thescientist--2020-10-21--Scientists Discover New Human Salivary Glands

ABOVE : A 3-D reconstruction from histological slides ( inset on right ) of the newly discovered tubarial gland ( yellow ; ducts in light blue ) .
The torus tubarius cartilage is colored dark blue and muscle is pink .
M. Valstar et al.
, Radiotherapy & Oncology , doi:10.1016/j.radonc.2020.09.034 , 2020 .
Doctors don ’ t regularly come across undiscovered bits of human anatomy , but a team of physicians recently reported a never-before-described set of salivary glands in patients ’ necks .
The first hint of this new gland emerged while Wouter Vogel , a radiation oncologist @ @ @ @ @ @ @ ) , was probing for damage to salivary glands after radiotherapy for cancer in the head , neck , or brain—injuries that can lead to issues such as problems with digestion , speech , and an increase in oral infections .
While going through these scans , he found something usual .
Vogel was using a new technique for detecting cells in the salivary glands—PSMA PET/CT , a form of combined positron emission tomography ( PET ) and computed tomography ( CT ) that uses a radioactive tracer that binds to a prostate-specific @ @ @ @ @ @ @ method is typically used to detect prostate cancer , but in a prior study , Vogel and his colleagues had found that it also labels salivary gland cells , where PSMA is also expressed .
Humans have three major salivary glands and approximately 1,000 minor ones .
“ This scan is extremely sensitive for the salivary glands , ” Vogel says .
“ So we can see more than ever before.
” What he saw was an unexpectedly high level of labeling in the upper section of the throat known as the nasopharynx @ @ @ @ @ @ @ supposed to be found .
When Vogel first observed the unanticipated signal , he says he was confused—salivary gland cells were not thought to be abundant in this location .
Immediately , he sought a second opinion from his colleague Matthijs Valstar , an oral and maxillofacial surgeon at the NCI .
“ You never believe something until you have some feedback from others , ” Vogel tells The Scientist .
“ But we agreed that it really was an unexpected and significant signal that requires further investigation.
” To examine further , @ @ @ @ @ @ @ more than a dozen researchers from NCI and three other medical centers in the Netherlands .
Together , they went through the PSMA PET/CT scans of more than 100 patients with prostate or urethral gland cancer and found similar signals in the nasopharynx region in those individuals as well .
This assessment also revealed that the glands existed as a pair and had an average length of four centimeters .
The group then dissected two human cadavers to confirm that this was , indeed , salivary gland tissue .
They dubbed these newly @ @ @ @ @ @ @ ” based on their location above the torus tubarius , the section of the nasopharynx just behind the pharynx .
These findings appeared last week ( October 16 ) in Radiotherapy & Oncology .
According to Vogel , there are likely two main reasons the tubarial glands haven ’ t been found before : researchers had not previously used PSMA PET/CT to look for salivary glands , and the newly discovered glands are located in a region that ’ s hard to access with standard surgical procedures .
“ With the other salivary @ @ @ @ @ @ @ by either with your hand or see them during surgery , ” Vogel explains .
“ The location we ’ re describing now , you can only see it with a nasal endoscopy.
” Nasal endoscopy is a method in which a tube with a tiny camera and light are used to image the nose and sinuses .
Based on the tubarial glands ’ similarities to the volume and draining system of the sublingual gland—one of the three major salivary glands—the authors suggest that the new glands should be classified as a fourth @ @ @ @ @ @ @ note that some might disagree with this categorization , because the new glands share similarities with minor glands as well .
Because salivary glands are at risk of damage from radiotherapy , the team also set out to investigate whether radiotherapy exposure to the tubarial glands would affect patients .
After examining data from a cohort of more than 700 head and neck cancer patients , they reported that the radiotherapy dose to the gland area was associated with dry mouth and swallowing difficulties after treatment .
Vincent Vander Poorten , an otorhinolaryngologist @ @ @ @ @ @ @ ) in Belgium who was not involved in this study but has collaborated with the authors on other projects , says that while he agrees that the authors have found a new cluster of minor glands , whether the tubarial gland is truly a separate , major gland is somewhat controversial .
“ Of course , you could say that it ’ s just a cluster of minor salivary glands that are all over the place in the mucous membranes of the head and neck.
” “ I don ’ t think there @ @ @ @ @ @ @ tissue that has been discovered.
” Chris Nutting , an oncologist at the Royal Marsden Hospital in the UK who was not involved in this study , tells The Scientist .
“ One of the areas that we are very keen on pursuing is trying to identify salivary tissue and avoiding it because it causes one of the main complications of radiotherapy.
” The question is how much sparing this gland will actually improve patient outcomes , he adds .
The authors conducted a retrospective study , which looks back at previously collected @ @ @ @ @ @ @ study , which enrolls participants and observes the outcomes of an exposure over time , will be important .
Vogel , too , notes that whether radiotherapy to spare the tubarial glands will actually make a difference in patient outcomes is an open question .
“ That is the reason that we can not just implement this new finding into treatment today , ” he adds .
“ We have to do prospective evaluations to see if it really helps patients .
This is something that we envision [ doing in ] the @ @ @ @ @ @ @ , “ The tubarial salivary glands : A potential new organ at risk for radiotherapy , ” Radiotherapy & Oncology , doi:10.1016/j.radonc.2020.09.034 , 2020 .

ABOVE: A 3-D reconstruction from histological slides (inset on right) of the newly discovered tubarial gland (yellow; ducts in light blue). The torus tubarius cartilage is colored dark blue and muscle is pink.
M. Valstar et al., Radiotherapy & Oncology, doi:10.1016/j.radonc.2020.09.034, 2020.
Doctors don’t regularly come across undiscovered bits of human anatomy, but a team of physicians recently reported a never-before-described set of salivary glands in patients’ necks. The first hint of this new gland emerged while Wouter Vogel, a radiation oncologist at the Netherlands Cancer Institute (NCI), was probing for damage to salivary glands after radiotherapy for cancer in the head, neck, or brain—injuries that can lead to issues such as problems with digestion, speech, and an increase in oral infections. While going through these scans, he found something usual.
Vogel was using a new technique for detecting cells in the salivary glands—PSMA PET/CT, a form of combined positron emission tomography (PET) and computed tomography (CT) that uses a radioactive tracer that binds to a prostate-specific membrane antigen (PSMA). This method is typically used to detect prostate cancer, but in a prior study, Vogel and his colleagues had found that it also labels salivary gland cells, where PSMA is also expressed. Humans have three major salivary glands and approximately 1,000 minor ones. “This scan is extremely sensitive for the salivary glands,” Vogel says. “So we can see more than ever before.”
What he saw was an unexpectedly high level of labeling in the upper section of the throat known as the nasopharynx, where only minor salivary glands are supposed to be found.
When Vogel first observed the unanticipated signal, he says he was confused—salivary gland cells were not thought to be abundant in this location. Immediately, he sought a second opinion from his colleague Matthijs Valstar, an oral and maxillofacial surgeon at the NCI. “You never believe something until you have some feedback from others,” Vogel tells The Scientist. “But we agreed that it really was an unexpected and significant signal that requires further investigation.”
I don’t think there is any doubt this is new salivary tissue that has been discovered. —Chris Nutting, Royal Marsden Hospital
To examine further, Vogel and Valstar assembled a team of more than a dozen researchers from NCI and three other medical centers in the Netherlands. Together, they went through the PSMA PET/CT scans of more than 100 patients with prostate or urethral gland cancer and found similar signals in the nasopharynx region in those individuals as well. This assessment also revealed that the glands existed as a pair and had an average length of four centimeters. The group then dissected two human cadavers to confirm that this was, indeed, salivary gland tissue. They dubbed these newly identified glands as “tubarial glands,” based on their location above the torus tubarius, the section of the nasopharynx just behind the pharynx. These findings appeared last week (October 16) in Radiotherapy & Oncology.
According to Vogel, there are likely two main reasons the tubarial glands haven’t been found before: researchers had not previously used PSMA PET/CT to look for salivary glands, and the newly discovered glands are located in a region that’s hard to access with standard surgical procedures. “With the other salivary glands, you can just feel them by either with your hand or see them during surgery,” Vogel explains. “The location we’re describing now, you can only see it with a nasal endoscopy.” Nasal endoscopy is a method in which a tube with a tiny camera and light are used to image the nose and sinuses. Based on the tubarial glands’ similarities to the volume and draining system of the sublingual gland—one of the three major salivary glands—the authors suggest that the new glands should be classified as a fourth major gland. However, they also note that some might disagree with this categorization, because the new glands share similarities with minor glands as well.
Because salivary glands are at risk of damage from radiotherapy, the team also set out to investigate whether radiotherapy exposure to the tubarial glands would affect patients. After examining data from a cohort of more than 700 head and neck cancer patients, they reported that the radiotherapy dose to the gland area was associated with dry mouth and swallowing difficulties after treatment.
Vincent Vander Poorten, an otorhinolaryngologist at University Hospital Leuven (UZ Leuven) in Belgium who was not involved in this study but has collaborated with the authors on other projects, says that while he agrees that the authors have found a new cluster of minor glands, whether the tubarial gland is truly a separate, major gland is somewhat controversial. “Of course, you could say that it’s just a cluster of minor salivary glands that are all over the place in the mucous membranes of the head and neck.”
See “New Discoveries in Human Anatomy”
“I don’t think there is any doubt this is new salivary tissue that has been discovered,” Chris Nutting, an oncologist at the Royal Marsden Hospital in the UK who was not involved in this study, tells The Scientist. “One of the areas that we are very keen on pursuing is trying to identify salivary tissue and avoiding it because it causes one of the main complications of radiotherapy.” The question is how much sparing this gland will actually improve patient outcomes, he adds. The authors conducted a retrospective study, which looks back at previously collected data, but Nutting says a prospective study, which enrolls participants and observes the outcomes of an exposure over time, will be important.
Vogel, too, notes that whether radiotherapy to spare the tubarial glands will actually make a difference in patient outcomes is an open question. “That is the reason that we cannot just implement this new finding into treatment today,” he adds. “We have to do prospective evaluations to see if it really helps patients. This is something that we envision [doing in] the coming years.”
Antoni Van Leeuwenhoek
M. Valstar et al., “The tubarial salivary glands: A potential new organ at risk for radiotherapy,” Radiotherapy & Oncology, doi:10.1016/j.radonc.2020.09.034, 2020.


