People Generate Their Own Oxidation Field Changing Air Chemistry

The indoor environment is usually more dangerous than the outdoors, with 90% of people’s time spent indoors. Chemicals from a variety of sources such as outdoor pollutants can seep into your home and cause problems for you there too! When it comes to health risks our bodies are constantly being bombarded by new chemicals – some good (like oxygen), others bad such as viruses or bacteria which want nothing better then an opportunity to live off of us. You might be surprised to learn that we are extremely harmful traveling emission sources of chemicals, including those found in our skin and breath.

The answer to why our atmosphere bothers cleaning up after us is that it’s a living thing. Atmospheric chemicals react with each other and rain to disappear. The sun UV light and water vapor in the air react with each other, forming molecules which then attach themselves (and any dirt) onto these reactive ingredients as “detergents.” These detergent-like components are mostly made when solar radiation strikes oxygen or hydrogen gas present amongst other things found on earth.

Indoor air is affected by rain and direct sunlight. UV rays are mainly filtered out through glass windows, so it’s been assumed that concentration of OH radicals in indoor environments isn’t as high compared to outdoor ones. This may be due mostly because there are no strong sources like solar radiation or wild fires burning nearby which can produce abundant quantities of ultra-violet light (which we know cause damage). It also seems likely than any ozone leaking into a building from outdoors will combine with other chemicals found inside a building.

OH radicals are a byproduct of skin oils and the ozone, which can be created indoors just due to people. It has now been discovered that humans are able to transform these reactive chemicals themselves- meaning we have even more control than previously thought over how much damage will be done or protective measures taken against it! The shape and strength of its oxidation field can be determined by things like ventilation patterns or space configuration. The research team found that even outside daytime concentrations of OHs were comparable.

The reaction of unsaturated fats and oil with ozone can be quite harmful to your skin, releasing a host of squalene degradation products. One type in particular is double-bonded gas phase chemicals that react further when exposed to the airfield generating OH radicals which have been shown as an important factor for aging signs such as wrinkles or age spots due their ability to damage DNA molecules by breaking apart hydrogen bonds between bases pairs. This study measured each individual level while also determining how much total reactivity there was so we could quantify what impact this has overall over time.

When scientists tested four different people to see how well they responded in an environment with higher indoor levels of ozone, they found that not only did all participants experience adverse effects such as headaches and difficulty breathing but even those who arrived without any pre-existing medical conditions experienced these same symptoms. The team monitored each individual’s OH value before their stay began along side assessments made at regular intervals during it.

To understand how the human activated OH field compared under a variety of conditions, results from an elaborate multiphase chemical kinetic model were connected with computational fluid dynamics models. The modeling team found that the human generated field varied under a variety of conditions, beyond those tested in lab. From their results it is clear OH radicals are abundant and present forming durable spatial gradients.

The model developed by this team has been the first of its kind that can accurately predict chemical processes happening at both molecular scales (in terms of individual molecules) as well room-sized regions. It does make sense why OH would be generated from your skin reaction when reacting with air particles; they’re essentially just small versions of you!

The team’s work has found that OH can oxidize many more spaces than ozone, which creates a myriad of products right in our immediate surroundings. These impacts on health are unknown as they have not yet been studied experimentally or clinically but could be serious due to how much time we spend near chemical signals like those present from plastics and other chemicals.

The research published today has implications for our health. Chemical emissions from a variety of furniture and materials are being tested before they can be approved to sell. It would also be wise to conduct tests in the presence of ozone because oxidation processes may generate respiratory irritants such as 4-oxopentanal or other OH radical generated oxygenated species that could have negative effects, especially on children.

To view the original scientific study click below:
The human oxidation field

Eating More Protein Will Not Enlarge Muscles Without Exercise

It has been found from reviewing 49 studies from 1800 weightlifters that increasing protein intake by double the amount increased strength by 9% and added about 1 lb of muscle growth. The participants worked out for 6 weeks and lifted weights at least twice per week.

The amount of protein used in the studies was the recommended dietary allowance (RDA), which is 0.4 grams for the average person per pound of body weight. When working out with strength training and increasing protein intake it was found that any additional gain in muscle strength levels off at 0.7 grams. The extra protein consumed presented less muscle growth with aging.

