By 1973, just nine years after the start of an antimosquito campaign, the Aedes aegypti will be eradicated from the United States. The mosquito, a potential carrier of yellow fever, dengue and hemorrhagic fever, has been the target of a $23 million attack launched in 1964…. The carrier of these viral diseases can still be found in 10 southern states, Hawaii, the Virgin Islands and Puerto Rico. — Science News, May 20, 1967
Update The eradication program, which used chemical sprays and eliminated breeding sites, never came close to getting rid of A. aegypti. Today, the virus-carrying insect’s potential range includes more than 20 states and other U.S. territories. And some carrying the Zika virus have been found in the continental United States. Researchers are investigating new ways to conquer A. aegypti, by inserting faulty genes into its DNA or dosing it with a sterilizing bacterium (SN: 4/1/17, p. 10).
Health care quality and availability improved globally from 1990 to 2015, but the gap between the haves and the have-nots widened in those 25 years, researchers report online May 18 in the Lancet.
As an approximate measure of citizens’ access to quality health care, an international team of researchers analyzed mortality rates for 32 diseases and injuries that are typically not fatal when effective medical care is available. The team summarized this data as a number on a scale from zero to 100, called the Healthcare Access and Quality Index, for 195 countries and territories. Places with the highest scores in 2015 include Canada, Australia, Japan and much of Europe, while some African countries as well as India, Pakistan, Afghanistan and Papua New Guinea have the lowest scores. The countries with the greatest improvement since 1990 include South Korea, Peru and China.
The growing gap between countries with the highest and lowest scores suggests that health care inequalities due to geography may be on the rise, the authors say.
A molecule that could help build otherworldly life is present on Saturn’s moon Titan, researchers have discovered.
Vinyl cyanide, a compound predicted to form membranelike structures, is created in Titan’s upper atmosphere, scientists report July 28 in Science Advances. There’s enough vinyl cyanide (C2H3CN) in the moon’s liquid methane seas to make about 10 million cell-like balls per cubic centimeter of ocean, researchers calculate. On Earth, about a million bacteria are found in a cubic centimeter of ocean water near shore. “It’s very positive news for putative-Titan-life studies,” says Jonathan Lunine, a planetary scientist at Cornell University who was not involved in the new study.
Titan has no water, usually considered a prerequisite for life. Instead of water, freezing-cold Titan has liquid methane. There’s even a methane cycle that mimics Earth’s water cycle (SN: 3/21/15, p. 32). But Titan is so cold — usually about –178° Celsius — that the smallest unit of life on Earth, the cell, would shatter in the moon’s subzero seas. In 2015, Lunine and Cornell colleagues James Stevenson and Paulette Clancy proposed a way life might exist in methane. Computer simulations predicted that vinyl cyanide (also called acrylonitrile or propenenitrile) could make flexible bubbles called azotosomes that would be stable in liquid methane (SN: 4/30/16, p. 28). Those bubbles might act much as cell membranes do on Earth, sheltering genetic material and concentrating biochemical reactions needed for life. When the Cornell researchers suggested the presence of azotosomes on Titan, carbon, hydrogen and nitrogen had already been detected in abundance in the moon’s atmosphere. But no one knew whether those atoms joined to make vinyl cyanide there. The Saturn probe Cassini had detected a molecule of the right mass to be vinyl cyanide, but couldn’t definitively identify the molecule’s chemical makeup.
But evidence for the chemical compound was buried in archived data from a large radio telescope, Maureen Palmer of Catholic University of America in Washington, D.C., and colleagues discovered. Palmer, an astrochemistry and astrobiology researcher, combed data collected by the Atacama Large Millimeter/submillimeter Array, or ALMA, in Chile between February 22 and May 27, 2014.
Astronomers point ALMA at Titan to calibrate the telescope because the moon has known brightness levels, says Palmer, who also works at NASA’s Goddard Space Flight Center in Greenbelt, Md. The team used that calibration data to detect the signature of vinyl cyanide at specific wavelengths of light and calculate its abundance.
“This is a pretty secure detection,” says Ralph Lorenz, a planetary scientist at the Johns Hopkins University Applied Physics Lab in Laurel, Md.
Even with confirmation of vinyl cyanide, researchers can’t say that azotosomes form on Titan. That’s probably not something telescopes can determine, Lunine says. A probe would need to sample Titan’s seas to detect the structures.
And even detecting azotosomes would not mean there’s life on Titan, says Lorenz. The moon’s extreme cold may hamper metabolism. What’s more, no one knows whether liquid methane can take the place of water for supporting life, he says. “If I were a betting man, I’d say Titan does not have life.”
