The only cigarette is your last one.
Duane Alan Hahn .................................
You own yourself, so if you want to do something that destroys yourself, go ahead. Just dont harm others when you do.
Jim Goebel .................................
To see what is right, and not do it, is want of courage, or of principle.
Confucius .................................
If you resolve to give up smoking, drinking and loving, you dont actually live longer; it just seems longer.
Clement Freud .................................
Smoking is a custom loathsome to the eye, hateful to the nose, harmful to the brain, dangerous to the lungs, and in the black, stinking fume thereof nearest resembling the horrible Stygian smoke of the pit that is bottomless.
King James I of England .................................
Smoking kills. If youre killed, youve lost a very important part of your life.
Brooke Shields .................................
Ill tell you why I like the cigarette business. It cost a penny to make. Sell it for a dollar. Its addictive. And theres a fantastic brand loyalty.
Warren Buffett .................................
If you resolve to give up smoking, drinking and loving, you dont actually live longer; it just seems longer.
Clement Freud .................................
Giving up smoking is the easiest thing in the world. I know because Ive done it thousands of times.

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Latitude 41 N Veggie Burgers Makes 12 servings
1 1/2 cups cooked brown rice
4 teaspoons bulgur wheat
1 cup rolled oats
1 1/2 cups boiling water, divided use
1 1/2 pounds mushrooms, stemmed, cleaned and quartered
2 cups diced onion
1 cup shredded mozzarella cheese
4 teaspoons shredded cheddar cheese
4 teaspoons cottage cheese
1/2 teaspoon salt
1 teaspoon garlic powder
1/4 teaspoon black pepper
4 teaspoons cornstarch
Canola oil
Cook's notes: Because they are so cheesy, do not try to cook these directly on a grill. You need to pan fry, either on stovetop or grill.
Preliminaries: Prepare the brown rice, using your favorite recipe, or buy some of the new, pre-cooked ready-to-eat rice sold in bowls in the supermarket's grocery aisle.
Hydrate other grains: In separate bowls, add the half-cup of boiling water to the oats and let them soak for 10 minutes. Drain excess water, if necessary. Meanwhile, add 1 cup boiling water to the bulgur wheat and let sit for about 1 hour. Drain excess water.
Prepare the mushrooms: Steam the mushrooms and onions for about 10 minutes.
Combine ingredients: In work bowl of food processor, combine plumped grains with onions, mushrooms, rice, cheeses and spices.
Pulse on-off 5 times or until ingredients are finely chopped but not pureed.
Make a slurry with the cornstarch by adding an equal amount of water, then add to mixture to thicken.
Shape and cook the patties: Form mixture into 4-ounce patties and brown in skillet on both sides, waiting until one side is well-browned before you turn it over (carefully).
Presentation: Serve hot.
Source: Adapted recipe from Latitude 41 N restaurant, Cleveland.


D'Vine Veggie Sliders Make 12-14 patties
1 tablespoon roasted garlic (see procedure, below)
1 pound raw, shelled edamame beans, roughly ground in blender or food processor
1/4 cup carrots, shredded
2 ribs celery, finely diced
1 red bell pepper, finely diced
1/2 cup finely chopped mushrooms, preferably portobello or cremini
1 cup panko (Japanese style) bread crumbs
2 eggs, lightly beaten
Salt, freshly ground pepper to taste
Your favorite rolls and grated or melting cheese (optional) for topping
Cook's notes: Make a mini version of these for an elegant cocktail appetizer.
Roast the garlic: Heat oven to 375 degrees. Using a whole head of garlic, slice off the tips of each clove. Place in a sheet of aluminum foil and drizzle with olive oil. Wrap tightly and bake for 1 hour in preheated oven. When cool, squeeze out roasted cloves.
Make patty mixture: Combine all ingredients (except toppings) in a bowl and mix by hand until well incorporated.
Shape the patties: Form mixture into firmly packed, 2-ounce patties.
Fry or grill the patties: Heat skillet and add 1 tablespoon of olive oil. When oil is hot, add patties a few at a time. When well-browned on one side, carefully flip and cook for an additional minute. Or, grill on an oiled, preheated, fine-mesh grate set over a medium-hot grill, first spraying each burger with oil before placing it on the grill.
Presentation: Put sliders on your favorite roll and, if you wish, top with cheese.
Source: Adapted recipe from D'Vine Wine Bar, Cleveland.


Moxie Crispy Black Bean Burger With Corn Aioli Makes 4 servings
For the burgers:
1 tablespoon olive oil, plus more as needed
1/2 cup onion, minced or grated
1 teaspoon kosher salt
1/2 teaspoon ground black pepper
2 cloves garlic, minced
2 cups canned whole black beans, drained and rinsed
1 tablespoon fresh cilantro, chopped
1 lime, zested finely and juiced
2 teaspoons cumin, ground
3/4 cup panko (Japanese-style) bread crumbs
1 egg
Canola or olive oil for frying

To assemble the sandwiches:
Corn Aioli (see accompanying recipe)
8 zucchini slices, big enough to cover each burger
4 kaiser rolls
1 ripe tomato, sliced
1/2 romaine lettuce heart, chopped
8 slices of white cheddar (such as Adam's Reserve), optional
Cook's notes: In advance, prepare the Corn Aioli; cover and refrigerate the mixture while you prepare everything else. You will need a grill at some point in this process, whether gas or charcoal, as well as a nonstick skillet that can be used on the grill -- or just use a ridged cast-iron grill pan (for use on the stovetop).
Saute the vegetables: In a nonstick pan, combine olive oil, onion, salt, pepper and garlic. Cook over low heat until vegetables are tender.
Make burger mixture: Scrape onion mixture into a medium-size bowl, and combine with all other burger ingredients. Using your fingers, crush the beans as you thoroughly combine all the ingredients. Form into 4 patties and set aside.
Prepare the grill: Heat gas grill or light briquettes for a medium-hot fire. Otherwise, have available a grill pan for stovetop use.
Grill the zucchini: Toss the zucchini in a mixing bowl and coat with a dab of olive oil and a pinch of salt. Grill slices to desired doneness.
Cook the burgers: Place a nonstick pan over the hottest part of the grill and add approximately 1 tablespoon of canola or olive oil per patty. Once pan is hot, add the patties to fit. Cook for 3-4 minutes on each side or until very crispy on the surface.
Top the patties: As burgers are done, top with cheese and let melt. Toast the buns on the coolest part of the grill.
Assembly: Place patties on bottom half of each bun, then top each one with portion of zucchini, then tomato, lettuce and aioli. Stab with a sandwich pick -- the burgers can get messy.
Source: Adapted recipe from chef Anthony Hamilton, Moxie the Restaurant, Beachwood.