The researchers found that the type of protein consumed, whether dietary or from supplements, made no difference in the amount of muscle gained. You do need more protein when trying to increase muscle growth, but consuming more than double the RDA did not change the outcome.

To add additional muscle growth, it was found that going to the gym and performing resistance exercises is what increases muscle growth. It could be beneficial to consume up to twice the protein but any extra amounts of protein from any source did not grow larger muscles. Maximum muscle can be gained from eating protein up to 50-70 grams per day.

From 15 previous studies it was shown the supplementing protein for older weightlifters offered no benefit. You cannot just eat extra protein and expect to increase muscle. With aging, almost any person will lose muscle strength and size. But you can decrease this loss brought on by aging with performing resistance exercises on a regular basis.

When you work a muscle it breaks down. In order for it to heal and grow any combination of foods that contain protein and sugar will promote healing. Protein can be found in nuts and seeds, beans and all animal products such as dairy products, eggs, fish, poultry and meat. A variety of these foods can meet the protein needs for muscle growth.

To view the original scientific study click below:
A systematic review, meta-analysis and meta-regression of the effect of protein supplementation on resistance training-induced gains in muscle mass and strength in healthy adults

Regenerating Muscle Repair with Hyaluranic Acid

New research has identified how cells communicate to repair muscle damage. When a muscle is damaged, stem cells and immune cells work together to repair the damage. But how these cells interact to complete the removal process of dead tissue and make new muscle fibers had been a mystery. Scientists have discovered that hyaluranic acid is the essential molecule that contributes to this interaction.

Hyaluranic acid is a natural substance and is currently used in beauty treatments and osteoarthritis injections. The new study shows it is the secret ingredient that communicates to muscle cells when to start repair. When muscle cells are damaged, it is critical for immune cells to rapidly enter the tissue to remove any damage so that stem cells can begin the repair process.

The research shows that the stem cells in muscles are prepared to begin repair instantly, but the immune cells keep the stem cells in a state of rest while they complete the cleanup job. This takes approximately 40 hours. Once this process is complete there is an internal alarm that wakes up the muscle stem cells and communicates to them to begin the repair process.

The damaged muscle stem cells must work in unison with immune cells to complete the process of repair. It is important for immune cells to quickly enter the tissue to remove the damage before stem cells can begin repair. When damage to muscles occur, stem cells begin coating and producing themselves with hyaluranic acid. When this coating is thick enough, it shuts down the immune cells sleep signal and wakes up the muscle stem cells.

From the use of human and mouse tissues, the team additionally discovered how stem cells in muscle control production of hyaluranic acid using epigenetic marks on the Has2 gene.

Aging is linked with muscle weakness, chronic inflammation, and a decreased ability of muscle stem cells to start the repair of any damage. If a way can be found to enhance the production of hyaluranic acid in the muscle stem cells of aged adults it might assist with repairing the muscle.

The team notes that the regenerative benefit of hyaluranic acid might depend on its production by the stem cells in the muscle. They are now examining drugs that can regulate the epigenetics of stem cells in muscle that may be used to increase the production of hyaluranic acid.

To view the original scientific study click below:
JMJD3 activated hyaluronan synthesis drives muscle regeneration in an inflammatory environment

Hip Implants from Cartilage Grown from Stem Cells

A new study has found a way to program stem cells in order to grow new cartilage on a 3-D template of the hip joint ball. This cartilage releases anti-inflammatory molecules that assist in fending off new arthritis occurrences. The new technology could supply an alternative to traditional hip replacement surgery and could remove the need for surgery for joint replacement surgery in some people.

The team has developed a means to resurface an arthritic joint with a person’s very own stem cells to grow new cartilage. When combined with gene therapy it can release molecules that are anti-inflammatory in an effort to stave off arthritis. Hopefully this could delay or prevent the normal plastic or metal prosthetic joint replacement.

The cartilage is made with the person’s own stem cells which are taken from fat found beneath the skin. A 3-D biodegradable synthetic scaffold is then molded into the shape of the joint of the patient. It is then covered with the cartilage and implanted onto the arthritic joint surface. The process helps to alleviate pain from arthritis and might delay or remove the necessity for hip replacement surgery.

