what is a demand fee

een What is a 'Demand Deposit'A demand deposit consists of funds held in an account from which deposited funds can be withdrawn at any time from the depository institution, such as a checking or savings account, accessible by a teller, ATM or online banking.

What is a 'Demand Deposit'

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In contrast, a term deposit is a type of account that cannot be accessed for a predetermined period of time. M1 is a category of the money supply that includes demand deposits as well as physical money and negotiable order of withdrawal (NOW) accounts that have no maturity period but limited withdrawals or transfers. Next Up Bank Deposits Call Deposit Account Deposit Interest Rate Term Deposit BREAKING DOWN 'Demand Deposit'Demand deposits provide the money consumers need for paying daily expenses. If depositors were required to notify their financial institutions before withdrawing funds, the depositors would have challenges making everyday purchases and paying bills. Characteristics of Demand Deposit Accounts Demand deposit accounts (DDAs) may have joint owners. Both owners must sign when opening the account, but only one owner must sign when closing the account. Either owner may deposit or withdraw funds and sign checks without permission from the other owner. Financial institutions typically create minimum balances for demand deposit accounts. Accounts falling below the minimum value typically are assessed a fee each time the balance drops below the required value. NOW Accounts, MMAs and Demand Deposits Although negotiable order of withdrawal (NOW) accounts and money market accounts (MMAs) let holders deposit and withdraw funds on demand and typically pay market interest rates, they are not DDA accounts. MMAs typically limit withdrawals, or transactions including deposits, withdrawals and transfers, to six per month. Fees may apply if the limit is exceeded. Cash Reserves and Demand Deposits The amount of cash reserves a financial institution is keeping either in its vault or deposited with the Federal Reserve depends on the amount of demand deposits the institution is holding. The greater the amount of demand deposits, the more cash the institution reserves. Regulation Q and Demand Deposits Federal Reserve Regulation Q prohibits financial institutions from paying interest on demand deposits. However, the institution may give an account holder cash or credit payments or merchandise when opening an account. The account holder may not receive more than two payments annually, and the value of each payment may not exceed $10 for deposits under $5,000 and $20 for deposits exceeding $5,000. Example of a Demand Deposit In July 2016, Bank First reported net income for the second quarter of 2016 of $3.76 million, or $0.60 per share. The numbers represented an 11% increase in quarterly earnings over the same quarter the previous year. The increase was partly due to growth in demand deposit balances, which are a low-cost source of funding for the bank.


arcadis phone number

it5Arcadis - San Antonio351 Killarney Drive, San Antonio TX 78223Phone Number: (210) 337-0502

Arcadis Locations & Hours near San Francisco

1Arcadis - Petaluma625 2nd Street Suite 210, Petaluma CA 91761Phone Number: (707) 769-9977Store Hours Hours may fluctuate Distance: 374.84 miles Edit2Arcadis - Phoenix8222 South 48th Street Suite 140, Phoenix AZ 85281Phone Number: (602) 438-0883Store Hours Hours may fluctuate Distance: 661.46 miles Edit3Arcadis - Tucson285 West 18th Street, Tucson AZ 85701Phone Number: (520) 903-2393Store Hours Hours may fluctuate Distance: 754.09 miles Edit4Arcadis - Helena1610 B Street, Helena MT 59601Phone Number: (406) 449-7001Store Hours Hours may fluctuate Distance: 800.76 miles Ed

Store Hours Hours may fluctuate Distance: 1,499.34 miles Edit6Arcadis - Lufkin2710 South Medford Drive, Lufkin TX 75901Phone Number: (936) 632-9722Store Hours Hours may fluctuate Distance: 1,637.52 miles Edit7Arcadis - Montgomery6009 Monticello Drive Suite A, Montgomery AL 35553Phone Number: (334) 272-3834Store Hours Hours may fluctuate Distance: 1,969.42 miles Edit8Arcadis - Chattanooga1210 Premier Drive, Chattanooga TN 37421Phone Number: (423) 756-7193Store Hours Hours may fluctuate Distance: 2,071.50 miles Edit9Arcadis - Dublin6397 Emerald Parkway Suite 150, Dublin OH 44804Phone Number: (614) 764-2310Store Hours Hours may fluctuate Distance: 2,074.69 miles Edit10Arcadis - Oak Ridge97 Midway Lane, Oak Ridge TN 37830Phone Number: (865) 481-3000Store Hours Hours may fluctuate Distance: 2,101.51 miles Edit1 2 View all Arcadis locations »Show Map Arcadis Avg. Customer Rating No reviews yet Useful Links Add a Arcadis Store


3/5 of 60

ment3/5 = 60/1 3*60 = 5*1 180/5 = 36*1 answer = 36D

What is 3/5 of the number 60?

Science & Mathematics Mathematics What is 3/5 of the number 60? Follow 11 answers Answers Relevance Rating Newest Oldest Best Answer: 36. Divide 60 by 5, then multiply by 3. Levi · 8 years ago1 0 Comment There are two ways in which you could do this problem: 1. 3/5 x 60 Cancel out the 5 and 60 and the 60 becomes a 12. 12 x 3 = 36 2. 3/5 x 60 Multiply the numerators --> 180/5 = 36confuzzledchee · 8 years ago0 0 Comment5 X 60Source (s):https://shorte.im/a9K0bemberger · 1 year ago0 0 Com

ean · 8 years ago0 0 Comment3/5 of 60 = 60 * 3/5 ==>36Govind 3i · 8 years ago0 1 Comment36Lara · 8 years ago0 0 Comment36? · 8 years ago0 0 Comment36Victor L · 8 years ago0 0 Comment36eagle · 8 years ago0 0 Comment (3*60)/5 = 180/5 = 36Guillermo · 8 years ago0 1 Comment1 2 next Maybe you would like to learn more about one of these? Find the best luxury cars Need Home Equity Loan Options? Look For Franchises For Sale Find Moving Container Services


which are the organs inside of our body

s. Vital organs Humans have five vital organs that are essential for survival. These are the brain, heart, kidneys, liver and lungs. The human brain is the body's control center, receiving and sending signals to other organs through the nervous system and through secreted hormones.

Live Science Health Reference: The Human Body: Anatomy, Facts & Functions By Rachael Rettner, Senior Writer | March 10, 2016 01:45pm ETMOREError setting up player: Invalid license key

The human body is everything that makes up, well, you. The basic parts of the human body are the head, neck, torso, arms and legs.

[ Image Gallery: The Bio Digital Hu

man]Body systems Our bodies consist of a number of biological systems that carry out specific functions necessary for everyday living. The job of the circulatory system is to move blood, nutrients, oxygen, carbon dioxide, and hormones, around the body. It consists of the heart, blood, blood vessels,arteries and veins. The digestive system consists of a series of connected organs that together, allow the body to break down and absorb food, and remove waste. It includes the mouth, esophagus, stomach, small intestine, large intestine, rectum, and anus.

The liver and pancreas also play a role in the digestive system because they produce digestive juices. The endocrine system consists of eight major glands that secrete hormones into the blood. These hormones, in turn, travel to different tissues and regulate various bodily functions, such as metabolism, growth and sexual function. The immune system is the body's defense against bacteria, viruses and other pathogens that may be harmful. It includes lymph nodes, the spleen, bone marrow, lymphocytes (including B-cells and T-cells), the thymus and leukocytes, which are white blood cells. The lymphatic system includes lymph nodes, lymph ducts and lymph vessels, and also plays a role in the body's defenses. Its main job is to make is to make and move lymph, a clear fluid that contains white blood cells, which help the body fight infection. The lymphatic system also removes excess lymph fluid from bodily tissues, and returns it to the blood. The nervous system controls both voluntary action (like conscious movement) and involuntary actions (like breathing), and sends signals to different parts of the body. The central nervous system includes the brain and spinal cord. The peripheral nervous system consists of nerves that connect every other part of the body to the central nervous system. The body's muscular system consists of about 650 muscles that aid in movement, blood flow and other bodily functions. There are three types of muscle: skeletal muscle which is connected to bone and helps with voluntary movement, smooth muscle which is found inside organs and helps to move substances through organs, and cardiac muscle which is found in the heart and helps pump blood. The reproductive system allows humans to reproduce. The male reproductive system includes the penis and the testes, which produce sperm. The female reproductive system consists of the vagina, the uterus and the ovaries, which produce eggs. During conception, a sperm cell fuses with an egg cell, which creates a fertilized egg that implants and grows in the uterus. [Related: Awkward Anatomy: 10 Odd Facts About the Female Body]Our bodies are supported by the skeletal system, which consists of 206 bones that are connected by tendons, ligaments and cartilage. The skeleton not only helps us move, but it's also involved in the production of blood cells and the storage of calcium. The teeth are also part of the skeletal system, but they aren't considered bones. The respiratory system allows us to take in vital oxygen and expel carbon dioxide in a process we call breathing. It consists mainly of the trachea, the diaphragm and the lungs. The urinary system helps eliminate a waste product called urea from the body, which is produced when certain foods are broken down. The whole system includes two kidneys, two ureters, the bladder, two sphincter muscles and the urethra. Urine produced by the kidneys travels down the ureters to the bladder, and exits the body through the urethra.

The skin, or integumentary system, is the body's largest organ. It protects us from the outside world, and is our first defense against bacteria, viruses and other pathogens. Our skin also helps regulate body temperature and eliminate waste through perspiration.

