TIME neuroscience

This Alzheimer’s Breakthrough Could Be a Game Changer

Scientists recreated what goes on in the brains of Alzheimer’s patients in a 3D culture dish that could speed development of new drugs for the disease

Researchers have overcome a major barrier in the study of Alzheimer’s that could pave the way for breakthroughs in our understanding of the disease, a new report shows—and that new understanding could, in turn, pave the way for drugs that treat or interrupt the progression of the neurodegenerative condition.

For decades, animals have been the stand-ins for studying human disease, and for good reason. Their shorter lifespans mean they can model human conditions in weeks or months, and their cells can be useful for testing promising new drug treatments.

But they haven’t been so helpful in studying Alzheimer’s disease. Two factors contribute to the neurodegenerative condition — the buildup of sticky plaques of the protein amyloid, and the toxic web of another protein, tau, which strangles healthy nerve cells and leaves behind a tangled mess of dead and dying neurons. Despite attempts by scientists to engineer mice who exhibit both factors, they haven’t been able to generate the tau tangles that contribute to the disease.

Now, Dr. Rudolph Tanzi and Dr. Doo Kim at the Mass General Institute for Neurodegenerative Diseases at Massachusetts General Hospital, have devised a work-around that doesn’t involve animals. They have developed a way to watch the disease progress in a lab dish.

“In this new system that we call ‘Alzheimer’s-in-a-dish,’ we’ve been able to show for the first time that amyloid deposition is sufficient to lead to tangles and subsequent cell death,” said Tanzi in a statement.

MORE: Blood Test for Alzheimer’s

While autopsies showed evidence of both amyloid and tau in the brain, Alzheimer’s experts have been debating for years which came first — do amyloid plaques trigger the formation of tau tangles, or does the presence of tau cause amyloid to get stickier and bunch together in the brain? Tanzi and his colleagues showed definitively for the first time that amyloid is the first step in the Alzheimer’s process, followed by tau tangles. When he blocked the formation of amyloid in the culture with a known amyloid inhibitor, tau tangles never formed.

The disease-in-a-dish model is an emerging way of understanding conditions that either can’t be recapitulated accurately in animals, or diseases that make it difficult to study and test in human patients. In recent years, for example, scientists have successfully recreated the process behind amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, using stem cells from patients and allowing them to develop into the motor neurons that are affected by the disease. The technique led to a breakthrough in understanding that a certain population of nerve cells known as glial cells poison the motor neurons and impede their normal function. Now experts are focusing on finding ways to control the glial cell activity as possible treatment for ALS.

MORE: How Moodiness and Jealousy May Lead to Alzheimer’s

Tanzi and his team are hoping that something similar will come from their model of Alzheimer’s.

While the genes responsible for the inherited form of Alzheimer’s differ slightly from those involved in the more common form that affects people as they age, the end result — the build up of amyloid plaques and tau tangles — are the same. So now that they can see both the clumps of amyloid and the tau tangles, form, they can start to tease apart the processes that link the two processes together.

That will open the way toward finding drugs or other ways of interrupting the process more quickly than they could working with animals. It took six to eight weeks for the cells in the dish to form plaques and then tangles, compared to a year or so in mice. “We can now screen hundreds of thousands of drugs in this system that recapitulates both plaques and tangles…in a matter of months,” Tanzi said. “This was not possible in mouse models.” The system also makes it possible to test these drug compounds at one-tenth the cost of evaluating them in mice, he said. And that means that finding a way to prevent Alzheimer’s may come both faster and cheaper than scientists had expected.

TIME Obesity

How Family Dynamics at the Dinner Table Affect Kids’ Weight

A stock photograph of a family dinner
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It's not just what kids eat, but who they eat with that matters when it comes to their weight

“Eat together” is a mantra that doctors and nutritionists use regularly when they talk with families about eating healthy and maintaining normal weight. Children who eat regular family meals tend to have lower rates of obesity and eat more nutritiously. A new study published Monday morning in the journal Pediatrics takes a novel look at why.

