High Blood Pressure And Accelerated Bone Aging

Recent research has found that mice with high blood pressure lose more bone than those without the condition. As humans age, their bones become weaker and more brittle as a result of chronic inflammation which can lead to osteoporosis-related fractures when not treated properly. The team suggests treatments for this type of hypertension throughout early adulthood might help prevent further damage during later years. However, they also say it’s important we find out how prevalent these traits are among younger individuals so treatment options exist if needed.

High blood pressure is a common disease that can also be associated with osteoporosis. In this study, researchers found inflammation to exist in mice that was linked to high blood pressure. From inducing young mice with high blood pressure they showed bone loss and osteoporosis related damage to bones comparable to older mice.

The team discovered that more pro-inflammatory immune cells in the bone marrow might be leading to damage on bones. That finding could lead towards developing treatments for osteoporosis and fragility fractures, as well as protecting people from having a lower quality of life because they have increased risks due to their high blood pressure levels.

Following inducing hypertension to young mice the researchers compared them to older mice without the condition. This was to assess whether high blood pressure is associated with bone aging. After six weeks, the mice that had received the drug angiotensin II had progressed more rapidly than a control group of 12 younger animals and they showed increased evidence for wrinkles on their bones. Bone health was determined by density of strength of the bone. Mathematical algorithms were used to estimate the possible effects of aging and hypertension on the strength and microstructure of the bone in the mice.

When compared to the young mice without hypertension, the young mice with induced hypertension had a 24% reduction in bone volume fraction, 18 percent less thickness of the sponge like trabecular bone which is located at end long bones such as spinal column and femurs and a 34% reduction in likely failure force. The estimated failure force for these younger animals was much higher than those that were elderly or had been given hypertension injections. This may be because they haven’t experienced enough wear-and tear on their bodies yet so there isn’t any major risk factors involved other then age itself.

The researchers found that when older mice were given an angiotensin II infusion, they did not show signs of bone loss like the younger ones did. However, during this same experiment with either high blood pressure or not-hypertensive but still aging factors present in their system, these animals’ osteoporosis was treated as if it was 15 – 25 human years old.

This heightened elevation in active immune cells told them that the older mice are overall more inflamed and that an ongoing inflammation level, whether they had high blood pressure or not, might be a determining factor on bone health. It seemed that high blood pressure was changing the remodeling process of bone towards loss of bone rather than gain of bone or equilibrium of bone in the hypertensive younger mice. This resulted in bone that will be weaker, leading to an increase for fragility fractures and osteoporosis. This may mean that we should be screening people for osteoporosis who have high blood pressure.

These exciting findings could help further our understanding of the immune cells and mechanisms that play a role in human bone health. This knowledge may lead to new approaches for preventing osteoporosis before adulthood, bringing us one step closer towards healthy bones.

To view the original scientific study click below:
High blood pressure may accelerate bone aging

Extra Exercise Could Extend Your Lifespan

Getting more than the minimum recommended amount of exercise could help you live a healthier and longer life according to a new study. The current guidelines recommend 75 to 300 minutes of exercise on a weekly basis to benefit health. By doing more, you are linked to even a lower risk of issues with heart health and other risk factors. Up to 5 hours of exercise that is vigorous and 10 hours of moderate exercise such as walking may help decrease the risk of early death.

Data was evaluated from more than 100,000 participants over a 30-year period. In follow up, researchers compared the self-reported habits of exercise with the risk of dying from any cause.

Moderate activities were weightlifting, walking, and body weight workouts, while exercise that was vigorous included swimming, running, aerobics and biking. Current guidelines from the Health Department recommend a minimum of 150 minutes of moderate exercise per week, 75 minutes of exercise that is vigorous, or combining them.

The team discovered that participants meeting the minimum guidelines had less all cause mortality by 21% throughout the study than the participants who had less exercise.

However, data from the more avid athletes has suggested that the participants that did 150 to 300 minutes of vigorous exercise weekly had a 21 to 23% lower chance of death. And moderate exercise such as walking from 300 to 600 minutes per week showed better results with 26 to 31% lower mortality risk.

Earlier research has discovered that an intense workout, such as triathlon and marathon training, might increase the health of heart risks, but this was not the finding in this study. While it wasn’t beneficial to get more than 10 hours per week of moderate exercise, or 6 hours of intense exercise, there were no side effects from it.

