- More defects found in Green Line tracks, so trolleys will keep running as slow as, well, you know Universal Hub
- MBTA lifts some speed restrictions for trolleys and trains WCVB Channel 5 Boston
- MBTA Lifts Last Full Trolley Line Speed Restriction, But Delays Remain NBC10 Boston
- MBTA lifts global speed restrictions on Green Line as repairs continue on some tracks Boston News, Weather, Sports | WHDH 7News
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Tag Archives: defects
Why a Widely Used Drug Causes Birth Defects and Autism
Researchers discovered how valproic acid, a medication commonly used to treat epilepsy, migraines, and bipolar disorder, causes birth defects when taken during pregnancy.
Researchers determined that valproic acid prevents nervous system cells from properly developing and dividing
When used during pregnancy, the drug valproic
Three mouse embryos, representative of the study that describes how the teratogenic drug Valproic acid can cause neurodevelopmental birth defects in mice, including microcephaly and exencephaly. The embryo on the left is a normal embryo, with no exposure to Valproic acid. The embryo in the middle is smaller and has microcephaly, while the embryo on the right exhibits exencephaly. The middle embryo and the one on the right were both exposed to Valproic acid. Credit: Muriel Rhinn (CC-BY 4.0)
Keyes and colleagues examined embryonic exposure to VPA in the new study by using both human organoids—three-dimensional collections of human cells generated in the lab—and mice. They found that neuroepithelial cells, which are the stem cells that give rise to the central nervous system, undergo cellular senescence as a result of VPA. The researchers also identified p19Arf as the specific molecule that caused this VPA-induced senescence. Although VPA exposure during pregnancy still resulted in other abnormalities, the scientists found that it no longer produced microcephaly (a small head size) or alterations to gene expression patterns linked to autism spectrum disorder in mice missing the p19Arf gene.
The work is one of the first to associate cellular senescence with developmental defects, the authors say. “Overall, the discovery that atypical activation of senescence in the embryo can perturb development raises the intriguing possibility that it may also contribute to defects in developmental contexts beyond those we studied here.”
Muriel Rhinn, the first author of the study, adds, “While cellular senescence has long been associated with aging and age-related disease, we now show that aberrant induction of senescence can also contribute to developmental defects. As valproic acid is strongly linked to cognitive defects and Autism Spectrum Disorder, this study now introduces an exciting link with senescence, supporting how additional studies are needed.”
This study was funded by grants from La Fondation pour la Recherche Medicale (FRM) (AJE20160635985), Fondation ARC pour la Recherche sur le Cancer (PJA20181208104), IDEX Attractivité – University of Strasbourg (IDEX2017), La Fondation Schlumberger pour l’Education et la Recherche FSER 19 (Year 2018)/FRM, Agence Nationale de la Recherche (ANR) (ANR-19-CE13-0023-03) and Ligue Contre le Cancer (all to W.M.K.). I.Z.B. was supported by a 4th-year fellowship from the Fondation ARC pour la Recherche sur le Cancer and a Ph.D. fellowship from INSERM and Conseil Regional Grand-Est. A.K. was supported by a fellowship from Eur IMCBiO. The work was also supported by an institutional grant to the IGBMC, ANR-10-LABX-0030-INRT, a French State fund managed by the Agence Nationale de la Recherche under the frame program Investissements d’Avenir ANR-10-IDEX-0002-02. Sequencing was performed by the GenomEast platform, a member of the “France Génomique” consortium (ANR-10-INBS-0009). The funders had no role in the study’s design, data collection, and analysis, decision to publish, or preparation of the manuscript.
Reference: “Aberrant induction of p19Arf-mediated cellular senescence contributes to neurodevelopmental defects” by Muriel Rhinn, Irene Zapata-Bodalo, Annabelle Klein, Jean-Luc Plassat, Tania Knauer-Meyer and William M. Keyes, 14 June 2022, PLoS Biology.
DOI: 10.1371/journal.pbio.3001664
Diabetes drug metformin linked to birth defects in baby boys, study finds
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A popular diabetes drug could be linked to major birth defects, according to researchers.
In a study from Stanford University, the University of Southern Denmark and Copenhagen University, published Tuesday in the Annals of Internal Medicine, the authors wrote that the offspring of male patients who were taking metformin three months before conception were impacted.
Sons born to those men were more than three times as likely to have a genital birth defect as unexposed babies, with metformin associated with a 1.4 times greater risk of birth defects in boys whose fathers were taking it versus those who were not.
