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Maryland running back Javon Leake (20) rushes past a group of Illinois defenders for a touchdown in the first half of an NCAA college football game, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)

Maryland running back Javon Leake (20) rushes past a group of Illinois defenders for a touchdown in the first half of an NCAA college football game, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)


Maryland interim head coach Matt Canada, at right in gray, stands on the sideline in the first half of an NCAA college football game against Illinois, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)


Maryland wide receiver Jahrvis Davenport scores a touchdown in the first half of an NCAA college football game against Illinois, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)


Leake scores 4 TDs to help Maryland beat Illinois 63-33

By DAVID GINSBURG

AP Sports Writer

Saturday, October 27

COLLEGE PARK, Md. (AP) — Maryland opened up its passing game and fortified an already formidable running attack with seldom-used Javon Leake.

The result was a feel-good 63-33 rout over Illinois, one that was definitely worth singing about well into Saturday night.

“The locker room, we’re in there singing that (Maryland fight) song, those guys are excited,” interim coach Matt Canada said. “We found a way to win. We played good on offense, good on defense, good on special teams.”

Leake rushed for three touchdowns and scored on a 97-yard kickoff return , Kasim Hill had the best passing game of his career and Maryland held the Fighting Illini without a touchdown until late in the third quarter.

Leake is the first Maryland player to score four TDs in a game since D.J. Adams in the 2010 Military Bowl. Leake, a sophomore, finished with 140 yards rushing, including scores of 64, 27 and 43 yards.

“The offensive line did a great job today,” Leake said. “They just set me up to make plays.”

Prior to Saturday, Leake had 16 career carries, just nine this season.

“He was not at the top of the list in the running back room as the season began,” Canada said. “He continued to practice hard.”

The victory left the Terrapins (5-3, 3-2 Big Ten) one win short of becoming bowl eligible, no small feat for a team that was rocked by the death of offensive lineman Jordan McNair and has been playing under Canada since August.

Despite of the uncertainty surrounding the program, Maryland has already exceeded its win total (4) from last year.

“The whole point of the story is, our guys have checked their egos and just want to win,” Canada said. “We’re sitting here 5-3 with a bunch of kids who are playing so hard for each other and care for each other.”

Canada, the team’s offensive coordinator, took over for DJ Durkin, who is on administrative leave during an investigation of the culture of the program.

The probe began soon after McNair collapsed on the practice field and died of heatstroke in June. The report is complete. Now, after the commission determined there are problems with the culture of the program, the school and the football team await the fallout.

Reggie Corbin ran for 155 yards and a touchdown for the Fighting Illini (3-5, 1-4). Illinois had yielded 158 points during a three-game skid, and its streak of forcing a turnover in 21 consecutive games came to an end.

“It’s kind of beyond words the feelings we have right now,” coach Lovie Smith said. “There’s been some cracks that we’ve seen, but not like this. We knew what was at stake, just thought we would play a lot better. I thought our preparation was good, but as you can see it was not.”

Starting quarterback M.J. Rivers was knocked from the game in the second quarter on a hit by Tre Watson, who was ejected for targeting. Rivers went 3 for 13 for 45 yards.

Leake’s kickoff return and 64-yard run, along with two touchdown passes by Hill , provided Maryland with a 28-9 halftime lead. The Terrapins tacked on three touchdowns in the third quarter, including a 27-yard run by Leake and Hill’s third touchdown pass.

Hill was removed from the game late in the third quarter with the score 49-19. He went 11 for 19 for a career-high 265 yards, and his three TD passes tied a career best.

Playing Illinois for the first time, Maryland set a school record for most points in a Big Ten game since joining the conference in 2014. The Terps finished with 712 yards in offense.

It was a redemptive performance for a team that mustered only 115 yards one week earlier in a 23-0 loss to Iowa.

WATSON DISQUALIFIED

Watson leads the Terps in tackles and is tied for the team lead in interceptions, but this is the second time he’s been booted for targeting.

Watson played three seasons for Illinois before coming to Maryland this year.

