep were shown the faces from the front, but to test how well they recognised the faces, the researchers next showed them the faces at an angle. As expected, the sheep’s performance dropped, but only by about 15% — a figure comparable to that seen when humans perform the task.

Finally, the researchers looked at whether sheep were able to recognise a handler from a photograph without pre-training. The handlers typically spend two hours a day with the sheep and so the sheep are very familiar with them. When a portrait photograph of the handler was interspersed randomly in place of the celebrity, the sheep chose the handler’s photograph over the unfamiliar face seven out of ten times.

During this final task the researchers observed an interesting behaviour. Upon seeing a photographic image of the handler for the first time — in other words, the sheep had never seen an image of this person before — the sheep did a ‘double take’. The sheep checked first the (unfamiliar) face, then the handler’s image, and then unfamiliar face again before making a decision to choose the familiar face, of the handler.

“Anyone who has spent time working with sheep will know that they are intelligent, individual animals who are able to recognise their handlers,” says Professor Jenny Morton, who led the study. “We’ve shown with our study that sheep have advanced face-recognition abilities, comparable with those of humans and monkeys.

“Sheep are long-lived and have brains that are similar in size and complexity to those of some monkeys. That means they can be useful models to help us understand disorders of the brain, such as Huntington’s disease, that develop over a long time and affect cognitive abilities. Our study gives us another way to monitor how these abilities change, particularly in sheep who carry the gene mutation that causes Huntington’s disease.”

Professor Morton’s team recently began studying sheep that have been genetically modified to carry the mutation that causes Huntington’s disease.

Huntington’s disease affects more than 6,700 people in the UK. It is an incurable neurodegenerative disease that typically begins in adulthood. Initially, the disease affects motor coordination, mood, personality and memory, as well as other complex symptoms including impairments in recognising facial emotion. Eventually, patients have difficulty in speech and swallowing, loss of motor function and die at a relatively early age. There is no known cure for the disease, only ways to manage the symptoms.


Story Source:

Materials provided by University of Cambridge. The original story is licensed under a Creative Commons LicenseNote: Content may be edited for style and length.

Journal Reference:

  1. Franziska Knolle, Rita P. Goncalves, A. Jennifer Morton. Sheep recognize familiar and unfamiliar human faces from two-dimensional imagesRoyal Society Open Science, 2017; 4 (11): 171228 DOI: 10.1098/rsos.171228


Source: University of Cambridge. “Sheep are able to recognize human faces from photographs.” ScienceDaily. ScienceDaily, 8 November 2017. <>.

November 7, 2017

University of Chicago

Scientists aren’t normally treated to fireworks when they discover something about the universe. But a team of researchers found a show waiting for them at the atomic level — along with a new form of quantum behavior.


Jets of atoms shoot off together like fireworks from a central disc in a new quantum phenomenon discovered by UChicago scientists (color added for illustration).
Credit: Courtesy of Cheng et al./University of Chicago



Scientists aren’t normally treated to fireworks when they discover something about the universe. But a team of University of Chicago researchers found a show waiting for them at the atomic level — along with a new form of quantum behavior.

“This is a very fundamental behavior that we have never been seen before; it was a great surprise to us,” said study author and professor of physics Cheng Chin. Published Nov. 6 in Nature, the research details a curious phenomenon — seen in what was thought to be a well-understood system — that may someday be useful in quantum technology applications.

Chin’s lab studies what happens to particles called bosons in a special state called a Bose-Einstein condensate. When cooled down to temperatures near absolute zero, bosons will all condense into the same quantum state. Researchers applied a magnetic field, jostling the atoms, and they began to collide — sending some flying out of the condensate. But rather than a uniform field of random ejections, they saw bright jets of atoms shooting together from the rim of the disk, like miniature fireworks.

“If you’d asked almost anyone to predict what would happen, they would have said that these collisions would just send atoms flying off in random directions,” said postdoctoral fellow Logan Clark, the first author of the study; he and co-author and postdoctoral fellow Anita Gaj were the first to see the phenomenon. “But what we see instead are thousands of bosons bunching together to leave in the same direction.”

“It’s like people forming a consensus and leaving in groups,” Chin said.

The tiny jets may show up in other systems, researchers said — and understanding them may help shed light on the underlying physics of other quantum systems.

Moreover, the jets, like other new quantum behaviors, may be of interest in technology. “For example, if you sent a particular atom in one direction, then a bunch more would follow in that same direction, which would help you amplify small signals in the microscopic world,” Clark said.

Since there’s energy delivered to the system and the particles are not at their ground states, it falls under the category of a particularly hot area of quantum engineering research called “driven” quantum systems, the authors said. The physics of systems in these quantum states is not well understood, but essential for engineering useful technologies.

However, Bose-Einstein condensates are a generally well-studied area, so they were excited to see a never-before-documented behavior, the scientists said.

“If you see something crazy in this simple experiment, it makes you wonder what else is out there,” said graduate student Lei Feng, also a co-author.

Story Source:

Materials provided by University of Chicago. Original written by Louise Lerner. Note: Content may be edited for style and length.

Journal Reference:

  1. Logan W. Clark, Anita Gaj, Lei Feng, Cheng Chin. Collective emission of matter-wave jets from driven Bose–Einstein condensatesNature, 2017; DOI: 10.1038/nature24272


Source: University of Chicago. “Fireworks from atoms at ultra-low temperatures.” ScienceDaily. ScienceDaily, 7 November 2017. <>.

November 6, 2017

University of East Anglia

New research reveals how immune systems can evolve resistance to parasites. The study solves the enigma of how species can adapt and change their immune system to cope with new parasitic threats — whilst at the same time showing little or no evolutionary change in critical immune function over millions of years. It help to explain why we humans have some immune genes that are almost identical to those of chimpanzees.


New findings help to explain why we humans have some immune genes that are almost identical to those of chimpanzees.
Credit: © ussatlantis / Fotolia



New research from the University of East Anglia (UEA), UK, and Dalhousie University, Canada, reveals how immune systems can evolve resistance to parasites.

