These Baby High Chairs Will Give Them the Safe Boost They Need

Aside from diapers and baby formula, the other constant in your life as a parent of a baby is going to be a reliable baby high chair. Whether you’re eating at home, at a relative’s, or at a restaurant, you’re going to need something to give them a boost while keeping them safely contained so you can eat too. The best baby high chairs come in a variety of shapes, sizes, and colors that you can match to their favorite outfits or colors. Many high chairs come with different features, so it’s important to consider what’s the best option for you and your little one.

When you’re picking out a baby high chair, you’ll first want to determine where you’re going to use it most. If you’re looking for a travel-friendly version, you’ll want a compact one that’s easy to fit in the car. To avoid buying high chairs as they grow out of them, one that easily adjusts as they grow up is a must. Some high chairs even convert into a step stool, so that’s another smart thing to consider. Ahead, we’ve rounded up the best baby high chairs to meet your needs.

1. Infantino High Chair

They (and you) won’t be able to resist this darling fox baby high chair. This four-in-one baby high chair is also smart too by saving space in your home. It converts from a booster into a toddler chair with ease so it will grow with them as they outgrow their baby high chair. It’s also easy to clean and has an easy release food tray for fuss-free cleaning. You can wipe down the soft cushioning without a problem, too. With front wheels, you can reposition the chair to face however you’d like.

2. Graco Everystep High Chair

If you want a baby high chair that does more than let your little one safely sit, then this convertible option will meet your needs. This smart high chair easily converts from a high chair to a kids step stool for when they need to reach for the counter. With seven total growing stages, you can keep this high chair for years without having to replace it as they get bigger. It’s narrowed down to three stages: the infant high chair with three reclining positions, fully featured baby high chair with seven height positions and dishwasher-safe tray insert, and infant booster seat that brings them right up to the table by attaching to the table.

3. Fisher Price SpaceSaver High Chair

Whether you have tight quarters at home or travel often with baby, this compact baby high chair is going to save a ton of valuable space wherever you go. Not to mention, it has a stylish neutral design that will look great in your home. It may be smaller, but it still packs in all the features of a full size high chair. It even transforms from an infant booster to a toddler one too, so you don’t have to purchase a new one as they get older. There’s two height adjustments and three recline positions for ultimate comfort, and the machine-washable seat pad makes clean ups a breeze. The deep-dish tray prevents food from falling over the edge, too.


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Should you fly yet? An epidemiologist and an exposure scientist walk you through the decision process

We don’t know about you, but we’re ready to travel. And that typically means flying.

We have been thinking through this issue as moms and as an exposure scientist and infectious disease epidemiologist. While we’ve decided personally that we’re not going to fly right now, we will walk you through our thought process on what to consider and how to minimize your risks.

Why the fear of flying?

The primary concern with flying—or traveling by bus or train—is sitting within six feet of an infected person. Remember: Even asymptomatic people can transmit. Your risk of infection directly corresponds to your dose of exposure, which is determined by your duration of time exposed and the amount of virus-contaminated droplets in the air.

A secondary concern is contact with contaminated surfaces. When an infected person contaminates a shared armrest, airport restroom handle, seat tray or other item, the virus can survive for hours though it degrades over time. If you touch that surface and then touch your mouth or nose, you put yourself at risk of infection.

Before you book, think

While there is no way to make air travel 100% safe, there are ways to make it safer. It’s important to think through the particulars for each trip.

One approach to your decision-making is to use what occupational health experts call the hierarchy of controls. This approach does two things. It focuses on strategies to control exposures close to the source. Second, it minimizes how much you have to rely on individual human behavior to control exposure. It’s important to remember you may be infectious and everyone around you may also be infectious.

The best way to control exposure is to eliminate the hazard. Since we cannot eliminate the new coronavirus, ask yourself if you can eliminate the trip. Think extra hard if you are older or have preexisting conditions, or if you are going to visit someone in that position.

If you are healthy and those you visit are healthy, think about ways to substitute the hazard. Is it possible to drive? This would allow you to have more control over minimizing your exposures, particularly if the distance is less than a day of travel.

You’re going, now what?

If you choose to fly, check out airlines’ policies on seating and boarding. Some are minimizing capacity and spacing passengers by not using middle seats and having empty rows. Others are boarding from the back of the plane. Some that were criticized for filling their planes to capacity have announced plans to allow customers to cancel their flights if the flight goes over 70% passenger seating capacity.

Federal and state guidance are changing constantly, so make sure you look up the most recent guidance from government agencies and the airlines and airport you are using for additional advice, and current policies or restrictions.

While this may sound counterintuitive, consider booking multiple, shorter flights. This will decrease the likelihood of having to use the lavatory and the duration of exposure to an infectious person on the plane.

After you book, select a window seat if possible. If you consider the six-foot radius circle around you, having a wall on one side would directly reduce the number of people you are exposed to during the flight in half, not to mention all the people going up and down the aisle.