Utilizing gene therapy, the developers were able to place anti-inflammatory molecules in the hip to fend off arthritis reoccurrence. As inflammatory molecules rise, cartilage in joints can be destroyed leading to an increase in pain, which this gene therapy can help deter.

If a patient has inflammation, they can be given a simple drug activating the gene that has been implanted, to decrease the joint inflammation. The drug can be stopped at any moment, which will turn off the gene.

The scaffold is made utilizing a weave of about 600 biodegradable fiber bundles. The weaving pattern gives the scaffold the properties and structure that can be found in normal cartilage. The implants have the ability to load up to 10 times a person’s body weight.

Currently, customized implants are being tested in lab animals using the stem cell based tissue. If they are successful, we could see some devices ready for human testing in 3 to 5 years.

To view the original scientific study click below:
Anatomically shaped tissue-engineered cartilage with tunable and inducible anticytokine delivery for biological joint resurfacing

New Discovery For Hair Follicle Life and Death

Hair follicle cells divide and die. But a new study has discovered a single chemical called TGF-beta that determines when this happens. It could ultimately treat baldness and may speed wound healing. Since follicles are a stem cell source they have the unique capability to be able to turn into other types of cells. This stem cell adaptability creates a path for repair of tissues and organs that have been damaged.

Hair follicles are the one organ in the human body that automatically regenerate periodically without injury. Therefore, this was the ideal organ for the research team to study. They determined how TGF-beta, which is a type of protein, controls the division of hair follicles or orchestrates its death.

TGF-beta has two roles at play in the hair follicle. The first role is to divide and produce new life in the hair follicle and the second is that it helps orchestrate cell death. The team found that the amount of this chemical is what makes the difference in life or death of the hair follicle. A certain amount and the cell divides, but too much and it causes apoptosis, or death.

But the death of a hair follicle does not kill the stem cell reservoir. The cell eventually receives a signal to regenerate and then it divides, makes a new cell and a new follicle is developed. If the scientists can figure out how TGF-beta activates cell division through communicating with other distinct genes, there is the possibility to activate follicle stem cells and stimulate hair growth.

The researchers hope in the future they can precisely determine how the TGF-beta activates the cell to divide. It could potentially lead to a cure of baldness and a variety of other problems.

To view the original scientific study click below:
A probabilistic Boolean model on hair follicle cell fate regulation by TGF-B

Relational Memory Benefits From Sleep

While we sleep there are brain circuits and neuron learning connections that are active. They help us establish differences between items that are unrelated. The ability to remember indirect or arbitrary links between people, objects or events is called relational memory. This is what helps you put names with faces, find your keys or remember to turn off the stove before you leave the house.

It has been established that human and animal memory receives benefits from quality and sufficient sleep. New research is showing the hidden mechanisms that create or strengthen new relational memories while you sleep.

The researchers made an artificial model of 2 different areas of the brain. The cortical, which is involved in learning, memory and making decisions, and the thalamic, which has to do with prior sensory processing. The model simulated 2 major states of the brain. The first is awake, when the neurons are automatically optimized and active to generate sensory input. The second is deep sleep, when inherent oscillations of electrical activity is processed, such as waves that are slow.

The network model properties were able to be changed to generate transitions from asleep activity and awake activity comparable to brain activity every day.

In the region that is cortical, the neuron connections were able to become weaker or stronger dependent on their activity. This is called synaptic plasticity, and reflects the primary biological mechanism of the way memories are erased or formed.

The team modeled the cortex following visual processing, with one cortical layer which represented primary visual cortex and another layer which represented associative cortex. Each time one sees the exact object, the same neurons in the cortex that was visual was active. If someone sees two objects in the exact context, then these links might be learned in the cortex that is associative through strengthening connections between neurons that represent the two objects.

The team trained the network in the awake mode to determine direct links, such as A+B or B+C but not A+C, then found that in sleep, the model made indirect associations of A+C.

This occurred because during sleep the neurons which represented all three related items (A, B & C), automatically fired in close order that was temporal. This phenomenon is known as sleep replay and triggers synaptic plasticity and leads to the formation of powerful synaptic connections between all the neurons. This means that following sleep, activating any one of the groups such as A, activated all the other related groups – B and C.