Corn Aioli Makes about 6 servings
2 ears of corn, shucked and cleaned
1 tablespoon olive oil
1/2 teaspoon kosher salt
1/2 cup mayonnaise
Procedure: Slice the corn off the cob and add to a nonstick pan with the olive oil and salt. Cook over low heat until the kernels are tender. Remove from heat and let cool. Once cool, combine with mayonnaise in a small mixing bowl.
Presentation: Cover and set aside if using within an hour or two, or else refrigerate until ready to use.
Source: Adapted recipe from chef Anthony Hamilton, Moxie the Restaurant, Beachwood.


Falafel Burgers Makes 6 to 10 servings

For the tahini sauce:
1/3 cup tahini paste
2/3 cup plain yogurt
Juice of 1/2 lemon
2 teaspoons ground cumin
2 teaspoons paprika

For the burgers:
2 red potatoes, boiled and peeled
3 cups cooked chickpeas, drained
2 tablespoons tahini (sesame paste)
1 tablespoon plain yogurt
1/2 cup bread crumbs
1 medium red onion, finely chopped
2 cloves garlic, finely minced
1 tablespoon ground cumin
1 tablespoon sweet paprika
Dash cayenne pepper
1/4 cup fresh cilantro, minced

Pita rounds or hamburger buns, and your choice of greens to serve
Cook's notes: Tahini paste is made from ground sesame seeds and is available at Mediterranean stores as well as some supermarkets.
Make tahini sauce: Whisk together the tahini and yogurt, then whisk in other sauce ingredients. Cover and chill.
Prepare the burger mixture: Use a manual potato masher or an electric mixer set on low to mash together all ingredients. Do not mix or puree too finely, or mixture will get too mushy.
Heat the grill: Light gas or charcoal grill until medium-hot.
Shape, grill the patties: Divide mixture and form into 6 to 10 patties.
Grill over medium-hot heat until patties are browned on both sides, about 10 minutes total.
Or bake patties on a lightly oiled sheet in a preheated 375-degree oven for 10 minutes on one side, then 5 minutes on the other.
Presentation: Serve patties in pitas or on burger buns. Serve with tahini sauce and greens of your choice.
Source: Adapted recipe from "Vegetarian Entertaining" by Diane Shaw (Harmony Books, 1991).

Yam and Nut Burgers Makes 4 servings

For the burger mixture:
About 1 pound yams or sweet potatoes, enough to make 1 cup puree
1/4 cup chickpea flour or whole-wheat flour (see cook's notes)
2 cups coarsely chopped nuts (your choice of cashews, pistachios, almonds, sunflower seeds)
1 tablespoon heavy cream or sour cream
1 teaspoon fresh lemon juice
1/2 cup golden raisins, finely chopped
1/3 cup chopped fresh cilantro
1 teaspoon freshly ground white pepper
1/2 teaspoon garam masala or ground coriander
1/4 teaspoon ground cardamom
1/2 teaspoon salt, or more to taste
3 tablespoons unsalted butter, melted

To assemble the burgers:
Naan, pita or lavash
Lemon wedges
Sliced fresh onions, cucumbers, tomatoes, chile peppers
Cook's notes: Instead of baking, you can grill the yams, using the indirect heat method, placing a drip pan underneath the yams and using a cover on top. The burger mix will need at least three hours to chill and firm up; it can be prepared in advance and chilled overnight. Chickpea flour, garam masala and cardamom are available at many East Indian grocery stores, natural foods stores and some specialty stores, such as Mediterranean Foods at the West Side Market, Cleveland.
Prepare the yams: Bake in heated 400-degree oven until soft, about 40 minutes to 1 hour. Let cool. Peel, mash by hand and set aside.
Toast flour and nuts: Bring a dry skillet to medium heat and cook the chickpea flour until lightly toasted and fragrant, about two minutes. Add to yams. Toast the nuts in the same skillet for 3 to 5 minutes and add to yams.
Make the burger mixture: Add the rest of the burger ingredients to the yams, except the melted butter. Blend thoroughly. Taste and adjust seasonings. Chill mixture for at least 3 hours, or overnight.
Shape the patties: Divide burger mixture into four equal portions. Wet your hands and shape into four patties no more than 1-inch thick. Place on oiled baking sheet, cover with plastic wrap and refrigerate until you're ready to grill.
Grill the patties: Prepare a hot fire. If using charcoal, wait until all briquettes are covered with white ash. Get your grate hot, then brush it with a paper towel dipped into vegetable oil held with long-handled tongs. Apply melted butter to one side of burgers. Place buttered side down on grill and apply butter to other side before turning. Cook until lightly browned on both sides.
Presentation: Serve hot, tucked into pita, naan or lavash. Let guests choose their own garnishes, and squeeze lemon juice over portions if they wish.
Source: Adapted recipe from "The Barbecue Bible" by Steven Raichlen (Workman Publishing, 2008).


Barbecued Tempeh Sandwiches Makes 4 servings
1 8-ounce package tempeh, cut into 3/8-inch-thick strips
1/2 cup tomato-based barbecue sauce
8 slices whole wheat bread or 4 whole-wheat rolls, halves
Garnishes: Lettuce leaves, tomato slices, onion slices
Cook's notes: Tempeh, a fermented soybean product, is available in specialty natural food stores and sometimes in the produce section of your supermarket. A lightly oiled vegetable grill rack is recommended.
Marinate the tempeh: Layer the tempeh slices in a bowl, and cover each layer with some of the barbecue sauce.
Prepare the fire: Prepare a medium-hot fire (if using charcoal, all coals should be covered with white ash for about 5 minutes).
Grill the tempeh: Cook tempeh on grill (lightly coat grill with oil beforehand) until heated through and crusty, about 4 to 6 minutes per side. Lightly toast the bread on the grill, about 2 minutes per side. Watch carefully and turn occasionally, to prevent burning.
Presentation: Serve tempeh on bread or rolls, and top with lettuce, tomato and onion as desired.
Source: Adapted recipe from "The New Vegetarian Grill" by Andrea Chesman (Harvard Common Press, 2008).