Also, check out your airline to see their engineering controls that are designed or put into practice to isolate hazards. These include ventilation systems, on-board barriers and electrostatic disinfectant sprays on flights.

When the ventilation system on planes is operating, planes have a very high ratio of outside fresh air to recirculated air – about 10 times higher than most commercial buildings. Plus, most planes’ ventilation systems have HEPA filters. These are at least 99.9% effective at removing particles that are 0.3 microns in diameter and more efficient at removing both smaller and larger particles.

How to be safe from shuttle to seat

From checking in, to going through security to boarding, you will be touching many surfaces. To minimize risk:

Bring hand wipes to disinfect surfaces such as your seat belt and your personal belongings, like your passport. If you cannot find hand wipes, bring a small washcloth soaked in a bleach solution in a zip bag. This would probably freak TSA out less than your personal spray bottle, and viruses are not likely to grow on a cloth with a bleach solution. But remember: More bleach is not better and can be unsafe. You only need one tablespoon in four cups of water to be effective.

Bring plastic zip bags for personal items that others may handle, such as your ID. Bring extra bags so you can put these things in a new bag after you get the chance to disinfect them.

Wash your hands or use hand sanitizer as often as you can. While soap and water is most effective, hand sanitizer is helpful after you wash to get any parts you may have missed.

Once you get to your window seat, stay put.

Wear a mask. If you already have an N95 respirator, consider using it but others can also provide protection. We do not recommend purchasing N95 until health care workers have an adequate supply. Technically, it should also be tested to make sure you have a good fit. We do not recommend the use of gloves, as that can lead to a false sense of security and has been associated with reduced hand hygiene practices.

If you are thinking about flying with kids, there are special considerations. Getting a young child to adhere to wearing a mask and maintaining good hygiene behaviors at home is hard enough; it may be impossible to do so when flying. Children under 2 should not wear a mask.

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The cholera outbreak in a Victorian asylum that anticipated the coronavirus crisis in care homes

In 1849, a cholera epidemic that was sweeping through Britain reached West Riding Asylum in Wakefield, West Yorkshire. The deadly disease soon spread through the wards. Searching for the source of the outbreak, the consulting physician eventually settled on an individual who had been admitted while ill. The doctor described this unfortunate patient as the “unconscious messenger of death”.

Over a century and a half later, a care-home owner in Devon—alarmed by the fact that local care homes could admit residents with COVID-19—expressed his fears in a strikingly similar way. In early April 2020, the government issued guidelines that permitted taking in new residents even if sick. This, the care-home owner argued, would be “tantamount to importing death”.

Care homes are the epicentre of the COVID-19 pandemic in the UK. Compared to all other settings, they have seen the biggest relative increase in deaths since the start of the outbreak. Most of the vast asylums of the Victorian era closed in the 20th century, as attitudes to treating mental health changed. Yet there are haunting parallels to be seen. Responses to, and experiences of, an outbreak of disease at one of these asylums back in the 19th century are disturbingly resonant today.

Cholera, an acute diarrhoeal disease, claimed the lives of more than 100 patients at West Riding Asylum in 1849. Such was the scale of the tragedy that the consulting physician, Thomas Giordani Wright, was commissioned by the asylum’s regulators to investigate and account for this disaster. The result, a report published in 1850, allows us to reconstruct the story of the cholera outbreak in minute detail. It is a story which foreshadows our own.

Cholera grips the asylum

The 19th century witnessed a huge expansion in the number of asylums in England.

In 1808, the British government passed legislation that allowed counties to collect and spend taxes on building asylums for those unable to pay for private treatment for mental illness. While most counties didn’t begin construction until they were forced to by further legislation in 1845. Yorkshire was quick off the mark. West Riding Asylum opened its doors in November 1818, initially with a view to accommodating 150 patients. By the middle of the century, extensions and a second building meant that more than 500 patients filled its wards.

Global cholera pandemics were a repeated problem throughout the 19th century. When the disease hit Britain in the autumn of 1848, Yorkshire was initially spared. But by September 1849, it had reached Wakefield. In his report, Wright conjures an image of the institution besieged, with “the spread of the pestilence all around the asylum”.

Some of those who had been attached to the asylum for a long time, like Wright himself, might have taken confidence from the fact it had escaped disaster during the previous cholera pandemic to hit England, in 1832. In 1849, sadly, it would not be so lucky.

In his report, Wright sought to understand how the disease had infiltrated the institution. He was doing so a few years before John Snow’s discovery that cholera was waterborne. Yet an inspection of both the drainage and ventilation did take place at West Riding Asylum; both were given a clean bill of health. Indeed, the inspectors—Messrs West and Dawson—were left to conclude that “the visitation, fatal as it has been to many, must be considered either as the immediate infliction of Divine Providence, or as dependent on causes of which nothing as yet is known”.

Wright looked elsewhere for causes. And in spite of his admission that “the laws of contamination are, in fact, little known”, he set his sights on one Elizabeth Fenton—his “unconscious messenger of death”.

