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AnemiaIron deficiency; Pernicious anemia
Anemia is the name applied to many different conditions that are all characterized by an abnormally low number of healthy red blood cells. There are many different causes and types of anemia.
Iron-deficiency anemia, the most common type, is usually treated with dietary changes and iron supplement pills. Other types of anemia, such as those associated with chronic diseases or cancer, may need more aggressive treatment.
Preventing Iron Deficiency in Infants and Toddlers
The American Academy of Pediatrics' guidelines for preventing iron deficiency and iron deficiency anemia in infants and young children include:
- Full-term infants who are healthy and exclusively breastfed should receive an oral iron supplement beginning at 4 months of age. The supplement should be continued until iron-containing solid foods, such as cereals, are introduced. Breast milk itself contains very little iron, but most healthy babies are born with iron stores sufficient for their first 4 months.
- Preterm infants who are breastfed should receive an iron supplement by 1 month of age.
- Formula-fed infants get adequate iron from iron-fortified formula. For all babies, cow's milk should not be introduced before age 12 months.
- Toddlers ages 1 - 3 years should get their iron from foods such asred meats, iron-rich vegetables, and fruits that are rich in vitamin C. (Vitamin C helps boost iron absorption.)
Anemia Drug for Dialysis Patients Approved and Recalled
In March 2012, the FDA approved the erythropoiesis-stimulating drug peginesatide (Omontys) specifically for patients receiving kidney dialysis. In February 2013, the drug's manufacturers issued a voluntary recall of the drug due to reports of serious and fatal allergic reactions.
Anemia is an abnormal reduction in red blood cells.
Anemia is not a single disease but a condition, like fever, with many possible causes and many forms. Causes of anemia include nutritional deficiencies, inherited genetic defects, medication-related side effects, and chronic disease. It can also occur because of blood loss from injury or internal bleeding, the destruction of red blood cells, or insufficient red blood cell production. The condition may be temporary or long term, and can manifest in mild or severe forms.
This report focuses on the most common forms of anemia:
- Iron deficiency anemia
- Anemia of chronic disease (ACD)
- Treatment-related anemia (chemotherapy, medication, radiation therapy)
- Megaloblastic anemia (caused by deficiencies in the B vitamins folate, vitamin B12, or both)
Blood has two major components:
- Plasma is a clear yellow liquid that contains proteins, nutrients, hormones, electrolytes, and other substances. It constitutes about 55% of blood.
- White and red blood cells and platelets make up the balance of blood. The white cells are the infection fighters for the body. Platelets are necessary for blood clotting. The important factors in anemia, however, are red blood cells.
Red blood cells (RBCs), also known as erythrocytes, carry oxygen throughout the body to nourish tissues and sustain life. Red blood cells are the most abundant cells in our bodies. On average, men have about 5.2 million red blood cells per cubic millimeter of blood, and women have about 4.7 million per cubic millimeter of blood.
Hemoglobin and Iron
Each red blood cell contains 280 million hemoglobin molecules. Hemoglobin is a complex molecule, and it is the most important component of red blood cells. It is composed of protein (globulin) and a molecule (heme), which binds to iron.
In the lungs, the heme component binds to oxygen in exchange for carbon dioxide. The oxygenated red blood cells are then transported to the body's tissues, where the hemoglobin releases the oxygen in exchange for carbon dioxide, and the cycle repeats. The oxygen is used in the mitochondria, the power source within all cells.
Red blood cells typically circulate for about 120 days before they are broken down in the spleen. Most of the iron used in hemoglobin can be recycled from there and reused.
Structure and Shape of Red Blood Cells
Red blood cells -- the erythrocytes -- are extremely small and look something like tiny, flexible discs. This unique shape offers many advantages:
- It provides a large surface area to absorb oxygen and carbon dioxide.
- Its flexibility allows it to squeeze through capillaries, the tiny blood vessels that join the arteries and veins.
Abnormally shaped or sized erythrocytes are typically destroyed and eliminated.
Blood Cell Production (Erythropoiesis)
The actual process of making red blood cells is called erythropoiesis. (In Greek, erythro means "red," and poiesis means "the making of things.") The process of manufacturing, recycling, and regulating the number of red blood cells is complex and involves many parts of the body:
- The body carefully regulates its production of red blood cells so that enough are manufactured to carry oxygen but not so many that the blood becomes thick or sticky (viscous).
- Most of the work of erythropoiesis occurs in the bone marrow. In children younger than 5 years old, the marrow in all the bones of the body is enlisted for producing red blood cells. As a person ages, red blood cells are eventually produced only in the marrow of the spine, ribs, and pelvis.
- If the body needs more oxygen (at high altitudes, for instance), the kidney triggers the release of the hormone erythropoietin (EPO), a hormone that acts in the bone marrow to increase the production of red blood cells.
- The lifespan of a red blood cell is 90 - 120 days. The liver and the spleen remove old red blood cells are removed from the blood by the liver and spleen.
- When old red blood cells are broken down for removal, iron is returned to the bone marrow to make new cells.
Iron Deficiency Anemia
Iron deficiency anemia occurs when the body lacks mineral iron to produce the hemoglobin it needs to make red blood cells. In general, there are three stages leading from iron deficiency to anemia:
- First, there is an insufficient supply of iron, which causes iron stores in the bone marrow to be depleted. This stage generally has no symptoms.
- Second, iron deficiencies develop and begin to affect hemoglobin production. (Tests will show low hemoglobin and hematocrit levels.)
- Hemoglobin production declines to the point where anemia develops.
Most of the iron used in the body can be recycled from blood and reused. Nevertheless, iron deficiency can occur from a number of conditions.
Inadequate Iron Intake. A healthy diet easily provides enough iron. In general, most people need just 1 mg of extra iron each day. (Menstruating women need 2 mg each day.) This means that lack of iron in the diet is not a common cause of iron deficiency anemia, except in infants. In fact, most American adults may be consuming too much iron in their diet. Iron-poor diets are a cause of anemia only in people with existing risks for iron deficiency. Children who have not yet eaten iron-fortified formulas or iron-enriched cereal may also become anemic.
Blood Loss. Iron deficiencies most commonly occur from internal blood loss due to other conditions that vary in severity. These conditions include:
- Very heavy periods (menorrhagia), the most common causes of anemia in menstruating women
- Peptic ulcers, which may be caused by H. pylori infections, or use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen.
- Chronic gastritis, caused by long-term use of NSAIDs, although it is rarely significant enough to cause anemia.
- Duodenal ulcers
- Hemorrhoids, though rare
- Colon polyps
- Colon, stomach, and esophageal cancer
- Bleeding from esophageal varices, often present in alcoholics
Impaired Absorption of Iron. Impaired absorption of iron is caused by:
- Certain intestinal diseases (inflammatory bowel disease, celiac disease)
- Surgical procedures, particularly those involving removal of parts of the stomach and small intestine, can impair the ability of the stomach or intestine to absorb iron. (Such conditions also often impair vitamin B12 absorption.)
- Pica, the craving for non-food substances such as ice, starch, or clay, is a possible cause of iron deficiency in young children. To complicate matters, pica (particularly ice cravings) may also be a symptom, rather than a cause, of anemia.
- Certain intestinal infections, such as hookworm and other parasites.
Genetic Causes. Some people are born with iron deficiency. Certain cases may be due to a mutation of the Nramp2 gene, which regulates a protein responsible for delivering iron to the cells.
Anemia of Chronic Disease (ACD)
Anemia of chronic disease (ACD), also called anemia of chronic inflammation (ACI), is a common condition associated with a wide variety of persistent inflammatory diseases. It can be very severe and require transfusions.
The Inflammatory Process and ACD. In ACD, iron is not efficiently recycled from blood cells and red blood cells do not survive for as long as normal. In addition, there is impaired response to erythropoietin, the hormone that acts in the bone marrow to increase the production of red blood cells.
Diseases Associated with ACD and Inflammation. The chronic diseases that are associated with this process include:
- Certain cancers. Examples include lymphomas and Hodgkin's disease.
- Autoimmune diseases. Examples include rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease, and polymyalgia rheumatica.
- Long-term infections. Examples include chronic or recurrent urinary tract infections, osteomyelitis, HIV/AIDS, hepatitis C.
- Liver disease. Cirrhosis can reduce the production of red blood cells. Gastrointestinal bleeding may also contribute to blood loss.
- Heart failure. Many patients with heart failure also have anemia. Anemia is associated with a higher risk of death in patients with heart failure. However, it is unclear whether anemia actually causes or worsens heart failure. Recent research suggests it may actually be a sign (marker) of heart failure. Iron deficiency in heart failure can be due to a number of factors. It may be caused by a lack of nutrients in a person's diet or by the body's inability to absorb nutrients from food.
- Chronic kidney disease. The hormone erythropoietin (EPO) is produced in the kidneys and stimulates the bone marrow production of red blood cells. Diseased kidneys do not release sufficient amounts of EPO. Anemia can result and is universal in end-stage renal disease (kidney failure). Chronic kidney disease is a common complication of diabetes.
Not all chronic diseases involve the inflammatory process and anemia. For example, high blood pressure is a chronic disease, but it does not affect red blood cells.
Treatment-Related Anemia
Treatment-related anemia results from the therapies used to treat conditions. For example, anemia is a common side effect of cancer treatments. Chemotherapy and radiation can impair the bone marrow's production of red blood cells and contribute to the extreme fatigue that many patients experience during cancer therapy. Patients with hepatitis C frequently receive combination therapy of ribavirin and interferon; ribavirin can induce anemia. Hepatitis C also affects many patients with HIV or AIDS. In addition to ribavirin, patients with HIV or AIDS can develop anemia as a result of highly active anti-retroviral therapy (HAART) and, in particular, from the drug AZT.
Other medications that increase the risk for anemia are certain antibiotics, some antiseizure medications (phenytoin), immunosuppressive drugs (methotrexate, azathioprine), antiarrhythmic drugs (procainamide, quinidine), and anti-clotting drugs (aspirin, warfarin, clopidogrel, heparin).
Megaloblastic Anemia
Megaloblastic anemia results from deficiencies in the B vitamins folate or vitamin B12 (also called cobalamin). Such deficiencies produce abnormally large (megaloblastic) red blood cells that have a shortened lifespan. Neurologic problems may be associated with vitamin B12 deficiency.
Causes of Vitamin B12 Deficiency. Conditions that cause vitamin B12 deficiencies include:
- Vitamin B12 deficiency from diet is very rare, because the liver stores over a 3-year supply. It usually does not occur even in alcoholism, strict vegetarianism, or in malnourished people with kidney failure or cancer. Since animal products are the chief source, however, vegan vegetarians may need a supplement, fortified food, or appropriate food selection known to contain adequate amounts of this vitamin
- Pernicious anemia. Pernicious anemia is an autoimmune disease in which antibodies are tricked into attacking stomach cells. This results in impaired production of intrinsic factor (IF), a compound that is critical for absorption of vitamin B12. Pernicious anemia is diagnosed in about 1% of people over age 60, with women having a higher risk than men.