A study, published in Nature Communications, solves the enigma of how species can adapt and change their immune system to cope with new parasitic threats — whilst at the same time showing little or no evolutionary change in critical immune function over millions of years.

The findings help to explain why we humans have some immune genes that are almost identical to those of chimpanzees.

Scientists from UEA and Dalhousie University studied how Guppy fish (Poecilia reticulata) adapt to survive by studying their immune genes, known as the Major Histocompatibility Complex or MHC genes.

They found that guppies fine-tune these genes in each location, enabling them to adapt and survive in many different and extreme environments. Despite this adaptation, genes maintained critical function of tens of millions of years.

The discovery could improve scientists’ understanding of how related species can adapt and change their immune system to cope with new threats from parasites while simultaneously sharing similar function.

Dr Jackie Lighten from UEA led the study. He said: “Guppies are a small, colourful fish native to South America, Trinidad and Tobago. They are a fantastic model for researching the ecology and evolution of vertebrates.

“MHC genes are an important line of defence in the immune system in vertebrates, including humans. Because parasites evolve quicker than their vertebrate hosts, immune genes need to be highly diverse to keep up with parasites and prevent infections.

“MHC genes produce protein structures that are on the external surface of cells. These genes are diverse and so produce an array of proteins, each of which presents a specific part of a parasite or pathogen that has attempted to infect the body. The specific shape of the protein dictates which parasites it can recognize, and signals to the immune system to prevent infection.”

The study looked at MHC genetic variation in 59 guppy populations across Trinidad, Tobago, Barbados, and Hawaii. The authors found hundreds of different immune variants, but these so called ‘alleles’ appear to be clustered in a smaller number of functional groups or ‘supertypes’.

Prof van Oosterhout, also from UEA’s School of Environmental Sciences, said: “Each supertype protects the host against a specific group of parasites, and these supertypes were common across populations, and species, irrespective of the location.

“However, the alleles that make up a supertype track the rapid evolution of the parasites, and they too are evolving rapidly. These alleles are largely specific to each population, and they help in the ‘fine-tuning’ of the immune response to the specific (local) parasites that attack the host in that population.”

Before this study, scientists debated how these immune genes can evolve rapidly (which is necessary to keep up with the fast-evolving parasites), whilst also showing little or no evolutionary change in their function over millions of years, as observed between humans and chimpanzees. This study resolves that debate.

Prof Bentzen from Dalhousie University said: “Although this study focused on MHC genes in vertebrates, the evolutionary dynamics described in it likely apply to other gene families, for example resistance genes and those which prevent self-fertilization in plants (self-incompatibility loci) that are caught up in their own evolutionary races.”

Dr Lighten added: “It is an important step forward in understanding the evolutionary genetics of the immune system, and can help explain some of the puzzling observations observed in previous studies of many other organisms.”

Story Source:

Materials provided by University of East AngliaNote: Content may be edited for style and length.

Journal Reference:

  1. Jackie Lighten, Alexander S. T. Papadopulos, Ryan S. Mohammed, Ben J. Ward, Ian G. Paterson, Lyndsey Baillie, Ian R. Bradbury, Andrew P. Hendry, Paul Bentzen, Cock van Oosterhout. Evolutionary genetics of immunological supertypes reveals two faces of the Red QueenNature Communications, 2017; 8 (1) DOI: 10.1038/s41467-017-01183-2


Source: University of East Anglia. “Fish provide insight into the evolution of the immune system.” ScienceDaily. ScienceDaily, 6 November 2017. <>.

Attack in New York City


This week, NYC was attacked again, this time by a deranged van driver, killing 8 people, and injuring many others. Our hearts and prayers go out to the families of those who were killed and injured. When it comes to tolerance, our city is open, gentle, and a true melting pot welcoming all to the American Dream.  Hopefully, the day will come, when Martin Luther King’s dream will become a reality, where we tolerate differences, share ideas, listen to each other and compromise.


Let freedom ring! Freedom Tower has replaced the WTC Towers – © Target Health Inc.


For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 165). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website.


Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor



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Study Shows How Memories Ripple Through the Brain


NIH-funded study suggests increased communication between key brain areas during sleep


Posterior and inferior cornua of left lateral ventricle exposed from the side. The hippocampus is located in the medial temporal lobe of the brain. In this lateral view of the human brain, the frontal lobe is at left, the occipital lobe at right, and the temporal and parietal lobes have largely been removed to reveal the hippocampus underneath.

Graphic credit: Henry Vandyke Carter – Henry Gray (1918) Anatomy of the Human Body (See “Book“ section below) Gray’s Anatomy, Plate 739; Public Domain, Wikipedia



The hippocampus (named after its resemblance to the seahorse, from the Greek “seahorse“ from hippos, “horse“ and kampos, “sea monster“) is a major component of the brains of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the 1) ___. The hippocampus belongs to the limbic system and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation. The hippocampus is located under the cerebral 2) ___ (allocortical) and in primates in the medial temporal lobe. It contains two main interlocking parts: the hippocampus proper (also called Ammon’s horn) and the dentate gyrus. The hippocampus is widely thought to turn new information into permanent memories while we sleep


In Alzheimer’s disease (and other forms of dementia), the hippocampus is one of the first regions of the brain to suffer damage. Short-term memory loss and disorientation are included among the early symptoms. Damage to the hippocampus can also result from oxygen starvation (hypoxia), encephalitis, or medial temporal lobe epilepsy. People with extensive, bilateral hippocampal damage may experience anterograde amnesia (the inability to form and retain new 3) ___. In rodents as model organisms, the hippocampus has been studied extensively as part of a brain system responsible for spatial memory and navigation. Many neurons in the rat and mouse hippocampus respond as place cells: that is, they fire bursts of action potentials when the animal passes through a specific part of its environment. Hippocampal place 4) ___ interact extensively with head direction cells, whose activity acts as an inertial compass, and conjecturally with grid cells in the neighboring entorhinal cortex. Since different neuronal cell types are neatly organized into layers in the hippocampus, it has frequently been used as a model system for studying neurophysiology. The form of neural plasticity known as long-term potentiation (LTP) was first discovered to occur in the hippocampus and has often been studied in this structure. LTP is widely believed to be one of the main neural mechanisms by which memories are stored in the brain.