Walls can get the best of clumsy TV sitcom characters and bats alike.
New lab tests suggest that smooth, vertical surfaces fool some bats into thinking their flight path is clear, leading to collisions and near misses.
The furry fliers famously use sound to navigate — emitting calls and tracking the echoes to hunt for prey and locate obstacles. But some surfaces can mess with echolocation.
Stefan Greif of the Max Planck Institute for Ornithology in Seewiesen, Germany, and colleagues put bats to the test in a flight tunnel. Nineteen of 21 greater mouse-eared bats (Myotis myotis) crashed into a vertical metal plate at least once, the scientists report in the Sept. 8 Science. In some crashes, bats face-planted without even trying to avoid the plate. Smooth surfaces act as acoustic mirrors, the team says: Up close, they reflect sound at an angle away from the bat, producing fuzzier, harder-to-read echoes than rough surfaces do. From farther away, smooth surfaces don’t produce any echoes at all.
Infrared camera footage of wild bat colonies showed that vertical plastic plates trick bats in more natural settings, too.
Crash reel This video shows three experiments into how smooth surfaces affect bat flight. In one lab test, a vertical metal plate gave a bat the illusion of a clear flight path, causing it to crash into the barrier. In a second lab test, a horizontal metal plate created the illusion of water; the bat dips to surface to take a sip. Finally, near a natural bat colony, a bat collides with a vertically hung plastic plate, showing that smooth surfaces could impact bats in the wild, as well.
To the residents of Donora, Pa., a mill town in a crook of the Monongahela River, the daily haze from nearby zinc and steel plants was the price of keeping their families fed. But on October 27, 1948, the city awoke to an unusually sooty sky, even for Donora. The next day, the high school quarterbacks couldn’t see their teammates well enough to complete a single pass.
The town was engulfed in smog for five days, until a storm finally swept the pollution out of the valley. By then, more than one-third of the population had fallen ill and 20 people were dead. Another 50 perished in the following months.
After the Donora tragedy, the federal government began to clamp down on industries that release pollutants into the air. Environmental advocates in the coming decades fought for, and won, tighter regulations. As a result, combined emissions of six common air pollutants have dropped by about 70 percent nationwide since the 1970 passage of the Clean Air Act, which regulates U.S. emissions of hazardous air pollutants. In 35 major U.S. cities, the total number of days with unhealthy air has fallen by almost two-thirds just since 2000. “It’s one of the great success stories of public health,” says Joel Kaufman, a physician and epidemiologist at the University of Washington School of Public Health in Seattle.
Our bodies feel the difference. One study, reported in JAMA last year, followed 4,602 children in Southern California between 1993 and 2012 to see how lung health correlated with three common air pollutants. As levels of ozone, nitrogen dioxide and particulate matter fell over time, so did the number of children who reported a daily cough, persistent congestion and other symptoms of irritated lungs. At the start of the study, 48 percent of children with asthma had reported bronchitis symptoms in the previous year. In communities with the greatest drop in pollutants during the study period, bronchitis prevalence fell by as much as 30 percent in children with asthma. But the air pollution story isn’t over. Researchers from the Harvard T.H. Chan School of Public Health in Boston recently reported on links between air quality and mortality throughout the entire U.S. Medicare population (more than 60 million people who are age 65 and older or disabled). The analysis looked at levels of two common air pollutants and death rates from 2000 to 2012, while accounting for factors that might confound the results, such as race and socioeconomic status. The analysis, published in June in the New England Journal of Medicine, found that when pollutant levels rose (but remained at levels below national standards), so did death rates.
Even with vast improvements in air quality since the ’70s, people haven’t stopped dying from the air they breathe. An analysis published in 2013 from researchers at MIT estimated that about 200,000 premature deaths occur each year in the United States because of fine particulate air pollution. A study published in January in Environmental Health Perspectives reported that daily deaths over a decade in metropolitan Boston peaked on days when concentrations of three common air pollutants were at their highest, even though those levels would currently satisfy the U.S. Environmental Protection Agency.
“We’ve made these improvements in exposure,” Kaufman says, “but what more do we need to clean up?”
So despite a half-century of progress, airborne grime is still a menace — probably in ways the people of Donora never imagined. Researchers are now finding that more than the lungs are at risk, as dirty air may in fact be an accomplice to some of the greatest threats to public health, including diabetes, obesity and even dementia. Those studies are likely to inform the ongoing debate over antismog rules. The U.S. House of Representatives voted this summer to delay implementation of updated standards for the Clean Air Act.