Consistency is the key no matter how much you are exercising for long term benefits. The study establishes evidence to help guide people to select the right intensity and amount of physical activity they need over their life in order to maintain their health overall.

A limitation of the study is the participants were primarily white and were gathered from 2 large surveys of medical professionals, so it isn’t clear if the results would apply to other demographics.

Extensive earlier research confirms the benefits of exercise to health in many ways from improving heart health, building muscle, boosting mood, and prevention from age related decline. In conclusion, to get the best results, include of mix of strength training and cardio in your exercise routine.

To view the original scientific study click below:
Long-Term Leisure-Time Physical Activity Intensity and All-Cause and Cause-Specific Mortality: A Prospective Cohort of US Adults

Consistency Improves Health

A new study by researchers at the Univ. of Pittsburgh has found that people who are consistently active throughout the day tend to be happier and their performance on cognitive tests are better than those who have an irregular activity pattern. The findings suggest that patterns of activity, not just the intensity of the activity, are critical for healthy mental health and aging.

This suggests that it’s important to maintain a consistent routine each day, with regular periods of activity and rest. The exciting thing about these findings is that health and wellness could be improved by voluntary and intentional activity patterns.

For the study, 1,800 older adults over 65 were recruited to identify if there were any links associated with their activity pattern and their cognition and mental health. They all wore accelerometers for 7 days which measured their activity. They also answered questionnaires to determine any symptoms of depression and to access their cognitive function. It was shown that 37.6% of the participants were early risers, kept consistent routines and remained active all day.

Whereas, another group of the participants (32.6%) also had daily routines but were only active for about 13.4 hours everyday. This was because they woke up later in the morning and retired earlier during the evening. They tended to have more symptoms of depression and their cognition was poorer.

The rest of the participants (29.8%) had disrupted activity patterns, exhibited erratic behavior throughout the day and their activity levels were inconsistent from day to day. These adults were more likely to experience depression and perform worse on cognitive tests.

Research suggests that the duration of activity, rather than intensity, may be more important for health. The relationship between mental health and activity patterns is bidirectional. Depression or cognitive impairment can make it more difficult to have a consistent routine, and conversely having a disrupted activity rhythm could make these symptoms worse. However, simply staying engaged with activities throughout the day can be beneficial for mental health.

People who want to get better sleep should develop a consistent routine. This includes waking up at the same time each day, no matter how tired you are. It’s also important to have a realistic plan to keep active throughout the day by incorporating activities you enjoy. If you are finding it difficult to get back into an exercise routine, it is important to be patient and reasonable with yourself. One way to make the process easier is to compile a list of activities that you enjoy and can do safely. Some examples might be swimming, biking, or taking a nature walk. By choosing something that you enjoy, you are more likely to stick with it in the long run.

Our internal clock can help us create a stable routine by setting time cues for things like sunlight, exercise, and eating. A healthy lifestyle is essential for everyone, and that includes getting enough sleep and exercise, as well as having a meaningful day filled with activities that you enjoy. It’s important to have something to look forward to each morning and to feel productive and satisfied by the end of the day. Whether it’s spending time with family and friends, working on a hobby, or volunteering in the community, finding purpose in your daily routine is key to living a happy and healthy life.

To view the original scientific study click below:
Association of 24-Hour Activity Pattern Phenotypes With Depression Symptoms and Cognitive Performance in Aging

Sleep exerts lasting effects on hematopoietic stem cell function and diversity

The impact of insufficient sleep on our health is largely unknown. However, a new study has found that people who consistently lose up to 1 1/2 hours per night are at increased risk for immune disorders such as cardiovascular disease or inflammatory conditions like arthritis.

Sleep is a time for the body to rejuvenate and heal itself, but did you know that lack of sleep can actually change how your DNA looks? The research shows immune cells are affected by changes in structure during rest. This could have long term effects on inflammation which leads to chronic diseases. And, it turns out catching up on sleep doesn’t fix what was lost from not getting enough. Instead we need quality sleep each night so our bodies stay as healthy as possible throughout life.

The study shows that sleep plays an important role in determining how well you are protected from immunological health on a long term basis. When we don’t get enough rest or our bedtime is interrupted by outside forces like stress, the immune system becomes weakened and less able to fight off infections. This can cause serious complications such as inflammation which makes matters worse if it occurs during a time when your body needs all its strength for fighting off illness.