Just recently, using an innovative “NeuroGrid“ technology, invented by the study authors, it was showed that sleep boosts communication between two brain regions whose connection is critical for the formation of memories. The NeuroGrid consists of a collection of tiny electrodes linked together like the threads of a blanket, which is then laid across an area of the brain so that each electrode can continuously monitor the activity of a different set of neurons. One of the features of the device, is that it provides for ability to look at multiple areas of the brain at the same time. The study, published in Science, was partially funded by the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, a project of the 5) ___ ___ of ___ devoted to accelerating the development of new approaches to probing the workings of the brain.


Previous work revealed high-frequency bursts of neural firing called ripples in the 6) ___ during sleep and suggested they play a role in memory storage. The current study confirmed the presence of ripples in the hippocampus during sleep and found them in certain parts of association neocortex, an area on the brain’s surface involved in processing complex sensory information. Using the NeuroGrid system, along with recording electrodes placed deeper into the brain, the researchers examined activity in several parts of rats’ brains during NREM or 7) ___-___ ___ ___ sleep, the longest stage of sleep. The team was also surprised to find that the ripples in the association neocortex and hippocampus occurred at the same time, suggesting the two regions were communicating as the rats were 8) ___. Because the association neocortex is thought to be a storage location for memories, the authors theorized that this neural dialogue could help the brain retain information. To test that idea, they examined brain activity during NREM sleep in rats trained to locate rewards in a maze and in rats that explored the 9) ___ in a random fashion. In the latter group of animals, the ripples in the hippocampus and cortex were no more synchronized before exploring the maze than afterwards. In the trained rats, however, the learning task increased the cross-talk between those areas, and a second training session boosted it even more, further suggesting that such communication is important for the creation and storage of memories.


The group hopes to use the NeuroGrid in people undergoing brain surgery for other reasons to determine if the same ripples occur in the 10) ___ brain. The group also plans to investigate if manipulating that neural firing in animals can boost or suppress memory formation in order to confirm that ripples are important for that process. According to the authors, identifying the specific neural patterns that go along with memory formation may provide a way to better understand memory and potentially even address disorders of memory.


The study was funded by NINDS (NS099705, NS090583) and the National Institute of Mental Health (MH107396). The National Institute of Neurological Disorders and Stroke (NINDS) <> is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. References: Khodagholy et al. Learning-enhanced coupling between ripple oscillations in association cortices and hippocampus. Science. October 20, 2017. doi: 10.1126/science.aan6203.


ANSWERS: 1) brain; 2) cortex; 3) memories; 4) cells; 5) National Institutes of Health; 6) hippocampus; 7) non-rapid eye movement; 8) sleeping; 9) maze; 10) human


Approximately 65 Years Ago, Eugene Aserinsky Discovered REM Sleep

REM Sleep, outlined in red, above. Below the REM Sleep, are slow EEG waveforms of brain activity during non-REM sleep. – By en:User:MrSandman – Own work, Public Domain,


It was Sigmund Freud who stated, “Dreams are the royal road to the unconscious.”


Eugene Aserinsky (May 6, 1921 – July 22, 1998), a pioneer in sleep research, was a graduate student at the University of Chicago in 1953 when he discovered REM sleep. Aserinsky the son of a dentist of Russian – Jewish descent, like many great scientists, was of an immigrant family. Aserinsky made his discovery after hours spent studying the eyelids of sleeping subjects. Aserinsky and his PhD adviser, Nathaniel Kleitman, went on to demonstrate that this “rapid-eye movement“ was correlated with dreaming and a general increase in brain activity. Aserinsky and Kleitman pioneered procedures that have now been used with thousands of volunteers using the electroencephalograph. Because of these discoveries, Aserinsky and Kleitman are generally considered the founders of modern sleep research.


In 1953, for his Ph.D. in physiology at the University of Chicago, Dr. Aserinsky produced his ground-breaking thesis, ”Eye Movements During Sleep.” His discovery of rapid eye movement, or R.E.M. — the periodic, rapid, jerky movement of the eyeballs under the lids during stages of sleep associated with dreaming — showed that the brain was in a state of some alertness for about 22% of total sleep time. In a long career, he taught at Jefferson Medical College in Philadelphia, Marshall University Medical School and West Virginia University.


Eugene Aserinsky, died on July 22, 1998, when his car hit a tree north of San Diego. He was 77 and lived in Escondido, Calif. Nathaniel Kleitman lived to be 104 years old.


Editor’s note: All the Eugene Aserinsky sources we searched through, were quite limited – dry facts only. Then we discovered a fascinating write-up in the Smithsonian Magazine, by Chip Brown, that is such a fascinating account of Eugene Aserinsky, we have included the whole article, below.


Night after night Eugene Aserinsky had been working late. He’d dragged an ancient brain-wave machine, an Offner Dynograph, from the basement to the physiology lab on the second floor of Abbott Hall at the University of Chicago. He had tinkered with it long enough to think it might not be totally unreliable. And now, late one December evening in 1951, his 8-year-old son, Armond, came over to the lab and sat patiently on an Army cot while his father scrubbed his scalp and the skin around his eyes with acetone, taped electrodes to the boy’s head and plugged the leads into a switch box over the bed. From the adjacent room, Aserinsky calibrated the machine, telling Armond to look left, right, up and down. The ink pens jumped in concert with the boy’s eyes. And then it was lights out, the sharp smell of acetone lingering in the darkness. Armond fell asleep; his father tried not to. Sustained by pretzels and coffee, Aserinsky sat at a desk under the hellish red eyes of a gargoyle-shaped lamp. He was 30 years old, a trim, handsome man of medium height, with black hair, a mustache, blue eyes and the mien of a bullfighter. When he was not in his lab coat, he usually wore a bow tie and a dark suit. He was a graduate student in physiology, and his future was riding on this research. He had nothing but a high school degree to fall back on. His wife, Sylvia, was pregnant with their second child. They lived on campus in a converted Army barracks heated by a kerosene stove. Money was so tight Aserinsky would eventually have to accept a small loan from his dissertation advisor, Nathaniel Kleitman, and then be obliged to feign enthusiasm for the distinguished man’s suggestion that he economize by eating chicken necks.


