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Thousands of lawsuits over baby formula should stay where filed, court says

Thousands of lawsuits over baby formula should stay where filed, court says

Reutersa day ago

CHICAGO, June 4 (Reuters) - An Illinois appeals court said on Tuesday that thousands of lawsuits claiming baby formula made by Abbott Laboratories and a Reckitt Benckiser subsidiary causes a dangerous disease in preterm infants should stay in the court where they were filed, a venue considered plaintiff friendly.
The Appellate Court of Illinois' 5th District upheld, opens new tab a lower court's ruling rejecting Abbott and Mead Johnson's motions to transfer the lawsuits out of Madison County, Illinois. The decision allows the claims to move forward in what is often viewed as a plaintiff-friendly county court. Madison County is often flagged by tort reform groups as a jurisdiction known for outsize jury verdicts against corporate defendants.
The appellate court, however, reversed the lower court's ruling denying the companies' separate motion to transfer or dismiss the lawsuits based on their argument that the cases were filed in an inconvenient location. The appeals court sent that ruling back to the lower court for reconsideration.
A representative for Mead Johnson said in a statement that the company will continue to pursue dismissal of the cases in Madison County, many of which don't involve Mead Johnson products or injuries that occurred in the county. The representative said that plaintiffs' lawyers were trying to "coerce settlement by building a large inventory of claims, even when plaintiffs' lawyers have no intention of ever trying them,' the company said.
A spokesperson for Abbott Laboratories did not respond to a request for comment.
Tor Hoerman, one of the attorneys for the plaintiffs said in a statement that the ruling "reinforces the importance of corporate accountability and helps ensure that families impacted by these tragic injuries can seek justice in the appropriate forum."
All of the lawsuits allege that the companies failed to warn that their specialized formulas used by newborn intensive care units in hospitals could cause necrotizing enterocolitis, a disease that almost exclusively affects premature infants and has an estimated mortality rate of more than 20%.
The companies have denied the claims, saying that while breast milk protects against NEC, formula does not cause it, and that the benefits of breast milk have long been known to clinicians.
In addition to state court cases in Illinois, Missouri and Pennsylvania, a federal multidistrict litigation with more than 700 cases over the claims is moving forward in Chicago, according to court records.
The same Illinois appeals court is also considering a similar dispute over transferring more cases over the preterm formula that are currently pending in St. Clair County, Illinois, another court targeted by tort reformers for being plaintiff-friendly.
In 2024, a jury in St. Clair County ordered Mead Johnson to pay $60 million to the mother of a premature baby who died after being fed the company's Enfamil baby formula. A few months later, a St. Louis, Missouri, jury ordered Abbott to pay $495 million in damages in another case.
Both companies prevailed in the most recent trial, in October. However, the judge in that case in March ordered a new trial, finding that lawyers for the defendants had acted improperly.
The case is Jupiter v. Mead Johnson and Co LLC, Appellate Court of Illinois, Fifth District, No. 230248.
For the plaintiffs: Ashley Keller and Benjamin Whiting of Keller Postman; Tor Hoerman of TorHoerman Law; and David Cates of Cates Law Firm
For Abbott Laboratories: Linda Coberly and Stephen D'Amore of Winston & Strawn; Thomas Kilbride and Adam Vaught of Kilbride & Vaught; and W. Jason Rankin and Emilee Bramstedt of HeplerBroom
For Mead Johnson: Joel Bertocchi of Akerman; Anthony Anscombe and Darlene Alt of Steptoe & Johnson; and Donald Flack of Bartholomew, Shevlin & Flack

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The mystery rise of lung cancer in non-smokers
The mystery rise of lung cancer in non-smokers