MORE THAN HALF OF US ABORTIONS DONE WITH PILLS, NOT SURGERY
The mothers in both groups had no history of diabetes or hypertension.
In addition, the fathers who used metformin during sperm development were less likely to have boys than girls compared with the general population.
Stanford said in a Monday release that its conclusions suggest that metformin affects men’s reproductive health in a way that can harm their sons, “though the mechanisms are still unclear.”
To reach these results, the group used health-registry data from Denmark that tracked more than 1 million births from 1997 to 2016.
The offspring were considered to be exposed if their father filled one or more prescriptions for a diabetes drug during the development of fertilizing sperm, and sex and frequencies of major birth defects were compared across drugs, times of exposure and siblings.
Of the more than 1.1 million babies included in the study, 3.3% had at least one major birth defect and 51.4% were boys.
Among the 1,451 babies exposed to metformin, 49.4% were male and the rate of birth defects was 5.2%.
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Stanford explained that the rates mean metformin use may account for two additional babies born with birth defects every year.
The college noted that the oral treatment is increasingly popular for Type 2 diabetes, but is known to have effects on the reproductive system.
The researchers also compared exposure to metformin with exposure to two other common diabetes drugs, insulin and sulfonylureas.
Exposure to insulin did not affect the rate of birth defects or sex ratio; exposure to sulfonylureas showed numbers trending in the same direction as metformin exposure, but they lacked a consistent pattern.
Lastly, men who filled metformin prescriptions before or after the three-month period of sperm development did not have offspring with a higher incidence of birth defects and unexposed siblings did not have increased rates of birth defects.
Limitations to the study include that information on underlying disease status was limited, as well as whether fathers took the drug as prescribed.
The authors called for further research that clarifies the causation of these defects.
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“I think that it’s a single study, so it’s hard to change clinical practice based on that,” Dr. Michael Eisenberg, senior author and professor of urology at Stanford, said. “But, for somebody considering fatherhood, this study emphasizes the importance of a father’s health on the health of a child.”
Ultimately, he said it will be important to uncover the biological mechanisms at work and to expand the study.
Data from Statista shows that 86 million prescriptions for metformin were written in the U.S. by 2019.
Major Birth Defects Linked With Fathers’ Use of Diabetes Drug Metformin
A large cohort study found that babies born to men who took metformin during the period of sperm development were at increased risk for birth defects, specifically genital defects in boys. These finding suggest that men with diabetes who are taking metformin should talk to their doctors about whether they should switch to another treatment when trying to conceive a child. However, because diabetes control also affects sperm quality, discontinuing metformin treatment could also affect birth outcomes. The findings are published in Annals of Internal Medicine.
Diabetes increasingly occurs in people of reproductive age, compromises sperm quality, and is associated with impaired male fertility. Some diabetes drugs may also affect male reproductive health.
Researchers from the University of Southern Denmark and Stanford University studied data from nation-wide national registries of births, patients, and prescriptions to evaluate whether the risk for birth defects varied among offspring born to men treated with insulin, metformin, or sulfonylureas prior to conception. Babies were considered exposed to a diabetes drug if their father filled at least 1 prescription during the 3 months when the fertilizing sperm were developing.
The researchers compared birth defects in the babies across diabetes drugs, different times of taking the drug relative to development of fertilizing sperm, and with unexposed siblings of the babies. Babies whose fathers took insulin had no increased risk for a birth defect compared with the general group.
Babies whose fathers took metformin had an increased risk for birth defects. There were too few babies whose fathers took sulfonylureas to determine risks for birth defects with any certainty. Taking metformin before or after sperm development did not increase the risk for birth defects. Unexposed siblings were also not at increased risk.
According to the authors, the size of the diabetes pandemic suggests that treatment of prospective fathers with diabetes, including pharmacologic management and counseling on diet, physical exercise, and weight loss, should be subject to further study.
An editorial from Germaine M. Buck Louis, PhD, MS at George Mason University emphasizes the importance of corroborating the findings, given the prevalence of metformin use as first-line therapy for type 2 diabetes. The author also calls for guidance from clinicians to help couples planning pregnancy weigh the risks and benefits of paternal metformin use relative to other medications.
