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We have all seen movies where right before the hero starts fighting, he cracks his knuckles and makes it look like the coolest thing in the world! But then our parents told us that you should not crack your knuckles because that weakens your grip and hand strength. But is that true? While many people do say that they experience a small loss in strength immediately after they crack their knuckles, but are their long-term effects to it? And what is the sound actually coming from?
The reason why people crack their fingers is because the evident and sharp crack noise causes a sense of relief. Many people also do it when they have done an activity that required them to work with their hands a lot like typing or sewing, giving themselves a sense of satisfaction, similar to stretching after doing hard work. That "crack" sound can make some people cringe, while others find it strangely satisfying. Cracking your knuckles is a pretty common habit, but there are a lot of misunderstandings about it. Some people do it without even thinking, others can't stand the noise, and some can't crack their knuckles at all. You might have been told as a kid that it causes arthritis or makes your fingers swell up. But those are just old wives' tales. There's a real science behind this habit, and it's more interesting than you may think.
The "crack" isn't actually bones breaking or anything bad happening to your joints. It's a normal thing called "crepitus." This just means harmless popping, snapping, or grinding sounds that come from your joints. The main reason you hear this sound is because of gas bubbles in the fluid that cushions your joints. This fluid is called synovial fluid. When you move or stretch, these tiny bubbles form and then pop, making the sound. It's totally normal and doesn't hurt you. Sometimes, especially in bigger joints like your knees, shoulders, or ankles, the sound can also happen when the stretchy tissues that connect your bones (ligaments and tendons) move slightly and then snap back into place.
After you crack your knuckles, you can't usually do it again right away. You have to wait a bit. That's because the gas bubbles in your joint fluid have already popped, and it takes a little while for them to build up again. While cracking your knuckles doesn't give you arthritis, doing it too much might cause some problems. Doctors say that cracking them too often could make your joints a little wobbly and might even make your grip weaker. Also, if the stretchy tissues in your joints keep snapping over your bones, they can get irritated and sore.
Sometimes, a pop in your joint is just like cracking your knuckles, nothing to worry about. But other times, it can be a sign of something else. As we get older, the cushiony stuff in our joints, called cartilage, can start to wear down. This cartilage helps your bones move smoothly. When it gets thin or uneven, the bones can rub together, and that can make a grinding or popping sound. This is different from the pop you get from gas bubbles. If this grinding sound happens along with pain, it could be a sign of osteoarthritis. This is a type of joint problem that's more common in older people, but younger people can get it too, especially after a joint injury. If your joints hurt, especially in the morning or after you've been sitting still for a while, feel wobbly, or are hard to move, it's a good idea to see a doctor.
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In June 2022, the U.S. Supreme Court issued a landmark decision in Dobbs v. Jackson Women’s Health Organization, overturning the 1973 Roe v. Wade ruling that had established a constitutional right to abortion. With the Dobbs ruling, the authority to regulate abortion returned to individual states—setting off a wave of legislative action that continues to reshape access to abortion care across the country.
Three years later, the national abortion landscape is more fragmented than ever. Some states have implemented near-total bans, while others have enshrined protections into their constitutions. As legal battles unfold and ballot measures continue to appear, access to abortion has become heavily dependent on geography.
As of mid-2025, abortion is nearly banned in 13 states, with limited exceptions such as life endangerment or cases of rape or incest.
In over 25 other states, gestational limits range from six to 26 weeks. These restrictions are particularly concentrated in the South and Midwest, where legislative action following the Dobbs decision was swift.
Conversely, several states have moved to protect or expand abortion rights.
Since 2022, voters in California, Michigan, Ohio, and Vermont have passed constitutional amendments guaranteeing the right to abortion.
In states like Kansas, Kentucky, and Montana, voters rejected ballot measures that would have added new abortion restrictions.
In Missouri—a state that implemented one of the country’s strictest abortion bans immediately after the Dobbs ruling—voters passed a measure in 2024 to enshrine abortion access in the state constitution.
However, that decision was followed by further legal disputes. The Missouri Supreme Court later blocked abortion access again, and lawmakers have approved another referendum for 2026 that could reverse the constitutional amendment.
As access has narrowed in certain states, more people are traveling long distances to obtain abortion care. According to data from The Brigid Alliance, an organization that provides travel and logistical support to abortion-seekers, average travel distances have increased nearly 50% since the Dobbs ruling. Today, many patients are traveling more than 1,400 miles round trip to reach a provider.
The group also reports that average travel-related expenses have risen to more than $2,300 per patient—reflecting the rising cost of transportation, lodging, and time away from work. The majority of their clients seeking assistance now come from states like Texas, Florida, Georgia, and North Carolina, where laws have become increasingly restrictive.
