way to stop smoking

[druidy]

-666- Wrote:hmm....
now i'm trying not to smoke once after 8pm....
i tried out for 1 day oledi .. haha
although is abit tough but feels like its working ^^
hope everything gonna be fine ^^
anyhow thanks alot guys...

thats a good start -666- you can cut it down slowly, and be proud of yourself later on. just like you play the MMORPG you look back when you spent so much time playing it you feel it is waste of time and energy.... (the reason i said that because i used to play a lot too and feel stupid too)

ps: is ur portrait a character in ragnarok?

[-666-]

^^ hehe yeah ... its a high priest in ragnarok online ^^
starting to cut down liao my smoke habit ...^^
cool

[druidy]

Researchers are starting clinical trials in humans of what they hope may be the first effective treatment for “smoker’s lung� - the UK’s fourth biggest killer - after the therapy showed success in mice.

Chronic obstructive pulmonary disease (COPD) is a condition describing a range of severe inflammatory diseases of the lungs including chronic bronchitis and emphysema. More than 90% of cases are caused by cigarette smoking, and even when a smoker quits the habit, the disease continues, becoming progressively worse – often until the patient dies from respiratory failure.

COPD currently kills more than 30,000 people in the UK every year and is predicted to kill over six million worldwide by 2020, becoming the world’s third biggest killer.

To date, it has only been possible to ease the symptoms of COPD. Researchers have failed to understand why steroids – an effective treatment for asthma-related lung inflammation – have proved ineffective in treating COPD. Now, scientists at Imperial College London, UK, have taken the first step towards a cure for the fatal disease by discovering why it is resistant to steroid treatment.

Peter Barnes, professor of thoracic medicine, and colleagues examined the role of an enzyme in the lung cells called HDAC2, which “switches off� the genes responsible for causing inflammation. Usually, steroidal drugs are able to facilitate this process by providing a molecular pathway between HDAC2 and the appropriate genes. But Barnes discovered that levels of HDAC2 were very low in COPD patients, which was why steroids had little effect.
Cheap drug

“Smoking causes oxidative stress in the cells, which results in reduced production of HDAC2 and much of the enzyme is in a deactivated form so it doesn’t respond to treatment by steroids,� Barnes explains.

He realised that by administering low doses of a cheap and widely available drug – theophylline – he could boost the levels of the enzyme, and therefore enable steroids to treat COPD. “Theophylline is a bronchodilator that has been used for the past 70 years in asthma and COPD patients, but until now it has always been administered in very high doses. We found that in very low doses the drug has a different effect – it appears to activate HDAC2 and increase its production.

“We should be able to prevent people with COPD getting worse and hopefully allow them to recover,� Barnes says.

Steve Connellan, chair of the British Thoracic Society COPD consortium, calls the research exciting, but cautions: “Time will tell as to whether this research which analyses complex changes down at the cellular level of our bodies will be successfully translated into real benefits for patients with smoking-related lung disease.�

The UK team has successfully tested the two-drug treatment in mice and is about to begin clinical trials in 40 patients.

And the therapy may have further benefits. “We are collaborating with researchers in other inflammatory diseases such as rheumatoid arthritis and psoriasis, where patients have ceased to respond to steroids, to see whether low doses of theophylline could potentially benefit these patients too,� Barnes says.

The research will be presented at the British Endocrine Society meeting in Harrogate, UK, on 6 April.

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[Bernard]

....... I wonder if they can find something similar to treat throat cancer brought about by "passive smoking" ?

kerry from truro
smoking should be banned from pubic places because it is bad for your health and can coss lung canser and heart attcackc .... and maik you hilliterate

Grace from oz
umm smoking really does damage your health your skin and everthing about yourself...i mean why throw yourself away like that..why not just stop smoking!!

Russell Exeter
My brother died threeweeks ago from lung cancer brought about by working in an office for 15 years with three heavy smokers, My bro at 35 had never smoked himself. The automsy shows that his lungs had the amount of tar etc of a middling smoker. The doctor told us that in Britain and Europe between a fifth and a third of smoking related deaths are attributable to passive smoking.Be warned.

[druidy]

Pregnant smokers increases grandkids' asthma risk
22:00 11 April 2005
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Gaia Vince


Women who smoke when pregnant may spark asthma in their grandchildren decades later, a new study discovers.

A child whose maternal grandmother smoked while pregnant may have double the risk of developing childhood asthma compared with those with grandmothers who never smoked, say researchers from the University of Southern California, US. And the risk remains high even if the child’s mother never smoked.

It has been known for some time that smoking while pregnant can increase the risk of the child developing asthma, but this is the first time that the toxic effects of cigarette smoke have been shown to damage the health of later generations. The researchers believe that the tobacco may be altering which genes are switched “on� or “off� in the fetus’s reproductive cells, causing changes that are passed on to future generations.

Frank Gilliland, professor of preventative medicine at the Keck School of Medicine in Los Angeles, US, and colleagues interviewed the parents of 338 children who had asthma by the age of five and a control group of 570 asthma-free children. They found that children whose mothers smoked while pregnant were 1.5 times more likely to develop asthma that those born to non-smoking mothers.

But children whose grandmothers smoked when pregnant had, on average, 2.1 times the risk of developing asthma than children with grandmothers who never smoked. Even if the mother did not smoke, but the grandmother did, the child was still 1.8 times more likely to develop asthma. Those children whose mother and grandmother both smoked while pregnant had their risk elevated by 2.6 times.
Two-pronged effect

Gilliland believes the trans-generational repercussions of smoking indicate that tobacco chemicals are having a two-pronged effect: by directly damaging the female fetus’s immature egg cells - putting future children at risk - and also by damaging parts of the fetus’s cells that are responsible for determining which genes will be expressed.

This second type of effect - called an epigenetic effect - could potentially alter which genes are expressed in the child’s immune system which, in turn, Gilliland suspects, may increase the child’s susceptibility to asthma.

“We did not study epigenetic changes directly, but this is one suggested mechanism that could account for our findings,� he told New Scientist.
Stress hormones

But Marcus Pembrey, an epigenetics expert and director of genetics at the Avon Longitudinal Study of Parents and Children in Bristol, UK, says that the results Gilliland found were unlikely to have an epigenetic basis. “Since the effect has passed down the mother’s line, the increase in asthma risk is more likely to be due to other factors. For example, the mother can pass stress hormones, metabolites or immune cells (lymphocytes) to the fetus while it is in utero, so these are more likely to affect the child’s health later on.�

“The epigenetic theory is a bit far-fetched in this case,� he told New Scientist.

Gilliland admits that one of the limitations of his study was that the children may have acquired their asthma through passive smoking as a result of living in a smoky household where their mother, grandmother or other relatives smoked.

“Other studies suggest that in-utero exposure has an independent effect from second-hand smoke, but second-hand smoke may also play a role that we could not separate in this study,� he comments, adding that further studies are needed.

Martyn Partridge, chief medical adviser to Asthma UK says: “The suggestion of an association with grand-maternal smoking is intriguing and whilst the authors’ postulated explanations for this are very reasonable, confirmation of the association in other studies should be the next step.�

Journal reference: Chest (vol 127, p 1232)