E-cigarettes flavours are toxic

Sugar and spice are not healthy when it comes to vaping or inhalation. Exposure to e-cigarette flavoring chemicals and liquids can cause significant inflammation to monocytes, a type of white blood cell and many flavoring compounds are also toxic, with cinnamon, vanilla and buttery flavors among the worst. That's the finding of new research published in open-access journal
Frontiers in Physiology, which also found that mixing e-cigarette flavors has a much worse effect than exposure to just one.

The use of e-cigarettes has exploded in the past decade as traditional cigarette consumption has declined. Vaping exposes the lungs to flavoring chemicals when the e-liquids are heated and inhaled. Since the flavoring chemicals are considered safe to eat, e-cigarettes are often considered and advertised as a healthier alternative to traditional cigarettes.

This new study, led by researchers at the University of Rochester Medical Centre in the United States, wanted to test the assumption that vaping nicotine-free flavored e-liquids is safer than smoking conventional cigarettes. Previous studies show that flavors used in e-cigarettes cause inflammatory and oxidative stress responses in lung cells.

Users of e-cigarettes also show increased levels oxidative stress markers in the blood compared to non-smokers. The new study extends this to assess the effects of commonly used flavoring chemicals, as well as e-liquids without nicotine, directly on immune cells-a type of white blood cell called monocytes.

Exposure to the e-cigarette flavoring chemicals and e-liquids led to higher production of two well-established biomarkers for inflammation and tissue damage mediated by oxidative stress. Furthermore, many of the flavoring chemicals caused significant cell death with some flavors being more toxic than others.
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Selenium protects interneurons in the brain

A team led by Dr. Marcus Conrad, research group leader at the Institute of Developmental Genetics (IDG) at Helmholtz Zentrum München, showed for the first time why selenium is a limiting factor for mammals. The scientists have been investigating for years the processes of a novel type of cell death, known as ferroptosis. The enzyme GPX4, which normally contains selenium in the form of the amino acid selenocysteine, plays an important role.

In order to better understand the role of GPX4 in this death process, they established and studied mouse models in which the enzyme was modified.In one of these models, they observed that mice with a replacement of selenium to sulfur in GPX4 did not survive for longer than three weeks due to neurological complications.

In their search for the underlying reasons, the researchers identified a distinct subpopulation of specialized neurons in the brain, which were absent when selenium-containing GPX4 was lacking.
Furthermore, the scientists were able to show that ferroptosis is triggered by oxidative stress, which is known to occur for instance during high metabolic activity of cells and high neuronal activity.

 Selenium-containing GPX4 protects these specialized neurons from oxidative stress and from ferroptotic cell death. Selenoenzymes are essential in some organisms, including mammals, whereas they are dispensable in other organisms, such as fungi and higher plants.
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Effects of obesity on bone marrow cells

According to new research, obesity causes durable and harmful changes to the hematopoietic stem cell compartment-the blood-making factory in human body. Blood stem cell compartment is made up of numerous cell subsets, age and environmental stresses can lessen the healthy diversity of cells in human blood-making machinery. This can include skewing blood cell formation toward myeloid cells and possibly promoting pre-leukemic fates.

Obesity related stresses alter the cellular architecture of the hematopoietic stem cell compartment and reduce its long-term functional fitness. Tests in obese mice show these effects are progressive and that some of the harmful manifestations persist even after researchers normalize the animals' weight through dietary controls. Alterations of the body's blood-making system appear to be linked to over- expression of a transcription factor called Gfi1- a regulatory gene that controls other genes. The researchers show that oxidative stresses in the body caused by obesity drive overexpression of Gfi1.

 This produces a lasting alteration of hematopoietic stem cell compartment and molecular mayhem. The study also provides groundwork to investigate how lifestyle choices, such as diet, can durably impact blood formation and may contribute to the development of blood cancer. Hematopoietic stem cells are an important tool for treating leukemia and other blood diseases.
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Gene expression for youthful skin

Some individuals' skin appears more youthful than their chronologic age. Although many people try to achieve this with creams, lotions, injections, and surgeries, new research indicates that increased expression of certain genes may be the key to intrinsically younger looking and younger behaving skin. It's not just the genes you are born with, but which ones turn on and off over time,wide range of processes in the skin affected by aging, and specific gene expression patterns in women who appear younger than their chronologic age.

Reseachers collected and integrated data at the molecular, cellular, and tissue levels from the sun-exposed skin (face and forearm) and sun-protected skin (buttocks) of  white women between 20 to 70 years. As part of the study, the team looked for gene expression patterns common in women who appeared years younger than their chronologic age.The physical appearance of facial skin was captured through digital images and analysis. Skin samples were processed for analysis and saliva samples were collected for genotyping.

