Credits: Canva
Every year on the second Thursday of March, we observe World Kidney Day to raise awareness about kidney health and its essential role in our overall well-being. This year, the day falls on March 13. Such health days are important as it highlights the need for paying attention to each part and organ of our body, which is essential to keep us going.
The kidneys are two bean-shaped organs which act as body's most essential and primary filtration system. They remove waste products and excess fluid from the blood.
The day is important to highlight because more often than you think, kidney diseases go unnoticed. Max Healthcare, a hospital chain in India states that 8 to 10% of adults are affected with some form of kidney damage. However, not many know about it, until severe complications arise. Each year, millions die prematurely from such conditions, this is why early detection is important as it can make a significant difference.
Theme For World Kidney Day
This is what has reflected in this year's theme for World Kidney Day: "Are Your Kidneys OK? Detect Early, Protect Kidney Health". This year's theme aims to target the importance of regular checkups for early detection and intervention at the right time to prevent any kidney disease.
As per the National Institutes of Health (NIH), the kidneys are important to maintain a healthy balance of water, salts, and minerals. These are extremely essential for regulating blood pressure, producing red blood cells, and ensuring overall body equilibrium.
When kidneys fail to perform its primary function, which is to filter out the waste and produce erythropoietin, which is a hormone that stimulates red blood cell production, it can lead to health complications. Your body gets filled with extra water and waste products, this condition is called uremia. As a result, your hands and feet may also swell. At the time of complete and irreversible kidney failure, your kidneys stop working completely. This condition is called End-stage renal disease or ESRD.
This day was for the first time observed in 2006 as a joint initiative by the Internal Society of Nephrology (ISN) and the International Federation of Kidney Foundations (IFKF). The aim back then too was to raise awareness about kidney health and to promote preventive measures to reduce the burden of kidney diseases worldwide. Since then, it has been observed on every second Thursday of March, every year.
The significance of World Kidney Day lies in its role in addressing the growing prevalence of kidney diseases. Many of the cases go undiagnosed. Other than that there are many cases among children where parents do not know whether it is a kidney disease or an unrelated infection. Thus this day also highlights the importance of paying attention to your child's health for any pediatric kidney issues. As this disease is often associated with adults only, but not always is this the case.
ALSO READ: Why Do Cases Of Pediatric Kidney Issues Go Unnoticed?
Credits: Wikimedia Commons
Björn Borg, the 11-time Grand Slam champion, a name the world is not unknown from has shocked everyone with his autobiography, where he revealed that he has been living with prostate cancer. His autobiography, Heartbeats is due for release on September 18, however, some of the details from his books were leaked on Thursday.
The details, which has been shared with The Athletic, Borg talks about his life-saving surgery that he had got done a couple years ago. He explained that "there never really was a choice because the cancer turned out to be extremely aggressive".
He reveals that his cancer was picked up because he would self examine regularly even though he did not have the symptoms. He revealed that the operation was necessary because "it turned out I was in the most advanced stage".
He said: "The fear comes and goes. But that's life, isn't it? You never really know what's coming. You just have to make the most of each day."
Also Read: Joe Biden Is Diagnosed With Aggressive Prostate Cancer: All That You Need To Know
As per the National Cancer Institute, USA, prostate cancer is the most common cancer and the second leading cause of cancer death among men in the United States. Prostate cancer usually grows very slowly, this is why finding it and treating it before symptoms occur could improve men's health.
The National Health Service (NHS), UK, notes that this affects the prostate gland under the bladder and usually is common among men over 50 years old. The prostate is a small, walnut-size gland under the bladder, which produces a thick, white fluid that mixes with sperm to make semen.
How aggressive the cancer is depends on if it has spread to other parts of the body. However, early diagnosis could help it treat successfully.
The NHS, UK notes that prostate cancer usually do not have signs at first, but it could have certain symptoms later on. The best way is to get regular screenings done to identify early, especially if you are in your late 40s.
Also Read: Olympic Cyclist Sir Chris Hoy Shares His Diagnosis Of Prostate Cancer From A Common Shoulder Pain
As per the US Centers for Disease Control and Prevention (CDC), these are the symptoms common in prostate cancer. Speak to your doctor if you experience any such symptom:
Weak or interrupted flow of urine
Urinating often, especially at night
Trouble emptying the bladder completely
Pain or burning during urination
Blood in the urine or semen
Pain in the back, hips, or pelvis that doesn't go away
Painful ejaculation
Another video interview from a couple days ago shows Borg excited about his book launch that he has written with his wife Patricia. He, in the interview, described many near-death experiences and even talked about his cocaine addiction after his early retirement from tennis in his mid-20s.
Read: Can Omega-3-rich Food Slow Prostate Cancer Growth?
However, he is now focused as he calls himself a "family man". He now lives in Stockholm, and regularly spends time in Ibiza. "I have two beautiful sons, Robin and Leo [a pro tennis player once ranked No. 334]. I have two beautiful grandchildren, aged 12 and 10. And I’m kind of a family man, and I want to spend a lot of time with the family. And that’s important for me. Stay involved with tennis, to travel, to watch tennis, to spend time with my tennis friends, with the people who love tennis, but to be with the family, with the kids, with the grandchildren, that’s very important to me."