In addition to skin, the integumentary system includes hair and nail

It is responsible for our thoughts, feelings, memory storage and general perception of the world. The human heart is a responsible for pumping blood throughout our body. The job of the kidneys is to remove waste and extra fluid from the blood. The kidneys take urea out of the blood and combine it with water and other substances to make urine. The liver has many functions, including detoxifying of harmful chemicals, breakdown of drugs, filtering of blood, secretion of bile and production of blood-clotting proteins. The lungs are responsible for removing oxygen from the air we breathe and transferring it to our blood where it can be sent to our cells. The lungs also remove carbon dioxide, which we exhale. Fun facts The human body contains nearly 100 trillion cells. There are at least 10 times as many bacteria in the human body as cells. The average adult takes over 20,000 breaths a day. Each day, the kidneys process about 200 quarts (50 gallons) of blood to filter out about 2 quarts of waste and water Adults excrete about a quarter and a half (1.42 liters) of urine each day. The human brain contains about 100 billion nerve cells Water makes up more than 50 percent of the average adult's body weight Ready for Med School? Test Your Body Smarts You use your eyes to see, your ears to hear and your muscles to do the heavy lifting. Well, sort of. In fact, most body parts are far more complicated than that, while some seem to have no business being inside there at all. Start the Quiz0 of 10 questions complete Editor’s Note: If you’d like more information on this topic, we recommend the following book (available on amazon.com): Human Body: An Illustrated Guide Related pages Systems of the human body Circulatory System: Facts, Function & Diseases Digestive System: Facts, Function & Diseases Endocrine System: Facts, Functions and Diseases Immune System: Diseases, Disorders & Function Lymphatic System: Facts, Functions & Diseases Muscular System: Facts, Functions & Diseases Nervous System: Facts, Function & Diseases Reproductive System: Facts, Functions and Diseases Respiratory System: Facts, Function & Diseases Skeletal System: Facts, Function & Diseases Skin: Facts, Diseases & Conditions Urinary System: Facts, Functions & Diseases Parts of the human body Bladder: Facts, Function & Disease Human Brain: Facts, Anatomy & Mapping Project Colon (Large Intestine): Facts, Function & Diseases Ears: Facts, Function & Disease Esophagus: Facts, Function & Diseases How the Human Eye Works Gallbladder: Function, Problems & Healthy Diet Human Heart: Anatomy, Function & Facts Kidneys: Facts, Function & Diseases Liver: Function, Failure & Disease Lungs: Facts, Function & Diseases Nose: Facts, Function & Diseases Pancreas: Function, Location & Diseases Small Intestine: Function, Length & Problems Spleen: Function, Location & Problems Stomach: Facts, Function & Diseases The Tongue: Facts, Function & Diseases You'd Also Like Lymphatic System: Facts, Functions & Diseases Live Science Muscular System: Facts, Functions & Diseases Live Science Diagram of the Human Lymphatic System (Infographic)Live Science Immune System: Diseases, Disorders & Function Live Science Latest on The Human Body: Anatomy, Facts & Functions This Pouched Rat Can Sniff Out Tuberculosis in Kids A Man Ate the 'World's Hottest' Pepper. Then the 'Thunderclap' Headaches Started Did You Buy Bitcoins? Your Brain's Anatomy Might Be to Blame Scientists Find Very Young Cells in Even Very Old Brains Tiny, Lab-Grown Minibrains Sprout Blood Vessels Brain-Uploading Company Has No Immediate Plans to Upload Brains More from Live Science Late to Bed, Early to Die? Night Owls May Die Sooner Gallbladder: Function, Problems & Healthy Diet Here's What Causes Some People's Bones to 'Drip' Like Candle Wax Synthetic Marijuana Tainted with Rat Poison Linked to 3 Deaths After Death, Your Microbiome Could Still Help the Living If You Want Your Friend to Vaccinate Their Kids, Don't Try to Change Their Mind This Pouched Rat Can Sniff Out Tuberculosis in Kids Restroom Hand Dryers Are Blowing Bacteria Everywhere Author Bio Rachael Rettner, Senior Writer Rachael has been with Live Science since 2010. She has a masters degree in journalism from New York University's Science, Health and Environmental Reporting Program. She also holds a Bachelor of Science in molecular biology and a Master of Science in biology from the University of California, San Diego. Rachael Rettner, Senior Writer on


what are the benefits of eating special dark chocolate

Dark chocolate contains polyphenols, a powerful type of antioxidant that is also found in foods like berries, green and black tea, and red wine. These polyphenols help to defend the body’s cells against free radicals from environmental toxins and diseases, including heart disease, cancer, and chronic inflammation.

The Health Benefits and Risks of Dark Chocolate

By Heidi Hackler Do you love chocolate? What if you could eat it every day for your health? It might sound too good to be true, but research shows that there are some excellent health gains associated with eating dark chocolate. There are, however, also some potential risks. Before we look at the health benefits and risks of dark chocolate, let’s take a look at how dark chocolate is made. From Bean to Bar Chocolate is made from cocoa beans that grow on cacao trees, originally native to Central America and now grown in tropical climates throughout the world. A single cacao tree produces 20 to 30 cocoa pods per year, and each pod contains around 40 cocoa beans. It takes one year’s yield from a single tree to produce about five dark chocolate bars. Cocoa pods mature on the vine and are hand-harvested, then cut open to dry. The cocoa beans, covered in a white pulp, are laid out in the sun to ferment, and the chocolate flavor starts to emerge. Different types of fermentation processes result in different flavors of chocolate. The dried beans are then cracked open, the shells are removed, and the remaining cocoa nibs are roasted. The roasting process also affects the flavor of the cocoa nibs. Roasted nibs are ground into a liquid called cocoa liquor, which is free of alcohol and contains 50 to 60 percent cocoa butter. From there the cocoa liquor can be further refined into cocoa powder, or other ingredients like sugar, vanilla, nuts, fruits, or milk can be added to the cocoa liquor to make chocolate bars. Dark chocolate contains 60 percent or more cocoa, and no milk. Milk chocolate only contains 5 to 7 percent cocoa, and white chocolate doesn’t contain any cocoa at all—just cocoa butter and milk. As with berries and leafy greens, the darker the color of the chocolate, the more antioxidants it contains and the better it is for you. Also, milk binds to the antioxidants eliminating their ability to fight free radicals, so eating milk chocolate or drinking milk with dark chocolate has few to no health benefits. Health Benefits of Dark Chocolate Chocolate has been used for its healing properties for more than 3,000 years, and dates back to the early Mayans. Now researchers are finding scientific evidence for those healing properties.

In fact, one study by Yale University Prevention Research Center indicated that chocolate contains more phenolic antioxidants than any other food. It’s Good for the Circulatory System Studies done at the University of Southern California, the Institute of Cardiology in Russia, and the University of Guadalajara, Mexico, showed that consumption of dark chocolate helps lower blood pressure, lowers LDL blood cholesterol, improves vascular function, and reduces the risk of stroke. According to a study of overweight men done at Wageningen University in the Netherlands, consuming dark chocolate daily for four weeks helped restore flexibility to arteries while also preventing white blood cells from sticking to the walls of blood vessels. This is significant because arterial rigidity and white blood cell adhesion are both factors in heart disease. It’s Good for Cognition and Your Mood The same study mentioned above by Yale University Prevention Research Center showed that dark chocolate has significant positive effects on cognitive function. Results from a study done in the UK confirmed that eating dark chocolate provides an acute improvement in visual and cognitive functions. A study done at Swinburne University in Melbourne, Australia, revealed “significantly increased self-rated calmness and contentedness relative to placebo” in participants who consumed a dark-chocolate drink mix for 30 days. It’s High in Minerals Dark chocolate is a mineral powerhouse. One ounce of dark chocolate—recommended daily serving—contains the following daily recommended doses of minerals: copper (25 percent), calcium (2 percent), iron (19 percent), magnesium (16 percent), potassium (6 percent), and zinc (6 percent). It Has Anti-inflammatory Properties Phytochemicals in dark chocolate have also been shown to have anti-inflammatory properties. Just keep an eye on the sugar content, as sugar is an inflammatory food. To get the most anti-inflammatory benefits from chocolate, go for the high cocoa content and least amount of sugar. It Improves Insulin Sensitivity New research from Queen Margaret University in the U. K. shows that dark chocolate improves insulin sensitivity and decreases glucose levels in non-diabetic adults. Health Risks of Eating Dark Chocolate Although there are many great health benefits of eating dark chocolate, there are also some downsides. It Contains Caffeine Dark chocolate contains 35 milligrams of caffeine per ounce compared to 145 milligrams for an 8-ounce cup of black coffee. Consider that if you’re trying to watch your caffeine intake or not hinder your ability to fall asleep at night. It Can Increase the Risk of Kidney Stones Dark chocolate contains a component found in many plants and animals called oxalates, which can increase the risk of kidney stones. If you’re prone to getting kidney stones you may want to watch your dark-chocolate consumption. It Can Bring on Migraines Dark chocolate has been implicated in some migraines. However, there are also people who are prone to migraines and don’t seem to be affected by dark chocolate, so the jury is still out. If you have a tendency to get migraines you may want to cut dark chocolate out of your diet to see if it helps. Moderation Is Key As with any sweet treat, moderation is key. Some dark chocolates contain more sugar and fat than others, although it’s typically a healthy fat from cocoa butter. Generally the higher the percentage of cocoa the less sugar it will contain, but this is not always the case. Read the labels to ensure just what your dark chocolate contains. And strive to not exceed 1 ounce per day. Consult your healthcare practitioner if you’re concerned about caffeine, kidney stones, or migraines. For the best dark chocolate, shop at local chocolatiers, and buy organic and/or fair-trade whenever possible. *Editor’s Note: The information in this article is intended for your educational use only; does not necessarily reflect the opinions of the Chopra Center's Mind-Body Medical Group; and is not a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health providers with any questions you may have regarding a medical condition and before undertaking any diet, supplement, fitness, or other health program. At our signature Perfect Health program you'll experience a week-long wellness immersion that will nourish your mind, body, and spirit and empower you with knowledge and practical tools taht will help you create vibrant health and wellbeing for the rest of your life. Click here for dates and more information. Share This Article Section: Nutrition & Recipes Topics: Healthy Eating Nutrition About the Author Heidi Hackler Holistic Health Coach and Health Writer Heidi Hackler is a Certified Holistic Health Coach (CHHC) and blogger, who received her training from the Institute for Integrative Nutrition (IIN). She inspires healthy habits on her happiness and wellness blog, and through her holistic health coaching programs. Heidi quenches her thirst for knowledge through continuing education courses at Chopra Center Certifications, Dogwood School of Botanical Medicine, and Andrea Beaman’s New Healers Master Coaching program. Heidi lives with her husband and two kittens aboard their 40-foot sailboat. They have a zest for living the... Read more


proton pump used for what

004Clinical Use Proton pump inhibitorsare orally active and used for the therapy of gastric ulcer, duodenal ulcer, gastroesophageal reflux disease, Zollinger-Ellison syndrome, and, combined with antibiotics, for eradication of Helicobacter pylori. The primary effect of these proton pump inhibitors is gastric acid suppression.