The work emphasizes the importance that adults need to consistently sleep seven to eight hours per day to help prevent inflammation and disease.

When researchers tracked the health of 14 adults over six weeks, they found that those who got eight hours sleep each night had more robust immune cells than people that had gotten less sleep. After six weeks with no change in bedtime rituals or work schedules, this group’s resting blood cells were more active than before. Then the same group reduced their sleep by 90 minutes per night for six weeks. They had their blood and immune cells reanalyzed.

The researchers were surprised to find that after six weeks of restricted sleep it had changed the immune cells in people’s bodies. The lack of rest caused more inflammation, which is an adverse effect on our body’s natural defense system. It also altered DNA structure for some participants who had less than eight hours per night throughout their study period.

The team also analyzed sleep in mice. The mice with sleep fragmentation had increased rates of immune system decline, while those who slept unaltered experienced less harmful effects on their bodies. The team also found that this pattern was consistent across humans and mice – both species share similar findings following disrupted slumber patterns over time periods ranging from two weeks to ten months.

The findings from this study show that sleep fragmentation leads to an increase in the production of immune cells, which can result in inflammation and disease. Despite recovering fully after a period without restorative sleep, these mice continued producing more white blood proteins than usual while their original amount remained unaltered . This suggests some kind of rewiring had occurred as well during those interrupted nights, which is a notable finding considering its relevance across all species

The researchers found that even after weeks of sleeping better, their immune systems were still reacting to sleep in an unhealthy way. This is because poor-quality interrupted slumber leaves behind a molecular imprint on stem cells which causes them trouble and leads back into disease or inflammation

The researchers were surprised to find that not all clusters of stem cells responded in the same way. Some grew and developed, while others decreased or aged rapidly. This variation is an important factor in determining who will develop cardiovascular disease as well inflammation-related illnesses like arthritis. It shows how sleep patterns can affect our immune system by varying cell growth rates depending on where they’re located within bodily tissues. The team noticed large differences between groups, while some types prospered despite limited rest whereas other greatly reduced responses when given more opportunity.

To view the original scientific study click below:
Sleep exerts lasting effects on hematopoietic stem cell function and diversity

Physical Activity May Play a Stronger Role Than Genes In Longevity

A recent study has asked whether there are links between a person being physically active or being sedentary can be associated with a higher risk of death. The question became – does the risk change at all if a person is genetically predisposed to live a longer life? Earlier research has indicated that low physical activity and more time spent sitting are linked with a higher risk of death.

The study’s goal was to see if there is an association between sedentary time and physical activity with death varied, based on a variety of levels with a person living a longer life based on genetic predisposition.

For this research, a team in 2012, began to measure the physical activity of 5,446 women in the U.S. who were 63 years of age of older. They followed them for 8 years to determine their mortality. The women wore a research grade accelerometer for up to 7 days measuring the amount of time they were sedentary, moving and the intensity of their physical activity and sedentary time.

The ensuing study discovered that a higher level of light activity and moderate to vigorous activity were linked to the risk of death at a lower level. The findings also found that a higher sedentary time was linked with death at a higher risk. These links were consistent among women who had a variety of levels of genetic predisposition for a longer life.

The study indicated that even if a person isn’t likely to live long based on their genes, they can still extend their lifespan by participating in positive lifestyle behaviors such as sitting less and regular exercise. Conversely, even in a person’s genes predispose them to a long life, being physically active is still crucial to achieve a longer life.

With the aging population in the U.S. and longer time spend participating in lower intensity activities, the study supports recommendations for older women to participate in physical activity of any intensity to reduce their risk of disease and premature death.

To view the original scientific study click below:
Associations of Accelerometer-Measured Physical Activity and Sedentary Time With All-Cause Mortality by Genetic Predisposition for Longevity

Reprogramming Skin Cells Into Neurons For Brain Disorders

A new study has developed a novel method for studying age related disorders of the brain. The team has focused on the neurodegenerative disorder Huntington’s Disease for the research.

The difficulty in recreating adequate animal or cellular models of disease is an issue that has limited progress towards new treatment. For example, Huntington’s disease, which affects about 30 thousand people globally, is characterized by uncontrollable jerky movements of specific limbs. This makes it difficult to study because there are no human cell cultures available for research purposes. However, one way around these obstacles could be through reprogramming cells again rather than using traditional methods.