JOHNSON OUT

Johnson, Maryland’s leading rusher, missed the second half with a leg injury. He ranks fourth on the team career list with 2,597 yards.

THE TAKEAWAY

Illinois: The Illini have a bad defense, plain and simple, especially when unable to force turnovers.

“Big plays are really hurting us,” Smith conceded.

Maryland: Well, for one game at least, the Terrapins proved they can pass as well as throw. That should be an asset in upcoming games against Michigan State, Ohio State and Penn State.

UP NEXT

Illinois hosts Minnesota, which defeated Indiana 38-31 Saturday for its first Big Ten win of the season.

Maryland faces visiting Michigan State (5-3, 3-2), which defeated Purdue 23-13 on Saturday.

More AP college football coverage: https://apnews.com/tag/Collegefootball and https://twitter.com/AP_Top25

The Conversation

What the flu does to your body, and why it makes you feel so awful

February 12, 2018

Author

Laura Haynes

Professor of Immunology, University of Connecticut

Disclosure statement: Laura Haynes receives funding from the National Institutes of Health.

Partners: University of Connecticut provides funding as a member of The Conversation US.

Every year, from 5 to 20 percent of the people in the United States will become infected with influenza virus. An average of 200,000 of these people will require hospitalization and up to 50,000 will die. Older folks over the age of 65 are especially susceptible to influenza infection, since the immune system becomes weaker with age. In addition, older folks are also more susceptible to long-term disability following influenza infection, especially if they are hospitalized.

We all know the symptoms of influenza infection include fever, cough, sore throat, muscle aches, headaches and fatigue. But just what causes all the havoc? What is going on in your body as you fight the flu?

I am a researcher who specializes in immunology at the University of Connecticut School of Medicine, and my laboratory focuses on how influenza infection affects the body and how our bodies combat the virus. It’s interesting to note that many of the body’s defenses that attack the virus also cause many of the symptoms associated with the flu.

How the flu works its way into your body

Influenza virus causes an infection in the respiratory tract, or nose, throat and lungs. The virus is inhaled or transmitted, usually via your fingers, to the mucous membranes of the mouth, nose or eyes. It then travels down the respiratory tract and binds to epithelial cells lining the lung airways via specific molecules on the cell surface. Once inside the cells, the virus hijacks the protein manufacturing machinery of the cell to generate its own viral proteins and create more viral particles. Once mature viral particles are produced, they are released from the cell and can then go on to invade adjacent cells.

While this process causes some lung injury, most of the symptoms of the flu are actually caused by the immune response to the virus. The initial immune response involves cells of the body’s innate immune system, such as macrophages and neutrophils. These cells express receptors that are able to sense the presence of the virus. They then sound the alarm by producing small hormone-like molecules called cytokines and chemokines. These alert the body that an infection has been established.

Cytokines orchestrate other components of the immune system to appropriately fight the invading virus, while chemokines direct these components to the location of infection. One of the types of cells called into action are T lymphocytes, a type of white blood cell that fights infection. Sometimes, they are even called “soldier” cells. When T cells specifically recognize influenza virus proteins, they then begin to proliferate in the lymph nodes around the lungs and throat. This causes swelling and pain in these lymph nodes.

After a few days, these T cells move to the lungs and begin to kill the virus-infected cells. This process creates a great deal of lung damage similar to bronchitis, which can worsen existing lung disease and make breathing difficult. In addition, the buildup of mucous in the lungs, as a result of this immune response to infection, induces coughing as a reflex to try to clear the airways. Normally, this damage triggered by arrival of T cells in the lungs is reversible in a healthy person, but when it advances, it is bad news and can lead to death.

The proper functioning of influenza-specific T cells is critical for efficient clearance of the virus from the lungs. When T cell function declines, such as with increasing age or during use of immunosuppressive drugs, viral clearance is delayed. This results in a prolonged infection and greater lung damage. This can also set the stage for complications including secondary bacterial pneumonia, which can often be deadly.

