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This topic would be in a Category for Health or Medicine, if we had one.
The focus of the topic is intended to be knowledge about bone loss and mitigation.
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This post is reserved for an index to posts that may be contributed by NewMars members.
Index:
Post #3: Article about research to counter bone loss on Earth
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This post is about research to attempt to prevent bone loss on Earth.
https://www.msn.com/en-us/health/medica … 5b3a&ei=67
June 12th is the release date for the report cited.
Here is a bit of text at the link above:
Stanford scientists discover enzyme that reverses arthritis in humans
Stanford Medicine researchers published a landmark study in the journal Science on June 12, 2026, revealing that blocking the aging enzyme 15-PGDH completely reverses cartilage loss in aged mice, prevents post-injury arthritis development, and — critically — regenerates human knee tissue obtained from joint replacement surgeries. The discovery represents what scientists call a potential paradigm shift in treating osteoarthritis, which affects more than 32 million American adults and costs the U.S. healthcare system over $300 billion annually. Researchers say a targeted therapy blocking 15-PGDH could be in human clinical trials within three years. WooGlobe Ref : WGA792247
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The counter measurements are after the signs of indications of weakness to which these increase with those in bed rest and a counter to this is changing head angle, The same principles for on orbit apply for indication and treatment.
Bed Rest Countermeasures: Exercise and Muscle Tone Preservation
Chronic bed rest leads to significant muscle atrophy, reduced resting muscle tone (HRMT), and changes in tendon/fascia properties, especially in lower limb muscles Frontiers+1. Countermeasures aim to maintain muscle health, prevent deconditioning, and support functional recovery.1. Exercise Countermeasures
NASA and space medicine research have evaluated isotonic (resistance) and isokinetic (constant-speed) exercise to counteract bed rest effects on:Work capacity (peak oxygen uptake)
Muscular strength
Orthostatic tolerance
Posture, equilibrium, and gait NASA Technical Reports Server (NTRS)+1
Key findings:Reactive jumps (e.g., on a sledge system) preserved HRMT in thigh, calf, and postural muscles, with minimal change in shoulder muscles Frontiers+1.
Exercise groups showed better maintenance of tendon/fascia biomechanical properties and reduced collagen-I changes in soleus muscle compared to non-exercise controls Frontiers.
Functional tests (e.g., one-leg jumps, EMG) showed trends toward preserved leg muscle activation Frontiers.
2. Non-Invasive Muscle Tone Monitoring
The MyotonPRO device measures dynamic oscillation mechanosignals (Hz, N/m, log decrement, ms) to assess:Resting muscle tone
Tendon/fascia stiffness and viscoelasticity
Changes in global and postural muscle groups Frontiers+1
This allows objective tracking of HRMT changes during and after bed rest, guiding personalized countermeasure prescriptions.
3. Reconditioning After Bed Rest
Studies show that structured exercise programs (e.g., reactive jumps, resistance training) can:Restore muscle tone and tendon properties
Improve functional performance
Support recovery in clinical and space medicine contexts Frontiers+1
4. Practical Applications
Spaceflight: Exercise devices (treadmills, resistance machines) and jump training are integrated into astronaut regimens to maintain muscle and bone health NASA Technical Reports Server (NTRS).Clinical rehab: Reactive jump training and resistance exercises can be adapted for patients with prolonged immobility (e.g., post-surgery, spinal injury) to prevent deconditioning Frontiers+1.
Monitoring: MyotonPRO or similar tools can be used to track progress and adjust training intensity.
In summary: Effective bed rest countermeasures combine targeted exercise (especially reactive jumps and resistance training) with objective muscle tone monitoring to preserve muscle and tendon health, improve functional outcomes, and support reconditioning Frontiers+3.
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For SpaceNut re #4...
Thank you for your substantial contribution to this topic!
Your post appears (as I read it) to be about using exercise to try to reduce the rate of bone loss for space travelers or for folks confined to bed.
The article cited in Post #3 is about something completely different. I realized after reading Post #4 that no one was actually reading the link at Post #3.
I went to the original source:
https://www.sciencedaily.com/releases/2 … 021604.htm
If anyone actually reads the article, I'd be interested in comments upon the actual research.
Science Newsfrom research organizations
Stanford scientists regrow lost cartilage and reverse arthritis in major breakthrough
Scientists may have found a way to regrow aging cartilage and stop arthritis before it starts, potentially making joint replacements far less common.