- Complications of gastrointestinal surgery. Surgeries such as stomach bypass or stapling, which remove part or all of the stomach, pose a risk of causing vitamin B12 deficiencies.
- Overgrowth of intestinal bacteria
- Tropical sprue (an acquired malabsorption disease occurring in tropical climates)
Causes of Folate Deficiency. The body stores only about 100 times its daily requirements for folate and can exhaust this supply within about 3 months if the diet is deficient in folate.
- Poor diet coupled with alcoholism is the most common cause of folate deficiency. Alcohol abuse not only contributes to malnutrition but also causes chemical changes that can result in lower folate levels.
- Any condition that disturbs the small intestine and impairs its absorption ability can cause a deficiency. Such disorders include inflammatory bowel disease or celiac sprue (a sensitivity reaction to gluten), as well as gastric bypass weight-loss surgery.
- Parasitic diseases such as giardiasis
- Short bowel syndrome
- Deficiencies can also arise due to high demand for folic acid caused by conditions such as cancer, pregnancy, severe psoriasis, severe hyperthyroidism, and hemolytic anemia.
- Some drugs, including phenytoin, methotrexate, trimethoprim, and triamterene, may also hinder folate absorption.
Risk Factors
Among Americans with iron deficiency anemia, young children have the highest risk followed by premenopausal women. Adolescent and adult men and postmenopausal women have the lowest risk. Men, in fact, are at risk for iron overload, probably because of their high meat intake and minimal iron loss.
Infants and Children
Up to 20% of American children and 80% of children in developing countries become anemic at some point during their childhood and adolescence. Iron deficiency is the most common cause in children, but other forms of anemia, including hereditary blood disorders, can also cause anemia in this population.
Hispanic American children have double the rates of iron deficiency as African-American and Caucasian children. Children in lower-income homes are at higher risk than those in higher income homes. However, children in any income group can develop iron deficiency.
Children need to absorb an average of 1 mg per day of iron to keep up with the needs of their growing bodies. Since children only absorb about 10% of the iron they eat, most children need to receive 8 - 10 mg of iron per day. Breast milk contains very little iron. Babies who are exclusively breastfed should get a daily oral iron supplement starting at age 4 months and continued until iron-rich solid foods are introduced.
An iron-poor diet is a common cause of iron deficiency. Drinking too much cow's milk (usually more than 2 cups per day) is a common cause of iron deficiency in young children because cow's milk contains little iron and can get in the way of iron absorption. Cow's milk also can cause problems in the intestine that lead to blood loss and increased risk of anemia. Babies should not get cow's milk before they are 12 months old.
Iron deficiency most commonly affects babies 9 - 24 months old. All babies should have a screening test for iron deficiency at around age 12 months. Babies born prematurely may need to be tested earlier. Other factors associated with iron-deficiency anemia in infants and small children include:
- Stopping breastfeeding too early or using formula that isn't iron-fortified.
- Bottle-feeding too long. Bottle-fed babies who are 7 - 9 months old should be weaned from bottles and given sippy cups. By the age of 12 months, all children should be using a cup instead of a bottle.
- Toddlers' preferences for iron-poor food. Parents should make sure that their children eat iron-rich foods such as beans, meat, fortified cereals, eggs, and green leafy vegetables
Premenopausal Women
Up to 10% or more of adolescent and adult women under age 49 years are iron deficient. Anemia among premenopausal women typically occurs from:
- Heavy menstruation for longer than 5 days
- Abnormal uterine bleeding, such as from fibroids
- Pregnancy (see below)
Older Adults
Causes of anemia in adults age 65 years and older include nutritional deficiencies, chronic inflammatory disease, and chronic renal disease.
People with alcoholism are at risk for anemia both from internal bleeding as well as folate- and vitamin B deficiency-related anemias.
Iron-Poor Diets
Although most Americans probably consume too much iron in their diets, some people may be at risk for diet-related iron deficiencies, including:
- People whose diets are high in processed foods and lack any meat.
- Strict vegetarians. Vegans and other vegetarians who avoid all animal products may have a slightly higher risk for deficiencies in iron and some B vitamins. Although dried beans and green vegetables often contain iron, it is less easily absorbed from plants than from meat. Fortunately, most commercial cereals and grain products are fortified with an easily absorbed form of vitamin B12 and with folic acid (the synthetic form of folate).
Although nutritional iron-deficiency anemia has declined in industrialized nations, it still affects about 2 billion people worldwide. Even in the U.S., iron deficiency is the most prevalent nutritional deficiency. It is highly associated with poverty. People in lower socioeconomic groups have double the risk of those who are middle or upper class.
Chronic or Critical Illnesses
Anyone with a chronic disease that causes inflammation or bleeding is at risk for anemia. Critical illness in the intensive care unit is also highly associated with anemia.
Pregnancy is associated with fluid retention, which in turn may produce high volumes of plasma (the fluid component of blood). This process can dilute red blood cells, which may lead to lower hemoglobin and hematocrit levels. These changes by themselves can be considered a normal alteration of pregnancy. However, other factors increase the risk for anemia during pregnancy:
- Pregnancy increases the body's demand for folic acid, which poses a risk for folate deficiency and, therefore, megaloblastic anemia.
- Pregnancy increases the body's demand for iron, thus posing a risk for iron deficiency anemia. Pregnant women need 27 mg of iron per day.
- During delivery, heavy bleeding or multiple births can cause postpartum anemia. Postpartum anemia can last 6 - 12 months after giving birth.
Most cases of anemia are mild, including those that occur as a result of chronic disease. Nevertheless, even mild anemia can reduce oxygen transport in the blood, causing fatigue and a diminished physical capacity. Moderate-to-severe iron-deficiency anemia is known to reduce endurance. Some studies indicate that even iron deficiency without anemia can produce a subtle but still lower capacity for exercise.
Because a reduction in red blood cells decreases the ability to absorb oxygen from the lungs, serious problems can occur in prolonged and severe anemia that is not treated. Anemia can lead to secondary organ dysfunction or damage, including heart arrhythmias and heart failure.
Effects of Anemia in Pregnant Women
Pregnant women with significant anemia may have an increased risk for poor pregnancy outcomes, particularly if they are anemic in the first trimester. Mild-to-moderate anemia does not pose any increased risk.
Complications from Anemia in Children and Adolescents
In children, severe anemia can impair growth and motor and mental development. Children may exhibit a shortened attention span and decreased alertness. Children with severe iron-deficiency anemia may also have an increased risk for stroke.
Effects of Anemia in the Elderly
Anemia is common in older people and can have significantly more severe complications than anemia in younger adults. Effects of anemia in the elderly include decreased strength and increased risk for falls. Anemia may have adverse effects on the heart and increase the severity of cardiac conditions, including reducing survival rates from heart failure and heart attacks. Even mild anemia may possibly lead to cognitive impairment or worsen existing dementia.
Effects of Vitamin B12 Deficiencies and Pernicious Anemia
In addition to anemia, vitamin B12 deficiency can cause neurologic damage, which can be irreversible if it continues for long periods without treatment.
Anemia in Patients with Cancer
Anemia is particularly serious in cancer patients. In people with many common cancers, the presence of anemia is associated with a shorter survival time.
Anemia in Patients with Kidney Disease
Anemia is associated with higher mortality rates and possibly heart disease in patients with kidney disease.
Anemia in Patients with Heart Failure
The combination of anemia and heart failure can increase the risk of hospitalization or death. Patients with heart failure whose hemoglobin levels decline do worse than patients with stable levels.
Effects of Excess Iron
Patients with certain types of anemia need frequent blood transfusions. These transfusions can cause iron overload. [For more information, see "Transfusions" in Treatment section of this report.]
Symptoms of anemia vary depending on the severity of the condition. Anemia may occur without symptoms and be detected only during a medical examination that includes a blood test. When they occur, symptoms may include:
- Weakness and fatigue are the most common symptoms
- Shortness of breath on exertion
- Rapid heartbeat
- Lightheadedness or dizziness
- Headache
- Ringing in the ears (tinnitus)
- Irritability and other mood disturbances
- Pale skin (however, healthy-looking skin color does not rule out anemia)
- Mental confusion
- Loss of sexual drive
- Restless legs syndrome may betriggered byiron deficiency
Unusual Symptoms
Pica. One odd symptom, which in some cases is also a cause of iron deficiency, is pica. This is the habit of eating unusual substances, such as ice (called pagophagia), clay, cardboard, foods that crunch (such as raw potatoes, carrots, or celery), or raw starch. The pica often stops, particularly in children, when iron supplements are given.
Symptoms of Megaloblastic Anemia and its Causes
Symptoms of Megaloblastic Anemia. The symptoms of megaloblastic anemia from vitamin B12 or folic acid deficiencies include not only standard anemic symptoms but also:
- Inflammation of the mouth (stomatitis)
- Inflammation of the tongue (glossitis), which involves shrinkage at the surface and edges of the tongue
Over time, psychiatric and neurologic problems develop. Vitamin B12 deficiencies can cause neurologic symptoms (numbness and tingling, depression, memory loss, and irritability).
Symptoms of Pernicious Anemia. Early neurologic symptoms of pernicious anemia, which is a form of megaloblastic anemia, are due to B12 deficiency. They include numbness and tingling, depression, memory loss, and irritability. Advanced nerve damage can cause loss of balance and staggering, confusion, dementia, spasticity, loss of bladder control, and erectile dysfunction. Folic acid deficiency does not cause neurologic damage, although people with this deficiency can be irritable, forgetful, and experience personality changes.
Because anemia may be the first symptom of a serious illness, it is very important to determine its cause. This may be difficult, particularly in the elderly, malnourished, or people with chronic diseases, whose anemia may be caused by one or more factors. A detailed medical, personal, and dietary history should report:
- Any family or personal history of anemia
- A history of gallbladder disease, jaundice, or enlarged spleen
- Heavy menstrual bleeding in women
- Any occurrence of blood in the stool or other signs of internal bleeding
- Dietary history, particularly in people who are elderly, poor, or both
The doctor should check for swollen lymph nodes, an enlarged spleen,or pale skin and nail color.
A complete blood count (CBC) blood test is performed to determine the presence of anemia. Other iron status blood tests are also used.
Complete Blood Count (CBC)
A complete blood count (CBC) is a panel of tests that measures red blood cells, white blood cells, and platelets. For diagnosis of anemia, the CBC provides critical information on the size, volume, and shape of red blood cells (erythrocytes). CBC results include measurements of hemoglobin, hematocrit, and mean corpuscular volume.
Hemoglobin. Hemoglobin is the iron-bearing and oxygen-carrying component of red blood cells. The normal value for hemoglobin varies by age and gender. Anemia is generally considered when hemoglobin concentrations fall below 11 g/dL for pregnant women, 12 g/dL for non-pregnant women, and 13 g/dL for men.
The severity of anemia is categorized by the following hemoglobin concentration ranges:
- Mild anemia is considered when hemoglobin is between 9.5 - 13.0 g/dL
