Your handwriting can reveal your personality traits, as it comes through the central nervous system, says a new study.
Your handwriting can tell if you have a personality similar to Isaac Newton or Queen Victoria, say scientists who have decoded character traits of some of Britain’s most famous names by decoding their writing style. Researchers from Royal Mail in the UK along with Tracey Trussell, a leading handwriting analyst studied letters and notes from UK’s defining figures such as Rosalind Franklin, Isaac Newton, Queen Victoria, Florence Nightingale, Millicent Fawcett, Charles Darwin and Elizabeth Fry.
The subjects were chosen as they were all keen letter writers and appeared in the 100 Greatest Britons or 100 Great Black Britons lists. “Handwriting is like ‘brain writing’ because it comes through the central nervous system. It’s a snapshot in time,” said Tracey Trussell, handwriting analyst in the UK.
Slant is an emotional barometer that measures people’s social stance. A marked right slant such as that in the writing style of Queen Victoria and Issac Newton indicates that a person is enthusiastic, responsive and that they do not want to hold back and tend to be highly proactive.
Writing consists of three zones — upper, middle and lower. The upper zone focuses on the parts of the letters that extend up wards like b, d, f, h and k, researchers said. People with a large and dominant upper zone have rich imaginations, creative mindsets and big aspirations. They are also intellectually savvy, ethical and have high standards, like Claudia Jones, Ignatius Sancho and Charles Darwin, researchers said.
A person with long and high t-bars is a take-charge sort of person, like Queen Victoria and feminist leader Millicent Fawcett. They are decision makers and perfectionists, they said. Narrow or non-existent right margin is when the end of a sentence leaves no space on the right hand side of the page. Words appear to fall off the edge of the page or dip down like in the cases of Isaac Newton and Charles Darwin. The size of the right hand margin shows the writer’s real feelings towards the future. Those that leave no right margin are outgoing and engaging. They are also impulsive, goal-orientated and driven, researchers said.
A noticeably large (or inflated) letter ‘k’ shows people who are resourceful and defiant like Charles Darwin, Ignatius Sancho and Claudia Jones. They like to get their own way and follow their own path in life, researchers said. “It is amazing to think that something we do every day can reveal so much about us,” said David Gold from Royal Mail — a postal and delivery provider service.
Fabric softener ads often portray an image of comfort, freshness and sweetness. Yet most fabric softeners contain a grim list of known toxins which can enter your body through the skin and by inhalation, causing a wide range of health problems, particularly for young children.
Here are some of the harmful ingredients commonly found in liquid or sheet fabric softeners include:
• Chloroform: This substance was used as an anesthesia in the 1800s up through the early 1900s when its potential for causing fatal cardiac arrhythmia was discovered. A carcinogenic neurotoxin, it is on the EPA’s Hazardous Waste list. Inhaling its vapors may cause loss of consciousness, nausea, headache, vomiting, and/or dizziness, drowsiness. It may aggravate disorders of the heart, kidneys or liver. Its effects worsen when subjected to heat.
• A-Terpineol: Causes Central Nervous System (CNS) disorders, meaning problems relating to the brain and spine such as Alzheimer’s disease, ADD, dementia, Multiple Sclerosis, Parkinson’s disease, seizures, strokes, and Sudden Infant Death Syndrome. Early symptoms of CNS problems include aphasia, blurred vision, disorientation, dizziness, headaches, hunger, memory loss, numbness in face, pain in neck and spine. A-Terpineol also irritates the mucous membranes and, if aspirated into the lungs, can cause respiratory depression, pneumonia or fatal edema.
• Benzyl Alcohol: This upper respiratory tract irritant can cause central nervous system (CNS) disorders, headache, nausea, vomiting, dizziness and dramatic drops in blood pressure.
• Benzyl Acetate: This substances has been linked to pancreatic cancer. Its vapors can be irritating to eyes and respiratory passages and it can also be absorbed through the skin.
• Ethanol: Another fabric softener ingredient which is on the EPA’s Hazardous Waste list and linked to CNS disorders.
