What Is In A Cigarette? Chemicals and Ingredient List Confirm How Dangerous Smoking Really Is.


Over 3,200 Americans under the age of 18 smoke their first cigarette every day, and most of them are unaware of what they are getting into. Many new smokers may not realize how quickly their new habit can lead to heart disease, stroke, diabetes, lung diseases, and certain types of cancer. If you’re looking for an explanation as to why cigarette smoke results in more than 480,000 deaths each year in the United States, look no further than its ingredients. The average cigarette contains upward of 600 different ingredients on top of over 7,000 chemicals produced by cigarette smoke. Where these ingredients and chemicals also show up may shock some smokers into quitting once and for all.

Cigarette Ingredients

“One of the issues with cigarettes is that they have hundreds of added ingredients, not just what is naturally in the tobacco plant,” environmental health scientist with Mount Sinai School of Medicine, Dr. Luz Claudio told Medical Daily in an email. “What complicates this even more is that when these chemicals burn, they form other chemicals that may have additional effects on health.”

While tobacco companies like R.J. Reynolds insist that a lot of the ingredients found in cigarettes are also found in Food and Drug Administration-approved foods and beverages, a few of these ingredients are also found in products that you would never think to put in your body otherwise. Take for example arsenic, an inorganic substance found in wood preservatives and rat poison. On the FDA’s Established List of Harmful and Potentially Harmful Constituents in Tobacco Products and Tobacco Smoke, arsenic’s dangers include: carcinogen, cardiovascular toxicant, and reproductive or developmental toxicant.

Some of cigarettes’ harmful ingredients and chemicals are more familiar, such as carbon monoxide, which can be found in car exhaust fumes, and nicotine, also found in insecticides. There’s also formaldehyde, a cancer-causing ingredient of embalming fluid. Others may not seem so dangerous by name alone like cadmium, an active ingredient in batteries, or hexamine, sometimes found in barbecue lighters. Approximately 70 of the chemicals and ingredients found in a cigarette are considered carcinogenic, meaning they have the potential to cause cancer. Almost all of these ingredients can lead to death in some way or another.

“Cigarette smoke can affect the flow of oxygen within our bodies in two ways,” pulmonologist specializing in pulmonary rehab with City of Hope, Dr. Brian Tiep told Medical Daily. “First, carbon monoxide grabs on to the hemoglobin molecule, which prevents the transport of oxygen through red blood cells. Secondly, cyanide hinders tissue’s ability to take up and utilize oxygen. Tissue cannot function without this steady flow of oxygen.”

According to the American Cancer Society, cigarette smoke accounts for at least 30 percent of all cancer-related deaths in the U.S. This includes 87 percent of lung cancer deaths among men and 70 percent of among women. Cigarette smoke can also lead to certain lung diseases including emphysema, bronchitis, and chronic airway obstruction. There are currently more than 16 million Americans suffering from a disease that was caused by smoking. If appropriate prevention strategies are not put in place to curb the number of young Americans who pick up smoking, an estimated 5.4 million people under the age of 18 will die prematurely due to a smoking-related illness.

Medical Miracle:Blind man restored vision after having a TOOTH implanted into his eye


Martin Jones, a 42-year-old builder, was left blind after an accident at work more than a decade ago. But a remarkable operation – which implants part of his tooth in his eye – has pierced his world of darkness. The procedure, performed fewer than 50 times before in Britain, uses the segment of tooth as a holder for a new lens grafted from his skin.


Mr Jones, from Rotherham, South Yorkshire, married his wife Gill, 50, four years ago.
By that time he had already spent eight years without his sight after a tub of white hot aluminium exploded in his face at work in a scrapyard.
He suffered 37 per cent burns and had to wear a special body stocking for 23 hours a day. He also had his left eye removed.
But surgeons were able to save the right eye, even though he was unable to see through it.
At first specialists in Nottingham tried to save his sight using stem cells from a donor but the attempt failed.
It was only when a revolutionary new operation was pioneered at the Sussex Eye Clinic in Brighton that he was given a chance to have his sight back.