- Moderate anemia is considered when hemoglobin is between 8.0 - 9.5 g/dL
- Severe anemia is considered for hemoglobin concentrations below 8.0 g/dL
Hematocrit. Hematocrit is the percentage of blood composed of red blood cells. People with a high volume of plasma (the liquid portion of blood) may be anemic even if their blood count is normal because the blood cells have become diluted. Like hemoglobin, a normal hematocrit percentage depends on age and gender. In general, doctors diagnose anemia when hematocrit falls below:
- 33% for children 6 months - 5 years
- 35% for children 5 - 12 years
- 36% for children 12 - 15 years
- 39% for adult men
- 36% for adult non-pregnant women
- 33% for adult pregnant women
Other hemoglobin measurements, such as mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) may also be calculated.
Mean Corpuscular Volume. Mean corpuscular volume (MCV) is a measurement of the average size of red blood cells. The MCV increases when red blood cells are larger than normal (macrocytic) and decreases when red blood cells are smaller than normal (microcytic). Macrocytic cells can be a sign of anemia caused by vitamin B12 deficiency, while microcytic cells are a sign of iron-deficiency anemia.
Other Iron Status Blood Tests
Serum Ferritin. Ferritin is a protein that binds to iron and helps to store iron in the body. Low levelssuggest reduced iron stores. Normal values are generally 12 - 300 ng/mL for men and 12 - 150 ng/mL for women. Lower than normal levels of ferritin are a sign of iron-deficiency anemia, while higher than normal levels may indicate hemolytic anemia or megaloblastic anemia.
Serum Iron. Serum iron measures the amount of iron in the blood. A normal serum iron is 60 - 170 mcg/dL. Lower levels may indicate iron-deficiency anemia or anemia of chronic disease, while higher levels may indicate hemolytic anemia or vitamin B12 deficiency.
Total Iron Binding Capacity. Total iron binding capacity (TIBC) measures the level of transferrin in the blood. Transferrin is a protein that carries iron in the blood. TIBC calculates how much or how little the transferrin in the body is carrying iron. A higher than normal TIBC is a sign of iron-deficiency anemia. A lower than normal level may indicate anemia of chronic disease, sickle cell, pernicious anemia, or hemolytic anemia.
Reticulocyte Count. Reticulocytes are young red blood cells, and their count reflects the rate of red blood cell production. The upper normal limit is about 100,000/mL. A low count, when bleeding isn't the cause, suggests production problems in the bone marrow. An abnormally high count indicates that red blood cells are being destroyed in high numbers and indicates hemolytic anemia. Recent research suggests that the reticulocyte hemoglobin content (CHr) test may be more accurate than a standard hemoglobin test for detecting iron deficiency in infants.
Vitamin Deficiencies. The doctor may order tests for vitamin B12 and folate levels. The Schilling test is used to determine whether the body absorbs vitamin B12 normally.
Other Diagnostic Tests
If internal bleeding is suspected as the cause of anemia, the gastrointestinal tract is usually the first possible source. A diagnosis in these cases can often be made if the patient has noticed blood in the stools, which can be black and tarry or red-streaked. Often, however, bleeding may be present but not visible. If so, the patient needs stool tests for this hidden (occult) blood. The patient may need additional tests to diagnose the precipitating condition. Endoscopy, in which a fiber optic tube is used to view into the gastrointestinal tract, is helpful in many patients, particularly when the source of bleeding is unclear. A colonoscopy may also be recommended to rule out colorectal cancer.
If the patient's diet suggests low iron intake and other causes cannot be established using inexpensive or noninvasive techniques, the patient may simply be given a monthly trial of iron supplements. If the patient fails to respond, further evaluation is needed.
Dietary Factors
Iron found in foods is either in the form of heme iron (attached to hemoglobin molecule) or non-heme iron:
- Heme Iron. Foods containing heme iron are the best sources for increasing or maintaining healthy iron levels. Such foods include (in decreasing order of iron-richness) clams, oysters, organ meats, beef, pork, poultry, and fish.
- Non-Heme Iron. Non-heme iron is less well-absorbed. About 60% of the iron in meat is non-heme (although meat itself helps absorb non-heme iron). Eggs, dairy products, and iron-containing vegetables have only the non-heme form. Such vegetable products include dried beans and peas, iron-fortified cereals, bread, and pasta products, dark green leafy vegetables (such as chard, spinach, mustard greens, and kale), dried fruits, nuts, and seeds.
The absorption of non-heme iron often depends on the food balances in meals. The following foods and cooking methods can enhance absorption of iron:
- Meat and fish not only contain heme iron -- the best form for maintaining stores -- but they also help absorb non-heme iron.
- Increasing intake of vitamin-C rich foods, such as orange juice, may enhance absorption of non-heme iron, although it is not clear if it improves iron stores in iron-deficient people. In any case, vitamin-C rich foods are healthy and include broccoli, cabbage, citrus fruits, melon, tomatoes, and strawberries.
- Riboflavin (vitamin B2) may help enhance the response of hemoglobin to iron. Food sources include dairy products, liver, and dried fortified cereals.
- Cooking methods can enhance iron stores. Cooking in cast iron pans and skillets can help increase the iron content of food.
- Vitamins B12 and folate are important for prevention of megaloblastic anemia and for good health in general. The only natural dietary sources of B12 are animal products, such as meats, dairy products, eggs, and fish (clams and oily fish are very high in B12). As is the case with other B vitamins, however, B12 is added to commercial dried cereals. The recommended daily allowance (RDA) for adults is 2.4 mcg a day.Older peoplemay have trouble absorbing natural vitamin B12 and require the more easily absorbed synthetic form of B12 from fortified foods or supplements.
- Folate is found in avocado, bananas, orange juice, cold cereal, asparagus, fruits, green, leafy vegetables, dried beans and peas, and yeast. The synthetic form, folic acid, is now added to commercial grain products. Vitamins are usually made from folic acid, which is about twice as potent as folate. The recommended daily amount of folic acid or folate for teenagers and adults is 400 mcg. Women who are pregnant need 600 mcg per day and women who are breastfeeding need 500 mcg daily.
Recommended Daily Allowance for Iron
The Recommended Daily Allowance (RDA) of iron for people who are not iron deficient varies by age group and other risk factors. (Iron supplements are rarely recommended in people without evidence of iron deficiency or anemia.) The RDA for iron intake is:
- Infants 0 - 6 months: 0.27 mg
- Infants 7 - 12 months: 11 mg
- Children 1 - 3 years old: 7 mg
- Children 4 - 8 years old: 10 mg
- Children 9 -13 years old: 8 mg
- Teenage boys (14 - 18 years): 11 mg
- Teenage girls (14 - 18 years): 15 mg
- Men 19 - 50 years old: 8 mg
- Women 19 - 50 years old: 18 mg
- Pregnant women: 27 mg
- Older men and women (over age 50): 8 mg
Preventing Anemia in Infants and Small Children
The main source of iron for an infant from birth to 1 year of age is from breast milk, iron-fortified infant formula, or cereal.
Breastfeeding and Iron-Supplemented Formulas. Mothers should be encouraged to breastfeed their babies for their first year. The American Academy of Pediatrics (AAP) recommends exclusively breastfeeding for a minimum of 4 months, but preferably 6 months, then gradually adding solid foods while continuing to breastfeed until at least the baby's first birthday. Because human breast milk contains very little iron, the AAP recommends that full-term healthy infants receive a daily oral iron supplement of 1 mg/kg beginning at age 4 months and continuing until iron-rich complementary foods, such as iron-fortified cereals, are introduced. Preterm infants who are breastfed should receive an iron supplement of 2 mg/kg by the time they are 1 month old.
Infants who are not breastfed should receive iron-fortified formulas (4 - 12 mg/L for their first year of life). Parents should discuss the best formula with their doctor. The AAP does not recommend cow's milk for children under 1 year old. The baby will begin drinking less formula or breast milk once solid foods become a source of nutrition. At 8 - 12 months of age, a baby will be ready to try strained or finely chopped meats. When cereals are begun, they should be iron fortified.
Recommendations for Toddlers. Toddlers who did not have iron supplements during infancy should be checked for iron deficiency. After the first year, children should be given a varied diet that is rich in sources of iron, B vitamins, and vitamin C. Good sources of iron include iron-fortified grains and cereals, egg yolks, red meat, potatoes (cooked with skin on), tomatoes, molasses, and raisins. Milk does not contain enough iron and can decrease children's appetite for iron-rich foods. Toddlers older than 1 year should not drink more than 2 cups of milk a day. Fruits that are rich in vitamin C can help boost iron absorption. Most children will receive adequate iron from a well-balanced diet, but some toddlers may benefit from liquid supplements or chewable multivitamins.
Oral iron supplements are the best way to restore iron levels for people who are iron deficient, but they should be used only when dietary measures have failed. Iron supplements cannot correct anemias that are not due to iron deficiency.
Iron replacement therapy can cause gastrointestinal problems, sometimes severe ones. Excess iron may also contribute to heart disease, diabetes, and certain cancers. Doctors generally advise against iron supplements in anyone with a healthy diet and no indications of iron deficiency anemia.
Treatment of Anemia of Chronic Disease. In general, the best treatment for anemia of chronic diseases is treating the disease itself. In some cases, iron deficiency accompanies the condition and requires iron replacement. Erythropoietin, most often administered with intravenous iron, is used for some patients.
Oral Iron Supplements
Supplement Forms. There are two forms of supplemental iron: ferrous and ferric. Ferrous iron is better absorbed and is the preferred form of iron tablets. Ferrous iron is available in three forms: ferrous fumarate, ferrous sulfate, and ferrous gluconate.
The label of an iron supplement contains information both on the tablet size (which is typically 325 mg) and the amount of elemental iron contained in the tablet (the amount of iron that is available for absorption by the body.) When selecting an iron supplement, it is important to look at the amount of elemental iron.
A 325 mg iron supplement contains the following amounts of elemental iron depending on the type of iron:
- Ferrous fumarate. 108 mg of elemental iron
- Ferrous sulfate. 65 mg of elemental iron
- Ferrous gluconate. 35 mg of elemental iron
Dosage. Depending on the severity of your anemia, as well as your age and weight, your doctor will recommend a dosage of 60 - 200 mg of elemental iron per day. This means taking one iron pill 2 - 3 time during the day. Make sure your doctor explains to you how many pills you should take in a day and when you should take them. Never take a double dose of iron.
Side Effects and Safety. Common side effects of iron supplements include:
- Constipation and diarrhea are very common. They are rarely severe, although iron tablets can aggravate existing gastrointestinal problems such as ulcers and ulcerative colitis.
- Nausea and vomiting may occur with high doses, but taking smaller amounts of medicine can control the problem. Switching to ferrous gluconate may help some people with severe gastrointestinal problems.
- Black stools are normal when taking iron tablets. In fact, if they do not turn black, the tablets may not be working effectively. This problem tends to be more common with coated or long-acting iron tablets.
- If the stools are tarry looking as well as black, if they have red streaks, or if cramps, sharp pains, or soreness in the stomach occur, gastrointestinal bleeding may be causing the iron deficiency. The patient should call the doctor promptly.
- Acute iron poisoning is rare in adults but can be fatal in children who take adult-strength tablets. Keep iron supplements out of the reach of children. If your child swallows an iron pill, immediately contact a poison control center.
Other Tips for Safety and Effectiveness. Other tips for taking iron are as follows:
