Tag Archives: Delay

Manchin pushes to delay tax credits for electric vehicles

WASHINGTON (AP) — Ratcheting up his criticism, Democratic Sen. Joe Manchin on Wednesday moved to delay new tax credits for electric vehicles, a key feature of President Joe Biden’s landmark climate law.

Manchin said guidelines issued by the Treasury Department allow manufacturers in Europe and other countries to bypass requirements that significant portions of EV batteries be produced in North America.

The climate law, officially known as the Inflation Reduction Act, “is first and foremost an energy security bill,” Manchin said, adding that the EV tax credits were supposed “to grow domestic manufacturing and reduce our reliance on foreign supply chains for the critical minerals needed to produce EV batteries.″

Manchin’s bid to delay the tax credits surfaced as Energy Secretary Jennifer Granholm and White House climate adviser Ali Zaidi visited the Washington, D.C., Auto Show on Wednesday to highlight the administration’s efforts to boost electric vehicles and related infrastructure.

EV sales have tripled since Biden, a Democrat, took office two years ago, Granholm said. There are now more than 2 million EVs and 100,000 chargers on U.S. roadways, with more than $100 billion invested or pledged for EVs and their supply chains, including batteries, she said.

While batteries and components have long been manufactured in China, “we’re going to bring that manufacturing home,″ Granholm told reporters.

“We’re going to give Americans the chance to drive American vehicles made by American workers — and that is only going to compound as Americans start to drive these vehicles and realize how great they are,″ she said. “The demand is going to go very high. We expect that by 2030, half of all the vehicles sold in the United States will be electric.″

Granholm and the White House declined to comment on Manchin’s bill, but the measure by the West Virginia lawmaker is unlikely to gain traction in the Senate, where Democrats hold a slim majority and have shown no inclination to reopen a bill they just passed on a party-line vote. During the midterm election campaign, Republicans criticized Biden and other Democrats for supporting electric vehicles, citing their relative high costs and batteries made in China.

Tax credits of up to $7,500 per vehicle are intended to spur EV sales and domestic production of vehicles and batteries while reducing planet-warming greenhouse gas emissions. European and Asian allies, including French President Emmanuel Macron, have criticized the rules as unfair to foreign manufacturers.

While Macron applauded Biden’s efforts to curb climate change, he said during a visit to Washington that subsidies in the new law could be an enormous problem for European companies.

Biden acknowledged “glitches” in the legislation but said “there’s tweaks we can make” to satisfy allies.

Manchin’s bill follows a decision by the Treasury Department to delay rules on battery contents and minerals until March, while allowing the rest of the program to be implemented on Jan. 1. The Manchin bill directs Treasury to stop issuing tax credits for vehicles that don’t comply with battery requirements.

“The United States is the birthplace of Henry Ford, who revolutionized the automotive industry,″ Manchin said, calling it “shameful that we rely so heavily on foreign suppliers, particularly China, for the batteries that power our electric vehicles.″

Manchin, chairman of the Senate Energy and Natural Resources Committee, was a crucial vote in passing the climate law, which was adopted without support from any Republican in the House or Senate. He has said exemptions approved by the Treasury — including one that allows tax credits for EVs purchased for commercial use, such as leasing or ride-sharing, even if they are foreign-made — undermine the law’s intent to reduce U.S. dependence on foreign countries, including adversaries, and create jobs in the United States.

At the World Economic Forum in Davos, Switzerland, last week, Manchin said he did not realize the European Union does not have a free trade agreement with the U.S. when Democrats passed the EV restrictions. He told reporters at the Capitol this week that European countries should reconsider their own policies for promoting clean energy, and the U.S. could work on a trade deal.

“Whether I realized it or not, they need to hopefully get that together and let’s get a free trade agreement,” Manchin said.

Senate Finance Committee Chairman Ron Wyden, D-Ore., has said he has no interest in reopening the climate law, which passed after more than a year and a half of sometimes contentious negotiations.

John Bozzella, president of the Alliance for Automotive Innovation, an industry trade group, said Manchin’s bill would only add confusion to an already complicated EV tax credit that many drivers — and even some car dealers — don’t fully understand.

“We want to make sure we don’t increase confusion for customers who might be confused already about what qualifies for a tax credit,” Bozzella said, “so I’m not quite sure what the value of the new legislation is.”

___

Follow the AP’s coverage of electric vehicles at https://apnews.com/hub/electric-vehicles.