• Pentane: A chemical known to be harmful if inhaled.
• Ethyl Acetate: This substance, which is on the EPA’s Hazardous Waste list, can be irritating to the eyes and respiratory tract. It may also cause severe headaches and loss of consciousness, as well as damage to the liver and kidneys.
• Camphor: Another substance on the EPA’s Hazardous Waste list. It is easily absorbed through body tissue, causing irritation of eyes, nose and throat. Camphor can also cause dizziness, confusion, nausea, twitching muscles and convulsions.
• Linalool: A narcotic known to cause respiratory problems and CNS disorders. In animal testing, exposure to linalool has resulted in death.
• Phthalates: Used in scented products to help the scent last longer, phthlates have been linked to breast cancer and reproductive system problems.
• Limonene: This known carcinogen can cause irritation to eyes and skin.
• Also, if you follow a vegan lifestyle, you should be aware that many fabric softener sheets are made using tallow, a form of animal fat.
Manufacturers are aware that the products contain toxic chemicals. The packaging on many brands include a warning that the product should not be used on children’s sleepwear. Since some of the same brands also have large images of children and toys, however, consumers may miss the small print message.
Making your own fabric softener is very easy and cost effective . Additionally, using homemade cleaning products helps keep harmful chemicals away. Vinegar is cheap and nontoxic. It naturally removes soap residue, and helps with static reduction during drying. Vinegar contains small amounts of sodium and potassium, which help soften hard water. Homemade fabric softener ingredients are combined with water to make a solution you can store in a container and use each time you do the wash.
Natural Homemade Fabric Softener
Mix ingredients together and pour into a storage container.
Background Nicotine is known as the drug that is responsible for the addicted behaviour of tobacco users, but it has poor reinforcing effects when administered alone. Tobacco product design features enhance abuse liability by (A) optimising the dynamic delivery of nicotine to central nervous system receptors, and affecting smokers’ withdrawal symptoms, mood and behaviour; and (B) effecting conditioned learning, through sensory cues, including aroma, touch and visual stimulation, to create perceptions of pending nicotine reward. This study examines the use of additives called ‘pyrazines’, which may enhance abuse potential, their introduction in ‘lights’ and subsequently in the highly market successful Marlboro Lights (Gold) cigarettes and eventually many major brands.
Methods We conducted internal tobacco industry research using online databases in conjunction with published scientific literature research, based on an iterative feedback process.
Results Tobacco manufacturers developed the use of a range of compounds, including pyrazines, in order to enhance ‘light’ cigarette products’ acceptance and sales. Pyrazines with chemosensory and pharmacological effects were incorporated in the first ‘full-flavour, low-tar’ product achieving high market success. Such additives may enhance dependence by helping to optimise nicotine delivery and dosing and through cueing and learned behaviour.
Conclusions Cigarette additives and ingredients with chemosensory effects that promote addiction by acting synergistically with nicotine, increasing product appeal, easing smoking initiation, discouraging cessation or promoting relapse should be regulated by the US Food and Drug Administration. Current models of tobacco abuse liability could be revised to include more explicit roles with regard to non-nicotine constituents that enhance abuse potential.
While searching for the origin of our brain, biologists at Heidelberg University have gained new insights into the evolution of the central nervous system (CNS) and its highly developed biological structures. The researchers analysed neurogenesis at the molecular level in the model organism Nematostella vectensis. Using certain genes and signal factors, the team led by Prof. Dr. Thomas Holstein of the Centre for Organismal Studies demonstrated how the origin of nerve cell centralisation can be traced back to the diffuse nerve net of simple and original lower animals like the sea anemone. The results of their research will be published in the journal “Nature Communications”.
Like corals and jellyfish, the sea anemone – Nematostella vectensis – is a member of the Cnidaria family, which is over 700 million years old. It has a simple sack-like body, with no skeleton and just one body orifice. The nervous system of this original multicellular animal is organised in an elementary nerve net that is already capable of simple behaviour patterns. Researchers previously assumed that this net did not evidence centralisation, that is, no local concentration of nerve cells. In the course of their research, however, the scientists discovered that the nerve net of the embryonic sea anemone is formed by a set of neuronal genes and signal factors that are also found in vertebrates.