- For best absorption, iron should be taken between meals. Iron may cause stomach and intestinal disturbances, however. Low doses of ferrous sulfate can be taken with food and are still absorbed but with fewer side effects.)
- Drink a full 8 ounces of fluid with an iron pill. Taking orange juice with an iron pill can help increase iron absorption. (Some doctors also recommend taking a vitamin C supplement with the iron pill.)
- If constipation becomes a problem, take a stool softener such as docusate sodium (Colace).
- Certain medications, including antacids, can reduce iron absorption. Iron tablets may also reduce the effectiveness of other drugs, including the antibiotics tetracycline, penicillin, and ciprofloxacin and the Parkinson's disease drugs methyldopa, levodopa, and carbidopa. At least 2 hours should elapse between doses of these drugs and iron supplements.
- Avoid taking milk, caffeine, antacids, or calcium supplements at the same time as an iron pill as they can interfere with iron absorption.
- Tablets should be kept in a cool place. (Bathroom medicine cabinets may be too warm and humid, which may cause the pills to disintegrate.)
The hematocrit should return to normal after 2 months of iron therapy. However, iron supplementation should be continued for another 6 - 12 months to replenish the body's iron stores in the bone marrow.
Intravenous or Injected Iron
In some cases, iron is administered through muscular injections or intravenously. Intravenous iron has the advantage of causing less gastrointestinal discomfort and inconvenience. It may be in the form of iron dextran (Dexferrum, InFed), sodium ferric gluconate complex in sucrose (Ferrlecit), or iron sucrose (Venofer). Ferrlecit or Venofer are equally effective and generally safer than iron dextran.
Candidates. The injected or intravenous forms should be limited to the following patients with iron deficiency:
- People with iron deficiency anemia in whom oral therapy has clearly failed.
- Patients with bleeding disorders in which blood loss continues to exceed the rate at which oral iron is absorbed.
- In emergencies, when people need red blood cells but transfusion is not appropriate or available.
- In people with serious gastrointestinal disorders, such as inflammatory bowel disease, who cannot take iron therapy by mouth.
- People undergoing hemodialysis who receive supplemental erythropoietin therapy. Sodium ferric gluconate complex in sucrose (Ferrlecit) or iron sucrose (Venofer) is specifically approved as first-line therapy for these patients.
Certain patients, even if they meet these qualifications, may not be appropriate candidates or should be monitored closely for complications. They include:
- Patients with any underlying autoimmune disease.
- Malnourished patients who also have an underlying infection.
- Patients who are at risk for iron overload.
Side Effects. Some side effects differ depending on how the iron is administered and include the following:
- Muscular injections include pain at the site.
- Intravenous administration can cause pain in the vein, flushing, and metallic taste, all of which are brief.
For both methods, side effects and serious complications can include:
- Blood clots
- Fever
- Joint aches
- Headache
- Rashes
- A delayed reaction of joint and muscle aches, headache, and malaise occurs 1 - 2 days after the infusion (most commonly with iron dextran) in about 10% of patients. These symptoms respond quickly to NSAIDs, such as ibuprofen or naproxen, in most people.
- Iron toxicity. Symptoms include nausea, dizziness, and a sudden drop in blood pressure. Sodium ferric gluconate in sucrose (Ferrlecit) or iron sucrose (Venofer) may pose a lower risk for toxicity than iron dextran.
- Allergic reactions. Allergic reactions that occur with intravenous iron can be very serious and, in rare cases, even fatal. Iron dextran appears to pose a much higher risk than sodium ferric gluconate complex in sucrose or iron sucrose, although allergic reactions can also occur with the latter forms.
Oral and injected iron should never be given at the same time. Intravenous iron therapy may be appropriate for some pregnant women who meet these requirements, depending on the pregnancy term and other factors.
Blood Transfusions
Transfusions are used to replace blood loss due to injuries and during certain surgeries. They are also commonly used to treat severely anemic patients who have thalassemia, sickle cell disease, myelodysplastic syndromes, or other types of anemia. Some patients require frequent blood transfusions. Iron overload can be a side effect of these frequent blood transfusions. If left untreated, iron overload can lead to liver and heart damage.
Iron chelation therapy is used to remove the excess iron caused by blood transfusions. Patients take a drug that binds to the iron in the blood. The excess iron is then removed from the body by the kidneys.
Deferasirox (Exjade) is a drug that is given as a once-daily treatment for iron overload due to blood transfusions. It does not require injections. Patients mix the deferasirox tablets in liquid and drink the medicine.
Erythropoiesis-Stimulating Drugs
Erythropoietin is the hormone that acts in the bone marrow to increase the production of red blood cells. It has been genetically engineered as recombinant human erythropoietin (rHuEPO) and is available as epoetin alfa (Epogen, Procrit, and Eprex). Novel erythropoiesis stimulating protein (NESP), also called darbepoetin alfa (Aranesp), lasts longer in the blood than epoetin alfa and requires fewer injections. These medications are also called "erythropoiesis-stimulating drugs."
Levels of erythropoietin are reduced in anemia of chronic disease. Injections of synthetic erythropoietin can help increase the number of red blood cells in order to avoid receiving blood transfusions. Synthetic erythropoietin can cause serious side effects, including blood clots, and is approved only for treating patients with anemia related to the following conditions:
- Cancer. For select patients, erythropoietin is used to treat the anemia associated with chemotherapy.
- Chronic kidney disease. Erythropoietin is an important anemia treatment for patients with chronic kidney disease, including those with end-stage renal disease who are on dialysis. In 2012, the FDA approved a new erythropoiesis-stimulating drug peginesatide (Omontys) specifically for patients on kidney dialysis. The manufacturer recalled the drug a year later due to serious and fatal allergic reactions.
- HIV/AIDS. Erythropoietin helps treat the anemia caused by zidovudine (AZT) therapy.
Erythropoiesis-Stimulating Drugs and Cancer. Erythropoietin may be used to treat anemia caused by chemotherapy. Erythropoietin treatment does not help prolong survival, but can improve quality of life during cancer treatment by improving anemia.
However, these drugs can shorten lifespan and cause some tumors to grow faster. In general, the lowest effective dose should be used. The risks of early death and increased tumor growth are greatest when these drugs are used to boost the hemoglobin level to10 - 12 g/dL or higher. The American Society of Clinical Oncology and the American Society of Hematology recommend starting erythropoietin only if a patient's hemoglobin level is less than 10 g/dL.)
Discuss with your doctor whether an erythropoiesis-stimulating drug is appropriate for you.
Erythropoiesis-Stimulating Drugs and Chronic Kidney Disease. For patients with chronic kidney disease or kidney failure, the FDA currently recommends that erythropoiesis-stimulating drugs be used to maintain hemoglobin levels between 10 - 12 g/dL. (The exact level within this range varies by individual.) There is a greater risk of death and serious cardiovascular events, such as heart attack, stroke, and heart failure when these drugs are used to achieve higher hemoglobin levels (13.5 - 14g/dL) compared to lower hemoglobin levels (10 - 11.3 g/dL).
Warning Symptoms. Contact your doctor if you have any of the following symptoms while being treated with an erythropoiesis-stimulating drug:
- Pain or swelling in the legs
- Worsening in shortness of breath
- Increases in blood pressure (be sure to regularly monitor your blood pressure)
- Dizziness or loss of consciousness
- Extreme fatigue
- Blood clots in hemodialysis vascular access ports
Vitamin Replacement for Megaloblastic Anemia
Megalobastic anemia is marked by abnormally large red blood cells. (Pernicious anemia is a type of megaloblastic anemia). It is caused by impaired absorption or insufficient intake of vitamin B12 or folate. If folate deficiency is responsible, treatment usually involves taking a daily oral folic acid supplement for at least several months as well as increasing intake of foods rich in folate. When vitamin B12 deficiency is responsible, vitamin B12 may be administered in tablets, injections of cyanocobalamin or hydroxocobalamin, or as a nasal spray.
- www.anemia.org -- National Anemia Action Council
- www.nhlbi.nih.gov -- National Heart, Lung and Blood Institute
- www.irondisorders.org -- Iron Disorders Institute
- www.healthychildren.org -- Healthy Children (American Academy of Pediatrics)
Alleyne M, Horne MK, Miller JL. Individualized treatment for iron-deficiency anemia in adults. Am J Med. 2008 Nov;121(11):943-8.
American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 95: anemia in pregnancy. Obstet Gynecol. 2008 Jul;112(1):201-7.
Baker RD, Greer FR; Committee on Nutrition American Academy of Pediatrics. Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0-3 years of age). Pediatrics. 2010 Nov;126(5):1040-50. Epub 2010 Oct 5.
Bennett CL, Silver SM, Djulbegovic B, Samaras AT, Blau CA, Gleason KJ, et al. Venous thromboembolism and mortality associated with recombinant erythropoietin and darbepoetin administration for the treatment of cancer-associated anemia. JAMA. 2008 Feb 27;299(8):914-24.
Bohlius J, Schmidlin K, Brillant C, Schwarzer G, Trelle S, Seidenfeld J, et al. Recombinant human erythropoiesis-stimulating agents and mortality in patients with cancer: a meta-analysis of randomised trials. Lancet. 2009 May 2;373(9674):1532-42.
Brotanek JM, Gosz J, Weitzman M, Flores G. Iron deficiency in early childhood in the United States: risk factors and racial/ethnic disparities. Pediatrics. 2007 Sep;120(3):568-75.
Bunn H. Approach to the anemias. In: Goldman L, Schafer AI, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 161.
Clement FM, Klarenbach S, Tonelli M, Johnson JA, Manns BJ. The impact of selecting a high hemoglobin target level on health-related quality of life for patients with chronic kidney disease: a systematic review and meta-analysis. Arch Intern Med. 2009 Jun 22;169(12):1104-12.
Goddard AF, James MW, McIntyre AS, Scott BB; British Society of Gastroenterology. Guidelines for the management of iron deficiency anaemia. Gut. 2011 Oct;60(10):1309-16. Epub 2011 May 11..
Groenveld HF, Januzzi JL, Damman K, van Wijngaarden J, Hillege HL, van Veldhuisen DJ, et al. Anemia and mortality in heart failure patients a systematic review and meta-analysis. J Am Coll Cardiol. 2008 Sep 2;52(10):818-27.
Janus J, Moerschel SK. Evaluation of anemia in children. Am Fam Physician. 2010 Jun 15;81(12):1462-71.
Killip S, Bennett JM, Chambers MD. Iron deficiency anemia. Am Fam Physician. 2007 Mar 1;75(5):671-8.
KDOQI. Kidney Disease: Improving Global Outcomes (KDIGO) Anemia Work Group. KDIGO Clinical Practice Guideline for Anemia in Chronic Kidney Disease. Kidney Inter. Suppl. 2012 Aug; 2(4):279–335..
Ludwig H, Crawford J, Osterborg A, Vansteenkiste J, Henry DH, Fleishman A, et al. Pooled analysis of individual patient-level data from all randomized, double-blind, placebo-controlled trials of darbepoetin alfa in the treatment of patients with chemotherapy-induced anemia. J Clin Oncol. 2009 Jun 10;27(17):2838-47. Epub 2009 Apr 20.
Mabry-Hernandez IR. Screening for iron deficiency anemia -- including iron supplementation for children and pregnant women. Am Fam Physician. 2009 May 15;79(10):897-8.
Rizzo JD, Brouwers M, Hurley P, Seidenfeld J, Arcasoy MO, Spivak JL, et al. American Society of Hematology/American Society of Clinical Oncology clinical practice guideline update on the use of epoetin and darbepoetin in adult patients with cancer. Blood. 2010 Nov 18;116(20):4045-59. Epub 2010 Oct 25
Rodgers GM 3rd, Becker PS, Bennett CL, Cella D, Chanan-Khan A, Chesney C, et al. Cancer- and chemotherapy-induced anemia. National Comprehensive Cancer Network. 2010.v.2.
Stabler SP. Clinical practice. Vitamin B12 deficiency. N Engl J Med. 2013 Jan 10;368(2):149-60.
Unger EF, Thompson AM, Blank MJ, Temple R. Erythropoiesis-stimulating agents - time for a reevaluation. N Engl J Med. 2010 Jan 21; 362(3):189-192.
Review Date: 3/18/2013�
Reviewed By: Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.