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Hypertension Drug Could Be Repurposed to Delay Aging

Summary: Rilmenidine, a drug commonly prescribed to help treat hypertension can help slow the effects of aging and extend lifespan, a new study reports.

Source: University of Liverpool

Researchers have found that the drug rilmenidine can extend lifespan and slow aging.

Published in Aging Cell, the findings show that animals treated with rilmenidine, currently used to treat hypertension, at young and older ages increases lifespan and improves health markers, mimicking the effects of caloric restriction.

They also demonstrate that the healthspan and lifespan benefits of rilmenidine treatment in the roundworm C. elegans are mediated by the I1-imidazoline receptor nish-1, identifying this receptor as a potential longevity target.

Unlike other drugs previously studied for this purpose by the researchers, the widely-prescribed, oral antihypertensive rilmenidine has potential for future translatability to humans as side-effects are rare and non-severe.

To date, a caloric restriction diet has been considered the most robust anti-aging intervention, promoting longevity across species. However, studies of caloric restriction in humans have had mixed results and side effects, meaning finding medications like rilmenidine that can mimic the benefits of caloric restriction is the most reasonable anti-aging strategy.

Unlike other drugs previously studied for this purpose by the researchers, the widely-prescribed, oral antihypertensive rilmenidine has potential for future translatability to humans as side-effects are rare and non-severe. Image is in the public domain

Professor João Pedro Magalhães, who led the research whilst at the University of Liverpool and is now based at the University of Birmingham, said: “With a global aging population, the benefits of delaying aging, even if slightly, are immense. Repurposing drugs capable of extending lifespan and healthspan has a huge untapped potential in translational geroscience.

“For the first time, we have been able to show in animals that rilmenidine can increase lifespan. We are now keen to explore if rilmenidine may have other clinical applications.”

Funding: This study was undertaken by researchers from the University of Liverpool, ETH Zürich and Harvard Medical School, and funded by the Swiss National Science Foundation, LongeCity and the Biotechnology and Biological Sciences Research Council.

About this pharmacology and aging research news

Author: Jennifer Morgan
Source: University of Liverpool
Contact: Jennifer Morgan – University of Liverpool
Image: The image is in the public domain

Original Research: Open access.
“Rilmenidine extends lifespan and healthspan in C. elegans via a nischarin I1- imidazoline receptor” by João Pedro Magalhães et al. Aging Cell


Abstract

Rilmenidine extends lifespan and healthspan in C. elegans via a nischarin I1- imidazoline receptor

See also

Repurposing drugs capable of extending lifespan and health span has a huge untapped potential in translational geroscience.

Here, we searched for known compounds that elicit a similar gene expression signature to caloric restriction and identified rilmenidine, an I1-imidazoline receptor agonist and prescription medication for the treatment of hypertension.

We then show that treating Caenorhabditis elegans with rilmenidine at young and older ages increases lifespan. We also demonstrate that the stress-resilience, health span, and lifespan benefits of rilmenidine treatment in C. elegans are mediated by the I1-imidazoline receptor nish-1, implicating this receptor as a potential longevity target.

Consistent with the shared caloric-restriction-mimicking gene signature, supplementing rilmenidine to calorically restricted C. elegans, genetic reduction of TORC1 function, or rapamycin treatment did not further increase lifespan. The rilmenidine-induced longevity required the transcription factors FOXO/DAF-16 and NRF1,2,3/SKN-1. F

urthermore, we find that autophagy, but not AMPK signaling, was needed for rilmenidine-induced longevity. Moreover, transcriptional changes similar to caloric restriction were observed in liver and kidney tissues in mice treated with rilmenidine.

Together, these results reveal a geroprotective and potential caloric restriction mimetic effect by rilmenidine that warrant fresh lines of inquiry into this compound.

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Dolphins coach – Thought we had 1st before delay flag on 4th-and-1

ORCHARD PARK, N.Y. — Miami Dolphins coach Mike McDaniel offered an explanation for a critical delay of game penalty his team incurred on its final offensive possession in a 34-31 loss to the Buffalo Bills on Sunday.

Facing fourth-and-1 from their own 48-yard line with 2:28 remaining in the game, the Dolphins failed to get a play off in time and were flagged for delay of game. The penalty pushed them back to fourth-and-6, and they were unable to convert on a Skylar Thompson pass attempt to tight end Mike Gesicki.

McDaniel said afterward it was communicated to him that the Dolphins had picked up a first down on the prior play, and he didn’t immediately have a fourth-down play ready.