thescientist--2020-10-21--Book Excerpt from The Nature of Fear

Book Excerpt from The Nature of Fear

My journey to understand the nature of fear began in 1986 , in Kenya .
After spending a month studying monkey behavior in Kakamega National Park , a spectacular remnant of the West African rain forests , I took a train to Nairobi , then to Mombasa , and started the first long leg of a cycling trip .
My mountain bike was overloaded .
A sleeping bag was secured to the top of the rear rack and a tent tied to the top of the front rack .
My bike was wobbly and the road was bumpy , so @ @ @ @ @ @ @ sandy roadside as I cycled toward Tanzania .
Unlike the trans-African highway or streets around Nairobi , this road felt reasonably safe .
There was little traffic .
Periodically , a heavily laden lorry or an occasional bus passed by , belching black diesel exhaust .
Late in the afternoon I was pedaling slowly up a long , straight hill at that interminable speed every cyclist knows—moving , but barely faster than a walk .
Ahead I saw three young men squatting on the side of the road .
As I approached , @ @ @ @ @ @ @ ( “ hello ” in Swahili ) .
One of the men was hunched over as I passed , just a few feet away , and I saw out of the side of my eye a glare from another .
A split second later a rock the size of a soccer ball hurtled toward my head , thrown by one of the men .
I ducked , putting up a shoulder to block the rock .
Astonishingly , even though my mountain bike was so heavy , I was not knocked over .
@ @ @ @ @ @ @ The rock struck a shoulder I ’ d dislocated only a few weeks prior .
With a grimace of pain , I turned to look behind me and saw the men sprinting toward me .
Adrenalin surged through my body .
I pedaled furiously .
Somehow , I found the strength to cycle up the hill and escape .
I kept riding .
A few miles later , I heard a truck behind me .
Unsure of whether the men would be on the truck , or if someone on the truck might @ @ @ @ @ @ @ making my decision .
I jumped off my bike and stood , gasping , in the middle of the road , waving frantically .
Thankfully , the driver and his passenger stopped .
I explained what had happened and asked for a ride .
They hoisted my bike into the back of the truck and told me that the area was very dangerous .
People were frequently attacked by thieves .
I was still shaking with after-effects of the adrenaline when they dropped me off after a few miles .
After thanking them @ @ @ @ @ @ @ along a sandy track .
The next day , despite the spectacular location , the coral reef I explored , and the delicious fresh fish that I ate , I found it difficult to relax .
My thoughts kept returning to the event .
Long after the adrenaline response gave my body the energy to pedal away and survive , fear continued to occupy my thoughts .
I looked at strangers with a newfound apprehension , worried about cycling alone .
I was no longer confident in my ability to estimate the risks @ @ @ @ @ @ @ to tuck this experience away at the back of my mind , I still had many questions about it .
Why did it affect me so profoundly—both physically and psychologically ?
I was genuinely afraid that I was going to be severely beaten or killed .
I ’ d not had such an intense , fearful experience like that before .
It was a sharp departure from my day-to-day emotional responses .
The surge of adrenaline was overpowering , but it was also empowering ; it likely saved my life !
What happened @ @ @ @ @ @ @ surge ?
How did this massive physiological response come about ?
What other sorts of events could elicit it ?
Why did I keep replaying this traumatic event in my mind ?
Can events like this trigger recurring nightmares and post-traumatic consequences ?
How long should I have let this influence my behavior ?
To understand why I responded the way I did , but more importantly , to understand why we , as humans , respond to fearful situations , we must understand our evolutionary history .
Over millions of years fear @ @ @ @ @ @ @ human ancestors but our nonhuman ancestors too .
My adrenaline response had its origins about 550 million years ago in the evolution of specialized nervous systems in worms .
This specialization required a variety of neurochemicals to selectively modulate and coordinate activity , such as the control of responses to life-threatening experiences and situations .
Whether balling up to hide or slithering away from a threat , animals evolved the ability to have more complex and , ultimately , conditional escape behavior .
About 250 million years ago , the origin of sociality @ @ @ @ @ @ @ much like predators , threatened an individual ’ s ability to survive and reproduce .
These social stressors included dominant individuals within a social group .
The costs of being subordinate involved losing access to food and other important resources .
Humans must account for more subtle social stressors in the survival and reproduction equation , like the risk of losing socioeconomic status or status among friends .
Social position is related to the ability to access resources to care for yourself and your family .
Even though these stressors may seem far @ @ @ @ @ @ @ with what it has rather than creating entirely de novo traits .
When social threats arise , they engage some of the same physiological and psychological systems that previously ensured safety from predators .
Thus it is reasonable to assert that it was the evolution of the ability to deal with predatory threats that generated a suite of chemicals and stress responses , as well as fears and anxieties , that enabled our ancestors to survive and reproduce .
In other words , we humans are the descendants of a long line of @ @ @ @ @ @ @ Our primate lineage diverged from its tree shrew–like ancestors about 55–65 million years ago , and our most recent ancestors are the chimpanzees and bonobos , from which we diverged about 7 million years ago .
Our primate ancestors inherited the physiological abilities to respond appropriately to threats from their ancestors , and those ancestors inherited skills from the ancestors that preceded them .
Thus , after generations and generations we have a wonderfully diverse set of antipredator adaptations , including neurochemical , behavioral , physical , and lifehistory responses .
Many of @ @ @ @ @ @ @ specialized nervous system .
We can view our fears and our responses to fearful situations as part of the great tapestry of life that both preceded us and surrounds us .
And , just as we learn from evolutionary history , I believe that we can learn a great deal by observing the life around us today .
Excerpt adapted from The Nature of Fear : Survival Lessons from the Wild by Daniel T. Blumstein , published by Harvard University Press .
Copyright © 2020 by the President and Fellows of Harvard College @ @ @ @ @ @ @ reserved .

My journey to understand the nature of fear began in 1986, in Kenya. After spending a month studying monkey behavior in Kakamega National Park, a spectacular remnant of the West African rain forests, I took a train to Nairobi, then to Mombasa, and started the first long leg of a cycling trip. My mountain bike was overloaded. A sleeping bag was secured to the top of the rear rack and a tent tied to the top of the front rack. My bike was wobbly and the road was bumpy, so I straddled the line between tarmac and sandy roadside as I cycled toward Tanzania. Unlike the trans-African highway or streets around Nairobi, this road felt reasonably safe. There was little traffic. Periodically, a heavily laden lorry or an occasional bus passed by, belching black diesel exhaust.
Late in the afternoon I was pedaling slowly up a long, straight hill at that interminable speed every cyclist knows—moving, but barely faster than a walk. Ahead I saw three young men squatting on the side of the road. As I approached, I greeted them with an enthusiastic jambo (“hello” in Swahili). One of the men was hunched over as I passed, just a few feet away, and I saw out of the side of my eye a glare from another. A split second later a rock the size of a soccer ball hurtled toward my head, thrown by one of the men. I ducked, putting up a shoulder to block the rock. Astonishingly, even though my mountain bike was so heavy, I was not knocked over. But I was hurt and scared. The rock struck a shoulder I’d dislocated only a few weeks prior. With a grimace of pain, I turned to look behind me and saw the men sprinting toward me.
Adrenalin surged through my body. I pedaled furiously. Somehow, I found the strength to cycle up the hill and escape. I kept riding. A few miles later, I heard a truck behind me. Unsure of whether the men would be on the truck, or if someone on the truck might help me, I hesitated—just a moment—before making my decision. I jumped off my bike and stood, gasping, in the middle of the road, waving frantically. Thankfully, the driver and his passenger stopped. I explained what had happened and asked for a ride. They hoisted my bike into the back of the truck and told me that the area was very dangerous. People were frequently attacked by thieves. I was still shaking with after-effects of the adrenaline when they dropped me off after a few miles. After thanking them profusely, I rode toward Tiwi Beach along a sandy track.
The next day, despite the spectacular location, the coral reef I explored, and the delicious fresh fish that I ate, I found it difficult to relax. My thoughts kept returning to the event. Long after the adrenaline response gave my body the energy to pedal away and survive, fear continued to occupy my thoughts. I looked at strangers with a newfound apprehension, worried about cycling alone. I was no longer confident in my ability to estimate the risks I was taking.
While I attempted to tuck this experience away at the back of my mind, I still had many questions about it. Why did it affect me so profoundly—both physically and psychologically? I was genuinely afraid that I was going to be severely beaten or killed. I’d not had such an intense, fearful experience like that before. It was a sharp departure from my day-to-day emotional responses. The surge of adrenaline was overpowering, but it was also empowering; it likely saved my life! What happened to my body when I had this surge? How did this massive physiological response come about? What other sorts of events could elicit it? Why did I keep replaying this traumatic event in my mind? Can events like this trigger recurring nightmares and post-traumatic consequences? How long should I have let this influence my behavior?
To understand why I responded the way I did, but more importantly, to understand why we, as humans, respond to fearful situations, we must understand our evolutionary history. Over millions of years fear has kept our ancestors alive—not only our human ancestors but our nonhuman ancestors too.
My adrenaline response had its origins about 550 million years ago in the evolution of specialized nervous systems in worms. This specialization required a variety of neurochemicals to selectively modulate and coordinate activity, such as the control of responses to life-threatening experiences and situations. Whether balling up to hide or slithering away from a threat, animals evolved the ability to have more complex and, ultimately, conditional escape behavior.
About 250 million years ago, the origin of sociality in termites introduced social stressors that, much like predators, threatened an individual’s ability to survive and reproduce. These social stressors included dominant individuals within a social group. The costs of being subordinate involved losing access to food and other important resources. Humans must account for more subtle social stressors in the survival and reproduction equation, like the risk of losing socioeconomic status or status among friends. Social position is related to the ability to access resources to care for yourself and your family. Even though these stressors may seem far removed from escape behavior, evolution works with what it has rather than creating entirely de novo traits. When social threats arise, they engage some of the same physiological and psychological systems that previously ensured safety from predators. Thus it is reasonable to assert that it was the evolution of the ability to deal with predatory threats that generated a suite of chemicals and stress responses, as well as fears and anxieties, that enabled our ancestors to survive and reproduce.
In other words, we humans are the descendants of a long line of fearful ancestors who successfully survived predators. Our primate lineage diverged from its tree shrew–like ancestors about 55–65 million years ago, and our most recent ancestors are the chimpanzees and bonobos, from which we diverged about 7 million years ago. Our primate ancestors inherited the physiological abilities to respond appropriately to threats from their ancestors, and those ancestors inherited skills from the ancestors that preceded them. Thus, after generations and generations we have a wonderfully diverse set of antipredator adaptations, including neurochemical, behavioral, physical, and lifehistory responses. Many of these stem from the beginning of a specialized nervous system. We can view our fears and our responses to fearful situations as part of the great tapestry of life that both preceded us and surrounds us. And, just as we learn from evolutionary history, I believe that we can learn a great deal by observing the life around us today.
Excerpt adapted from The Nature of Fear: Survival Lessons from the Wild by Daniel T. Blumstein, published by Harvard University Press. Copyright © 2020 by the President and Fellows of Harvard College. Used by permission. All rights reserved.