A team led by Jerica Berge, in the department of family medicine and community health at University of Minnesota, asked the families of 120 children aged 6 to 12 to record eight days of meals. The families didn’t have to eat every meal together, and didn’t even have to eat dinner together every one of those nights, but did have to share at least three meals during that time. Half of the children were overweight or obese, and half were normal weight.

To tease out what features of the family meal might be influence weight, Berge’s team laboriously coded the interactions occurring at the table into two broad groups — those relating to the emotional atmosphere at the meal, such as how much the family members seemed to be enjoying the time together, how much hostility the diners showed one another, and how many uncomfortable silences or awkward pauses occurred — and those involving food specifically, including how much hostility emerged from discussions about food, including weight issues, and how much the parents controlled or limited what and how much children ate.

Children who were overweight or obese had family meals that included more negative emotional interactions — hostility, poor quality interactions, little communication and more controlling behavior from their parents — compared to children who weren’t obese. Their meals tended to have a warmer, more communicative atmosphere. For example, these children were given positive reinforcements to eat, and were encouraged to eat foods to get stronger or run faster, while heavier children experienced more negative pressures including threats and made to feel guilty about those in the world who can’t afford to eat three meals a day. If parents or caregivers talked constantly throughout the meal about food, and lectured about homework or attempted to control what the children ate, the youngsters were also more likely to be heavy.

“I was surprised by how consistent the patterns were,” says Berge. “Almost every single one of the emotional factors we coded were in the right direction, and there were really clear patterns in how much positive or negative interactions were associated with overweight and non overweight.”

The analysis also revealed other things that distinguished the family meals of overweight children and normal weight youngsters. Heavier children tended to have shorter meals — spending 13.5 minutes on average eating with their family compared to 18.2 minutes for non obese kids. Children who weren’t obese were also more likely to have a father or step-father at the table. The reason, says Berge, may be practical. “It might be a matter of having one more person at the table for crowd control, another person to help make the meal and be a model for children to emulate,” she says.

The team only coded the types of interactions between the family members during the meal, and did not include an in-depth look at what the families were eating. But that’s the focus of their next study.

In the meantime, the current data suggests that simply sitting down at the same table at the same time isn’t enough to influence obesity. And it’s up to pediatricians and family doctors to help families understand how to take full advantage of breaking bread together. “There is clear evidence that family meals are important in protecting kids against overweight,” says Berge, “so it’s important to start the conversation with families. It’s important to focus on making the meal environment more positive.” And, as her study showed, it doesn’t take lengthy repasts either — just 20 minutes as many times a week as possible.

Read next: Why I Don’t Eat With My Kids

TIME Obesity

Why Brown Fat May Be the Key to Weight Loss

brown fat
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Can you think your way thinner?

Not all fats we eat are created equal. We all know that, trying to dodge the less healthy ones that come from animals and dairy products and load up on those less likely to clog our arteries and add to our waistlines.

But it turns out that even after we consume fat, we store it in different forms as well, and scientists reporting in the journal Cell have identified a pathway in the brain that can direct our bodies to convert stubborn waistline-growing fat into a different fat that’s easier to burn off.

MORE: Having The Right Kind of Fat Can Protect Against Diabetes, Study Says

Brown fat, so-called because it is rich in the darker hued energy factories of cells known as mitochondria, is a calorie-hungry machine. It consumes a lot of energy and generates just as much, mostly in the form of heat. That’s why brown fat is more common in newborns, who need to be protected from getting chilled after nine months in the toasty womb. As we age and are better able to regulate our body temperature, we lose brown fat, and until recently scientists thought most adults had little brown fat, if any.

Now researchers at Yale School of Medicine have identified the process that turns white fat, the more common kind in the average adult body and the primary culprit in weight gain, into the energy-consuming brown fat.

