Neuroscience

Recording waves, reading minds – Science Magazine

Our brains, each of which thrums with enough electrical energy to power a low-wattage light bulb, can now be measured and explored much better than ever beforea boon for doctors seeking better medical treatments and a thrill for inventors crossing neuroscience thresholds, but a warning, too, as our personalities and thoughts become less private and potentially more exploitable. In Electric Brain, R. Douglas Fields details scientists' quest to understand brain waves throughout history, covering a good deal of unsettling material in the process and touching on today's emerging technology and most pressing ethical questions.

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Recording waves, reading minds - Science Magazine

Neuroscience

Hanover author urges us to give our brains a workout – Valley News

Think your brain is destined to shrivel bit by bit as the years go by?

Think again, says John Randolph.

In his new book, The Brain Health Book, the Hanover neuropsychologist presents a sunny view of gray matter, making the case that our brains are not only able to withstand the forces of aging but capable of regeneration and even growth later in life.

We really do have a fair amount of control over our brain health, Randolph said in a recent telephone interview. What the science says is that the things that matter the most are the lifestyle choices that are free or inexpensive and available to all of us.

These choices range from intuitive techniques such as doing crossword puzzles and sudoku to strategies less obviously connected to cognition, such as exercising, maintaining social connections and even defining your core values. Randolph, who conducts research at the Geisel School of Medicine at Dartmouth College and has his own practice as a brain health coach and consultant in Lebanon, also emphasizes preventive measures including proper nutrition, adequate sleep and stress management.

If such a regimen sounds a bit overwhelming, Randolph recommends tackling the techniques one at a time. Read just a few chapters and let those chapters simmer a bit, he said. Its important to be realistic. Making even a 10-15% change in one area of your life can make a huge difference.

The book offers a laypersons look at some of the latest research in neuroscience, along with checklists, quizzes and stories from Randolphs practice, where he treats people with cognitive challenges as well as those who are simply interested in improving and preserving their cognitive skills.

Randolph, who is scheduled to discuss his book at the Norwich Bookstore on Wednesday, believes that latter group is beginning to grow.

Its sort of like investing, he said. I think the wave of the future is to be thinking about how our brains are functioning right now and how that plots onto our future even decades down the road.

For that reason, the book may be most relevant not to people in their 70s and 80s although its never too late to think about brain health but to those in their 40s, 50s and 60s. Many of the studies presented in the book demonstrate how lifestyle factors in middle age affect brain function in the later years.

For example, one evidence-based study showed that women who were the most physically fit in middle age were 88% less likely to develop Alzheimers disease or other forms of dementia than women who were moderately fit.

The importance of exercise in maintaining brain health really cannot be overemphasized, Randolph writes. It reduces inflammation, which has been linked to Alzheimers; lowers stress, which affects a variety of cognitive functions; boosts neurochemicals that help us focus, learn and remember new things; and even promotes growth in the hippocampus and frontal cortex.

There is simply no better intervention to date that impacts the brain so profoundly and completely as exercise, he writes.

The book also shows how social connections are closely linked to brain health. The amount of time we spend socializing, the size of our social networks and the degree of support we feel in those networks all play a role in cognition as we age. Conversely, negative relationships and isolation hurt the brain. Studies found that cognitive skills declined 20% faster among people who described themselves as lonely and that particularly isolated people have a 60% higher risk of cognitive decline than people with a large social network.

The book also demonstrates how stimulating mental activities such as playing games, reading and playing instruments improve brain health. One particularly compelling study examined sets of twins in which one played a musical instrument and one didnt. The twins who played instruments were 64% less likely to develop dementia than those who didnt.

Randolph, who moved to the Upper Valley from the West Coast 18 years ago to complete clinical and research fellowships in neuropsychology and neuroimaging at Dartmouth, has applied much of the research to his own life. He tries to eat a mostly Mediterranean-style diet high in whole grains, fish, fruit, vegetables and legumes and stays active by running, playing racquetball, snowboarding, skiing and kayaking. At 48, hes in the prime age bracket to invest in his brain health.