Proton Pump Inhibitors

Proton Pump Inhibitors Jai Moo Shin, George Sachs, in Encyclopedia of Gastroenterology, 2

The degree of acid suppression correlates with healing rates for reflux esophagitis and peptic ulcer. Rabeprazole is fast-acting with pain relief. Pantoprazole shows a longer half-time of restoration of acid secretion. Omeprazole and pantoprazole show an increase in acid inhibitory effect over several days of repeated administration. Lansoprazole shows maximal inhibition after the first day. There is poor correlation between maximal plasma drug concentration ( C max) and the degree of acid suppression. Instead, the area under the plasma concentration–time curve (AUC) correlates with acid suppression. Amongproton pump inhibitors, omeprazole 20 mg and rabeprazole 20 mg showed a significantly lower AUC than pantoprazole 20 and 40 mg and lansoprazole 30 mg. However, all proton pump inhibitors used clinically, omeprazole, lansoprazole, pantoprazole, and rabeprazole, show approximately equivalent potency for gastric acid suppression. Pantoprazole is available for intravenous use and is used to suppress acid secretion in intensive care situations. All proton pump inhibitorsare extensively metabolized in liver by P450 cytochromes. People with hepatic impairment have shown a 7- to 9-fold increase in the AUC with a prolongation of the plasma half-life to 4–8h. Approximately 3% of the population with a genetic polymorphism are poor metabolizers and show a 5- to 10-fold increase of AUC. Elderly people showed a 50–100% increase in the AUC since hepatic metabolism was poor. All four proton pump inhibitors are metabolized mainly by CYP 2C19 and CYP 3A4. CYP 2C19 generates hydroxylation of proton pump inhibitor, which is responsible for 80% of clearance in the case of omeprazole. CYP 3A4 generates sulfonylation ofproton pump inhibitors. Recently, S-omeprazole became available for clinical use. Omeprazole is a racemate consisting of S- and R- enantiomers. The R-form of omeprazole is sensitive to CYP 2C19 and CYP 3A4 enzymes and the S-form is less sensitive to these CYP enzymes. S-omeprazole has a longer plasma half-life than omeprazole, providing longer acid suppression. Acid suppression correlates with healing rates for reflux esophagitis and peptic ulcer. Good healing for reflux esophagitis was achieved when the intragastric p H was greater than 4 for 16 h/day and healing for peptic ulcer was best achieved when the intragastric p H was greater than 3. In patients with reflux esophagitis, lansoprazole 30 mg provided faster symptom relief than omeprazole 20 mg; however, no significant difference was observed compared to omeprazole 40 mg in terms of healing rates and symptom relief. Rabeprazole 20 mg and pantoprazole 40 mg provided equivalent healing rates and symptom relief compared to omeprazole 20 mg. In peptic ulcer disease and duodenal ulcers, all four proton pump inhibitors showed very similar efficacy, whereas rabeprazole and lansoprazole claimed a little fast symptom relief. H. pylori has been successfully eradicated by triple-therapy regimens: clarithromycin, amoxycillin, and proton pump inhibitor. There are no significant differences among four proton pump inhibitors, omeprazole, lansoprazole, pantoprazole, and rabeprazole, when used for this purpose. See Also the Following Articles Duodenal Ulcer; Gastric Acid Secretion; Gastric H + ,K + -ATPase; Gastric Ulcer; Gastrinoma; Gastroesophageal Reflux Disease (GERD); Helicobacter pylori; Pharmacology, Overview Read full chapter


lasik surgery how long to wear goggles at night

How long are LASIK goggles worn? LASIK goggles will be worn for roughly four days, though there are different instructions to consider during the healing process. For the first 24 hours after LASIK, the LASIK goggles should be worn at all times in order to avoid harm to the eyes. Medicated eye drops should be the only thing that comes into contact with the eyes in that first day of surgery. In the three to four days following surgery, patients will usually only be instructed to wear their LASIK goggles at night to avoid accidental rubbing and contact. When outdoors, patients should wear sunglasses in order to protect the eyes from the harshness of the light.

How Patients Should Use LASIK Goggles After Surgery By Gordon Wong, OD on May 30, 2014LASIK surgery is one of the most popular options for vision correction available today, though many people have misunderstandings about the treatment process and what is involved. Optometrists and eye care specialists can determine if LASIK or another vision correction option is right for you during a consultation. Right now, we would like to look at LASIK in basic terms and then consider the need for special goggles to be worn after the surgery in order to ensure proper and complication-free healing. About LASIK Surgery LASIK is a refractive surgery procedure that is performed in order to address myopia (nearsightedness), hyperopia (farsightedness), and astigmatism. The LASIK laser carefully reshapes the cornea so that light properly passes through it and focuses on the retina, the light-sensitive tissue located at the back of the eyes. What are LASIK goggles? Also known as eye shields, special goggles are worn after LASIK surgery as a protective measure. These goggles help prevent patients from making accidental contact with their eyes, such as rubbing their eyes at night while they sleep or having foreign objects accidentally come into contact with the eyes. Are LASIK goggles necessary? Yes, they actually are a crucial part of the healing process. During LASIK, a small flap is created in the cornea in order for the corneal reshaping to be performed. This flap is set down to heal, but it is very delicate and can easily be shifted out of position. The LASIK goggles will make sure that the eyes are given proper opportunity to heal without incidental or accidental contact that may affect the corneal flap. Are LASIK goggles comfortable? Even though LASIK goggles look funny, you'll be happy to know that they are quite comfortable, all things considered.

Alternatives to LASIK Surgery Though LASIK is right for many patients, it may not be the most ideal solution for you. There are many other eye care solutions to consider, including other forms of refractive surgery, traditional glasses, and contact lenses. We would be more than happy to discuss all eye care treatments in greater detail during your visit. Schedule a Consultation with Our Eye Care Specialists If you would like to learn more about LASIK surgery and how it may be of great benefit to you and your needs, be sure to contact our La Jolla eye care and vision correction doctors today. Our entire team looks forward to meeting you in person and helping you achieve the very best with regard to your eye health and total wellness. Related to This All Blog Posts Lasik Laser Eye Surgery


does sugarless gum cause diarrhea

It is manufactured from corn syrup. Sorbitol has only 50 percent of the relative sweetness of sugar which means twice as much must be used to deliver a similar amount of sweetness to a product. It has less of a tendency to cause diarrhea compared to mannitol. It is often an ingredient in sugar-free gums and candies. Xylitol is also called ""wood sugar"" and occurs naturally in straw, corncobs, fruit, vegetables, cereals, mushrooms and some cereals. Xylitol has the same relative sweetness as sugar.

Eat Any Sugar Alcohol Lately?

"Eat Any Sugar Alcohol Lately? If you've looked lately at the ""Nutrition Facts"" panel on a pack of sugar-free gum or candy, you might be surprised to see that it contains ""sugar alcohol."" Don't let the name fool you. These ingredients were given this consumer-friendly name because part of their structure resembles sugar and part is similar to alcohol. Not One in the Same Don't be confused. Although they share a similar name, sugar alcohol and alcoholic beverages do not have the same chemical structure. Sugar alcohol does not contain ethanol, which is found in alcoholic beverages. What is Sugar Alcohol?

Sugar alcohols, also know as polyols, are ingredients used as sweeteners and bulking agents. They occur naturally in foods and come from plant products such as fruits and berries. As a sugar substitute, they provide fewer calories (about a half to one-third less calories) than regular sugar.

This is because they are converted to glucose more slowly, require little or no insulin to be metabolized and don't cause sudden increases in blood sugar. This makes them popular among individuals with diabetes; however, their use is becoming more common by just about everyone. You may be consuming them and not even know it. Identifying Them Common sugar alcohols are mannitol, sorbitol, xylitol, lactitol, isomalt, maltitol and hydrogenated starch hydrolysates (HSH). Sugar alcohols are not commonly used in home food preparation, but are found in many processed foods. Food products labeled ""sugar-free,"" including hard candies, cookies, chewing gums, soft drinks and throat lozenges often consist of sugar alcohols. They are frequently used in toothpaste and mouthwash too. Check Carbohydrates So why are sugar alcohols used so often? For one thing, they help to provide the sweet flavor to food in many products marketed towards individuals with diabetes. But, beware! There is often the misconception that all sugar alcohol-containing products are ""free foods."" Some of these products may still contain significant amounts of carbohydrates. It's important to check the food label for the total carbohydrate contained in the product and talk with a registered dietitian to determine how it will best fit into your meal plan. If a manufacturer uses the term ""sugar free"" or ""no added sugar,"" they must list the grams of sugar alcohols. If more than one sugar alcohol is used in a product, the ""Nutrition Facts"" panel will list the amount of sugar alcohol it contains under the total carbohydrate. If just one sugar alcohol is used, the label will list its specific name, for example, ""mannitol"" or ""hydrogenated starch hydrolysates. ""

Pros and Cons of Sugar Alcohols On the positive side, sugar alcohols contain less calories (1.5 - 3 calories per gram) than sugar (4 calories per gram), and they do not cause tooth decay like sugar does. Therefore, many ""sugar-free"" gums including Trident® and Extra® are made with sugar alcohols.

Sugar alcohols also add texture to foods, retain moisture better and prevent foods from browning when they are heated. Unfortunately, there are some negatives associated with sugar alcohols

. The most common side effect is the possibility of bloating and diarrhea when sugar alcohols are eaten in excessive amounts. There is also some evidence that sugar alcohols, much like fructose (natural fruit sugar) in fruit and fruit juice can cause a ""laxative effect."

" Weight gain has been seen when these products are overeaten. The American Diabetes Association claims that sugar alcohols are acceptable in a moderate amount but should not be eaten in excess. Some people with diabetes, especially Type I diabetics, have found that their blood sugars rise if sugar alcohols are eaten in uncontrolled amounts. Sugar Alcohols vs. Artificial Sweeteners

Sugar alcohols and artificial sweeteners, such as saccharin (Sweet & Low®) and aspartame (Equal® or Nutrasweet®), are not one and the same. One difference between the two types of sugar substitutes is that the artificial sweeteners contain zero calories whereas sugar alcohols contain about 2.6 calories per gram.

Another issue is diabetes management. Artificial sweeteners do not contain carbohydrates so they do not cause blood sugar to elevate, whereas, sugar alcohols have some effect on blood sugar. Overall, both can be useful in diabetes management when used properly. Forms of Sugar Alcohol Mannitol occurs naturally in pineapples, olives, asparagus, sweet potatoes and carrots. It is extracted from seaweed for use in food manufacturing. Mannitol has 50-70 percent of the relative sweetness of sugar, which means more must be used to equal the sweetness of sugar. Mannitol lingers in the intestines for a long time and therefore often causes bloating and diarrhea. Sorbitol is found naturally in fruits and vegetables.

It is found in chewing gums. Lactitol has about 30-40 percent of sugar's sweetening power, but its taste and solubility profile resembles sugar so it is often found in sugar-free ice cream, chocolate, hard and soft candies, baked goods, sugar-reduced preserves and chewing gums. Isomalt is 45 - 65 percent as sweet as sugar and does not tend to lose its sweetness or break down during the heating process. Isomalt absorbs little water, so it is often used in hard candies, toffee, cough drops and lollipops. Maltitol is 75 percent as sweet as sugar. It is used in sugar-free hard candies, chewing gum, chocolate-flavored desserts, baked goods and ice cream because it gives a creamy texture to foods. Hydrogenated starch hydrolysates (HSH) are produced by the partial hydrolysis of corn. HSH are nutritive sweeteners that provide 40 - 90 percent of the sweetness of sugar. HSH do not crystallize and are used extensively in confections, baked goods and mouthwashes. For more information on this topic, visit: Calorie Control Council American Diabetes Association Artificial sweeteners, Maryland Cooperative Extension, University of Maryland All about polyols, SPI Polyols, Inc. "


what percent of the world's population is india and china

China's population is estimated to be around 1,373,541,278 and India’s population is estimated to be around 1,266,883,598. Combined population of China and India is around 2,640,424,876 which is around 36% of the world population. World population as of today is estimated to be around 7,359,928,000.