The analyses revealed progressive changes from the 20s to the 70s in pathways related to oxidative stress , energy metabolism, senescence (aging) and skin barrier. These changes were accelerated in the 60s and 70s. Comparing sun-exposed and sun-protected skin samples revealed that certain genetic changes are likely due to photoaging. The gene expression patterns from the women in the study who were younger appearing were similar to those in women who were actually younger in age. These women had increased activity in genes associated with basic biologic processes, including DNA repair, cell replication, response to oxidative stress, and protein metabolism.

Women with exceptionally youthful-appearing facial skin in older age groups also had higher expression of genes associated with mitochondrial structure and metabolism, overall epidermal structure, and barrier function in their facial epidermal samples, as well as dermal matrix production.A better understanding of the genes associated with youthful-appearing skin may point to new strategies to enhance factors that slow the skin's aging process. This work also confirmed that ultraviolent (UV) exposure is a main driver and accelerator of skin aging.
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Brain oxidative stress can cause migraine

Migraine are an integrated mechanism by which the brain protects and repairs itself. Migraine can be triggered by diet, stress, sleep disruption, noise and air pollution. It can increase brain oxidative stress, an imbalance between the production of free radicals and the ability of the body to counteract their harmful effects.

Oxidative stress is a useful signal of impending harm because a number of unfavorable conditions in the brain can give rise to it, targeting oxidative stress might prevent or preempt migraines. An interruption in blood supply each of the components is protective: strengthening antioxidant defenses, lowering the production of oxidants, lowering energy requirements and, especially, releasing growth factors into the brain that protect existing neurons and support the birth and development of new neurons.

There are feedback loops between these components of a migraine attack that tie them together into an integrated system, migraine attacks are not triggered by oxidative stress, they actively protect and repair the brain from it. The pain, nausea, and sensitivity to light and sound, fever and pain, or cough are not the disease itself but part of the body's defense against migraine.
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E-cigarette with nicotine changes adrenaline in nonsmokers heart

Healthy nonsmokers experienced increased adrenaline levels in their heart after taking one electronic cigarette with nicotine but there were no increased adrenaline levels when the study subjects used a nicotine-free or empty e-cigarette.

Unlike cigarettes, e-cigarette have no combustion or tobacco. Instead, these electronic, handheld devices deliver nicotine with flavoring and other chemicals in a vapor instead of smoke.
E-cigarettes produce fewer carcinogens than tar of tobacco cigarette smoke, they also produce nicotine.

E-cigarette users have elevated sympathetic nerve activity which increases adrenaline directed to the heart and are more susceptible to oxidative stress. Researchers used heart rate variability obtained from a prolonged, non-invasive heart rhythm recording. Heart rate variability is calculated from the degree of variability in the time between heartbeats.

This variability may be indicative of the amount of adrenaline on the heart.
heart rate variability test to link increased adrenaline activity in the heart with increased cardiac risk. People with known heart disease and people without known heart disease who have this pattern of high adrenaline levels in the heart have increased risk of death.

In the first study to separate the nicotine from the non-nicotine components when looking at the heart impact of e-cigarettes on humans, researchers studied healthy adults who were not smoking. Researchers measured cardiac adrenaline activity by assessing heart rate variability and oxidative stress in blood samples by measuring the enzyme plasma paraoxonase PON1.

They discovered that exposure to e-cigarettes with nicotine, but not e-cigarettes without nicotine, led to increased adrenaline levels to the heart, as indicated by abnormal heart rate variability. Acute electronic cigarette use with nicotine increases cardiac adrenaline levels. And it's in the same pattern that is associated with increased cardiac risk in patients who have known cardiac disease and even in patients without known cardiac disease.
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Cocoa may delay Type 2 diabetes

Insulin is the hormone that manages glucose, the blood sugar that reaches unhealthy levels in diabetes patients is caused by insulin not working properly.

Failure of beta cells to produce insulin can leads to diabetes, the body of diabetes patients either doesn't produce enough insulin or doesn't process blood sugar properly.

Researchers have discovered certain compounds in cocoa that can aid the release of more insulin and respond to increased blood glucose. Beta cells work better and remain stronger with an increased presence of epicatechin monomers, compounds found in cocoa.

Researchers fed animals with the cocoa compound, they discovered that adding the compound to their diet decreases the level of obesity in the animals and increases their ability to regulate increased blood glucose levels.

This showed that cocoa compounds called epicatechin monomers enhanced beta cells' ability to secrete insulin by protecting the cells and increase their ability to deal with oxidative stress.

The epicatechin monomers are making the mitochondria in the beta cells stronger, which produces more ATP which leads to more production of insulin.
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