The hours crept by in the spooky gray-stone gloom of Abbott Hall. While the long banner of graph paper unfurled, Aserinsky noticed that the pens tracking his son’s eye movements – as well as the pens registering brain activity – were swinging back and forth, suggesting Armond was alert and looking around. Aserinsky went in to check on his son, expecting to find him wide awake. But Armond’s eyes were closed; the boy was fast asleep. What was going on? Yet another problem with the infernal machine? Aserinsky didn’t know what to think, standing in bewildered excitement, on the threshold of a great discovery.


The existence of rapid eye movement (REM) and its correlation with dreaming was announced 50 years ago last month in a brief, little-noted report in the journal Science. The two-page paper is a fine example of the maxim that the eye can see only what the mind knows: for thousands of years the physical clues of REM sleep were baldly visible to anyone who ever gazed at the eyelids of a napping child or studied the twitching paws of a sleeping dog. The association of a certain stage of sleep with dreaming might have been described by any number of observant cave men; in fact, if the 17,000-year-old Lascaux cave painting of a presumably dreaming Cro-Magnon hunter with an erect penis is any indication, maybe it was. But scientists had long been blinkered by preconceptions about the sleeping brain. It remains an astonishing anachronism in the history of science that Watson and Crick unraveled the structure of DNA before virtually anything was known about the physiological condition in which people spend one-third of their lives. As Tom Roth, the former editor of the journal Sleep, put it: “It’s analogous to going to Mars with a third of the Earth’s surface still unexplored.“ The REM state is so important that some scientists have designated it a “third state of being“ (after wakefulness and sleep), yet the phenomenon itself remained hidden in plain sight until September 1953, when the experiments conducted in Chicago by Aserinsky were published.


His now-classic paper, coauthored by advisor Kleitman, was less important for what it revealed than what it began. REM opened the terra incognita of the sleeping brain to scientific exploration. Before REM, it was assumed that sleep was a passive state; absent stimulation, the brain simply switched off at night like a desk lamp. After REM, scientists saw that the sleeping brain actually cycled between two distinct electrical and biochemical climates – one characterized by deep, slow-wave sleep, which is sometimes called “quiet sleep“ and is now known as non-REM or NREM sleep, and the other characterized by REM sleep, also sometimes called “active“ or “paradoxical“ sleep. The mind in REM sleep teems with vivid dreams; some brain structures consume oxygen and glucose at rates equal to or higher than in waking. The surprising implication is that the brain, which generates and evidently benefits from sleep, seems to be too busy to get any sleep itself.


The discovery of REM launched a new branch of medicine, leading to the diagnosis and treatment of sleep disorders that afflict tens of millions of people. It also changed the way we view our dreams and ourselves. It shifted scientists’ focus from the dreaming person to the dreaming brain, and inspired new models in which the chimerical dramas of the night were said to reflect random neural fireworks rather than the hidden intentions of unconscious conflict or the escapades of disembodied souls. By showing that the brain cycles through various neurodynamic phases, the discovery of REM underscored the view that the “self“ is not a fixed state but reflects fluctuating brain chemistry and electrical activity. Many researchers continue to hope that REM may yet provide a link between the physical activity of the brain during a dream and the experience of dreaming itself. It’s hard to overestimate the importance of Aserinsky’s breakthrough, said Bert States, an emeritus professor of dramatic arts at the University of California at Santa Barbara and the author of three books on dreams and dreaming: “The discovery of REM sleep was just about as significant to the study of cognition as the invention of the telescope was to the study of the stars.“


In 1950, when Aserinsky knocked on Nathaniel Kleitman’s office door, Kleitman, then 55, was considered the “father of modern sleep research.“ A Russian emigre, he had received a doctorate from the University of Chicago in 1923 and joined the faculty two years later. There he set up the world’s first sleep lab. The cot where research subjects slept was pitched under a metal hood formerly used to suck out noxious lab fumes. At the time, few scientists were interested in the subject. Despite research on the electrical activity of the brain in the late 1920s, the understanding of sleep hadn’t advanced much beyond the ancient Greeks, who viewed Hypnos, the god of sleep, as the brother of Thanatos, the god of death. Sleep was what happened when you turned out the lights and stopped the influx of sensation. Sleep was what the brain lapsed into, not what it actively constructed. On the face of it, dull stuff.


Kleitman was intrigued nonetheless, and began to explore the physiology of the body’s basic rest-activity cycle. A painstaking researcher, he once stayed up 180 hours straight to appraise the effects of sleep deprivation on himself. In 1938, he and fellow researcher Bruce Richardson moved into Mammoth Cave in Kentucky for more than a month to study fluctuations in their body temperatures and other darkness-engendered changes in their normal sleep-wake cycle – pioneering work in the now booming field of circadian rhythm research. Kleitman backed his fieldwork with formidable scholarship. When he published his landmark book Sleep and Wakefulness in 1939, he apologized for being unable to read in any language other than Russian, English, German, French and Italian. At the office door, Aserinsky found a man with “a grey head, a grey complexion and a grey smock.“ As the younger scientist wrote years later, “there was no joy in this initial encounter for either of us. For my part I recognized Kleitman as the most distinguished sleep researcher in the world. Unfortunately, sleep was perhaps the least desirable of the scientific areas I wished to pursue.“