And those investments arent limited to physical concerns like exercise and diet. Randolph also makes the case that our outlook and values have a profound effect on our brains, clearing out mental clutter and sharpening our focus on what matters.

When we have a stronger purpose in life, when we have a good sense of what drives us day to day, that improves how the brain works, he said. Gratitude would be another example. When people engage in gratitude exercises on a regular basis, their brain health tends to be stronger.

John Randolph will be at the Norwich Bookstore on Wednesday at 7 p.m. For information or to save a seat, call 802-649-1114 or email info@norwichbookstore.com.

Sarah Earle can be reached at searle@vnews.com or 603-727-3268.

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Hanover author urges us to give our brains a workout - Valley News

Neuroscience

Brain and Brawn: Hitting the Gym Slows Neurodegeneration in Older People At Risk of Alzheimer’s – Technology Networks

For the first time, an intervention - lifting weights - has been able to slow and even halt degeneration, over a long period, in brain areas particularly vulnerable to Alzheimer's disease.

Researchers have found that six months of strength training (lifting weights) can help protect brain areas especially vulnerable to Alzheimers disease up to one year later.

The team, led by researchers at the University of Sydney, conducted a clinical trial for older people at high risk of Alzheimers disease due to mild cognitive impairment.

Mild cognitive impairment involves a decline in memory and other thinking skills despite generally intact daily living skills, and is one of strongest risk factors for dementia. People with mild cognitive impairment are at a one-in-10 risk of developing dementia within a year.

Study participants were randomly allocated to do computerised brain training, strength training, combined computer and strength training, which they did for just six months followed by their usual activity for 12 months.

The long-term study found that strength training led to overall benefits to cognitive performance, benefits linked to protection from degeneration in specific subregions of the hippocampus. The hippocampus is a complex structure in the brain with a major role in learning and memory.

The hippocampus subregions targeted by the strength training were those especially vulnerable to Alzheimers disease. In the control condition, where no strength training was undertaken hippocampal subregions shrunk by 3-4 percent over the 18-months, whilst those undergoing strength training saw only 1-2 percent reductions, and in some areas, none at all.

The findings have been published this month in the specialist journal Neuroimage: Clinical.

Strength training is a type of physical exercise that requires repetitive contraction of the major muscle groups against an opposing force, typically a free weight or using gym equipment. Participants in this study did supervised strength training for just 90 minutes in total each week, over two or three weekly sessions.

Dr Kathryn Broadhouse, now with the University of the Sunshine Coast, who led the analysis while at the University of Sydney, said the data showed that strength training could exert important biological effects.

Our research shows that strength training can protect some hippocampal subregions from degeneration or shrinkage for up to 12-months after the training has stopped, Dr Broadhouse said.

To arrive at their conclusions, the team conducted MRI brain scans of the participants three times over an 18-month period and used some of the latest advances in image analysis to quantify changes to subregions within the hippocampus, the brains memory hub.

Hippocampal segmentation is difficult because the borders between structures are sometimes unclear and even anatomists will debate where to draw the line, so we restricted our analysis to those subregions where the data is consistent, Dr Broadhouse said.

Professor Michael Valenzuela, leader of the Regenerative Neuroscience Group at the University of Sydneys Brain and Mind Centre and the senior author of the study, believes the finding should change the dementia prevention message.

This is the first time any intervention, medical or lifestyle, has been able to slow and even halt degeneration in brain areas particularly vulnerable to Alzheimers disease over such a long time, said Professor Valenzuela, from the Sydney Medical School in the Faculty of Medicine and Health.

Given this was also linked to protection from cognitive decline, the message is clear: resistance exercise needs to become a standard part of dementia risk-reduction strategies, he said.

Professor Valenzuela is one of the leaders of the multi-million-dollar Australian Maintain your Brain online trial (www.maintainyourbrain.org) that will test if a tailored program of lifestyle modification, including resistance exercise, can prevent cognitive loss in a group of 6,000+ older adults.