Demographics of China Demographics of India Population of India India-China Relations Populations Demographics China India What percent of the world's population does China and India make up?ad by UC Berkeley Extension Introduction to statistics at UC Berkeley Extension. Learn basic concepts of statistics - available in classroom & online formats. Learn More at extension.berkeley.edu5 Answers Sam Qwato Answered Dec 15, 2016 · Author has 2.4k answers and 2.6m answer views Q. What percent of the world's population does China and India make up? (1) World population: 7.4b (Aug 2016)China: 1.4b (2015)India: 1.3b (2016)China/India % of world: 36.5% (2) Here’s a thought... If we draw a map of the world, and plot the population ‘ center of gravity ’ point, it will pan out per below, underpinned by the massive populations of China, India, Indonesia ( and ASEAN in aggregate ). This is where the center of humanity is.4.7k Views · View Upvoters Related Questions More Answers Below Will India end up having a Muslim majority in the future? What will be the social, economical and political consequences if that happens? Do Asian people really make up 60 percent of the worlds population? Why are countries like India and China so densely populated? What are the circumstances and reasons? What percentage of the world's land do China, India, and Indonesia, make up? Can India replace China as the factory of the world? Ask New Question Vishnu Veen, Student Answered Dec 11, 2016China and India are the 2 most populated countries in the world China has 1.39 Billion people India has 1.27 Billion people They both combine total of 36.41% of total world population of 7,243,784,121 and counting.. In short Every 1 in 6 people of world population is INDIAN&Every 1 in 5 people of world population is CHINESSE. ( All figures are approximate )1.6k Viewspromoted by Truth Finder Have you ever googled yourself? Do a “deep search” instead. Americans are shocked about how this new site can reveal so much more. Enter a name to begin. Learn More at truthfinder.com Raghu MAnswered Jan 6, 2017

http://www.uspopulations.com/WOR...1.3k Views Denis Havlik Answered Dec 11, 2016 · Author has 3.2k answers and 2.4m answer views World population is currently around 7.4 billion India plus china is about 2.5 billion.that's roughly 1/3rd of the total world population. 33℅881 Views Arushi Gupta, B. Sc Economic Hons. from Lovely Professional University- LPU (2019)Answered Feb 20, 2018Roughly, they both make up of 36.5% of world’s population.206 Views Related Questions Can India defeat China in a full-fledged war? If you combine China and Indias population how much of the worlds population would it take up? How can we explain the fact that 40 percent of the world lives in only two countries, China and India? How did these two civilizations manage ... As a foreigner, which country is better to work and live for several years, China or India? Why are India and China are the most populated in the world? Is India stronger than China? What is 7 percent of the world's population? What would happen if China declared war on India today? What are the reasons behind the poor performance of India in Olympics? Will India catch up to China? Ask New Question Related Questions Will India end up having a Muslim majority in the future? What will be the social, economical and political consequences if that happens? Do Asian people really make up 60 percent of the worlds population? Why are countries like India and China so densely populated? What are the circumstances and reasons? What percentage of the world's land do China, India, and Indonesia, make up? Can India replace China as the factory of the world? Can India defeat China in a full-fledged war? If you combine China and Indias population how much of the worlds population would it take up? How can we explain the fact that 40 percent of the world lives in only two countries, China and India? How did these two civilizations manage ... As a foreigner, which country is better to work and live for several years, China or India? Why are India and China are the most populated in the world? Ask New Question


how to find a slit

The attempt at a solution ok i used the above equatiob to find the d, slit separation as d=m*lambda/sin (theta) but im getting the wrong answer....and im not able to figure out the problem....plez som1 help.....!

Homework Help: How to find slit separation?

May 16, 2009#1patelpalak1. The problem statement, all variables and given/known data The green line of gaseous mercury at 546nm fals on a double-slit apparatus. If the fifth dark fringe is at 0.150 degree from the centerline, what is the slit separaton? 2. Relevant equations d sin (theta) = m* lambda 3.

!Phys.org - latest science and technology news stories on Phys.org• A different spin on superconductivity—Unusual particle interactions open up new possibilities in exotic materials• How pathogenic bacteria prepare a sticky adhesion protein• Nova-like explosion of spinning live bacteria explained May 17, 2009#2tiny-tim Science Advisor Homework Helper Hi patelpalak! (have a lambda: λ and a theta: θ) Show us your full calculations, and then we can see what went wrong, and we'll know how to help!May 17, 2009#3patelpalakok here's what i did d sin (theta) =m*lamdba therefore, d=m*lambda/ sin (theta) m=5, since its fifth fringe lambda= 546*10^-9 theta = 0.150 degrees so, d= (5) (546*10^-9)/sin (0.150) and i get 0.001042 meters but it gives me wrong answer....!!!! thats all i did ... May 18, 2009#4tiny-tim Science Advisor Homework Helper Hi patelpalak! (whatever happened to that λ and θ I gave you? )patelpalak said: ↑ok here's what i did d sin (theta) =m*lamdba … theta = 0.150 degrees so, d= (5) (546*10^-9)/sin (0.150)erm … θ has to be in radians!May 18, 2009#5tyco05Hmmm.... If it is a dark fringe, isn't the equation something like: dsinθ = (m+0.5)λ ? Also, if my memory serves me correctly, you need to be careful with the order of your minimum. The first minimum has an m value of 0. Last edited: May 18, 2009May 19, 2009#6patelpalakok thanx all i got the answer.... appriciate your help....thanx once again! !


acute myelogenous leukemia age

t? Acute myeloid leukemia (AML) presents at all ages, but is mainly a disease of the elderly, with a median age of 69 years in the white US population. 1 In the Swedish Acute Leukemia Registry, 68% of patients diagnosed with AML since 1973 were over age 60 years; between 1997 and 2005, 75% was aged 60 years or more.

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ASH Home ASH Store ASH Academy My Account Sign In Skip to main page content About Hematology Subscriptions CME and MOC FAQs Current Issue Archives Advanced Search Treating the Elderly Patient with Acute Myelogenous Leukemia Selina M. Luger 1+ Author Affiliations1Hematologic Malignancies and Stem Cell Transplant Program, Hematology-Oncology Division, University of Pennsylvania Medical Center, Philadelphia, PANext Section Abstract Decisions regarding the optimal treatment of acute myelogenous leukemia in the elderly patient requires the consideration of multiple factors. Population-based studies have demonstrated that, for all age groups, aggressive therapy results in improved survival and quality of life when compared with palliative care. The optimal induction and postremission regimen for older patients has yet to be determined. Furthermore, not all patients are candidates for such therapy. Consideration of patient and disease-related factors can help to determine the appropriateness of intensive therapy in a given patient. For those patients for whom aggressive induction therapy does not seem to be in their best interest, novel agents are being investigated that will hopefully address the issues of induction death and early relapse associated with these patient populations. Previous Section Next Section How Is Acute Myeloid Leukemia in the Elderly Differen