Slow burn As it has for more than a century, air pollution in America largely arises from power plants, industries, vehicles and other sources of fuel burning. The pollution is generally a mixture of gases — such as carbon monoxide, sulfur dioxide and nitrogen oxides — and particulate matter, microscopic solids or droplets that can be inhaled into the lungs. The pollutant that has declined the least is ozone, a hard-to-control noxious gas formed when nitrogen oxides and volatile organic compounds react with sunlight. Ozone pollution tends to soar on hot, windless summer days as the sun blazes.
Particulates come from tail pipes and smokestacks, but also consist of tiny fragments shed from tires, roads and brake pads. Fine particulates (less than 2.5 micrometers wide, or about a quarter of the width of the smallest grain of pollen) are of greatest concern because they can penetrate deeply into the lungs to reach the body’s innermost nooks and crannies. A study in April in the journal ACS Nano demonstrated that fact. Fourteen healthy volunteers intermittently riding exercise bikes inhaled gold nanoparticles — stand-ins for particulates — and 15 minutes later, the nanoparticles were detected in the bloodstream and remained present in the body for as long as three months.
While events in Donora showed that air pollution can have immediate consequences, it took decades for researchers to realize that deaths from smog could be going undetected, lost in the background noise of mortality statistics. In 1993, Harvard University scientists published a study in the New England Journal of Medicine looking at mortality rates among adults in six U.S. cities. The researchers studied more than 8,000 people for 14 to 16 years. In areas with higher levels of sulfate particles in the air, a measure of pollution, mortality rates were higher. Dozens of similar studies have followed, including one published in 2003 that looked at death rates across 20 of the largest U.S. cities. That research found that the highest death rates occurred the day after particulate concentrations reached their highest levels, though the levels were subtle enough to go unnoticed at the time. Scientists now know that inhaling pollutants triggers a flurry of physiological coping mechanisms throughout the body. “Until 20 years ago, we thought that air pollution affected only the respiratory system,” says Petros Koutrakis, an environmental chemist who heads the EPA Harvard Center for Ambient Particle Health Effects. By 2004, the American Heart Association published a consensus statement in Circulation laying out “a strong case that air pollution increases the risk of cardiovascular disease,” the leading cause of U.S. deaths. More studies followed that statement, including one from Kaufman and colleagues in the New England Journal of Medicine in 2007. The researchers studied 65,893 women, looking for a link between exposure to fine particulates and death from heart attack or stroke, or even nonfatal heart attacks or the need for artery-clearing procedures. In the end, each increase of 10 micrograms of fine particulates per cubic meter of air increased the risk of any cardiovascular health event by 24 percent and the risk of dying from heart attack or stroke by 76 percent. In 2010, the American Heart Association updated its position: “The overall evidence is consistent with a causal relationship between [fine particulate] exposure and cardiovascular morbidity and mortality.” While the mechanism is still under study, research points to inflammation, heart rate variability and blood vessel damage.
Evidence keeps accumulating. A study by Koutrakis and colleagues, published in 2012 in Archives of Internal Medicine, found similar results. When particulate concentrations rose even to mild levels — those classified as a “moderate health concern for a very small number of people” by EPA standards — the risk of stroke rose by 34 percent within a day of exposure.
Pounds and pollution Lately, studies have moved from cardiovascular disease into more unexpected territory. And they’ve turned up compelling evidence that air quality may contribute to excess body weight. Frank Gilliland, an environmental epidemiologist at the University of Southern California in Los Angeles, became intrigued when laboratory studies suggested that certain pollutants in the environment might function as “obesogens,” contributing to weight gain by mimicking or disrupting the action of hormones, or having other effects. Still, he says, “I was very skeptical.”
Out of curiosity, he began to look for a link between childhood obesity and living close to a major roadway. His first study, published in 2010, examined over 3,000 children across California. Although the researchers found an association, they couldn’t rule out other explanations that would also lead back to cars. “Maybe the kids aren’t getting exercise because there’s a lot of traffic out,” he says. Newer findings are more convincing, including a 2014 study by Gilliland and colleagues. They studied body mass index among children exposed to traffic-related air pollution. Of course, as the children grew over the five-year study period, their BMIs increased from an average of 16.8 to 19.4 kilograms per square meter. But children exposed to the most air pollution, compared with those least exposed, had a 14 percent larger BMI increase, which meant an additional 0.4 kg/m2 increase in BMI by age 10. Adults, too, appear to be affected. Researchers from Harvard Medical School and elsewhere published a study in 2016 in the journal Obesity looking at whether adults living with constant exposure to traffic are more likely to be overweight. In particular, people who lived within 60 meters of a major road had a higher BMI, by 0.37 kg/m2, and more fat tissue than those who lived 440 meters from a busy road. The healthy range for an adult’s BMI is 18.5 to 25 kg/m2.