“There was some communication that we’d gotten first down,” he said. “So then we were deploying a group of players for the first-and-10 call. Then it was articulated that no, it was fourth down … I had gotten conflicted information that it was a first down; I don’t really know exactly who it was from. It’s probably the first time all year that that had happened. You try to do your best. As it was, I thought we had a fourth-and-6 opportunity we were unable to come up with.

“You just have to adjust to any variables out there, and I thought we had a chance at fourth-and-6, as well.”

The Dolphins entered Sunday’s contest 14-point underdogs but held a one-score lead midway through the third quarter. The Bills answered with 14 straight points to take a 10-point lead with two minutes remaining in the third quarter.

Miami cut its deficit to three points after a Jeff Wilson Jr. touchdown run with 11 minutes left in the game and got the ball back with four minutes remaining with an opportunity to tie it or take the lead.

Thompson completed a 14-yard pass to Jaylen Waddle on second-and-15 to bring up third-and-1, but Salvon Ahmed’s rushing attempt did not result in a first down. McDaniel said he believes someone on his headset communicated to him that Ahmed had converted, however, and the coach said he called a play to reflect that before realizing the actual down and distance.

The Dolphins did not have any timeouts remaining and could not stop the clock after the Bills took over on downs.

Sunday’s contest was the Dolphins’ first playoff appearance since the 2016 season. The five-year playoff drought marked the third-longest in franchise history.

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How 6 Minutes of Exercise Could Delay Alzheimer’s and Parkinson’s Disease

According to a new study, just six minutes of high-intensity exercise could extend the lifespan of a healthy brain and delay the onset of neurodegenerative disorders such as Alzheimer’s and Parkinson’s. The research found that a short but intense bout of cycling increases the production of a protein that is essential for brain formation, learning, and memory, and could protect the brain from age-related cognitive decline.

Six minutes of high-intensity exercise could extend the lifespan of a healthy brain and delay the onset of neurodegenerative disorders, such as

Lead author Travis Gibbons from University of Otago, New Zealand said, “BDNF has shown great promise in animal models, but pharmaceutical interventions have thus far failed to safely harness the protective power of BDNF in humans. We saw the need to explore non-pharmacological approaches that can preserve the brain’s capacity which humans can use to naturally increase BDNF to help with healthy aging.”

To tease apart the influence of fasting and exercise on BDNF production the researchers, from the University of Otago, New Zealand, compared the following factors to study the isolated and interactive effects:

  • Fasting for 20 hours,
  • Light exercise (90-minutes of low-intensity cycling),
  • High-intensity exercise (a six-minute bout of vigorous cycling),
  • Combined fasting and exercise.

They found that brief but vigorous exercise was the most efficient way to increase BDNF compared to one day of fasting with or without a lengthy session of light exercise. BDNF increased by four to five-fold (396 pg L-1 to 1170 pg L-1) more compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L-1 to 390 pg L-1).

The cause for these differences is not yet known and more research is needed to understand the mechanisms involved. One hypothesis is related to the cerebral substrate switch and glucose metabolism, the brain’s primary fuel source. The cerebral substrate switch is when the brain switches its favoured fuel source for another to ensure the body’s energy demands are met, for example, metabolizing lactate rather than glucose during exercise. The brain’s transition from consuming glucose to lactate initiates pathways that result in elevated levels of BDNF in the blood.

The observed increase in BDNF during exercise could be due to the increased number of platelets (the smallest blood cell) which store large amounts of BDNF. The concentration of platelets circulating in the blood is more heavily influenced by exercise than fasting and increases by 20%.

12 physically active participants (six males and six females aged between 18 and 56 years) took part in the study. The balanced ratio of male and female participants was to provide a better representation of the population rather than indicate sex differences.

Further research is underway to delve deeper into the effects of calorie restriction and exercise to distinguish the influence on BDNF and the cognitive benefits.

Travis Gibbons said, “We are now studying how fasting for longer durations, for example up to three days, influences BDNF. We are curious whether exercising hard at the start of a fast accelerates the beneficial effects of fasting. Fasting and exercise are rarely studied together. We think fasting and exercise can be used in conjunction to optimize BDNF production in the human brain.”