The work is primarily conceptual, but the team states the work has implications that are real world. One that is important in the study is in informing studies of disease in the future – such as autism spectrum disorder and schizophrenia. Studies show that people who have these conditions do worse on relational memory tasks and also have sleep that is disrupted and that is slow wave.

The study has suggested the focus on improving sleep that is slow wave, which would alleviate some of the symptoms that are cognitive and associated with theses conditions, might be a more fruitful forward path rather than focusing exclusively on the cognitive symptoms.

The team notes that sleep quality and memory function do decline with the aging process, however current or even new technologies that augment sleep oscillations might help improve and protect functions of memory in the older population.

To view the original scientific study click below:
Role of Sleep in Formation of Relational Associative Memory

This Exercise Can Help Reduce Effects of Aging on Stem Cells

As we age, we lose muscle mass and the risk of dementia, heart disease, and immune function decreases. As the years go by, it becomes more difficult for humans to rebound from injury, a workout or illness. Aging takes a big toll on muscle tissue. Scientists have discovered that one type of activity in particular puts this process in reverse.

Exercise that is consistent can help slow down the process of degeneration. According to a new study on mice, aerobic exercise may have the ability to reverse aging’s effect on muscle stem cells that are essential in the involvement of tissue regeneration.

Translating the study that was done on mice to people, it means that cycling, swimming and other aerobic exercises can help the older population recover as efficiently and quickly as their once younger selves. In the future, this discovery could help contribute to the development of a drug that de-ages muscle stem cells.

Researchers have been aware for a long time that exercise does help promote lifespan which gives people extra years free from disease.

This new discovery is very different. It is somewhat like a person who has already acquired diseases through aging, reversing the process.

The research has suggested that aerobic exercise can cause cells that are old to start behaving and gaining attributes of young cells. In the study, the team used old and young mice and had them run on a wheel for 3 weeks. Using a variety of tests, they analyzed how the mouse’s stem cells and tissue that are muscle responded. They compared the mice that were running to a group that were non-exercising with a stationary wheel that was locked restricting their ability to run.

Within one week, both old and young mice with the wheels that were running were able to establish a routine. They ran about 4.9 and 10 kilometers per night, respectively.

The equivalent to humans from the mice on the running wheel would be similar to consistent aerobic exercise such as cycling, running, and swimming, but no weight lifting or strength training involved.

At the end of the three week period of voluntary running on the wheel, the mice were then relocated to cages that didn’t have wheels. Then, the team injured various muscles and than looked at whether the mice could rebuild the tissue that was injured.

They additionally transplanted muscle stem cells from older mice into the injured mice and observed if the cells functioned well. Compared to young donor muscle stem cells, old donor muscle stem cells formed fewer and smaller fibers in the mice that were injured. However, old muscle stem cells from mice that exercised performed much like young muscle stem cells and formed many fibers than old muscle stem cells and were non-exercising.

Overall, the older mice that were allowed to exercise experienced accelerated repair of muscle tissue and improvement of the function of the muscle stem cells.

The older mice that were active did not produce more stem cells that are muscle. Instead, exercising had a rejuvenating effect on the old cells. The team noted it helped the mice operate more like their once younger selves.

The benefits did disappear after one week after the mice were put in cages without wheels which suggests that the rejuvenating effect is consistent exercise. This indicates that voluntary aerobic exercise may have benefits that are above and beyond preventing age related diseases and may really improve function of tissue directly.

The idea is that the older humans would recover more efficiently and faster just like younger humans do as a response to injury.

The team notes that surprisingly the younger mice who ran on the wheel did not experience muscle repair that was improved. This puzzled the team. Its seems young mice have already plateaued. They will lose function with age and they can get back to that baseline, but it is hard to get them better with more exercise.

The effects of exercise on stem cells that are muscle and repair of tissue is dependent on a tiny protein known as cyclin D1. Voluntary aerobic exercise was able to restore cyclin D1 levels in stem cells that were dormant back to a more youthful state.

Discovering cyclin D1’s crucial role means scientists might be able to target the protein therapeutically or even develop a new drug with the ability to create these positive de-aging effects. However, before any prescribed exercise routine or anti-aging pill can be verified, research on humans needs to be done.