BBC News

timean hour ago

  • BBC News

The mystery rise of lung cancer in non-smokers

The number of lung cancer cases in people who have never smoked is increasing. The disease is different from lung cancer caused by smoking, so what causes it? Martha first realised that something was wrong when her cough changed and the mucus in her airways became increasingly viscous. Her doctors put it down to a rare disorder she had that caused her lungs to become chronically inflamed. "No worry, it must be that," she was told. When she finally had an X-ray, a shadow was detected on her lung. "That set the ball rolling," Martha recalls. "First, a CT scan was done, then a bronchoscopy [a procedure that involves using a long tube to inspect the airways in a person's lungs] to take tissue samples." After the tumour was removed, about four months after she'd first reported symptoms to her GP, she received the diagnosis: Stage IIIA lung cancer. The tumour had infiltrated the surrounding lymph nodes but had not yet spread to distant organs. Martha was 59 years old. "It was a total shock," says Martha. Although she would occasionally light up a cigarette at a party, she never considered herself a smoker. Lung cancer is the most common cancer worldwide and the leading cause of cancer death. In 2022, about 2.5 million people were diagnosed with the disease and more than 1.8 million died. Although tobacco-related lung cancers still account for the majority of diagnoses worldwide, smoking rates have been declining for several decades. As the number of smokers continues to fall in many countries around the world, the proportion of lung cancer occurring in people who have never smoked is on the rise. Between 10 and 20% of lung cancer diagnoses are now made in individuals who have never smoked. "Lung cancer in never-smokers is emerging as a separate disease entity with distinct molecular characteristics that directly impact treatment decisions and outcomes," says Andreas Wicki, an oncologist at the University Hospital Zurich, Switzerland. While the average age at diagnosis is similar to that of smoking-related lung cancers, younger patients with lung cancer are more likely to have never smoked. "When we see 30- or 35-year-olds with lung cancer, they are usually never-smokers," he says. Another difference is the type of cancer being diagnosed. Until the 1950s and 1960s, the most common form of lung cancer was squamous cell carcinoma – a type which begins with the cells that line the lungs. In contrast, lung cancer in never-smokers is almost exclusively adenocarcinoma – a type which starts in mucus-producing cells – which is now the most common form of lung cancer in both smokers and never-smokers. Like other forms of lung cancer, adenocarcinoma is usually diagnosed at an advanced stage. "If there's a 1cm (0.4in) tumour hidden somewhere in your lungs, you won't notice it," says Wicki. The early symptoms, which include persistent coughing, chest pain, shortness of breath or wheezing, often only appear when the tumour is larger or has spread. In addition, the historically strong link between smoking and lung cancer may inadvertently lead non-smokers to attribute symptoms to other causes, says Wicki. "Most cases in never-smokers are therefore only diagnosed at stage 3 or 4." Lung cancer in never-smokers is also more common in women. Women who have never smoked are more than twice as likely to develop lung cancer as male never-smokers. Aside from lung anatomy and environmental exposures, at least part of the answer may lie in genetic mutations that are more common in women, especially in Asian women. One of the most prevalent is a mutation known as EGFR. Lung cancer cells in people who have never smoked usually have a number of mutations that could be causing their cancer, explains Wicki – so-called driver mutations. These genetic changes drive tumour growth, such as the EGFR gene which codes for a protein on the surface of cells and is called epidermal growth factor receptor. The reasons why these driver mutations are more frequently found in female patients, particularly those of Asian descent, are not entirely understood. There is some evidence that female hormones may play a role, with certain genetic variants that affect oestrogen metabolism being more prevalent in East Asians. This could potentially explain the higher incidence of EGFR-mutant lung cancer in Asian women, although the data is very preliminary. Following the discovery of mutations which can lead to lung cancer in non-smokers, the pharmaceutical industry began to develop drugs that specifically block the activity of those proteins. For example, the first EGFR inhibitors became available around 20 years ago and most patients showed an impressive response. However, treatment often led to resistant cancer cells, resulting in tumour relapse. In recent years, much effort has been put into overcoming this problem, with newer types of drugs now entering the market. As a result, the prognosis for patients has steadily improved. "The median survival rate of patients who carry such driver mutations is now several years," Wicki explains. "We have patients who have been on