Southern states, in particular, have emerged as areas where abortion access is most limited. For example, Florida implemented a six-week abortion ban after a proposed constitutional amendment to protect abortion access narrowly failed, receiving just under the 60% threshold required for passage. This has redirected patients to other states with more permissive laws, such as Virginia.
Since the Dobbs ruling, many abortion-related measures have appeared on state ballots—either to protect or restrict access. In 2024 alone, voters in Arizona, Colorado, Maryland, Missouri, Montana, Nevada, and New York took up initiatives involving abortion rights. Most successful measures focused on preserving access until fetal viability, generally considered to occur around 24 weeks of pregnancy.
Not all efforts to expand abortion rights have succeeded. In Nebraska, voters faced competing ballot measures—one aiming to restrict abortion after the first trimester (which passed) and another to guarantee abortion access up to fetal viability (which failed). South Dakota also rejected a measure to protect abortion rights.
Three years after Dobbs, the U.S. remains sharply divided on abortion access, with legal and political fights continuing to play out across state lines. As more ballot measures are introduced and court rulings evolve, the future of abortion rights in America remains uncertain—shaped less by federal law than by the individual choices of state governments and their voters.
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A new study published in the Journal of the American Chemical Society offers critical insight into the biological mechanisms underlying type 2 diabetes. Researchers from the Indian Institute of Technology Bombay (IIT Bombay), in collaboration with IIT Kanpur and the Chittaranjan National Cancer Institute (CNCI), Kolkata, have identified a key trigger that accelerates the progression of this widespread disease: the structural protein collagen I.
Type 2 diabetes currently affects over 500 million people worldwide, and numbers are expected to rise sharply in the coming decades. The disease is primarily driven by a combination of genetics, lifestyle factors, and complex cellular mechanisms. At its core lies the dysfunction of pancreatic β-cells, the insulin-producing cells responsible for regulating blood sugar levels.
As diabetes develops, β-cells either fail to produce enough insulin or the body’s cells become resistant to it. A lesser-known yet crucial hormone, amylin, is also secreted by these β-cells and plays a vital role in managing blood sugar after meals. However, in diabetic conditions, excessive amylin production leads to misfolding and toxic clumping, which damages β-cells and accelerates disease progression.
In the latest study, the research team pinpointed fibrillar collagen I, a common component of the extracellular matrix, as a key factor driving the toxic aggregation of amylin. Found abundantly in connective tissues like skin and bones, collagen I is also present in the pancreatic environment—particularly in diabetic tissues where it is elevated.
“Every tissue is composed of cells and an extracellular matrix that provides structural support. In diabetic pancreatic tissue, this matrix, especially collagen I, becomes more prominent,” explained Prof. Shamik Sen, the study’s lead investigator from the Department of Biosciences and Bioengineering at IIT Bombay.
The researchers discovered that collagen I acts like a scaffold or platform, accelerating the misfolding and aggregation of amylin, which in turn damages β-cells. This discovery adds a new layer to understanding why the disease worsens over time, even with treatments targeting cellular pathways.
To investigate how collagen I interacts with amylin, the team used a suite of advanced biophysical tools. These included surface plasmon resonance to measure binding strength, atomic force microscopy to study molecular adhesion, thioflavin T fluorescence to track aggregation speed, and NMR spectroscopy to identify interacting regions of the molecules.
“Amylin almost coats the collagen fibres, forming stable, toxic aggregates that cells struggle to clear,” said Prof. Sen. The behavior of amylin on collagen fibres resembled trains moving on tracks—quickly and with destructive momentum.
Computer simulations by Prof. Prasenjit Bhaumik’s group at IIT Bombay confirmed that fibrillar collagen I accelerates the toxic aggregation process, offering further validation of the molecular interaction.
The team extended their study to biological samples from diabetic mice and humans. With the help of Prof. Hamim Zafar and Prof. Sai Prasad Pydi from IIT Kanpur, and Dr. Sankhadeep Dutta from CNCI, they analyzed single-cell data and tissue architecture.
The findings were striking: as diabetes progressed, both collagen and amylin levels rose, accompanied by damage to pancreatic islets—clusters of cells that house insulin-producing β-cells.
To test the functional impact, the researchers grew lab-engineered β-cells on collagen gels containing amylin. These cells showed increased oxidative stress, reduced insulin production, and higher rates of cell death, compared to controls grown without collagen or amylin.
This suggests that the extracellular environment, particularly collagen I, plays a central role in worsening β-cell dysfunction in diabetes.
The findings could explain why many diabetes treatments fall short—they overlook the external microenvironment contributing to disease progression. “Unless we disrupt the interaction between amylin and collagen, we may not be able to eliminate the toxic pancreatic environment,” said Prof. Sen.