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It has been seen that women are mostly unerect to assorted kinds of welfare problems as opposition to men because they are genetically divers and their hormones and reproductive meat are mostly the leading sources of their trouble. The eudaimonia of a female is essential because she is not exclusive answerable for her possess upbeat but as symptomless has to carry a child.
Hence it is really main that women obligate different steps to recognise statesman almost womens welfare and adjunctive issues so that they pot decide fitter tending of their embody and thus brace inaccurate from and foreclose these symptom and diseases.
There are different kinds of corporeal and psychic ailments that pass a class and these handle with issues specified as mamma constellation issues, diabetes issues and reproductive issues and nascence check issues. It has been seen that most of these subjects are intellectual and require prompt care.
It is real primary for women to translate that that their embody types and construction are not the Siamese same men and thence winning attention of their embody the con natural course that men do is not accomplishment to help. figure of the maximal issues that women screw to tackling today is the problems of vaporization and drinking.
It has been that the utilization of fuel in women has destroyed up drastically and this has resulted in different kinds of welfare problems and opposite neighboring issues.
Researches and studies finished examination practitioners as considerably ridicule that the even of punctuate is a most key businessperson to the boilersuit translation in the brain. This in amount endorse has the index to strike the gross psychogenic welfare and thus women are unerect to much kinds of diseases.
As asymptomatic the opposite most essential issues with women are mettle diseases, which is opposite to the preceding belief that women do not effectuate temperament diseases simply. formerly much the primary providers here are substance route of life, ventilation and drinking, which claims much lives for women as well.

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Its great that you have decided to go back to college or university to continue with or complete your degree! If you are in the category of what is referred to as adult learners or mature-age students, chances are you might be enrolled in coursework on a part time basis because you have a career and perhaps a family that you are are responsible for. Non-traditional students are more often than not passionate about succeeding in whatever they do. They also have a good grasp on time-management skills and they have very focused.

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DRA-diology

DOTmed was among the first outlets to report the impact of Deficit Reduction Act on Medicare reimbursement for non-hospital imaging procedures. Our first report from the ground was in April 2007.

A recent study from ACR confirms what we found anecdotally -- that the impact is adverse and diverse, with modalities including MR, interventional and ultrasound hit worst.

Read more about this ongoing challenge to radiology, along with other news about technologies, discoveries and business topics. And don't miss the June issue of DOTmed Business News, focusing on nuclear medicine. It's now online.

See you tomorrow.

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Breaking Boards For Breast Cancer Fundraiser
www.firstgiving.com/bonitaboutin.
The Gloria Gemma Breast Cancer Foundation is having a fundraiser at the Flames of Hope..a Celebration of Life Waterfire in Providence RI October 11th. My karate studio, Mastery Martial Arts, will be hosting a board breaking event. The chief instructors will break 1,000 boards. It is so cool. People can buy a board for $10 and write a positive affirmation on it. Then after all the boards are broken, they will be placed on the fire and all the positive affirmations of love, faith, and healing will be sent off into the universe.
Please help me help this wonderful cause. Go to my fundraising website at
www.firstgiving.com/bonitaboutin.
This is a huge event. There will be a pink ribbon made out of people on our state house steps. The state house will be lighted in pink!! This event is so large it is receiving national coverage. Please help. We all have known someone in our lives where breast cancer has touched theirs. Donate to this worthy cause.

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Its a classic case of, if youre not white-hot with rage, youre sure as heck not paying attention.

Last month The Australian reported that Julian Burnside QC (Queens Counsel) had produced in court internal Merck emails that contained a hit list of doctors, researchers and academics it needed to neutralize or discredit. In some cases it was noted that a doctor had already been neutralized. We may need to seek them out and destroy them where they live, it read. (One can only assume that the advice was not meant to be taken Mafia-style.)

Why discredit these people? Because they had criticized Vioxx or Merck.

Now it turns out that New Zealands Health Ministry may have picked up a few tips from Merck.

Just to refresh your memory, the Merck e-mails were presented in a class-action lawsuit against Merck over its anti-inflammatory drug Vioxx. Julian Burnside also produced evidence that Merck had attempted to intimidate researchers with implied threats of funding cut-offs or withdrawn academic appointments. An infuriated James Fries, professor of medicine at Stanford University, had apparently written to Merck back in 2000 to complain about the way it had treated some of his researchers who had been critical of Vioxx.

Even worse were allegations of Merck damage control by intimidationThis has happened to at least eight (clinical) investigators ... I suppose I was mildly threatened myself

Specific incidences of intimidation included one of Fries colleagues belief that his position had been put in jeopardy, and phone calls to another alleging his bias. Fries apparently told Merck that it had been systematically playing down the side effects of Vioxx and that its behavior "seriously impinges on academic freedom."

"In every possible way the company exerted itself to present the impression to the world at large that Vioxx did not provide any increased cardio risk ... when (a) it probably would and (b) it probably did," the letter went on to say.

So, on to Gardasil and New Zealands Ministry of Health.

New Zealand is having a bit of a problem with implementing its country-wide Gardasil vaccination program. The 3-shot HPV vaccine is being administered through schools, and 78 schools, about 5 percent, have declined to take part.

Furthermore, New Zealands self-described leading health and fitness magazine Fitness Life produced an article critical of Gardasil because, according to the publisher, the drug had been heavily promoted by a glowingly positive Ministry of Health and Merck, and no-one had publicly discussed potential long-term effects.

The article was publicized with a billboard in the middle of Auckland. The Ministry of Health promptly filed a complaint with the Advertising Standards Authority (ASA) on the grounds that both billboard and article were misleading, deceptive, and irresponsible.

The magazine countered that it would be deceptive and irresponsible to only talk Gardasil up, regardless of possible side-effectsThe advertisement and article were commissioned with a keen sense of social responsibility and with the hope that, by asking entirely valid questions, we are opening the floor to fresh debate on an issue that is of great importance to families and their daughters.

Fair enough. The ASA agreed on all counts and threw out the MoHs complaint.

Now, heres where it gets interesting.

The MoHs next cannon-ball was a written response to the article, available online, from the Immunisation Advisory Center.