Aserinsky had grown up in Brooklyn in a Yiddish- and Russian-speaking household. His mother died when he was 12, and he was left in the care of his father, Boris, a dentist who loved to gamble. Boris often had his son sit in on pinochle hands if the table was a player short. Meals were catch as catch can. Aserinsky’s son, Armond, recalled: “Dad once told me he said to his father, ?Pop, I’m hungry,’ and his father said, ?I’m not hungry, how can you be hungry?“ Eugene graduated from public high school at the age of 16 and for the next 12 years knocked about in search of his metier. At Brooklyn College, he took courses in social science, Spanish and premedical studies but never received a degree. He enrolled at the University of Maryland dental school only to discover that he hated teeth. He kept the books for an ice company in Baltimore. He served as a social worker in the Maryland state employment office. Though he was legally blind in his right eye, he did a stint in the U.S. Army as a high explosives handler. By 1949, Aserinsky, married and with a 6-year-old son, was looking to take advantage of the G.I. Bill of Rights to launch a science career. He aced the entrance exams at the University of Chicago and, though he lacked an undergraduate degree, persuaded the admissions office to accept him as a graduate student. “My father was courtly, intelligent and intensely driven,“ says Armond Aserinsky, 60, now a clinical psychologist in North Wales, Pennsylvania. “He could be extremely charming, and he had a fine scientific mind, but he had all kinds of conflicts with authority. He always wore black suits. I once asked him, ?Dad, how come you never wear a sports jacket?’ He looked at me and said, ?I’m not a sport.“


Kleitman’s first idea was to have Aserinsky test a recent claim that the rate of blinking could predict the onset of sleep. But after a number of vexing weeks trying to concoct a way to measure blink rates, Aserinsky confessed his lack of progress. Kleitman proposed that Aserinsky observe infants while they slept and study what their eyelids did. So he sat by cribs for hours but found that it was difficult to differentiate eyelid movements from eyeball movements. Once again he knocked on Kleitman’s door, something he was loath to do because of Kleitman’s austere and formal air. (Ten years after their famous paper was published, Kleitman began a letter to his colleague and coauthor, “Dear Aserinsky.“) Aserinsky had the idea of studying all eye movements in sleeping infants, and with Kleitman’s approval embarked on a new line of inquiry – one that, he would later confess, was “about as exciting as warm milk.“ Significantly, he did not at first “see“ REM, which is obvious if you know to look for it. Over months of monotonous observations, he initially discerned a 20-minute period in each infant’s sleep cycle in which there was no eye movement at all, after which the babies usually woke up. He learned to exploit the observation. During such periods, the fatigued researcher was able to nap himself, certain he would not miss any important data. And he was also able to impress mothers hovering near the cribs by telling them when their babies would wake up. “The mothers were invariably amazed at the accuracy of my prediction and equally pleased by my impending departure,“ he once wrote.


At home, Aserinsky was under considerable pressure. His daughter, Jill, was born in April 1952. His wife, Sylvia, suffered from bouts of mania and depression. Aserinsky couldn’t even afford the rent on the typewriter he leased to draft his dissertation. “We were so poor my father once stole some potatoes so we would have something to eat,“ recalls Jill Buckley, now 51 and a lawyer in Pismo Beach, California, for the American Society for the Prevention of Cruelty to Animals. “I think he saw himself as a kind of Don Quixote. Ninety percent of what drove him was curiosity – wanting to know. We had a set of Collier’s Encyclopedias, and my father read every volume.“ After studying babies, Aserinsky set out to study sleeping adults. At the time, no scientist had ever made all-night continuous measurements of brain-wave activity. Given the thinking of the era – that sleep was a featureless neurological desert – it was pointless to squander thousands of feet of expensive graph paper making electroencephalogram (EEG) recordings. Aserinsky’s decision to do so, combined with his adapting the balky Offner Dynograph machine to register eye movements during sleep, led to the breakthrough. His son, Armond, liked to hang out at the lab because it meant spending time with his father. “I remember going into the lab for the night,“ Armond says. “I knew the machine was harmless. I knew it didn’t read my mind. The set up took a long time. We had to work out some things. It was a long schlep to the bathroom down the hall, so we kept a bottle by the bed.“ Aserinsky did a second nightlong sleep study of Armond with the same results – again the pens traced sharp jerky lines previously associated only with eye movements during wakefulness. As Aserinsky recruited other subjects, he was growing confident that his machine was not fabricating these phenomena, but could it be picking up activity from the nearby muscles of the inner ear? Was it possible the sleeping subjects were waking up but just not opening their eyes? “In one of the earliest sleep sessions, I went into the sleep chamber and directly observed the eyes through the lids at the time that the sporadic eye movement deflections appeared on the polygraph record,“ he would recall in 1996 in the Journal of the History of the Neurosciences. “The eyes were moving vigorously but the subject did not respond to my vocalization. There was no doubt whatsoever that the subject was asleep despite the EEG that suggested a waking state.“ By the spring of 1952, a “flabbergasted“ Aserinsky was certain he had stumbled onto something new and unknown. “The question was, what was triggering these eye movements. What do they mean?“ he recalled in a 1992 interview with the Journal of NIH Research. In the fall of 1952, he began a series of studies with a more reliable EEG machine, running more than 50 sleep sessions on some two dozen subjects. The charts confirmed his initial findings. He thought of calling the phenomena “jerky eye movements,“ but decided against it. He didn’t want critics to ridicule his findings by playing off the word “jerk.“


Aserinsky went on to find that heart rates increased an average of 10% and respiration went up 20% during REM; the phase began a certain amount of time after the onset of sleep; and sleepers could have multiple periods of REM during the night. He linked REM interludes with increased body movement and particular brain waves that appear in waking. Most amazingly, by rousing people from sleep during REM periods, he found that rapid eye movements were correlated with the recall of dreams – with, as he noted in his dissertation, “remarkably vivid visual imagery.“ He later wrote, “The possibility that these eye movements might be associated with dreaming did not arise as a lightning stroke of insight. An association of the eyes with dreaming is deeply ingrained in the unscientific literature and can be categorized as common knowledge. It was Edgar Allan Poe who anthropomorphized the raven, ?and his eyes have all the seeming of a demon’s that is dreaming.’ “