According to Prof. Holstein, the origin of the first nerve cells depends on the Wnt signal pathway, named for its signal protein, Wnt. It plays a pivotal role in the orderly evolution of different types of animal cells. The Heidelberg researchers also uncovered an initial indication that another signal path is active in the neurogenesis of sea anemones – the BMP pathway, which is instrumental for the centralisation of nerve cells in vertebrates.
While the Wnt signal path triggers the formation of the primary body axis of all animals, from sponges to vertebrates, the BMP signal pathway is also involved in the formation of the secondary body axis (back and abdomen) in advanced vertebrates. “Our research results indicate that the origin of a central nervous system is closely linked to the evolution of the body axes,” explains Prof. Holstein.
The idea it gets worse before it gets better is applicable to certain antidepressants, according to a new paper published in the journal Trends in Cognitive Sciences.
Selective serotonin reuptake inhibitors (SSRIs) are among the most prescribed drugs (or overprescribed depending on who you talk to) for psychiatric disorders, including depression, anxiety, and eating disorders. They work to increase the brain’s level of serotonin — a chemical that work as a neurotransmitter and is responsible for maintaining mood balance — while inhibiting its reuptake (absorption) into the brain’s presynaptic cell. Chemical synapses are what allow neurons to form circuits within the central nervous system, as well as help connect to and control other systems of the body.
While serotonin can increase up to hours after an SSRI is taken, it takes two weeks before patients notice a subside in symptoms. It’s during this delay researchers from Otto-von-Guericke University believe depression gets worse before it gets better. Specifically, this delay stems from the different ways SSRI affects serotonin and another brain chemical called glutamate, which are both released from the serotonin neuron. Glutamate is the brain’s main excitatory neurotransmitter, and it’s important for neural communication, memory formation, learning and regulation.
Researchers culled data from existing studies and found when taking an SSRI, serotonin is immediately amplified while glutamate is suppressed. This balance is only restored after several days of drug treatment, Adrian Fischer, lead study author, said in a press release. Fischer added the serotonin component has been linked to motivation, while the glutamate component has been linked to pleasure and learning.
Put it another way: An SSRI immediately boosts motivation in depressed patients, while at the same time it’s hampering hedonic components (pleasure) of the reward system. The answer isn’t a higher dose of SSRIs either. Instead, researchers found this combination, whatever the dose, “could lead to the facilitation of suicidal thoughts or behavior in the early weeks of SSRI administration,” especially in young adults.
Pharmacology experts refer to this as a “paradoxical reaction.” Medical Daily previously reported this type of reaction is not uncommon among depression sufferers. One study was on par with the current study’s findings: 42 10- to 17-year-olds were compelled to self-harm after taking Prozac, four of which were hospitalized.
Fischer and his team concluded their paper “offers a framework of directly testable predictions for a better understanding and interpretation of studies employing SSRI challenges.” It also opens potentials for new drugs aiming to delay onset of SSRIs in depression. As always, consult with your doctor on the medication that is best suited for your particular symptoms; antidepressant, and otherwise prescription drugs, aren’t one size fits all. And if patients are prescribed medication, be sure to read up on possible side effects.
Source: Fischer A, Jocham G, Ullsperger M. Dual serotonergic signals: a key to understanding paradoxical effects? Trends in Cognitive Sciences. 2014.
Scientists have long wondered why sleep is restorative and why lack of sleep impairs brain function.
Now, new animal research suggests how the sleep state may help clear the body of potentially toxic central nervous system (CNS) metabolites.
Proteins linked to neurodegenerative diseases, including β-amyloid (Aβ), are present in the interstitial space surrounding cells in the brain. In a series of experiments, researchers tested the hypothesis that Aβ clearance is increased during sleep and that the sleep-wake cycle regulates the glial cell–dependent glymphatic system, which is responsible for clearing waste from the brain and spinal cord.