Why your head hurts so much

While the influenza virus is wholly contained in the lungs under normal circumstances, several symptoms of influenza are systemic, including fever, headache, fatigue and muscle aches. In order to properly combat influenza infection, the cytokines and chemokines produced by the innate immune cells in the lungs become systemic – that is, they enter the bloodstream, and contribute to these systemic symptoms. When this happens, a cascade of complicating biological events occur.

One of the things that happens is that Interleukin-1, an inflammatory type of cytokine, is activated. Interleukin-1 is important for developing the killer T cell response against the virus, but it also affects the part of the brain in the hypothalamus that regulates body temperature, resulting in fever and headaches.

Another important cytokine that fights influenza infection is something called “tumor necrosis factor alpha.” This cytokine can have direct antiviral effects in the lungs, and that’s good. But it can also cause fever and appetite loss, fatigue and weakness during influenza and other types of infection.

Why your muscles ache

Our research has also uncovered another aspect of how influenza infection affects our bodies.

It is well-known that muscle aches and weakness are prominent symptoms of influenza infection. Our study in an animal model found that influenza infection leads to an increase in the expression of muscle-degrading genes and a decrease in expression of muscle-building genes in skeletal muscles in the legs.

Functionally, influenza infection also hinders walking and leg strength. Importantly, in young individuals, these effects are transient and return to normal once the infection was cleared.

In contrast, these effects can linger significantly longer in older individuals. This is important, since a decrease in leg stability and strength could result in older folks being more prone to falls during recovery from influenza infection. It could also result in long-term disability and lead to the need for a cane or walker, limiting mobility and independence.

Researchers in my lab think that this impact of influenza infection on muscles is another unintended consequence of the immune response to the virus. We are currently working to determine what specific factors produced during the immune response are responsible for this and if we can find a way to prevent it.

Thus, while you feel miserable when you have an influenza infection, you can rest assured that it is because your body is fighting hard. It’s combating the spread of the virus in your lungs and killing infected cells.

The Conversation

The mystery of a 1918 veteran and the flu pandemic

November 9, 2017 7.22pm EST

Author

Ruth Craig

Emerita Professor, Pharmacology and Toxicology, Dartmouth College

Disclosure statement

Ruth Craig does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Vaccination is underway for the 2017-2018 seasonal flu, and next year will mark the 100-year anniversary of the 1918 flu pandemic, which killed roughly 40 million people. It is an opportune time to consider the possibility of pandemics – infections that go global and affect many people – and the importance of measures aimed at curbing them.

The 1918 pandemic was unusual in that it killed many healthy 20- to 40-year-olds, including millions of World War I soldiers. In contrast, people who die of the flu are usually under five years old or over 75.

The factors underlying the virulence of the 1918 flu are still unclear. Modern-day scientists sequenced the DNA of the 1918 virus from lung samples preserved from victims. However, this did not solve the mystery of why so many healthy young adults were killed.

I started investigating what happened to a young man who immigrated to the U.S. and was lost during World War I. Uncovering his story also brought me up to speed on hypotheses about why the immune systems of young adults in 1918 did not protect them from the flu.

The 1918 flu and World War I

Certificates picturing the goddess Columbia as a personification of the U.S. were awarded to men and women who died in service during World War I. One such certificate surfaced many decades later. This one honored Adolfo Sartini and was found by grandnephews who had never known him: Thomas, Richard and Robert Sartini.

The certificate was a message from the past. It called out to me, as I had just received the credential of certified genealogist and had spent most of my career as a scientist tracing a gene that regulates immune cells. What had happened to Adolfo?

A bit of sleuthing identified Adolfo’s ship listing, which showed that he was born in 1889 in Italy and immigrated to Boston in 1913. His draft card revealed that he worked at a country club in the Boston suburb of Newton. To learn more, Robert Sartini bought a 1930 book entitled “Newton War Memorial” on eBay. The book provided clues: Adolfo was drafted and ordered to report to Camp Devens, 35 miles from Boston, in March of 1918. He was later transferred to an engineer training regiment.