MORE: How Now, Brown Fat? Scientists Are Onto a New Way to Lose Weight

Working with mice, the scientists honed in on a set of neurons in the brain that regulate the body’s energy balance, including the breakdown of glucose, which is the primary source of fuel for most cells. When mice fast, for example, their bodies shift into a type of emergency mode, conserving energy and shutting off systems and cells that require high amounts of energy, such as the heat-generating brown fat cells. Fasting resembles times of starvation, so evolutionarily, this makes sense; when food is scarce, the body shunts its energy toward essential processes, such as keeping the heart pumping and getting oxygen to the brain.

Xiaoyong Yang, an associate professor of comparative medicine and physiology at Yale, showed that this switch to conserve energy is intimately tied to hunger signals in the brain. “We showed that hunger itself is a signal that controls the browning of white fat, so the brain can actually control the browning of white fat.”

That means it’s the brain that regulates what type of fat, and how much of it, is burned. In obese animals, Yang found, these hunger signals are dysfunction; overweight and obese mice eat regardless of whether they are hungry, so the normal physical signals from the stomach don’t function properly. Heavier animals continuously feel hungry, even if they’ve eaten enough for their energy needs. That perpetuates the cycle of obesity, since it shuts off the transformation of white fat into energy-consuming brown fat, and therefore keeps more fat in an inert, pound-packing form.

“Obese animals, and people, lose the response to hunger,” he says. “Although there is plenty of food and plenty of energy, the hunger neurons send a false message that the body needs to conserve energy, not burn it.”

Eventually, he says, it might be possible to intervene with the hunger signal anywhere along its journey from the brain to the fat cells, and that may shift the balance in favor of burning fat rather than storing it, which might open the door to weight loss. But calibrating the switch will be critical, since favoring the burning of fat can also lead to other physiological problems such as wasting and malnutrition. “You don’t want to set the body’s energy balance to zero,” says Yang. “You want to reset it to normal levels.”

TIME Cancer

Why Cancer Drugs May Work Better While You Sleep

The body doesn't process drugs in the same way throughout the day, so it's possible to time your doses to make anti-cancer meds more effective

It’s news to no one that your body works differently when you’re awake and when you’re sleeping. But could the different states also affect how your body processes certain life-saving drugs? Researchers, reporting Friday in the journal Nature Communications, found that when it comes to cancer drugs, the answer may be yes.

Researchers at the Weizmann Institute of Science discovered—by happy accident—that some of the body’s molecular functions during the day may interfere with the effectiveness of certain cancer medication. Specifically, they found that the normal day-time production of some steroid hormones in the body actually inhibited the work of epidermal growth factor (EGF) receptors—which are the proteins targeted by a class of anti-cancer drugs. Tumor cells plant these receptors on their surfaces to attract nutrients that help them survive and grow. Drugs, including the breast cancer agent lapatinib, can block these receptors on tumors, and such medications are a popular way to treat breast cancers expressing epidermal growth factor.

But Yosef Yarden, a professor in the department of biological regulation, and his team found that when the tumor cells simultaneously bind to something else—such as steroid hormones—the EGF receptors are less active, making drugs like lapatinib less potent.

The findings are still preliminary, but there is other evidence that the day-night cycle may be a potentially important factor in determining cancer treatment dosing in coming years. Some studies showed, for example, that when the 24-hour rest and activity cycle is broken metabolically, and the EGF receptors aren’t given enough time to be active, certain tumors in animals grow two to three times faster.

“The study developed out of a mistake. We accidentally omitted a synthetic steroid…from the medium in which we routinely grow mammary gland cells,” Yarden wrote in an email response to TIME. “And we noticed that the cells acquired a faster rate of migration when we followed them under a microscope.”

Intrigued, they turned to mice to answer some more questions. Knowing that steroid levels peak during the day and drop off during sleep, Yarden and his colleagues wondered whether the timing of anti-tumor drugs would affect tumor growth. So they gave a group of mice with breast cancer tumors lapatinib at different times over a 24-hour period and tracked any differences in the size and growth of the tumors.