thescientist--2020-10-22--Mexican Senate Votes to Cut Research Funding, Disaster Relief

The Mexican Senate voted on Wednesday ( October 21 ) to pass a bill that cuts funding from 109 public trust funds , which the government pays into .
These accounts provide consistent funding , unrelated to the national budget .
About one-third of the $ 68 billion pesos ( $ 2.5 billion US ) from the government that would ordinarily go into these trusts each year supports scientific research , and the rest is for sports , health initiatives , protections for journalists , and disaster relief .
As the Associated Press reports , Mexican President Andrés Manuel López @ @ @ @ @ @ @ April , citing widespread corruption and doubt that the funds actually reach and benefit Mexican citizens .
López Obrador has also said that the money is needed to support the country ’ s response to the COVID-19 pandemic and that his administration inherited a lot of debt when he took office in 2018 .
According to The Guardian , $ 3 billion pesos have been earmarked for pandemic response , among other reallocations .
Opponents of the bill have expressed worry that this is a power move intended to make researchers more reliant @ @ @ @ @ @ @ with political change and do not provide the stability of the trusts .
“ [ López Obrador ] has always referred to scientists as if we were a privileged group that lives in the comfort of our cubicles , enjoying advantages and far away from reality , ” Antonio Lazcano , an evolutionary biologist at the National Autonomous University of Mexico , told Science earlier this month .
“ [ Public trusts are ] clearly necessary for many scientific projects but also for keeping the arts going , and having a trust fund @ @ @ @ @ @ @ like a no-brainer—but go figure , ” Beatriz Rumbos , a mathematician at the Instituto Tecnológico Autonomo de México , tells Times Higher Education earlier in October .
The loss of the trusts will be an incredible hardship , some scientists claim .
“ It ’ s as if we were going back 20 , 40 years , ” María del Carmen Robles Domínguez , a chemist at the Center for Research and Advanced Studies , tells Science .
According to Mexico News Daily , many opponents of the cuts have taken to @ @ @ @ @ @ @ using the hashtag , # MásCienciaMenosObediencia , meaning “ more science , less obedience .
”

ABOVE: © ISTOCK.COM,
AGCUESTA
The Mexican Senate voted on Wednesday (October 21) to pass a bill that cuts funding from 109 public trust funds, which the government pays into. These accounts provide consistent funding, unrelated to the national budget. About one-third of the $68 billion pesos ($2.5 billion US) from the government that would ordinarily go into these trusts each year supports scientific research, and the rest is for sports, health initiatives, protections for journalists, and disaster relief.
As the Associated Press reports, Mexican President Andrés Manuel López Obrador called for the cuts back in April, citing widespread corruption and doubt that the funds actually reach and benefit Mexican citizens. López Obrador has also said that the money is needed to support the country’s response to the COVID-19 pandemic and that his administration inherited a lot of debt when he took office in 2018. According to The Guardian, $3 billion pesos have been earmarked for pandemic response, among other reallocations.
Opponents of the bill have expressed worry that this is a power move intended to make researchers more reliant on annual appropriations, which could fluctuate with political change and do not provide the stability of the trusts.
“[López Obrador] has always referred to scientists as if we were a privileged group that lives in the comfort of our cubicles, enjoying advantages and far away from reality,” Antonio Lazcano, an evolutionary biologist at the National Autonomous University of Mexico, told Science earlier this month.
“[Public trusts are] clearly necessary for many scientific projects but also for keeping the arts going, and having a trust fund for attending natural disasters seems to me like a no-brainer—but go figure,” Beatriz Rumbos, a mathematician at the Instituto Tecnológico Autonomo de México, tells Times Higher Education earlier in October.
The loss of the trusts will be an incredible hardship, some scientists claim. “It’s as if we were going back 20, 40 years,” María del Carmen Robles Domínguez, a chemist at the Center for Research and Advanced Studies, tells Science.
According to Mexico News Daily, many opponents of the cuts have taken to social media to voice their concerns, using the hashtag, #MásCienciaMenosObediencia, meaning “more science, less obedience.”


thescientist--2020-10-22--Traceable, Reliable, and Reproducible Science: TRACKMAN® Connected

TRACKMAN® Connected is a tablet with accessories and apps that makes pipetting faster and more verifiable , which improves reliability @ @ @ @ @ at the bench .

TRACKMAN® Connected is a tablet with accessories and apps that makes pipetting faster and more verifiable, which improves reliability, traceability, and reproducibility at the bench.


thescientist--2020-10-22--Proteintech Acquires ChromoTek, Expanding its Next Generation Antibody Tools

ChromoTek is the market leader in nanobodies — high-performance recombinant reagents used for breakthrough research discoveries .
The combined companies @ @ @ @ @ ’ s growing opportunities and challenges in single cell analysis , super resolution imaging , @ @ @ @ @ Our fit-for-purpose nanobody-based tools perfectly complement the comprehensive antibody coverage of the proteome that Proteintech @ @ @ @ @ Marion Jung , CEO of ChromoTek .
“ It is exciting to be working together @ @ @ @ @ our common values in reproducibility and quality for the benefit of research and beyond.
” @ @ @ @ @ of Proteintech said , “ This new partnership will deliver considerable value to the market @ @ @ @ @ three continents , not only will we serve the research market better , but we @ @ @ @ @ translational science and therapeutic applications .
”

ChromoTek is the market leader in nanobodies — high-performance recombinant reagents used for breakthrough research discoveries. The combined companies will better address the industry’s growing opportunities and challenges in single cell analysis, super resolution imaging, and multiplex assays.
“Our fit-for-purpose nanobody-based tools perfectly complement the comprehensive antibody coverage of the proteome that Proteintech offers,” said Dr. Marion Jung, CEO of ChromoTek. “It is exciting to be working together with a company that shares our common values in reproducibility and quality for the benefit of research and beyond.”
Dr. Jason Li, CEO of Proteintech said, “This new partnership will deliver considerable value to the market. With global manufacturing across three continents, not only will we serve the research market better, but we’ll also deeply impact translational science and therapeutic applications.”


thescientist--2020-10-22--SARS-CoV-2 Disables Key Components of Human Cells' Defense System