Reference: Broadhouse, K. M., Singh, M. F., Suo, C., Gates, N., Wen, W., Brodaty, H., Jain, N., Wilson, G. C., Meiklejohn, J., Singh, N., Baune, B. T., Baker, M., Foroughi, N., Wang, Y., Kochan, N., Ashton, K., Brown, M., Li, Z., Mavros, Y., Valenzuela, M. J. (2020). Hippocampal plasticity underpins long-term cognitive gains from resistance exercise in MCI. NeuroImage: Clinical, 25, 102182. https://doi.org/10.1016/j.nicl.2020.102182

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Brain and Brawn: Hitting the Gym Slows Neurodegeneration in Older People At Risk of Alzheimer's - Technology Networks

Neuroscience

Researchers decode the science behind good lighting – News-Medical.net

Researchers at UW Medicine have decoded what makes good lighting - lighting capable of stimulating the cone photoreceptor inputs to specific neurons in the eye that regulate circadian rhythms.

Their study, "A color vision circuit for non-image-forming vision in the primate retina," published in Current Biology Feb. 20, identifies a cell in the retina, which plays an important role in signaling our brain centers that regulate circadian rhythms, boost alertness, help memory and cognitive function, and elevate mood.

These effects have been attributed to a pigment in the eye called melanopsin, which is sensitive to blue light, but researchers say cone photoreceptors are a thousand times more sensitive to light than melanopsin. The cone photoreceptor inputs to the circadian circuity respond to short wavelength blue light, but they also respond strongly to long wavelength oranges and yellows and contrasting light - the colors at sunrise and sunset.

Lead author Sara Patterson, a graduate student in neuroscience at the University of Washington School of Medicine, said how we set our internal clocks to the external light-dark cycle has been studied a lot. But how the changes in the color of light affect our brain has not.

"Color vision used for something other than color perception was the most exciting part for me," she said.

In the study, Patterson and colleagues identified a cell known as an inhibitory interneuron or amacrine cell in the retina, which signals to photosensitive ganglion cells that affect our circadian brain centers. The researchers said these amacrine cells provide "the missing component of an evolutionary ancient color vision circuit capable of setting the circadian clock by encoding the spectral content of light."

Patterson said so little is known about rare retinal circuitry that it was possible to find a new blue cone cell. She said there is a lot more to be discovered about how blue cone cells are projecting to other areas of the brain.

While sunrise lights, blue lights and seasonal affective disorder (SAD) lights have all tried to capture benefits of natural light, they haven't been that effective because they are missing key science data, said corresponding author Jay Neitz, professor of ophthalmology at the UW School of Medicine, a scientist at the UW Medicine Eye Institute, and a well-known color vision researcher. He said the science behind SAD lights, for example, is to make lights hundreds of times brighter than normal lights to stimulate melanopsin.

This research all started because of our interest in the health benefits of having natural light that occurs at the right time of day that helps regulate our circadian clock and our mood and alertness."

Jay Neitz, professor of ophthalmology, UW School of Medicine

The University of Washington has licensed technology based on this discovery to TUO, a lighting technology company that will be selling white LED lightbulbs that will incorporate undetectable sunrise and sunset wavelengths for commercial use.

Source:

Journal reference:

Patterson, S.S., et al. (2020) A Color Vision Circuit for Non-Image-Forming Vision in the Primate Retina. Current Biology. doi.org/10.1016/j.cub.2020.01.040.

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Researchers decode the science behind good lighting - News-Medical.net

Biochemistry

First Clinical Evidence of Neuroprotection in Acute Stroke? – Medscape

LOS ANGELES A new potential neuroprotectant agent has been found to be beneficial for patients with acute ischemic stroke undergoing endovascular thrombectomy in a large placebo-controlled trial, but only for those patients who did not also receive thrombolysis.

There was no difference between groups on the primary outcome in the main analysis of the trial, lead author Michael Hill, MD, reported.

However, "In our study, we found a dramatic interaction of nerinetide with alteplase. There was a large benefit of nerinetide in patients not given thrombolysis, but in patients who received alteplase, this benefit was completely obliterated," Hill told Medscape Medical News.