Studies in animals have started to offer hints why this might be the case. Last year in the FASEB Journal, Chinese researchers described an experiment in which one group of pregnant rats was raised in filtered air scrubbed of pollutants, while another breathed the usual Beijinghaze. Though they were fed the same diet, the animals living in Beijing air were heavier at the end of their pregnancies, as were their offspring that continued to breathe the dirty air eight weeks after birth. Among later autopsy findings: Rats exposed to pollution experienced higher levels of inflammation, which is thought to be a contributor to weight gain and metabolic disruption.
The relationship is probably subtle, and interwoven with genetics and lifestyle. UCLA researchers who followed a large group of African-American women over 16 years found no association between weight and exposure to particulates. For now, the connection between obesity and pollution is still a subject of investigation. But given that 11 million Americans live along major roadways, even a small effect could have widespread consequences.
Links to diabetes For many people, diabetes goes hand in hand with obesity. One of the earliest compelling studies to suggest a relationship between diabetes and air pollution was an animal experiment published in 2009 in Circulation from researchers at Ohio State University and other institutions. The test was relatively simple: Two groups of mice were fed a high-fat diet for 24 weeks. One lived in clean, filtered air; the other group was housed in enclosures polluted with air containing fine particulates, at concentrations still within EPA standards. The mice breathed the polluted air for six hours per day, five days a week for 128 days. Even though they ate the same food, the mice living in dirty air developed metabolic changes characteristic of insulin resistance while the other mice did not. Similarly, a 2013 study from EPA scientists found that mice exposed to ozone can develop glucose intolerance, a precursor for diabetes.
In July in Diabetes, Gilliland and colleagues published data not only finding links between air pollution and diabetes in children, but also insight into the body’s physiological response. In the study, 314 overweight or obese children in Los Angeles were followed for an average of three years. At the end of the study, children who lived in neighborhoods with the highest concentrations of nitrogen dioxide and particulates had experienced greater declines in insulin sensitivity and had signs of impaired pancreatic beta cells, which produce insulin. As for adults, a study this year in Environment International, conducted by researchers from eight institutions, tracked more than 45,000 African-American women across the United States. Those who were exposed to the highest concentrations of ozone were about 20 percent more likely to develop diabetes, even after adjusting for other possible explanations such as diet and exercise levels.
Brain drain One of the latest lines of research suggests that poisons in the air might accelerate aging in the brain. Studies have long documented the connection between the nose and brain function. For reasons not yet known, for instance, one of the early signs of Parkinson’s disease is a loss of the ability to distinguish smells.
During her graduate studies at Harvard, Jennifer Weuve, now an epidemiologist at the Boston University School of Public Health, wondered if airborne pollutants might be bad for the brain. “There was really intriguing data from animal studies,” she says, which showed that inhaled pollutants had toxic effects on nerve cells. In 2012, she published the first study to note a faster-than-normal cognitive decline among people exposed to higher levels of particulates, both those smaller than 2.5 micrometers and even larger ones that are thought to be less harmful. Her study, published in Archives of Internal Medicine, analyzed data from the Nurses’ Health Study Cognitive Cohort, which included almost 20,000 women ages 70 to 81, and used geographic information and air-monitoring data to estimate pollution exposure.
More recently, researchers from Sweden examined the relationship between pollution exposure and dementia, studying the records of people in northern Sweden participating in a long-term study of memory and aging. In 2016 in Environmental Health Perspectives, the researchers reported that people with the most exposure to air pollution were also the most likely to be diagnosed with Alzheimer’s or other forms of dementia. In all, more than a dozen human studies have examined pollution’s link to dementia. Last year in NeuroToxicology, Weuve and colleagues reviewed 18 human studies published as of late 2015, and concluded that as a whole, the evidence was “highly suggestive” and in need of more exploration. “What is it going to take for more people to take this seriously?” Weuve asks.