Reference: “Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans” by Travis D. Gibbons, James D. Cotter, Philip N. Ainslie, Wickliffe C. Abraham, Bruce G. Mockett, Holly A. Campbell, Emma M. W. Jones, Elliott J. Jenkins and Kate N. Thomas, 11 January 2023, The Journal of Physiology.
DOI: 10.1113/JP283582



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Six Minutes of Daily High-Intensity Exercise Could Delay the Onset of Alzheimer’s Disease

Summary: Researchers report six minutes of high-intensity exercise on a regular basis can slow brain aging and delay the onset of neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. High-intensity exercise increases the production of BDNF, a protein implicated in memory, learning, and brain plasticity, which could protect the brain from age-related cognitive decline.

Source: The Physiological Society

Six minutes of high-intensity exercise could extend the lifespan of a healthy brain and delay the onset of neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease.

New research published in The Journal of Physiology shows that a short but intense bout of cycling increases the production of a specialized protein that is essential for brain formation, learning and memory, and could protect the brain from age-related cognitive decline.

This insight on exercise is part of the drive to develop accessible, equitable and affordable non-pharmacological approaches that anyone can adopt to promote healthy aging.

The specialized protein named brain-derived neurotrophic factor (BDNF) promotes neuroplasticity (the ability of the brain to form new connections and pathways) and the survival of neurons.

Animal studies have shown that increasing the availability of BDNF encourages the formation and storage of memories, enhances learning and overall boosts cognitive performance. These key roles and its apparent neuroprotective qualities have led to the interest in BDNF for aging research.

Lead author Travis Gibbons from University of Otago, New Zealand stated, “BDNF has shown great promise in animal models, but pharmaceutical interventions have thus far failed to safely harness the protective power of BDNF in humans.

“We saw the need to explore non-pharmacological approaches that can preserve the brain’s capacity which humans can use to naturally increase BDNF to help with healthy aging.”

To tease apart the influence of fasting and exercise on BDNF production, the researchers, from the University of Otago, New Zealand, compared the following factors to study the isolated and interactive effects:

  • Fasting for 20 hours
  • Light exercise (90-minute low intensity cycling)
  • High-intensity exercise (six-minute bout of vigorous cycling)
  • Combined fasting and exercise

They found that brief but vigorous exercise was the most efficient way to increase BDNF compared to one day of fasting with or without a lengthy session of light exercise. BDNF increased by four to five-fold (396 pg L-1 to 1170 pg L-1) more compared to fasting (no change in BDNF concentration) or prolonged activity (slight increase in BDNF concentration, 336 pg L-1 to 390 pg L-1).

The cause for these differences is not yet known, and more research is needed to understand the mechanisms involved. One hypothesis is related to the cerebral substrate switch and glucose metabolism, the brain’s primary fuel source.

The cerebral substrate switch is when the brain switches its favored fuel source for another to ensure the body’s energy demands are met, for example metabolizing lactate rather than glucose during exercise. The brain’s transition from consuming glucose to lactate initiates pathways that result in elevated levels of BDNF in the blood.

They found that brief but vigorous exercise was the most efficient way to increase BDNF compared to one day of fasting with or without a lengthy session of light exercise. Image is in the public domain

The observed increase in BDNF during exercise could be due to the increased number of platelets (the smallest blood cell), which store large amounts of BDNF. The concentration of platelets circulating in the blood is more heavily influenced by exercise than fasting and increases by 20%.

Twelve physically active participants (six males, six females aged between 18 and 56 years) took part in the study. The balanced ratio of male and female participants was to provide a better representation of the population rather than indicate sex differences.

Further research is underway to delve deeper into the effects of calorie restriction and exercise to distinguish the influence on BDNF and the cognitive benefits.

Travis Gibbons noted, “We are now studying how fasting for longer durations, for example up to three days, influences BDNF. We are curious whether exercising hard at the start of a fast accelerates the beneficial effects of fasting.

“Fasting and exercise are rarely studied together. We think fasting and exercise can be used in conjunction to optimize BDNF production in the human brain.”

About this exercise and dementia research news

Author: Press Office
Source: The Physiological Society
Contact: Press Office – The Physiological Society
Image: The image is in the public domain

See also

Original Research: Closed access.
“Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans” by Travis Gibbons et al. Journal of Physiology


Abstract

Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans

Intermittent fasting and exercise provide neuroprotection from age-related cognitive decline. A link between these two seemingly distinct stressors is their capability to steer the brain away from exclusively glucose metabolism. This cerebral substrate switch has been implicated in upregulating brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning and memory, and may underlie some of these neuroprotective effects.