"In patients not treated with thrombolysis, we found a large effect size with a 9.5% absolute improvement in patients having an independent outcome (modified Rankin Score [mRS] 0-2) and a number need to treat of 10 to 11," he said. "We also found a mortality benefit and a reduction in the size of strokes, with all other secondary outcomes going in the right direction.

"The drug works really well in patients who do not get thrombolysis, but it doesn't work at all in patients who have had thrombolysis. The thrombolytic appears to break the peptide down so it is inactive," he added.

"This is the first evidence that neuroprotection is possible in human stroke. This has never been shown before," Hill noted. "Many previous clinical trials of potential neuroprotectants have been negative. We think this is a major breakthrough. This is pretty exciting stuff with really tantalizing results."

Hill, who is professor of neurology at the University of Calgary, Alberta, Canada, presented results of the ESCAPE-NA1 trial today at the International Stroke Conference (ISC) 2020. The trial was also simultaneously published online in the Lancet.

The new agent known as NA1 or nerinetide is a 20 amino acid peptide with a novel mechanism of action; it inhibits signaling that leads to neuronal excitotoxicity. "It reduces endogenous nitric oxide generated inside the cell during ischemia, which is one of the main biochemical processes contributing to cell death," Hill explained. In a primate model of ischemia reperfusion that was published in Nature in 2012, it was highly protective, he added.

The drug is given just once at the time of thrombectomy. It is short lived in the blood but detectable in the brain for up to 24 hours, Hill said.

The trial included 1105 patients who had experienced acute ischemic stroke due to large-vessel occlusion within a 12-hour treatment window and for whom imaging results suitable for thrombectomy were available. The patients were randomly assigned to receive either intravenous nerinetide in a single dose of 2.6 mg/kg or saline placebo at the time of thrombectomy.

Patients were stratified by intravenous alteplase treatment and by declared endovascular device choice.

The primary outcome was a favorable functional outcome 90 days after randomization, defined as an mRS score of 02. In the main analysis of the whole population, this favorable outcome was achieved for 61.4% of the group that received nerinetide and for 59.2% of the placebo group, a nonsignificant difference. Secondary outcomes were also similar between the two groups.

But an exploratory analysis showed evidence that nerinetide's treatment effect was modified by alteplase treatment.

Among the patients who did not receive alteplase, use of nerinetide was associated with improved outcomes, whereas no benefit was found in the alteplase stratum. The difference in absolute risk slightly but not significantly favored placebo.

In the stratum that did not receive alteplase (40% of the trial population), the favorable mRS outcome was achieved by 59.3% of patients who received nerinetide, compared with 49.8% of those given placebo a significant difference (adjusted risk ratio, 1.18; 95% confidence interval, 1.01 1.38).

There was also a 7.5% absolute risk reduction in mortality at 90 days post treatment with nerinetide for the patients who did not receive thrombolysis. This resulted in an approximate halving of the hazard of death (adjusted hazard ratio, 0.56).

In addition, infarct size was reduced in those patients who received nerinetide but not thrombolysis.

Among the patients who received alteplase, the proportion of patients who achieved an mRS of 02 wassimilar between groups, as were median infarct volumes.

The observed treatment effect modification by alteplase was supported by reductions in peak plasma nerinetide concentrations in the alteplase stratum, the researchers report.

They say that the combination of the clinical results in the no-thrombolytic stratum and subsequent tests documenting that nerinetide is broken down by plasmin (which is generated by alteplase) "provide evidence that the clinical observation of effect modification is not a chance finding." But they add: "This novel observation will require additional confirmation, and we cannot draw a definitive conclusion on treatment effect in this study."

There is still more work to do, Hill said. "We don't fully understand the pharmacology, and we will certainly have to do another trial, but we believe this agent is going to shake the field up.

"This is a totally new drug, and we have to think carefully about where it could fit in," he said. "The obvious first group is those patients who do not receive thrombolysis. This is a large group, as most patients do not present in time for thrombolysis. Then we can work on the biochemistry and see if we can develop a version of nerinetide that is resistant to breakdown by thrombolysis."