The hunt for ‘patient zero’ begins

Elizabeth Fenton, a person with epilepsy, had been admitted to West Riding Asylum on 17 September 1849. She came from the nearby Gomersal Workhouse, where she had been for the past six years after her husband, a stonemason, abandoned her and their two children. Although her transfer had been recommended some weeks earlier, when the local official called at the workhouse to take her to the asylum, it took people at the workhouse by surprise.

Strokes of ill luck might, in part, explain the disastrous chain of events which followed. Two residents at the Gomersal Workhouse had died of cholera the night before Fenton was transferred; one of them normally slept in the same room as her. Yet authorities may have been lulled into a false sense of security by the fact that Fenton had not had direct contact with these residents before her transfer. She had suffered an unusually violent seizure that week, and so had spent most of her last nights in the workhouse restrained in a chair in another room. And the day before her transfer, she had been given a laxative to help relieve constipation. An early warning sign of cholera infection, diarrhoea, was thus concealed.

By the evening of her first day in the asylum, Fenton had developed symptoms. She was isolated immediately, as it had become clear that an outbreak was underway in Gomersal Workhouse. Her room was locked, and access restricted to a select few. But within a week, four more women had fallen ill. From that point on, the disease spread like wildfire through the female as well as male patient populations of the asylum.

Since the male cases were known not to have had any direct contact with any of the female cases, and the original four women were not even thought to have seen Fenton, Wright was stumped to explain whether the mode of transmission was “gaseous or solid, material or immaterial, vegetable or animal, magnetic or electrical”.

But he was firm in his conclusion that “infection was in some way brought into the asylum by that patient”. He cinched his argument by referring back to the 1832 pandemic, which the asylum had escaped unscathed. The only difference, he argued, between the two contexts was that no new patients from infected districts had been admitted in 1832, whereas in 1849, they had: Fenton. Case closed.

Yet Wright pursued this line of investigation further, with prosecutorial zeal, by turning his attention to Gomersal Workhouse. Fenton had brought the disease from Gomersal to West Riding Asylum—but how, in the first place, had it arrived at Gomersal?

From the medical officer at the workhouse, Wright learned that on 6 September “a dirty Irish woman, and her four children, were brought into the workhouse”. Showing signs of cholera, they had been taken to the workhouse hospital, where the mother had died just hours after arrival. One of her children died “a day or two after”; the exact timing was not thought worth recording. And just a day before Fenton was transferred to the asylum, two other women at the workhouse died.

As we know all too well from COVID-19, Aids and other recent pandemics, the hunt for the first person to fall ill—known as “patient zero”—collides with other vectors of stigmatisation. In the case of COVID-19, this has been clear above all in the horrifying rise in anti-Asian racism and xenophobia worldwide.

By 1849, the arrival in England of hundreds of thousands of Irish displaced by the Great Famine had contributed to wider anti-Irish sentiment, cementing a prejudicial association with poverty, dirt and disease. Forced into desperate living conditions, including dog kennels and cellars, this was an association which drew vicious strength from the staggeringly high death rates among the Irish during times of epidemic disease. As well as being epidemiologically unhelpful, Wright’s explicit identification of a local Irish patient zero fed into growing anti-Irish racism and a representation of the Irish as carriers, rather than fellow sufferers, of the disease.

The human cost rises

With cholera loose in the institution, the medical officers and attendants at West Riding Asylum tried to fight it using the full arsenal at their disposal: removal of patients to a separate cholera ward; improvements in diet—including “extra allowances of tea and brandy for supper”; fumigation of wards; and laundering of all bed sheets and clothes.

But as in the current pandemic, there was no cure, no vaccine. By the end of the year, more than 100 residents had died of cholera. Nineteen had died in just a single day towards the end of October.

In what Wright evidently considered to be a small mercy, the patients “generally did not appear to be much affected by fear, nor were they aware of the extent of the mortality”. But just as in today’s care homes, for the staff of the institution, it was traumatic. “It was a period of awful emergency, and the consternation of all was increased by the fearful mystery of the pestilence, the rapidity of its attack, without previous symptom or warning, and the little more than failure of every effort, to mitigate its course, or avert its progress.”

Amid this horror, it is unsurprising—particularly, unhappily, to us now—that residents were not the only fatalities. On November 4 1849, Mrs Reynolds, the chief nurse of the ward set up to tend to cholera cases, died of the disease.

In a separate report in November 1849, the director of the asylum quoted Reynolds as saying: “If I should die, I shall have the satisfaction on my death bed of knowing that I have done my duty.” Wright later wrote movingly of “her heroic and unremitting devotion to her duties” and “her kindness and humanity”.