ABOVE : A mammalian cell infected with SARS-CoV-2 , showing the formation of compartments where viral RNA is replicated ( top left ) and individual virions exiting the cell ( right ) EMILY BRUCE Viral proteins encoded by SARS-CoV-2 disrupt critical components of human cells ’ molecular machinery and disable responses to infection , according to a study published October 8 in Cell .
Researchers in the US describe how specific viral proteins bind to human RNAs involved in RNA splicing , protein translation , and protein trafficking , and in doing so suppress the host cell ’ s coordination @ @ @ @ @ @ @ the type I interferon response .
The study offers a possible mechanistic explanation for the blunted immune responses observed in some COVID-19 patients , says Benjamin Terrier , an immunologist at Cochin Hospital in Paris who was not involved in the work .
The researchers “ are clearly demonstrating how the virus is able to impair the production of proteins involved in [ this defense ] .
” In the type I interferon response , a cell that has detected foreign genetic material in its cytoplasm launches the production and secretion of interferons—signaling @ @ @ @ @ @ @ expression of hundreds of antiviral genes .
Studies by Terrier and others have reported that patients with severe COVID-19 often show a huge reduction in interferon production , suggesting that the virus ’ s success might in some cases be linked to an ability to disrupt this cellular defense .
See “ Cells ’ Response to SARS-CoV-2 Different from Flu , RSV ” Caltech biologist Mitchell Guttman , along with Dev Majumdar of the University of Vermont ’ s Larner College of Medicine and colleagues , discovered just how SARS-CoV-2 might be doing @ @ @ @ @ @ @ ’ s 27 known proteins and human RNA in vitro .
The researchers had inserted the genes for each of SARS-CoV-2 ’ s proteins into different sets of human cells , such that each cell would produce just one viral protein .
Then , the team had extracted those proteins along with whatever RNAs they ’ d bound to and studied the interactions between the molecules .
The researchers found that 10 of the virus ’ s proteins were bound to RNAs involved in critical cell processes such as RNA splicing , protein @ @ @ @ @ @ @ the team ’ s surprise , Guttman says , as many as four proteins bound specifically to structural noncoding RNAs that make up the cell machinery in charge of coordinating those processes .
The viral protein NSP16 , for example , bound to a host RNA sequence in the spliceosome in a way that rendered the complex unable to recognize RNA transcripts , let alone splice them properly .
NSP1 bound to the ribosome in a position that made it impossible for mRNAs to enter—essentially “ putting a cork ” in the protein-translating @ @ @ @ @ @ @ and NSP9 bound to and interfered with the signal recognition particle , a structure that helps transport newly translated proteins around the cell .
Based on these results , the team predicted that infection with SARS-CoV-2 would drastically reduce splicing , translation , and protein transport in human cells and would consequently suppress the interferon response , which relies on boosting these three processes .
Indeed , lung epithelial cells infected with the virus showed just that , the researchers report in their paper .
Christian Münch , a cell biologist at Goethe @ @ @ @ @ @ @ the work , praises the study ’ s comprehensive description of the basic biological mechanisms underlying these effects .
“ This is one of these nice examples where very nice methods were [ applied to ] this new virus to look at what actually happens in the cell after infection , ” he says .
As the researchers note in their paper , Münch adds , the study did not rule out a role for other pathways in helping SARS-CoV-2 evade host defenses or examine potential interactions among the viral proteins themselves .
@ @ @ @ @ @ @ more into how the effects develop over time from infection .
Guttman says the team is interested in possible therapeutic implications of the study ’ s results .
One route could be to target viral proteins such as NSP1 with drugs that stop them interacting with cellular apparatus .
The researchers are also investigating how the virus—which is dependent on the host to get its own RNA translated and its proteins transported—manages to replicate itself in such a severely compromised cell , says Majumdar .
“ We want to understand how the virus @ @ @ @ @ @ @ be able to engage ribosomes , be able to engage the trafficking machinery—all these things that have been shut off , ” Majumdar explains .
“ What are the signals being presented by the viral mRNAs to basically give it a ticket to ride on all of those machines ?
” Preliminary data indicate that distinctive loops in the structure of SARS-CoV-2 mRNAs could be acting as those signals , Majumdar says .
Hitting the loops with small-molecule drugs might help block viral activity inside infected cells , he adds .
Terrier notes @ @ @ @ @ @ @ on stopping the virus getting into cells , rather than dampening viral activity within already infected cells .
“ Since SARS-CoV-2 is really acute , I think the most important [ thing ] to do is to block the entry of the virus , ” he says .
“ If you are really efficient at that , you don ’ t need to be as efficient ” in targeting intracellular responses .
But the team ’ s data offer crucial mechanistic information to inform future research on this and closely related viruses such @ @ @ @ @ @ @ the 2003 SARS outbreak ) and Middle East respiratory syndrome coronavirus ( MERS-CoV ) , he adds .
“ Trying to [ understand ] how the virus could determine the severity of the disease , the fact that it could paralyze the immune system—clearly that ’ s very important.
” A.K .
Banerjee et al.
, “ SARS-CoV-2 disrupts splicing , translation , and protein trafficking to suppress host defenses , ” Cell , doi:10.1016/j.cell/2020.10.004 , 2020 .

ABOVE: A mammalian cell infected with SARS-CoV-2, showing the formation of compartments where viral RNA is replicated (top left) and individual virions exiting the cell (right)
EMILY BRUCE
Viral proteins encoded by SARS-CoV-2 disrupt critical components of human cells’ molecular machinery and disable responses to infection, according to a study published October 8 in Cell. Researchers in the US describe how specific viral proteins bind to human RNAs involved in RNA splicing, protein translation, and protein trafficking, and in doing so suppress the host cell’s coordination of a key antiviral defense known as the type I interferon response.
The study offers a possible mechanistic explanation for the blunted immune responses observed in some COVID-19 patients, says Benjamin Terrier, an immunologist at Cochin Hospital in Paris who was not involved in the work. The researchers “are clearly demonstrating how the virus is able to impair the production of proteins involved in [this defense].”
In the type I interferon response, a cell that has detected foreign genetic material in its cytoplasm launches the production and secretion of interferons—signaling proteins that go on to trigger the expression of hundreds of antiviral genes.
Studies by Terrier and others have reported that patients with severe COVID-19 often show a huge reduction in interferon production, suggesting that the virus’s success might in some cases be linked to an ability to disrupt this cellular defense.
Caltech biologist Mitchell Guttman, along with Dev Majumdar of the University of Vermont’s Larner College of Medicine and colleagues, discovered just how SARS-CoV-2 might be doing this while studying interactions between the virus’s 27 known proteins and human RNA in vitro.
The researchers had inserted the genes for each of SARS-CoV-2’s proteins into different sets of human cells, such that each cell would produce just one viral protein. Then, the team had extracted those proteins along with whatever RNAs they’d bound to and studied the interactions between the molecules.
We want to understand how the virus can disrupt host cell machinery and yet be able to engage ribosomes, be able to engage the trafficking machinery—all these things that have been shut off. —Dev Majumdar, University of Vermont Larner College of Medicine
The researchers found that 10 of the virus’s proteins were bound to RNAs involved in critical cell processes such as RNA splicing, protein translation, and protein transport. To the team’s surprise, Guttman says, as many as four proteins bound specifically to structural noncoding RNAs that make up the cell machinery in charge of coordinating those processes.
The viral protein NSP16, for example, bound to a host RNA sequence in the spliceosome in a way that rendered the complex unable to recognize RNA transcripts, let alone splice them properly. NSP1 bound to the ribosome in a position that made it impossible for mRNAs to enter—essentially “putting a cork” in the protein-translating structure, Guttman says. And NSP8 and NSP9 bound to and interfered with the signal recognition particle, a structure that helps transport newly translated proteins around the cell.
Based on these results, the team predicted that infection with SARS-CoV-2 would drastically reduce splicing, translation, and protein transport in human cells and would consequently suppress the interferon response, which relies on boosting these three processes. Indeed, lung epithelial cells infected with the virus showed just that, the researchers report in their paper.
Christian Münch, a cell biologist at Goethe University Frankfurt who was not involved in the work, praises the study’s comprehensive description of the basic biological mechanisms underlying these effects. “This is one of these nice examples where very nice methods were [applied to] this new virus to look at what actually happens in the cell after infection,” he says.
As the researchers note in their paper, Münch adds, the study did not rule out a role for other pathways in helping SARS-CoV-2 evade host defenses or examine potential interactions among the viral proteins themselves. He adds that future work could look more into how the effects develop over time from infection.
Guttman says the team is interested in possible therapeutic implications of the study’s results. One route could be to target viral proteins such as NSP1 with drugs that stop them interacting with cellular apparatus.
The researchers are also investigating how the virus—which is dependent on the host to get its own RNA translated and its proteins transported—manages to replicate itself in such a severely compromised cell, says Majumdar.
“We want to understand how the virus can disrupt host cell machinery and yet be able to engage ribosomes, be able to engage the trafficking machinery—all these things that have been shut off,” Majumdar explains. “What are the signals being presented by the viral mRNAs to basically give it a ticket to ride on all of those machines?”
Preliminary data indicate that distinctive loops in the structure of SARS-CoV-2 mRNAs could be acting as those signals, Majumdar says. Hitting the loops with small-molecule drugs might help block viral activity inside infected cells, he adds.
Terrier notes that most therapeutic strategies for SARS-CoV-2 focus on stopping the virus getting into cells, rather than dampening viral activity within already infected cells. “Since SARS-CoV-2 is really acute, I think the most important [thing] to do is to block the entry of the virus,” he says. “If you are really efficient at that, you don’t need to be as efficient” in targeting intracellular responses.
But the team’s data offer crucial mechanistic information to inform future research on this and closely related viruses such as SARS-CoV (the virus responsible for the 2003 SARS outbreak) and Middle East respiratory syndrome coronavirus (MERS-CoV), he adds. “Trying to [understand] how the virus could determine the severity of the disease, the fact that it could paralyze the immune system—clearly that’s very important.”
A.K. Banerjee et al., “SARS-CoV-2 disrupts splicing, translation, and protein trafficking to suppress host defenses,” Cell, doi:10.1016/j.cell/2020.10.004, 2020.


thescientist--2020-10-20--Targeting Proteins and Proteolysis to Counter Cancer

Cancer drug development tends to focus on inhibiting protein activity rather than modulating protein levels .
While this approach has @ @ @ @ @ comes with challenges , such as long-term resistance and toxicity .
Targeted protein degradation offers @ @ @ @ @ problem .
Protein degraders are small molecules that induce degradation and remove deleterious proteins from @ @ @ @ @ ligase ubiquitination activity .
In this webinar brought to you by The Scientist and sponsored @ @ @ @ @ discuss how small-molecule degraders work , key points of interest in their design , and @ @ @ @ @ laboratory and the clinic .
• Using proteolysis targeting chimera ( PROTAC ) technology to @ @ @ @ @ agents Daohong Zhou , MD Professor of Pharmacodynamics and Radiation Oncology Harry E. Innes Endowed @ @ @ @ @ Director for Translation and Drug Development University of Florida Health Cancer Center University of Florida @ @ @ @ @ PhD Alessio Ciulli Research Group Medicinal Chemist and Organic Chemistry Scientist Biological Chemistry and Drug @ @ @ @ @ Sciences University of Dundee

FREE Webinar
Thursday, November 19, 2020
2:30 - 4:00 PM, Eastern Time
Register Now
Cancer drug development tends to focus on inhibiting protein activity rather than modulating protein levels. While this approach has seen some success, it comes with challenges, such as long-term resistance and toxicity. Targeted protein degradation offers a potential solution to this problem.
Protein degraders are small molecules that induce degradation and remove deleterious proteins from afflicted cells by modulating E3 ligase ubiquitination activity. In this webinar brought to you by The Scientist and sponsored by PerkinElmer|Cisbio, researchers will discuss how small-molecule degraders work, key points of interest in their design, and their applications in both the laboratory and the clinic.
Topics to be covered
Using proteolysis targeting chimera (PROTAC) technology to overcome on-target toxicity of anticancer agents
Structure-based design approaches for developing PROTACs against cancer
Register Now
Meet the Speakers:
Daohong Zhou, MD
Professor of Pharmacodynamics and Radiation Oncology
Harry E. Innes Endowed Professor of Cancer Research
Associate Director for Translation and Drug Development
University of Florida Health Cancer Center
University of Florida at Gainesville
Aileen Frost, PhD
Alessio Ciulli Research Group
Medicinal Chemist and Organic Chemistry Scientist
Biological Chemistry and Drug Discovery, School of Life Sciences
University of Dundee


thescientist--2020-10-23--Physician Behind Surgisphere Scandal Switches Medical Licenses