During the procedure, a minute section of a patient’s tooth is removed, reshaped and chiselled through to grip the man-made lens which is then placed in its core.
It is implanted under an eyelid where it becomes covered in tissue.
The process requires a living tooth as an implant because doctors suggest there are chances the eye would reject a plastic equivalent.
So a canine – which is the best option due to its shape and size – was taken out of Mr Jones’ mouth.

A patch of skin is then taken from the inside of the cheek and placed in the eye for two months, where it gradually acquires its own blood supply.
The tooth segment is finally transplanted into the eye socket. The flap of grafted skin is then partially lifted from the eye and placed over its new sturdy base

 

Pill to switch off hunger on the horizon .


LONDON: The world’s first pill to make you stop eating is set to become a reality.

In a study led by Imperial College London and the Medical Research Council (MRC), an international team of researchers identified an anti-appetite molecule called acetate that is naturally released when we digest fibre in the gut. Once released, the acetate is transported to the brain where it produces a signal to tell us to stop eating.

The research confirms the natural benefits of increasing the amount of fibre in our diets to control overeating and could also help develop methods to reduce appetite.

The study found that acetate reduces appetite when directly applied into the bloodstream, the colon or the brain.

Dietary fibre is found in most plants and vegetables but tends to be at low levels in processed food. When fibre is digested by bacteria in our colon, it ferments and releases large amounts of acetate as a waste product. The study tracked the pathway of acetate from the colon to the brain and identified some of the mechanisms that enable it to influence appetite. This is the first demonstration that acetate released from dietary fibre can affect the appetite response in the brain.

Using positron emission tomography (PET) scans, the researchers tracked the acetate through the body from the colon to the liver and the heart and showed it eventually ended up in the hypothalamus region of the brain, which controls hunger.

“The average diet in Europe today contains about 15 g of fibre per day,” said lead author of the study Professor Gary Frost from Imperial College London. “In stone-age times we ate about 100g per day but now we favour low-fibre ready-made meals over vegetables, pulses and other sources of fibre. Unfortunately our digestive system has not yet evolved to deal with this modern diet and this mismatch contributes to the current obesity epidemic. Our research has shown that the release of acetate is central to how fibre suppresses our appetite and this could help scientists to tackle overeating.”

The study analyzed the effects of a form of dietary fibre called inulin that comes from chicory and sugar beets and is also added to cereal bars. Using a mouse model, researchers demonstrated that mice fed on a high fat diet with added inulin ate less and gained less weight than mice fed on a high fat diet with no inulin. Further analysis showed the mice fed on a diet containing inulin had a high level of acetate in their guts.

“The major challenge is to develop an approach that will deliver the amount of acetate needed to suppress appetite but in a form that is acceptable and safe for humans,” Professor Frost said. “Acetate is only active for a short amount of time in the body so if we focused on a purely acetate-based product we would need to find a way to drip-feed it and mimic its slow release in the gut.”

Professor David Lomas from MRC said: “It’s becoming increasingly clear that the interaction between the gut and the brain plays a key role in controlling how much food we eat. Being able to influence this relationship, for example using acetate to suppress appetite, may in future lead to new, non-surgical treatments for obesity.”

UK cancer care a national shame, says Macmillan charity.


Report finds patients diagnosed too late, abandoned after treatment and denied a dignified death.

 

Cancer patients receive chemotherapy at Harrogate district hospital

Cancer patients receive chemotherapy at Harrogate district hospital. Photograph: Christopher Thomond for the Guardian

Cancer care in Britain has been dubbed a national shame, and despite many people with the disease living longer, patients are being denied a dignified death, according to a leading charity.

Too many people are diagnosed too late, are shown a lack of compassion during their care and feel abandoned after treatment, said Ciarán Devane, chief executive of Macmillan Cancer Support.

His damning verdict accompanied the charity’s first state of the nation report which condemns UK governments for lagging behind western European countries and others on cancer survival rates.

“Any notions that cancer care in the UK is ‘fixed’ are rubbished by our findings,” said Devane. “While the NHS does amazing things every day, it is a national shame that our cancer survival rates are among the worst in Europe, that patients are being treated with a lack of dignity, or being denied a ‘good’ death.

“Cancer patients no longer either simply get cured or die. Many live a long time but struggle with serious health problems,” said Devane.