We examined the isolated and interactive effects of (1) 20-h fasting, (2) 90-min light exercise, and (3) high-intensity exercise on peripheral venous BDNF in 12 human volunteers.

A follow-up study isolated the influence of cerebrovascular shear stress on circulating BDNF. Fasting for 20 h decreased glucose and increased ketones (P ≤ 0.0157) but had no effect on BDNF (P ≥ 0.4637). Light cycling at 25% of peak oxygen uptake (${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$) increased serum BDNF by 6 ± 8% (independent of being fed or fasted) and was mediated by a 7 ± 6% increase in platelets (P < 0.0001).

Plasma BDNF was increased from 336 pg l−1 [46,626] to 390 pg l−1 [127,653] by 90-min of light cycling (P = 0.0128). Six 40-s intervals at 100% of ${dot V_{{{rm{O}}_{rm{2}}}{rm{peak}}}}$ increased plasma and serum BDNF, as well as the BDNF-per-platelet ratio 4- to 5-fold more than light exercise did (P ≤ 0.0044). Plasma BDNF was correlated with circulating lactate during the high-intensity intervals (r = 0.47, P = 0.0057), but not during light exercise (P = 0.7407).

Changes in cerebral shear stress – whether occurring naturally during exercise or induced experimentally with inspired CO2 – did not correspond with changes in BDNF (P ≥ 0.2730).

BDNF responses to low-intensity exercise are mediated by increased circulating platelets, and increasing either exercise duration or particularly intensity is required to liberate free BDNF.

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Delay in NFL postponement of a traumatic football game was unconscionable – Chicago Tribune

The date may only have been Jan. 2, but Monday Night Football may turn out to be the most excruciating hour of broadcast television Americans will see all year.

The fault did not lie with the ESPN broadcasters, who did their best to harness their own emotions and fill an hour of airtime following the on-field collapse of Buffalo Bills safety Damar Hamlin whose heart reportedly stopped, and who received CPR on the field, following a tackle during a game with the Cincinnati Bengals.

They tried to talk on, even saying the same things over and over again with no new information, without unduly exploiting the situation at hand. The issue was the absurd delay in the NFL postponing the game, even while players agonized at a fellow athlete facing a life-or-death situation. The pain on players’ faces was all too visible to the television audience.

On Tuesday morning, it was unclear why sportscaster Joe Buck made repeated reference to the players possibly restarting after a short break of just a few minutes, given that the NFL insisted it was never the league’s intent. And it’s certainly true that sudden, shocking events like this can cause breakdowns in decision-making and communication.

We’d like to think, though, that any scheduling or competitive issues with postponing a pivotal, late-season game did not come into play, given that a young player’s life was hanging in the balance.

Eventually, the famously cautious NFL Commissioner Roger Goodell did the right thing and let the players and fans go home with their minds not on football but on the health of Hamlin, who doctors say had suffered cardiac arrest. On Tuesday, he was reported as being in critical but stable condition.

But given the on-field ambulance and the CPR needed to restore Hamlin’s heartbeat, it sure took Goodell, who makes $63.9 million a year, a long time to turn a game “suspension” into a postponement, amplifying the emotional distress not just of a stadium full of fans and players but an entire nation watching on television and catching on far quicker than the NFL bosses that, when health is on the line in their dangerous game, football must be nothing more than an afterthought.

Instead of letting ESPN squirm in a vacuum, Goodell should have been personally on camera as quickly as possible, making that very point and turning everyone’s minds to a talented young man who clearly was fighting for his life.

Join the discussion on Twitter @chitribopinions and on Facebook.

Submit a letter, of no more than 400 words, to the editor here or email letters@chicagotribune.com.



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NFL’s Tennessee Titans delay game one hour as state deals with rolling power outages



CNN
 — 

The NFL’s Tennessee Titans delayed its scheduled noon CT game by an hour due to rolling blackouts in the region, which have since ended, stemming from the winter storm and brutal cold.

“Due to the extreme weather and power outages affecting our region, kickoff for today’s game has been postponed one hour to 1 p.m. CT,” the Titans said in a statement.

“This decision was made in partnership with the NFL, Office of Emergency Management, Nashville Electric Service and the Mayor’s Office in an abundance of caution to ensure that the game would not negatively impact our community in any way. We are exploring every possibility to minimize non-essential power around the stadium.”

The Titans (7-7), losers of four straight games, began their game against the Houston Texans (1-12-1) at Nissan Stadium in Nashville at 1 p.m. CT. The temperature was 22 degrees at kickoff, making it the coldest game in Nissan Stadium history, according to the CBS broadcast.