targeted therapy for more than 10 years. This is a huge step forward when you consider that the median survival rate was less than 12 months about 20 years ago." As the proportion of lung cancer in never-smokers increases, experts say it is crucial to develop prevention strategies for this population. A number of risk factors have been implicated. For example, studies have revealed that radon and second-hand smoke can elevate the risk of lung cancer in non-smokers. Additionally, exposure to cooking fumes or to stoves burning wood or coal in poorly ventilated rooms may also increase this risk. Since women traditionally spend more time indoors, they are particularly vulnerable to this type of indoor air pollution. However, outdoor air pollution is an even more significant factor in the development of lung cancer. In fact, outdoor air pollution is the second leading cause of all lung cancer cases after smoking. Studies have revealed that people who live in highly polluted areas are more likely to die of lung cancer than those who do not. Particulate matter less than 2.5 microns in diameter (about a 30th of the width of a human hair), typically found in vehicle exhaust and fossil fuel smoke, seems to play an important role. And intriguingly, research has shown a strong link between high levels of PM2.5 and lung cancer in individuals who have never smoked and who carry an EGFR mutation. How air pollution may trigger lung cancer in never-smokers carrying the EGFR mutation has been the focus of research at the Francis Crick Institute in London. "When we think about environmental carcinogens, we usually think about them as causing mutations in the DNA", says William Hill, a post-doctoral researcher in the cancer evolution and genome instability laboratory of the Francis Crick Institute. Cigarette smoke, for example, damages our DNA, thus leading to lung cancer. "However, our [2023] study proposes that PM2.5 doesn't directly mutate DNA, rather it wakes up dormant mutant cells sitting in our lungs and starts them on the early stages of lung cancer." In their experiments, the researchers showed that air pollutants are taken up by immune cells called macrophages. These cells normally protect the lung by ingesting infectious organisms. In response to PM2.5 exposure, macrophages release chemical messengers known as cytokines, which wake up cells carrying the EGFR mutation and causes them to proliferate. "Both air pollution and EGFR mutations are needed for tumours to grow," says Hill. Understanding how PM2.5 acts on the microenvironment of cells carrying EGFR mutations to promote tumour growth, he adds, could pave the way for new approaches to preventing lung cancer. The association between air pollution and lung cancer is not new. In a landmark paper establishing the link between smoking and lung cancer in 1950, the authors suggested outdoor pollutants from the burning of fossil fuels as a possible cause. But policies to date have focused almost exclusively on tobacco control. But 75 years later, air pollution is finally coming into focus. Air pollution levels in Europe and the US have fallen in recent decades. But the effect of changes on lung cancer rates has not yet become apparent. "It probably takes 15 to 20 years for changes in exposure to be reflected in lung cancer rates, but we don't know for sure," says Christine Berg, a retired oncologist from the National Cancer Institute in Maryland, US. Moreover, the picture is not static: climate change is likely to have an impact in the future. "With the increasing risk of wildfires, air pollution and PM2.5 levels are rising again in certain regions of the US," says Berg. "At least one study has shown an association between wildfire exposure and increased incidence of lung cancer. Transitioning away from coal, oil and gas is therefore crucial not only to slow global warming but also to improve air quality." In 2021, the WHO halved the annual mean air quality guideline for PM2.5, meaning it has adopted a more stringent approach to particulate matter. "But 99% of the world population lives in areas where air pollution levels exceed [these updated] WHO guideline limits," says Ganfeng Luo, a postdoctoral researcher at the International Agency for Research on Cancer (IARC) in Lyon, France. In a recent study, IARC researchers estimated that approximately 194,000 cases of lung adenocarcinoma worldwide were attributable to PM2.5 in 2022. "The highest burden is estimated in East Asia, especially in China," says Luo. In the future, the number of lung cancer deaths attributable to air pollution could increase in countries such as India, which currently has some of the highest levels of air pollution, according to the WHO. In Delhi, the average PM2.5 levels are above 100 micrograms per sq m, which is 20 times above the WHO air quality guidelines. In the UK, 1,100 people developed adenocarcinoma of the lung as a result of air pollution in 2022, the IARC study found. 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Mobility expert says you should swap stretching for this exercise to ease tight hips
Mobility expert says you should swap stretching for this exercise to ease tight hips