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Michael MacMunn, LICSW, LADC
Licensed Social Worker, Licensed Alcohol & Drug Counselor
30 Court Street, Westfield, Massachusetts 01085
Some aspect of your life is not working, otherwise you would not be on a site like this. I have 25+ years experience helping 1000s of folks with problematic issues just like yours. Let's talk!

subset: commoncrawl


text:
Cook earned the award after averaging 11.3 assists and 2.1 digs per set in road wins over No. 12 Purdue (3-0) and Indiana (3-2). She led the Huskers to a .348 hitting percentage on the weekend, including a .361 clip against the Boilermakers. Cook also dished out 52 assists against Indiana and 38 against Purdue.
The Huskers will face Wisconsin and Minnesota this weekend at the NU Coliseum. The Badgers will visit Lincoln on Friday, Oct. 12 at 7 p.m. in a match that can be seen on NET. The Gophers and the Huskers will face each other on Sunday, Oct. 14 at 2 p.m. That match will air nationally on ESPN2.


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Last week I finished my tenure as Editor in Chief of The Greyhound, Loyola University Maryland's student-run newspaper. During my time there, I served as columnist, copy editor, news staff writer, Opinions Editor, Copy Chief and Managing Editor, all before taking over as Editor in Chief in April 2010.
I inherited a paper that completed the bare minimum to put out a print product every week, an aggravating fact given the extremely privileged position in which college newspapers nationwide find themselves. (They're niche markets, for chrissakes–no advertising falling off there.) Our stories were stale; we covered lectures, and reports on campus events were boring re-tellings of what happened. Our website was stagnant and one-dimensional; it was, essentially, an article dump. We had no social media strategy, no policy on how often staff writers needed to contribute articles, no copy editing standards (no attention to fact checking as an integral piece of copy editing), and seemingly no interest in producing articles of feature length or quality.
In a year's time, with the help of a dedicated and talented staff, we implemented significant changes at The Greyhound, including:
- A website redesign and relaunch, facilitated by College Media Network and College Publisher 5 content management system.
- Social media presence–Facebook, Twitter–using HootSuite's excellent dashboard interface.
- Ticket giveaways to concerts via our PR contacts at Rams Head Live! in Baltimore; we started off giving away two pairs of tickets to see The Roots.
- Full-page, color front pages, which effectively removed columns of text from the front page of our print product. (An aesthetic choice, admittedly, but one we made–despite the "tabloid" feel and association–because we didn't think students would be more apt to pick up a large photo than columns of black and white text.)
- Several feature stories, in various sections of the paper, that broadened our content and coverage, and allowed us to view the print paper less as a round-up of the week's events and instead treat it as a weekly magazine. (In other words, lectures were now online-only content, and we reserved paper space for more interesting, more in-depth coverage of other stories.) One such story, printed as an insert, was our Greyhound Guide to Baltimore.
- One of these feature stories, a profile on basketball player Jamal Barney, was subsequently picked as a Mark of Excellence Award winner by the Virginia Chapter of the Society of Professional Journalists.
- Better management of our budget, a sore spot among Greyhound staffs of old. There was no soliciting or courting of advertisers; that ended this year, as we worked with our contacts at advertising "clearing houses" like Alloy Media to pull in advertising, in addition to our own proactive efforts to contact local businesses. (For instance, after reaching out to clothing store South Moon Under with a media kit, they began an advertising campaign with us.) Beyond that, we partnered with CampusAve to streamline classified advertising placement and to take the entire process online, which allowed advertisers to use their credit card to purchase ad space. (A first at The Greyhound.)
- Actual copy editing, with a Greyhound style guide outlining our house style.
I make these points not in a self-aggrandizing effort, but rather to highlight the opportunities college newspapers have to truly be laboratories of journalism. Like their professional counterparts, college newspapers oftentimes stay mired in the status quo, unwilling or unable to implement substantive, innovative change.
That has to end. The new Greyhounders coming in need to view the paper–in both its print and online forms–as an incubator for journalistic creativity and innovation…
It begins with putting a premium on your online content. Divide stories into online-only and print stories. Seek to publish at least one new article each day on the website. Hire bloggers who are feisty social media junkies to write online-only content. View the website as a means by which readers can be more involved in the campus conversation. This means encouraging people to check out the site, and then being open to commenters and engaging in dialogue with them.
Photos and videos. Rinse. Repeat. All digital cameras have a record function. Thirty-second video clips of live events go a long way in enhancing a reader's experience; iMovie software is simple enough to understand, and it's available in the Mac labs on campus. Photo albums–ones rife with photos, and not just three or four additional shots–should assist a reader looking to grasp a better sense of the surroundings in a particular story.
Everyone is a web editor. Everyone should be on Facebook and Twitter. Every editor should be running a section blog. Every editor–and all the writers–should take their cameras to each event they attend. The new "New New Journalism" places greater emphasis on having a conversation with readers. No longer can newspapers see their audience as people they are speaking to; social media and online commenting have broken those boundaries. Get online, and get to talking to people who read The Greyhound.
Take chances. Think of stories you want to cover, and then cover them. Working for a college newspaper gives you a unique chance to mess up and not ruin yourself professionally. That isn't to say be unethical, plagiarize, or manufacture a story or information. But it is to say that you can try out various story ideas and see if they work. You'll never learn otherwise.
Finally: have one editor learn WordPress, teach it to the other editors, and then make the switch. Because WordPress is open source, newsrooms have greater flexibility to create, manipulate, and transform their online operations, without the hassle of negotiating through a third-party organization. That, and WordPress is simple enough for everyone to use and infinitely more cost-efficient given College Media Network's new pricing plan. Look for newspaper WordPress themes online, and let the gears start churning.
As pithy as this sounds, making the above changes isn't going to easy, but it will be rewarding in the long run. Not only will you put out a better Greyhound, but you'll cultivate skills on a level of creativity that is absolutely vital to the newsrooms of today.
And always remember: When the going gets tough, you can always keep drinking.