To follow up, I posted a query on the “U.S. Militaria Forum.” Here, military history enthusiasts explained that the Army Corps of Engineers had trained men at Camp A. A. Humphreys in Virginia. Perhaps Adolfo had gone to this camp?

While a mild flu circulated during the spring of 1918, the deadly strain appeared on U.S. soil on Tuesday, Aug. 27, when three Navy dockworkers at Commonwealth Pier in Boston fell ill. Within 48 hours, dozens more men were infected. Ten days later, the flu was decimating Camp Devens. A renowned pathologist from Johns Hopkins, William Welch, was brought in. He realized that “this must be some new kind of infection or plague.” Viruses, minuscule agents that can pass through fine filters, were poorly understood.

With men mobilizing for World War I, the flu spread to military installations throughout the U.S. and to the general population. It hit Camp Humphreys in mid-September and killed more than 400 men there over the next month. This included Adolfo Sartini, age 29½. Adolfo’s body was brought back to Boston.

His grave is marked by a sculpture of the lower half of a toppled column, epitomizing his premature death.

The legacy of victims of the 1918 flu

The quest to understand the 1918 flu fueled many scientific advances, including the discovery of the influenza virus. However, the virus itself did not cause most of the deaths. Instead, a fraction of individuals infected by the virus were susceptible to pneumonia due to secondary infection by bacteria. In an era before antibiotics, pneumonia could be fatal.

Recent analyses revealed that deaths in 1918 were highest among individuals born in the years around 1889, like Adolfo. An earlier flu pandemic emerged then, and involved a virus that was likely of a different subtype than the 1918 strain. These analyses engendered a novel hypothesis, discussed below, about the susceptibility of healthy young adults in 1918.

Exposure to an influenza virus at a young age increases resistance to a subsequent infection with the same or a similar virus. On the flip side, a person who is a child around the time of a pandemic may not be resistant to other, dissimilar viruses. Flu viruses fall into groups that are related evolutionarily. The virus that circulated when Adolfo was a baby was likely in what is called “Group 2,” whereas the 1918 virus was in “Group 1.” Adolfo would therefore not be expected to have a good ability to respond to this “Group 1” virus. In fact, exposure to the “Group 2” virus as a young child may have resulted in a dysfunctional response to the “Group 1” virus in 1918, exacerbating his condition.

Support for this hypothesis was seen with the emergence of the Hong Kong flu virus in 1968. It was in “Group 2” and had severe effects on people who had been children around the time of the 1918 “Group 1” flu.

To 2018 and beyond

What causes a common recurring illness to convert to a pandemic that is massively lethal to healthy individuals? Could it happen again? Until the reason for the death of young adults in 1918 is better understood, a similar scenario could reoccur. Experts fear that a new pandemic, of influenza or another infectious agent, could kill millions. Bill Gates is leading the funding effort to prevent this.

Flu vaccines are generated each year by monitoring the strains circulating months before flu season. A time lag of months allows for vaccine production. Unfortunately, because the influenza virus mutates rapidly, the lag also allows for the appearance of virus variants that are poorly targeted by the vaccine. In addition, flu pandemics often arise upon virus gene reassortment. This involves the joining together of genetic material from different viruses, which can occur suddenly and unpredictably.

An influenza virus is currently killing chickens in Asia, and has recently killed humans who had contact with chickens. This virus is of a subtype that has not been known to cause pandemics. It has not yet demonstrated the ability to be transmitted from person to person. However, whether this ability will arise during ongoing virus evolution cannot be predicted.

The chicken virus is in “Group 2.” Therefore, if it went pandemic, people who were children around the time of the 1968 “Group 2” Hong Kong flu might have some protection. I was born much earlier, and “Group 1” viruses were circulating when I was a child. If the next pandemic virus is in “Group 2,” I would probably not be resistant.