The Independent

timean hour ago

  • The Independent

Mobility expert says you should swap stretching for this exercise to ease tight hips

As a coach and fitness writer, having tight hips is one of the most common complaints I hear about. People usually default to stretching to sort this out, but a specialist says there are more effective ways to address the problem. Movement mechanics expert and Training Stimulus founder Ash Grossmann says regular movement and developing stability around the joint are likely to yield better long-term results for those seeking to banish tightness. 'In terms of broad, generalised advice, we want to establish what is causing the tightness,' Grossmann says. 'There are indirect reasons why a muscle could be becoming tight – the clue is if you stretch it and the tightness keeps coming back, stretching isn't solving the tightness. 'In a lot of situations, stretching can actually make it feel worse because you get into a wrestling match with your nervous system. Your nervous system generally has your best interests at heart with the tools it has available, so it thinks it's doing you a favour by tightening the muscle. Yanking on that tight muscle [via stretching] can be hurting your bigger picture goal rather than the small muscle tightness you're dealing with.' Below, Grossmann explains the possible causes of muscle tightness, and an accessible protocol for combatting this around the hips. Possible causes of muscle tightness Protection 'The first role of the nervous system, when it comes to movement, is survival and protection,' Grossman says. Muscle tightness might be your nervous system's way of preventing you from accessing a position it perceives as dangerous. For example, you might not be able to complete a full squat because your body 'doesn't feel strong, stable or in control' in the bottom position. Habit If we do anything consistently, the body will adapt to get better at it. Sitting at a desk all day with a flexed hip sends a strong message that this is a position to prioritise. As a result, the nervous system might tighten the hip flexor muscles (which raise the knee towards the chest) to do you a favour and save some energy. Regular, varied movement is the obvious remedy to this – think desk breaks, walking, side bends and rotations (like you'll find in this three-move ab workout). Instability Alternatively, Grossmann says the nervous system can use tightness in the hip flexors as a way of compensating for other muscle's shortcomings and creating stability in an otherwise unstable joint. 'If the body perceives a joint as loose or unstable, it will tighten the muscles it has to hand or that it's familiar with to try and create stability, even if they are not the ideal muscles to get the job done,' he explains. If this is the case, your first course of action should be to recruit and strengthen other key players such as the glutes, adductors and glute medius. You might do this through traditional strength training, or any number of other methods. As Grossmann says: 'Anything that gets length and load through the tissues [around the hip] will help.' The exercise below allows you to do just that, as well as work the hip through a wide range of motion, making it a top option for most people suffering from hip stiffness. The best exercise for fixing stiff hips: The Stimulus Six Lunges The body operates on a use it or lose it basis, as far as movement is concerned. To persuade it to regain range of motion around the hips and banish tightness, we need to build a solid business case for doing so, says Grossmann. 'The body is pretty rational, so unless you give it a compelling case to say, 'Actually, we need length through our hip flexors quite often and for reasonable amounts of time', it won't buy into it.' Doing the Stimulus Six Lunges daily is a good way to go about this. It involves lunging in six different directions, recruiting all the main musculature of the hip and moving in all three planes of motion; sagittal, meaning up, down, forward and backward; frontal, meaning side-to-side; and transverse, meaning rotational. Doing this acts like a mini movement assessment in itself, as you can work out your weaknesses by observing which lunges you struggle with. 'If you don't like doing a side lunge, maybe the adductors are super tight,' he explains. 'If you don't like doing a crossover lunge, maybe the lateral hip or the glute medius is really tight,' Grossmann says. 'By regularly training those movements, we're telling the body, 'We're going to be doing these movements, so you'd better get used to getting length in these muscles'.' Done daily, this will help the hips of your average desk job worker feel 'way, way better', he says. 'There's obviously a lot more nuance you could dig into on an individual basis, but their hips are going to be exposed to more positions and ranges of motion than even a lot of people who go to the gym all the time,' Grossmann explains. 'A lot of gym rats will just do squats and deadlifts, only moving up and down, but not moving sideways or rotating. If you do the Stimulus Six Lunges, you are maintaining your body's ability to access all the joint motions of the hip.' If you simply want to maintain your mobility, doing the sequence daily will help. If you're looking to improve your body's strength and performance in these positions for sport, you can progressively overload them by adding weight, upping the number of reps or increasing the range of motion accessed in each direction. 'If you can only do a side lunge to 90cm at first, gradually working towards a wider side lunge is another way to track and improve, beyond adding weight,' says Grossmann. 'Whether you need to do this all comes back to what your goals are. Do you need more mobility, or are you just trying to keep those hips feeling good and not lose access to those joint positions?' Ultimately the best thing you can do is listen to your body but if you're struggling with tightness, it could be worth asking yourself why the feeling keeps returning and look to Grossmann's advice for help. By taking a slightly different approach you might start to see changes and hopefully, improvements too.