“With the number of people living with cancer set to increase, political parties must ask themselves – how will we cope with these growing numbers when we cannot even meet the needs of many people today? … With a UK cancer crisis looming, we must take action now.”

Macmillan’s report says one in three (32%) people with cancer die within a year of diagnosis, suggesting for many diagnosis is too late, and lambasts lack of information and support for patients and shortages of specialist cancer nurses. It says there is lack of compassion towards some patients when they are at their most vulnerable. Significant numbers of those with cancer “experience long-term physical, emotional, financial and work issues”.

Calling for a shift in funds from hospitals to community care, the charity calls for government focus on reducing late diagnosis, priority for patients’ experiences alongside clinical matters and to let patients spend their final days in the place of their choosing and with free social care.

Macmillan points to the disparity in patients’ wishes on where they want to die, shown in its own online survey in 2010, and where they do die, as recorded for England and Wales in 2012 by the Office for National Statistics. Thus while 73% of those with cancer want to die at home, more than a quarter elsewhere, and less than 1% in hospital, in reality only 30% die at home, 32% elsewhere and 38% in hospital, the report says.

It cites evidence from the British Journal of Cancer that one in four cancers in England are diagnosed via emergency admission to hospital, rather than through screening or GP referral, rising to half all cases of pancreatic and nearly two-thirds of brain or central nervous system cancers.

It also says that there is “a shocking postcode lottery” within the UK over survival rates, treatment and care for those with cancer.

The report also points to research on cancer survival published in the Lancet medical journal three years ago, for colorectal, lung, breast and ovarian cancer in Australia, Canada, Denmark, Norway, Sweden and Britain.

It was persistently lower in Denmark, England, Northern Ireland, and Wales, particularly in the first year after diagnosis and for patients aged 65 years and older.

The proportion of people with lung cancer dying within a year of diagnosis in the UK was 70%, compared with 65% in Denmark, 61% in Norway and 56% in Sweden.

The Department of Health in England said: “We want the UK to be the best place in the world to survive cancer. We have invested £750m over four years to support early diagnosis and improve access to screening and have already seen significant improvements in some cancer survival rates.

“The recent cancer experience survey has shown high levels of satisfaction with the care and compassion shown to patients. However, the NHS always works to improve standards. We are starting a review looking at the issue of choice in end-of-life care.”

Spinal cord neurons that control skilled limb movement identified .


Two types of neurons that enable the spinal cord to control skilled forelimb movement have been found by researchers. The first is a group of excitatory interneurons that are needed to make accurate and precise movements; the second is a group of inhibitory interneurons necessary for achieving smooth movement of the limbs. The findings are important steps toward understanding normal human motor function and potentially treating movement disorders that arise from injury or disease.

Normal mice move their limbs smoothly when reaching for food pellets. The limbs of mice without the GABAergic interneurons (red line) displayed severe tremors.
Credit: Nature and lab of Thomas M. Jessell, PhD

Researchers have identified two types of neurons that enable the spinal cord to control skilled forelimb movement. The first is a group of excitatory interneurons that are needed to make accurate and precise movements; the second is a group of inhibitory interneurons necessary for achieving smooth movement of the limbs. The findings are important steps toward understanding normal human motor function and potentially treating movement disorders that arise from injury or disease.

“We take for granted many motor behaviors, such as catching a ball or flipping a coin, that in fact require considerable planning and precision,” said Columbia University Medical Center’s (CUMC’s) Thomas M. Jessell, PhD, a senior author of both studies, which were published separately in recent issues of Nature. “While such motor acts seem effortless, they depend on intricate and carefully orchestrated communication between neural networks that connect the brain to the spinal cord and muscles.”

To move one’s hand to a desired target, the brain sends the spinal cord signals, which activate the motor neurons that control limb muscles. During subsequent movements, information from the limb is conveyed back to the brain and spinal cord, providing a feedback system that can support the control and adjustment of motor output.