Reynolds was not alone in being held up for praise. In 1851, the director of the asylum looked back on the service of all staff in these harrowing months “with gratitude and admiration”. And while noting that “no pecuniary recompense can adequately remunerate such services”, he drew attention to the princely sum of £264 which had been distributed among staff by the visiting justices, and a further—unspecified but “very large”—sum disbursed by a visiting magistrate (there to oversee Wright’s investigation) in a private capacity.

There is a poignant coda to this story, however. In contrast to the “substantial tokens of public approbation” the surviving officers and attendants had received, Wright used his report to draw attention to the sad inadequacy of Reynolds’s final resting place: a grave “without a mark to record her fate”. He pleaded with the magistrates and medical officers to make contributions so that her life and service could also be properly remembered.

Were lessons learnt?

Wright rounded off his report with a “lessons learnt” section—a genre with which we are likely to become all too familiar in the coming months and years.

While noting that changes to diet and fumigation appeared to bear some fruit, the lesson Wright was desperate to hammer home was the importance of “the precaution of not admitting into the asylum fresh patients from infected districts”. In that respect, his advice was much stricter than that issued by the Board of Health, the body charged with the control of epidemic disease, whose confident assurances—he suggested—had influenced people “to disregard all risk of communication”.

Wright concluded: “We have been fatally taught, that it is most important to use every possible vigilance to avert the approach of cholera; for, if it once find an entrance, no human resources are of much avail, to mitigate its intensity or abate its ravages.”

The colossal asylums of the 19th century may no longer be with us, but the parallels haunt us still. The risk to care homes was clear early in the contemporary crisis, according to chief scientific adviser Sir Patrick Vallance. And the vulnerability of institutionalised populations was not only foreseeable; doctors during the 1849 cholera outbreak tried to pass down lessons to future generations.

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Coronavirus: Big tobacco sees an opportunity in the pandemic

Over the last few months, as COVID-19 has spread around the world, big tobacco has exploited the pandemic to push its branding and products. The industry never misses a trick when it comes to exploiting the chaos of international crises, including wars. The current pandemic is no exception.

The strategy is to use the pandemic to try and shift their image from vilified industry to trusted health partner. The tactics they have employed to achieve this are shameless, even for an industry as controversial as tobacco. There are examples of tobacco companies offering assistance in the form of ventilators, gels, PPE and even cash. They are even involved in trying to develop a vaccine. While there is no doubt that these have been gratefully received by authorities struggling with a chronic lack of resources, the industry has been up to other tricks, too. And one British FTSE 100 company is proving particularly adept.

In March, as many governments began to lock down their populations, British American Tobacco (BAT) began co-opting universal health messages. These were then placed on branded face masks, which were subsequently handed out to social media influencers for free.

Instagram remains one of the key marketing platforms for the industry. In 2019, BAT paid Instagram influencers to promote glo, its heated tobacco device, among other products. One of the hashtags used was #todayiwill.

BAT’s Instagram campaign ran into trouble, though. In December 2019, in a landmark decision, the UK Advertising Standards Authority, ruled against BAT and three other firms for promoting an e-cigarette, Vype, on Instagram, after a complaint by ASH, Campaign for Tobacco-Free Kids and STOP, of which the University of Bath is a partner. Later that month, under pressure to act, Facebook and Instagram announced that “branded content that promotes goods such as vaping, tobacco products and weapons will not be allowed”.

Undaunted, BAT appeared to use the social media platform as a COVID-19 marketing tool, especially in countries where oversight was likely to be less stringent. BAT simply changed the #todayiwill hashtag to #todayIwillstayhome, to reflect the messaging from governments for people to stay at home. Evidence uncovered by the Campaign for Tobacco-Free Kids, which has been tracking BAT’s activities, found that in Kazakhstan among other countries, BAT provided influencers with “today I will stay home” glo masks. Other hashtags used included #glomask.

The company used other COVID-19 hashtags, too. An influencer appeared on one BAT Vype account in Spain, using #frenalacurva, the Spanish for “flatten the curve”. BAT employed similar tactics in Latin America and Europe. This meant if you were searching on Instagram for these government messages, you would come across BAT’s subliminal marketing.

Days before the glo-branded masks started appearing on social media and right in the middle of the pandemic, BAT launched a glossy rebranding exercise unveiling a new slogan “For a Better Tomorrow”. The company replaced its old tired leaf logo with bright rainbow colours.

‘New adults’, new market

BAT’s board told investors that its redefined mission was now “stimulating the senses of a new adult generation”. This essentially means entrapping a new generation of young people into nicotine addiction, from vaping, heated tobacco products to cigarettes.

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These Fruits and Veggies Could Last Months When Stored The Right Way

Any smart shopper would want their fresh produce to last as long as possible. If it doesn’t go bad fast, it means you can save more money because fresh fruits and vegetables can be pretty expensive. Having to throw away rotten ones and restock again can hurt your food budget and is also wasteful.

According to the Environmental Protection Agency, around 94% of food thrown away end up in landfills. This could be lessened just by knowing the right way to purchase, store, and prepare your fruits and vegetables so they will last for as long as possible. But you can also opt to stock up on these products that could last for longer than you would expect, as long as you store and use them correctly.