References:
“Preconception Antidiabetic Drugs in Men and Birth Defects in Offspring: A Nationwide Cohort Study” by Maarten J. Wensink, MD, PhD, Ying Lu, PhD, Lu Tian, PhD, Gary M. Shaw, DrPH, Silvia Rizzi, PhD, Tina Kold Jensen, PhD, Elisabeth R. Mathiesen, MD, Niels E. Skakkebæk, MD, DMSc, Rune Lindahl-Jacobsen, PhD and Michael L. Eisenberg, MD, 29 March 2022, Annals of Internal Medicine.
DOI: 10.7326/M21-4389
“Paternal Preconception Diabetes Drugs and Birth Defects in Offspring: A Call for More Conclusive Study” by Germaine M. Buck Louis, PhD, MS, 29 March 2022, Annals of Internal Medicine.
DOI: 10.7326/M22-0770
Men’s use of diabetes drug just before conception is linked to a 40% increase in birth defects, study finds
Metformin is a first-line drug in the treatment of type 2 diabetes.
The research, which was done out of Denmark, used national registries to follow over 1 million births between 1997 and 2016 and compared the risk of major birth defects in babies based on paternal exposures to diabetes medications. The study observed only children who were born to women under 35 and men under 40. Babies born to women with diabetes were excluded.
The researchers considered men exposed to metformin if they filled a prescription for it in the three months before conception, which is how long it takes the fertilizing sperm to fully mature.
According to the study, the frequency of birth defects in babies born to men who had a type 2 diabetes diagnosis but who were not taking metformin was 3.1% (1,594 children), but the frequency was 4.6% (788) in children with paternal exposure to metformin during the preconception period.
Genital birth defects, seen only in male babies, was the only birth defect in the study that was found to be associated with a statistically significant increased risk after paternal metformin use.
Men who took metformin before or after the three-month maturation period did not have an increased risk of having a baby with birth defects. Similarly, the babies’ unexposed siblings were not affected.
Because previous research has shown that diabetes can compromise sperm quality and impair male fertility, the researchers also compared the rates of birth defects in the babies of men who took insulin to those who took metformin in order to ensure that a diabetes diagnosis itself was not a contributing factor. They found that insulin use was not associated with a change in the birth defect rate.
The researchers did not find any significant association between birth defects and paternal exposure to diabetes medication other than metformin.
However, the authors note that they did not have data on other aspects of diabetes, such as glycemic control or medication compliance, as they assessed data only on when prescriptions were filled. In addition, babies who had paternal metformin exposure also tended to have parents who were older and of a lower socioeconomic status, which may play a role.
In an editorial published alongside the study, Germain Buck Louis, a reproductive and perinatal epidemiologist at George Mason University who was not involved in the research, said there is evidence from past studies to suggest that “altered testosterone levels may be an underlying mechanism raising concern about the antiandrogenic activity of oral diabetes pharmacologic agents, including metformin” to explain these findings.
Louis also noted that due to the limitations of this study, further research is needed to find out whether men taking metformin should make any considerations, especially given the high prevalence of diabetes that may require metformin use.
There are currently no US Food and Drug Administration warnings against the use of metformin by men planning to have children.
“Clinical guidance is needed to help couples planning pregnancy weigh the risks and benefits of paternal metformin use relative to other medications,” Louis wrote.
Rare genital defects seen in sons of men taking major diabetes drug | Science
Metformin, a first-line diabetes drug used for decades, may boost the risk of birth defects in the offspring of men who took it during sperm development, according to a large Danish study. Sons born to those men were more than three times as likely to have a genital birth defect as unexposed babies, according to the paper, published in the Annals of Internal Medicine today.
The genital defects, such as hypospadias, when the urethra does not exit from the tip of the penis, were relatively rare, occurring in 0.9% of all babies whose biological fathers took metformin in the 3 months before conception. But epidemiologists say the findings are important because tens of millions of people worldwide take metformin, chiefly for type 2 diabetes.
“When I saw the paper … I thought: ‘Yup, this is gonna go viral,’” says Germaine Buck Louis, a reproductive epidemiologist at George Mason University who wrote an editorial accompanying the report. “[Metformin] is widely used even by young men because of the obesity issue that we have. So that is potentially a huge source of exposure for the next generation.”
However, Buck Louis and every other scientist interviewed for this article stressed that the paper’s findings are preliminary and observational and need to be corroborated; they add that factors besides metformin may have influenced the findings. The scientists cautioned men with diabetes against abruptly stopping metformin before trying to conceive.