How di simple habit of removing your shoes wen you enta house fit contribute to your good health
How di simple habit of removing your shoes wen you enta house fit contribute to your good health

BBC News

time2 hours ago

  • BBC News

How di simple habit of removing your shoes wen you enta house fit contribute to your good health

My mother always get one rule: no shoes inside her house. E no mata who you be. Family member, neighbour or guest, you gatz comot your shoe bifor you enta house. Wen I dey small, I bin tink say na one of di many manners. But as I grow older (and wiser), I realise say no be obsession wit cleanliness. Na about health, safety and hygiene. Cleanliness dey often associated wit dirty wey eye fit see. But wen, if na shoes, wetin dey under di surface dey microscopic and dem dey far more dangerous dan mud or dry grass. Outdoor shoes dey carry bacteria, allergens, and toxic chemicals, e dey lead to serious health problems. Tink about wia your shoes go evri day: public restrooms, sidewalks, hospital hallways, and lawns wey dem don treat wit chemicals like herbicides and insecticides to control weeds and pests. According to one study by di University of Arizona in di United States, 96% of shoes test positive for coliform bacteria, wey dem dey commonly find inside poo poo. And even more worryingly, 27% contain "E. coli," one bacteria linked to various infections, some of dem dey potentially deadly. While some strains of E. coli dey harmless, odas dey produce Shiga toxins, wey fit cause bloody diarrhoea and lead to hemolytic uremic syndrome, one potentially deadly condition wey fit cause kidney failure. Children under five dey at risk due to dia developing immune systems and di fact say dem dey always put dia hands for dia mouths. But E. coli no be di only germ wey dey enta your living room. Shoes dey also collect clostridium, one bacteria wey pipo know to dey cause painful and sometimes severe diarrhea, and Staphylococcus aureus, including MRSA, one drug-resistant "superbug" wey fit cause deep skin infections, pneumonia, or even deadly bloodstream infections. No be only germs Di health risks go beyond bacteria. Shoe also dey act as carrier of chemicals and allergens. Studies don show say outdoor footwear fit contain pesticides, herbicides and heavy metals like lead, e dey pose serious health risks, especially for young children and pets. Exposure to lead, wey dem find inside dust or soil, dey harmful for children becos e fit affect dia brain development and cause lifelong cognitive problems. In addition, allergens such as pollen fit stick to di di soles, causing allergies and respiratory problems. Even more alarming, di asphalt sealants wey dem dey use on roads contain carcinogenic compounds. One U.S. study reveal say di dem fit find dis chemicals indoors and e go dey for in di indoor dust, sometimes at levels 37 times higher dan di one wey dem find outdoors. And e dey spend di most time for ground. Children and pets. Children crawl, play and dey often put dia hands to dia mouths. Pets dey lick dia paws afta dem walk on contaminated surfaces. Wearing outdoor shoes indoors fit increase dia exposure to harmful substances. Clean floors, healthy homes Based on my evidence, my mother rules no dey bad anymore. In fact, na one of di simplest and most effective public health measures you fit adopt for your house. Comot your shoes wen you enta, no be only dirt you dey prevent from staining di carpet, but you also significantly reduce your family exposure to germs and harmful chemicals. And e no dey difficult to do. Leave one space for shoes near di entrance. You fit also put shoe rack or basket, or even comfortable slippers for guests. To tell pipo to comot dia shoe before dem enta your house fit dey somehow at first, but e dey easy to forget say sometin as routine as to enta di house fit carry hidden risks. *Manal Mohammed na Professor of Medical Microbiology at di University of Westminster, UK. We publish dis article in The Conversation and reproduce am here under di Creative Commons license.

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