2 Prognosis worsens every decade beginning at age 30 to 40. 1, 3 A report by the German Acute Myeloid Leukemia Cooperative Group looked at patients 16 to 85 years of age enrolled in two consecutive trials in 1992 and 1999 with no upper age limit who had AML. 4 In a multivariate analysis of prognostic factors, age ≥ 60 years was a statistically significant poor prognostic factor for complete remission (CR), overall survival (OS), remission duration, and relapse-free survival (RFS). Population-based studies have reported 3- and 5-year survival rates of only 9% to 10% and 3% to 8%, respectively, in patients over age 60, compared with 5-year survival rates of up to 50% for younger patients. 2, 5, 6 Poorer outcome has traditionally been considered to be the result of less intensive therapy in this population, concurrent comorbidities, a higher likelihood of underlying hematopoietic disorders, and biologically poor risk disease. Moreover, because of the perception that older adults are less likely to do well with standard therapy, clinicians are less likely to treat these patients aggressively or refer them to centers that do so. As such, lower levels of aggressive treatment may compound underlying prognostic differences associated with patient factors and disease biology. In a retrospective analysis of 968 adults with AML in five Southwest Oncology Group (SWOG) trials to understand the nature of how AML changes with age, differences were noted in performance status (PS), presenting white blood cell (WBC) count, percentage marrow blasts, expression of multidrug resistance (MDR), and karyotype. 7 ( Table 1 ). When compared with disease in patients younger than age 56, those age ≥ 56 are are more likely to have unfavorable cytogenetics and less likely to have favorable cytogenetics. Differences in disease biology are also apparent. For example, in an analysis of oncogenic pathway dysresgulation in 425 patients with AML, there is a statistically significant difference in the expression of E2F and PI3 (phosphoinositide 3) kinase activation, but a higher probability of RAS, TNF (tumor necrosis factor), Src, and EPI (extrinsic pathway inhibitor) pathway activation. 8 In younger patients, a similar profile is of poor prognostic significance and portends for decreased sensitivity to anthracycline. View this table: In this window In a new window Table 1. Patient and disease characteristics at presentation of AML, by age Previous Section Next Section What Is the Standard Therapy for the Older Patient With AML? The combination of an anthracycline and cytarabine (3+7), with or without other agents, is considered the standard induction regimen for patients under age 60, followed by consolidation therapy that often uses high-dose cytarabine. 9 – 11 As noted previously, the use of the standard 3+7 regimen in elderly patients does not yield results similar to those seen in younger patients. Recent studies have, therefore, focused on dose intensification of anthracyclines and/or postremission therapy ( Table 2 ). View this table: In this window In a new window Table 2. Intensive regimens for elderly AMLIn a recently published cooperative group study, Lowenberg et al 12reports the results of a comparison of induction therapy with daunorubicin (DNR) at a dose of 45 mg/m 2 or 90 mg/m 2 in 813 patients over age 60 with previously untreated AML. Although CR rates were improved in the group that received the higher dose of DNR (64% vs 54%, P = .002), there was no significant difference in the two induction groups with respect to OS and event-free survival (EFS). Thirty-day mortality was 11% to 12% in both groups. Two-year probabilities of relapse after CR and death during CR for the standard versus intensified DNR groups were 61% versus 54% for relapse and 10% versus 16% for death. Exploratory post-hoc analysis of patients aged 60 to 65 (n = 299), however, demonstrated a difference in the two dose groups with respect to CR (51% vs 73%), 2-year EFS (14% vs 29%, P = .002), and 2-year OS (23% vs 38%, P < .001). In the subgroup with core binding factor abnormalities (n = 33), escalated dose was associated with increased CR and decreased risk of disease progression or death (CR, 74% vs 93%; disease-free survival [DFS], 31% vs 62%). Although the study by Lowenberg et al 12would suggest that intensification of DNR leads to superior CR rates with no difference in toxicity, the use of high-dose DNR by the French Cooperative Group in ALFA (Acute Leukemia French Association)-9801 did not demonstrate similar results. 13 In their study, DNR at 80 mg/m 2 /day was compared with standard or high-dose idarubicin (IDA) during induction therapy of patients ages 50 to 70. Neither high-dose DNR nor high-dose IDA demonstrated any clinically relevant superiority over standard dose IDA in this population of patients. Multivariate analysis revealed age > 60 or < 60 to be of prognostic significance for OS, but not for CR or EFS. WBCs and cytogenetics significantly influenced EFS and OS in multivariate analysis. Although the superiority of higher dose anthracycline as induction is not clearly established by these trials, they do demonstrate that there is no increased toxicity with these regimens. In addition, dose-reduced anthracycline led to inferior CR rates in the Lowenberg study, and survival was not as good in certain subgroups of patients. As such, although there is no clear evidence that dose intensification is needed, there does not seem to be any reason to attenuate doses of anthracycline in patients over age 60. Doses of DNR at 60 mg/m 2 or IDA at 12 mg/ 2 for 3 days together with cytarabine would be appropriate to use. In the National Cancer Research Institute (NCRI) AML 14 trial, randomizations were conducted of anthracycline dose and cytarabine dose in induction, the use of an MDR modulator (PSC 833) in induction, and a number of postremission courses. 14 No benefit was seen to any of the interventions tested. The PSC 833 arm was closed prematurely because of an increased early death rate because of infection. A randomized trial by the Eastern Cooperative Oncology Group (ECOG) similarly showed no benefit to the addition of the MDR modulator zosuquidar to induction therapy with DNR 45 mg/m 2 and cytarabine. 15 The question of whether the short infusion time of zosuquidar in this study inadequately blocked the polyglycoprotein pump has been raised by a subsequent study. 16 A review of sequential SWOG studies that differed by the addition of cyclosporine to DNR and cytarabine demonstrated that CR rates were the same with and without cyclosporine (38% vs 44%), with a median OS of 6 months versus 7 months and an RFS of 14 months versus 8 months. 17 The lack of benefit of these agents suggests that they are either not effective at inhibiting MDR or that MDR inhibition, even if effective, cannot overcome the drug resistance. Clofarabine, an agent that was initially approved for use with patients with acute lymphoblastic leukemia, has recently been studied in patients with relapsed and refractory AML, as well as untreated elderly patients with AML. 18 – 20 Results of phase II trials are encouraging. The upcoming phase III ECOG trial for elderly patients with AML will randomize patients to induction therapy with DNR and cytarabine versus single-agent clofarabine. Once CR has been obtained, there is no standard postremission strategy in these patients. No prospective randomized study has ever established the benefit of postremission therapy in older adults; however, all large studies of AML have included postremission therapy, presumably because of the concern that patients are all destined to relapse without postremission therapy. Cycles of high-dose cytarabine, which is felt to be of benefit in younger patients, has not been demonstrated to be of benefit in this age group and is thought to be too toxic. 21 Single cycles of high-dose cytarabine have, however, been well tolerated in cooperative group studies. 13, 22 Recent studies of gemtuzumab, as well as studies of interleukin-2 as postremission therapy, have not demonstrated any benefit. 23, 24 In the EORTC-GIMEMA (European Organization for Research and Treatment of Cancer-Gruppo Italiano Malattie e Matologiche dell'Adulto) AML 13 trial, in which postremission therapy was randomized between two cycles of intensive intravenous therapy versus oral therapy, no difference in DFS was demonstrable between the two groups. 25, 26 The median DFS was 9 months for the noninfusional therapy versus 10.4 months for the intravenous regimen and 3-year DFS 13 versus 21% ( P = .15). Although no OS benefit was seen, the only patients who enjoyed prolonged DFS had received postremission chemotherapy. This study also offered autologous hematopoetic stem cell transplant (HSCT) as a postremission therapy, and no benefit was demonstrated to HSCT. 23 Of the 61 patients with AML in CR in this study who underwent stem cell harvest after first consolidation, 33 of 61 patients had HSCT with a median 3-year OS of 39% and a DFS of 28% for the 33 patients who underwent HSCT and a DFS of 21% for the 61 patients who underwent stem cell harvest. Although randomized trials have not been done to unequivocally establish the need for consolidation therapy, randomized trials have evaluated duration and types of postremission therapy. The AML 11 trial demonstrated that there was no benefit when four cycles, rather than 1 cycle, of moderate intensity postremission therapy were given. 27 In the ALFA 9803 trial comparing a cycle of intensive consolidation versus 6 months of lower dose therapy, prolonged consolidation was associated with improved OS (56% vs 37%) and DFS (28% vs 17%). 28 Repeated courses of low-intensity chemotherapy were also associated with shorter hospitalization and fewer transfusions. Age, AML type, and cytogenetics were associated with longer DFS. In the AML HD98 study, in which patients who achieved a CR and after one intensive consolidation were randomized to either a second intensive consolidation with IDA/etoposide or mild oral maintenance with the same drugs, there was a lower relapse rate and superior survival in the group that received the more intensive therapy (median survival 22.3 vs 14.3 months). 29 In addition to supporting the use of high-dose consolidation, this study suggests that more than one cycle of consolidation was superior when this regimen was used. Like other studies in the elderly, only 29% of the initial patient cohort was randomized after first consolidation. Moreover, only 2 of 96 randomized patients had high-risk cytogenetics, highlighting the selection bias in many of these trials. One of the other major issues for studies of postconsoldation is that many patients do not receive their assigned therapy, making the trials difficult to interpret. Until there is a randomized trial demonstrating that there is no benefit to postremission therapy, I feel that it should be offered to those patients who achieve a CR and are able to tolerate it. Recent analyses have further tried to elucidate the prognostic importance of cytogenetics and molecular prognostic factors in elderly patients. As in younger patients, core binding factor abnormalities have a more favorable prognosis. In a retrospective French study of 147 patients who received at least one dose of induction chemotherapy, 60 had t (8;21) and 87 had inversion (16). There was an 88% CR rate and a 10% 8-week early death rate. 30 With a median follow-up of 48 months, the 5-year probability of OS and leukemia-free survival (LFS) was 31% and 27%, respectively. On multivariate analysis, high WBC count, poor PS, and del (9q) were of negative impact, and trisomy 22 and intensive consolidation—when compared with maintenance therapy—were of positive impact. Despite a CR rate of 88%, median LFS was only 18 months. In the t (8;21) group, the difference in survival following intensive consolidation was statistically significant when compared with maintenance (not yet reached vs 10 months). In a recent analysis of the impact of NPM1 (nucleophosmin) mutation in elderly patients in 148 patients ≥ 60 years of age, with de novo cytogenetically normal AML enrolled onto CALGB (Cancer and Leukemia Group B) 9720 and 10201, those patients with NPM1 mutations have a higher CR (84 vs 48) and longer 3-year DFS (DFS 23 vs 10) and OS (35 vs 8). In multivariate analysis, this was particularly true in patients ≥ 70 years of age (CR 87% vs 39%, DFS 30% vs 7%, and OS 49% vs 5%). Several investigators have suggested that, in determining therapy for older patients with AML, it would be appropriate to wait for results of cytogenetic and perhaps molecular studies before discussing therapeutic options. 31Overall, these studies demonstrate that results of intensive therapy in elderly patients remain poor. Although CR rates of 40% to 80% can be achieved, in highly selected populations, long-term survival is poor. Even in patients with favorable cytogenetics who have 80% CR rates, relapse rates are high. As such, novel strategies are needed. With the use of reduced-intensity conditioning regimens, allogeneic transplantation has become a valid option. Recent reports have suggested that age, at least up to 70, does not impact outcome of reduced-intensity transplant and that reduced intensity transplantation may yield better outcomes than chemotherapy in patients aged 60 to 70. Retrospective registry studies have demonstrated that age does not appear to be a factor in transplant outcome. In a retrospective analysis of 629 reduced-intensity allogeneic transplants reported to the French transplant registry, outcomes (OS, transplant-related mortality, and acute graft-versus-host disease [GVHD]) in patients over age 65 were comparable with those for patients who were between ages 60 and 65. 32 Two-year OS was 48% vs 47% for the two age groups. Similarly, data from the Center for International Blood and Marrow Transplant Research (CIBMTR) on 1080 patients undergoing reduced-intensity conditioning transplant for AML or myelodysplastic syndrome (MDS) demonstrated no difference in nonrelapse mortality, grade 2 to 4 GVHD, chronic GVHD, or relapse, when patients ages 60 to 64 or over age 65 were compared with patients aged 40 to 59. 33 Although 2-year survival rates were lower in patients over age 60, 2-year survival rates were greater than 30% in all age groups, and multivariate analysis revealed no significant impact of age on DFS or OS. In a prospective study of the feasibility of transplant in patients over age 50 at M. D. Anderson who entered CR, outcome for those patients who underwent an allogeneic transplant with reduced-intensity conditioning had a superior RFS and OS when compared with those who received postremission chemotherapy. 