Sapan Desai , the embattled vascular surgeon and CEO of the now-defunct Surgisphere Corporation , has inactivated his medical license in one state and obtained a license in another .
Each US state has its own licensing board , and generally a doctor requires an in-state license to practice medicine there—although Illinois is one of many states that is granting emergency authorization to some out-of-state physicians in response to the COVID-19 crisis , provided they have an active license and are in good standing .
According to public records held by the Illinois Department of Financial and Professional Regulation ( @ @ @ @ @ @ @ , which was issued to the South Barrington–based surgeon in 2013 , was recently inactivated—a change requested voluntarily by the licensee that prohibits them from practicing medicine in the state .
The license isn ’ t set to expire until 2023 .
On September 25 , according to records held by the State Medical Board of Ohio , a new medical license was issued to a Sapan Desai based in South Barrington , Illinois , with a specialty in vascular surgery .
That license is valid until 2022 .
Desai became the focus @ @ @ @ @ @ @ Surgisphere provided data for several high-profile studies on COVID-19 patients .
Those studies were quickly retracted after scientists and journalists raised questions about the provenance of the data , and independent auditors were refused access to the company ’ s database .
The company disappeared shortly thereafter , and Desai stopped responding to requests for comment .
See The Scientist ’ s Investigation into Surgisphere Corporation Over the summer , The Scientist spoke to a number of former colleagues and supervisors who described long-standing concerns about Desai ’ s conduct as a physician @ @ @ @ @ @ @ false information about patients .
See “ The Surgisphere Scandal : What Went Wrong ?
” Desai resigned from his latest position as a physician at Northwest Community Hospital in February this year following the filing of a string of medical malpractice lawsuits against him in Cook County , Illinois .
He told The Scientist in May that he deemed any lawsuit naming him to be unfounded and that he left Northwest for personal reasons .
An employee at IDFPR ’ s complaints center tells The Scientist that the department can not confirm @ @ @ @ @ @ @ into a particular physician ’ s actions , and says that no information about ongoing investigations is shared publicly or with medical boards in different states unless and until an investigation results in disciplinary action .
Contacted by The Scientist , an employee at the American Board of Surgery confirms that Desai is still certified with the board , but notes that the medical license on file is the Illinois license , not the Ohio one .
Surgeons are required to contact the board themselves with any changes in license status .
The @ @ @ @ @ @ @ chief communications officer confirms in an email to The Scientist that Desai ’ s license in Ohio is active and shows no board disciplinary action .
She adds that applicants for licenses are required to undergo background checks and report any malpractice settlements or disciplinary actions against them .

ABOVE: ISTOCK.COM, ANDREI_R
Update (November 2): Sapan Desai has requested that his newly obtained Ohio medical license be inactivated, according to documents obtained by The Scientist. In correspondence sent a few days after this story was published, Desai wrote to the State Medical Board of Ohio that he would “not be practicing medicine in the state of Ohio.”
Sapan Desai, the embattled vascular surgeon and CEO of the now-defunct Surgisphere Corporation, has inactivated his medical license in one state and obtained a license in another.
Each US state has its own licensing board, and generally a doctor requires an in-state license to practice medicine there—although Illinois is one of many states that is granting emergency authorization to some out-of-state physicians in response to the COVID-19 crisis, provided they have an active license and are in good standing.
According to public records held by the Illinois Department of Financial and Professional Regulation (IDFPR), Desai’s license, which was issued to the South Barrington–based surgeon in 2013, was recently inactivated—a change requested voluntarily by the licensee that prohibits them from practicing medicine in the state. The license isn’t set to expire until 2023.
On September 25, according to records held by the State Medical Board of Ohio, a new medical license was issued to a Sapan Desai based in South Barrington, Illinois, with a specialty in vascular surgery. That license is valid until 2022.
Desai became the focus of a scandal earlier this year after Surgisphere provided data for several high-profile studies on COVID-19 patients. Those studies were quickly retracted after scientists and journalists raised questions about the provenance of the data, and independent auditors were refused access to the company’s database. The company disappeared shortly thereafter, and Desai stopped responding to requests for comment.
Over the summer, The Scientist spoke to a number of former colleagues and supervisors who described long-standing concerns about Desai’s conduct as a physician, including firsthand experiences of Desai providing false information about patients.
Desai resigned from his latest position as a physician at Northwest Community Hospital in February this year following the filing of a string of medical malpractice lawsuits against him in Cook County, Illinois. He told The Scientist in May that he deemed any lawsuit naming him to be unfounded and that he left Northwest for personal reasons.
An employee at IDFPR’s complaints center tells The Scientist that the department cannot confirm or deny whether any investigations are underway into a particular physician’s actions, and says that no information about ongoing investigations is shared publicly or with medical boards in different states unless and until an investigation results in disciplinary action.
Contacted by The Scientist, an employee at the American Board of Surgery confirms that Desai is still certified with the board, but notes that the medical license on file is the Illinois license, not the Ohio one. Surgeons are required to contact the board themselves with any changes in license status.
The State Medical Board of Ohio’s chief communications officer confirms in an email to The Scientist that Desai’s license in Ohio is active and shows no board disciplinary action. She adds that applicants for licenses are required to undergo background checks and report any malpractice settlements or disciplinary actions against them.


thescientist--2020-10-23--Wyatt Technology Announces Breakthrough in Field Flow Fractionation (FFF) Separation Technology

This completely new line of separation instrumentation and software was designed for the widest range of analytes including proteins , polymers , viruses , gene vectors , liposomal drug nanoparticles , and more .
Covering a range of sizes from 1 nm to 10 µm , the Eclipse offers programmable separation power for enhanced resolution within any size range .
The system incorporates sophisticated micro-controllers and sensors with built-in intelligence and an intuitive interface to ensure simple use , reliability and repeatability across research , development and quality control environments .
The introduction of Mobility™ implements electrical/asymmetric-flow FFF for determining @ @ @ @ @ @ @ Control Module™ ( DCM ) increases sample concentrations up to 10x , for higher sensitivity and fraction titer .
Improved channel design provides unique and accurate temperature control for higher sample recovery , reproducibility and pressure stability .
Geofrey Wyatt , CEO of Wyatt Technology , said , “ To say that I ’ m proud of the accomplishments of Team Wyatt in developing the new Eclipse and Mobility hardware products , and VISION software package would be an understatement .
Add in the complexities of coordinating so many contributors during a pandemic @ @ @ @ @ @ @ our hands .
The complete execution of a product redesign is difficult enough under ordinary circumstances , but in this case it was re-imagining of what FFF is and how it can be made more accessible to more scientists .
The resulting products , their novelty and their utility move FFF from a relatively obscure area of separation science into the mainstream.
” Developing reliable means of separation and characterization methods is just one more way that Wyatt Technology fulfills its mission : to help ensure our customers ’ success in providing leading-edge @ @ @ @

This completely new line of separation instrumentation and software was designed for the widest range of analytes including proteins, polymers, viruses, gene vectors, liposomal drug nanoparticles, and more. Covering a range of sizes from 1 nm to 10 µm, the Eclipse offers programmable separation power for enhanced resolution within any size range. The system incorporates sophisticated micro-controllers and sensors with built-in intelligence and an intuitive interface to ensure simple use, reliability and repeatability across research, development and quality control environments.
The introduction of Mobility™ implements electrical/asymmetric-flow FFF for determining size-resolved zeta potential. The new Dilution Control Module™ (DCM) increases sample concentrations up to 10x, for higher sensitivity and fraction titer. Improved channel design provides unique and accurate temperature control for higher sample recovery, reproducibility and pressure stability.
Geofrey Wyatt, CEO of Wyatt Technology, said, “To say that I’m proud of the accomplishments of Team Wyatt in developing the new Eclipse and Mobility hardware products, and VISION software package would be an understatement. Add in the complexities of coordinating so many contributors during a pandemic and we have an extraordinary story on our hands. The complete execution of a product redesign is difficult enough under ordinary circumstances, but in this case it was re-imagining of what FFF is and how it can be made more accessible to more scientists. The resulting products, their novelty and their utility move FFF from a relatively obscure area of separation science into the mainstream.”
Developing reliable means of separation and characterization methods is just one more way that Wyatt Technology fulfills its mission: to help ensure our customers’ success in providing leading-edge, life-enhancing products.


thescientist--2020-10-24--California Voters to Decide Future of Stem Cell Funding Agency