Indeed, the mice given the drug while they slept showed significantly smaller tumors after seven days than those who received the drug during the day. Yarden suspects that the lower levels of steroid hormones circulating at night allows more of the EGF-targeting drug to hone in on its receptors on the tumor cells and inhibit their growth. Not only that, but the tumors in the mice taking the drug at night looked different; they showed less blood vessel infiltration which meant they were less robust.

Does that mean it’s better to get cancer therapy at night? So far, the results only apply to animal models, and to cancers driven by EGF. More work needs to be done, but if it’s validated, shifting therapies to just before bed “seems logical,” says Yarden. Especially since drugs like lapatinib come in pill form, so it would be relatively easy to take medications before turning in rather than in the morning.

TIME diabetes

Type 1 Diabetes Treatment Gets Boost from Stem Cells

Human stem cell derived beta cells
Insulin-making cells grown from stem cells glow green two weeks after they are transplanted into mice (c) Douglas Melton 2014

Scientists started with stem cells and created the first insulin-making cells that respond to changes in glucose

Scientists are closer to a potential stem cell treatment for type 1 diabetes.

In a new article in the journal Cell, Douglas Melton, co-director of the Harvard Stem Cell Institute (and one of the 2009 TIME 100) and his colleagues describe how they made the first set of pancreatic cells that can sense and respond to changing levels of sugar in the blood and churn out the proper amounts of insulin.

It’s a critical first step toward a more permanent therapy for type 1 diabetics, who currently have to rely on insulin pumps that infuse insulin when needed or repeated injections of the hormone in order to keep their blood sugar levels under control. Because these patients have pancreatic beta cells that don’t make enough insulin, they need outside sources of the hormone to break down the sugars they eat.

MORE: Stem-Cell Research: The Quest Resumes

Melton started with two types of stem cells: those that come from excess embryos from IVF procedures, and those that can be made from skin or other cells of adults. The latter cells, known as iPS cells, have to be manipulated to erase their developmental history and returned back to an embryonic state. They then can turn into any cell in the body, including the pancreatic beta cells that produce insulin. While the embryonic stem cells from IVF don’t require this step, they aren’t genetically matched to patients, so any beta cells made from them may cause immune reactions when they are transplanted into diabetic patients.

Both techniques, however, produced similar amounts of insulin-making beta cells—something that would have surprised Melton a few years ago. But advances in stem cell technology have made even the iPS cells pretty amenable to reprogramming into beta cells. Melton’s group tested more than 150 different combinations of more than 70 different compounds, including growth factors, hormones and other signaling proteins that direct cells to develop into specific cell types, and narrowed the field down to 11 factors that efficiently turned the stem cells into functioning beta cells.

MORE: Woman Receives First Stem Cell Therapy Using Her Own Skin Cells

The two populations of stem cells churned out hundreds of millions of insulin-making cells, which is the volume of cells that a patient with type 1 diabetes would need to cure them and free them from their dependence on insulin. An average patient, says Melton, would need one or two “large coffee cups” worth of cells’, each containing about 300 million cells. Melton and his team then conducted a series of tests in a lab dish to confirm that the cells were functioning just like normal beta cells by producing more insulin when they were doused with glucose, and less when glucose levels dropped. That was a huge advance over previous efforts to make beta cells from stem cells—those cells could produce insulin, but they didn’t respond to changing levels of glucose and continuously pumped out insulin at will.

Next, the scientists transplanted about five million of the stem cell derived beta cells into healthy mice, and two weeks later, gave them an injection of glucose. About 73% of the mice produced enough insulin to successfully break down the sugar. What’s more, that was similar to the proportion of mice responding to glucose after getting a transplant of beta cells from human cadavers. That was especially encouraging since some type 1 diabetics currently receive such transplants to keep their diabetes under control. “We’ve now shown that we can produce an inexhaustible source of beta cells without having to do to cadavers,” he says.