After an unprofessionally snarky introduction, it counters some errors, such as a statement in the Fitness Life article that Gardasil contains a dead virus (its neither dead nor alive; it in fact uses a new genetically-engineered process that produces virus-like particles). It clears up some and reiterates the CDCs stance that, regardless of VAERS data (which is raw and often unverified data, both under-reported and over-reported) Gardasil has not been found to increase the risk of any of the serious conditions (other than anaphylaxis) noted in Wheatons article.m certainly not opposed to correcting statements of fact. As a writer, I do my damndest to get my facts straight, and Im happy to correct any factual error that I might make. I get positively crabby, actually, when people do the Chinese-whispers thing with some fairly outrageous suggestionsand that certainly has been known to happen with Gardasil. Because Fitness Life is not online, I have no clue what the article actually said.

But what sticks in my craw, apart from the pettish tone of the response, is the rather blatant attempt to shut down debate.

And what really, truly sticks in my craw like a bowling ball in a drinking straw. is the little zinger at the end.

A note on Diane Harper: After involvement with Merck and Gardasil clinical trials, Diane Harper disappeared and was found working for GSK on the Cervarix clinical trials. Her position on Gardasil may not be neutral.

Wow. That comes straight out of Mercks playbook.

I dont know Harper from Adam. But Ive liked the seemingly very realistic and sensible statements Ive heard from her. She has said, pretty much, that Gardasil is a great vaccine that is very valuable for most women, BUT that it was marketed too aggressively, introduced too rapidly, and could be a no-no for people with a family or personal history of auto-immune disorder. In other words, shed have liked to see Merck and medical authorities proceeding a little more cautiously with a brand-new vaccine. Which sounds completely reasonable to me.

Oh wait. Its partially critical.

So lets discredit her.

Yep. Sounds like good old New Zealand has been getting some advice from Merck.

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1: Int J Cancer. 2009 Mar 3. [Epub ahead of print] Tumor microvasculature supports proliferation and expansion of glioma-propagating cells. Borovski T, Verhoeff JJ, Ten Cate R, Cameron K, de Vries NA, van Tellingen O, Richel DJ, van Furth WR, Medema JP, Sprick MR. Laboratory for Experimental Oncology and Radiobiology, LEXOR, CEMM, AMC, University of Amsterdam, 1105AZ Amsterdam, The Netherlands. Glioblastoma multiforme (GBM) is the most common and aggressive primary brain tumor. The identification of 'cancer stem cells' (CSC) has shed new light on the potential mechanism of therapy resistance of these tumors. Because these cells appear to be more resistant to conventional treatments, they are thought to drive tumor regrowth after therapy. Therefore, novel therapeutic approaches that target these cells are needed. Tumor cells interact with their microenvironment. It has been reported that close contact between CSCs and tumor microvascular endothelium in GBM is important for CSCs to preserve their undifferentiated state and self-renewal ability. However, our understanding of this interaction is still rudimentary. This is in part due to a lack of suitable in vitro models that accurately represent the in vivo situation. Therefore, we set up a co-culture system consisting of primary brain tumor microvascular endothelial cells (tMVECs) and glioma propagating cells (GPCs) derived from biopsies of GBM patients. We found that tMVECs support the growth of GPCs resulting in higher proliferation rates comparing to GPCs cultured alone. This effect was dependent on direct contact between the 2 cell types. In contrast to GPCs, the FCS-cultured cell line U87 was stimulated by culturing on tMVEC-derived ECM alone, suggesting that both cell types interact different with their microenvironment. Together, these results demonstrate the feasibility and utility of our system to model the interaction of GPCs with their microenvironment. Identification of molecules that mediate this interaction could provide novel targets for directed therapy for GBM. (c) 2009 UICC. PMID: 19431144 [PubMed - as supplied by publisher] 2: Int J Cancer. 2009 Feb 27. [Epub ahead of print] The induction of autophagy by gamma-radiation contributes to the radioresistance of glioma stem cells. Lomonaco SL, Finniss S, Xiang C, Decarvalho A, Umansky F, Kalkanis SN, Mikkelsen T, Brodie C. William and Karen Davidson Laboratory of Cell Signaling and Tumorigenesis, Department of Neurosurgery, Hermelin Brain Tumor Center, Henry Ford Hospital, Detroit, MI. Malignant gliomas are characterized by a short median survival which is largely impacted by the resistance of these tumors tochemo- and radiotherapy. Recent studies suggest that a small subpopulation of cancer stem cells, which are highly resistant to gamma-radiation, has the capacity to repopulate the tumors and contribute to their malignant progression. gamma-radiation activates the process of autophagy and inhibition of this process increases the radiosensitivity of glioma cells; however, the role of autophagy in the resistance of glioma stem cells (GSCs) to radiation has not been yet reported. In this study we examined the induction of autophagy by gamma-radiation in CD133+ GSCs. Irradiation of CD133+ cells induced autophagy within 24-48 hr and slightly decreased the viability of the cells. gamma-radiation induced a larger degree of autophagy in the CD133+ cells as compared with CD133- cells and the CD133+ cells expressed higher levels of the autophagy-related proteins LC3, ATG5 and ATG12. The autophagy inhibitor bafilomycin A1 and silencing of ATG5 and beclin1 sensitized the CD133+ cells to gamma-radiation and significantly decreased the viability of the irradiated cells and their ability to form neurospheres. Collectively, these results indicate that the induction of autophagy contributes to the radioresistance of these cells and autophagy inhibitors may be employed to increase the sensitivity of CD133+ GSCs to gamma-radiation. (c) 2009 UICC. PMID: 19431142 [PubMed - as supplied by publisher] 3: Mol Cell Biochem. 2009 May 9. [Epub ahead of print] Telomerase downregulation in cancer brain stem cell. Shervington A, Lu C, Patel R, Shervington L. Brain Tumour North West, Faculty of Science and Technology, University of Central Lancashire, Preston, UK, aashervington@uclan.ac.uk. Cancer stem cells (CSCs) are a minute sub-population of self-renewing, immortal cells, which can be responsible for chemoresistance observed in the treatment of cancer. CSCs are similar to cancer cells requiring telomerase activity or alternative mechanisms for their proliferation and regeneration. This study explored the correlation between CD133 (stem cell marker) and telomerase expression using CD133+ cells isolated from the glioma GOS-3 cell line with magnetic affinity cell sorting (MACS). GOS-3 CD133+ showed a transcription downregulation of hTERT ( approximately 100-fold decrease) compared with CD133- cells. In order to further substantiate the novel finding, serum deprivation was adopted to enrich CD133 expression in GOS-3 cells. A pronounced upregulation of cd133 and downregulation of telomerase expression were produced as a consequence of decreasing serum supplement levels in GOS-3 cells. These findings showed for the first time that telomerase is downregulated in brain cancer stem cells compared to cancer cells. PMID: 19430894 [PubMed - as supplied by publisher] 4: J Neurooncol. 2009 May;93(1):49-60. Epub 2009 May 9. Origins and clinical implications of the brain tumor stem cell hypothesis. Zaidi HA, Kosztowski T, DiMeco F, Quiñones-Hinojosa A. The Johns Hopkins Hospital, Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21231, USA. With the advent of the cancer stem cell hypothesis, the field of cancer research has experienced a revolution in how we think of and approach cancer. The discovery of "brain tumor stem cells" has offered an explanation for several long-standing conundrums on why brain tumors behave the way they do to treatment. Despite the great amount of research that has been done in order to understand the molecular aspects of malignant gliomas, the prognosis of brain tumors remains dismal. The slow progress in extending the survival of patients with malignant CNS neoplasms is very likely due to poor understanding of the cell of origin in these tumors. This review article discusses the progress in our understanding of brain tumor stem cells as the cell of origin in brain cancers. We review the different proposed mechanisms of how brain tumor stem cells may originate, the intracellular pathways disrupted in the pathogenesis of BTSCs, the molecular markers used to identify BTSCs, the molecular mechanisms of cancer initiation and progression, and finally the clinical implications of this research. Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't PMID: 19430882 [PubMed - in process] 5: Acta Biochim Biophys Sin (Shanghai). 2009 May;41(5):341-51. The role of autophagy in sensitizing malignant glioma cells to radiation therapy. Zhuang W, Qin Z, Liang Z. Department of Pharmacology, Soochow University School of Medicine, Suzhou, China. Malignant gliomas represent the majority of primary brain tumors. The current standard treatments for malignant gliomas include surgical resection, radiation therapy, and chemotherapy. Radiotherapy, a standard adjuvant therapy, confers some survival advantages, but resistance of the glioma cells to the efficacy of radiation limits the success of the treatment. The mechanisms underlying glioma cell radioresistance have remained elusive. Autophagy is a protein degradation system characterized by a prominent formation of double-membrane vesicles in the cytoplasm. Recent studies suggest that autophagy may be important in the regulation of cancer development and progression and in determining the response of tumor cells to anticancer therapy. Also, autophagy is a novel response of glioma cells to ionizing radiation. Autophagic cell death is considered programmed cell death type II, whereas apoptosis is programmed cell death type I. These two types of cell death are predominantly distinctive, but many studies demonstrate a cross-talk between them. Whether autophagy in cancer cells causes death or protects cells is controversial. The regulatory pathways of autophagy share several molecules. PI3K/Akt/mTOR, DNA-PK, tumor suppressor genes, mitochondrial damage, and lysosome may play important roles in radiation-induced autophagy in glioma cells. Recently, a highly tumorigenic glioma tumor subpopulation, termed cancer stem cell or tumor-initiating cell, has been shown to promote therapeutic resistance. This review summarizes the main mediators associated with radiation-induced autophagy in malignant glioma cells and discusses the implications of the cancer stem cell hypothesis for the development of future therapies for brain tumors. Publication Types: Research Support, Non-U.S.