Date:
June 12, 2026
Source:
Stanford MedicineSummary:
A new treatment that blocks an aging-related protein restored lost cartilage in old mice and helped prevent arthritis after knee injuries. Human cartilage samples showed similar signs of regeneration, raising hopes for a future drug that could repair joints instead of replacing them.Scientists Regrow Cartilage & Stop Arthritis
Scientists have found a way to regenerate worn-out joint cartilage by blocking an aging-related protein called 15-PGDH. Credit: Shutterstock
A treatment that targets a protein linked to aging has restored lost knee cartilage in older mice and prevented arthritis from developing after serious joint injuries, according to a Stanford Medicine-led study.
Researchers also found encouraging results in human tissue. Samples collected during knee replacement surgeries began producing new, functional cartilage when exposed to the treatment.
The findings raise the possibility that damaged cartilage caused by aging or osteoarthritis could one day be repaired with either a local injection or an oral medication. If successful in people, the approach could reduce the need for knee and hip replacement surgeries.
An oral version of the treatment is already being tested in clinical trials for age-related muscle weakness.
Targeting the Root Cause of Osteoarthritis
Osteoarthritis is the most common form of arthritis and affects about one in five adults in the United States. The disease gradually breaks down cartilage in the joints, causing pain, stiffness, and swelling. It is estimated to generate roughly $65 billion in direct health care costs each year.
Current treatments focus mainly on pain relief and, in severe cases, joint replacement surgery. No approved medication can slow, stop, or reverse the underlying disease process.
The new treatment works by blocking a protein called 15-PGDH, which researchers describe as a "gerozyme." This class of proteins becomes more abundant with age and contributes to declining tissue function throughout the body.
The same research team first identified gerozymes in 2023. Previous studies showed that 15-PGDH plays a major role in age-related muscle decline in mice. When researchers block the protein, older animals gain muscle mass and endurance. When the protein is artificially increased in young mice, their muscles become weaker and smaller.
Scientists have also linked 15-PGDH to the regeneration of bone, nerve, and blood cells.
A Different Type of Tissue Regeneration
In many tissues, regeneration occurs because stem cells multiply and develop into new specialized cells. Cartilage appears to work differently.
Instead of relying on stem cells, cartilage-producing cells called chondrocytes seem able to shift their gene activity and return to a more youthful state.
"This is a new way of regenerating adult tissue, and it has significant clinical promise for treating arthritis due to aging or injury," said Helen Blau, PhD, professor of microbiology and immunology. "We were looking for stem cells, but they are clearly not involved. It's very exciting."
Blau, director of the Baxter Laboratory for Stem Cell Biology and the Donald E. and Delia B. Baxter Foundation Professor, and Nidhi Bhutani, PhD, associate professor of orthopedic surgery, are the senior authors of the study, which was published in Science. Instructor of orthopedic surgery Mamta Singla, PhD, and former postdoctoral scholar Yu Xin (Will) Wang, PhD, are the lead authors. Wang is now an assistant professor at the Sanford Burnham Institute in San Diego.
Remarkable Cartilage Regrowth
"Millions of people suffer from joint pain and swelling as they age," Bhutani said. "It is a huge unmet medical need. Until now, there has been no drug that directly treats the cause of cartilage loss. But this gerozyme inhibitor causes a dramatic regeneration of cartilage beyond that reported in response to any other drug or intervention."
The human body contains three main forms of cartilage. Elastic cartilage provides flexibility in structures such as the outer ear. Fibrocartilage is tough and shock-absorbing, found in places like the discs between vertebrae. Hyaline cartilage is smooth and slippery, allowing joints such as the knees, hips, shoulders, and ankles to move freely.
Osteoarthritis primarily damages hyaline cartilage, also called articular cartilage.
As joints age or experience injury or excess stress from obesity, chondrocytes begin producing inflammatory molecules and breaking down collagen, the main structural component of cartilage. As collagen disappears, cartilage becomes thinner and softer. Inflammation then triggers the pain and swelling associated with osteoarthritis.
Unlike many other tissues, articular cartilage rarely repairs itself. While researchers have identified possible cartilage-producing stem cells in bone, similar cells have not been successfully identified in articular cartilage.
Why Researchers Focused on 15-PGDH
Earlier work from Blau's laboratory showed that prostaglandin E2 is critical for muscle stem cell function. The protein 15-PGDH breaks down prostaglandin E2.
When researchers inhibit 15-PGDH or increase prostaglandin E2 levels, damaged muscle, nerve, bone, colon, liver, and blood tissues regenerate more effectively in young mice.
The team wondered whether the same mechanism might influence cartilage aging.
When they compared cartilage from young and old mice, they found that levels of 15-PGDH approximately doubled with age.