It’s early days for understanding how prior exposure affects flu susceptibility, especially for people born in the last three to four decades. Since 1977, viruses of both “Group 1” and “Group 2” have been in circulation. People born since then probably developed resistance to one or the other based on their initial virus exposures. This is good news for the near future since, if either a “Group 1” or a “Group 2” virus develops pandemic potential, some people should be protected. At the same time, if you are under 40 and another pandemic is identified, more information would be needed to hazard a guess as to whether you might be susceptible or resistant.

The Conversation

The ‘greatest pandemic in history’ was 100 years ago – but many of us still get the basic facts wrong

January 11, 2018

Influenza victims crowd into an emergency hospital near Fort Riley, Kansas in 1918. AP Photo/National Museum of Health

Author

Richard Gunderman

Chancellor’s Professor of Medicine, Liberal Arts, and Philanthropy, Indiana University

Disclosure statement

Richard Gunderman does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Partners: Indiana University provides funding as a member of The Conversation US.

This year marks the 100th anniversary of the great influenza pandemic of 1918. Between 50 and 100 million people are thought to have died, representing as much as 5 percent of the world’s population. Half a billion people were infected.

Especially remarkable was the 1918 flu’s predilection for taking the lives of otherwise healthy young adults, as opposed to children and the elderly, who usually suffer most. Some have called it the greatest pandemic in history.

The 1918 flu pandemic has been a regular subject of speculation over the last century. Historians and scientists have advanced numerous hypotheses regarding its origin, spread and consequences. As a result, many of us harbor misconceptions about it.

By correcting these 10 myths, we can better understand what actually happened and learn how to prevent and mitigate such disasters in the future.

1. The pandemic originated in Spain

No one believes the so-called “Spanish flu” originated in Spain.

The pandemic likely acquired this nickname because of World War I, which was in full swing at the time. The major countries involved in the war were keen to avoid encouraging their enemies, so reports of the extent of the flu were suppressed in Germany, Austria, France, the United Kingdom and the U.S. By contrast, neutral Spain had no need to keep the flu under wraps. That created the false impression that Spain was bearing the brunt of the disease.

In fact, the geographic origin of the flu is debated to this day, though hypotheses have suggested East Asia, Europe and even Kansas.

2. The pandemic was the work of a ‘super-virus’

The 1918 flu spread rapidly, killing 25 million people in just the first six months. This led some to fear the end of mankind, and has long fueled the supposition that the strain of influenza was particularly lethal.

However, more recent study suggests that the virus itself, though more lethal than other strains, was not fundamentally different from those that caused epidemics in other years.

Much of the high death rate can be attributed to crowding in military camps and urban environments, as well as poor nutrition and sanitation, which suffered during wartime. It’s now thought that many of the deaths were due to the development of bacterial pneumonias in lungs weakened by influenza.

3. The first wave of the pandemic was most lethal

Actually, the initial wave of deaths from the pandemic in the first half of 1918 was relatively low.

It was in the second wave, from October through December of that year, that the highest death rates were observed. A third wave in spring of 1919 was more lethal than the first but less so than the second.

Scientists now believe that the marked increase in deaths in the second wave was caused by conditions that favored the spread of a deadlier strain. People with mild cases stayed home, but those with severe cases were often crowded together in hospitals and camps, increasing transmission of a more lethal form of the virus.

4. The virus killed most people who were infected with it

In fact, the vast majority of the people who contracted the 1918 flu survived. National death rates among the infected generally did not exceed 20 percent.

However, death rates varied among different groups. In the U.S., deaths were particularly high among Native American populations, perhaps due to lower rates of exposure to past strains of influenza. In some cases, entire Native communities were wiped out.

Of course, even a 20 percent death rate vastly exceeds a typical flu, which kills less than one percent of those infected.

5. Therapies of the day had little impact on the disease

No specific anti-viral therapies were available during the 1918 flu. That’s still largely true today, where most medical care for the flu aims to support patients, rather than cure them.

One hypothesis suggests that many flu deaths could actually be attributed to aspirin poisoning. Medical authorities at the time recommended large doses of aspirin of up to 30 grams per day. Today, about four grams would be considered the maximum safe daily dose. Large doses of aspirin can lead to many of the pandemic’s symptoms, including bleeding.