Potatoes

It’s ideal to store potatoes in 40 degrees Fahrenheit. These veggies don’t like light, so the perfect storage conditions for potatoes is in the basement or a cellar. Light can also make them turn green.

Storing potatoes in this condition keeps them from rotting for around 2 to 4 months. However, keep them away from apples and onions as both of these food items emit gases that could make potatoes ripen faster.

Cabbage

Although cabbage tastes best when it’s fresh, it can also last for up to 2 months if you plan to stock up on it. However, it should be placed inside the fridge and wrapped in plastic. Since cabbages can last longer than lettuce or other delicate leafy greens, it can be used as a stand-in as an ingredient of your salads. Most greens that are frequently used in salads wilt in a matter of days because of their high water content.

Cabbages can be alternatives to salad greens that wilt quickly.

Apples

According to the University of Maine, no other tree fruit could last longer than apples and pears. Under the right conditions, these could last up to 4 months. Apples could thrive in a storage temperature of around 32 degrees Fahrenheit, except for the Honeycrisp variant that should be stored at 36 degrees Fahrenheit because it tends to get a chilling injury.

Among your bunch of apples, consume the largest one first since these are usually the first ones to go bad. Store apples inside a plastic bag and stow it inside the fruit crisper drawer of your refrigerator to prolong it for weeks. Just make sure that you keep them away from veggies. Other vegetables ripen faster when exposed to ethylene gas, which apples emit.

Beets

Beets can be used in a variety of ways. You can slice them up for salads or snack on baked beet chips. It’s a good thing that these veggies can last between 2 to 4 months in your refrigerator if stored properly. If there are still greens attached to the beets, make sure to remove them. After that, place it in a perforated plastic bag and inside the vegetable crisper.

Garlic

These kitchen staples can last the longest when stored at around 60 to 65 degrees Fahrenheit. These should be okay to store inside a dark kitchen cabinet.

A whole bulb could last for months stored inside a paper bag in the fridge. However, all your other food items might taste like garlic if you store them with already cut ones. Once you refrigerate the garlic bulb, you should keep it inside until you are about to use it. Days after it has been taken out from the cold and into room temperature, it will start sprouting.

You should only store unopened bulbs inside the fridge and not sliced ones if you don’t want other food items to acquire a garlicky taste.

Carrots

Carrots give off plenty of moisture, so you have to keep them dry if you intend to use it much later. This is because the moisture makes the carrots rot quicker. If they came in a plastic bag when you bought them from the grocery store, just put in a paper towel inside so it can absorb any moisture from the carrots. Once the paper towel gets saturated, replace it with a new one so you can keep your carrots fresh for up to a few months.

Onions

Onions can last up to a year as long as these are stored in a dry area with a temperature between 30 to 50 degrees Fahrenheit. If you don’t have the proper storage place, just keep it in mesh bags, like the ones used to pack onions sold by the grocery stores. If you store them inside a dark cabinet, they can last to a month or even longer.

Winter Radish

The white-colored daikon variety you see in your local grocery store is more pungent than the red ones you use for spring salads. So, if you’re looking for a healthy supply of fresh produce, don’t store too many of these. Storage for winter radishes is similar to that of carrots. After you remove the greens, place the radishes inside a plastic bag with a paper towel to absorb moisture. That way, these could last for about a month.

You can use shredded or thinly shaved winter radish for your slaw or salad.

Winter Squash

Varieties of winter squash, including pumpkins and butternut squash, can last around 2 to 6 months if stored inside a dark cabinet. Just make sure that you arrange them in a single layer so that air can circulate better. Stocking up on these versatile vegetables is a smart choice since these are packed with nutrients and can be used in a number of recipes.

Frozen Vegetables

Aside from your fresh produce, also hit the frozen foods aisle and stock up on a couple of packs of frozen vegetables. It may be healthier than fresh asparagus, spinach, peas, and other veggies with a short shelf life as these were frozen just hours after being harvested. Plus, you don’t have to worry too much about expiration as long as you keep it inside your freezer.

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Individualized mosaics of microbial strains transfer from the maternal to the infant gut

Microbial communities in the intestine—also known as the gut microbiome—are vital for human digestion, metabolism and resistance to colonization by pathogens. The gut microbiome composition in infants and toddlers changes extensively in the first three years of life. But where do those microbes come from in the first place?

Scientists have long been able to analyze the gut microbiome at the level of the 500 to 1,000 different bacterial species that mainly have a beneficial influence; only more recently have they been able to identify individual strains within a single species using powerful genomic tools and supercomputers that analyze massive amounts of genetic data.

Researchers at the University of Alabama at Birmingham now have used their microbiome “fingerprint” method to report that an individualized mosaic of microbial strains is transmitted to the infant gut microbiome from a mother giving birth through vaginal delivery. They detailed this transmission by analyzing existing metagenomic databases of fecal samples from mother-infant pairs, as well as analyzing mouse dam and pup transmission in a germ-free, or gnotobiotic, mouse model at UAB, where the dams were inoculated with human fecal microbes.