To test the idea, researchers treated older mice with a small molecule drug that blocks 15-PGDH activity. Some animals received injections into the abdomen, exposing the whole body to the treatment. Others received injections directly into the knee joint.
Both approaches produced striking results. Cartilage that had become thinner and less functional with age grew thicker across the joint surface. Additional testing showed the regenerated tissue was hyaline cartilage, the type needed for healthy joint function, rather than the less effective fibrocartilage.
"Cartilage regeneration to such an extent in aged mice took us by surprise," Bhutani said. "The effect was remarkable."
Preventing Arthritis After ACL-Type Injuries
The researchers also investigated whether the treatment could protect joints after injury.
They used a mouse model that mimics ACL tears, a common sports injury seen in activities such as soccer, basketball, and skiing that involve sudden stopping, pivoting, or jumping.
Although ACL injuries can be surgically repaired, roughly half of affected people develop osteoarthritis in the injured joint within about 15 years.
Mice that received the gerozyme inhibitor twice weekly for four weeks after injury were far less likely to develop osteoarthritis. In contrast, untreated animals showed 15-PGDH levels that were about twice as high as those of uninjured mice and developed osteoarthritis within four weeks.
Treated mice also walked more normally and placed more weight on the injured limb.
"Interestingly, prostaglandin E2 has been implicated in inflammation and pain," Blau said. "But this research shows that, at normal biological levels, small increases in prostaglandin E2 can promote regeneration."
Reprogramming Aging Cartilage Cells
A closer look at cartilage cells revealed important differences between young and old joints.
Older chondrocytes were more likely to activate genes linked to inflammation and unwanted conversion of cartilage into bone. They were less likely to express genes associated with healthy cartilage formation.
The treatment appeared to reverse many of these age-related changes.
One group of chondrocytes that produced 15-PGDH and expressed genes involved in cartilage breakdown dropped from 8% of cells to 3% after treatment. Another group associated with fibrocartilage production fell from 16% to 8%.
Meanwhile, a population of cells involved in building hyaline cartilage and maintaining the extracellular matrix increased from 22% to 42%.
Overall, the results suggest the treatment shifts cartilage toward a younger, healthier state without requiring stem or progenitor cells.
Human Cartilage Also Responded
The team then examined cartilage removed from people undergoing total knee replacement surgery for osteoarthritis.
After one week of treatment with the 15-PGDH inhibitor, the tissue showed fewer cartilage-degrading cells and lower activity of genes linked to cartilage breakdown and fibrocartilage production. The samples also began generating new articular cartilage.
"The mechanism is quite striking and really shifted our perspective about how tissue regeneration can occur," Bhutani said. "It's clear that a large pool of already existing cells in cartilage are changing their gene expression patterns. And by targeting these cells for regeneration, we may have an opportunity to have a bigger overall impact clinically."
Blau added, "Phase 1 clinical trials of a 15-PGDH inhibitor for muscle weakness have shown that it is safe and active in healthy volunteers. Our hope is that a similar trial will be launched soon to test its effect in cartilage regeneration. We are very excited about this potential breakthrough. Imagine regrowing existing cartilage and avoiding joint replacement."
Researchers from the Sanford Burnham Prebys Medical Discovery Institute also contributed to the study.
The research was funded by the National Institutes of Health (grants R01AR070864, R01AR077530, R01AG069858 and R00NS120278), the Baxter Foundation for Stem Cell Biology, the Li Ka Shing Foundation, the Stanford Cardiovascular Institute, the Milky Way Research Foundation, the Canadian Institutes of Health Research, a Stanford Translational Research and Applied Medicine Pilot grant, a GlaxoSmithKline Sir James Black Postdoctoral Fellowship, and a Stanford Dean's Postdoctoral Fellowship.
Blau, Bhutani, and several co-authors are inventors on Stanford University patent applications involving 15-PGDH inhibition for cartilage repair and tissue rejuvenation that have been licensed to Epirium Bio. Blau is a co-founder of Myoforte/Epirium and holds equity and stock options in the company.
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Story Source:Materials provided by Stanford Medicine. Note: Content may be edited for style and length.
Journal Reference:
Mamta Singla, Yu Xin Wang, Elena Monti, Yudhishtar Bedi, Pranay Agarwal, Shiqi Su, Sara Ancel, Maiko Hermsmeier, Nitya Devisetti, Akshay Pandey, Mohsen Afshar Bakooshli, Adelaida R. Palla, Stuart Goodman, Helen M. Blau, Nidhi Bhutani. Inhibition of 15-hydroxy prostaglandin dehydrogenase promotes cartilage regeneration. Science, 2026; 391 (6789): 1053 DOI: 10.1126/science.adx6649
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