Another possibility would be to withhold thrombolysis and give nerinetide instead. "It may be that thrombolysis is not needed if patients are receiving thrombectomy this is being suggested now in initial studies," Hill stated.

They also chose a very select group of patients those undergoing thrombectomy, who represent only 10% to 15% of stroke patients. "We have to work out how to expand that population," he said.

Hill noted that there have been many examples in the past of potential neuroprotectantagents that have worked in animal models of ischemia-reperfusion but that failed in humans with acute stroke.

"Until recently, we have not had a reliable ischemia-reperfusion model in humans, but now with endovascular therapy, we have a situation where the blood flow is reliably restored, which is an ideal situation to test new neuroprotectant agents. That may be another factor that has contributed to our positive findings," he said.

In an accompanying comment in the Lancet, Graeme J. Hankey, MD, the University of Western Australia, Perth, notes that although endovascular thrombectomy after use of intravenous alteplase improves reperfusion and clinical outcomes for a fifth of patients with ischemic stroke caused by large-artery occlusion, half of patients do not recover an independent lifestyle. Cytoprotection aims to augment the resilience of neurons, neurovascular units, and white matter during ischemia until perfusion is restored.

Hankey also points out that numerous cytoprotection strategies have been reported to reduce brain infarction in preclinical models of ischemic stroke but have not been found to improve clinical outcomes in clinical trials involving patients with ischemic stroke.

The advent of thrombectomy provides an opportunity to reassess cytoprotection as an adjunctive therapy for patients with types of temporary brain ischemia that align more closely with successful preclinical models of ischemia, cytoprotection, and reperfusion, he adds.

On the results of the current study and the benefit in the no-thrombolysis group, Hankey states: "Although this result might be a chance finding or confounded by the indication for alteplase, complementary pharmacokinetic data in a small number of patients treated with nerinetide showed that alteplase lowered plasma concentrations of nerinetide, probably by converting plasminogen to plasmin, which cleaves peptide bonds not only in fibrin but also in the eicosapeptide nerinetide."

He says the ESCAPE-NA1 trial "informs the study of cytoprotection as an adjunct therapy to reperfusion in acute ischemic stroke" and suggests that researchers who have reported encouraging results of other cytoprotective therapies for ischemic stroke should test their compounds for interactions with concurrent thrombolytic therapies.

The ESCAPE-NA1 trial was sponsored by NoNO, the company developing nerinetide. Hill has received grants from NoNO for the conduct of the study, is named on a US patent for systems and methods for assisting in decision making and triaging for acute stroke patients, and owns stock in Calgary Scientific. Other coauthors are employees of NoNO or have stock options in the company. Hankey has received personal honoraria from the American Heart Association, AC Immune, Bayer, Bristol-Myers Squibb, and Medscape outside the area of work that he commented on.

International Stroke Conference (ISC) 2020: Abstract LB2. Presented February 20, 2020.

Lancet. Published online February 20. Abstract, Comment

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First Clinical Evidence of Neuroprotection in Acute Stroke? - Medscape

Biochemistry

Teacher, 26, died after accidentally taking too many painkillers and being told to make her own way to hospital – Telegraph.co.uk

A young science teacher who dialled 999 after complaining she could barely walk died just hours later after an operator mistakenly advised her to make her own way to A&E, an inquest heard.

Amber Hickford, 26, said she was experiencing dizziness and blurred vision after falling into a bedside cabinet, but her 999 call was "coded" incorrectly on the scale of the emergency and no ambulance was sent to her address.

Instead Miss Hickford was advised to take herself to hospital, which involved navigating two flights of stairs. But she refused to go despite being offered help by her boyfriend, Jason Hanmer.

Miss Hickford tried to sleep it off, but when Mr Hanmer found her unresponsive in bed around 99 minutes later, he called 999 again. He began CPR while an ambulance was dispatched to their apartment in Rochdale, Greater Manchester.

Three ambulances arrived at the property within 10 minutes of Mr Hanmer's call being made but Miss Hickford was pronounced dead shortly afterwards. Tests showed she had inadvertently taken a toxic level of paracetamol for severe stomach pains she had been experiencing following a urinary infection.