“The results of our analysis demonstrate that multiple strains of maternal microbes—some that are not abundant in the maternal fecal community—can be transmitted during birth to establish a diverse infant gut microbial community,” said Casey Morrow, Ph.D., professor emeritus in UAB’s Department of Cell, Developmental and Integrative Biology. “Our analysis provides new insights into the origin of microbial strains in the complex infant microbial community.”

The study used a strain-tracking bioinformatics tool previously developed at UAB, called Window-based Single-nucleotide-variant Similarity, or WSS. Hyunmin Koo, Ph.D., UAB Department of Genetics and Genomics Core, led the informatics analysis. The gnotobiotic mouse model studies were led by Braden McFarland, Ph.D., assistant professor in the UAB Department of Cell, Developmental and Integrative Biology.

Morrow and colleagues have used this microbe fingerprint tool in several previous strain-tracking studies. In 2017, they found that fecal donor microbes—used to treat patients with recurrent Clostridium difficile infections—remained in recipients for months or years after fecal transplants. In 2018, they showed that changes in the upper gastrointestinal tract through obesity surgery led to the emergence of new strains of microbes. In 2019, they analyzed the stability of new strains in individuals after antibiotic treatments, and earlier this year, they found that adult twins, ages 36 to 80 years old, shared a certain strain or strains between each pair for periods of years, and even decades, after they began living apart from each other.

In the current study, several individual-specific patterns of microbial strain-sharing were found between mothers and infants. Three mother-infant pairs showed only related strains, while a dozen other infants of mother-infant pairs contained a mosaic of maternal-related and unrelated microbes. It could be that the unrelated strains came from the mother, but they had not been the dominant strain of that species in the mother, and so had not been detected.

Indeed, in a second study using a dataset from nine women taken at different times in their pregnancies showed that strain variations in individual species occurred in seven of the women.

To further define the source of the unrelated strains, a mouse model was used to look at transmission from dam to pup in the absence of environmental microbes. Five different females were given transplants of different human fecal matter to create five unique humanized-microbiome mice, which were bred with gnotobiotic males. The researchers then analyzed the strains found in the human donors, the mouse dams and their mouse pups. They found four different patterns: 1) The pup’s strain of a particular species was related to the dam’s strain; 2) The pup’s strain was related to both the dam’s strain and the human donor’s strain; 3) The pup’s strain was related to the human donor’s strain, but not to the dam’s strain; and, importantly, 4) No related strains for a particular species were found between the pup, the dam and the human donor. Since these animals were bred and raised in germ-free conditions, the unrelated strains in the pups came from minor, undetected strains in the dams.

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How does the brain link events to form a memory? Study reveals unexpected mental processes

A woman walking down the street hears a bang. Several moments later she discovers her boyfriend, who had been walking ahead of her, has been shot. A month later, the woman checks into the emergency room. The noises made by garbage trucks, she says, are causing panic attacks. Her brain had formed a deep, lasting connection between loud sounds and the devastating sight she witnessed.

This story, relayed by clinical psychiatrist and co-author of a new study Mohsin Ahmed, MD, Ph.D., is a powerful example of the brain’s powerful ability to remember and connect events separated in time. And now, in that new study in mice published today in Neuron, scientists at Columbia’s Zuckerman Institute have shed light on how the brain can form such enduring links.

The scientists uncovered a surprising mechanism by which the hippocampus, a brain region critical for memory, builds bridges across time: by firing off bursts of activity that seem random, but in fact make up a complex pattern that, over time, help the brain learn associations. By revealing the underlying circuitry behind associative learning, the findings lay the foundation for a better understanding of anxiety and trauma- and stressor-related disorders, such as panic and post-traumatic stress disorders, in which a seemingly neutral event can elicit a negative response.

“We know that the hippocampus is important in forms of learning that involve linking two events that happen even up to 10 to 30 seconds apart,” said Attila Losonczy, MD, Ph.D., a principal investigator at Columbia’s Mortimer B. Zuckerman Mind Brain Behavior Institute and the paper’s co-senior author. “This ability is a key to survival, but the mechanisms behind it have proven elusive. With today’s study in mice, we have mapped the complex calculations the brain undertakes in order to link distinct events that are separated in time.”

The hippocampus—a small, seahorse-shaped region buried deep in the brain—is an important headquarters for learning and memory. Previous experiments in mice showed that disruption to the hippocampus leaves the animals with trouble learning to associate two events separated by tens of seconds.

“The prevailing view has been that cells in the hippocampus keep up a level of persistent activity to associate such events,” said Dr. Ahmed, an assistant professor of clinical psychiatry at Columbia’s Vagelos College of Physicians and Surgeons, and co-first author of today’s study. “Turning these cells off would thus disrupt learning.”