While the relationship is far from established, animal data may help clarify the results. One study published this year in Neurobiology of Aging, from researchers at the University of Southern California, examined brain changes in mice exposed to particulate air pollution at levels commonly found near freeways. After exposure to the pollution for five hours per day, three days a week for 10 weeks, the animals showed accelerated aging in the hippocampus, a region of the brain associated with memory. And a 2015 study of older women exposed to high levels of particulate matter, at levels common in the eastern half of the United States and in parts of California, showed a small decrease in the volume of white matter, the myelin-coated nerve cell projections called axons. Parkinson’s disease may also be linked to pollution. Danish researchers, with colleagues in the United States and Taiwan, published a study last year in Environmental Health Perspectives looking at people with and without Parkinson’s and their exposure to nitrogen dioxide, a marker for traffic-polluted air. The scientists identified 1,828 people in Denmark with Parkinson’s diagnosed between 1996 and 2009, and compared them with about the same number of randomly selected healthy people. Those exposed to the highest levels of air pollution had the greatest risk of developing the disease. The data, the researchers wrote, “raise concern given the increase in vulnerable aging populations.”
If science bears out the connection between pollution and brain health, or pollution and metabolism, environmental advocates and businesses may have even more reason to push for cleaner air. Researchers hope in the future to have more data on which pollutants cause the greatest harm, and why. In Donora, the site of one of the country’s biggest air pollution disasters, a sign at the Smog Museum now reads “Clean Air Started Here.” No one can yet say how clean is clean enough.
Light-sensitive cells in the eyes of some fish do double-duty. In pearlsides, cells that look like rods — the stars of low-light vision — actually act more like cones, which only respond to brighter light, researchers report November 8 in Science Advances. It’s probably an adaptation to give the deep-sea fish acute vision at dawn and dusk, when they come to the surface of the water to feed.
Rods and cones studding the retina can work in tandem to give an animal good vision in a wide variety of light conditions. Some species that live in dark environments, like many deep-sea fish, have dropped cones entirely. But pearlside eyes have confused scientists: The shimmery fish snack at the water’s surface at dusk and dawn, catching more sun than fish that feed at night. Most animals active at these times of day use a mixture of rods and cones to see, but pearlside eyes appear to contain only rods. “That’s actually not the case when you look at it in more detail,” says study coauthor Fanny de Busserolles, a sensory biologist at the University of Queensland in Australia.
She and her colleagues investigated which light-responsive genes those rod-shaped cells were turning on. The cells were making light-sensitive proteins usually found in cones, the researchers found, rather than the rod-specific versions of those proteins.
These rodlike cones still have the more elongated shape of a rod. And like regular rods, they are sensitive to even small amounts of light. But the light-absorbing proteins inside match those found in cones, and are specifically tuned to respond to the blue wavelengths of light that dominate at dawn and dusk, the researchers found. The fish don’t have color vision, though, which relies on having different cones sensitive to different wavelengths of light.
“Pearlsides found a more economical and efficient way of seeing in these particular light conditions by combining the best characteristics of both cell types into a single cell,” de Busserolles says. A few other animals have also been found to have photoreceptors that fall somewhere between traditional rods and cones, says Belinda Chang, an evolutionary biologist at the University of Toronto who wasn’t involved in the study. Chang’s lab recently identified similar cells in the eyes of garter snakes. “These are thought to be really cool and unusual receptors,” she says.
Together, finds like these begin to challenge the idea that rods and cones are two separate visual systems, de Busserolles says. “We usually classify photoreceptors into rods or cones only,” she says. “Our results clearly show that the reality is more complex than that.”
Overtime is going to look a little bit different in college football games during the 2021 season. The NCAA has once again made some minor tweaks to its overtime rules.
Why? It's all in the name of bringing the game to a quicker conclusion. The NCAA has made shortening overtime its mission since Texas A&M beat LSU 74-72 in a seven overtime game during the 2018 season. As exciting as that game was, it was long. More than 200 snaps were played, which is certainly not ideal for the players on the field.
So, how is the NCAA changing its overtime rules for 2021? Here's everything you need to know about the differences in overtime this season and how it compares to previous seasons. College football overtime rules 2021 The NCAA amended its overtime rules in 2021 in an attempt to lessen the number of plays run in an overtime period. Teams are now required to run a two-point conversion after a touchdown beginning in the second overtime period. Previously, that began in the third overtime period.
Additionally, teams will begin running alternating two-point conversion attempts if the game reaches a third overtime. So, it's essentially a one-play drive. The goal of this is to limit the number of plays run from scrimmage by each team.
Here are the rest of the college football overtime rules for the 2021 season.
