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January 24th, 2008:

FREE Smoking Cessation Counseling Service

Message from Department of Nursing Studies

Wanna quit smoking but need help quitting? Have you tried to quit but can’t quite knock the habit? The Department of Nursing Studies is now offering a FREE smoking cessation counseling service for youth, young adults, and women! We care about your health and will do our best to help you quit. If you have friends that smoke, feel free to introduce them too. All personal information will be kept confidential.

Youth Quitline

Trained peer counsellors will help you quit and answer your questions via telephone.

If you are:

1. A 12-25 year-old smoker
2. Want to quit smoking
3. Can communicate in Cantonese

We will

1. Provide counselling service up to 5 times via telephone
2. Provide a basic body check-up to quitters after 6 months
3. An incentive will be given to those who come to the body check.

Please call 2855-9557 to make an appointment.


Senior trained nurses will help you to quit through either a face-to-face interview or telephone interview at your convenience.

If you are:

1. Over 18 years old, female, and a smoker
2. Want to quit smoking
3. Can communicate in Cantonese

We will:

1. Provide quitting techniques specially designed for women
2. Provide Nicotine Replacement Therapy and a basic body check-up

Please contact Miss Tracy Cheung at 2819-2692/ 6752-6266 to make appointment.

For more details, please visit

Professor Sophia Chan
Department of Nursing Studies
The University of Hong Kong

Cigarettes Leave Deadly Path By Purging Protective Genes

ScienceDaily (Jan. 24, 2008) — A University of Rochester scientist discovered that the toxins in cigarette smoke wipe out a gene that plays a vital role in protecting the body from the effects of premature aging. Without this gene we not only lose a bit of youthfulness — but the lungs are left open to destructive inflammation and diseases such as chronic obstructive pulmonary disease (COPD) and lung cancer.

By identifying the Sirtuin (SIRT1) gene’s role in pulmonary disease, scientists also hope to find ways to restore it and jump-start lung healing. They’ve begun testing the powerful antioxidant resveratrol, which is extracted from red grape skins, to develop a treatment to target SIRT1 and reverse lung damage, or at least enhance the way standard COPD therapies work.

“This novel protein will allow us to program our body’s immune-inflammatory system against lung damage and premature aging. The hallmark of this discovery is that we may be able to provide remedies to millions of smokers who would like to quit but cannot kick their addiction, and millions of former smokers who, despite quitting, remain at risk for illness as they age,” said Irfan Rahman, Ph.D., associate professor of Environmental Medicine and an investigator in the University of Rochester’s Lung Biology and Disease Program.

Approximately 23 million Americans have COPD, which is induced by inflammation and results in progressive breathlessness. By the year 2020, it is expected to be the third leading cause of death worldwide; today at least 9 percent of the elderly population is estimated to suffer from debilitating lung conditions.

Rahman has spent years studying how the 4,700 toxic chemical compounds in cigarettes assault lung tissue. He also focuses on why some people seem genetically predisposed to develop lung diseases while others are more fortunate, despite being smokers.

SIRT1 plays a pivotal role in the puzzle. It belongs to a class of genes that regulate chronic inflammation, cancer and aging. When SIRT1 is highly active, or over-expressed in mice, worms and fruit flies, their life spans are greatly increased. Recent studies also show that SIRT1 plays a positive role in stress resistance, metabolism, apoptosis and other processes involved in premature aging. However, environmental stress such as cigarette smoke or pollution can decrease production of SIRT1 in the lungs.

In collaboration with Vuokko L. Kinnula, M.D., at Helsinki University Hospital in Finland, Rahman’s team studied the levels of SIRT1 in the lungs of nonsmokers and smokers with and without COPD. Thirty-seven patients from Helsinki who were undergoing either a lung resection for suspected cancer or a lung transplant, volunteered to provide tissue samples for the study. Researchers confirmed that SIRT1 was significantly lower in smokers who had COPD and in smokers who did not have disease, compared to nonsmokers.

The next step was to investigate what pathways lead to the depletion of SIRT1. Researchers found that Sirtuin also plays a role in regulating the entire chemical signaling system that protects the lungs from smoke and pollution. They investigated how SIRT1 relates to another key protective molecule, Nrf2, a transcription factor. Just as in the case of SIRT1, an airway deficient in Nrf2 is weak and inflamed and more prone to conditions such as COPD, researchers found.

Nrf2 was also important because it directly regulates several antioxidant genes such as gluthathione (GSH), the most abundant cellular antioxidant responsible for detoxifying the airways. Therefore, the pathway from SIRT1 to Nrf2 ultimately leads to the depletion of GSH, exacerbating the organ’s aging process.

“You can be 45 years old and look great on the outside, but if you are a smoker or former smoker, your lungs can easily be 60 years old because of the chemical assault,” Rahman said.

Other University of Rochester research teams are investigating the Nrf2 pathway and various ways to boost fundamental genetic changes in the body that would arm it with amplified natural antioxidants. The result could be the development of a target for new drugs that would protect us from age-related diseases such as cancer and emphysema.

Although he was not involved in the study, James D. Crapo, M.D., a leading expert in the field of lung disease and a professor of Medicine at the National Jewish Medical and Research Center, University of Colorado Health Sciences Center in Denver, said Rahman’s novel finding opens new doors. “This is certainly an important breakthrough in understanding the persistent lung damage and inflammation that occur in patients with COPD, and therapies can now be directed towards this protein.”

The research was published in two separate studies, in the American Journal of Respiratory Critical Care Medicine, appearing online Jan. 3, 2008, and in the American Journal of Physiology, appearing Dec. 27, 2007.

The Environmental Health Sciences Center of the University of Rochester, which is partially funded by the National Institute of Environmental Health Sciences (NIEHS), supported the research. In addition, the University of Rochester has filed a patent to protect the identification of a novel molecular target to treat the progression of COPD and emphysema by inducing the Sirtuin1 gene.

How Tobacco Ages

Take a look at how you will look after a few too many cigarettes. This game will let you upload your own picture and add the realistic effects of smoking: