Autoimmune kidney disease

Monash researchers have solved a mystery, revealing how certain immune cells work together to instigate autoimmune kidney disease.The study, led by Professor Michael Hickey and Professor Richard Kitching from Monash University's Centre for Inflammatory Diseases. In glomerulonephritis, an immune disease of the kidney, rogue immune cells damage the kidney via a misdirected inflammatory attack.

Special cells called monocytes continuously patrol the glomeruli by crawling within its blood vessels. Monocytes are very good at 'picking up and removing rubbish' and being on the lookout for signs of infection and tissue injury. However in autoimmunity, some immune cells in the circulation are highly reactive to molecules picked up in the kidney.

Patrolling monocytes can display these molecules to the reactive immune cells in the bloodstream, resulting in the rogue cells remaining in the kidney and turning on an unnecessary and damaging inflammatory attack. This autoimmune damage to the kidney can severely impact on the normal function of the kidney, if left untreated.

 This damage occurs while the cells are moving around in the kidney blood vessels. This process, known as intravascular antigen recognition, has never been described before for the key helper T cells that direct and control the immune response.
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Exercise changes gut microbiota

What we eat affects the microbes that live in our intestine, collectively known as the gut microbiota. According to two new studies, however, exercise has the same effect. Two new studies suggest that exercise independent of diet can alter the composition of gut microbiota. In mouse and human experiments, researchers discovered that physical activity independent of diet alters the composition of gut microbiota in a way that increases the production of short-chain fatty acids (SCFAs) that are beneficial for health.

The diversity of gut bacteria can be modified through exercise alone. The study included three groups of mice: one group of mice was sedentary, the other group had access to a running wheel (the exercise group), while the remaining group was sedentary and germ-free, meaning that they did not possess any gut microbiota due to being bred in a sterile environment.

The researchers took fecal material from both the exercise and sedentary groups and transplanted it into the colons of the germ-free mice. Exercise increased beneficial gut microbes
As a result of fecal transplantation, the previously germ-free mice developed gut microbiota that had comparable composition to their donor groups.

The germ-free mice that received fecal material from the exercise group had higher levels of gut microbes that produce an SCFA called butyrate, which is known to reduce inflammation and promote gut health. Additionally, when these mice were given a chemical that triggers colitis, or inflammation of the colon, the researchers witnessed a surprising response. There was a reduction in inflammation and an increase in the regenerative molecules that promote a faster recovery.

Exercise-induced modifications in the gut microbiota can mediate host-microbial interactions with potentially beneficial outcomes for the host.
Researchers included 32 sedentary adults, of whom 18 were lean and 14 were obese. The participants took part in a supervised exercise program, which involved 30–60 minutes of endurance exercise, 3 days per week, for a total of 6 weeks. Once the 6-week exercise program ceased, subjects were asked to revert to sedentary behavior for 6 weeks.

Fecal samples were obtained from each participant before and after the exercise training program, and before and after the 6-week sedentary period.
Throughout the study period, subjects continued with their usual diets.
The researchers found that all participants experienced an increase in SCFA levels especially butyrate, following the 6-week exercise program, but these levels declined when subjects reverted to sedentary behavior.

With the help of genetic testing, the researchers found that the increase in SCFA levels correlated with alterations in the levels of gut microbes that produce SCFAs, including butyrate.
The greatest increases in SCFA-producing gut microbes after exercise, the team reports, noting that their levels were much lower at baseline. Subjects who were obese experienced "modest" increases in gut microbes that produce SCFAs.
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Women are more fit than men

Women can process oxygen more quickly than men during exercise. Quick oxygen uptake places less strain on the body's cells and is considered an important measure of aerobic fitness.

The study compared oxygen uptake and muscle oxygen extraction between young men and women of similar age and weight during treadmill exercise. Women consistently outperformed men with around 30 per cent faster oxygen handling throughout the body.