To view the original scientific study click below:
Exercise rejuvenates quiescent skeletal muscle stem cells in old mice through restoration of Cyclin D1

Immune System and Intestinal Flora Balance

There are trillions of benign bacteria that live in our intestines. The immune system keeps them in constant balance which in turn ensures they are harmless to humans. A team has been able to demonstrate how some natural antibodies keep them in check. Their discoveries could make a substantial contribution to developing superior vaccines.

The bacteria that live in the intestine comprise from 500 to 1000 different species. They are known as intestinal flora which play a key role in the digestive process and also preventing infections. They are not like pathogens which invade the body from the outside. The body’s immune system tolerates them and, therefore, they are harmless.

It is unknown how the immune system is able to maintain this very delicate balance. But it is known that IgA or type A immunoglobulins play a significant role. These substances naturally defend parts of the immune system and will recognize an exogenous pathogen.

The researchers recently have shown that IgA antibodies from a mouse model specifically will limit the fitness of any benign bacteria at a variety of levels. This will enable the immune system to tweak the microbial balance in the intestines and successfully demonstrates that the immune system will recognize and specifically restrict these bacteria.

The most common antibodies in the immune system are IgA antibodies and are secreted by special cells in the mucous membranes. They make up about 65% of human immunoglobulins. Interestingly, most IgA antibodies that are produced by the body are directed towards benign bacteria found in the intestinal flora. By not having this immune protection these microorganisms could have a negative effect on a person’s health and cause diseases of the intestines. It has remained unsolved however, the way IgA antibodies regulate the consensual coexistence in the intestines.

Until now, studying IgA antibodies found in their natural form in mouse models was not possible. In the team’s experiment, they were able to conquer this hurdle. They were able to succeed in producing sufficient amounts of IgA antibodies specifically administered against a type of Escherichia Colo Bacteria which is a typical bacterium in the intestine. The antibodies were able to recognize and bound a building block on the microorganism’s membrane.

They succeeded in tracking the in-viva and the in-vitro effect in germ free mouse intestines with exact accuracy. The antibodies affected the fitness of the bacteria in a variety of ways. For example, the mobility of the bacteria was restricted or they were able to hinder the uptake of sugar building blocks for the bacteria’s metabolism. This signifies that the immune system is able to influence the benign bacteria through a variety of approaches on a simultaneous basis or IgA parallelism.

Why the immune system is able to achieve an equilibrium with the benign bacteria while also being able to destroy pathogenic invaders seems to have been conclusively clarified. The experiment shows that IgA antibodies can fine-tune the balance between the intestinal flora and the human organism.

The discoveries do not only build on some of the basic understanding of the intestine’s immune system, they can help contribute to developing vaccines. Through understanding where and how antibodies recognize intestinal microorganisms will also help in developing vaccines against pathogenic organisms on a more accurate basis.

To view the original scientific study click below:
Parallelism of intestinal secretory IgA shapes functional microbial fitness

Immune Aging Accelerated By Stress

A new study demonstrates that stress from things like job strain, traumatic events, discrimination, and everyday occurrences can accelerate immune system aging. This can possibly increase people’s chances of cardiovascular disease, cancer and illness due to infections. The study could offer an explanation in disparities in health that are age related which include the diverse toll of the COVID-19 pandemic and determine possible avenues for intervention.

Because the worldwide population of aging people is increasing, the understanding of disparities in health that are age related is essential. The study helps to identify mechanisms connected to immune aging that is accelerated.

As we age, our immune system will naturally start a dramatic downturn which is a condition known as immunosenescence. As advanced age occurs, a person’s immune system will weaken and include many white blood cells that are not circulating and not enough that are naive and can take on new invaders.

The aging of the immune system is linked not only to cancer, but also with a heightened risk of cardiovascular disease, pneumonia, and reduced efficacy of aging organs.

The team wanted to see if they might be able to coax out a link between a life long exposure to stress, which is a known precursor to health that is poor, and declining intensity of the immune system.

They cross referenced and queried an enormous amount of data sets from the Univ. of Michigan and Retirement Study, which was a national study of the status of health, economic, marital and family position, and private and public support systems of Americans that were older.

To determine exposure to a variety of social stressors, the team studied answers from a national sampling of 5,744 individuals over age 50. A questionnaire was designed for the participants to answer that assessed respondents experiences with social stress that included chronic stress, life events that are stressful, ongoing discrimination and everyday discrimination.