Credits: iStock
A fading sense of smell may do more than hint at aging—it could be one of the earliest warning signs of Alzheimer’s disease. New research from DZNE and Ludwig-Maximilians-Universität München reveals that immune cells in the brain mistakenly target and destroy nerve fibers critical for odor perception, offering fresh clues into how the disease begins and how it might be diagnosed sooner.
Patients and families may notice that scents seem muted or distorted, sometimes years before other symptoms. Until now, the exact cause behind this early warning sign remained elusive.
A new study led by researchers at the German Center for Neurodegenerative Diseases (DZNE) and Ludwig-Maximilians-Universität München (LMU) sheds fresh light on the mystery. The findings, published in Nature Communications, suggest that the brain’s own immune system mistakenly destroys nerve fibers vital for processing odors. This breakthrough could open the door to earlier diagnosis—and possibly earlier treatment—of Alzheimer’s.
Smell perception begins in the olfactory bulb, a small but complex structure in the forebrain that receives input from sensory receptors in the nose. But the olfactory bulb doesn’t work alone. It relies on nerve fibers extending from the locus coeruleus, a brainstem region that helps regulate attention, blood flow, and sensory processing.
The new study shows that in early Alzheimer’s disease, this communication line is disrupted. Microglia—immune cells that normally act as the brain’s cleanup crew—start dismantling the nerve fibers linking the locus coeruleus and olfactory bulb. This immune-driven attack deprives the brain of crucial odor-processing pathways, leading to smell loss.
“Our study suggests that in early Alzheimer’s disease, changes occur in the nerve fibers linking the locus coeruleus to the olfactory bulb. These alterations signal to the microglia that affected fibers are defective or superfluous. Consequently, the microglia break them down,” explained Dr. Lars Paeger of DZNE and LMU.
At the heart of this immune misfire lies an unusual molecular change. Researchers observed that phosphatidylserine, a fatty acid normally tucked inside the protective membrane of neurons, shifts to the cell’s outer surface in affected nerve fibers.
When this happens, microglia interpret it as an “eat-me” signal. Under normal conditions, this signal supports a healthy process called synaptic pruning, where unnecessary or damaged connections are cleared away. But in Alzheimer’s, this mechanism seems to go awry.
Paeger explained that hyperactive neurons—cells firing abnormally due to early disease changes—appear to trigger this membrane shift. Once flagged as dysfunctional, these otherwise critical smell-related fibers are targeted and destroyed.
PET imaging scans in living patients, which confirmed damage to smell-related nerve circuits in people with Alzheimer’s or mild cognitive impairment.
“Smell issues in Alzheimer’s disease and damage to the associated nerves have been discussed for some time. However, the causes were unclear until now. Our findings point to an immunological mechanism as cause for such dysfunctions – and, in particular, that such events already arise in the early stages of Alzheimer’s disease,” said Prof. Joachim Herms, senior researcher on the study.
More than 6 million Americans currently live with Alzheimer’s disease, a number projected to rise sharply as populations age. Yet diagnosis often comes late, when memory loss and cognitive decline are already advanced.
Smell loss offers an earlier red flag. If the biological mechanisms behind it can be mapped and measured, doctors could potentially screen for Alzheimer’s years before symptoms interfere with daily life. This could be especially critical as new treatments, such as amyloid-beta antibodies, are designed to work best in the earliest phases of disease progression.
“Our findings could pave the way for the early identification of patients at risk of developing Alzheimer’s, enabling them to undergo comprehensive testing to confirm the diagnosis before cognitive problems arise,” Herms noted. “This would allow earlier intervention with amyloid-beta antibodies, increasing the probability of a positive response.”
The study also highlights the often-overlooked locus coeruleus, a small cluster of neurons deep in the brainstem. Beyond smell, this structure regulates blood flow, sleep-wake cycles, and stress responses through widespread connections.
Damage to the locus coeruleus is one of the earliest detectable signs of Alzheimer’s, even before amyloid plaques and tau tangles spread widely. The new findings underscore that its breakdown may not only affect memory and attention but also disrupt sensory pathways, making smell loss one of the first noticeable symptoms.
While the research answers critical questions, it also raises new ones. If immune cells misidentify smell-related fibers as expendable, can this process be slowed or stopped? Could therapies aimed at stabilizing neuron membranes prevent the fatal “eat-me” signal from being displayed in the first place?
Future studies will likely explore whether drugs that regulate microglial activity—or protect the integrity of phosphatidylserine positioning—could preserve nerve connections in early Alzheimer’s.
Meanwhile, incorporating smell testing into routine checkups for older adults may become a more practical step. Inexpensive scratch-and-sniff exams already exist and could serve as a noninvasive screening tool to identify people who may need further evaluation.
For families watching loved ones struggle with subtle changes—whether misplaced keys, unusual forgetfulness, or an inability to smell morning coffee—the findings offer clarity. Smell loss is not just an odd, isolated symptom but a biological signal that Alzheimer’s is affecting the brain long before dementia sets in.