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The Manville Trust was established in 1974 to settle asbestos claims for injuries resulting from exposure to asbestos products extracted or manufactured by Johns-Manville Corporation and its affiliates. In 1978, a judge was "a conscious effort by the [asbestos] industry in 1930 to minimize or even eliminate the dissemination of information to employees and the public for fear of the promotion of justice. "After this statement, the EPA announced its intention to issue a rule banning all uses of asbestos.

First government of Ban Asbestos

OSHA tightened asbestos-exposure standard in 1986. In 1989, EPA banned asbestos in most applications. However, a federal law suit with asbestos in 1991, companies in the EPA reversed a ban on asbestos. OSHA tightened standards for asbestos exposure in 1994. Finally, in 1999, the Florida Supreme Court ruled that Owens Corning willfully retained information on the dangers of working with the company for asbestos products stating, "It would be difficult to have a more serious case of figure ... a blatant disregard of safety involving large numbers of people whose lives are in danger. "

In 2003, Senator Orrin Hatch (R-Utah) introduced legislation to $ 108 billion national trust fund to compensate asbestos victims, cap business liability and ease the presentation of an action justice.

Choosing a Mesothelioma Attorneys

Now that you know the above, charges for mesothelioma litigation, to consider some key points concerning the selection of asbestos lawyer.

* Mesothelioma Cancer Network recommendation - If you arrive at the list of mesothelioma or cancer in general? If so, ask for personal recommendations. Why choose the person mesothelioma lawyer? How was their attention? What is their experience in resolving cases of asbestos? etc.etc.etc. Lawyers depend on good relations with customers and by word of mouth advertising is planned for a good deal. But do not expect any form of guarantee, just because another patient mesothelioma in May and have done in their case - all the circumstances are different, and therefore the results.

* Check files - Check, experience, disciplinary measures for any potential candidate mesothelioma lawyer. Many states currently require all lawyers to obtain a degree from the University and Law School, passing a written examination, a test of physical fitness and character, and they practice law in May In addition, many lawyers remain legal education courses each year. You will find many circles mesothelioma lawyers legal source control books in your local library or the public library legislation.

* Consider mesothelioma lawyer by training and experience - Ask if the lawyer has dealt with issues similar to asbestos, and what were the results. Ask if the lawyer has legal training on asbestos and mesothelioma lititgation legislation.

Consider specialisation mesothelioma, You'll find that the lawyers/attorneys to focus exclusively or almost exclusively on the representation of individuals and families of people with mesothelioma and lung cancer.