At the end of regulation, the referee will toss a coin to determine which team will possess the ball first in overtime. The visiting team captain will call the toss. The winner gets to choose to either play offense or defense first or chooses which side of the field to play on. The decision cannot be deferred. The teams that loses the coin toss must exercise the remaining option. They will then have the chance to choose first from the four categories in the second overtime and subsequent even-numbered OT periods. The team that wins the toss will have the same options in odd-numbered OT periods. In each of the first two overtime periods, teams are granted one possession beginning at the opponent's 25-yard line, unless a penalty occurs to move them back. The offense can place the ball anywhere on or between the hash marks. Each team is granted one timeout per overtime period. Timeouts do not carry over from regulation nor do they carry over between overtime periods. Each team retains the ball until it fails to score, fails to make a first down or turns the ball over. Beginning with the second overtime period, teams must attempt a two-point conversion after scoring a touchdown. Beginning with the third overtime period, teams will begin to run alternating two-point conversion plays instead of offensive possessions. The college football overtime rules are the same in both the regular and postseason. College football overtime rule change proposals The most recent overtime rule change proposal was passed by the NCAA in 2021. It was made in the name of shortening games and limiting offensive reps, as previously stated.
Below are the rule changes that were ratified for 2021:
Beginning with the second overtime period, teams must attempt a two-point conversion after scoring a touchdown. Beginning with the third overtime period, teams will begin to run alternating two-point conversion plays instead of offensive possessions. History of college football overtime rules Up until 1996, most NCAA games did not go to overtime. They simply ended in a tie. However, the governing body adopted overtime rules after pushback on some important matchups ending all square.
The initial overtime rules were in place for quite a while. Each team got the ball at the opponent's 25-yard line and retained the ball until it failed to score, failed to make a first down or turned the ball over. Teams alternated possessions until a team emerged as a victor.
Then, in 2019, the NCAA made a couple of changes in the name of shortening the game. That's when they added the two-point conversion rule, so teams had to start attempting a two-point conversion starting in the third overtime. Then, after five overtimes, teams would start running alternating two-point conversion plays. These changes were, basically, a direct response to the Texas A&M vs. LSU game.
In 2021, the rules were tweaked again, as teams must run two-point conversions in the second overtime period and will begin alternating two-point plays when the third overtime begins.
For the first time all season, Columbus, Ohio will host "College GameDay" in what will be a massive game between the fourth-ranked Buckeyes and No. 7 Michigan State.
Rece Davis, Kirk Herbstreit, Lee Corso, Desmond Howard, David Pollack and Co. will head to Ohio Stadium to preview a game that will not only affect the Big Ten championship race, but also the College Football Playoff rankings. Should the Spartans pull off the upset in Columbus, they will have only Penn State and the Big Ten West division champion standing between them and a playoff berth. Things are slightly more complicated for Ohio State which, even with a win on Saturday, has a tough road to a fifth playoff appearance. They must then face No. 6 Michigan in The Big House before heading to Indianapolis for the Big Ten championship game. The Buckeyes then have to contend with their Week 2 loss to Oregon, yet another team that is in the playoff chase. This game could be a contrast of styles as Ohio State quarterback C.J. Stroud seeks to lead the Buckeyes to victory. He has completed 68.8 percent of his passes for 3,036 yards and 30 touchdowns to five interceptions. He has no shortage of skill position weapons to use in Jaxon Smith-Njigba (59 receptions, 1,027 yards, five touchdowns), Garrett Wilson (53 receptions, 813 yards, nine touchdowns) or Chris Olave (51 receptions, 708 yards, 11 touchdowns). Running back TreVeyon Henderson (141 rushes, 1,035 yards, 14 touchdowns) is a home run threat as well.
There's no question who Michigan State's offense runs through: running back Kenneth Walker III. The junior leads all FBS in rushing yards (1,483 yards) and ties the national lead in rushing touchdowns (17) and touchdowns from scrimmage (18). He is also coming off three straight games with at least 143 yards and one score. In fact, he only has three games rushing for fewer than 100 yards this season.
Which play style will win out on Saturday? Only one way to find out. Until then, Sporting News has you covered on how to watch "College GameDay" preview the massive Big Ten meeting. Where is 'College GameDay' location for Week 12? Location: Columbus, Ohio Matchup: No. 7 Michigan State at No. 4 Ohio State The Buckeyes will make their 51st all time appearance on "GameDay" on Saturday, giving them one more than second-place Alabama for most all time. It will also be Ohio State's 20th time hosting "GameDay," a scenario in which the Buckeyes are 14-5 all time. More impressive is that all but one of those games took place between ranked teams (the lone exception was a 38-24 win over unranked Penn State in 2010).