“But feedback from muscles is not quick enough to permit the most rapid real-time adjustments of fine motor control,” said Dr. Jessell, “suggesting that there may be other, faster, systems at play.” Dr. Jessell is the Claire Tow Professor of Motor Neuron Disorders in the Departments of Neuroscience and of Biochemistry and Molecular Biophysics, co-director of the Mortimer B. Zuckerman Mind Brain Behavior Institute, co-director of the Kavli Institute for Brain Science, and a Howard Hughes Medical Institute investigator, all at Columbia.

Researchers had suspected that one rapid form of feedback might derive from a group of interneurons in the cervical spinal cord called propriospinal neurons (PNs). Like many other neurons, PNs send signals to motor neurons that innervate arm muscles and trigger movement. But this subset of neurons also has a distinct output branch that projects away from motor neurons towards the cerebellum. Through this dual-branched anatomy, these neurons have the potential to carry internal copies of motor output signals up to the brain.

However, the nature of this internal feedback pathway and whether it has any impact on movement have not been clear. “If PNs were indeed sending copies of outgoing motor commands to the brain, they could provide a conveniently rapid means of adjusting ongoing movements when things go awry,” said Eiman Azim, PhD, a postdoctoral fellow in Dr. Jessell’s lab and lead author of the first paper. “But without a way to selectively target the copy function of PNs, there was no way to test this theory.”

The CUMC team, in collaboration with Bror Alstermark, PhD, a professor in integrative medical biology at Umeå University in Sweden, overcame this technical barrier by developing a genetic method for accessing and eliminating PNs in mice, abolishing both motor-directed and copy signals sent by the neurons. When the researchers quantified the limb movements of the PN-deprived mice in three dimensions as they reached for food pellets, they found that the mice’s ability to reach for the target accurately was badly compromised. “Basically, their movements were uncoordinated,” said Dr. Azim. “The PN-deprived mice consistently over- or under-reached.”

But with both PN output signals gone, the precise role of the PN copy signal remained unclear. The researchers then turned to optogenetics — the use of light to control neuronal activity. They selectively activated the copy axonal branch alone, decalibrating this copy signal from the version sent to motor neurons. With the copy signal altered, the animals’ ability to reach was severely compromised, indicating that the PN copy pathway is capable of influencing the outcome of goal-directed reaching movements.

The PN copy signal also works blazingly fast. It takes just 4 to 5 milliseconds for motor neuron activity to be altered after transmission of a PN copy signal. “These reaching movements typically take 200 to 300 milliseconds, so the PN copy signal pathway appears well equipped to correct arm movements,” said Dr. Azim. The researchers think that this copy signal represents just one of many similar internal feedback pathways that the spinal cord and brain use to validate and correct movements throughout the body.

Are these findings relevant to human motor performance? Many of the pathways and circuits that influence reach and grasp in monkeys and humans are conserved in mice. “We need to learn more about these pathways before we can evaluate how their dysfunction contributes to deficits seen after spinal cord injury and neurodegenerative disease,” said Dr. Azim.

In the second Nature study, CUMC researchers examined how spinal circuits regulate sensory feedback from muscles to control movement. The simplest form of this feedback system involves a reflex pathway (such as the knee-jerk reflex), in which sensory endings in muscles convey signals to the motor system through direct monosynaptic connections with motor neurons. Signals from motor neurons, in turn, cause muscles to contract, completing the reflex cycle.

Researchers have long wondered how the strength of this sensory signal might be regulated. Studies had shown that spinal interneurons — in particular those that release the neurotransmitter GABA, inhibiting neuronal activity — play a key role in this process. But most GABA-releasing interneurons exert their effects postsynaptically, by blocking the excitation of neurons on the receiving end of a synapse (the gap across which two neurons communicate).

“We knew that such neurons are unlikely to be responsible for fine-tuning the sensory signal,” said lead author Andrew J. P. Fink, PhD, a former graduate student in Dr. Jessell’s lab. “Postsynaptic inhibition affects the entire neuron, and motor neurons receive many different inputs. So a mechanism that shut down the motor neuron to all of its inputs would lack refinement.”

Researchers have long speculated that one subset of GABAergic interneurons might regulate movement by controlling the strength of sensory feedback signals from muscles. “These particular neurons are known to work presynaptically, by forming direct connections with the terminals of sensory neurons and suppressing the release of sensory neurotransmitter,” said Dr. Fink. For technical reasons, the function of these interneurons, if any, in motor behavior has remained elusive.