Inquiries revealed she had been discharged from hospital just two days earlier and given stronger codeine painkillers. The call handler who fielded Miss Hickford's 999 call has since been given "feedback" over the error.

The inquest was told Miss Hickford, who taught at Oulder Hill Community School in Rochdale, had been "extremely caring" and "always put other people's needs before her own". After attaining a 2:1 in biochemistry at Leeds University, she passed her teaching exams and undertook voluntary work for Barnado's children's charity.

The tragic events began on April 19 last year after Miss Hickford was admitted to Fairfield Hospital in Bury with stomach problems. Doctors gave her codeine and sent her home, with advice to attend a follow-up appointment. But on April 21, she rang the NHS 111 service at around 8.40pm saying she was struggling to walk.

Mr Hanmer told the inquest in Heywood: "As I got home Amber was sat in the hallway, and she said she was feeling drowsy. I made her tea, but later that evening she fell into a shoe cabinet and into the bedside table.

"She couldn't walk at all and went drowsy every time she stood up. I could tell she was very unsteady. I rang 111, and the operator said they would not to talk to me and asked to speak to Amber herself.

"They told her to ring 999, but when she rang, the call handler told her to go to A&E. We live up two flights of stairs and I couldn't get her down safely by myself. Her parents arrived but Amber stated that she didn't want to go to the hospital and her parents left.

"I went out to move my car and went straight back to the bedroom and Amber was in there making snoring noises.

"I moved her on to her side and was only gone again 10 minutes before I went back to check on her. I shouted out but didn't get a response and rushed over to her, and she was cold. I listened to see but she wasn't breathing.

"I pulled her on to the floor and called 999, and they talked me through CPR. The paramedics arrived and then came into the room but said Amber wasn't breathing and her heart had stopped and machines were doing it for her. They called another ambulance for help getting her downstairs. Amber passed away later in hospital. We had been together for two years."

Miss Hickford's father, Neil, said: "She had mentioned that she did have some stomach pains but she had just started a new job and felt some of that might be down to nerves.

"At around 9pm that evening, Jay rang saying they had called the emergency services and asked us to help him convince Amber to go to hospital as she wasn't listening to him.

"When we got there, Amber was standing and dressed but still didn't want to go to hospital. We stayed there until around 10pm, and we were almost home and Jay phoned again around 10.20pm saying he had rung the ambulance and wanted us to go back. There were three ambulances outside, and the paramedics were working on Amber on the floor in the bedroom. It was devastating to be told she could not be resuscitated.

"Amber was a science teacher and would be aware of the nature of the medication she was taking and the effects that may have. She would never have knowingly taken more than she should have."

Angela Lee, Deputy Sector Manager for the North West Ambulance Service, said: "On April 21, an emergency call was received, and although Amber's abdominal pain seemed to have subsided, she was now struggling to walk and experiencing dizziness, drowsiness and blurred vision when stood.

"At 10.24pm - around two hours later - a further call was received from Amber and three emergency response vehicles were allocated.

"The initial emergency call was coded a category four but should have been coded as a category two response. When I listened to the emergency call, I didn't hear anything that gave me cause for concern that it was coded correctly, but if the call had been categorised as a category two, there may have been an emergency ambulance to attend to Amber.

"The call handler who handled the call has received feedback, which revolved around a one-to-one session."

When questioned by Amber's family about why the callhandler had not dispatched an ambulance following the first 999 call, Ms Lee said: "They have a couple of seconds to make that decision and it's a very difficult task. The call was passed to a clinician who spoke to Jay and then to Amber and the clinician gave the advice to attend the emergency department."

Coroner Michael Salt adjourned the hearing for further inquiries but said: "I accept that the call was coded incorrectly. I need to know more about the potential effect of the delay in the arrival of the ambulance and what could have been achieved in the time - that seems to me at least an hour and 36 minutes.

"I have heard about the way in which the categorisation error came about in a very difficult situation. A judgement needs to be made very quickly, and I don't in any way criticise the call taker.