Looking ahead, the team is working on cryo-electron microscopy (cryo-EM) models to visualize how amylin and collagen interact at the molecular level. They are also exploring 3D tissue engineering strategies to restore pancreatic function by replicating healthy extracellular conditions.
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As wildfires become an all-too-familiar headline across the globe, their visible devastation—scorched forests, lost homes, and displaced communities—often overshadows a more insidious threat: the impact of wildfire smoke on human health. While the immediate dangers of flames and evacuations are clear, a new study published in Nature Medicine reveals that wildfire smoke does far more than irritate eyes and throats. It can fundamentally alter the immune system, potentially making people more susceptible to illness long after the smoke has cleared.
The study, led by researchers from the Harvard T.H. Chan School of Public Health, found that people exposed to wildfire smoke exhibit changes in gene expression and immune function, even if they’re otherwise healthy. This suggests that the health consequences of wildfires may extend far beyond the immediate coughing, wheezing, and watery eyes that so many experience during fire season.
The research, led by Dr. Kari Nadeau of the Harvard T.H. Chan School of Public Health, provides the most detailed look yet at how wildfire smoke affects the body on a cellular level. By analyzing blood samples from 31 firefighters and civilians exposed to wildfire smoke and comparing them to 29 unexposed individuals, the study uncovered a complex web of immune changes.
People exposed to wildfire smoke showed a marked increase in memory immune cells—cells that typically provide long-term immunity. At first glance, this might seem beneficial, but the study also found elevated biomarkers of inflammation and immune activity, as well as changes in dozens of genes linked to allergies and asthma. In short, the immune system was not just activated—it was thrown into overdrive, potentially increasing vulnerability to illness.
Dr. Mary Johnson, the study’s lead researcher, explains, “Our findings demonstrate that the immune system is extremely sensitive to environmental exposures like fire smoke, even in healthy individuals. Knowing exactly how may help us detect immune dysfunction from smoke exposure earlier and could pave the way for new therapeutics to mitigate, or prevent altogether, the health effects of smoke exposure and environmental contaminants.”
Wildfire smoke is a toxic brew. It contains:
The ultra-fine PM2.5 particles are particularly dangerous. At less than 2.5 micrometers in diameter, they are 28 times smaller than the width of a human hair and can be inhaled deep into the lungs, enter the bloodstream, and affect organs throughout the body.
“These findings suggest that even short-term exposure to wildfire smoke can act as a biological stressor with long-lasting effects,” said Dr. Mary Johnson, lead researcher and environmental health scientist at Harvard. “That’s especially concerning as wildfire seasons grow longer and smoke plumes travel farther.”
One of the most striking findings of the study was the alteration of 133 genes related to allergies and asthma in those exposed to wildfire smoke. This genetic shift may help explain why people living in wildfire-prone areas often report more respiratory problems, even months after the fires have ended.
The study also found that smoke-exposed individuals had more immune cells affected by toxic metals, further increasing inflammation and the risk of immune dysfunction. These changes may make people more susceptible to infections, worsen existing respiratory conditions, and potentially contribute to the development of new allergies or asthma.
The United States, particularly western states like California, has witnessed a dramatic increase in wildfire frequency and severity. In 2023 alone, California experienced over 7,000 wildfires, with the California Department of Forestry and Fire Protection responding to nearly 590,000 related emergencies. The devastating January 2025 fire in Los Angeles County, which claimed 30 lives and scorched 40,000 acres, underscored the deadly toll of these disasters.
Climate change is a major driver, creating hotter, drier conditions that fuel longer and more intense fire seasons. As wildfires become more common, understanding and mitigating the health risks of smoke exposure is more urgent than ever.
Wildfire smoke can trigger a range of symptoms, from burning eyes and runny noses to persistent coughs and breathing difficulties. For people with pre-existing conditions like asthma, COPD, or eczema, exposure can lead to dangerous flare-ups.
But the risks extend beyond the lungs. Fine particulate matter (PM2.5) can enter the bloodstream, causing inflammation throughout the body. Studies have linked wildfire smoke to increased emergency room visits for heart attacks and coronary heart disease within 24 hours of exposure. There is also emerging evidence that PM2.5 can impair cognitive functions such as memory and attention, likely by inducing inflammation in the brain.
Experts emphasize the need for proactive measures as wildfire season peaks:
If evacuation orders are issued, follow them promptly—not just for safety from flames, but from the health threats the smoke carries.
As wildfires continue to reshape landscapes and communities, their invisible legacy—on our immune systems and overall health—demands urgent attention. The message from scientists is clear: wildfire smoke is not just an environmental nuisance, but a profound health hazard that can affect anyone, anywhere the wind blows. Proactive measures, informed guidelines, and continued research are essential to protect public health in an increasingly fiery world.
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