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Detection
There are often no symptoms in the early stages. Women should be aware of the screening recommendations and follow them. There are varieties of symptoms that may appear as the tumor grows such as:
- The breast changing in size or shape
- Breast skin becomes pitted or ridged
- Thickening or lump in the underarm or breast
- Discharge from nipple or the nipple turns inward
- Skin on the breast becomes red or scales
If you have any of these symptoms, have yourself examined by a medical professional. This does not mean you have cancer but you defiantly want to have this checked.
Before the age of twenty, is very rare to get it and not often diagnosed in women less than twenty-five years old. The chances of contacting climbs steadily after 25 and peaks around menopause age in women. It increases less after menopause but as they age, the risk to older women gradually increases.
Risk Factors
Nobody really knows what causes this cancer. Some of the elements that are thought to increase the risk are:
Gender: There are more cases of women than men
Weight: Overweight women are at higher risk
Age: From 25 to menopause, the chances increases.
Children: If a woman has not had a child, or had a child after 30
Family History: Women that have a family member that have or had it are at risk.
Male Breast Cancer
Yes, it really does happen. It is certainly not as common as in women but approximately one to 1.5% happens to men. Older men most often diagnosed with it and are between sixty and seventy years old. If a man has had previous exposure to radiation, such as for cancer treatment, their risk increases. Approximately 20% of men with a mother, sister or other close female relatives with breast cancer are certainly at higher risk. Some of the symptoms in men includes swelling or a breast lump, retracted nipple or discharge and scaling or redness of the breast skin or nipple.
Statistics
The statistics are frightening. Each and ever year, over 182,000 women and 16,000 men are diagnosed with breast cancer. Over 400 men and 43,300 women will die from this terrible disease. During their lifetime, one woman out of eight has or will get breast cancer. Most people have family or friends that have or had breast cancer. Always give them your support and encouragement.

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Nano changes rise to macro importance in a key electronics material
By combining the results of a number of powerful techniques for studying material structure at the nanoscale, a team of researchers from the National Institute of Standards and Technology (NIST), working with colleagues in other federal labs and abroad, believe they have settled a long-standing debate over the source of the unique electronic properties of a material with potentially great importance for wireless communications.

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VIENNA: The United Nations' crime and drug watchdog has indications that money made in illicit drug trade has been used to keep banks afloat in the global financial crisis, its head was quoted as saying on Sunday.

Vienna-based UNODC Executive Director Antonio Maria Costa said in an interview released by Austrian weekly Profil that drug money often became the only available capital when the crisis spiralled out of control last year.

"In many instances, drug money is currently the only liquid investment capital," Costa was quoted as saying by Profil. "In the second half of 2008, liquidity was the banking system's main problem and hence liquid capital became an important factor."

The United Nations Office on Drugs and Crime had found evidence that "interbank loans were funded by money that originated from drug trade and other illegal activities," Costa was quoted as saying. There were "signs that some banks were rescued in that way."

Profil said Costa declined to identify countries or banks which may have received drug money and gave no indication how much cash might be involved. He only said Austria was not on top of his list, Profil said.

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I will tell you a story. About 2 years ago, I was on a panel of highly trained dentists to evaluate certain new products that are going to be introduced to the market by one of the big supply companies. They introduced a new material that will help to bond or glue on the white fillings to the teeth. Now, there are 10 different quality of materials in general that can be used for this, each one has its own indications based on the type of the filling, the quality of the tooth and how deep and big the cavity is. And to make it more complicated, there are subcategories of these materials. This company has had a bonding agent material that has served well and does a great job for certain specific situations. One of the issues is that most dentists only carry one type of these materials in their office and use the same thing for all instances. Why? Because most often they do not know that there is a difference between the strength of this materials in different situations. The sales reps know enough to sell the material, but are not dentists and do not know when a dentist should use these material. Back in that meeting, this company introduced a new version of this same bonding agent to us. Instead of having two little bottles and putting one drop of each on the tooth and place the filling over it. The new material, instead of two bottles, is in a beautiful pen like applicator and it auto mixes the material, so it can conserve the material.

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Jarod Steenwyk, who is in his fourth year on the varsity, and his Ellsworth teammates will play in a Class D state quarterfinal game 7 p.m. Tuesday at Traverse City Central High School. The Lancers are 24-0 and in the state quarters for the first time since 1993. They’ll play defending state champion Muskegon Western Michigan Christian, 21-4, for a berth in the state semifinals at Michigan State University’s Breslin Center.

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breast cancer patients who lack vitamin D in their bodies are much more likely to have their cancer spread and to die from the disease, articulated a new study in United States. The researchers studied more than 500 women with breast cancer and found that women deficient in vitamin D were 94 percent more likely to have their cancer spread and 73 percent more likely to die from their cancer.