“Basically, we found a new function of sleep,” said study lead author Lulu Xie, PhD, Division of Glial Disease and Therapeutics, Center for Translational Neuromedicine, Department of Neurosurgery, University of Rochester Medical Center, New York.
“When mice are awake, the brain cells continuously produce toxic waste. This waste can build up in the spaces between the brain cells and damage them. However, during sleep, the spaces between brain cells increase, which may help the brain flush out the toxic waste. Therefore, a good sleep can clear the brain.”
“Sleep changes the cellular structure of the brain. It appears to be a completely different state,” Maiken Nedergaard, MD, DMSc, codirector of the Center for Translational Neuromedicine at the University of Rochester Medical Center, who is a leader of the study, said in a statement from the National Institute of Neurological Disorders and Stroke, which supported the study.
The new research was published October 18 in Science.
Sleeping vs Awake Brain
The researchers infused fluorescent dye into the cerebrospinal fluid (CSF) of mice and observed it flow through the brain. At the same time, they monitored electrical brain activity and wakefulness with electrocorticography (EcoG) and electromyography (EMG)..
“In the sleeping brain, we found the CSF flushed into the brain very quickly and broadly,” said Dr. Xie. “After half an hour, we woke the mice up by gently touching their tails, and injected another color of dye. But what we saw is that CSF barely flowed when the same mice were awake.”
These results suggest that the awake brain may have more resistance to CSF influx, which leads to the assumption that the path of CSF flow into the brain is smaller in the awake brain, said Dr. Xie.
Next, the scientists inserted electrodes into the brain to directly measure the space between brain cells, and found that it increased by around 60% when the mice were asleep.
“Theoretically, big spaces lead to easier fluid influx,” said Dr. Xie. “So we presumed that the clearance of the toxic protein between cells will become more efficient.”
To test this assumption, they infused radio-labeled Aβ into the brain and measured how long it stayed in both the sleeping brain and the awake brain.
We found Aβ disappeared 2-fold faster in the sleeping mice brains as compared with awake mice,” noted Dr. Xie. “Based on this experiment, we can see that the sleeping brain is more capable of clearing out the toxic protein.”
Technically, it might be relatively easy to study these processes in humans, possibly using magnetic resonance imaging. However, Dr. Xie said she does not know when human trials, which involve “a lot more concerns” than animal experiments, might come about.
“These results may have broad implications for multiple neurological disorders,” said Jim Koenig, PhD, a program director at the National Institute of Neurological Disorders and Stroke (NINDS), which funded the study, in a statement. “This means the cells regulating the glymphatic system may be new targets for treating a range of disorders.”
In animal study, inflammation stops cells from accessing iron needed for brain development
Researchers exploring the link between newborn infections and later behavior and movement problems have found that inflammation in the brain keeps cells from accessing iron that they need to perform a critical role in brain development.
Specific cells in the brain need iron to produce the white matter that ensures efficient communication among cells in the central nervous system. White matter refers to white-colored bundles of myelin, a protective coating on the axons that project from the main body of a brain cell.
The scientists induced a mild E. coli infection in 3-day-old mice. This caused a transient inflammatory response in their brains that was resolved within 72 hours. This brain inflammation, though fleeting, interfered with storage and release of iron, temporarily resulting in reduced iron availability in the brain. When the iron was needed most, it was unavailable, researchers say.
What’s important is that the timing of the inflammation during brain development switches the brain’s gears from development to trying to deal with inflammation,” said Jonathan Godbout, associate professor of neuroscience at The Ohio State University and senior author of the study. “The consequence of that is this abnormal iron storage by neurons that limits access of iron to the rest of the brain.”
The cells that need iron during this critical period of development are called oligodendrocytes, which produce myelin and wrap it around axons. In the current study, neonatal infection caused neurons to increase their storage of iron, which deprived iron from oligodendrocytes.