However, death rates seem to have been equally high in some places in the world where aspirin was not so readily available, so the debate continues.

6. The pandemic dominated the day’s news

Public health officials, law enforcement officers and politicians had reasons to underplay the severity of the 1918 flu, which resulted in less coverage in the press. In addition to the fear that full disclosure might embolden enemies during wartime, they wanted to preserve public order and avoid panic.

However, officials did respond. At the height of the pandemic, quarantines were instituted in many cities. Some were forced to restrict essential services, including police and fire.

7. The pandemic changed the course of World War I

It’s unlikely that the flu changed the outcome of World War I, because combatants on both sides of the battlefield were relatively equally affected.

However, there is little doubt that the war profoundly influenced the course of the pandemic. Concentrating millions of troops created ideal circumstances for the development of more aggressive strains of the virus and its spread around the globe.

8. Widespread immunization ended the pandemic

Immunization against the flu as we know it today was not practiced in 1918, and thus played no role in ending the pandemic.

Exposure to prior strains of the flu may have offered some protection. For example, soldiers who had served in the military for years suffered lower rates of death than new recruits.

In addition, the rapidly mutating virus likely evolved over time into less lethal strains. This is predicted by models of natural selection. Because highly lethal strains kill their host rapidly, they cannot spread as easily as less lethal strains.

9. The genes of the virus have never been sequenced

In 2005, researchers announced that they had successfully determined the gene sequence of the 1918 influenza virus. The virus was recovered from the body of a flu victim buried in the permafrost of Alaska, as well as from samples of American soldiers who fell ill at the time.

Two years later, monkeys infected with the virus were found to exhibit the symptoms observed during the pandemic. Studies suggest that the monkeys died when their immune systems overreacted to the virus, a so-called “cytokine storm.” Scientists now believe that a similar immune system overreaction contributed to high death rates among otherwise healthy young adults in 1918.

10. The 1918 pandemic offers few lessons for 2018

Severe influenza epidemics tend to occur every few decades. Experts believe that the next one is a question not of “if” but “when.”

While few living people can recall the great flu pandemic of 1918, we can continue to learn its lessons, which range from the commonsense value of handwashing and immunizations to the potential of anti-viral drugs. Today we know more about how to isolate and handle large numbers of ill and dying patients, and we can prescribe antibiotics, not available in 1918, to combat secondary bacterial infections. Perhaps the best hope lies in improving nutrition, sanitation and standards of living, which render patients better able to resist the infection.

For the foreseeable future, flu epidemics will remain an annual feature of the rhythm of human life. As a society, we can only hope that we have learned the great pandemic’s lessons sufficiently well to quell another such worldwide catastrophe.

Maryland running back Javon Leake (20) rushes past a group of Illinois defenders for a touchdown in the first half of an NCAA college football game, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)
https://www.sunburynews.com/wp-content/uploads/sites/48/2018/10/web1_121659348-b85c4881fcc14db09829e4e8546092c8.jpgMaryland running back Javon Leake (20) rushes past a group of Illinois defenders for a touchdown in the first half of an NCAA college football game, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)

Maryland interim head coach Matt Canada, at right in gray, stands on the sideline in the first half of an NCAA college football game against Illinois, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)
https://www.sunburynews.com/wp-content/uploads/sites/48/2018/10/web1_121659348-01962dda75dc47338bccea849a216c63.jpgMaryland interim head coach Matt Canada, at right in gray, stands on the sideline in the first half of an NCAA college football game against Illinois, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)

Maryland wide receiver Jahrvis Davenport scores a touchdown in the first half of an NCAA college football game against Illinois, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)
https://www.sunburynews.com/wp-content/uploads/sites/48/2018/10/web1_121659348-b821b81f55464be9b1caa785847a9cd4.jpgMaryland wide receiver Jahrvis Davenport scores a touchdown in the first half of an NCAA college football game against Illinois, Saturday, Oct. 27, 2018, in College Park, Md. (AP Photo/Patrick Semansky)
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