Samples of blood from the participants were then analyzed through flow cytometry, a lab technique that classifies and counts blood cells as they flow one by one in a narrow stream by a laser.

As was expected, participants with a high stress score had older immune profiles with a lower percentage of disease fighters and a high percentage of white blood cells that were worn out. The association between stressful life events and fewer, ready to respond T cells, continued to be strong even following controlling of smoking, education, BMI, race, drinking and ethnicity.

T cells are critical components of immunity develop in the thymus gland, which is in front and above the heart. As we age, the tissue in the thymus gland diminshes and is replaced by fatty tissue which results in decreased production of immune cells. Earlier research has suggested that this process is sped up by lifestyle factors like low exercise, poor diet, which are both linked with social stress.

In the study, after the team statistically controlled for low exercise and poor diet, the association between stress and increased immune aging wasn’t as strong. This means people who go through more stress have poor exercise and diet habits, which partly explains why they have increased aging. Improving exercise and diet habits in older people might help counteract the immune aging linked with stress.

Also, CMV (cytomegaloovirus) may be a point for intervention. It is usually asymptomatic and a common virus in people and is known to have a powerful effect on increased immune aging. Similar to cold sores and shingles, CMV is mostly dormant but can occur when a person experiences high stress.

In the study, statistically controlling CMV positivity also decreased the link between accelerated immune aging and stress.

To view the original scientific study click below:
Social stressors associated with age-related T lymphocyte percentages in older US adults: Evidence from the US Health and Retirement Study

Researchers Can Identify What You Are Eating

Researchers have developed a new method called untargeted metabolomics that identifies the large number of molecules that come from our food. Most of these molecules appear in our blood and stool and had previously been unknown. This method can provide a direct way to detect hundreds of thousands of molecules that may now be used to make a diet profile of individuals and provide clues as to health outcomes.

The scientists consisted of an international team that were able to match all metabolism products in a specimen to a vast database of samples. Where available, they used chemical inventories to provide a remarkable catalog of the signatures of molecules created by eating food or by processing in the gut.

The ability to determine how what we consume translates into byproducts and products of metabolism has important implications for the health of humans. The approach can be be used to get diet information scientifically and to understand the relationships to outcomes in the clinic. It is possible to link molecules in the diet to outcomes of health not per occurrence, but all at once which has previously not been possible.

Metabolomics consists of the comprehensive measuring of all the metabolites in a specimen that are biological. Metabolites are substances that are typically small molecules used or made when an organism breaks down drugs, food, and chemicals in the tissues. They are metabolism byproducts. In addition, the research used a relevant technique called metagenomics, which measures genetic material in samples that are biological and characterize microbes that are present.

Currently metabolomics research identifies only 10% of molecular features in specimen samples leaving 90% of the material to be unknown. The novel approach uses RDD, which is reference data driven analysis to match data from metabolomics that has been obtained from tandem mass spectrometry or MS/MS. This is an analytical tool which measures molecular weight utilizing two analyzers opposed to one against metadata annotated data that is a pseudo MS/MS reference library.

Eventually, every molecule is left without its electrons to charge it. The ion that is charged is weighted utilizing a scale that is very sensitive, then shattered into pieces and these pieces are weighed which creates a fingerprint that is unique for every molecule. These pieces of fragmentation spectra can be matched between the analyzed sample and a reference database. However, it has been a very challenging process until now.

This new research investigated thousands of foods that were assembled by people around the globe from an initiative launched 7 years ago by US San Diego called Global FoodOmics. The team has increased their data output more than five fold over techniques that were conventional. More notable was the new method allowed the untargeted metabbolomics to be utilized to infer the diet based on blood or stool samples.

It truly shows how crucial getting both clinical samples from people around the globe and food specimens are to be able to determine how microbes and molecules work together in order to degrade or improve health based on the foods we eat.

The study additionally suggests the way towards using RDD to explain the dark matter found in our metabolome. Not only in terms of the foods we eat, but in exposures to chemicals found in the clothes we wear, the medications taken, the beauty products we use and the environments people are exposed to. It will substantially help the team explore chemical connections throughout our world and ourselves.

To view the original scientific study click below:
Enhancing untargeted metabolomics using metadata-based source annotation