The study on Huntington’s disease provides an innovative process by reprogramming skin cells into neurons. This allows them for the first time ever, not just at a cellular level but also on an emotional one too. This could be important when it comes down to studying age related brain disorders such as Alzheimer’s or Parkinson’s.

Researchers were able to reprogram skin cells from patients that have Huntington’s disease converting them into neurons. They then compared the “reprogrammed” brain cell samples against people that are healthy. The findings showed several defects unique only among those suffering from HD; namely an inability to break down certain proteins that may cause energy shortage or increased trafficking rates within the body’s system leading up toward illness onset (traffic overload).

They found that these reprogrammed neurons keep their biological age, which could make them an excellent model system This means they are old and can be used as a reference in studying other neurodegenerative disorders such Alzheimer’s or Parkinson’s disease. The findings are important for future studies using this model system and may also provide insight into how aging affects our health over time.

To find a cure for Huntington’s disease, scientists need to investigate the progression of this deadly condition in living organisms. Researchers are using cells taken from patients with HD and studying them outside their bodies- something that has never been done before.

The model was created for this purpose and so far it seems accurate. More research is needed on how useful these findings really are when applied towards human treatments or even prevention strategies.

To view the original scientific study click below:
Distinct subcellular autophagy impairments in induced neurons from patients with Huntington’s disease/a>

What Is The Best Way To Increase Muscle Strength?

The process of aging affects your body in many different ways, including the gradual loss of muscle mass and strength. It starts as early as age 30 and amounts to about 1% loss per year. In addition some people have a condition called sarcopenia where their muscles become weak more quickly than others after they reach an older age.

Resistance exercise using barbells, dumb bells, machines, or your own weight (push ups, chin ups, etc) increases strength. This can help make up for the loss that occurs with aging which can be significant by the age of 70 or older. Also it is a whole lot easier to maintain strength than try to regain it later on. This research study explored whether just a small amount of activity daily is more helpful than a lengthier exercise workout less often.

The study involved four weeks of training that consisted of 3 groups performing an exercise that consisted of arm resistance. Two of the groups performed 30 contractions each week, with one group doing six contractions per day for a period of five days per week (6×5), while the other group crammed all 30 into a single day (30×1). Another group performed just six contractions one day per week.

The exercise consisted of “maximal voluntary eccentric bicep contractions” that were performed on a machine that measures muscle strength in each contraction of the muscle that you would do at a gym. An eccentric contraction is when the muscle lengthens and in this case like lowering a heavy dumbbell in a bicep curl.

Changes in muscle strength and thickness were measured and compared. The researchers found that over four weeks, people who did six contractions per day had greater increases than those doing 30 in both muscle thickness and strength. The former also saw their power output increase while performing this exercise; they could lift heavier weights after only five days of training!

The group that did 30 contractions in one day showed no increase in muscle strength, but they did see an increase of 5.8% for thickness. The 6×5 exercise plan showed significant increases in muscle strength, more than 10% with an increase of thickness similar to the 30X1 group. The group that did the six contractions once a week did not show any changes in muscle thickness or strength.

The finding is important because it suggests that short, regular sessions of exercise can produce similar results to those seen after longer ones. The current thought is that you have to do lengthy sessions at the gym, noted Ken Nosaka from ECU’s College Of Health And Human Sciences, but this isn’t always necessary. Just lowering heavy dumbbells gently for 1-6 times per day will provide enough physical stimulation for your muscles without overdoing things and possibly doing more harm than good.

The bicep curl is a common exercise for weightlifters and bodybuilders, but recent research suggests it’s not the only muscle group you need to work out. While the research required participants to perform the maximum effort with this particular move early findings indicate similar results can be achieved without needing as hard or pushing up against limits.

The body seems to respond better when exercises involve eccentric contractions at smaller doses rather than bigger loads less frequently. There is still much research left to be done on why this happens, but one theory is that it may relate to how often our brain is asked to make muscles perform in a particular manner.

If we want to be effective in our fitness goals, it’s important for us not only to focus on the weekly minute goal but also make exercise a daily activity. If a person exercises once every week or ten days, the results will be different from someone who does their workout five times per week. This research together with previous studies suggests how crucial accumulating small amounts of physical activity throughout each day can become over time rather than spending hours working out all at one time.