In other mice, the scientists confirmed that neonatal E. coli infection was associated with motor coordination problems and hyperactivity two months later – the equivalent to young adulthood in humans. The brains of these same mice contained lower levels of myelin and fewer oligodendrocytes, suggesting that brief reductions in brain-iron availability during early development have long-lasting effects on brain myelination.
The timing of infection in newborn mice generally coincides with the late stages of the third trimester of pregnancy in humans. The myelination process begins during fetal development and continues after birth.
Though other researchers have observed links between newborn infections and effects on myelin and behavior, scientists had not figured out why those associations exist. Godbout’s group focuses on understanding how immune system activation can trigger unexpected interactions between the central nervous system and other parts of the body.
“We’re not the first to show early inflammatory events can change the brain and behavior, but we’re the first to propose a detailed mechanism connecting neonatal inflammation to physiological changes in the central nervous system,” said Daniel McKim, a lead author on the paper and a student in Ohio State’s Neuroscience Graduate Studies Program.
The neonatal infection caused several changes in brain physiology. For example, infected mice had increased inflammatory markers, altered neuronal iron storage, and reduced oligodendrocytes and myelin in their brains. Importantly, the impairments in brain myelination corresponded with behavioral and motor impairments two months after infection.
Though it’s unknown if these movement problems would last a lifetime, McKim noted that “since these impairments lasted into what would be young adulthood in humans, it seems likely to be relatively permanent.”
The reduced myelination linked to movement and behavior issues in this study has also been associated with schizophrenia and autism spectrum disorders in previous work by other scientists, said Godbout, also an investigator in Ohio State’s Institute for Behavioral Medicine Research (IBMR).
This current study did not identify potential interventions to prevent these effects of early-life infection. Godbout and colleagues theorize that maternal nutrition – a diet high in antioxidants, for example – might help lower the inflammation in the brain that follows a neonatal infection.
“The prenatal and neonatal period is such an active time of development,” Godbout said. “That’s really the key – these inflammatory challenges during critical points in development seem to have profound effects. We might just want to think more about that clinically.”
CD133+ cells have the potential to enhance histological and functional recovery from peripheral nerve injury. However, the number of CD133+ cells safely obtained from human peripheral blood is extremely limited. To address this issue, the authors expanded CD133+ cells derived from human peripheral blood using the serum-free expansion culture method and transplanted these ex vivo expanded cells into a model of sciatic nerve defect in rats. The purpose of this study was to determine the potential of ex vivo expanded CD133+ cells to induce or enhance the repair of injured peripheral nerves.
Phosphate-buffered saline (PBS group [Group 1]), 105 fresh CD133+ cells (fresh group [Group 2]), 105 ex vivo expanded CD133+ cells (expansion group [Group 3]), or 104 fresh CD133+ cells (low-dose group [Group 4]) embedded in atelocollagen gel were transplanted into a silicone tube that was then used to bridge a 15-mm defect in the sciatic nerve of athymic rats (10 animals per group). At 8 weeks postsurgery, histological and functional evaluations of the regenerated tissues were performed.
After 1 week of expansion culture, the number of cells increased 9.6 ± 3.3–fold. Based on the fluorescence-activated cell sorting analysis, it was demonstrated that the initial freshly isolated CD133+ cell population contained 93.22% ± 0.30% CD133+ cells and further confirmed that the expanded cells had a purity of 59.02% ± 1.58% CD133+ cells. However, the histologically and functionally regenerated nerves bridging the defects were recognized in all rats in Groups 2 and 3 and in 6 of 10 rats in Group 4. The nerves did not regenerate to bridge the defect in any of the rats in Group 1.
The authors’ results show that ex vivo expanded CD133+ cells derived from human peripheral blood have a therapeutic potential similar to fresh CD133+ cells for peripheral nerve injuries. The ex vivo procedure that can be used to expand CD133+ cells without reducing their function represents a novel method for developing cell therapy for nerve defects in a clinical setting.
Source: Journal of Neurosurgery.