The Tennessee Valley Authority, the federally owned electric utility company that powers seven states in the region, had directed local power companies to reduce their power load for periods on Friday and Saturday due to weather-related record-high demand and power generation issues.

Chief Operating Officer Don Moul said the agency “lost some generation” due to the extreme cold and high winds, and the authority urged residents to conserve power. Still, the TVA said Saturday it supplied more power in the past 24 hours than at any other time in its history.

The authority ended the rolling blackouts midday Saturday after temperatures rose slightly and the power system’s conditions improved, the TVA said.

“We recognize that these planned temporary disruptions are a challenge, but it was needed to maintain grid stability for 10 million people across seven states,” the authority said. “Thank you for doing your part, conserving energy, and helping us manage this extreme weather event.”

On Saturday morning, local power companies said that they were directed to interrupt power for short spurts. CDE Lightband, a power company out of Clarksville, Tennessee, said the TVA told it to interrupt power in 15-minute intervals.

Similarly, the Nashville Electric Service told customers Saturday morning to expect “rotating, intermittent power outages” in about 10-minute increments every one-and-a-half to two hours.

Amid the blackouts, Nashville Mayor John Cooper had urged the Titans to postpone their game, saying that “all non-essential businesses should reduce power usage.” He issued a follow-up tweet saying he appreciated the decision to delay the game an hour.

In general, prolonged cold snaps can overwhelm the power grid by simultaneously knocking out power supply and causing a sharp increase in demand as residents turn up the heat. For example, in Texas in February 2021, a winter storm and lengthy cold period caused mass outages in areas served by the Electric Reliability Council of Texas, leaving millions of residents in the cold and dark for nearly a week.

The TVA informed residents on Friday there would be rolling blackouts due to the winter storm, though that directive was later rescinded.

Memphis Mayor Jim Strickland told CNN on Friday hospitals and medical offices were exempt. The TVA did not anticipate the extent of the situation prior to the storm, he said.

“This is a real struggle. This has never happened in my lifetime, this hasn’t happened in Memphis in at least 50 years,” Strickland said Friday.

On Saturday morning, he said the rolling blackouts across Memphis impacted more than 50,000 people for about 30 to 60 minutes at a time, likely two to three times per day.

“TVA has always prided itself on reliability. This is the first time TVA has required rolling blackouts,” Strickland told CNN. “It’s going to take a deeper dive into the reasons this happened.”

Strickland said that temperatures are not expected to rise above 32 degrees Fahrenheit for at least the next two days.

The outages and rolling blackouts have affected much of the US, particularly the Southeast.

As of 11 a.m. ET Saturday, Tennessee has about 250,000 customers without power, and North Carolina has over 380,000 customers without power, according to the website PowerOutage.US. In Davidson County, Tennessee, which includes Nashville, more than 60% of customers were without power, the site says.

Duke Energy, the electric power company headquartered in Charlotte, North Carolina, on Saturday morning announced “emergency outages” as extremely cold temperature drive unusually high energy demand across the Carolinas.

“We have begun short, temporary power outages. These emergency outages are necessary to protect the energy grid against longer, more widespread outages. We appreciate your patience,” the energy provider said in a tweet.



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Odell Beckham Jr. removed from flight, causes delay at Miami airport after incident with crew, per police

Days before the official start of his in-season free agency tour, Odell Beckham Jr. has been grounded, literally. Set to travel from Miami to Los Angeles, the wide receiver was removed from an American Airlines flight on Sunday after an incident with the flight crew, according to the Miami-Dade Police Department:

At approximately 9:30 a.m., officers from the Miami-Dade Police Department were dispatched to a medical emergency at an American Airlines flight. The flight crew was concerned for a passenger (Mr. Odell Beckham), as they tried to wake him to fasten his seat belt, he appeared to be coming in and out of consciousness, prior to their departure. Fearing that Mr. Beckham was seriously ill, and that his condition would worsen through the expected 5 hour flight, the attendants called for police and fire rescue. Upon the officers arrival, the flight crew asked Mr. Beckham several times to exit the aircraft, which he refused. The aircraft was deplaned, at which time Mr. Beckham was asked by the officers to exit the plane, and did so without incident. Mr. Beckham was escorted to the non-secure area of the terminal by the officers where he made other arrangements. 