To view the original scientific study click below:
Greater effects by performing a small number of eccentric contractions daily than a larger number of them once a week

It Isn’t All In The Genes – Are We Inheriting More Than We Think?

Scientists have made a groundbreaking discovery about the mechanisms of healthy development in embryos, which could change our understanding on what we inherit from parents and how they shape us. The new research suggests that mothers may be passing on more of their DNA than we thought, with an epigenetic legacy for future generations.

It’s a recently discovered phenomenon called “epi-genetics”. The study, led by researchers from WEHI in Melbourne, Australia has significantly broadened our understanding of which genes have information passed down through generations and what proteins control this unusual process.

We all know that our genetics determine who we are, but what if there were other factors involved? DNA contains the instructions for producing all cells in your body. It’s really hard to change yourself and pass on these new changes because they happen through alterations of chromatin structure around genes which cause them not to be read by protein-coding regions any longer – so no products get made! This means you can have different versions or “epigenes” depending how much nutrition improves during development.

And it turns out that mothers can pass on their genes through epigenetics to a tiny extent. This means we need more research into how this works and what other factors come in play when determining whether or not an individual will have certain traits based off the DNA they’ve been given at birth. The new research has shown that a mother’s supply of protein can affect the genes which drive skeletal patterning in their offspring.

The discovery that mother’s DNA contains information passed on through generations has a deep impact on how we view ourselves. With this new understanding, there are many more questions than answers about what other types of environmental factors can affect our development and future health risks.

Researchers have recently discovered a new link between the mother’s eggs and her developing baby. This study focused on one protein, SMCHD1; it was found by Professor Blewitt back in 2008! The researchers wanted to see what would happen if they decreased or increased this level within an ovo- fertilized embryo before birth via maternal transfer. They monitored how many different types of Hox genes were activated throughout development as well because these play important roles during patterning for elegant structural formation.

It has been shown that mothers pass on their epigenetic information, rather than just the blueprint of genes. This is fascinating knowledge that we can now put to use. While there are more than 20,000 genes in our genome-the average human possesses around 150 of these coding regions which carry genetic information produced by mutation or choice over time. “This is the first time that we’ve seen this type of inheritance happen in human beings,” said Dr. Benetti, “and it gives us an idea about how few genes really matter over long periods.”

Research has shown that a gene called SMCHD1, which only exists in the fertilized egg after two days of conception and is unique to humans as well as other animals, can have an impact on life-long health problems. This discovery could help women with these variants live more comfortable lives by providing them opportunities for treatment options through our drug design efforts at WEHI.

To view the original scientific study click below:
Maternal SMCHD1 regulates Hox gene expression and patterning in the mouse embryo

Growing Transplantable Arteries From Stem Cells

From the early 1900’s blood banks have been crucial in medical care. A team is now wanting to take the concepts a step further by utilizing stem cells in creating new arteries for people that have cardiovascular diseases. They have discovered a drug that might help decrease complications in people who undergo bypass surgery.

There are 2 cellular building blocks of arteries that are functional, one of which is smooth muscle cells. A team was able to perfect the process of building them by using pluripotent stem cells along with a drug called RepSox. The identical compound may additionally lower the risk of a possibly dangerous complication that is frequently seen in people who undergo restorative surgeries like stents, balloon angioplasty and arterial disease bypass surgery.

The team used single cell CRISPR-Cas9 and single cell RNA sequencing to determine the pathways that can control differentiation of arterial endothelial cells, which are pillars of arteries. From manipulation of the pathways they were successful at generating arterial cells that were functional. They focused on cells that are smooth muscle.

Growth factors that have been widely used for production of smooth muscle cells from stem cells can account for an irregular thickening known as intimal hyperplasia. Initial hyperplasia can lead to blood vessel narrowing known as restenosis. It is a frequent problem in differentiation of smooth muscle cells and if you want an artery that is useful, you do not want this risk.

Restoring the contractile ability of cells that are smooth muscle and hence facilitate better flow of blood, the team utilized high throughput screening in order to find small molecules that can overcome the problem. RepSox emerged from 4,804 different drugs. In comparison to frequently used growth factors, they discovered that RepSox inhibited intimal hyperplasisa in a rat balloon model of injury and it is less expensive and more stable.