Recognizing this signal early could give patients and clinicians a window of opportunity: time to prepare, time to plan, and perhaps in the future, time to intervene with treatments that slow or alter the course of disease.
Alzheimer’s remains one of the greatest public health challenges of our time. While there is still no cure, understanding its earliest signals brings us closer to meaningful change. By uncovering how immune cells mistakenly dismantle smell pathways, this study not only solves a long-standing puzzle but also lays the foundation for earlier, more effective care strategies.
The sense of smell may be more than just a window to the world—it may be a window into the earliest changes of Alzheimer’s disease.
Credits: Canva/McAlpine Research Group, University of Minnesota
Spinal cord injuries have long posed one of the most stubborn challenges in medicine. Affecting more than 300,000 people in the United States alone, these injuries often lead to permanent paralysis because damaged nerve fibers fail to regenerate across the site of trauma. Traditional therapies focus largely on rehabilitation and symptom management rather than reversing the underlying injury. Now, a groundbreaking study from the University of Minnesota Twin Cities suggests that a combination of 3D printing, stem cells, and lab-grown tissues could change that narrative. Researchers have engineered tiny scaffolds that guide stem cells to form nerve fibers capable of bridging severed spinal cords. In rat models, this approach restored nerve connections and movement—offering a tantalizing glimpse into the future of paralysis treatment.
At the heart of this innovation are organoid scaffolds—microscopic 3D-printed structures designed to direct stem cell growth. These scaffolds contain a network of tiny channels that can be seeded with spinal neural progenitor cells (sNPCs). Originating from human adult stem cells, sNPCs have the potential to differentiate into the various types of neurons needed for spinal cord repair. The scaffold essentially provides a framework for these cells, ensuring they grow along the correct pathways to reconnect disrupted nerve circuits.
Guebum Han, a former postdoctoral researcher in mechanical engineering at the University of Minnesota and the study’s first author, explains, “We use the 3D printed channels of the scaffold to direct the growth of the stem cells, which ensures the new nerve fibers grow in the desired way. This method creates a relay system that, when placed in the spinal cord, bypasses the damaged area.”
To test their approach, the researchers transplanted the scaffolds into rats with completely severed spinal cords. Over time, the stem cells differentiated into mature neurons and extended their nerve fibers in both directions—toward the head (rostral) and toward the tail (caudal)—forming new connections with the host’s existing spinal circuitry.
The results were remarkable. Rats that received the organoid scaffolds showed significant functional recovery compared to controls, regaining movements that were previously impossible. The new neurons integrated seamlessly into the host tissue, demonstrating that lab-grown spinal tissue could not only survive transplantation but also restore communication across previously severed areas.
While the research is still in its early stages, the potential implications for human medicine are profound. Spinal cord injuries have been notoriously resistant to treatment because adult nerve cells rarely regrow once damaged. This study provides proof-of-concept that targeted, scaffold-guided stem cell growth can rebuild the neural network necessary for motor function.
Ann Parr, professor of neurosurgery at the University of Minnesota, emphasizes the significance: “Regenerative medicine has brought about a new era in spinal cord injury research. Our laboratory is excited to explore the future potential of our ‘mini spinal cords’ for clinical translation.” The team hopes to refine the technique, scale up scaffold production, and move toward clinical trials that could one day benefit people living with paralysis.
Despite the promising results, several hurdles remain before this technology can be applied to humans. Scaling the tiny lab-grown spinal cords to the size necessary for human injuries will require sophisticated bioengineering solutions. Immune rejection and integration into a complex, pre-existing nervous system present additional challenges. Moreover, safety and efficacy will need to be rigorously tested in larger animal models before human trials can proceed.
The ethical considerations of stem cell use and genetic manipulation also require careful navigation. While adult stem cells used in this study bypass some of the ethical debates associated with embryonic stem cells, clinical applications must still adhere to stringent regulatory standards.
The merging of 3D printing, stem cell science, and lab-grown tissue engineering represents a paradigm shift in regenerative medicine. The concept of “mini spinal cords” could open the door to therapies not only for spinal cord injuries but potentially for other neurodegenerative diseases that involve nerve degeneration, such as amyotrophic lateral sclerosis (ALS) or multiple sclerosis.
Moreover, these technologies exemplify the broader trend of personalized medicine. By tailoring organoid scaffolds to individual patients, it may become possible to repair nervous system injuries with unprecedented precision. This could drastically improve outcomes, reduce rehabilitation times, and enhance quality of life for patients who currently have few options.
The University of Minnesota study is an early but significant step toward reversing paralysis. By combining 3D-printed scaffolds, stem cell biology, and lab-grown spinal tissue, researchers have demonstrated that damaged neural pathways can be rebuilt and functional recovery is achievable—at least in animal models.
While human applications are still a way off, the research provides a blueprint for the future of spinal cord repair and regenerative neuroscience. For the millions affected by spinal cord injuries, these tiny lab-grown spinal cords could one day offer more than hope—they could offer a pathway to regained movement and independence.
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