Dr. Fink and his colleagues identified a way to access this subset of interneurons genetically in mice and then devised approaches to manipulate their function in a selective manner. In one experiment, they activated presynaptic inhibitory interneurons optogenetically, decreasing the strength of sensory-motor transmission. They also ablated these interneurons by making them selectively sensitive to a lethal toxin, abolishing their control over sensory feedback strength. Without sensory feedback regulation, forelimb movements were dominated by severe oscillatory tremors, drastically diminishing motor accuracy.

This finding, along with parallel modeling studies, indicates that presynaptic inhibitory neurons normally adjust the “gain” of sensory feedback at synapses with motor neurons and are therefore crucial for the smooth execution of movement. Understanding how these basic microcircuits regulate sensory input and motor output may, in the long run, provide insight into ways to combat the movement instability and tremor seen in many neurological disorders.

“These two studies shed new light on how discrete classes of spinal interneurons empower the nervous system to direct motor behaviors in ways that match the particular task at hand,” said Dr. Jessell.


Story Source:

The above story is based on materials provided by Columbia University Medical Center. Note: Materials may be edited for content and length.


Journal References:

  1. Andrew J. P. Fink, Katherine R. Croce, Z. Josh Huang, L. F. Abbott, Thomas M. Jessell, Eiman Azim. Presynaptic inhibition of spinal sensory feedback ensures smooth movement. Nature, 2014; 509 (7498): 43 DOI: 10.1038/nature13276
  2. Eiman Azim, Juan Jiang, Bror Alstermark, Thomas M. Jessell. Skilled reaching relies on a V2a propriospinal internal copy circuit. Nature, 2014; 508 (7496): 357 DOI: 10.1038/nature13021

New rapid synthesis developed for bilayer graphene and high-performance transistors


Researchers at University of California, Santa Barbara, in collaboration with Rice University, have recently demonstrated a rapid synthesis technique for large-area Bernal (or AB) stacked bilayer graphene films that can open up new pathways for digital electronics and transparent conductor applications.

The invention also includes the first demonstration of a bilayer double-gate field-effect transistor (FET), showing record ON/OFF transistor switching ratio and carrier mobility that could drive future ultra-low power and low-cost electronics.

https://i2.wp.com/cdn.physorg.com/newman/gfx/news/2014/newrapidsynt.png

Graphene is the thinnest known (~0.5 nanometer per layer) 2-dimensional atomic crystal. It has attracted wide interest due to its promising electrical and thermal properties and potential applications in electronics and photonics. However, many of those applications are significantly restricted by the zero band gap of graphene that results in leaky transistors not suitable for digital electronics.

“In addition to its atomically smooth surfaces, a considerable band gap of up to ~0.25 eV can be opened up in bilayer graphene by creating a potential difference between the two layers, and thereby breaking the inherent symmetry, if the two layers can be aligned along a certain (Bernal or AB) orientation” explained Kaustav Banerjee, professor of electrical and computer engineering and Director of the Nanoelectronics Research Lab at UCSB. “The dual-gated transistors were specifically designed to allow such potential difference to be established between the layers through one of the gates, while the second gate modulated the carriers in the channel,” he added. Banerjee’s research team also includes UCSB researchers Wei Liu, Stephan Kraemer, Deblina Sarkar, Hong Li and Professor Pulickel Ajayan of Rice University. Their study was recently published in Chemistry of Materials.

This is concept art of a schematic view of an AB-stacked graphene film synthesized by UC Santa Barbara researchers using a stoichiometry engineered bifunctional alloy catalyst. Credit: Peter Allen, UCSB

The graphene films were grown in a deterministic manner using an engineered bifunctional (Cu:Ni) alloy surface at a relatively low temperature of 920 °C. Large-area (> 3 inch x 3 inch) Bernal (or AB) stacked bilayer graphene growth was demonstrated within few minutes and with nearly 100% area coverage. The bilayer graphene films exhibited electron mobility as high as 3450 cm2/(V*s), which is comparable to that of exfoliated bilayer graphene, thereby confirming very high-quality. The quality of grown graphene was further corroborated by demonstration of high-performance FETs with record ON/OFF ratio that is a key requirement in low-power .