Researchers discovered that women's muscles extract oxygen from the blood faster, which, scientifically speaking, indicates a superior aerobic system.
By processing oxygen faster, women are less likely to accumulate molecules linked with muscle fatigue, effort perception and poor athletic performance.
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RNA modification and brain development

A chemical tag added to RNA during embryonic development regulates how the early brain grows, when this development goes wrong, it may cause psychiatric disorders in people. Researchers used animal models and mini-brains, made from human stem cells to relate their findings to conditions found in people.

Researchers have discovered chemical modifications to messenger RNA mRNA across the genome at certain sites and found that these changes are dynamic- a specific chemical group is added and taken off by enzymes in a regular, pattern. The chemical group studied in the Cell paper, m6A, is the most prevalent modification to mRNA in human cells.

The current thinking is that a tightly controlled molecular process guides the complicated development of the brain before birth and the process relies on a precise sequence of genes being turned on and off. However, even subtle mistakes in this process can become serious issue. The classic view of this control is that DNA codes for RNA, guiding which proteins will be made by cells. However, mRNA can be modified along the way so that it can produce proteins with many variations.

A new field called epitranscriptomics was discovered during the research. The Cell paper is the first study of epitranscriptomics in the embryonic mammalian brain, and the key is m6A, a marker for molecules bound for disposal within the cell. Normally, m6A-tagged mRNAs are related to such processes as cell replication and neuron differentiation, and m6A-tagging promotes their decay after they are no longer needed.

If m6A is not added on the correct time schedule to a garbage-bound molecule, the developmental train goes down the wrong tracks because developing brain cells get stuck at an earlier stage because the m6A cues for taking out the cellular trash are misread or not read at all. The researchers found that in a mouse model with depleted m6A, cell replication is prolonged, so that stem-cell differentiation, which normally reels out daughter cells in an orderly fashion, gets stuck. The knockout mouse develops less brain cells such as neurons and glia cells, and therefore has abnormal circuitry and a non-functioning brain.

Neuron development in the mini-brains that was developed is similar to what happens in people, modeling fetal brain development up to the second trimester. Human stem cells had a greater number of m6A tags compared to mouse cells. Many of the genes associated with genetic risk for certain conditions, such as schizophrenia and autism spectrum disorder, are only m6A-tagged in humans, not in mice, raising the possibility that dysregulation at this level of gene expression may contribute to certain human brain disorders.
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New molecules may prevent stroke and neurodegenerative diseases

Researchers have discovered a new class of molecules in the brain that synchronize cell-to-cell communication and immune activity in response to injury or diseases. Elovanoids ELVs are bioactive chemical messengers made from omega-3 very long chain polyunsaturated fatty acids VLC-PUFAs,n-3. They are released on demand when cells are damaged or stressed.

Working in neuronal cell cultures from the cerebral cortex and from the hippocampus and a model of ischemic stroke, the researchers found that elovanoids not only protected neuronal cells and promoted their survival, but maintained their integrity and stability.

This can proffer solution in the understanding of how the complexity and resiliency of the brain are sustained when confronted with adversities such as stroke, Parkinson's or Alzheimer's and neuroprotection signaling needs to be activated and how neurons communicate among themselves.

These novel molecules participate in communicating messages to overall synaptic organization to ensure an accurate flow of information through neuronal circuits. We know how neurons make synaptic connections with other neurons, however these connections have to be malleable to change strength appropriately.

Elovanoids might play a central role as synaptic organizers, especially important in conditions resulting from synaptic dysfunction such as autism or amyotropic lateral sclerosis, for which there is no therapeutic solutions.

The researchers discovered the structure and characteristics of two elovanoids - ELV-N32 and ELV-N34 - in the brain. Starting with neuron cell cultures and then an experimental model of stroke, they found that elovanoids were activated when cells underwent either oxygen deprivation or excitotoxicity - early events associated with stroke, epilepsy, Parkinson's, traumatic brain injury and other neurodegenerative diseases.