34 A retrospective analysis of over 1,000 elderly patients with AML in first CR who underwent HSCT or chemotherapy demonstrated improved OS and DFS in the HSCT group. 35 Further prospective studies are needed. Previous Section Next Section Who Should Not Receive Intensive Therapy? Selection criteria commonly used for inclusion into clinical studies have a major impact on reported outcome. Furthermore, the interpretation of clinical trials must be done with caution, in that not only are eligibility criteria different, but also investigator choice and patient preference clearly influence patient inclusion. In an analysis by the Swedish of 9729 patients diagnosed with AML in Sweden since 1973, the proportion of older patients who were considered eligible for intensive remission induction therapy decreased from 92% in those aged 60 to 64 years to 80%, 67%, 45%, 23%, and 4% in those aged 65 to 69, 70 to 74, 75 to 79, 80 to 84, and 85+ years, respectively. 2 Importantly, this report found that early death rates were improved with intensive treatment, compared with palliation alone. This was seen in all age groups and all PS levels. For example, within patients age 76 to 89, with a PS of > 2, those who received intensive treatment had a 36% early death rate, compared with 52% for those who received palliation alone. The assessment of eligibility for intensive therapy is, however, quite subjective, and the reason that certain patients within the cohort received intensive therapy whereas others did not is not available in this report. An analysis was done within the six Swedish health care regions among patients age 70 to 79 years. 2, 36 Percentage of patients who were deemed candidates for intensive therapy differed by region, probably because of physician and patient preferences, because baseline characteristics of the patients seem no different. In those regions in which only 40% of patients were felt to be eligible for intensive therapy, there was a 16% early death rate with intensive treatment, compared with 27% with palliation only. The early death rate was similar in those regions wherein 75% of patients were felt to be eligible for intensive treatment. When comparing regions where only 40% versus 75% were treated intensively, CR rates with intensive treatment were 41% and 49%, respectively, and CR rates for the entire group in the region was 19% versus 37%. Given the lower proportion of patients who received intensive therapy in those regions, the 2-year OS was decreased at 24% versus 50% and 5-year OS was 1% versus 13%. Furthermore, although PS is more predictive for early death rate than age, long-term survival may be achieved in patients with initial poor PS. Based on their report, they state that standard intensive treatment decreased early death rates in most patients up to age 80. The MRC (Medical Research Council) AML 11 trial allowed for the use of cytogenetic data to identify prognostic groups in older adults who were treated with intensive therapy on study. 37 More recently, investigators have become interested in developing tools to allow us to discriminate between patients who are likely to benefit from intensive chemotherapy versus those who should be candidates for less aggressive therapy ( Table 3 ). View this table: In this window In a new window Table 3. Prognostic scoring in elderly AMLPatients are now being considered “unfit for intensive therapy” and more appropriate for alternative or investigational therapy if there is either a high risk of early mortality or a poor chance of long-term DFS. In a retrospective analysis by Wheatley of the patients in the AML 11 trial, five risk factors were identified in AML patients that were weighted according to the values of their multivariate coefficients and used to define three subgroup risk classifications that were then able to be validated in the more recent MRC AML 14 trial. 38 Cytogenetic group, age, WBC count, PS, and de novo vs secondary AML were all found to be highly significant. Good, standard, and poor risk groups had a 1-year survival of 53%, 43%, and 16%, respectively ( P < .0001). In a retrospective analysis by Kantarjian et al 39 of 998 patients aged 60 or older who received intensive therapy at M. D. Anderson Cancer Center, a multivariate analysis was performed to calculate a prognostic score. They identified prognostic risk factors: age (≥ 75 years), unfavorable cytogenetics, poor PS (> 2), ≥ 12-month history of antecedent hematologic disorder (AHD), lactate dehydrogenase (LDH) > 600, elevated creatinine, and treatment outside a laminar flow room. Three risk subgroups were defined based on the number of poor prognostic factors. Those with none of the adverse risk factors have an expected CR rate of > 60%, induction mortality of 10%, and 1-year survival over 50%. A poor risk group with more than or equal to three poor prognostic risk factors had CR, induction mortality, and 1-year survival rates of < 20%, > 50%, and < 10%, whereas those in an intermediate risk group had rates of 50%, 30%, and 30%, respectively. Several reports have focused on the impact of comorbidities on decision making in AML. A refined Hematopoetic Cell Transplantation Comorbidity Index (HCTCI) has been found to be useful in identifying patients who are not candidates for intensive therapy. 40 Malfuson et al 41 analyzed 416 patients treated on the ALFA 9803 multicenter trial to identify independent prognostic factors that would impact on OS. Based on their analysis, they propose that, in those patients with unfavorable cytogenetics and the presence of two poor prognostic factors (age ≥ 75 years, PS ≥ 2, and WBC count ≥ 50 × 10 9 /L), the OS is only 19% at 12 months, and these patients should, therefore, not be considered for standard chemotherapy. In a recent analysis of the AML 96 trial of 909 patients with a median age of 67, univariate and multivariate analyses identified karyotype, NPM1 mutation status, WBC count, and LDH of independent prognostic significance for OS, DFS, and relapse. 42 Although favorable and poor cytogenetic risk groups had markedly different OS, those patients with intermediate risk karyotype could be subdivided based on CD34 expression, along with the abovementioned factors identified on multivariate analysis, allowing for the designation of four groups: (1) favorable cytogenetics, (2) intermediate cytogenetic with favorable features, (3) intermediate cytogenetics with adverse risk features, and (4) poor risk cytogenetics, with 3-year OS of 39.5%, 30%, 10.6%, and 3.3%, respectively. These scoring systems can be used to identify patients who are likely to respond to standard therapy, as well as those who are not likely to benefit and should therefore be considered for alternate or investigational therapy. Previous Section Next Section What Treatment Options Are Available for Patients Who Are Not Candidates for Intensive Induction Therapy? For those patients who are not considered to be candidates for intensive induction therapy, one would hope to identify agents and regimens that are more effective and less toxic to address the concerns regarding early induction death, inadequate response rate, and high risk of relapse. The NCRI AML 14 study was designed to allow for randomization of patients between intensive and nonintensive therapy, but only eight patients agreed to randomization. 14, 43 As such, data available on novel agents comes from a variety of pilot and phase II studies with differing eligibility criteria. When evaluating the outcomes, it is important to also look at the characteristics of patients who were ultimately enrolled. Table 4 reviews available data from some of these studies. View this table: In this window In a new window Table 4. Novel therapeutic regimens As part of the NCRI AML 14 study, 212 patients who were deemed unfit for intensive treatment options by the local investigator were randomized to receive supportive care alone with hydroxyurea or cytarabine 20 mg twice daily by subcutaneous injection for 10 days every 4 to 6 weeks. 43 Outcome was improved for the low-dose (LD) cytarabine arm when compared with supportive care with hydroxyurea alone. CR was 18% versus 1%, and median survival was 575 days for those who achieved CR, compared with 66 days in nonresponders. DFS for responders was 8 months. Survival benefit was seen in all age groups, even those over age 75. As none of the patients with adverse cytogenetics achieved a CR, no survival benefit was, however, seen in that group. The early death rate was 39% at 8 weeks. Although no criteria were used to define unfit patients, 78% were over age 70, 27% had secondary AML, 30% had PS ≥ 2, 27% had heart disease, 49% had other comorbidities, and 59% had a poor risk score by the Wheatley Risk Index. 38 Based on this study, LD cytarabine became the standard of care for the treatment of patients felt to be unfit for intensive chemotherapy, although one could argue that it should not be given to those with poor risk cytogenetics. The DNA methyltransferase inhibitors have been the subject of several recent studies. In a multicenter phase II study of 55 patients over age 60 with untreated AML, decitabine was administered for 5 days monthly until disease progression. 44 With a median of three cycles, the overall response rate was 24%, median survival was 7.7 months, and 30-day mortality was 7%. Responses were seen in all cytogenetic risk groups, as well as in those patients with prior MDS. An alternate schedule of decitabine was reported by Blum et al. 45, 46 Patients received an initial one to two courses of 10 days of decitabine, followed by a course over 3 to 5 days every 4 weeks for 1 year. Of the 53 patients with a median age of 74, 36% had secondary AML, and 34% had a complex karyotype. Eighteen patients had a HCTCI score of ≥ 3. There was a 64% response rate after a median of three cycles of therapy. CR occurred in all subsets, regardless of age, karyotype, presenting WBC, and prior AHD. One-year survival of poor risk patients was 30% (compared with 10% in patients with a similar Wheatley risk score in the AML 11 trial 38 ). In a study of azacitidine in AML with 20% to 30% blasts, patients who were deemed unfit for standard induction chemotherapy were randomized against either supportive care or LD cytarabine. 47 OS survival was superior in the azacitidine arm. There was a statistically significant difference seen in OS for patients with poor risk cytogenetics in favor of azacitidine, compared with conventional care regimens (12.3 vs 5.3 months, respectively, with 2-year OS of 38% vs 0%). Gemtuzumab ozogamicin (GO) has been the subject of a recent study by the EORTC and GIMEMA leukemia groups (AML 19). 48 In this randomized multicenter study, 84 patients were randomized to receive one of two schedules of GO at attenuated doses or best supportive care. The proportion of patients either achieving a response or maintaining stable disease was greater in patients who receive GO at a dose of 6 mg/m 2 on day 1 and 3 mg/m 2 on day 8, when compared with a schedule of GO 3 mg/m 2 on days 1, 3, and 5 (63% vs 38%, respectively). Results of the comparison with patients who were randomized to standard care are not yet available, and a phase III trial is ongoing. Clofarabine has been studied as an agent in elderly patients with AML. In a phase II study of the agent in 112 patients over age 60 with untreated AML with at least one unfavorable baseline prognostic factor, there was a 46% response rate. 49 The median age of the patients was 71. Twenty-two percent of patients had a baseline PS of 2, 47% had a prior hematologic disorder (AHD) or secondary AML, 55% had an unfavorable karyotype, and 62% were ≥ age 70. Overall response rate (ORR) was 395 for patients ≥ 70, 32% for PS 2, 51% for patients with AHD, 54% for intermediate karyotype and 42% for unfavorable karyotype, and 38% for patients with three risk factors. Median DFS was 37 weeks, and median OS was 41 weeks for all patients, 59 weeks for patients with CR/complete remission with incomplete platelet recovery (CRp), and 72 weeks for patients with CR. Early death rate (within 60 days) was 16%. In two consecutive European studies of 106 untreated older patients with AML who were considered unfit for chemotherapy, participants were given four to six 5-day courses of clofarabine. 18, 50 In the UWCM (University of Wales College of Medicine)-001 study, patients who were either over age 70 (68%) or over age 60, with a PS of 2 or cardiac comorbidity, were treated with clofarabine for 5 days every 28 days for 2 to 4 courses. In the BIOV-121 study, patients were treated for 5 days every 4 to 6 weeks for up to six courses. All patients were age ≥ 65 and deemed unfit for chemotherapy. Overall, 36% of patients had a PS ≥ 2, 30% had adverse risk cytogenetics, 46% had Wheatley poor risk disease, and 65% were age ≥ 70. The ORR was 48%, and the median OS was 19 weeks for all and 45 weeks for those who attained a CR/complete remission with incomplete blood count recovery (CRi). Responses were seen in patients with adverse cytogenetics (44% ORR), patients with secondary AML (31%), and patients age ≥ 70 (49%). The death rate within 30 days was 18%. A novel agent, laromustine (VNP40101M), a sulfonylhydrazine alkylating agent, has been studied in 85 patients with poor risk AML age ≥ 60 years. 51 Patients received one to two cycles of laromustine at a dose of 600 mg/m 2, followed by one cycle of cytarabine. Seventy-eight percent of patients were age ≥ 70, 47% had an adverse karytype, 41% had a PS of 2, 77% had pulmonary disease, 73% had cardiac disease, and 3% had hepatic disease. All patients with unfavorable karyotype or ECOG PS had at least one other risk factor at the time of enrollment. Seventy-five percent of patients had ≥ 3 risk factors. The ORR was 32% and was similar in patients over age 70 (32%), with a PS of 2 (32%), with baseline pulmonary or cardiac dysfunction (27%–34%). There was a 14% 30-day mortality. OS was 3.2 months (12.4 months for those with CR/CRp), and 1-year survival was 21% (52% for those with CR/CRp). These phase II studies are encouraging, in that responses are seen in all poor risk categories, and early death rates are acceptable. Randomized trials are needed. Although randomized trials of intensive versus nonintensive therapy have not been successful, the ongoing AML 16 trial was designed to randomize patients who are considered not fit for intensive treatment to LD cytarabine versus LD cytarabine with GO, LD cytarabine with arsenic trioxide or tipifarnib, or LD clofarabine. 