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Source: The Lancet, Volume 373, Issue 9665, Page 693, 28 February 2009
Author: editorial staff
Tensions between provision of and payment for health care are familiar. Though doctors assume principal responsibility for patients health, those who work for pharmaceutical companies view the patented medicines they design as key components of health care. Creative ways are continually found to make such drugs available to as many patients in high-income countries as possible, the profits contributing to future investment in development and leaving national drug budgets affordable, just. Yet, a few hours flying away, patients in developing countries usually have no access to these very same patented drugs.
GlaxoSmithKline (GSK) has grown in size and influence by successful drug development, timely takeovers, and shrewd management. Andrew Witty, who ascended to the vertiginous position of chief executive at GSK in the past year, has attracted attention by a surprising presentation at Harvard Medical School on Feb 13. He promises that GSK will now not only make its medicines available much more cheaply to patients in low-income countries, but also make a bolder commitment to research into neglected diseases. As one blogger puts it, “arise Sir Andrew Witty (or is it Saint Andrew?)”.
Does this announcement mark a sea change in pharmas attitude to the provision of drugs in poor countries, or could it be more reminiscent of the zany hybrid vehicles that distract attention from car manufacturers shamelessly polluting stock in trade? Wittys words were carefully weighed to cast a rosy glow around GSKs existing efforts. He namechecked the companys Spanish centre focused on research into “diseases of the developing world”, including tuberculosis, and the companys malaria vaccine programme (a vaccine that will in any event need to find its main markets in low-income and middle-income regions). But a statement of intent was made, and some clear ideas put forward. In the 50 poorest countries, patented medicines are to be sold at no more than a quarter of their price in developed countries, and a commitment has been made to reinvest 20% of GSKs developing-country profits back into local health-care infrastructure. Most intriguingly, the idea of a patent pool has been floated, by which holders of intellectual property rights would share them with others to invigorate research into neglected diseases.
GSK has made philanthropic gestures in the past—witness its ancestor SmithKlineBeechams donation of albendazole for treatment of lymphatic filariasis—and positive publicity might help to lift some of the dark clouds that have been gathering on pharmas horizon, including depleted development pipelines and increased regulatory oversight. To be sure, Witty is not intending to alarm shareholders. GSK (2007 annual revenue £22·7 billion, profit after tax £5·5 billion) currently earns annual revenues of just US$43 million in the poorest countries, suggesting that the money to be reinvested locally will be less than 0·1% of overall profits. Flaws have been spotted in Wittys new way too. Médecins Sans Frontières campaign for access to essential medicines notes that, despite a need for new pediatric and combination antiretroviral drugs to combat HIV, GSK does not plan to share its HIV patents with other researchers. Voluntary price reductions seem unlikely to match the dramatic falls in price, and consequent transformational increase in poor-country access, wrought by generic competition on antiretrovirals in the past decade.
Those committed to the forbidding task of improving health care in developing countries should commend Wittys stance, but continue to press for more, and broader, action. GSK is not offering to give away its drugs and vaccines—someone will need to pay for patented medicines that can now be made available to patients in poor countries more cheaply, and likewise development of patent-pooled orphan drugs is yet to be planned, pursued, and paid for. And who will pay, amid a financial ice age of unknown extent? To convert a promising soundbite into improved health for people in developing countries, GSK must work openly with funding bodies, governments, and other stakeholders to identify clinical and public health problems that offer the greatest potential benefit to human health. These efforts will need close scrutiny to ensure that they register measurable achievements and, given the substantial obstacles of unstable health systems and uncertain funding, gather momentum.
Now that Andrew Witty has chosen this particular agenda, as a test of GSKs resolve he can be presented with one straightforward preventive challenge—to make GSKs licensed human papillomavirus vaccine affordable for girls and young women in low-income countries, and work proactively with funding agencies to deliver the vaccine in countries with suitable health systems.

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FHCRC.org - Frequent and/or long-term marijuana use may significantly increase a mans risk of developing the most aggressive type of testicular cancer, according to a study by researchers at Fred Hutchinson Cancer Research Center. Even occasional users of marijuana - about weekly - had double the risk for testicular cancer compared to nonusers. Starting marijuana use as a teenager was particularly hazardous in terms of risk. The study results were published online February 9, 2009 in the journal Cancer.
The researchers found that being a marijuana smoker at the time of diagnosis was associated with a 70 percent increased risk of testicular cancer. The risk was particularly elevated (about twice that of those who never smoked marijuana) for those who used marijuana at least weekly and/or who had long-term exposure to the substance beginning in adolescence.
The results also suggested that the association with marijuana use might be limited to nonseminoma, a fast-growing testicular malignancy that tends to strike early, between ages 20 and 35, and accounts for about 40 percent of all testicular-cancer cases.
Since the 1950s, the incidence of the two main cellular subtypes of testicular cancer, nonseminoma and seminoma - the more common, slower growing kind that strikes men in their 30s and 40s -  has increased by 3 percent to 6 percent per year in the U.S., Canada, Europe, Australia and New Zealand. During the same time period, marijuana use in North America, Europe and Australia has risen accordingly, which is one of several factors that led the researchers to hypothesize a potential association.
Our study is not the first to suggest that some aspect of a mans lifestyle or environment is a risk factor for testicular cancer, but it is the first that has looked at marijuana use, said author Stephen M. Schwartz, M.P.H., Ph.D., an epidemiologist and member of the Public Health Sciences Division at the Hutchinson Center. The study was funded by the National Cancer Institute.
Established risk factors for testicular cancer include a family history of the disease, undescended testes and abnormal testicular development. The disease is thought to begin in the womb, when some fetal germ cells (those that eventually make sperm in adulthood) fail to develop properly and become vulnerable to malignancy. Later, during adolescence and adulthood, it is thought that exposure to male sex hormones coaxes these cells to become cancerous.
Just as the changing hormonal environment of adolescence and adulthood can trigger undifferentiated fetal germ cells to become cancerous, it has been suggested that puberty is a window of opportunity during which lifestyle or environmental factors also can increase the risk of testicular cancer, said senior author Janet R. Daling, Ph.D., an epidemiologist who is also a member of the Centers Public Health Sciences Division. This is consistent with the studys findings that the elevated risk of nonseminoma-type testicular cancer in particular was associated with marijuana use prior to age 18.
Chronic marijuana exposure has multiple adverse effects on the endocrine and reproductive systems, primarily decreased sperm quality. Other possible effects include decreased testosterone and male impotency. Because male infertility and poor semen quality also have been linked to an increased risk of testicular cancer, this further reinforced the researchers hypothesis that marijuana use may be a risk factor for the disease.
Daling first got the idea to explore a possible association between marijuana use and testicular cancer about eight years ago, when she attended a talk by a physician at the University of Washington who presented findings that only two organs, the brain and the testes, had receptors for tetrahydrocannabinol, or THC, the main psychoactive component of marijuana. Since then, a number of other sites have been found to contain THC receptors, including the heart, uterus, spleen and immune-system cells.
The male reproductive system also naturally produces a cannabinoid-like chemical that is thought to have a protective effect against cancer. The authors speculate that marijuana use may disrupt this anti-tumor effect, which could be another explanation for the possible link between marijuana and increased risk of testicular cancer.
Study participants were also asked about other habits that may be correlated with marijuana use, including smoking and alcohol consumption. Even after statistically controlling for these lifestyle factors, as well as other risk factors, such as first-degree family history of testicular cancer and a history of undescended testes, marijuana use emerged as a significant, independent risk factor for testicular cancer.
According to the National Cancer Institute, testicular cancer is the most common form of cancer in men between the ages of 15 and 34 and is most common in white men, especially those of Scandinavian descent.

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Clinicians have an important role to play in reducing hospital waste and should not be discouraged by lack of knowledge or the threat of legal liability, according to a paper published on bmj.com today.
In 2005-6, the NHS produced 408,218 tonnes of waste, 29% of which was clinical waste, and spent nearly £73m (€80m; $103m) on its disposal. Concerns about the risk of prion transmission and sterility have also led to large increases in both the amount of anaesthetic packaging and the use of disposable devices over the past 5-10 years.