“Achieving surface catalytic graphene growth mode and precise control of the surface carbon concentration were key factors for the favorable growth kinetics for AB stacked bilayer graphene,” explained Wei Liu, a post-doctoral researcher in Banerjee’s group and a co-author of the article. In 2011, Banerjee’s group demonstrated a large-area monolayer graphene synthesis method using a copper substrate as catalyst.

Bilayer graphene is close to monolayer graphene in terms of the film thickness with a hexagonal atomic structure and can be derived from its layered bulk form (graphite) in which adjacent layers are held together by relatively weak van der Waals forces. “However, apart from its tunability, bilayer graphene has some key advantages over monolayer graphene. It has higher density of states and suffers much less from interface effects, which are beneficial for improving the current carrying capability,” Liu continued.

“This demonstration is very impressive and should have far-reaching implications for the entire 2D materials community,” commented Professor Ali Javey, of University of California, Berkeley and a Co-Director of the Bay Area Photovoltaic Consortium (BAPVC).

Vitamin D Deficiency May Be Linked With Aggressive Prostate Cancer .


Vitamin D deficiency may increase the odds that some men who already are at high risk for prostate cancer will have an aggressive form of the disease, according to new research.

The study, published online today in Clinical Cancer Research, is the first to evaluate whether vitamin D deficiency might be associated with prostate cancer based on biopsy results from men who had abnormal findings on a prostate-specific antigen (PSA) test or digital rectal examination. Previous studies compared vitamin D levels only in men with or without prostate cancer.

Vitamin D may be a biomarker of more aggressive prostate cancer, particularly in African American men. (Image: ©iStock.com/areeya_ann)

Investigators enrolled 667 men aged 40 to 79 years who had their first prostate biopsy at 1 of 5 urology clinics in Chicago. About half were African American and the other half were European American. Their blood levels of 25-hydroxyvitamin D (25-OH D) were measured at enrollment to determine vitamin D deficiency.

European American men had higher 25-OH D levels (19.3 nanograms per milliliter [ng/mL] of blood) than African American men (16.7 ng/mL). Dark skin has more melanin, which blocks ultraviolent rays that trigger vitamin D production. The Institute of Medicine has concluded that a 25-OH D level below 12 ng/mL puts a person at risk for vitamin D deficiency and levels from 12 ng/mL to 20 ng/mL indicate insufficiency. But 20 ng/mL is considered adequate for most people.

Overall, 383 men in the study received a prostate cancer diagnosis. Among African American men, those with a 25-OH D level below 20 ng/mL were 2.4 times more likely to be diagnosed with prostate cancer than those with higher levels. African American men with 25-OH D levels below 12 mg/mL were nearly 5 times more likely to have aggressive prostate cancer and 4.2 times more likely to have a tumor stage T2b or higher, meaning that cancer is present in more than half of either the left or right side of the prostate.

Among European American men, 25-OH D levels weren’t related to overall prostate cancer risk. But those with levels below 12 ng/mL were 3.7 times more likely to have aggressive prostate cancer and 2.4 times more likely to have a tumor stage T2b or higher.

In both groups, low 25-OH D levels were linked with aggressive prostate cancer even after investigators accounted for diet, smoking habits, obesity, family medical history, and calcium intake.

“The stronger associations in African American men imply that vitamin D deficiency is a bigger contributor to prostate cancer in African American men compared with European American men,” lead author Adam Murphy, MD, said in a statement.

Murphy, an assistant professor of urology at Northwestern University’s Feinberg School of Medicine in Chicago, said vitamin D supplements may help prevent tumor progression in some men with prostate cancer. “It would be wise to be screened for vitamin D deficiency and treated,” he added.

Epidemic of ticks to hit Britain this summer after mild winter, experts warn.


An epidemic of blood-sucking ticks may hit Britain this summer after the mild, wet winter gave them perfect breeding conditions.