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The Sheridan Troopers lost to the Billings Scarlets 6-16.
REGIONAL SOCCER - The Bronc and Lady Bronc soccer teams finish up play today at the 4-A East regional tournament.
The Lady Broncs lost 4-0 against Laramie Friday night and will play Cheyenne Central for 3rd and 4th place today.
The Broncs lost 2-1 against Gillette and will play Central today for 3rd and 4th.
They will open play at the state tournament next Thursday in Rock Springs.
REGIONAL TRACK - Regional track and field competition concludes today after day one here are the team standings.
Former Lady Bronc and current Wyoming Cowgirl Taylor Gardner had a personal best in the 400 hurdles last Friday is 4th all time in UW history.
UW is at for UNLV this weekend for the conference outdoor meet.
Gardner will be running on the 4 X 100 team, the 4 X 400 team and in the 400 hurdles. Her time Friday of 59.8 in the 400 hurdles is second fastest in the MWC this year.
REGIONAL SOCCER - It was a wild night of region soccer for the Broncs and Lady Broncs both teams advanced to the regional tournament semi finals with both matches going to penalty kicks.
In Gillette the Lady Broncs and Camels were tied at 1-all after two overtime periods so the match went to penalty kicks the Lady Broncs came out on top 4-3. They will play Laramie tonight in one regional semi final.
The Broncs played Cheyenne East to a 1-all overtime tie and beat the T-Birds on penalties 4-3 they play Gillette tonight in the semi finals.
25 18
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DOWN Ref; Powder River Power
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DOWN Ref: Sheridan Jaycees
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DOWN Ref; Blacktooth Brewery
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SHERIDAN COLLEGE - The Sheridan college booster clubs has two big fund raising events scheduled over the next several weeks.
A week from tomorrow they host their annual golf tournament at the Powder Horn, the event has turned into one of the best early season golf outings in Sheridan, SC Athletic Director Steve Smiley.
They may have a few spots open if you are interested in playing or getting a team together you can contact smiley at the Sheridan college Men's basketball office.
TRACK AND FIELD - Regional track and field competition starts Friday in Gillette for all Eastern 1-A, 2-A and 4-A teams.
Sheridan high school head coach Art Bauers says they've had a good spring and are looking for good this in Gillette this week.
BRONC / LADY BRONC SOCCER - The Bronc and Lady Bronc soccer teams get ready for regional tournament elimination games tomorrow.
The Lady Broncs will play Gillette in Gillette at 5:00 the winner moves on to play Laramie in the semi finals Friday.
The Sheridan Lady Bronc volleyball camp will be held for three days May 20th-22nd. That's Monday through Wednesday
after school. The camp is open to all players in the 4th through 8th grades.
Campers will be split into two groups 4th - 6th grades will go each evening from 4:00 - 5:30 and 7th and 8th grades from 4:00 - 6:00.
Registration forms are available at all local schools clinicians will be the Lady Bronc coaching staff and players.
Our goal in allowing public comment on our web site is to provide an arena for open discussion on the issues. Following these simple guidlines will ensure that your comments remain posted.
The moderators of sheridanmedia.com reserve the right to monitor and screen all content submitted to the site and may delete content, and block or ban users at our discretion. For a full description see our User Agreement.


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After the evening's lecture, I trundled off to the men's room. When I returned, not five minutes later, nearly everyone had gathered at the front of the room. People were praying for each other, laying hands on each other, talking quietly with each other, while a pianist played riffs lightly in the background.This is the quintessence of the Vineyard movement, which began under the leadership of John Wimber in the 1970s. It's a strange—and inviting—mixture of Pentecostal and Quaker elements. T … [Read more...]
Intimacy with God and a Blindfolded Boy
April 10, 2014 by Leave a Comment


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Attending Mass in Rome not quite as easy as you'd think
posted at 7:25 am on March 10, 2013 by Ed Morrissey
A quick observation on my first Sunday here in Rome …
I had figured that it would be easy to find a church nearby my hotel in Rome, because … well, it's Rome, right? When I asked the hotel's clerk, however, she seemed a bit nonplussed. She suggested the Vatican at first, but that's nearly a mile away. I was hoping to give my sore legs and feet a little relief today after walking back and forth from the media center both Friday (twice) and Saturday (once, blessedly). Part of the reason for this is that my hotel is, I have discovered, off the beaten path for tourists and pilgrims, and is in more of a government-office section of town. It's nice, but not as active as Campo di Fiori or Piazza della Repubblica, where we stayed the last time.
The clerk then suggested a church here in the neighborhood, but I misunderstood her directions in English — my fault, not hers — and didn't see any church at all. I consulted my GPS system to find the nearest church, and it was 1.1 kilometers away, almost the same as walking to the Vatican. Finally, as I headed back, I realized the church she pointed out was practically in the same building as the hotel, just around the corner from the entrance, and looks nothing like a church from the outside.
I entered and waited for Mass to begin, at first with only a few elderly congregants in the pews. By the end of the half-hour, though, the place was packed, especially with children who had obviously just finished their Sunday school lessons. I tried to follow the service, very easily recognizing the structure as identical to those everywhere but failing to comprehend much of what was said. I offered my responses in English, quietly so as not to distract the people around me, and said "Pace" during the Sign of Peace. That must have worked; I got plenty of smiles and "pace" responses. Queuing for Communion turned out to be less organized than in most American churches, but I managed to go with the flow.
It's very comforting to know that one can travel and still be in communion with the Church and the people of the community, even if we don't understand a word each other are saying.


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By Aaron Lommers Herald Writer
EVERETT — After two games, it didn't look like any team in the National Lacrosse League could stop the Washington Stealth's offense.
At Comcast Arena on Sunday, it was the Edmonton Rush that couldn't be stopped. The two teams were tied 3-3 after the first quarter, but the Rush dominated the final three quarters to win 18-10.
"I don't think things were going all that well in the first quarter either," Stealth coach Chris Hall said after the game. "We gave up an easy goal on the first goal of the game and then they got up. Personally, I don't think we ever recovered from the first goal of the game."
That first goal of the game belonged to Edmonton forward Mark Matthews, who the Rush selected with the top overall pick in the 2012 NLL entry draft. Matthews has back-to-back hat tricks in his first two games in the NLL and finished with four goals and five assists on Sunday.
"Anytime your first shot of the game goes in the net you think, 'well, this is going to be a good night for me,'" Hall said. "We know he's going to get his points. He is a great lacrosse player, but we've got to get more stops."
The defense struggled to get stops and for the first time this season, the offense struggled to find the net. Forward Rhys Duch had his third hat trick of the season and forward Athan Iannucci and transition player Bob Snider each scored two goals, but outside of that there wasn't much offense to speak of.
"They put great pressure on us," Hall said. "They are very athletic and very quick. It was the best defense we have faced in three games. I thought they played superb defense and I thought we handled it poorly. You have to expend way more energy on offense when a defense is going to put that kind of pressure on you and I don't think we expended that energy."
The Rush also slowed down Cliff Smith, who had been nearly unstoppable his first two games with seven goals and eight assists, holding him to just one assist and without a goal. Perhaps even more impressive, Stealth forward Lewis Ratcliff had no points and just five shots.
"Lewis struggled tonight, there is no doubt about that," Hall said. "Don't forget we have Iannucci, Duch and Smith and other guys who can score. I don't think necessarily that they were totally limiting Lewis' game, I think they put pressure on him as well like they did on others."
The Stealth trailed the Rush 8-5 at halftime and Hall said he felt his team was lucky to be within three goals, but the Rush wasted little time extending that lead in the third period. Edmonton scored the first four goals of the third quarter and extended their lead to 12-5. With Washington goalkeeper Nick Patterson struggling, the Stealth went to Neil Tyacke, who the team signed on Saturday to try to turn things around. Tyacke, who was playing in just his second NLL game, held the Rush in check for the remainder of the third quarter, but Washington needed goals.
They finally got one in the final minute of the third quarter, when Duch scored his second of the game. The goal seemed to awaken the Stealth because Snider won the ensuing face off and ran through the center of the Rush defense to score another goal just eight seconds later. Iannucci added his second goal of the game with 13 seconds left in the quarter and the Stealth had cut the Rush lead to 12-8.
Within striking distance heading into the fourth, Hall said the Stealth needed to score quickly to make it a game. Instead, Edmonton scored the first three goals of the fourth quarter to take a seven-goal advantage again at 15-8. At that point, the Stealth went back to Patterson to finish the game.
After looking like a championship contender in its first two contests, it looked like it was just one of those nights for the Stealth, but Duch said the Stealth can't have that mentality.
"I don't think you can do that for any loss," Duch said. "Obviously, you can't expect to go 16-0 in a season, so you have to chalk it up to that is one of the losses we are allowed. But it's a good learning experience. That's a team you have to expect to see down the road. They are a good team. So I think we would be kind of stupid to just put it behind us and not learn anything, but that being said you have to have a short memory. You can't hold it against yourself. You have to take it as a learning experience and move forward."
For Washington, it was a missed opportunity to send two teams in its division to 0-2 while improving to 3-0 on the season. Instead, the Stealth find themselves just a half game up on Colorado (Washington's next game) and Edmonton with the Rush leading the season series 1-0.
"It's disappointing to miss the opportunity," Duch said. "That being said, we play them next. So if we win it still puts us three wins to their two losses."
Aaron Lommers covers the Washington Stealth for The Herald. Follow him on twitter @aaronlommers and contact him at email@example.com.
Rush 17, Stealth 10
Edmonton 3 5 4 6 — 18
Washington 3 2 3 2 — 10
1st Quarter — Scoring: EDM — Matthews Goal (Small, Knight) 0:29; WAS — Grimes Goal (Garrison) 2:59; EDM — Small Goal (PP) (Matthews, Knight) 5:09; WAS — Duch Goal (Patterson, Garrison) 12:18; EDM — Corbeil Goal (SH) (Rubisch) 13:08; WAS — Hill Goal (PP) (Duch, Smith) 13:35. Penalties: McElroy, WAS (Holding, Minor, 2 min) 4:05; Ward, EDM (Checking from Behind, Minor, 2 min) 7:08; Thompson, EDM (Holding The Stick, Minor, 2 min) 12:10. Goalie Changes: None.
2nd Quarter — Scoring: EDM — Ward Goal (PP) (Greer, Small) 1:25; EDM — Davis Goal (Conway, Greer) 4:16; EDM — Mydske Goal 5:34; WAS — Iannucci Goal (Hill, Buchanan) 7:09; EDM — Greer Goal (PP) (Matthews, Small) 8:42; EDM — Cornwall Goal 9:52; WAS — Bucktooth Goal (PP) (Duch) 14:25. Penalties: O'Dougherty, WAS (Holding, Minor, 2 min) 1:04; Henderson, WAS (Checking from Behind, Minor, 2 min) 8:13; Thompson, EDM (Holding, Minor, 2 min) 12:40. Goalie Changes: None.
3rd Quarter — Scoring: EDM — Matthews Goal (Ward, Conway) 0:53; EDM — Matthews Goal (Ward, Small) 4:26; EDM — Toll Goal (Bold) 6:45; EDM — Small Goal (Matthews) 10:16; WAS — Duch Goal (Snider) 14:15; WAS — Snider Goal 14:20; WAS — Iannucci Goal (Hill, Bucktooth) 14:46. Penalties: None. Goalie Changes: None.
4th Quarter — Scoring: EDM — Ward Goal (Conway, Matthews) 2:03; EDM — Knight Goal (Small, Matthews) 6:08; EDM — Mydske Goal (Cornwall) 6:35; WAS — Duch Goal (Buchanan, Hill) 9:33; EDM — Ward Goal (Greer, Davis) 10:20; WAS — Snider Goal 10:27; EDM — Thompson Goal (EN) (Bold) 11:54; EDM — Matthews Goal (PP) (Ward, Knight) 13:01. Penalties: Bucktooth, WAS (Roughing, Minor, 2 min) 10:20; Moleski, WAS (Holding, Minor, 2 min) 12:45. Goalie Changes: None.