Surprisingly, Ohio State has more nonconference losses in Ohio Stadium than conference losses; they have lost to Texas (2005), USC (2009) and Oklahoma (2017). In the Big Ten, only Penn State (2008) and Michigan State (2015) can claim "GameDay" victories in Columbus.
Michigan State is making its 16th all-time appearance on "GameDay," where it has gone 9-6 in its previous 15 matchups. That includes a 2-1 record as the road team, 9-2 record in ranked matchups and 2-2 record against Ohio State. 'College GameDay' schedule on ESPN TV channel: ESPN Start time: 9 a.m. ET Davis, Herbstreit, Howard and Pollack will preview Week 12 action live from Ohio Stadium starting at 9 a.m. ET. The game will be broadcast on ESPN, with kickoff set for 7 p.m. ET.
"GameDay" has three games to consider for its Week 13 visit, depending on how Week 12 plays out. The most obvious of those is No. 4 Ohio State at No. 6 Michigan. The game could very well determine the Big Ten East champion and, by extension, the Big Ten champion outright. Another option is Bedlam, between No. 13 Oklahoma and No. 9 Oklahoma State in Stillwater. It's possible the game features the Sooners and Cowboys as one-loss opponents; it could also be the first of two meetings this season. The meeting between No. 2 Alabama and Auburn in the Iron Bowl is also worth visiting, though the SEC West race could already be decided by then.
Week Matchup Location Guest Picker Corso's Headgear Outcome 0 Alcorn State vs. NCCU Atlanta Eddie George Braves NCCU 23, Alcorn State 14 1 No. 5 Georgia vs. No. 3 Clemson Charlotte, N.C. Kane Brown Bulldogs Georgia 10, Clemson 3 2 No. 10 Iowa at No. 9 Iowa State Ames, Iowa Ashton Kutcher Hawkeyes Iowa 27, Iowa State 17 3 No. 22 Auburn at No. 10 Penn State University Park, Pa. Saquon Barkley Nittany Lions Penn State 28, Auburn 20 4 No. 12 Notre Dame vs. No. 18 Wisconsin Chicago Danica Patrick Fighting Irish Notre Dame 41, Wisconsin 13 5 No. 8 Arkansas at No. 2 Georgia Athens, Ga. Harris English Bulldogs Georgia 37, Arkansas 0 6 No. 6 Oklahoma vs. No. 21 Texas Dallas Mark Cuban Longhorns Oklahoma 55, Texas 48 7 No. 11 Kentucky at No. 2 Georgia Athens, Ga. Jeff Foxworthy Bulldogs Georgia 30, Kentucky 13 8 No. 10 Oregon at UCLA Pasadena, Calif. Bill Walton Bruins Oregon 34, UCLA 31 9 No. 6 Michigan at No. 8 Michigan State East Lansing, Mich. Ken Jeong Wolverines Michigan State 37, Michigan 33 10 Tulsa at No. 6 Cincinnati Cincinnati Nick Lachey Bearcats Cincinnati 28, Tulsa 20 11 No. 11 Texas A&M at No. 15 Ole Miss Oxford, Miss. Lane Kiffin Rebels Ole Miss 29, Texas A&M 19 12 No. 7 Michigan State at No. 4 Ohio State Columbus, Ohio TBD TBD TBD Who is the guest picker on 'College GameDay' for Week 12? "GameDay" has yet to announce its celebrity guest picker for Week 12.
There was a moment in the first half, not even 20 minutes into the United States’ World Cup qualifier at Jamaica, that American midfielder Yunus Musah gathered the ball in the center of the field at Independence Park and contemplated one of his favored rampages toward the opposing goal. He had demolished Mexico with his physical strength and dribbling skill, and it was time to do the same to the Reggae Boyz.
As Musah advanced, though, the ball did not. The field — yes, the field — had other ideas. It’s not always the opposing fans or the refs or the pressure of the circumstance. Sometimes, it’s as simple as lacking the comforts of home. For a squad that included three teenagers and was the second-youngest the USMNT ever deployed for a qualifier, being unable to count on the ball rolling evenly was among the many reasons it left Jamaica with a 1-1 draw and a single point to add toward its total.
“We’re not looking at it as a disappointing result. We’re looking at it as a good result,” U.S. coach Gregg Berhalter told reporters. “Any time you can get a point away from home is a good thing in CONCACAF qualifying. I want to be very clear by saying that.
“I think for the guys to have their heads down because we wanted more is completely natural, but this is a point that we’ll absolutely take on the road.”