They determined the concentrations and therapeutic windows at which elovanoids conferred neuroprotection. They discovered that elovanoids overcame the damaging effects and toxicity of these early events. In the stroke model, elovanoids reduced the size of the damaged brain area, initiated repair mechanisms and improved neurological recovery.
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Tension strengthens the heart

Depleted heart tissue regenerates itself in a wave in zebrafish led by a front of fast-moving, supersized cells and trailed by smaller cells that multiply to produce others. The nature of this wavefront and the success of the tissue regeneration that follows is determined by mechanical tension that acts upon the cells.

Manipulating the mechanical tension of the cells may develop new translational approaches. Human heart can not fully heal itself after a heart attack but the zebrafish heart can easily replace cells lost to damage or disease.

The researchers measured a number of properties of the cells in the regenerative wavefront. They discovered that the bigger leader cells migrated across the surface of the heart at higher speeds than the smaller follower cells.

When they measured the levels of tension experienced by the cells, they found that leader cells recoiled faster than follower cells when tiny incisions were applied, much like the surface of an inflated balloon retracts after bursting. The mechanical tension seems to keep the cells from dividing after DNA replication.

The researchers plan to use the zebrafish heart explant culture system to screen for small molecules that could potentially increase the regenerative capacity of heart tissues. Such chemicals could form the basis for new drugs to repair the damage caused by a heart attack or other cardiovascular diseases.

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Stress hormone reduced the effectiveness of cancer treatment

Stress reduction therapy is very important for cancer patients, stress hormones during treatment can prevent the cancerous cells in the body from dividing and reacting.

These hormones prevent the growing tumors from being treated by the cancer drugs that are used for the patients. Stress reduction therapy is essential during cancer treatment to promote the success of the drugs and cancer treatment.

Chemotherapy method of cancer treatment targets rapidly dividing cells, cells exposed to stress hormones such as cortisol and norepinephrine generate destructive DNA damaging free radicals molecules.

This causes the cells temporarily to stop their relentless cell division as DNA repair mechanisms starts and protects the tumors from the lethal effects of chemotherapy.

Stressed mice with breast cancer produced higher levels of a nitric oxide-generating enzyme iNOS in their tumors. Greater iNOS activity leads to more aggressive breast cancer.
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Foods determined human gut germs

What you eat regularly or don't eat determined the germs in your digestive tract. Many microbial species exist in the human intestine, digest fiber, make vitamins and other molecules. They also strengthen the immune system and protect against harmful bacteria.

Antibiotics, cesarean sections and other lifestyle changes have also changed the composition of microbes in the human gut. People that are eating meat, berries, fruits and vegetables have gut bacteria different and more diverse than the gut bacteria of those that eat processed foods. What we eat can change the balance of microbes in our digestive tracts

Different gut microbes changes with the seasons and diet. Human microbiota can change significantly from day to day, or within hours, in response to what we have been eating.

Foods can increase the populations of some types of bacteria and reduce others, as their relative numbers change, they secrete different substances, activate different genes and absorb different nutrients.
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Cholesterol crystal are signs of impending heart attack

According to the latest research by cardiologist, cholesterol crystals are responsible for obstructing the coronary arteries of patients who had suffered a heart attack.

These crystals are released from plaque that can build up in the heart and is often made up of fat, calcium and other substances. When this material hardens over time in the arteries, it's known as atherosclerosis.

When cholesterol goes from a liquid to a solid, or crystal state, it expands in volume. This expansion inside the wall of the artery can tear it and block blood flow resulting into a heart attack or stroke.

Researchers discovered clusters of large crystals in the arteries of patients suffering from heart attack, this crystals are released into the heart and it damaged the heart by blocking blood flow.

Cholesterol crystals activated the production of inflammation molecules, known as Interleukin-1 beta, which inflame coronary arteries. The use of statin drugs can lower cholesterol. Canakinumab drug can also block the Interleukin-1 beta inflammation molecule and reduce the chances of a cardiac event.