To test this traditional view, the researchers imaged parts of the hippocampus of mice as the animals were exposed to two different stimuli: a neutral sound followed by a small but unpleasant puff of air. A fifteen-second delay separated the two events. The scientists repeated this experiment across several trials. Over time, the mice learned to associate the tone with the soon-to-follow puff of air. Using advanced two-photon microscopy and functional calcium imaging, they recorded the activity of thousands of neurons, a type of brain cell, in the animals’ hippocampus simultaneously over the course of each trial for many days.

“With this approach, we could mimic, albeit in a simpler way, the process our own brains undergo when we learn to connect two events,” said Dr. Losonczy, who is also a professor of neuroscience at Columbia’s Vagelos College of Physicians and Surgeons.

To make sense of the information they collected, the researchers teamed up with computational neuroscientists who develop powerful mathematical tools to analyze vast amounts of experimental data.

“We expected to see repetitive, continuous neural activity that persisted during the fifteen-second gap, an indication of the hippocampus at work linking the auditory tone and the air puff,” said computational neuroscientist Stefano Fusi, Ph.D., a principal investigator at Columbia’s Zuckerman Institute and the paper’s co-senior author. “But when we began to analyze the data, we saw no such activity.”

Instead, the neural activity recorded during the fifteen-second time gap was sparse. Only a small number of neurons fired, and they did so seemingly at random. This sporadic activity looked distinctly different from the continuous activity that the brain displays during other learning and memory tasks, like memorizing a phone number.

“The activity appears to come in fits and bursts at intermittent and random time periods throughout the task,” said James Priestley, a doctoral candidate co-mentored by Drs. Losonczy and Fusi at Columbia’s Zuckerman Institute and the paper’s co-first author. “To understand activity, we had to shift the way we analyzed data and use tools designed to make sense of random processes.”

Ultimately, the researchers discovered a pattern in the randomness: a style of mental computing that seems to be a remarkably efficient way that neurons store information. Instead of communicating with each other constantly, the neurons save energy—perhaps by encoding information in the connections between cells, called synapses, rather than through the electrical activity of the cells.

“We were happy to see that the brain doesn’t maintain ongoing activity over all these seconds because, metabolically, that’s not the most efficient way to store information,” said Dr. Fusi, who is also a professor of neuroscience at Columbia’s Vagelos College of Physicians and Surgeons. “The brain seems to have a more efficient way to build this bridge, which we suspect may involve changing the strength of the synapses.”

In addition to helping to map the circuitry involved in associative learning, these findings also provide a starting point to more deeply explore disorders involving dysfunctions in associative memory, such as panic and pos-ttraumatic stress disorder.

“While our study does not explicitly model the clinical syndromes of either of these disorders, it can be immensely informative,” said Dr. Ahmed, who is also a member of the Losonczy lab at Columbia’s Zuckerman Institute. “For example, it can help us to model some aspects of what may be happening in the brain when patients experience a fearful association between two events that would, to someone else, not elicit fright or panic.”

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A new plant-based system for the mass production of allergens for immunotherapy

Allergies can significantly affect health and quality of life. While allergen immunotherapy provides long-lasting therapeutic relief to people suffering from environmental allergies, the therapy can last several years and requires large amounts of allergen. Now, researchers from the University of Tsukuba developed a novel system that enables the mass production of the major birch pollen allergen Bet v 1 in plant leaves in just a matter of days. In a new study published in Frontiers in Plant Science, they showed that their system not only produces large amounts of Bet v 1, but the purified protein was also highly reactive towards the IgE antibodies in sera from individuals with birch pollen allergy.

“The idea of allergen immunotherapy is to desensitize the body’s response to the allergen by exposing patients to it in gradually increasing amounts,” says corresponding author of the study Professor Kenji Miura. “Because a significant drawback is the difficult, expensive and low-yield production of allergens, our goal was to develop a new system that allows for the rapid and massive production of allergens that can be used in the clinical setting.”

To achieve their goal, the researchers turned to their previously established “Tsukuba system,” which makes use of a method called agroinfiltration. They first introduced the gene for Bet v 1 into a specific type of bacteria called Agrobacterium tumefaciens and let them grow. They then immersed leaves of the plant Nicotiana benthamiana into the bacterial solution to bring the bacteria into close contact with the plant, so the bacteria could transfer the Bet v 1 gene to plant cells, which in turn started producing the protein. To test the quality of their product, the researchers also produced the protein in Brevibacillus brevis, which is a standard bacterial host for protein production.

“We were able to purify 1.2mg of Bet v 1 protein from 1g leaves in just 5 days,” explains Professor Miura. “This is a relatively large amount that is otherwise difficult to achieve using standard methods. Our next goal was to test whether our protein was immunogenic, which is a prerequisite for immunotherapy.”