Officers were initially dispatched to the airport for a “medical emergency,” with Beckham allegedly appearing to “come in and out of consciousness” while seated on the plane before the scheduled takeoff. Eventually, the aircraft was deplaned, and Beckham was escorted off — and through the airport — without incident.

The American Airlines crew was “concerned for … Beckham as they tried to wake him to fasten his seat belt,” the police said. “Fearing that Mr. Beckham was seriously ill, and that his condition would worsen through the expected five-hour flight, the attendants called for police and fire rescue.” Upon arrival, the officers allegedly asked Beckham several times to exit the plane, and the wide receiver refused. After all the other passengers were deplaned, however, Beckham agreed to exit and was seen walking with a police escort out of the gate area and into the terminal, “where he made other arrangements.”

Beckham was not officially cited or detained as part of the incident. Several people alleging to be on his flight, however, complained on social media about his behavior causing a delay. American Airlines released the following statement: “Flight 1228, with service from Miami to Los Angeles, returned to the gate before takeoff due to a customer failing to follow crew member instructions and refusing to fasten their seatbelt. The customer was removed and the flight re-departed at 10:54 a.m. local time,” roughly an hour and a half after its scheduled takeoff.

Beckham has only indirectly addressed the events via Twitter, tweeting Sunday: “Never in my life have I experienced what just happened to me … I’ve seen it all.” His attorney, Daniel Davillier, has since downplayed Beckham’s role in the incident:

Earlier today, Odell Beckham Jr. boarded a morning flight in Miami without any problems. The flight was delayed after boarding and prior to takeoff. Mr. Beckham fell asleep with his blanket over his head, which is his normal practice for long flights. He was awaken [sic] and told that the plane was back at the gate and that he needed to get off the plane because he did not put his seatbelt on when asked. He responded that he was asleep, and that he would put his seatbelt on at that time. He was informed that it was too late, and that either he would have to get off the plane or everyone would have to deplane.

The overzealous flight attendant insisted on removing everyone from the plane instead of simply allowing Mr. Beckham to fasten his seatbelt and proceed with the flight. At no time was Mr. Beckham disruptive or combative. He was willing to comply with the seatbelt requirement, but the flight attendant wanted to prove that he had the authority to have Mr. Beckham removed from the flight. The airline proceeded to send Mr. Beckham’s luggage to Los Angeles without him.

That incident was unnecessary. Sleeping on a plane should not be a cause for removal from a flight.

The off-field controversy comes just days ahead of his scheduled visit with the Cowboys, who have been publicly courting his services as he plans a return to the field. The former Rams standout, who’s yet to play in 2022 due to a torn ACL suffered in February, is also scheduled to visit the Giants and Bills in the near future.

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FDA approves first treatment to delay onset of type 1 diabetes



CNN
 — 

A biologic therapy that delays the onset of type 1 diabetes received approval from the US Food and Drug Administration on Thursday.

It is the first therapy approved for prevention of type 1 diabetes.

The monoclonal antibody teplizumab, which will be marketed under the brand name Tzield, from ProventionBio and Sanofi is given through intravenous infusion.

It is thought to work by turning down the body’s misdirected attack on its own insulin-producing cells. The idea is that protecting these cells buys people more time before they become dependent on insulin to manage their condition.

In clinical trials, Tzield delayed progression to full-blown diabetes by a little over two years. But the benefits have lasted much longer in some of the study participants.

One of them, Mikayla Olsten, was screened for diabetes after her 9-year old sister, Mia, suddenly developed a life-threatening episode of diabetic ketoacidosis and was diagnosed with diabetes. There was no history of diabetes in the family, and Mikayla wasn’t sick, but she had four of the five types of autoantibodies that doctors look for to assess a person’s risk.

“They told us when somebody has that many markers, it’s not if they’re going to develop diabetes, it’s when,” said her mom, Tracy.

Mikayla was 15 when she joined the study and received teplizumab. She’s now 21 and a senior in college. She gets an annual battery of tests to check her pancreas and blood markers, and Tracy Olsten says her condition hasn’t progressed in six years.

According to a scientific statement from the Juvenile Diabetes Research Foundation, the Endocrine Society and the American Diabetes Association, when a person has markers for autoimmune disease and episodes of uncontrolled blood sugar, the five-year risk for progression to insulin-dependent symptomatic disease is 75%. The lifetime risk of developing insulin-dependent diabetes is nearly 100%.

So far, Mikayla seems to be beating those odds.

Tracy said that for Mia, who is dependent on insulin, managing her diabetes is a constant chore.