 Controlling cholesterol by eating a healthy diet, engaging in exercise and taking statin medications as recommended could prevent crystals from forming and reduce the risk of heart attack.
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Triclocarbon in soaps can affects fetus lipid metabolism

Lipids are naturally occurring molecules that includes fats, waxes, fat-soluble vitamins, monoglycerides, diglycerides and triglycerides. Lipids stored energy and signal and act as structural components of cell membranes.

Triclocarban TCC is an antibacterial agent in daily care products like soaps and toothpaste. Exposure to TCC through the use of daily care products can affect fetus proper formation. This can cause irreversible changes to the developing fetuses.

 Researchers injected TCC laced with carbon-14 to trace how the contaminant distributed in organ systems of female mice and exposed offspring.
 Using accelerator mass spectrometry AMS. AMS fills a special niche in the biomedical field because it can measure very low concentrations of compounds with extreme accuracy and track bio-distribution and excretion over long periods of time.

This showed that TCC effectively transfer from mother to offspring through placenta and breastfeeding.
 Exposure to TCC during development may pose a health risk to the developing fetuses because they are more sensitive to alterations in hormone levels, which may leads to an irrelevant changes. TCC-related compounds were detected in the tissues of offspring with significantly higher concentrations in the brain, heart and fat.

Quantitative real-time polymerase chain reaction qPCR was used in the study to examine changes in gene expression in liver and adipose tissue in the exposed offspring. The results showed alterations in genes involved in lipid metabolism in exposed female offspring were consistent with the observed increase in fat weights and hepatic triglycerides. Exposed offspring were heavier in weight than unexposed.
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Early signs of cancer

Scientists have discovered how damage to the cell's genetic material can trigger inflammation. Cancerous cells are similar to other cells at early stage, so that they can be removed as part of the body's natural surveillance systems before tumours form.

A key molecule called cGAS is known to bind DNA, triggering inflammation.
When damage occurs, fragments of DNA can get separated from the nucleus and form structures micronuclei.

 cGAS can penetrate these micronuclei and bind to DNA, creating mechanisms that lead to inflammation. DNA damage is one of the early steps in the development of cancer.

Detection of micronuclei by cGAS could be an important early signal to the human body to detect and remove potentially cancerous cells.

Autoinflammatory diseases- when the immune system attacks the body's own tissues can also be an early sign of cancer, this could trigger an inflammatory diseases.
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Carpolobia lutea plant may be effective for treating Alzheimer’s disease

Carpolobia lutea is a small shrub found in Central and West Africa. Scientific studies have shown that Carpolobia lutea plant has antimicrobial, anti-inflammatory and analgesic properties.

The plant was effective in preventing the breakdown of acetylcholine when tested. At higher concentrations, its extract prevents acetylcholine breakdown than Ezerine drug, lowers free radicals and harmful molecules that damage brain cells.

Alzheimer’s patients experienced reduction in neurotransmitter acetylcholine leading to problems with memory and attention.

Carpolobia lutea plant could protect chemical messengers in the brain, reduces levels of free radicals and harmful molecules that destroy brain cells. It's extract could be used to produce new drugs for treating Alzheimer’s disease because of its anti-inflammatory properties.
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Cinnamon may reduce damage of high-fat diet

Cinnamon may lessen the risk of cardiovascular damage of a high-fat diet by enabling the body's antioxidant and anti-inflammatory systems and slowing the fat-storing process.

Researchers fed rats cinnamon supplements for 12 weeks along with a high-fat diet. They discovered that rats
weighed less and had less belly fat and healthier levels of sugar, insulin and fat in their blood, compared to rats that did not receive cinnamon with their high-fat foods.

Rats fed with cinnamon also had fewer molecules involved in the body's fat-storing process and more antioxidant and anti-inflammatory molecules that protect the body from the damages of stress. This shows that cinnamon may reduce the effects of a high-fat diet.