52 The arsenic arm has been closed because of ineffectiveness with CR/CRi of 29%, compared with 24% and a 12-month OS of 27%, compared with 41%. The other arms continue to accrue patients. Previous Section Next Section Approach to the Elderly Patient With AMLAML is a disease of the elderly, with the majority of patients over age 60. As our population ages, that percentage will only increase. Unfortunately, the standard regimens that are successful in treating younger patients will AML are not as beneficial in the majority of older patients with the disease. Figure 1 outlines my approach to the elderly patient with AML. Understanding of the disease biology, as well as the prognostic factors associated with the host, allows us to better determine which patients are likely to benefit from standard therapy and which require alternative approaches. Objective scoring systems are being developed that allow us to define patients unfit for intensive chemotherapy on the basis of increased risk of induction death, low response rate, and/or low long-term DFS. Optimal induction and postremission therapy for patients appropriate for intensive therapy have yet to be defined, again, because results are not satisfactory with our current regimens, even in those patients who do not have definable poor prognostic factors. When compared with young patients with similar disease-related features, outcomes are inferior. For patients who are not candidates for intensive therapy because of comorbid conditions, low-intensity therapies appear to be superior to palliative care alone. Whenever possible, patients should be enrolled in clinical trials that will allow us to address these issues. View larger version: In this page In a new window Download as Power Point Slide Figure 1. My approach to the patient over age 60 with AML. Previous Section Next Section Disclosures Conflict-of-interest disclosure: The author declares no competing financial interests. Off-label drug use: Use of gemtuzumab ozogamicin, clofarabine, and decitabine. Previous Section Next Section Correspondence Selina M. Luger, MD, Professor of Medicine, and Director, Leukemia Program, Hospital of the University of Pennsylvania, Perelman Center for Advanced Medicine, 3400 Civic Center Blvd., Philadelphia, PA 19104; Phone: (215) 614-1847; Fax: (215) 615-5888; e-mail: selina.luger@uphs.upenn.edu Previous Section References↵Surveillance Epidemiology and End Results (SEER) Program SEER Web site, Limited use-data (1973–2004). National Cancer Institute D, Surveillance Research Program, Cancer Statistics Branch. http://www.seer.cancer.gov. Accessed April 2007.↵Juliusson G, Antunovic P, Derolf A, et al. ( 2009) Age and acute myeloid leukemia: real world data on decision to treat and outcomes from the Swedish Acute Leukemia Registry. Blood 113: 4179 – 4187. Abstract / FREE Full Text↵Pulte D, Gondos A, Brenner H, Pulte D, Gondos A, and Brenner H ( 2008) Improvements in survival of adults diagnosed with acute myeloblastic leukemia in the early 21st century. Haematologica 93: 594 – 600. 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( 2007) Phase I/II study of the P-glycoprotein (Pgp) inhibitor zosuquidar administered by continuous infusion (CIV) with daunorubicin (DNR) and cytarabine (ARA-C) as primary therapy in older patients with Pgp-positive acute myeloid leukemia (AML) [abstract] Blood, 110. Google Scholar↵Chauncey TR, Gundacker H, Shadman M, et al. ( 2009) Sequential phase II Southwest Oncology Group studies (S0112 and S0301) of daunorubicin and cytarabine by continuous infusion, without and with ciclosporin, in older patients with previously untreated acute myeloid leukaemia. Br J Haematol148: 48 – 58. Medline Google Scholar↵Burnett A, Russell N, Kell J, et al. ( 2010) European development of clofarabine as treatment for older patients with acute myeloid leukemia considered unsuitable for intensive chemotherapy [abstract]J Clin Oncol, 28. Google Scholar↵Faderl S, Erba HP, Claxton DF, et al. ( 2009) Clofarabine produces durable remissions in older patients with AML with unfavorable prognostic factors and multiple comorbidities [abstract 4155] Blood, 114. Google Scholar↵Faderl S, Ravandi F, Huang X, et al. ( 2008) A randomized study of clofarabine versus clofarabine plus low-dose cytarabine as front-line therapy for patients aged 60 years and older with acute myeloid leukemia and high-risk myelodysplastic syndrome. Blood 112: 1638 – 1645. Abstract / FREE Full Text↵Mayer RJ, Davis RB, Schiffer CA, et al. ( 1994) Intensive postremission chemotherapy in adults with acute myeloid leukemia. N Engl J Med331: 896 – 903. Cross Ref Medline Google Scholar↵Rowe JM, Neuberg D, Friedenberg W, et al. ( 2004) A phase 3 study of three induction regimens and of priming with GM-CSF in older adults with acute myeloid leukemia. A trial by the Eastern Cooperataive Oncology Group. Blood 103: 479 – 485. Abstract / FREE Full Text↵Lowenberg B, Beck J, Graux C, et al. ( 2010) Gemtuzumab ozogamicin as postremission treatment in AML at 60 years of age or more: results of a multicenter phase 3 study. Blood 115: 2586 – 2591. Abstract / FREE Full Text↵Baer MR, George SL, Caligiuri MA, et al. ( 2008) Low-dose interleukin-2 immunotherapy does not improve outcome of patients age 60 years and older with acute myeloid leukemia in first complete remission: Cancer and Leukemia Group B Study 9720. J Clin Oncol 26: 4934 – 4939. Abstract / FREE Full Text↵Jehn U, Suciu S, Thomas X, et al. ( 2006) Non-infusional vs intravenous consolidation chemotherapy in elderly patients with acute myeloid leukemia: final results of the EORTC-GIMEMA AML-13 randomized phase III trial. Leukemia 20: 1723 – 1730. Cross Ref Medline Google Scholar↵Thomas X, Suciu S, Rio B, et al. ( 2007) Autologous stem cell transplantation after complete remission and first consolidation in acute myeloid leukemia patients aged 61–70 years: results of the prospective EORTC-GIMEMA AML-13 study. Haematologica 92: 389 – 396. Abstract / FREE Full Text↵Goldstone A, Burnett A, Wheatley K, Smith AG, Hutchinson M, and Clark R ( 2001) Attemps to improve treatment outcomes in acute myeloid leukemia (AML) in older patients: the results of the United Kingdon Medical Research Council AML11 trial. Blood 98: 1302 – 1311. Abstract / FREE Full Text↵Gardin C, Turlure P, Fagot T, et al. ( 2007) Postremission treatment of elderly patients with acute myeloid leukemia in first complete remission after intensive induction chemotherapy: results of the multicenter randomized Acute Leukemia French Association (ALFA) 9803 trial. Blood109: 5129 – 5135. Abstract / FREE Full Text↵Schlenk RF, Frohling S, Hartmann F, et al. ( 2006) Intensive consolidation versus oral maintenance therapy in patients 61 years or older with acute myeloid leukemia in first remission: results of second randomization of the AML HD98-B treatment trial. Leukemia 20: 748 – 750. Cross Ref Medline Google Scholar↵Prebet T, Boissel N, Reutenauer S, et al. ( 2009) Acute myeloid leukemia with translocation (8;21) or inversion (16) in elderly patients treated with conventional chemotherapy: a collaborative study of the French CBF-AML intergroup. J Clin Oncol 27: 4747 – 4753. Abstract / FREE Full Text↵Sekeres MA, Elson P, Kalaycio ME, et al. ( 2009) Time from diagnosis to treatment initiation predicts survival in younger, but not older, acute myeloid leukemia patients. Blood 113: 28 – 36. Abstract / FREE Full Text↵Chevallier P, Blaise D, Milpied N, et al. ( 2009) Reduced intensity conditioning (RIC) allogeneic stem cell transplantation for patients aged >=60 years: a retrospective study of 629 patients from the Societe Francaise De Greffe De Moelle et de therapie cellulaire (SFGM-TC) Blood114: 84 – 85. Google Scholar↵Röllig C, Thiede C, Gramatzki M, et al. ( 2010) A novel prognostic model in elderly patients with acute myeloid leukemia: results of 909 patients entered into the prospective AML96 trial. Blood 116: 971 – 978. Abstract / FREE Full Text↵Estey E, de Lima M, Tibes R, et al. ( 2007) Prospective feasibility analysis of reduced-intensity conditioning (RIC) regimens for hematopoietic stem cell transplantation (HSCT) in elderly patients with acute myeloid leukemia (AML) and high-risk myelodysplastic syndrome (MDS) Blood109: 1395 – 1400. Abstract / FREE Full Text↵Kurosawa S, Yamaguchi T, Uchida N, et al. ( 2009) Comparison of allogeneic hematopoietic cell transplantation and chemotherapy as post-remission strategy in elderly patients with non-M3 AML in CR1: retrospective analysis with 1036 patients [abstract 524] Blood, 114. Google Scholar↵Juliusson G, Billstrom R, Gruber A, et al. ( 2006) Attitude towards remission induction for elderly patients with acute myeloid leukemia influences survival. Leukemia 20: 42 – 47. Cross Ref Medline Google Scholar↵Grimwade D, Walker H, Harrison G, et al. ( 2001) The predictive value of hierarchical cytogenetic classification in older adults with acute myeloid leukemia (AML): analysis of 1065 patients entered into the United Kingdom Medical Research Council AML11 trial. Blood 98: 1312 – 1320. Abstract / FREE Full Text↵Wheatley K, Brookes CL, Howman AJ, et al. ( 2009) Prognostic factor analysis of the survival of elderly patients with AML in the MRC AML11 and LRF AML14 trials. Br J Haematol 145: 598 – 605. Cross Ref Medline Google Scholar↵Kantarjian H, O'Brien S, Cortes J, et al. ( 2006) Results of intensive chemotherapy in 998 patients age 65 years or older with acute myeloid leukemia or high-risk myelodysplastic syndrome: predictive prognostic models for outcome. Cancer 106: 1090 – 1098. Cross Ref Medline Google Scholar↵Giles FJ, Borthakur G, Ravandi F, et al. ( 2007) The haematopoietic cell transplantation comorbidity index score is predictive of early death and survival in patients over 60 years of age receiving induction therapy for acute myeloid leukaemia. Br J Haematol 136: 624 – 627. Cross Ref Medline Google Scholar↵Malfuson JV, Etienne A, Turlure P, et al. ( 2008) Risk factors and decision criteria for intensive chemotherapy in older patients with acute myeloid leukemia. Haematologica 93: 1806 – 1813. Abstract / FREE Full Text↵Rollig C, Aulitzky WE, Bodenstein H, et al. ( 2009) Risk stratification and prognostic factors in elderly AML patients—updated results of 909 patients entered into the prospective AML96 trial [abstract 329] Blood, 114. Google Scholar↵Burnett AK, Milligan D, Prentice AG, et al. ( 2007) A comparison of low-dose cytarabine and hydroxyurea with or without all-trans retinoic acid for acute myeloid leukemia and high-risk myelodysplastic syndrome in patients not considered fit for intensive treatment. Cancer 109: 1114 – 1124. Cross Ref Medline Google Scholar↵Cashen AF, Schiller GJ, O'Donnell MR, et al. ( 2010) Multicenter, phase II study of decitabine for the first-line treatment of older patients with acute myeloid leukemia. J Clin Oncol 28: 556 – 561. Abstract / FREE Full Text↵Blum W, Garzon R, Klisovic RB, et al. ( 2010) Clinical response and mi R-29b predictive significance in older AML patients treated with a 10-day schedule of decitabine. Proc Natl Acad Sci U S A 107: 7473 – 7478. Abstract / FREE Full Text↵Blum W, Klisovic R, Liu S, et al. ( 2008) Preliminary results of a phase II study of low dose decitabine as a single agent in older patients (age >=60) with previously untreated acute myeloid leukemia (AML) [abstract 2957]Blood, 112. Google Scholar↵Fenaux P, Mufti GJ, Hellstrom-Lindberg E, et al. ( 2010) Azacitidine prolongs overall survival compared with conventional care regimens in elderly patients with low bone marrow blast count acute myeloid leukemia. J Clin Oncol 28: 562 – 569. Abstract / FREE Full Text↵Amadori S, Suciu S, Selleslag D, et al. ( 2010) Randomized trial of two schedules of low-dose gemtuzumab ozogamicin as induction monotherapy for newly diagnosed acute myeloid leukaemia in older patients not considered candidates for intensive chemotherapy. (A phase II study of the EORTC and GIMEMEA leukaemia groups (AML-19). )Br J Haematol 149: 376 – 382. Cross Ref Medline Google Scholar↵Kantarjian HM, Erba HP, Claxton D, et al. ( 2010) Phase II study of clofarabine monotherapy in previously untreated older adults with acute myeloid leukemia and unfavorable prognostic factors. J Clin Oncol28: 549 – 555. Abstract / FREE Full Text↵Burnett AK, Baccarani M, Johnson P, et al. ( 2006) A phase II study (biov-121) of clofarabine monotherapy first line in patients aged 65 years or older with acute myeloid leukemia for whom standard intensive chemotherapy is not considered suitable [abstract 425] Blood, 108. Google Scholar↵Schiller GJ, O'Brien SM, Pigneux A, et al. ( 2010) Single-agent laromustine, a novel alkylating agent, has significant activity in older patients with previously untreated poor-risk acute myeloid leukemia. J Clin Oncol28: 815 – 821. Abstract / FREE Full Text↵Russell NH, Hills RK, Hunter AE, et al. ( 2009) Low dose ara-C versus low dose ara-C and arsenic trioxide: the UK NCRI AML16 “pick a winner” comparison [abstract 486] Blood, 114. Google Scholar Articles citing this article Hospital volume and acute myeloid leukemia mortality in Medicare beneficiaries aged 65 years and older Blood 2016 128: 872 - 874Full Text Full Text (PDF)DNMT3A Mutational Status Affects the Results of Dose-Escalated Induction Therapy in Acute Myelogenous Leukemia Clin. Cancer Res. 2015 21: 1614 - 1620Abstract Full Text Full Text (PDF)Hematologic malignancies in elderly patientshaematol 2014 99: 1124 - 1127Full Text Full Text (PDF)« Previous | Next Article »Table of Contents This Articledoi: 10.1182/asheducation-2010.1.62ASH Education Book December 4, 2010vol. 2010 no. 1 62-69Abstract Free» Full Text Full Text (PDF)- Classifications Series: Challenges in Acute Myeloid Leukemia Challenges in Acute Myeloid Leukemia- Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Pub Med Download to citation manager+ Citing Articles+ Google Scholar+ Pub Med+ Social Bookmarking Navigate This Article Top Abstract How Is Acute Myeloid Leukemia in the Elderly Different? What Is the Standard Therapy for the Older Patient With AML? Who Should Not Receive Intensive Therapy? What Treatment Options Are Available for Patients Who Are Not Candidates for Intensive Induction Therapy? Approach to the Elderly Patient With AMLDisclosures Correspondence References Current Issue December 8, 2017, 2017 (1)Alert me to new issues of Hematology ASH Education Program Access to Hematology 2017 is only available to active ASH Members, 2017 ASH Full Conference Attendees, and anyone else that has purchased a copy of Hematology 2017. Institutional subscriptions are also available. Please contact us for a quotation. Individual Access Institutional Access ASH On Demand Instantly access webcasts from ASH's many educational meetings and webinars.2021 L Street NW, Suite 900, Washington, DC 20036Phone 202-776-0544 | Fax 202-776-0545ASH Home Research Education Advocacy Meetings Publications ASH Store Copyright © 2018 by the American Society of Hematology Contact Us | Terms of Service | Privacy Policy