MORE: First Stem Cells Cloned From Diabetes Patient, Thanks to Egg Donors

Taking the tests even further, the group showed that even mice that were already diabetic showed improved blood sugar levels after receiving a transplant of the stem cell beta cells—in other words, the transplanted cells effectively cured their diabetes. “We showed you can give three sequential challenges of glucose—similar to breakfast, lunch and dinner—and the cells responded properly,” says Melton.

But he acknowledges that as exciting as the advance is, it only solves half the problem for those with type 1 diabetes. The reason their beta cells aren’t able to make enough insulin may be due to the fact that they are attacked by the body’s own immune system for reasons that scientists still don’t understand. So the next step in turning these findings into a potential therapy is to find ways to protect the beta cells from destruction, either by encapsulating them in a mesh-like device similar to a molecular tea bag, or finding ways to genetically modify them to carry ‘don’t attack me’ proteins, the same way that fetal cells do so that an expectant mother’s immune cells don’t attack the growing baby.

MORE: Stem Cell Miracle? New Therapies May Cure Chronic Conditions like Alzheimer’s

“It’s taken me 10 to 15 years to get to this point, and I consider this a major step forward,” says Melton, who began researching ways to treat type 1 diabetes when first his son, then his daughter were diagnosed with the condition more than two decades ago. “But the longer term plan includes finding ways to protect these cells, and we haven’t solved that problem yet.”

TIME ebola

See How Ebola Drugs Grow In Tobacco Leaves

The drug that saved the lives of American aid workers from Ebola was made by plants

It would be an understatement to call ZMapp a “sought after” drug. Ever since it brough tback two Ebola-infected aid workers from the brink of death, demand for the drug—which has not been approved by the Food and Drug Administration and was made available on an emergency use basis—has boomed. The trouble is, there’s no supply.

The doses administered to the U.S. aid workers exhausted a nearly nonexistent supply, according to its manufacturer, Mapp Biopharmaceuticals. But that’s not because it takes a long time to manufacture the antibodies that make up the ZMapp cocktail. ZMapp is taking longer to produce in large quantities because one of the three antibodies in the cocktail doesn’t grow well in the plants—which is how ZMapp is produced.

The process involves growing tobacco plants, not in the acres of fields earmarked by tobacco companies for their cigarettes, but in a controlled environment in a greenhouse, for six weeks. Then, the leaves of the plants are injected or infused with a plant bacterium that carries a valuable payload — the genes for the antibodies that can bind to and neutralize the Ebola virus. The plant cells treat the new genes as one of their own, and start making the antibody. It takes about 14g of these antibodies to treat a patient, says Yuri Gleba, CEO of Icon Genetics, the German company that pioneered the platform, and to produce that much requires around 78 tobacco plants and about seven to 10 days.

A team led by Gleba is helping Mapp Biopharmaceuticals to optimize that production and to make the entire process more efficient so it requires fewer plants. “If everything is properly optimized, those plants can be full of that antibody,” he says. (Mapp officials declined to comment for this article on the status of their ZMapp production.)

MORE: Ebola Treatment May Emerge From Drug For Another Virus

Why plants? The time it takes to grow a plant is less time than it takes to genetically engineer a mouse or other rodent to produce human antibodies, which is how such products have been made in the past. It’s also less expensive. Plant-based manufacturing represents a promising new way of producing drugs that could cut the time it takes to bring critical medications, such as a flu vaccine during a pandemic, to a large number of people. Researchers have used the technology to develop a vaccine against norovirus, the infection that plagues cruise ships, for example, that is being tested now.

Here’s what that process looks like.

MORE: Potential Vaccine Shows Some Promise, but the Spread of Ebola Is Accelerating

 

 

TIME Sex

Does Teen Sexting Lead to Earlier Sex?

teen sext text
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The latest research teases apart whether sexting promotes more sex, or whether having sex makes sexting more likely

While plenty of studies have linked the sending of sexually explicit messages or naked pictures to a higher incidence of sex and risky sexual behavior, most of those studies didn’t follow the same children over time. That means they studied sexting habits in one group of children, and sexual behaviors in another, older group a year or so later. So it’s possible that other factors could explain the relationship that had nothing to do with the sexting.