“She has a tremendous amount of juggling that her peers don’t have to do. She has to plan ahead when she has a basketball game or practice on making sure she carbs up and decreases her insulin levels,” Tracy said. “She cannot go a minute or a day without thinking about it nonstop, and to be able to give Mikayla the opportunity where she doesn’t have to think about it 24/7 is amazing.”

Aaron Kowalski, CEO of the Juvenile Diabetes Research Foundation, says the main challenge in prescribing Tzield will be finding people who need it. The drug is approved for people who don’t have any symptoms of the disease and may not know they’re on the road to getting it.

“Screening becomes a really big issue, because what we know is, about 85% of type 1 diagnoses today are in families that don’t have a known family history,” Kowalski said. “Our goal is to do general population screening” with blood tests to look for markers of the disease.

Tzield is approved for use in people 8 and older who are in stage 2 of their type 1 diabetes. In that stage, doctors can measure antibodies that attack insulin-producing beta cells in the person’s blood, and they have abnormal blood sugar levels, but their body can still make insulin.

“The way in which not just industry but our medical system go about managing autoimmune diseases, and especial type 1 diabetes, is really suboptimal in today’s day and age,” ProventionBio co-founder and CEO Ashleigh Palmer said. “What we do is, we wait until the symptoms of the disease present to doctors, and then doctors treat the patient’s symptoms chronically for a lifetime. The trouble is that in type 1 diabetes, when the symptoms first present, it’s too late.”

The treatment comes in a single 14-day course of infusions that each last 30 to 60 minutes.

The most common side effects reported in the trial participants were low white blood cells and lymph cells, rash and headache.

With type 1 diabetes, a person’s immune system attacks cells called beta cells in the pancreas that produce insulin, a hormone that helps blood sugar enter cells, where it’s used for energy. The attack can happen for years before any symptoms of diabetes appear. Without insulin, blood sugar can build up in the bloodstream and break down the body’s own fat and muscle.

Palmer says Tzield holds off the disease before symptoms appear by stopping the autoimmune disease process and the underlying destruction of beta cells. The treatment essentially reboots the immune system, preserving beta cell function.

“We really have no preventative measure for type 1 diabetes to date, and that is despite [the National Institutes of Health] funding hundreds of millions of dollars over the last 20-plus years of a program called TrialNet that has tested many, many different things, including this, and some of this came out of that work,” said Dr. Robert Gabbay, chief scientific and medical officer for the American Diabetes Association. “Finally, there is something that delays the onset of type 1 diabetes, and it’s so exciting.”

Unlike type 2 diabetes, which can be prevented with lifestyle changes like losing weight and exercising, type 1 is a genetic disease that has not had any prevention options until now.

“For some reason, we don’t screen for type 1 diabetes, even though there are biomarkers available to show that the autoimmune disease process is already underway,” Palmer said. He added that the hopes the drug will catalyze the medical system to start population-based screening during routine childhood well visits in order to intercept the disease and delay its onset.

With Tzield, doctors would screen individual family members of people with type 1 diabetes to see whether they have those specific antibodies. If antibody levels are high and it appears that the person is about to develop diabetes, the treatment will delay that process.

“If somebody has type 1, a common question that comes up is ‘well, what about my child? Are they going to develop type 1?’ It’s only about a 5% risk, so more often than not, they won’t, but if you could find the ones that would and treat them, that can make a big difference,” Gabbay said.

A delayed diagnosis of type 1 diabetes could have a significant impact.

“Obviously, the quality of life is substantially impacted, negatively impacted, if you are diagnosed with type 1 diabetes. It’s a disease that never goes away,” Palmer said.

People who are type 1 diabetics must monitor their blood glucose levels around the clock, affecting how they exercise and eat. High blood sugar can lead to diabetic ketoacidosis, in which the body starts to break down fat as its fuel, and can cause a buildup of acids called ketones in the bloodstream. That condition can lead to hospitalization, coma or death.

As of 2019, about 1.9 million people have type 1 diabetes in the United States, according to the American Diabetes Association, including 244,000 children and adolescents. Type 1 affects 8% of everyone with diabetes.

“The incidence of the type 1 is mainly in kids and teenagers, and when you are in the turmoil of adolescence, when you just want to forget that you have it,” said Olivier Bogillot, Sanofi’s head of US general medicines. “So when you have the ability with a treatment to just delay the onset of the disease, you can change the way the quality of life is impacted for families and for those kids.”

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