It’s a point more precious than American fans are likely to appreciate. The U.S. easily could have lost, given one blown opportunity at a wide-open tap-in for Jamaica’s Bobby Reid and a disallowed goal from his teammate, Damian Lowe, on an 84th-minute set piece.
The U.S. took a 1-0 lead on forward Timothy Weah’s inventive 11th-minute goal, which required a sweet feed from striker Ricardo Pepi, two nifty moves from Weah and a left-footed finish past ace goalkeeper Andre Blake. That was answered 11 minutes later, though, when Jamaica’s Michail Antonio — currently third in the Premier League in goals for West Ham United — drove to the left against U.S. midfielder Tyler Adams, stopped and cut back to his right foot and left Adams behind. He blasted a searing shot from 34 yards that found the top right corner, beyond the reach of goalkeeper Zack Steffen.
“Obviously, it was a rough game. Not the result that we wanted,” Weah said. “We knew it was going to be difficult.
“Conditions were rough, but that’s no excuse. We wanted to execute, but it wasn’t there today.”
It’s difficult to reconcile this torpid performance against the brilliance of Friday night’s victory over Mexico. But combining the two gives the USMNT four points from the two-game window in CONCACAF qualifying, and still leaves it in position to earn an automatic position in the 2022 World Cup field.
The Americans now have five points from four road games, slightly ahead of the “win your home games, draw on the road” standard that tends to assure qualification in this format. However, they’re also a couple points behind at home because of a 1-1 September draw against Canada. Their 15 points through eight games is three more than they earned in the entire 10-game qualifying round when failing to qualify for Russia 2018.
Qualifying will not be easy. Not that it ever has been.
“It was difficult conditions, it really was,” Berhalter said. “Controlling the ball, playing the ball was challenging. You can chalk it up to simply that. It was challenging field conditions, and the movements weren’t always clean. That’s something you can’t control.”
This is not something Musah would have encountered often while growing up in Italy or later England, where he trained in the Arsenal youth program. Pristine pitches predominated once he moved to Spain to join Valencia in 2019, and that’s what was in place in Cincinnati — even though it rained — when the USMNT dominated rival Mexico to earn a 2-0 victory and take over first place in the final round of World Cup qualifying.
After that moment in the 18th minute, though, Musah seemed to abandon the skill that had made him such a force against Mexico. With midfielder Weston McKennie out because of a yellow-card suspension — and with Musah muted and fellow teen Gianluca Busio just a shade hesitant in his first qualifying start — the Americans lacked the engine that had driven them four days earlier.
Berhalter allowed that he thought Musah was bothered by the conditions, then told Sporting News he also was bothered by a case of strep throat.
“We could tell that was taking a toll on him,” Berhalter told SN. “I don’t want this to be about the field, I really don’t. It was the same for both teams. We had enough time to be moving the ball. It was difficult, but we had enough time. And it’s just something you have to deal with. And we’re used to dealing with that.”
Are they, though? Most of the USMNT still has played in just a few CONCACAF road qualifiers. Hesitation was horrifically huge for many of those who played Tuesday. So many circumstances that could have been devastating developed because players expected balls to roll into their feet, only to see them die and be beaten to the play by the opposition. There were passes fed in the direction of teammates that lacked the necessary pace, including one to Steffen that traveled so slowly it nearly allowed Jamaica another simple scoring chance.
That’s what happened on the play that set Reid up, with U.S. right back DeAndre Yedlin waiting too long to pursue what should have been a simple clearance. Instead, Jamaica was able to feed a cross to the far post, where left back Antonee Robinson tried to clear it for the Americans. Instead, he knocked it directly across the goal to Reid. What should have been a simple tap-in was blasted over the crossbar because Reid panicked.
In the 84th minute, Jamaica’s corner kick was pursued by Lowe directly in front of the goal, but he was called for climbing over defender Walker Zimmerman’s back to head the ball past. Berhalter said he heard the whistle quickly, so he believed referee Juan Gabriel Calderon of Costa Rica was convinced of his call.
“When you think about the youth of this group, the inexperience of this group in CONCACAF qualifying, we’re on the right track,” Berhalter said. “Just thinking about it, you don’t often get where you’re in a qualifying competition, one venue is freezing cold, and the next venue is this tropical climate.
“Most continents, when they have qualifying, the weather’s consistent. So we’re going through a lot here, man. We’re learning on the fly. The guys have done a good job with that. We’ll take our position now and focus on 2022.”
To be clear, he meant the six games remaining in qualifying that will be played in the new year — not “Qatar 2022.”
The Americans are not there yet. And the road to get there will remain bumpy.