Over the course of its 16-year existence , the California Institute for Regenerative Medicine in Oakland has helped transform its state into an innovation hub of stem cell science .
But CIRM announced last year that its first $ 3 billion of funding has dried up , and now it ’ s up to voters to decide on November 3 whether to give the agency a second life .
The Stem Cell Research Institute Bond Initiative , Proposition 14 , would issue $ 5.5 billion in general obligation bonds for the agency to continue funding stem cell studies , training @ @ @ @ @ @ @ , with the aim of developing and testing treatments for a range of diseases .
The measure isn ’ t facing significant organized opposition , but it has drawn criticism from newspaper editorial boards and others for what they see as conflicts of interest between CIRM board members and institutions applying for funds .
Critics also question the state ’ s ability to afford the new funding amid a record wildfire season and a pandemic , and the necessity of CIRM given federal funding of stem cell research .
“ I have a @ @ @ @ @ @ @ if I didn ’ t have CIRM funding , and I may be able to treat people with Parkinson ’ s disease ” in the future , says Jeanne Loring , a stem cell biologist and professor emeritus at Scripps Research who last year launched the biotech company Aspen Neuroscience , which is developing a stem cell–based neuron replacement therapy for Parkinson ’ s .
But she says she has concerns about the proposition due to conflicts of interest on the board and other factors .
CIRM was created in 2004 as an @ @ @ @ @ @ @ funding for human embryonic stem cell research implemented by then-President George W. Bush .
At the time , the National Institutes of Health ( NIH ) was only allowed to fund research involving a limited number of pre-existing stem cell lines .
California voters approved a ballot measure that year that established a state constitutional right to conduct stem cell research and authorized the sale of $ 3 billion worth of bonds to fund the agency .
See “ Stem Cell Funding Agency CIRM Is Nearly Out of Funds ” The Bush-era restrictions @ @ @ @ @ @ @ presidency , but CIRM has continued to fund stem cell science , including research involving both induced pluripotent stem ( iPS ) cells and embryo- and blood-derived stem cells .
To Loring , who says she ’ s received nearly $ 30 million in CIRM grants over the years , the agency ’ s most important legacy is that it invested in physical infrastructure such as buildings and labs as well as training programs for early-career stem cell scientists .
For instance , the agency ran an internship program for undergraduate and master @ @ @ @ @ @ @ in a mentor ’ s lab to learn the ropes of stem cell research , through which Loring says she ’ s trained some 30 students , making them more employable in a thriving stem cell research field in California and beyond .
CIRM also offered pre-doctoral and postdoc training programs .
“ What worries me about the funding going forward is [ potentially losing ] the internship programs and the support for graduate students and postdocs .
I think those were the diamonds in that whole program , ” Loring says .
@ @ @ @ @ @ @ at the University of California , San Diego , says the agency has filled a critical funding gap by supporting the progression of interesting scientific discoveries to late-stage clinical trials .
Using CIRM funding—Goldstein has received some $ 21 million as a principal investigator , according to the agency ’ s website—he ’ s created an in vitro model of hereditary forms of Alzheimer ’ s disease using iPS cells and used it to identify drug candidates that target pathological processes in the disease .
He says the project was “ too risky @ @ @ @ @ @ @ CIRM funded “ most of the work , up to getting it to the point where we can get it into trials.
” Loring reckons that most of CIRM-supported early research didn ’ t take off beyond the first stages of development .
But according to a dataset available on the agency ’ s website , it has funded 66 ongoing , mostly early-stage clinical trials targeting a broad range of diseases , and has contributed to initial steps in the development of more than a dozen drugs .
These include the recently @ @ @ @ @ @ @ -approved small molecule inhibitors fedratinib and glasdegib to treat the cancer subtypes myelofibrosis and acute myeloid leukemia , respectively .
However , the editorial boards of the San Francisco Chronicle and the Los Angeles Times argue that CIRM-funded medical advancements have yet to live up to the rosy promises made to voters during the 2004 campaign to create the agency , which included curative treatments for a number of diseases .
Critics also argue that CIRM no longer fills an unmet funding need .
Jeff Sheehy , a longtime HIV/AIDS activist and the @ @ @ @ @ @ @ new proposition , points out that last year alone , the NIH put more than $ 2 billion toward stem cell research , including studies involving embryonic stem cells , dwarfing the $ 5.5 billion CIRM would spend over a number of years if the ballot measure passes .
“ The [ federal ] funding is not at risk—there ’ s no unmet need here , ” Sheehy says .
Goldstein , however , expresses concern that if reelected , President Donald Trump ’ s administration could enact new restrictions on stem cell @ @ @ @ @ @ @ Proposition 14 is , he says , that its language doesn ’ t address mitigating conflicts of interest that could arise given that the majority of CIRM ’ s 29 board members are executives at institutions that are competing for grants—an issue noted in a 2013 Institute of Medicine report requested by CIRM .
While board members can not vote directly on grants requested by their own institutions , “ it ’ s very hard for them not to try to exert some kind of influence .
It ’ s just human nature @ @ @ @ @ @ @ a recent blog post detailed a situation she says involved such influence .
Sheehy and Loring both say that a smaller board would make it easier to manage conflicts of interest , as would diversifying its members so that institutions competing for grants are less strongly represented .
The new proposition could worsen the situation by raising the number of board members to 35 , Loring adds .
Goldstein , however , says he thinks the board ’ s procedures , and the measure itself , manage the conflicts appropriately .
“ There @ @ @ @ @ @ @ in the practices that the board has developed.
” Sheehy also voices concern about the potential economic impact of approving the measure , especially at a time when the state is facing a huge pandemic-driven budget deficit .
Bonds are effectively loans that need to be paid back by taxpayers , with interest , over time .
The nonpartisan federal Legislative Analyst ’ s Office ( LAO ) estimates it would cost the state a total of $ 7.8 billion to pay off the bonds , or around $ 260 million annually over @ @ @ @ @ @ @ $ 327 million annually in debt payments the state is still paying off from the 2004 proposition ’ s bonds .
“ I have huge issues with paying for this with debt to begin with because stem cell research could get in line with everyone else : healthcare , education , housing , wildfire fighting and mitigation , ” not to mention managing the pandemic , Sheehy says .
“ Stem cell research should be judged in the context of all the other state needs.
” Given that it would effectively be funded @ @ @ @ @ @ @ wording that would allow the state to reap greater returns on its investment , Sheehy adds .
Figures from the LAO suggest that CIRM-funded inventions have brought far less revenue to the state than voters were initially promised with the 2004 measure , he notes in a recent opinion article .
Furthermore , the new proposition would require the state to put royalty revenues from CIRM-funded discoveries toward making stem cell therapies more affordable , in what Sheehy sees as a “ giant subsidy for pharmaceutical and biotech companies.
” Goldstein argues that @ @ @ @ @ @ @ s economy and aid its recovery from the pandemic : “ You ’ re putting money into the development of products and businesses that California will ultimately benefit from.
” He adds that a large part of California ’ s healthcare bill is driven by chronic diseases such as Alzheimer ’ s disease , and that investing in developing treatments will pay off in the long term .
“ These are reasonable investments [ and ] this is good for the state.
” There ’ s no organized opposition to Proposition 14 , @ @ @ @ @ @ @ stem cell research have waned over the years , Loring says .
According to California ’ s Secretary of State , the “ No on Proposition 14 ” committee has raised only $ 250 so far , whereas the campaign in support of it has raised more than $ 16 million .
Much of that comes from San Francisco real estate investor Robert N. Klein II , who spearheaded the measure , according to The New York Times .
“ I have mixed feelings ” toward the measure , Loring says .
If @ @ @ @ @ @ @ ’ ll be happy .
If it doesn ’ t , I ’ ll be fine.
” Clarification ( October 24 ) : This article has been edited to reflect the number of funded clinical trials listed on CIRM ’ s website , rather than the number given in the counter at the top of that webpage .