The countryside has become home to growing numbers of the bugs, which spread the potentially deadly Lyme disease, zoology experts have warned.

o

 

Up close: But hopefully nt personal – 3mm-long tick

Prof Richard Wall, of Bristol ­University, said ticks lurked in woods and grassland and posed “a considerable threat” – ­especially to dog walkers.

He added: “Ticks are most commonly found in woodland and long grass areas that are regularly used by dog walkers.

“Climate change can certainly be blamed for the increase as the warmer and damper weather provides a good ­environment for ticks.

“Another reason for the rise is the increase in deer as ticks feed on deer.

“They pose a considerable threat as they pass on many diseases, such as babesiosis in dogs and Lyme disease in humans.”

The arachnid parasites, which are about 3mm long, feed on mammals and birds.

Their numbers have surged in the UK during the past 20 years and Prof Wall estimated there were now up to 20 ticks in every square metre of ­woodland.

But he warned the creatures were becoming such a threat they could spread to parks in towns and cities.

 

SWNS Ticks
Warning: Prof Richard Wall

He urged dog owners to check ­themselves and their pets after every walk and added: “Ticks are often found tucked up in creases of the body – the armpits or behind the ears.

“The best way to remove them is to use tweezers and put them close to the skin and press and twist out.”

Prof Wall, who heads Europe’s leading centre for research into veterinary ectoparasites, and fellow experts, Paul Sands, a specialist veterinary dermatologist from the Pride Veterinary Hospital in Derbyshire, and veterinary advisor Renata Turlej, will host a live broadcast tomorrow night with staff and pets from Bristol’s Highcroft Veterinary Practice.

The team will be demonstrating how to check for ticks and telling pet owners what they can do to combat the problem.

The show marks the launch of MyPetonline’s Big Flea Guarantee, a campaign set to run this summer with vet practices across the country offering free flea and tick checks and advice.

The broadcast begins at 8:30pm and can be viewed by visiting www.mypetonline.co.uk , where pet owners can also download a voucher for a free flea check.

Anyone struggling to remove a tick should see their doctor or take their pet to a vet.

Nasty infection starts with bite

A tick can feed for days before dropping off and the longer it stays, the greater the risk of Lyme disease.

The infection usually starts with a rash around the bite. If untreated, unpleasant symptoms can develop later including muscle or joint pain and even facial paralysis.

There are 3,000 cases in England and Wales each year.

It is treated with antibiotics but is best prevented by using insect repellent and covering up to avoid bites.

Start Seeing the Good When Things Look Bad


It’s well known that storm-tossed waves often expose new treasures along the shoreline; there is unexpected wealth to be collected by those who know the secret value of rough seas. And yet, even though most of us have little tolerance for anything that “rocks our boat,” the truth of the matter is self-evident:

Unwanted moments introduce us to parts of ourselves that would otherwise never get healed were it not for the difficulties that first reveal them and that lead us to release their pain.

When things go “badly” for us, we’re not intended to “return” to who and what we have been. To see the good in this idea, we must be willing to see that the pain in unwanted moments can either be a rock into which we crash time and time again — a tempest without termination — or that same suffering can be used as an inflection point, a place of real change that exists only when all seems lost.

Let me share three ideas with you about this strange and wonderful kind of spiritual goodness that seems to arrive in a package marked: “Caution! Contents under pressure!” Welcome this light into your life and you will learn to exchange resistance to unwanted moments for being receptive to the lessons they bring with them. Soon you will know, without taking thought, the greatest secret in the universe:

All things good come to those for whom the Good is all things.

1. Even though we may feel badly when we lose whatever we hold near and dear to ourselves, it is good to see that nothing in this world — or that we can imagine — is permanent. Learning to welcome events that foster this understanding helps liberate us from painful attachments to relationships, possessions, and of course, our own bodies. What follows is freedom from all forms of false dependency and their attending fears.

2. Even though we may feel badly when our sense of self-worth is shaken by events, it is good to see in these experiences that any sense of Self derived through images, social powers, acclaim, or peer approval is not who we really are. Learning to welcome events that reveal this truth helps free us from the impossible task of trying to be all things to all people and strengthens our intention to realize our unshakable original Self.