“Metformin is a safe drug, it’s cheap, and it does what it needs to do” by controlling blood sugar levels, says the paper’s first author, Maarten Wensink, an epidemiologist and biostatistician at the University of Southern Denmark. Any change in medication “is a complex decision that [a couple] should take together with their physicians,” he says.
Use of metformin, a synthetic compound that lowers blood sugar by boosting insulin sensitivity, has skyrocketed with the obesity epidemic and attendant diagnoses of type 2 diabetes. In the United States in 2004, 41 million prescriptions for the drug were written; by 2019 that number was 86 million.
The drug has been in use since the 1950s, but this is the first large study to rigorously analyze any paternally mediated impact on human birth defects. Although metformin’s use skews toward older people, the rise in diabetes means more men in their reproductive years are taking the drug. In the United States, prescriptions to 18- to 49-year-olds with type 2 diabetes grew from fewer than 2200 in 2000 to 768,000 in 2015.
The researchers analyzed records from more than 1.1 million babies born in Denmark between 1997 and 2016, using the country’s comprehensive medical registries to connect data on births, paternal metformin prescriptions, and birth defects. In the 1451 offspring of men who filled metformin prescriptions during the 90 days before conception, the period when sperm are being made, the team found a 5.2% rate of birth defects, compared with 3.3% among unexposed babies. That translated to 1.4 times higher odds of at least one major birth defect, including genital, digestive, urinary, and heart defects, after adjustments for paternal age and other factors.
For genital defects alone, the increased risk—only seen in male infants—was much larger. Among exposed babies, 0.9% had genital defects, compared with 0.24% in unexposed babies.
The numbers were small—13 metformin-exposed boys were born with genital defects. But after the researchers adjusted for factors including parental ages and maternal smoking status, they found a 3.39-fold rise in the odds of a genital defect. “The rate per se was surprisingly high,” Wensink says.
Reassuringly, the researchers saw no effect in offspring of men who took the drug earlier in life or in the year before or after the 90-day window of sperm production. “It really has to do with taking it in that window when the sperm … is being developed,” says senior author Michael Eisenberg, a urologist at Stanford Medicine.
The team also found no additional risk in unexposed siblings of metformin-exposed babies, or in infants of diabetic fathers who took insulin or were not on metformin. All those findings suggest it’s the drug’s impact on sperm formation, rather than diabetes or another factor intrinsic to the men, that’s responsible.
But the researchers acknowledge that men with diabetes who took metformin and those who didn’t may have differed in attributes such as obesity or how well their disease was controlled—data that were not accessible to the researchers.
Nor are scientists sure exactly how the drug may be impacting sperm. Studies in fish and mice suggest metformin can disrupt the development of male reproductive organs, and one small study found metformin reduced serum testosterone levels in men.
The caveats make scientists cautious about drawing conclusions from the paper. “This paper is the first word, not the last word,” says Russell Kirby, a birth defects epidemiologist at the University of South Florida. “It’s definitely going to require additional research.”
Exclusive: SEC probes Tesla over whistleblower claims on solar panel defects
SAN FRANCISCO, Dec 6 (Reuters) – The U.S. securities regulator has opened an investigation into Tesla Inc (TSLA.O) over a whistleblower complaint that the company failed to properly notify its shareholders and the public of fire risks associated with solar panel system defects over several years, according to a letter from the agency.
The probe raises regulatory pressure on the world’s most valuable automaker, which already faces a federal safety probe into accidents involving its driver assistant systems. Concerns about fires from Tesla solar systems have been published previously, but this is the first report of investigation by the securities regulator.
The U.S. Securities and Exchange Commission disclosed the Tesla probe in response to a Freedom of Information Act request by Steven Henkes, a former Tesla field quality manager, who filed a whistleblower complaint on the solar systems in 2019 and asked the agency for information about the report.
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“We have confirmed with Division of Enforcement staff that the investigation from which you seek records is still active and ongoing,” the SEC said in a Sept. 24 response to Henkes, declining his request to provide its records. The SEC official said the letter should not be taken as an indication by the agency that violations of law had occurred. Reuters independently confirmed the SEC letter was legitimate.
Henkes, a former Toyota Motor quality division manager, was fired from Tesla in August 2020 and he sued Tesla claiming the dismissal was in retaliation for raising safety concerns. Tesla did not respond to Reuters’ emailed questions, while the SEC declined to comment.