The researchers isolated sera from individuals with birch pollen allergy and mixed them with Bet v 1 protein purified from plants and bacteria. In both cases, the researchers were able to show that Bet v 1-specific IgE from the patients’ sera, which is the antibody causing the allergy, was strongly reactive to their proteins.

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We may be able to eliminate coronavirus, but we’ll probably never eradicate it. Here’s the difference

Compared to many other countries around the world, Australia and New Zealand have done an exceptional job controlling COVID-19.

As of May 7, there were 794 active cases of COVID-19 in Australia. Only 62 were in hospital.

The situation in New Zealand is similar, with 136 active cases, only two of whom are in hospital.

If we continue on this path, could we eliminate COVID-19 from Australia and New Zealand?

Control –> elimination –> eradication

In order to answer this question, we first to need to understand what elimination means in the context of disease, and how it differs from control and eradication.

Disease control is when we see a reduction in disease incidence and prevalence (new cases and current cases) as a result of public health measures. The reduction does not mean to zero cases, but rather to an acceptable level.

Unfortunately, there’s no consensus on what is acceptable. It can differ from disease to disease and from jurisdiction to jurisdiction.

As an example, there were only 81 cases of measles reported in Australia in 2017. Measles is considered under control in Australia.

Conversely, measles is not regarded as controlled in New Zealand, where there was an outbreak in 2019. From January 1, 2019, to February 21, 2020, New Zealand recorded 2,194 measles cases.

For disease elimination, there must be zero new cases of the disease in a defined geographic area. There is no defined time period this needs to be sustained for—it usually depends on the incubation period of the disease (the time between being exposed to the virus and the onset of symptoms).

For example, the South Australian government is looking for 28 days of no new coronavirus cases (twice the incubation period of COVID-19) before they will consider it eliminated.

Even when a disease has been eliminated, we continue intervention measures such as border controls and surveillance testing to ensure it doesn’t come back.

For example, in Australia, we have successfully eliminated rubella (German measles). But we maintain an immunization schedule and disease surveillance program.

Finally, disease eradication is when there is zero incidence worldwide of a disease following deliberate efforts to get rid of it. In this scenario, we no longer need intervention measures.

Only two infectious diseases have been declared eradicated by the World Health Organisation – smallpox in 1980 and rinderpest (a disease in cattle caused by the paramyxovirus) in 2011.

Polio is close to eradication with only 539 cases reported worldwide in 2019.

Guinea worm disease is also close with a total of just 19 human cases from January to June 2019 across two African countries.

What stage are we at with COVID-19?

In Australia and New Zealand we currently have COVID-19 under control.

Importantly, in Australia, the effective reproduction number (Reff) is close to zero. Estimates of Reff come from mathematical modelling, which has not been published for New Zealand, but the Reff is likely to be close to zero in New Zealand too.

The Reff is the average number of people each infected person infects. So a Reff of 2 means on average, each person with COVID-19 infects two others.

If the Reff is greater than 1 the epidemic continues; if the Reff is equal to 1 it becomes endemic (that is, it grumbles along on a permanent basis); and if the Reff is lower than 1, the epidemic dies out.

So we could be on the way to elimination.

In both Australia and New Zealand we have found almost all of the imported cases, quarantined them, and undertaken contact tracing. Based on extensive community testing, there also appear to be very few community-acquired cases.

The next step in both countries will be sentinel surveillance, where random testing is carried out in selected groups. Hopefully in time these results will be able to show us COVID-19 has been eliminated.

It’s unlikely COVID-19 will ever be eradicated

To be eradicated, a disease needs to be both preventable and treatable. At the moment, we neither have anything to prevent COVID-19 (such as a vaccine) nor any proven treatments (such as antivirals).

Even if a vaccine does become available, SARS-CoV-2 (the virus that causes COVID-19) easily mutates. So we would be in a situation like we are with influenza, where we need annual vaccinations targeting the circulating strains.

The other factor making COVID-19 very difficult if not impossible to eradicate is the fact many infected people have few or no symptoms, and people could still be infectious even with no symptoms. This makes case detection very difficult.

At least with smallpox, it was easy to see whether someone was infected, as their body was covered in pustules (fluid-containing swellings).

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The role of miRNAs in glioblastoma multiforme

Glioblastoma multiforme is one of the most malignant tumors of the central nervous system. It is characterized by the fast growth and high malignancy. Although surgery combined with radiation therapy and chemotherapy has been widely used for the treatment of glioblastoma, the prognosis is still very poor. Furthermore, chemoresistance and radioresistance are the typical hallmarks of the recurrent glioblastoma. Thus, it is necessary to identify all the potential therapeutic targets for glioblastoma and to clarify its underlying mechanism.

In recent years, attention has been paid to the role of microRNAs in the development, diagnosis, and prognosis of gliomas. Thus, the team of researchers from the Cancer Hospital of China Medical University revealed that miR-129-5p, and ZFP36L1 gene were functionally involved in the hallmarks glioblastoma. This includes the tumor proliferation, migration, and tumor colony-forming abilities.

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