ABOVE: © ISTOCK.COM, CIPHOTOS
Over the course of its 16-year existence, the California Institute for Regenerative Medicine in Oakland has helped transform its state into an innovation hub of stem cell science. But CIRM announced last year that its first $3 billion of funding has dried up, and now it’s up to voters to decide on November 3 whether to give the agency a second life.
The Stem Cell Research Institute Bond Initiative, Proposition 14, would issue $5.5 billion in general obligation bonds for the agency to continue funding stem cell studies, training scientists, and building new research facilities, with the aim of developing and testing treatments for a range of diseases.
The measure isn’t facing significant organized opposition, but it has drawn criticism from newspaper editorial boards and others for what they see as conflicts of interest between CIRM board members and institutions applying for funds. Critics also question the state’s ability to afford the new funding amid a record wildfire season and a pandemic, and the necessity of CIRM given federal funding of stem cell research.
“I have a company now that would not have existed if I didn’t have CIRM funding, and I may be able to treat people with Parkinson’s disease” in the future, says Jeanne Loring, a stem cell biologist and professor emeritus at Scripps Research who last year launched the biotech company Aspen Neuroscience, which is developing a stem cell–based neuron replacement therapy for Parkinson’s. But she says she has concerns about the proposition due to conflicts of interest on the board and other factors.
CIRM was created in 2004 as an apparent rebuke to the federal restrictions on funding for human embryonic stem cell research implemented by then-President George W. Bush. At the time, the National Institutes of Health (NIH) was only allowed to fund research involving a limited number of pre-existing stem cell lines. California voters approved a ballot measure that year that established a state constitutional right to conduct stem cell research and authorized the sale of $3 billion worth of bonds to fund the agency.
See “Stem Cell Funding Agency CIRM Is Nearly Out of Funds”
The Bush-era restrictions were lifted during Barack Obama’s presidency, but CIRM has continued to fund stem cell science, including research involving both induced pluripotent stem (iPS) cells and embryo- and blood-derived stem cells. To Loring, who says she’s received nearly $30 million in CIRM grants over the years, the agency’s most important legacy is that it invested in physical infrastructure such as buildings and labs as well as training programs for early-career stem cell scientists.
For instance, the agency ran an internship program for undergraduate and master’s students to spend a year in a mentor’s lab to learn the ropes of stem cell research, through which Loring says she’s trained some 30 students, making them more employable in a thriving stem cell research field in California and beyond. CIRM also offered pre-doctoral and postdoc training programs. “What worries me about the funding going forward is [potentially losing] the internship programs and the support for graduate students and postdocs. I think those were the diamonds in that whole program,” Loring says.
Larry Goldstein, a stem cell scientist at the University of California, San Diego, says the agency has filled a critical funding gap by supporting the progression of interesting scientific discoveries to late-stage clinical trials. Using CIRM funding—Goldstein has received some $21 million as a principal investigator, according to the agency’s website—he’s created an in vitro model of hereditary forms of Alzheimer’s disease using iPS cells and used it to identify drug candidates that target pathological processes in the disease. He says the project was “too risky” to attract NIH funding, but CIRM funded “most of the work, up to getting it to the point where we can get it into trials.”
Loring reckons that most of CIRM-supported early research didn’t take off beyond the first stages of development. But according to a dataset available on the agency’s website, it has funded 66 ongoing, mostly early-stage clinical trials targeting a broad range of diseases, and has contributed to initial steps in the development of more than a dozen drugs. These include the recently Food and Drug Administration (FDA)-approved small molecule inhibitors fedratinib and glasdegib to treat the cancer subtypes myelofibrosis and acute myeloid leukemia, respectively.
However, the editorial boards of the San Francisco Chronicle and the Los Angeles Times argue that CIRM-funded medical advancements have yet to live up to the rosy promises made to voters during the 2004 campaign to create the agency, which included curative treatments for a number of diseases.
The [federal] funding is not at risk—there’s no unmet need here. —Jeff Sheehy, CIRM board member
Critics also argue that CIRM no longer fills an unmet funding need. Jeff Sheehy, a longtime HIV/AIDS activist and the only CIRM board member to oppose the new proposition, points out that last year alone, the NIH put more than $2 billion toward stem cell research, including studies involving embryonic stem cells, dwarfing the $5.5 billion CIRM would spend over a number of years if the ballot measure passes. “The [federal] funding is not at risk—there’s no unmet need here,” Sheehy says. Goldstein, however, expresses concern that if reelected, President Donald Trump’s administration could enact new restrictions on stem cell research.
Another reason why Sheehy opposes Proposition 14 is, he says, that its language doesn’t address mitigating conflicts of interest that could arise given that the majority of CIRM’s 29 board members are executives at institutions that are competing for grants—an issue noted in a 2013 Institute of Medicine report requested by CIRM. While board members cannot vote directly on grants requested by their own institutions, “it’s very hard for them not to try to exert some kind of influence. It’s just human nature,” says Loring, who in a recent blog post detailed a situation she says involved such influence.
Sheehy and Loring both say that a smaller board would make it easier to manage conflicts of interest, as would diversifying its members so that institutions competing for grants are less strongly represented. The new proposition could worsen the situation by raising the number of board members to 35, Loring adds. Goldstein, however, says he thinks the board’s procedures, and the measure itself, manage the conflicts appropriately. “There are enough protections in the measure and in the practices that the board has developed.”
Sheehy also voices concern about the potential economic impact of approving the measure, especially at a time when the state is facing a huge pandemic-driven budget deficit. Bonds are effectively loans that need to be paid back by taxpayers, with interest, over time. The nonpartisan federal Legislative Analyst’s Office (LAO) estimates it would cost the state a total of $7.8 billion to pay off the bonds, or around $260 million annually over 30 years, in addition to the $327 million annually in debt payments the state is still paying off from the 2004 proposition’s bonds.
“I have huge issues with paying for this with debt to begin with because stem cell research could get in line with everyone else: healthcare, education, housing, wildfire fighting and mitigation,” not to mention managing the pandemic, Sheehy says. “Stem cell research should be judged in the context of all the other state needs.”
Given that it would effectively be funded with debt, the measure should include wording that would allow the state to reap greater returns on its investment, Sheehy adds. Figures from the LAO suggest that CIRM-funded inventions have brought far less revenue to the state than voters were initially promised with the 2004 measure, he notes in a recent opinion article. Furthermore, the new proposition would require the state to put royalty revenues from CIRM-funded discoveries toward making stem cell therapies more affordable, in what Sheehy sees as a “giant subsidy for pharmaceutical and biotech companies.”
You’re putting money into the development of products and businesses that California will ultimately benefit from. —Larry Goldstein, UC San Diego
Goldstein argues that the measure could stimulate the state’s economy and aid its recovery from the pandemic: “You’re putting money into the development of products and businesses that California will ultimately benefit from.” He adds that a large part of California’s healthcare bill is driven by chronic diseases such as Alzheimer’s disease, and that investing in developing treatments will pay off in the long term. “These are reasonable investments [and] this is good for the state.”
There’s no organized opposition to Proposition 14, in part because public concerns around embryonic stem cell research have waned over the years, Loring says. According to California’s Secretary of State, the “No on Proposition 14” committee has raised only $250 so far, whereas the campaign in support of it has raised more than $16 million. Much of that comes from San Francisco real estate investor Robert N. Klein II, who spearheaded the measure, according to The New York Times.
“I have mixed feelings” toward the measure, Loring says. If it’s approved, “I’ll be happy. If it doesn’t, I’ll be fine.”
Clarification (October 24): This article has been edited to reflect the number of funded clinical trials listed on CIRM’s website, rather than the number given in the counter at the top of that webpage.


thescientist--2020-10-26--More SARS-CoV-2 Reinfections Reported, But Still a Rare Event

At least 285 individuals in Mexico appear to have contracted the novel coronavirus twice , according to a preprint posted October 18 on medRxiv .
The study , which has not yet been peer reviewed , is the largest to date to assess the possibility of SARS-CoV-2 reinfection .
It fuels an ongoing discussion among researchers about how long immunity to the virus lasts after an initial infection and how that length of immunity may affect the way vaccines against the virus are administered in the future .
“ If we find that our immunity is poor , or nonexistent @ @ @ @ @ @ @ big problem for vaccination policies , ” study coauthor Carlos Hernandez-Suarez , a researcher at Universidad de Colima in San Sebastian , Mexico , tells The Scientist , adding that no conclusions can be made from the current data about the strength of survivors ’ immunity or the protection offered by future vaccines .
In his team ’ s analysis of hospital records of 100,432 individuals infected with SARS-CoV-2 between March and July 2020 , only 285 ( 0.26 percent ) presented signs that they ’ d contracted the virus twice .
Hernandez-Suarez @ @ @ @ @ @ @ frequency of reinfections among the patients .
They ’ d read several studies pointing to possible reinfections and also an August letter to the editor in the Journal of Infection by Julian Tang , a clinical virologist at the University of Leicester in the UK , and colleagues laying out criteria for defining reinfection .
The definition included an initial PCR-confirmed infection with SARS-CoV-2 , then clinical recovery and a negative SARS-CoV-2 PCR test , and then a confirmed SARS-CoV-2 PCR-positive test at least 28 days after the initial positive test .
The @ @ @ @ @ @ @ least 28 days after the initial ones because evidence suggests it takes that long for viral shedding to begin to taper off and because certain SARS-CoV-2 antibodies start to drop off at that point , according to another study posted to medRxiv in July .
Following that definition , Hernandez-Suarez and colleagues dug into the hospital records and identified the 285 patients obtaining medical care after a second positive PCR-confirmed SARS-CoV-2 infection .
For the majority of patients , “ we didn ’ t have the test in between , ” the negative @ @ @ @ @ @ @ did have that test for 14 individuals , and it was negative , but for the rest , the patients ’ second positive test came 28 days or more after the first , in some cases 60 or 70 days later , he explains .
“ The average was 66 days , with no complications , no problems , and then they went to the hospital again with [ respiratory ] problems.
” To the team , that was an indication of a second infection , rather than a prolonged initial illness .
@ @ @ @ @ @ @ more data , such as negative tests in between positive ones , if the cases are in fact reinfections or long-lasting illnesses from a single infection , says Tang , who was not involved in the work .
Still , the latest results align with other studies and case reports that indicate reinfection is rare .
“ This reinfection thing is not new .
It ’ s not unusual , not dramatic , or scary , or whatever you want to call it .
It ’ s very normal , ” Tang tells @ @ @ @ @ @ @ such as respiratory syncytial virus ( RSV ) can cause repeated reinfections .
Whether it happens frequently with SARS-CoV-2 , though , he says , is not yet clear .
The first indications that reinfection could occur came from case reports out of Hong Kong and Europe , and then Nevada .
What distinguished some of these cases as clear reinfections rather than lingering initial infections is that the genomes of the viruses causing the first and second infections weren ’ t identical .
“ You can really only prove reinfection ” if @ @ @ @ @ @ @ second positive swabs are different , notes Angela Rasmussen , a virologist at Columbia University in New York , “ because it ’ s very unlikely that you would be infected with the exact same variants a second time.
” SARS-CoV-2 has an RNA genome , which has a higher mutation rate than a DNA viral genome .
The mutation rate is so fast , in fact , that “ even within an individual host who ’ s infected , you may have multiple variants that are just emerging as the virus replicates @ @ @ @ @ @ @ explains .
The genetic changes that SARS-CoV-2 has so far accumulated seem to be functionally inconsequential , and “ in the population , when you think about how many millions of different coronavirus cases there are , different variants have emerged .
.
.
[ so ] it ’ s very unlikely that you would get the exact same one.
” A study posted September 28 to medRxiv confirms four reinfections in Qatar using genetic sequencing data that found distinct viral variants between the first and second infections .
These are among 133,266 @ @ @ @ @ @ @ a doctor with the Ministry of Public Health in Doha , and colleagues analyzed .
It ’ s possible there were more reinfections , as the authors note that 243 individuals had positive PCR tests at least 45 days apart , but only 12 patients had sufficient viral genome data at both time points .
Two of the cases had identical viral genomes on the first and second positive test , suggesting a lingering infection that never cleared in the weeks between the two positive tests , and the six others didn ’ @ @ @ @ @ @ @ a firm conclusion about reinfection .
Regardless , Bertollini and his colleagues conclude in their report that “ the risk for documented reinfection was very rare at about 1-2 reinfections per 10,000 infected persons.
” The researchers further note that the “ findings suggest that most infected persons do develop immunity against reinfection that lasts for at least [ a ] few months , and that reinfections ( if they occur ) are well tolerated and no more symptomatic than primary infections.
” Contracting the virus twice within the span of a few @ @ @ @ @ @ @ data collected so far suggest .
That ’ s if SARS-CoV-2 acts anything like seasonal coronaviruses , according to a paper published September 14 .
In that study , Arthur Edridge of the University of Amsterdam and colleagues analyzed stored blood samples of 10 healthy individuals that were taken , on average , every few months for the past 35 years .
The team tested the samples for an increase in antibodies to a specific region of the structural capsid protein of each seasonal coronavirus .
Antibody levels spiked and dropped at regular @ @ @ @ @ @ @ four seasonal coronaviruses are common and frequently occur after about a year , ” Edridge writes in an email to The Scientist .
Reinfection is therefore a “ common human coronavirus feature , ” he explains , and SARS-CoV-2 would most likely be no exception .
See “ Does the Common Cold Protect You from COVID-19 ?
” Rasmussen , who was not involved with any of the studies , says that reinfection is certainly possible , but she ’ s less convinced that SARS-CoV-2 will act like other coronaviruses that cause colds @ @ @ @ @ @ @ because those viruses only cause a mild infection and don ’ t elicit a strong immune response with lots of long-lasting antibodies .
SARS-CoV-2 could be very different , she says .
That immune durability should really be the focus of reinfection studies , Tang explains .
Researchers need to look at the longevity of antibodies after infection or vaccination , because if they start to wane , then there may be a need for vaccine boosters several months after the initial shot is given .
The case reports and preliminary studies contribute @ @ @ @ @ @ @ immunity and its implication for vaccination , he explains , “ but there ’ s a long way to go .
”