To address that issue, Jeff Temple, from the department of obstetrics and gynecology at University of Texas Medical Branch, collected data from a group of nearly 1,000 high school students in Texas over six years. The students answered questions about dating, dating violence and other behaviors as sophomores and then as juniors. Temple then compared the answers.

MORE: Review: Men, Women & Children Shows How Sexting Is Ruining America

Reporting in the journal Pediatrics, he says that those who sexted as sophomores were 32% more likely to have had sex in the following year than those who did not, supporting earlier data. But Temple was also able to break down the types of sexts the students primarily used, from those who actively sent naked pictures to those who only received or asked for them. Those who only received sexts did not show a statistically significant higher risk of having sex, but those who asked for a sext were nearly 10 times more likely and those who were sent a sex were 5.3 times more likely to send one themselves. And students who sent sexts were the most likely to have sex in the following year.

“So basically if a parent saw his kid had asked for a sext, that in and of itself isn’t related to sexual behavior unless that kid also sent naked pictures of himself,” says Temple.

The data also showed that sending sexts, while associated with a higher chance of having sexual intercourse, was not linked to an increased incidence of risky sexual behavior, such as unprotected sex, having multiple sexual partners, or using alcohol or drugs before sex. “That was surprising but it might mean that sexting is not limited to just at-risk kids,” he says. “Sexting may be becoming part of sexual development, and therefore it involves a cross section of all adolescents.”

MORE: Sexting in Middle School Means More Sex for Preteens and Teens

Temple admits that the data need to be confirmed with other studies; the reports on sexting and sex were self-reported by the students, which could affect their reliability. But the rates of sexting, along with sexual intercourse, fall in line with national surveys so are likely to be valid, he says.

MORE: Non-Consensual Sexting: The Hot New Way to Make Someone Really Uncomfortable

If sexting is indeed part of the new normal of sexual development, then it could be a sign of those who are more ready for sexual activity or more receptive to it, he says. Studies show that up to a third of adolescents are involved in sexting, and they may be good candidates for education about safe sex and the dangers of unprotected sex. “If sexting does predate sex, then it’s of public health importance. It becomes a marker of sexual activity and it could be a good opportunity to talk to them about safe sex prior to them having sex and preventing early sexual debut and risky sexual behavior,” he says.

TIME medicine

New Genes Found that Determine Your Height

The latest analysis doubles the number of genes connected to height

How tall you are is strongly related to the genes you inherit, and previous studies suggested that as much as 80% of the variance in height among people is due to their DNA.

And in the largest genetic study of height-related genes to date, scientists involved in the appropriately titled GIANT consortium (Genetic Investigation of Anthropometric Traits) identified 423 genetic regions connected to height — which could explain as much as 60% of that genetic component.

Dr. Joel Hirschhorn, leader of the GIANT consortium at Boston Children’s Hospital, Harvard Medical School and the Broad Institute of MIT says that for a trait like height, which isn’t determined by a single gene but likely the combined effects of multiple genes involved in multiple different processes from bone growth to cell growth, the new findings are like finding biggest nuggets of gold in a riverbed. The latest analysis, published in the journal Nature Genetics, describes the gene variants most commonly shared among people (not the rare mutations) that likely contribute to height.

They emerged from a sweep of the genomes of more than 250,000 people of various heights, and from correlating their stature with their genetics. Many of the known and familiar factors related to height, including those dealing with skeletal growth and collagen that are mutated in people with medically short stature, for example, appeared in the study, confirming their role in determining how tall people get.

But there were also some surprises — genetic regions that previous had never been thought to be related to height, including a gene known to be involved in cell growth but not in skeletal functions. “It’s a mix ranging from completely known things, to those that make sense to things that are completely surprising and things we don’t even know what to think about them,” says Hirschhorn.