Aserinsky had little patience for Freudian dream theory, but he wondered if the eyes moving during sleep were essentially watching dreams unfold. To test that possibility, he persuaded a blind undergraduate to come into the lab for the night. The young man brought his Seeing Eye dog. “As the hours passed I noticed at one point that the eye channels were a little more active than previously and that conceivably he was in a REM state,“ Aserinsky wrote. “It was imperative that I examine his eyes directly while he slept. Very carefully I opened the door to the darkened sleeping chamber so as not to awaken the subject. Suddenly, there was a low menacing growl from near the bed followed by a general commotion which instantaneously reminded me that I had completely forgotten about the dog. By this time the animal took on the proportions of a wolf, and I immediately terminated the session, foreclosing any further exploration along this avenue.“ (Other researchers would later confirm that blind people do indeed experience REM.) In any event, Aserinsky wasn’t much interested in the meaning of dreams, said his daughter Jill, adding: “He was a pure research scientist. It always irritated him when people wanted him to interpret their dreams.“


But a future colleague of Aserinsky’s was intrigued. William Dement was a medical student at Chicago, and in the fall of 1952 Kleitman assigned him to help Aserinsky with his overnight sleep studies. Dement recounted his excitement in his 1999 book, The Promise of Sleep. “Aserinsky told me about what he had been seeing in the sleep lab and then threw in the kicker that really hooked me: ?Dr. Kleitman and I think these eye movements might be related to dreaming.’ For a student interested in psychiatry, this offhand comment was more stunning than if he had just offered me a winning lottery ticket. It was as if he told me, ?We found this old map to something called the Fountain of Youth.’ “ By Aserinsky’s account, Dement ran five overnight sessions for him starting in January 1953. With a camera Kleitman had obtained, Dement and Aserinsky took 16-millimeter movie footage of subjects in REM sleep, one of whom was a young medical student named Faylon Brunemeier, today a retired ophthalmologist living in Northern California. They were paying three dollars a night, he recalled, “and that was a lot to an impecunious medical student.“ Kleitman had barred women as sleep study subjects, fearing the possibility of scandal, but Dement wheedled permission to wire up his sweetheart, a student named Pamela Vickers. The only provision was that Aserinsky had to be on hand to “chaperon“ the session. While the sleep-deprived Aserinsky passed out on the lab couch, Dement documented that Vickers, too, experienced REM. Next, Dement says he recruited three other female subjects, including Elaine May, then a student at the University of Chicago. Even if she had not become famous a few years later as part of the comedy team Nichols and May, and had not gone on to write Heaven Can Wait and other movies, she would still have a measure of fame, in the annals of sleep science.


From 1955 to 1957, Dement published studies with Kleitman establishing the correlation between REM sleep and dreaming. Dement went on to help organize the first sleep research society and started the world’s first sleep clinic at Stanford in 1970. With a collaborator, Howard Roffwarg, a psychiatrist now at the University of Mississippi Medical Center, Dement showed that even a 7-month-old premature infant experiences REM, suggesting that REM may occur in the womb. Dement’s colony of dogs with narcolepsy – a condition of uncontrollable sleep – shed light on the physiological basis of the disorder, which in people had long been attributed to psychological disturbances. Dement became such an evangelist about the dangers of undiagnosed sleep disorders that he once approached the managers of the rock band R.E.M., seeking to enlist the group for a fundraising concert. The musicians brushed him off with a shaggy story about the acronym standing for retired english majors.


When Aserinsky left the University of Chicago, in 1953, he turned his back on sleep research. He went to the University of Washington in Seattle and for a year studied the effects of electrical currents on salmon. Then he landed a faculty position at Jefferson Medical College in Philadelphia, where he explored high-frequency brain waves and studied animal respiration. In 1957, his wife’s depression came to a tragic conclusion; while staying at a mental hospital in Pennsylvania, Sylvia committed suicide. Two years later, Aserinsky married Rita Roseman, a widow, and became stepfather to her young daughter, Iris; the couple remained together until Rita’s death in 1994.


In the early 1960s, Armond Aserinsky urged his father, then in his 40s, to return to the field he had helped start. Aserinsky finally wrote to Kleitman, who had retired from the University of Chicago. Kleitman replied, “It was good to learn that you have renewed work on rapid eye movements during sleep. The literature on the subject is quite extensive now. I believe that you have ability and perseverance but have had personal hard knocks to contend with. Let us hope that things will be better for you in the future.“ Kleitman also took the opportunity to remind his former student that he still owed him a hundred dollars. In March 1963, Aserinsky went home to Brooklyn to attend a meeting of sleep researchers. “People were shocked,“ his son recalled. “They looked at him and said, ?My God, you’re Aserinsky! We thought you were dead!’ “


Delving into the night again in an unused operating room at the Eastern Pennsylvania Psychiatric Institute in Philadelphia, Aserinsky worked on the physiology of REM and non-REM sleep, but he had prickly encounters with colleagues. He took offense when he did not receive an invitation to a prestigious dinner at a 1972 meeting of sleep researchers. He was often stung when Dement and Kleitman got credit he felt belonged to him. (For his part, Dement said he resented that Aserinsky never acknowledged all the work he did as low man on the lab totem pole. “I was so naive,“ he told me.) In 1976, after more than two decades at Jefferson MedicalCollege, Aserinsky was passed over for the chairmanship of the physiology department. He left, becoming chairman of physiology at Marshall University in Huntington, West Virginia. He retired in 1987. “He could be a deeply suspicious and impolitic person,“ Armond Aserinsky said. Narrating his version of events in the Journal of the History of the Neurosciences, Aserinsky criticized Dement’s contention that the discovery of REM was a “team effort,“ saying, “If anything is characteristic about the REM discovery, it was that there was no teamwork at all. In the first place, Kleitman was reserved, almost reclusive, and had little contact with me. Secondly, I myself am extremely stubborn and have never taken kindly to working with others. This negative virtue carried on throughout my career as evidenced by my resume, which reveals that I was either the sole or senior author in my first thirty publications, encompassing a period of twenty-five years.“ That stubbornness spilled into his family relations as well. Years passed in which he had no contact with Armond. To younger sleep scientists, Aserinsky was only a name on a famous paper, an abstraction from another time. And such he might have remained if not for a license plate and a chance encounter in 1989. Peter Shiromani, then an assistant professor of psychiatry at the University of California at San Diego, had just nosed his Datsun 310 into the parking lot of a Target department store in Encinitas, California. His custom license plates advertised what had been his scientific obsession since his undergraduate days at City College in New York City: REM SLEP. “A woman walked up to me and said, ?I really love your plates! Did you know my father discovered REM sleep?’ “ Shiromani recalled. “I said, ?You must be Eugene Aserinsky’s daughter!’ She was very pleased. I think she felt a lot of pride in her father’s accomplishment, and here was someone who recognized her father’s name. We chatted briefly with much enthusiasm about REM sleep. Fortunately, I had the presence of mind to ask for her father’s address.“ Shiromani passed the address along to Jerry Siegel, a sleep researcher at UCLA and the Sepulveda Veterans Affairs medical center in suburban Los Angeles, who invited Aserinsky to address the June 1995 meeting of the Associated Professional Sleep Societies in Nashville. Siegel was organizing a symposium in honor of Kleitman, who had recently turned 100. “It was very difficult to get Aserinsky to come,“ Siegel recalls. “People who knew him in the early days said, ?Don’t invite him.’ But my dealings with him were very pleasant.“ Despite their rivalry, it was Dement who introduced Aserinsky to the crowd of 2,000 people in the ballroom at the OpryLand Hotel. They gave him a standing ovation. And when he finished a witty, wide-ranging talk on the history of REM, the audience again rose to its feet. “It was one of the high points of his life,“ recalls his daughter Jill, who had accompanied her father to the meeting along with his stepdaughter, Iris Carter. “He wore a name tag, and people would stop and point and say, ?There’s Aserinsky!’ “ says Carter.