"The question is whether something could have been achieved in the time that might have been available. The important thing is to try to find out whether the delay contributed to death and whether it was a missed opportunity."

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Teacher, 26, died after accidentally taking too many painkillers and being told to make her own way to hospital - Telegraph.co.uk

Anatomy

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Anatomy

Fund Drive Special The Anatomy of Fascism – KPFA – 94.1FM

Robert Paxton talks about the history of fascism and why it is relevant in contemporary America. Paxton is a political scientist and historian specializing in the World War II era. He is a professor emeritus at Columbia University.

BOOK: Anatomy of Fascism $100

Book: Tyrant: Shakespeare on Politics by Stephen Greenblatt $100

Book: Barracoon: The Story of the Last Black Cargo Edited by Deborah Plant $100

COMBO: All three books $250

Letters and Politic The Tyranny Pack MP3 CD $100

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Fund Drive Special The Anatomy of Fascism - KPFA - 94.1FM

Anatomy

Greys Anatomy-season 16: one knows when will be released the series on TF1 ! – The Saxon

Season 16 of Greys Anatomy arrives soon on TF1. More is known about its release date and it tells you everything !

The 16th season of Greys Anatomy arrives soon on our small screens. Heres what we know about its release date on TF1.

Season 16 of Greys Anatomy will soon be broadcasted on TF1. It was about time ! In fact, in the United States they are already at the 14th episode of the 16th season. It is well overdue ! In France, Meredith and his small band are conspicuously absent. But the wait is soon over. What good news !

For those who follow Greys Anatomy in French, TF1 will broadcast the first episodes of the last season from the 11th of march next. Always from 21h05. Save the date ! What to bring joy to the fans of the series medical.

We cant wait to discover the new adventures of our surgeons preferred ! Moreover, it seems that there is going to be bustle. You do not remember the end of season 15 ? No worries, you refreshes the memory. Bailey vire Meredith, Alex and Richard to the result of an insurance fraud. It is not all ! Deluca has also been found in prison after being denounced. Season 16 of Greys Anatomy will bring lot of change for everyone. We cant wait !

Also, during the last few episodes aired on TF1, a thick fog descended on Seattle after a storm. Maggie had also lost Jackson after yet another argument between the two. However, the intrigue surrounding his disappearance will be quickly raised. The other hand, it will also detect the breakage of the two surgeons. Some reconciliations will be expected to be in the coming episodes of Greys Anatomy. As well as a love story. Suspense ! New heads are also added to the cast. We wont say no more. See you march 11 at 21h05 on TF1 to discover more !

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Greys Anatomy-season 16: one knows when will be released the series on TF1 ! - The Saxon

Embryology

4-H Incubation and Embryology Program – News – New Jersey Herald

WednesdayFeb19,2020at2:00AM

MIDDLETOWN Orange County 4-H is looking for schools to participate in the 2020 Incubation and Embryology Program. They are looking for classrooms in grades one through three to spend twenty-five days learning all about the importance of incubation and embryology. Teachers and students will participate in this great hands-on science activity and physically watch the transformation of embryo to chick. Classrooms will be able to explore and learn all about the life cycle, a vital curriculum in their grade levels through the world of feathers.

Two free training sessions will be offered at Cornell Cooperative Extension Orange County located at 18 Seward Avenue, Suite 300, Middletown. Training will be offered on March 4 starting at 4 p.m. and March 9 starting at 6:30 p.m.

In the training you will be given a sample of the activities and materials that 4-H can provide for your group of youth. Then explore and discuss the world of incubation and embryology and how your club or class can be a part of the hatching madness. The session will finish with exploring the package offered by Orange County 4-H to your classroom. Our program is called Incubation with your Teachers.

Projects and packages run from April- June in twenty-five day sessions, however please note that space is limited.

If your school district or classroom is interested in taking part in the hatching madness, call 344-1234 or email mms426@cornell.edu by March 3.

For more information call Cornell Cooperative Extension Orange County at 344-1234 or visit cceorangecounty.org.

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4-H Incubation and Embryology Program - News - New Jersey Herald