3. Even though we may feel badly when we run into a limitation of some kind, it is good to see that, apart from the certainty behind our own pressing demands on life, nothing else stands in our way. Learning to welcome events that illuminate this new understanding reveals two key lessons about limitless living: The more we resist seeing our own limitations, the greater they become! And when we realize this truth, we see that limitations are illusions: They exist only for as long as we resist going through what we must to prove them false.

There is an old proverb that goes something like this: “God never takes anything from us without giving us something greater in return.” The task for those of us who seek the life divine — those who seek to live from their original fearless Self — is to prove the trust of this timeless idea. Through it, we are set free.

Taking a Shot at a Tropical Killer


A vaccine against the disease leishmaniasis could save tens of thousands of lives every year. Now, scientists report that they have used snippets of DNA to spur mice to fight back against the parasites responsible for the illness, an approach they hope to soon begin testing in people.

Leishmaniasis is caused by microscopic parasites of the genus Leishmania; some 20 different species can sicken humans. Leishmaniasis hits poor residents of tropical countries the hardest. The sandflies that spread the disease are silent and smaller than a mosquito. After a sandfly’s bite injects them into the body, Leishmania cells can attack the skin or mucous membranes, causing ulcers or disfiguring lesions. In an often lethal variety of the disease, they damage the liver, spleen, and bone marrow. Although the disease’s toll isn’t certain, estimates suggest there are about 1.3 million new cases and up to 40,000 deaths each year.

Leishmania parasites are tricky foes, and so far no vaccine has received approval for use in humans. One challenge is that the parasites lay low inside our cells, out of reach of the antibodies triggered by most other vaccines. The key to eradicating these sheltered invaders, researchers suspect, is stimulating the immune cells known as T cells. Although two experimental leishmaniasis vaccines that use this strategy have undergone preliminary safety and effectiveness tests in people, the best method for enlisting T cells isn’t clear.

Immunologist Peter Walden of Charité University Medicine Berlin and colleagues decided to try a DNA vaccine, a type of vaccine that is good at inciting T cells. Such vaccines contain DNA strands coding for proteins from a pathogen. Cells in the vaccine recipient’s body absorb the DNA and start churning out the proteins—also called antigens—which alert the immune system and prime it to attack if a real infection occurs.

First, the researchers had to choose the right antigens. They settled on five different proteins that vary little across Leishmania samples from a range of species found around the world. To determine whether the antigens galvanize human T cells, the team obtained blood samples from people in India and Tunisia who had recovered from the disease or had been exposed to it without getting sick. They found that portions of all five proteins sparked a response by T cells from the blood samples.

The researchers’ final vaccine mixture, which they tested in mice, contained five kinds of DNA strands, each coding for all or part of one of the proteins. The vaccine stimulated the mice to produce defenses against leishmaniasis parasites, Walden and colleagues report online today in Science Translational Medicine. T cells from the vaccinated animals reacted vigorously to Leishmania antigens. To confirm that the vaccine helped the animals combat the invaders, the researchers injected the mice with cells of one Leishmania species. Three weeks later, mice that received the highest vaccine dose carried 94% fewer parasites in their liver than did mice that received a control shot. Although some parasites remained in the mice that received the largest dose, Walden says there weren’t enough of them to cause disease symptoms.

Colorful killers. A new vaccine protects mice against parasites that cause leishmaniasis.

“We are ready for human trials,” he says. The vaccine should provide protection against different human Leishmania species, he adds, because the selected antigens are the same across species.

Immunologist Paul Kaye of the University of York in the United Kingdom agrees that the time for human trials has come. “There is every reason to believe that they should move forward as soon as possible,” says Kaye, who’s excited that there are now three vaccines to try in humans. Kaye and colleagues’ own vaccine candidate, which stimulates T cells with a harmless virus that carries sections of two Leishmania genes, has already undergone a safety study in people, but the results have not yet been published.

“This is a significant advance,” says vector biologist Jesus Valenzuela of the National Institute of Allergy and Infectious Diseases in Rockville, Maryland. Walden’s group deserves credit for using human blood samples to identify the antigens, he says; other vaccine developers have used rodents.

Leishmaniasis is one of the neglected tropical diseases for which research cash is hard to obtain. Still, Walden is hopeful that he and his colleagues will find financing for safety trials.