One July day three years later, Aserinsky, driving down a hill in Carlsbad, California, collided with a tree and was killed. He was 77. An autopsy could not determine the cause of the accident. It’s possible he fell asleep at the wheel.


Today it’s well established that normal sleep in human adults includes between four and six REM periods a night. The first starts about 90 minutes after sleep begins; it usually lasts several minutes. Each subsequent REM period is longer. REM sleep is characterized by not only brain-wave activity typical of waking but also a sort of muscle paralysis, which renders one incapable of acting on motor impulses. (Sleepwalking most often occurs during non-REM sleep.) In men and women, blood flow to the genitals is increased. Parts of the brain burn more energy. The heart may beat faster. Adults spend about two hours a night in REM, or 25% of their total sleep. Newborns spend 50 percent of their sleep in REM, upwards of eight hours a day, and they are much more active than adults during REM sleep, sighing and smiling and grimacing. After 50 years, researchers have learned a great deal about what REM isn’t. For example, it was once thought that people prevented from dreaming would become psychotic. That proved not to be the case; patients with injuries to the brainstem, which controls REM, do not go nuts without it. Still, if you deprive a person of REM sleep, they’ll recoup it at the first chance, plunging directly into the REM phase – a phenomenon discovered by Dement and called REM rebound.


Studies of animals have yielded insights into REM, sometimes. In the early 1960s, Michel Jouvet, a giant of sleep research and a neurophysiologist at the University Claude Bernard in Lyon, France, mapped the brain structures that generate REM sleep and produce the attendant muscle paralysis. Jouvet, who coined the term “paradoxical sleep“ as a substitute for REM sleep, also discovered that cats with lesions in one part of the brainstem were “disinhibited“ and would act out their dreams, as it were, jumping up and arching their backs. (More recently, University of Minnesota researchers have documented a not-dissimilar condition in people; REM sleep behavior disorder, as it’s called, mainly affects men over 50, who kick, punch and otherwise act out aggressive dream scenarios while they sleep. Researchers believe that REM sleep disorder may be a harbinger of Parkinson’s disease in some people.) Paradoxical sleep has been found in almost all mammals tested so far except for some marine mammals, including dolphins. Many bird species appear to have short bursts of paradoxical sleep, but reptiles, at least the few that have been assessed, do not. Jouvet was especially interested in penguins, because they stay awake for long periods during the brooding season. Hoping to learn more about their physiology, he went to great trouble to implant a costly radio-telemetry chip in an emperor penguin in Antarctica. The prize research subject was released into the sea, only to be promptly gobbled up by a killer whale.


In 1975, Harvard’s Allan Hobson and Robert McCarley proposed that many properties of dreams – the vivid imagery, the bizarre events, the difficulty remembering them – could be explained by neurochemical conditions of the brain in REM sleep, including the ebb and flow of the neurotransmitters norepinephrine, serotonin and acetylcholine. Their theory stunned proponents of the idea that dreams were rooted not in neurochemistry but psychology, and it has been a starting point of dream theorizing for the past 25 years. The once-popular description of REM as “dream sleep“ is now considered an oversimplification, and debate rages over questions of what can be properly claimed about the relation of dreaming to the physiology of REM sleep. (In 2000, an entire volume of the journal Behavioral and Brain Sciences was devoted to the debate.) To be sure, you can have REM without dreaming, and you can dream without experiencing REM. But most researchers say that dreaming is probably influenced and may be facilitated by REM. Still, dissenters, some of whom adhere to psychoanalytic theory, say that REM and dreaming have little connection with each other, as suggested by clinical evidence that different brain structures control the two phenomena. In the years to come, new approaches may help clarify these disagreements. In a sort of echo of Aserinsky’s first efforts to probe the sleeping brain with EEG, some researchers have used powerful positron brain-scanning technology to focus on parts of the brain activated during REM.


This past June, more than 4,800 people attended the Associated Professional Sleep Societies’ annual meeting in Chicago. The scientists took time out to mark REM’s golden anniversary. With mock solemnity, Dement echoed the Gettysburg Address in his lecture: “Two score and ten years ago Aserinsky and Kleitman brought forth on this continent a new discipline conceived at night and dedicated to the proposition that sleep is equal to waking.“ But to paraphrase the physicist Max Planck, science advances funeral by funeral. Kleitman died in 1999 at the age of 104, and though he was a coauthor of the milestone REM study, he never really accepted that REM was anything other than a phase of especially shallow sleep. “Kleitman died still believing there was only one state of sleep,“ Dement told me. Aserinsky had his own blind spots; he never relinquished his doubts that sleeping infants exhibit REM. To honor the research done in Kleitman’s lab five decades ago, the Sleep Research Society commissioned a 65-pound zinc plaque. It now hangs in the psychiatry department at the University of Chicago Medical Center, adjacent to Abbott Hall. To be sure, the inscription – “Commemorating the 50th Anniversary of the Discovery of REM Sleep by Eugene Aserinsky, Ph.D., and Nathaniel Kleitman, Ph.D., at the University of Chicago“ – doesn’t speak to the poetry of a lyric moment in the history of science, a moment when, as Michel Jouvet once said, humanity came upon “a new continent in the brain.“ If it’s the poetry of REM you want, you need wait only until tonight.