In the SEC complaint, Henkes said Tesla and SolarCity, which it acquired in 2016, did not disclose its “liability and exposure to property damage, risk of injury of users, fire etc to shareholders” prior and after the acquisition.
Tesla also failed to notify its customers that defective electrical connectors could lead to fires, according to the complaint.
Tesla told consumers that it needed to conduct maintenance on the solar panel system to avoid a failure that could shut down the system. It did not warn of fire risks, offer temporary shutdown to mitigate risk, or report the problems to regulators, Henkes said.
Tesla shares fell 5.5% at $960.25 on Monday after the Reuters report.
EX-TOYOTA QUALITY MANAGER BLOWS THE WHISTLE
More than 60,000 residential customers in the U.S. and 500 government and commercial accounts were affected by the issue, according to his lawsuit filed in November last year against Tesla Energy over wrongful termination.
It is not clear how many of those remain after Tesla’s remediation program.
Henkes, a longtime manager at Toyota’s North American quality division, moved to SolarCity as a quality engineer in 2016, months before Tesla acquired SolarCity. After the acquisition, his duties changed and he became aware of the widespread problem, he told Reuters.
Henkes, in the SEC complaint, said he told Tesla management that Tesla needs to shut down the fire-prone solar systems, report to safety regulators and notify consumers. When his calls were ignored, he proceeded to file complaints with regulators.
“The top lawyer cautioned any communication of this issue to the public as a detriment to the Tesla reputation. For me this is criminal,” he said in the SEC complaint.
Litigation and concerns over faulty connectors and Tesla solar system issues stretch back several years. Walmart in a 2019 lawsuit against Tesla said the latter’s roof solar system led to seven store fires. Tesla denied the allegations and the two settled.
Business Insider reported Tesla’s program to replace defective solar panel parts in 2019.
Several residential customers or their insurers have sued Tesla and parts supplier Amphenol (APH.N) over fires related to their solar systems, according to documents provided by legal transparency group PlainSite.
Henkes also filed a complaint with he U.S. Consumer Product Safety Commission, which CNBC reported this year was investigating the case. CPSC and Amphenol didn’t respond to request for comment.
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Reporting by Hyunjoo Jin; Additional reporting by Chris Prentice in Washington and Shreyashi Sanyal in Bangalore; Editing by Peter Henderson and Nick Zieminski
Our Standards: The Thomson Reuters Trust Principles.
Vascular defects appear to underlie the progression of Parkinson’s disease
In an unexpected discovery, Georgetown University Medical Center researchers have identified what appears to be a significant vascular defect in patients with moderately severe Parkinson’s disease. The finding could help explain an earlier outcome of the same study, in which the drug nilotinib was able to halt motor and non-motor (cognition and quality of life) decline in the long term.
The researchers say their finding, detailed in a study published November 12, 2021, in Neurology Genetics, suggests that blood vessel walls called the blood brain barrier, which normally act as a crucial filter to protect the brain against toxins as well as allow passage of nutrients to nourish it, doesn’t work correctly in some Parkinson’s patients: It prohibits toxins from leaving the brain and inhibits nutrients such as glucose from entering. Perhaps even more damaging, the dysfunctional barrier allows inflammatory cells and molecules from the body to enter and damage the brain.
The research, the first longitudinal study to use such advanced genomics, now provides investigators with a new target for therapeutic intervention in Parkinson’s disease, says the study’s senior author, Charbel Moussa, MBBS, Ph.D., director of the Medical Center’s Translational Neurotherapeutics Program.
The new discovery comes from the second part of a Phase II clinical trial that featured next generation whole genome sequencing of the cerebrospinal fluid of 75 Parkinson’s patients, before and after treatment with a repurposed leukemia drug, nilotinib, or a placebo.
This study lasted 27 months; the initial trial was double-blinded and patients were randomized to either placebo, or 150mgs or 300mgs nilotinib for 12 months. The patients had severe Parkinson’s disease; all treated with optimal standard of care and many (30%) had also used the most sophisticated treatments possible, such as deep brain stimulation. The second part of the study employed an adaptive design and all participants had a 3-month drug washout period before re-randomization to either 150mgs or 300mgs for an additional 12 months. After 27 months, nilotinib was found to be safe, and patients who received nilotinib showed a dose-dependent increase of dopamine, the chemical lost as a result of neuronal destruction.
“It appeared nilotinib halted motor and non-motor decline in the patients taking the 300mgs higher dose,” says Moussa. The clinical outcomes of this study were published in Movement Disorders in March 2021.