text:
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Kristofer Helgen
Illustration by Andrew Howley/NGS
Photograph by Bruce M. Beehler
Dr. Kristofer Helgen discovers new animals. Deep in a New Guinea rain forest. High on an Andean mountainside. Resting in a museum's specimen drawer.
"Conventional wisdom would have it that we know all the mammals of the world," he notes. In fact, we know so little. Unique species, profoundly different from anything ever discovered, are out there waiting to be found." His own efforts prove this. Helgen himself has discovered approximately 100 new species of mammals previously unknown to science. To date, about 25 have been confirmed in published scientific papers.
"Since I was three years old, I've been transfixed by animals," he recalls. "Even then, my excitement revolved around figuring out how many different kinds there were. Every time I picked up a book and learned about a new species, I would add it to my list. In some very real way that's exactly what I still do today. Making these discoveries is the most personally rewarding thing I could ever hope to do."
Helgen's search plunges him into the wild on almost every continent. Yet about three times as many new finds are made within the walls of museums. "An expert can go into any large natural history museum and identify kinds of animals no one knew existed," he explains. When only a few specimens of a species exist, and reside in museums scattered across the globe, sheer logistics often prevent researchers from connecting the dots and pinpointing a new find. "Collections build up over centuries," he says, "It's virtually impossible to fully interpret that wealth of material. Every day brings surprises."
As Curator of Mammals for the Smithsonian Institution's National Museum of Natural History, he oversees not only the collection's use as an invaluable research resource, but also its continued expansion through new exploration.
One such expedition, to the Foja Mountains of New Guinea, yielded extraordinary results. Helgen describes the remote region as "one of the few places in the world with no villages, no roads, no human population at all. Animals there were much more abundant and far less afraid of people since the area has such a fantastic history of being uninhabited." Helgen identified a number of new species including mice, rats, and a "beautiful little grey-brown wallaby I hope to name within the next year." He also documented viable populations of animals previously thought to be in major decline, or possibly even extinct.
Another exploratory trip to the Andes in Ecuador was inspired by an unusual set of skins and skulls Helgen noticed in a museum collection. He recognized it as a type of Olingo (a long-tailed cat-like animal related to raccoons) which had never received a scientific name. "I could have simply described it as a new species based on the specimens in the museum. But I wanted to go a step further and find it in the wild. We brought back film, photographs, and a much better understanding of how and where it lives." In fact, its cloud forest habitat is being rapidly cleared for agriculture and other development. Helgen hopes that publicity surrounding the announcement, as well as the animal's inherent appeal, will generate concern for its threatened forest home.
Even discoveries made without leaving the confines of museums can have far reaching impact. A case in point is the hog badger. Long thought to be a single widespread species, Helgen's study of museum specimens revealed it is in fact three distinct species, two of which face serious threats from hunting and logging. "No one thought it was endangered before," he says. "Now, we need to reassess that." The finding could also guide zoos in captive breeding programs, and would have been valuable in previous studies considering hog badgers as potential vectors of disease such as SARS.
Sometimes, the wisest conservation policies stem from proving a species should not be protected. Helgen's research showed that raccoons which have been protected as endangered endemic Caribbean mammals are actually an invasive species introduced to the islands in recent centuries. What's more, they threaten native ground-nesting birds and sea turtles; and can spread disease among wildlife and humans. So strategies should contain, rather than protect, this potentially destructive animal.
"Some of these conservation-related discoveries are just as exciting as finding a new species," he notes. When my findings interact with the real world through epidemiology, economics, and conservation, it really fuels me onward."
Latest Explorer News
- What 'Planet of the Apes' & Caesar Show Us About Our Own Evolution
- The Camargue: Wild West of France
- Everglades Restoration: Alterations of Downstream Biodiversity
- Exploring Everglades National Park by Kayak
- Bald Eagle Celebrated by National Geographic Photo Ark for Independence Day
- Paddleboarding with Polar Bears & Contributing to Conservation
- A Family of Explorers in Search of Some of Earth's Oldest Fossils
- Hōkūleʻa Returns Home
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Inside National Geographic Magazine
Discovery in the Foja Mountains
Expeditions Council grantees discover a world of bizarre creatures.
Nat Geo E-Team
What are Kristofer Helgen and the rest of the National Geographic Explorers up to? Meet the E-Team and learn about their projects in this interactive mural.
In Their Words
It constantly surprises me how little we know about the mammals of the world. Making discoveries about this overlooked wealth of biodiversity feels absolutely fantastic.
Kristofer Helgen
New Species Photos: Olinguito and Kin
Kris Helgen led the study that discovered the world's newest carnivore, the olinguito.
The Future of Exploration
Discovering new species, animal-borne recorders, and even plagues are daily routines for National Geographic explorers.
Our Explorers in Action
Famous Women Explorers
Meet female explorers who have pushed the limits in adventure, science, and more.
Meet All Our Explorers
Explorers A-Z
At the heart of our explorers program is the quest for knowledge through exploration and the people who make it possible.
Explorers by Category
Browse our different areas of exploration and discover the fascinating people behind the projects.


text: Posted November 20, 2012 Which of the two do you guys think is the bigger problem for us this season? I know that there isn't really much to say for either sides of the ball here, but I would have to go with the offense being our weakest point right now. As bad as our defense as been at closing out games this season, i think our offense is worse. Not only is our running game virtually non existing, but it also doesn't intimidate anyone. Without our running game we are just airing it out half that time, and aside from smith we have yet to really solidify a number 2 WR (not saying LaFell can't step up). I just think that as bad as our defense has played in closing moments of the game, they have kept us in plenty of games, it is our offense that seems to choke whenever they need to pull a win. They can't convert when it matters, cant run when it matters, cant catch when it matters. The defense can't hold off a team forever when they are constantly going back after our offense keeps getting 3 and outs. Just wanted to see what everyone else thought, Feel free to share. Share this post Link to post Share on other sites


text: Ryan Kenny's photos seem to be about quiet moments of youthful exploration. Like those days when the city just boils over and you head up to Ojai to catch your breath for an afternoon. You and your favorite people are driving through those oak trees and no one's really talking but that's how it needs to be. These images are like that–catching your breath.


text:
You don't know which channel your ap is using?
First thing, when you run airodump it will still pickup AP's that are strong enough no matter what channel your on. I think this has to do with a high signal strength along with the small gap between the channel frequencies.
Next, You might want to set your card to channel 7.
iwconfig wlan4 channel 7
Also make sure that any other wireless interfaces are not channel hopping while your trying to do this. Best to just take them down like this:
ifconfig wlan0 down
ifconfig wlan1 down
I'm not sure if this will work but you might want to try entering the ESSID with quotes.
Another thing that I'm unsure if it works or not but I never enter the BSSID using capital letters.
You can also shorten your commands by using -c instead of --channel and -w instead of --write
This makes things slightly quicker and easier to type.


text:
Did you Prepare the Kernel Headers?
I'm trying to:
make install
in the mad-wifi directory.
I get this as soon as i type: make
/bin/sh: line 0: cd: /lib/modules/220.127.116.11/build: No such file or directory
Makefile.inc:66: *** /lib/modules/188.8.131.52/build is missing, please set KERNELPATH. Stop.
I've installed linux-headers and linux-source
It looks like they've been installed into: /usr/src/
I've also tried reinstalling the packages.
The command: uname -r returns:
Does anybody have any idea on how i can get make && make install working??
UPDATE: Solved With:
root@bt:~# prepare-kernel-sources
root@bt:~# cd /usr/src/linux
root@bt:~# cp -rf include/generated/* include/linux/
Last edited by g0bl1n; 10-26-2011 at 10:12 PM. Reason: Format Error
Did you Prepare the Kernel Headers?
Have you...g0tmi1k?
copy this code and paste it into console:
if you get error like"module.symvers is missing" during driver installation and you would like to fix that than after you prepare kernel headers do this:Code:cd /lib/modules/18.104.22.168/ ln -s /usr/src/linux build
however this action may take 2 hours and it's not very important.Code:cd /usr/src/linux/ make modules
important is to make symbolic link in your /lib/modules/$(uname -r)/
Thanks man, it worked.. I appreciate the help!


text:
Danielle O'Connor
Theatre Director/Productions Manager
- Email:
- Phone: (812) 535-5286
Danielle earned her Bachelors of Arts at Saint Mary-of-the-Woods College in 2011. She returned in the fall of 2011 to direct Little Women as the guest artist; the next spring she stage managed and assisted directed under Prof. Sharon Ammen, Ph. D. for The Sound of Music. O'Connor taught at a private Catholic school near Indianapolis last year, but chose to return to The Woods when offered the position of Theatre Director/Productions Manager.