What the group has identified are gene regions of interest, and a new round of studies will have to delve deeper into those areas to isolate specific genes — and the proteins they make, such as growth factors, enzymes, or other agents — that are actually responsible for determining height. But it’s a critical first step, and could lead to potential new ways of treating medical conditions of short stature or gigantism that can have health negative health effects on the heart and joints.

TIME ebola

Ebola Contact Found By Dallas Law Enforcement

A scanning electron micrograph of Ebola virus budding from the surface of a Vero cell of an African green monkey kidney epithelial cell line.
A scanning electron micrograph of Ebola virus budding from the surface of a Vero cell of an African green monkey kidney epithelial cell line. NIAID—EPA

"This person has not committed a crime; he is a low risk individual"

Updated Sunday, Oct. 5

A once-missing homeless man believed to have had some level of contact with Dallas Ebola patient Thomas Duncan was found Sunday, NBC news reports.

The man’s temperature was taken yesterday, and he was asked to remain available for temperature checks today and for 21 days, but left, said Judge Clay Jenkins, who is leading Dallas’ emergency response efforts. The Dallas County sheriff’s office and police department were searching for the man.

“This person has not committed a crime; he is a low risk individual. We want to move him to a comfortable, compassionate place, and care for his every need while we monitor him throughout the monitoring period,” said Jenkins during a news conference Sunday. “He is asymptomatic. We are doing this as a precautionary measure.”

The man belongs to a group of 38 people who are having their temperatures taken twice a day and asked about any possible Ebola symptoms for 21 days, since they may have had contact of any kind, even indirect, with Duncan. Centers for Disease Control (CDC) director Dr. Tom Frieden said that 10 people who had more direct contact with Duncan are being watched the same way.

Seven of the 10 are health care workers who were at the hospital while Duncan was treated, and three are from his family or community. Four of Duncan’s close relations, including his female partner and three young men living in the apartment where he stayed prior to falling ill, have been quarantined. One of these individuals, however, did not have direct contact with Duncan; however, he may have wanted to stay with his family.

The four were moved on Saturday to a more secure location and none are showing any symptoms of infection. One of the young men is able to play basketball at the new residence, said Jenkins.

Duncan’s condition worsened on Saturday, and he is now in critical condition at Texas Health Presbyterian. Frieden said any decisions about whether Duncan would be treated with any experimental therapies would be decided by Duncan, his family and his doctors. One potential treatment initially makes patients worse before they improve, and none have been approved by Food and Drug Administration because none have been tested for safety and efficacy in human patients.

The news about the missing contact in Dallas comes on the same day that health officials ruled out a potential case of Ebola in a traveler arriving at Newark airport. That passenger’s symptoms and tests did not indicate he was infected with Ebola, said Frieden. But concern about the disease has escalated since Duncan’s diagnosis. The CDC received an average of 50 calls or emails daily from doctors, hospitals or health departments about potential Ebola cases, before Duncan’s case, and that volume has jumped to about 800 inquiries a day.

Frieden stressed that keeping Ebola from spreading in the U.S. will require a combination of strong public health efforts within the country — making sure health care providers ask about recent travel history for any patients presenting with fever and other symptoms of Ebola, and quickly isolating them if they have been to West Africa — and maintaining efforts to stop the epidemic in Guinea, Liberia and Sierra Leone as well.

So far, CDC-trained screeners at airports in the three affected countries have removed 77 from boarding planes headed to the U.S., and those temperature-taking efforts, along with asking passengers about any potential contact with Ebola patients, remain critical, said Frieden. But aid efforts to help health officials in Africa are just as essential to protecting the U.S. as well.

If people are prevented from leaving or entering the three countries struggling with the Ebola epidemic, he said, then the disease will continue to rage there and potentially pose a larger threat to the global community in coming months. “As long as cases continue there, there is the possibility that someone will travel, and infect someone else in this country or other countries,” he said. “An outbreak anywhere is potentially a threat everywhere.”

Frieden will meet with President Obama this week to discuss global efforts to contain Ebola in Africa.

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