The current part of the study, just published, examined the cerebrospinal fluid of patients via epigenomics, which is a systematic analysis of the global state of gene expression, in correlation with continuing clinical outcomes. The new analysis helps explain the clinical findings.
Nilotinib inactivated a protein (DDR1) that was destroying the ability of the blood brain barrier to function properly. When DDR1 was inhibited, normal transport of molecules in and out of the brain filter resumed, and inflammation declined to the point that dopamine, the neurotransmitter depleted by the disease process, was being produced again.
Moussa and his team have long been working on the effects that nilotinib (Tasigna) may have on neurodegeneration, including Alzheimer’s and Parkinson’s diseases. The drug was approved in 2007 for chronic myelogenous leukemia (CML), but Moussa reasoned that its mechanism of action may help the brain destroy toxins that develop in the brains of patients with neurodegenerative disorders.
“Not only does nilotinib flip on the brain’s garbage disposal system to eliminate bad toxic proteins, but it appears to also repair the blood brain barrier to allow this toxic waste to leave the brain and to allow nutrients in,” Moussa explains. “Parkinson’s disease is generally believed to involve mitochondrial or energy deficits that can be caused by environmental toxins or by toxic protein accumulation; it has never been identified as a vascular disease.”
“To our knowledge, this is the first study to show that the body’s blood brain barrier potentially offers a target for the treatment for Parkinson’s disease,” Moussa says. “Much work remains to be done, but just knowing that a patient’s brain vascular system is playing a significant role in the progression of the disease is a very promising discovery.”
Researchers decode how cancer drug works in brains of Parkinson’s disease patients
More information:
CSF MicroRNAs Reveal Impairment of Angiogenesis and Autophagy in Parkinson Disease, Neurology Genetics (2021). DOI: 10.1212/NXG.0000000000000633
CSF MicroRNAs Reveal Impairment of Angiogenesis and Autophagy in Parkinson Disease, Neurology Genetics (2021). DOI: 10.1212/NXG.0000000000000633
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Justin Long, the ‘I’m a Mac’ actor, defects from Apple in new Intel ad
Nearly two decades ago, Long extolled the benefits of Mac computers while playing one opposite John Hodgman’s PC in Apple’s iconic “Get a Mac” commercials. Now, in a pointed jab at Apple (AAPL), Long is featured in a new Intel (INTC) ad where he appears much more excited about new Intel-based PCs than the latest Mac laptops.
“Hello, I’m a — Justin. Just a real person, doing a real comparison between Mac and PC,” Long says in the new Intel commercial, an obvious play on the “Hello, I’m a Mac” intro to the old Apple ads.
“These are all PCs,” Long says as he surveys a collection of laptops in the new ad. “Oh yeah, Intel! Nice. My face just unlocked that, that’s so cool. And I’ve never seen a screen like that on a laptop.”
He moves on to look at the Mac lineup: “So these are the newer Macs? Okay. So, gray and gray-er.”
The new commercial is the latest exchange of not-so-friendly fire between Intel and Apple in recent months.
Last fall, Apple went from being an Intel customer to competitor when it replaced the semiconductor giant’s x86 chips with its own M1 chips in the newest Mac lineup. Apple claimed its new chips make Macs significantly faster and quieter and give them longer battery life compared to previous Mac models and rival laptops.
In fact, reviving the theme of the old Apple ads was the iPhone maker’s idea. When it announced the new M1 Macs in November, Apple brought back Hodgman to again star as “PC guy” in a new ad.
“Hi, I’m a PC,” Hodgman says in Apple’s November ad. “Is there a time for questions? Good, because I have one. Why? Why make all these advancements? What’s the point?”
Moves like Apple’s to make its own chips pose a real threat to Intel, which has long relied on dominating the PC business. In recent years, Intel has lost share in the PC market, among other challenges, and the company recently hired new CEO Pat Gelsinger to help right the ship.
At an Intel staff meeting in January, after Gelsinger was named the incoming CEO but before officially taking over the role, he told employees that the company has to “deliver better products” for PCs than anything “a lifestyle company in Cupertino” makes, a likely reference to Apple, according to a report from The Oregonian.
The new commercial may be another indicator of how aggressive Gelsinger plans to be in countering Apple and other competitors as he attempts to return Intel to its former glory. Whether the ad convinces people to buy more PCs remains to be seen, but at least Intel now has Long’s support.