ABOVE: SARS-COV-2 virus particles (yellow) infect a cell (blue)
FLICKR, NIAID
At least 285 individuals in Mexico appear to have contracted the novel coronavirus twice, according to a preprint posted October 18 on medRxiv. The study, which has not yet been peer reviewed, is the largest to date to assess the possibility of SARS-CoV-2 reinfection. It fuels an ongoing discussion among researchers about how long immunity to the virus lasts after an initial infection and how that length of immunity may affect the way vaccines against the virus are administered in the future.
“If we find that our immunity is poor, or nonexistent . . . this will be a big problem for vaccination policies,” study coauthor Carlos Hernandez-Suarez, a researcher at Universidad de Colima in San Sebastian, Mexico, tells The Scientist, adding that no conclusions can be made from the current data about the strength of survivors’ immunity or the protection offered by future vaccines. In his team’s analysis of hospital records of 100,432 individuals infected with SARS-CoV-2 between March and July 2020, only 285 (0.26 percent) presented signs that they’d contracted the virus twice.
Hernandez-Suarez and colleagues set out to pinpoint the frequency of reinfections among the patients. They’d read several studies pointing to possible reinfections and also an August letter to the editor in the Journal of Infection by Julian Tang, a clinical virologist at the University of Leicester in the UK, and colleagues laying out criteria for defining reinfection. The definition included an initial PCR-confirmed infection with SARS-CoV-2, then clinical recovery and a negative SARS-CoV-2 PCR test, and then a confirmed SARS-CoV-2 PCR-positive test at least 28 days after the initial positive test. The suspected second infections need to be at least 28 days after the initial ones because evidence suggests it takes that long for viral shedding to begin to taper off and because certain SARS-CoV-2 antibodies start to drop off at that point, according to another study posted to medRxiv in July.
Following that definition, Hernandez-Suarez and colleagues dug into the hospital records and identified the 285 patients obtaining medical care after a second positive PCR-confirmed SARS-CoV-2 infection. For the majority of patients, “we didn’t have the test in between,” the negative test, Hernandez-Suarez notes.
The team did have that test for 14 individuals, and it was negative, but for the rest, the patients’ second positive test came 28 days or more after the first, in some cases 60 or 70 days later, he explains. “The average was 66 days, with no complications, no problems, and then they went to the hospital again with [respiratory] problems.” To the team, that was an indication of a second infection, rather than a prolonged initial illness.
It’s hard to know without more data, such as negative tests in between positive ones, if the cases are in fact reinfections or long-lasting illnesses from a single infection, says Tang, who was not involved in the work. Still, the latest results align with other studies and case reports that indicate reinfection is rare.
“This reinfection thing is not new. It’s not unusual, not dramatic, or scary, or whatever you want to call it. It’s very normal,” Tang tells The Scientist, noting that other viruses such as respiratory syncytial virus (RSV) can cause repeated reinfections. Whether it happens frequently with SARS-CoV-2, though, he says, is not yet clear.
The genetic evidence for reinfection
The first indications that reinfection could occur came from case reports out of Hong Kong and Europe, and then Nevada. What distinguished some of these cases as clear reinfections rather than lingering initial infections is that the genomes of the viruses causing the first and second infections weren’t identical.
“You can really only prove reinfection” if the viral variants from the first and second positive swabs are different, notes Angela Rasmussen, a virologist at Columbia University in New York, “because it’s very unlikely that you would be infected with the exact same variants a second time.”
SARS-CoV-2 has an RNA genome, which has a higher mutation rate than a DNA viral genome. The mutation rate is so fast, in fact, that “even within an individual host who’s infected, you may have multiple variants that are just emerging as the virus replicates itself and makes mistakes,” she explains. The genetic changes that SARS-CoV-2 has so far accumulated seem to be functionally inconsequential, and “in the population, when you think about how many millions of different coronavirus cases there are, different variants have emerged . . . [so] it’s very unlikely that you would get the exact same one.”
A study posted September 28 to medRxiv confirms four reinfections in Qatar using genetic sequencing data that found distinct viral variants between the first and second infections. These are among 133,266 confirmed SARS-CoV-2 cases that Roberto Bertollini, a doctor with the Ministry of Public Health in Doha, and colleagues analyzed. It’s possible there were more reinfections, as the authors note that 243 individuals had positive PCR tests at least 45 days apart, but only 12 patients had sufficient viral genome data at both time points. Two of the cases had identical viral genomes on the first and second positive test, suggesting a lingering infection that never cleared in the weeks between the two positive tests, and the six others didn’t have enough genetic changes to make a firm conclusion about reinfection.
Regardless, Bertollini and his colleagues conclude in their report that “the risk for documented reinfection was very rare at about 1-2 reinfections per 10,000 infected persons.” The researchers further note that the “findings suggest that most infected persons do develop immunity against reinfection that lasts for at least [a] few months, and that reinfections (if they occur) are well tolerated and no more symptomatic than primary infections.”
Insights into immunity from reinfection cases
Contracting the virus twice within the span of a few months may be more common than the data collected so far suggest. That’s if SARS-CoV-2 acts anything like seasonal coronaviruses, according to a paper published September 14. In that study, Arthur Edridge of the University of Amsterdam and colleagues analyzed stored blood samples of 10 healthy individuals that were taken, on average, every few months for the past 35 years. The team tested the samples for an increase in antibodies to a specific region of the structural capsid protein of each seasonal coronavirus.
Antibody levels spiked and dropped at regular intervals, showing “reinfections with all four seasonal coronaviruses are common and frequently occur after about a year,” Edridge writes in an email to The Scientist. Reinfection is therefore a “common human coronavirus feature,” he explains, and SARS-CoV-2 would most likely be no exception.
Rasmussen, who was not involved with any of the studies, says that reinfection is certainly possible, but she’s less convinced that SARS-CoV-2 will act like other coronaviruses that cause colds. Those other coronavirus reinfections may happen because those viruses only cause a mild infection and don’t elicit a strong immune response with lots of long-lasting antibodies. SARS-CoV-2 could be very different, she says.
That immune durability should really be the focus of reinfection studies, Tang explains. Researchers need to look at the longevity of antibodies after infection or vaccination, because if they start to wane, then there may be a need for vaccine boosters several months after the initial shot is given. The case reports and preliminary studies contribute to that overall picture of understanding SARS-CoV-2 immunity and its implication for vaccination, he explains, “but there’s a long way to go.”


thescientist--2020-10-26--NYU Langone to Drop Sackler Name from Biomedical Institute

New York University ’ s Langone Medical Center will remove the Sackler family name from its Institute of Graduate Biomedical Sciences after the US Department of Justice announced last week ( October 21 ) that Purdue Pharma , founded by the Sackler family , would plead guilty to three criminal charges for its role in the opioid epidemic .
“ Given the Sackler family ’ s association with Purdue Pharma and its role in encouraging opioid overuse , we view continuing to use the Sackler name as inconsistent with our institution ’ s values and incompatible with our mission , @ @ @ @ @ @ @ , according to the Associated Press .
Purdue , which makes the painkiller OxyContin , will plead guilty to conspiring to defraud the United States and violating federal anti-kickback laws as part of a settlement for more than $ 8 billion .
The deal does not release the company ’ s executives , nor the Sacklers , from criminal liability , and a criminal investigation is ongoing .
Daniel Connolly , a lawyer for members of the Sackler family , criticized the decision by New York University ( NYU ) .
“ As @ @ @ @ @ @ @ will show the company ’ s history and that members of the Sackler family who served on the board of directors always acted ethically and lawfully , so it is disappointing that NYU is rushing to judgment , ” Connolly tells the AP .
Named after the family since its founding in 1980 , the institute formally ceased accepting new donations from the Sacklers last summer .
In stripping the Sackler name , NYU joins institutions such as the Louvre and Tufts University , which was one of the first major institutions to @ @ @ @ @ @ @ increasingly faced pressure to rename buildings and return money from patrons with disgraceful behavior .

ABOVE: © ISTOCK.COM,
CRIBBVISUALS
New York University’s Langone Medical Center will remove the Sackler family name from its Institute of Graduate Biomedical Sciences after the US Department of Justice announced last week (October 21) that Purdue Pharma, founded by the Sackler family, would plead guilty to three criminal charges for its role in the opioid epidemic.
“Given the Sackler family’s association with Purdue Pharma and its role in encouraging opioid overuse, we view continuing to use the Sackler name as inconsistent with our institution’s values and incompatible with our mission,” university officials wrote in a statement, according to the Associated Press.
Purdue, which makes the painkiller OxyContin, will plead guilty to conspiring to defraud the United States and violating federal anti-kickback laws as part of a settlement for more than $8 billion. The deal does not release the company’s executives, nor the Sacklers, from criminal liability, and a criminal investigation is ongoing.
Daniel Connolly, a lawyer for members of the Sackler family, criticized the decision by New York University (NYU). “As soon as Purdue documents are released they will show the company’s history and that members of the Sackler family who served on the board of directors always acted ethically and lawfully, so it is disappointing that NYU is rushing to judgment,” Connolly tells the AP.
Named after the family since its founding in 1980, the institute formally ceased accepting new donations from the Sacklers last summer.
In stripping the Sackler name, NYU joins institutions such as the Louvre and Tufts University, which was one of the first major institutions to do so last December. Universities have increasingly faced pressure to rename buildings and return money from patrons with disgraceful behavior.