The team thinks RepSox may additionally serve as a medication to treat restenosis in people after surgery. At the present, there are 2 FDA approved medications to address the problems and they are not cell type specific leading to side effects. The team found that RepSox suppresses intimal hyperplasia with fewer side effects.

It is hard to repair the cardiac system when damages occur, therefore, scientists are looking into various regenerative methods. One team discovered a protein known as CXCL12 could grow ancillary arteries when the major arteries of the heart are blocked. It has been found that the Hippo signaling pathway, which controls the size of organs and cell death, can prevent damage to heart muscles from repairing themselves. When the team silenced it, the heart’s ability to pump in mouse models that had heart failure was restored.

From this study the team is now nearing their goal of building arteries, but there is still lots of work ahead. This cell type is an improvement from earlier efforts, but it still isn’t mature. The team needs to generate these cells to become more mature which would make them like a native artery and make it more functional.

To view the original scientific study click below:
A Human Pluripotent Stem Cell-Based Screen for Smooth Muscle Cell Differentiation and Maturation Identifies Inhibitors of Intimal Hyperplasia

New Way to Generate Human Heart Cells from Stem Cells

A new study is trying to understand early heart disease and development in relation to the mechanisms that determine cell fate. PSCs, or human pluripotent stem cells can conceivably produce a tissue the human body needs for repair. But developing technology for this to happen for a specialized cell, for example a beating heart muscle cell, has required intricate knowledge of developmental pathways and regulatory factors.

Although there has been important technological advances, types of cells that are obtained from human PSCs are still functionally immature. For example, in a human beating heart muscle cell (cardiomyocyte), the applications are limited in disease modeling and regenerative medicine. The cells that are generated don’t fully portray those that are found in the adult heart but are instead more similar to a fetal heart that is 20-weeks old.

The team utilized mouse embryo and cardiomyocytes to look into mechanisms that determine the fate of cells by modulating the peroxisome proliferator activated receptor (PPAR) signaling pathway. It plays a vital role in the development of cardiomyocytes to repeat in culture, and the cell in the womb to maturate and to progress to its specialization.

They were able to identify a response from isoform specific maturation, where PPARdelta signaling activation had the ability to augment the structural, metabolic and contractile maturation of hPSC-CMs. This being the first incident where PPAR signaling has been decoded in such an isoform specific way.

The specificity of PPARdelta, however, not PPARalha to show such an efficient effect on cardiac maturation was unexpected. The new strategy for maturation provided an easy and robust way to generate in culture mature heart cells. These can be used for a variety of applications such as disease modeling, drug screening or therapy for cell replacement in failing hearts.

The researchers were able to identify how the protein PPARdelta played a role by inducing a metabolic receptor from glycolysis to fatty acid oxidation in a heart muscle that was lab generated. This is a vital step in the controls and maturation no matter if these cells produce energy from fatty acids or glucose.

They showed that the signaling of PPARdelta plays an important role. It has the ability to turn on gene regulatory networks which increase the organization and number of mitochondria and peroxisomes, fatty acid oxidation, myofibril lay out, the contractility and the size of heart muscle cells.

To purify hPSC-CMs they are exposed to lactate and this treatment will trigger an independent molecular reaction for maturation of heart cells. In the study, the team exhibited lactate treatment along with activation of PPARdelta that increased further oxidative metabolism which allows energy generation from both fatty acids and carbohydrates.

The team developed a publicly and comprehensive accessible gene expression dataset of transcriptomic changes in hPSC-CMs which might be valuable to scientists studying PPAR lactate selection, PPAR signaling, or screening targets for drug or research testing.

The team is interested in analyzing disorders of fatty acid oxidation. This will depend on having CMs that primarily utilize fatty acid oxidation as a source of energy. They will investigate using the mature hPSC-CMs in transplants following an infarct.

The work will expand opportunities to further research biology of the human heart through multi-disciplinary avenues that incorporate transcriptomics, developmental biology, drug testing, and contractile measurements. They are headed to understanding how to use their knowledge of human development in order to improve access to human cell types that are mature.

To view the original scientific study click below:
PPARdelta activation induces metabolic and contractile maturation of human pluripotent stem cell-derived cardiomyocytes

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