is death a natural disaster

Introduction- What is a natural disaster? The definition of natural disasters is any catastrophic event that is caused by nature or the natural processes of the earth. The severity of a disaster is measured in lives lost, economic loss, and the ability of the population to rebuild. Events that occur in unpopulated areas are not considered disasters. So a flood on an uninhabited island would not count as a disaster, but a flood in a populated area is called a natural disaster. All natural disasters cause loss in some way. Depending on the severity, lives can be lost in any number of disasters.

Natural Disasters

Natural Disasters Natural Disasters

Falling buildings or trees, freezing to death, being washed away, or heat stroke are just some of the deadly effects. Some disasters cause more loss of life than others, and population density affects the death count as well. Natural Disasters– Asteroid– Avalanche– Blizzard– Thunderstorm– Earthquake– Flood– Gamma-Ray Burst– Volcano Eruption– Heat Wave– Hurricane– Landslide– Solar Flare– Drought– Tornado– Tsunami– Hail– Wildfire Then there is loss of property, which affects people’s living quarters, transportation, livelihood, and means to live. Fields saturated in salt water after tsunamis take years to grow crops again. Homes destroyed by floods, hurricanes, cyclones, landslides and avalanches, a volcanic eruption, or an earthquake are often beyond repair or take a lot of time to become livable again. Personal effects, memorabilia, vehicles, and documents also take a hit after many natural disasters. The natural disasters that really affect people worldwide tend to become more intense as the years go on. Frequency of earthquakes, mega storms, and heat waves has gone up considerably in the last few decades. Heavy population in areas that get hit by floods, cyclones, and hurricanes has meant that more lives are lost. In some areas, the population has gotten somewhat prepared for the eventuality of disasters and shelters are built for hurricanes and tornadoes. However, loss of property is still a problem, and predicting many natural disasters isn’t easy. Scientists, geologists, and storm watchers work hard to predict major disasters and avert as much damage as possible. With all the technology available, it’s become easier to predict major storms, blizzards, cyclones, and other weather related natural disasters. But there are still natural disasters that come up rather unexpectedly, such as earthquakes, wildfires, landslides, or even volcanic eruptions. Sometimes, a time of warning is there, but it’s often very short with catastrophic results. Areas that are not used to disasters affected by flash floods or sudden hail storms can be affected in an extreme way. Flood- Natural disaster However, despite the many natural disasters the world over, mankind has shown amazing resilience. When an area or country is badly affected by a natural disaster, the reaction is always one of solidarity and aid is quick to come. There are organizations set up with the primary goal of being prepared for natural disasters. These groups work on global and local scale rescue work. Aside from those who have chosen to make disaster relief their life-work, when disasters hit, it’s the individuals who step in who help to make a difference. Many people talk about when a disaster has hit and their neighbors and countrymen have come to aid, often to their own loss. People will step in and donate items, time, and skills in order to help those affected by a natural disaster. Celebrities will often do what they can to raise money through concerts, phone marathons, and visiting affected areas with aid. People have also shown that they can rebuild, lives can be remade or start over. Trauma is a big after effect of natural disasters and getting counseling has been the focus of aid—to heal emotionally as well as physically. It’s clear that natural disasters are a part of life as we know it. However, science is making it more possible to predict, aid is faster at coming, and people are learning how to rebuild in safer areas. Natural Disasters Videohttpvh://www.youtube.com/watch?v=3Ehj PQCQi BI


how cucumbers are grown in a greenhouse

"Planting Cucumbers in a Greenhouse Growing cucumbers in a greenhouse starts off with sowing the seeds, 2cm (¾in) deep, in 8cm (3in) pots around April or May time. Keep the pots indoors (or in a heated greenhouse) until all risk of frost has passed (ie. the very low temperatures are over).

Planting Cucumbers in a Greenhouse

Starting them off in pots and planting out when they are small plants, helps to protect them from slug and snail damage. When you plant them out, make sure you water them in well. Cucumber Plant Care – Greenhouse Cucumbers grown in a greenhouse need one thing above all else, regular watering! You’ll need to water them daily to keep up with their intake. Their leaves are large and plentyful, resulting in their high water requirement. There is a balance though. Try not to over-water them, regular rather than sporadic but heavy watering is the key. style=""display:inline-block;width:320px;height:100px"" data-ad-client=""ca-pub-6979934380247289"" data-ad-slot=""1741063807""> You’ll need to provide support for your greenhouse cucmbers, so erect a trellis type system, preferably one that keeps the leaves away from the windows of the greenhouse. Greenhouse cucumbers can be planted either in growbags, pots or direct into the greenhouse soil. Train the leading stem up to the top of your support and then pinch out the growing tip to encourage branching below. Check the variety of your cucumbers. A lof of modern cucumber varieties are ‘All Female’ varieties, which do not require pollinating (in fact don’t want pollinating). If this is the case, then remove any rogue male flowers (the flowers that do not have a mini cucumber behind them) that grow, as pollination can lead to bitter cucumbers.1. Growing Cucumbers in a Greenhouse – QUICKSTART GUIDE 2. Planting Cucumbers in a Greenhouse – How and when to plant cucumbers in a greenhouse3. Picking and Preserving Cucumbers – How and when to harvest and preserve cucumbers 4. Cucumber Growing Tips – Some tips to help you grow greenhouse cucumbers 5. Cucumber Pests, Problems and Diseases – Help is at hand for troublesome greenhouse cucumbers Back to main Growing Vegetables page "