Fifty years ago, Eugene Aserinksy discovered rapid eye movement and changed the way we think about sleep and dreaming



Sources: Smithsonian Magazine, October 2003, By Chip Brown;;; Wikipedia

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For your sheer pleasure, British tenor, John Owen-Jones sings, Music of the Night, from Phantom of the Opera.


CHAPLE Disease and Possible Treatment With a Repurposed Drug


CHAPLE disease is also known as CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy. The disease is a form of primary intestinal lymphangiectasia (PIL), or Waldmann’s disease, and was first described in 1961 by Thomas A. Waldmann, M.D., an NIH Distinguished Investigator at the National Cancer Institute, at NIH. Children with the condition can experience severe gastrointestinal distress and deep vein blood clots. No effective treatments are available to ameliorate or prevent these life-threatening symptoms. Now, 56 years later, a genetic cause and potential treatment strategy for a CHAPLE disease has been identified.


In a study published in the New England Journal of Medicine (2017; 377:52-6), genes were analyzed from 11 children with CHAPLE disease and their families. Results showed that each child had two copies of a defective CD55 gene that prevented them from producing a cell surface protein of the same name. The CD55 protein helps regulate the immune system by blocking the activity of complement, a group of immune system proteins that can fight infections by punching holes in the cell membranes of bacteria and other infectious agents. However, complement also can damage the body’s tissues. The study found that in CHAPLE disease, uninhibited complement resulting from a lack of CD55 protein damaged blood and lymph vessels along the lower digestive tract, leading to the loss of protective immune proteins and blood cells. In many patients, this process caused a range of symptoms, such as abdominal pain, bloody diarrhea, vomiting, problems absorbing nutrients, slow growth, swelling in the legs, recurrent lung infections, and blood clots.


After discovering that complement hyperactivity was driving these severe symptoms, the authors tested drugs already approved by the U.S. Food and Drug Administration for the treatment of other diseases to see if they block this process in samples of patient immune cells. The authors found that complement production decreased when cells were exposed to eculizumab, a therapeutic antibody approved to treat another rare condition called paroxysmal nocturnal hemoglobinuria. The NIAID team and their collaborators plan to study eculizumab in people with CHAPLE disease with the hope that the therapeutic could become the first effective treatment for the disorder.


CAPTION: This light microscope image shows the gut tissue of a child with CHAPLE disease. The large white areas in the bottom right corner are enlarged lymphatic vessels, which can contribute to intestinal distress.



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Experimental HIV Vaccine


According to the results from an early-stage clinical trial called APPROACH, presented at the 9th International AIDS Society Conference on HIV Science in Paris, an investigational HIV vaccine regimen was well-tolerated and generated immune responses against HIV in healthy adults. The APPROACH findings, as well as results expected in late 2017 from another early-stage clinical trial called TRAVERSE, will form the basis of the decision whether to move forward with a larger trial in southern Africa to evaluate vaccine safety and efficacy among women at risk of acquiring HIV. The ongoing TRAVERSE trial is comparing Ad26-based regimens containing three mosaic antigens (trivalent) with Ad26-based regimens containing four mosaic antigens (tetravalent).


The experimental vaccine regimens evaluated in APPROACH are based on “mosaic“ vaccines designed to induce immunological responses against a wide variety of HIV subtypes responsible for HIV infections globally. Different HIV subtypes, or clades, predominate in various geographic regions around the world. The Ad26-based mosaic vaccines were initially developed by scientists at NIAID and Janssen Pharmaceuticals. In pre-clinical studies, regimens incorporating these mosaic vaccines protected monkeys against infection with an HIV-like virus called simian human immunodeficiency virus (SHIV). The most effective prime-boost regimen reduced the risk of infection per exposure to SHIV by 94% and resulted in 66% complete protection after six exposures. The vaccine-induced immune responses that correlated with this protection were identified and characterized.


APPROACH involved nearly 400 volunteers in the United States, Rwanda, Uganda, South Africa and Thailand who were randomly assigned to receive one of seven experimental vaccine regimens or a placebo. APPROACH found that different mosaic vaccine regimens were well-tolerated and capable of generating anti-HIV immune responses in healthy, HIV-negative adults. Notably, the vaccine regimen that was most protective in pre-clinical studies in animals elicited among the greatest immune responses in the study participants. However, further research will be needed because the ability to elicit anti-HIV immune responses does not necessarily indicate that a candidate vaccine regimen can prevent HIV acquisition.


In APPROACH, study participants received four vaccinations over 48 weeks: two doses of an initial, or “prime,“ vaccine, followed by two doses of a booster vaccine. The experimental regimens all incorporated the same vaccine components in the prime vaccination, known as Ad26.Mos.HIV. The vaccine uses a strain of common-cold virus (adenovirus serotype 26, or Ad26), engineered so that it does not cause illness, as a vector to deliver three mosaic antigens created from genes from many HIV variants. The booster vaccination included various combinations of the Ad26.Mos.HIV components or a different mosaic component, called MVA-Mosaic, and/or two different doses of clade C HIV gp140 envelope protein containing an aluminum adjuvant to boost immune responses. Following the third vaccination, most APPROACH participants had developed antibody and cellular immune responses against HIV. The different boost vaccines altered the magnitude and character of these immune responses, with the regimen that showed greatest protection in monkey studies also eliciting among the greatest immune responses in humans. The anti-HIV immune responses increased after the fourth vaccination.


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