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Grok Didnt Take Supplements So Why Should I?
Robert Chon asks:
Id be interested to know Mark and Richards take on the newest wave of miracle supplements.
Im speaking of course of those which generally perform the function known as colon cleansing.
The purveyors make many claims, mostly regarding the removal of toxins from the body and of course, substantial weight-loss claims.
I’m inherently skeptical of quick fixes – especially when specifically marketed as such. It makes me think of some conman hightailing it out of Dodge, suitcase of money in hand. A few of these guys are suggesting that many of us have a ten-foot-long layer of plaque in our colon that’s been there for years! It’s all BS. I say if you’re eating clean, whole foods as ordained by evolutionary biology, you won’t need to cleanse yourself of toxins. These supplements – I’m just guessing here, as I’m not sure which you’re referring to – may help you lose weight in the short term, but I’d imagine it would be via a combination of starvation and frequent trips to the bathroom. Many of these are just high-fiber preparations that might even be dangerous. Why not just stick to eating good fats and proteins and cutting carbs?
Next are three questions around the same issue. First, Meese asks:
Ive been puzzling over Lyle McDonalds posts on leptin and had the following 2 questions:
1) On a primal/paleo/evfit type of lifestyle in which one consumes relatively constrained amounts of carbohydrates, could falling or low leptin still become a problem as both carbohydrate metabolism and fat storage would tend to decrease, possibly prompting hormonal responses to guard against starvation? For instance, I notice when I am fasting, I am not particularly hungry or weak (insulin levels good!), but I am extremely and uncomfortably cold.
2) McDonald seems to recommend brief(ish) carb-heavy to bring leptin levels back to baseline after dieting. As fat and protein dont seem to have appreciable effects on leptin, and fat and sugar stores tend to decrease on a primal lifestyle, how can a recovering dieter/non-bodybuilder raise leptin levels? Assuming one already gets adequate sleep, is there a better way than controlled carb binges?
Then... Madmax:
Id like to know how Mark approaches Intermittent Fasting; ie how often he does it and for how long.
I too second Meeses questions regarding Lyle McDonalds carb re-feeding idea. McDonald is an interesting case. Hes heavy into the science aspect but he does not recommend a paleo/primal lifestyle. In fact, I get the impression that he thinks its and unscientific. Lyle is also no fan of Gary Taubes. I would usually dismiss someone like him but for those that know Lyle, they know that he knows his science. This makes ignoring him out of hand difficult.
And... Richard:
At the risk of just re-hashing Meese and Madmax, here goes: can there be potential value in intermittent/random higher carb days? Nothing ridiculous, but Im thinking something like ratcheting from, say 100g or less per day, to the occasional 200-300g per day. Aside from the leptin issue noted by Meese above (which I did not know about), Im wondering whether this could simply be a valuable form of variation/randomizing that the body in a productive way.
Lyle (whom I greatly respect) seems to attribute a whole lot more to leptin than I do. I’d say insulin is the more significant driver (by a factor of 10, even). While leptin has it’s function, it, as Lyle says, has a lot to do with regulating appetite – it’s an “anti-starvation” hormone. But if you’re doing a true Primal eating program, appetite doesn’t really ever become an issue.
As you lose body fat, leptin may decrease. If hunger pangs set in, eat a bit more. Once you’re down to 10% body fat (for a guy) or 15% (for a gal) and you feel the need for more carbs in your life, have at it! Just make them healthy sources. At that level, maintaining your body composition shouldn’t be an issue, and eating all the protein and fat you want with 100-150g/day of carbs from veggies and fruits shouldn’t change it.
And finally, if leptin is mostly an “anti-starvation” hormone and you don’t feel like you’re starving, where’s the problem? If you do feel like you’re starving yourself, try to up the fat and protein first, then bump up the carbs to 100-150g/day. Still feeling it? Go for a “refeed” day or two. Even then, get your carbs from healthy sources (think yams, roots, vegetables, fruits) and try not to exceed 300 grams a day.
Chris asks:
1. Mark, how does someone with very fair skin, who easily burns, handle sun exposure? Maybe 15-20 minutes exposure before you break out the Chernobyl strength suncreen?
2. What would you suggest for those of us Primals who go on a cruise? Go for the fruity drinks with all that sugar, or stick to the beer or wine?
(1) 15-20 minutes of good sun exposure a day is a perfect amount (in fact, for the ultra-fair skinned – think Nordic maidens – 3-15 minutes is plenty). You don’t want to burn, but you do need to give your skin enough time to absorb the good stuff. Fifteen minutes seems to be an optimum level to shoot for. Then just find shade, cover up with clothing or apply a good sunblock.
(2) I’d say go for the wine. Although you probably aren’t thinking about nutrients and healthy stuff on a cruise, red wine is loaded with antioxidants and has actually been deemed healthy by CW (I know, I know, not exactly a sterling endorsement, but still…).

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Risk factors are factors that are increasing the risk of lung cancer. This deadly form of cancer is taking more than million lives each year so it very good to know what factors increase the risk of getting this horrible disease. This article will give you some basic information. The major risk factor for lung cancer is off course smoking tobacco, and this not only among smokers but also among secondhand smokers. If we take a look at United States data we can see that about 90% of lung cancer deaths in men and almost 80% of lung cancer deaths in women are result of smoking. Smoking is the biggest lung cancer risk factor, in fact the people who smoke are 10 to 20 times more likely to get lung cancer or die from lung cancer than people who do not smoke. Factors that additionally increase the risk are also number of cigarettes that person smokes per day, and of course years of smoking.

Many people want to know what happens if they quit smoking at some time, is the risk for getting the lung cancer then lower or the same compared to if they didn't stop smoking at all. It has to be said here that the people who quit smoking have a lower risk of lung cancer than if they had continued to smoke, but their risk is still significantly higher compared to the risk for people who never smoke. Smoking does not only cause lung cancer but some other forms of cancer as well, including cancer of the mouth and throat, esophagus, bladder, kidney, pancreas, cervix, and stomach. This is really no surprising when you consider that hat cigarette smoke contains over 60 known carcinogens, so each cigarette means more risk. Secondhand smokers also have increased lung cancer risk compared to people that are not frequently surrounded by smokers. Secondhand smoking each year takes away around 3000 lives.

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