text:
November 11, 2011 – March 11, 2012
- View a slide show and comment about the exhibition!
- See if the exhibition is visiting your hometown
- Tour the galleries on Flickr
- Go behind-the-scenes with the museum's blog , Eye Level
- Read articles about the exhibition
Multiplicity features 83 works from the museum's permanent collection by such outstanding contemporary artists as John Baldessari, John Cage, Vija Celmins, Chuck Close, R. Luke DuBois, Sol LeWitt, Brice Marden, Julie Mehretu, Martin Puryear, Susan Rothenberg, Kiki Smith, and Kara Walker. The concept of making multiple images from the same matrix has been integral to printmaking ever since the earliest prints were pulled from woodblocks and metal plates in the fifteenth century. Each impression is considered to be an original work of art.
Many of the artists in this exhibition have expanded the idea of multiplicity beyond editions of identical impressions by creating series, sequences, and images that comprise numerous parts. They explore repetition, pairing, and variations on a theme as artistic strategies. Implicit in their exploration of multiplicity is a challenge to rarity and uniqueness as determinants of value.
This exhibition brings together a selection of prints by artists for whom the concept of multiplicity in its many forms provides a touchstone for their artistic expression. These prints are the result of collaboration between the artist and professional printers who help realize the artist's vision. They question the authority of the unique masterpiece and alter the stereotype of the artist working alone in the studio.
Nearly half of the prints included in the exhibition are recent acquisitions. Joann Moser, senior curator, selected the works for display.
Free Public Programs
November 16, 2011, Washington Printmakers
December 1, 2011, Curator Gallery Talk
January 19, 2012, Take 5! Printmaking Demonstration
January 21, 2012, Multi-Prints Family Day
February 8, 2012, Curator Gallery Talk
February 11, 2012, 21st Century Consort, Multiplicity
February 16, 2012, Take 5! Printmaking Demonstration
March 10, 2012, Identifying and Collecting Fine Prints
The Museum's blog, Eye Level
Seeing Double: On Multiplicity, January 3, 2012
Multiplicity: Five Questions with Joann Moser, November 29, 2011
In the News
WETA, Februrary 2012, Around Town
Smithsonian Magazine, November 21, 2011, Around the Mall, "The Many Angles and Perspectives of 'Multiplicity' at the American Art Museum" by Joseph Stromberg
National Tour
Multiplicity is touring the United States after closing at the Smithsonian American Art Museum. Venues include:
Arkansas Arts Center in Little Rock, Arkansas (September 20, 2012–January 6, 2013)
Patty & Jay Baker Naples Museum of Art in Naples, Florida (April 6, 2013–July 7, 2013)
Akron Art Museum in Akron, Ohio (November 23, 2013–March 16, 2014)
Virginia Museum of Contemporary Art in Virginia Beach, Virginia (May 29, 2014–August 18, 2014)
Multiplicity is organized by the Smithsonian American Art Museum with support from the William R. Kenan, Jr. Endowment Fund. The C.F. Foundation in Atlanta supports the museum's traveling exhibition program, Treasures to Go.


text:
Calendar of Events
Sep 8
NSW: Life After Carleton
11:15 am – 12:15 pm / Recreation Center
Wait! You just got here! Why should you think about life after Carleton? Because if you make career planning and development an integral part of your Carleton education right from the beginning, you will graduate with more knowledge, skills, and confidence in relation to what will come next in your life. Come meet staff and peer leaders from the Career Center and learn about the amazing opportunities and resources available to you.
Sponsored by New Students 2016. Contact: Sarah Wojnicki, x4462
Students, Faculty, Staff, Alumni, Families, Prospective Students, New Students, Faculty Emeriti


text:
Krauss homers twice, drives in six
D-backs prospect pilots Mobile's 20-3 stomping of Pensacola
By Andrew Pentis / Special to MLB.com | July 8, 2012 5:14 PM ET
The D-backs' No. 20 prospect lifted two longballs and drove in a career-high six runs in the BayBears' 20-3 shellacking of the host Pensacola Blue Wahoos. The 20 runs and 18 hits represented season highs for the Southern League South Division's first-half title holders.
Batting cleanup and playing right field, Krauss flew out to right and singled in the fourth for just one of three hits against Blue Wahoos spot starter David Serrano over the game's first four innings. But when Serrano -- who took Futures Game participant Kyle Lotzkar's spot in the rotation -- exited, the BayBears feasted.
In between left fielder Bobby Borchering's grand slam in the fifth and pinch-hitter Daniel Kaczrowski's slam in the ninth, the left-handed hitting Krauss went deep twice. He smacked a three-run shot in the sixth off of left-hander Chris Manno and a three-run blast in the seventh off of righty Curtis Partch.
"I got some help with the wind on the first one. The second one I hit well," said Krauss, who pulled a 2-2 fastball in the sixth and an 0-2 changeup in the seventh. "They still have to throw another strike to you with two. That's the way I look at it."
Krauss' third multi-homer game of his four-year career was his first since June 25, 2010, when he was at Class A Advanced Visalia. He also collected his previous single-game best in RBIs (five) in a June 29, 2010 game. These dates aren't so coincidental. While he went deep 16 times in 2011, it was something of a lost season. He told MLB.com in March that his campaign was, in part, less than stellar because of a lack of physical conditioning.
Listed at 235 pounds these days, Arizona's second-round draftee in 2009 appears plenty fit. The numbers bear this out.
"I feel a lot better at the plate than I did last year," he said. "I just got back to the basics in the offseason. I'm not trying to do too much."
First baseman Kyle Greene (three runs) and shortstop Chris Owings (two runs) matched Krauss with a game-high three hits apiece.
David Holmberg (2-1) pitched six innings of two-run ball. The D-backs' No. 7 prospect gave up five hits and struck out five.
"David had a good sinker going today," Krauss said. "He's going to get a lot of his outs that way."
Blue Wahoos right-hander Brian Pearl, who preceded fellow relievers Manno and Partch, was charged with the BayBears' first five runs. Pearl (0-1) recorded two outs before exiting in the fifth.
Lotzkar, the Reds' No. 18 prospect, pitched a scoreless inning for the Futures' World Team. In his absence, the Blue Wahoos were forced to employ all seven members of their bullpen.
Andrew Pentis is a contributor to MLB.com. Follow him on Twitter at AndrewMiLB. This story was not subject to the approval of the National Association of Professional Baseball Leagues or its clubs.View More


text:
Intrauterine growth restriction (IUGR) refers to the poor growth of a baby while in the mother's womb during pregnancy. Specifically, it means the developing baby weighs less than 90% of other babies at the same gestational age.
Intrauterine growth retardation; IUGR
Many different things can lead to intrauterine growth restriction (IUGR). An unborn baby may not get enough oxygen and nutrition from the placenta during pregnancy because of:
Congenital or chromosomal abnormalities are often associated with below-normal weight. Infections during pregnancy that affect the developing baby, such as rubella, cytomegalovirus, toxoplasmosis, and syphilis can also affect the weight of the developing baby.
Risk factors in the mother that may contribute to IUGR include:
If the mother is small, it may be normal for her baby to be small, but this is not due to IUGR.
Depending on the cause of IUGR, the developing baby may be symmetrically small, or have a head that is normal size for gestational age, while the remainder of its body is small.
A pregnant woman may feel that her baby is not as big as it should be. The measurement from the mother's pubic bone to the top of the uterus will be smaller than expected for the baby's gestational age. This measurement is called the uterine fundal height.
Intrauterine growth restriction (IUGR) may be suspected if the size of the pregnant woman's uterus is small. The condition is usually confirmed by ultrasound.
Further tests may be needed to screen for infection or genetic problems if IUGR is suspected.
IUGR increases the risk that the baby will die inside the womb before birth. If your doctor thinks you might have IUGR, you will be closely monitored with regular pregnancy ultrasounds to measure the baby's growth, movements, blood flow, and fluid around the baby.
Non-stress testing will also be done.
Depending on the results of these tests, delivery of your baby may be necessary.
After delivery, growth and development of the newborn depends on the severity and cause of IUGR. The baby's outlook should be discussed with your obstetrician and pediatrician.
Depending on the specific cause, IUGR increases the risk of pregnancy and newborn complications. Babies may have an abnormal fetal heart rate during labor, requiring delivery by C-section.
Contact your provider right away if you are pregnant and notice that the baby is moving less than usual.
Also call your health care provider if your infant or child does not seem to be growing or developing normally.
Do not drink alcohol, smoke, or use recreational drugs. Eat healthy foods. Get regular prenatal care. If you have a chronic medical condition or take prescribed medications regularly, see your doctor before you get pregnant. This can help reduce any effects of your medical condition on your pregnancy and the baby.
Baschat AA, Galan HL, Ross MG, Gabbe SG. Intrauterine growth restriction. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: Normal and Problem Pregnancies. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 31.
Carlo WA. Prematurity andintrauterine growth restriction. In: Kliegman RM,Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Elsevier Saunders;2011:chap 91.
Figueras F, Gardosi J. Intrauterine growth restriction: newconcepts in antenatal surveillance, diagnosis, and management. Am J Obstet Gynecol. 2011;204(4):288-300.


text:
Image Gallery
07.11.2017 'Nathan Bridges Dune' on a Martian Mountain
07.11.2017 'Ireson Hill' on Mount Sharp, Mars
06.29.2017 Traction control testing
06.21.2017 A.I. laser targeting
06.01.2017 Diagram of Lake Stratification on Mars
03.21.2017 Break in Raised Tread on Curiosity Wheel
02.27.2017 Swirling Dust in Gale Crater, Mars, Sol 1613
02.27.2017 Dust Devil Passes Near Martian Sand Dune
02.27.2017 Sand Moving Under Curiosity, One Day to Next
12.13.2016 Now and Long Ago at Gale Crater, Mars
12.13.2016 Where's Boron? Mars Rover Detects It
10.03.2016 Curiosity Self-Portrait at 'Murray Buttes'
10.03.2016 Butte 'M9a' in 'Murray Buttes' on Mars
09.19.2016 Ribbon Cutting
09.09.2016 Farewell to Murray Buttes (Image 5)
09.09.2016 Farewell to Murray Buttes (Image 4)
09.09.2016 Farewell to Murray Buttes (Image 3)
09.09.2016 Farewell to Murray Buttes (Image 2)
09.09.2016 Farewell to Murray Buttes (Image 1)
08.26.2016 Out-of-this-World Records
03.30.2016 Erisa Hines
03.30.2016 Buzz Aldrin
02.12.2016 Women in Science
02.09.2016 Adam Steltzner, a JPL engineer
01.27.2016 Night Close-up of Martian Sand Grains
01.27.2016 Curiosity Self-Portrait at Martian Sand Dune
12.17.2015 Alteration Effects at Gale and Gusev Craters
Curiosity Rover's Location for Sol 545This map shows the route driven by NASA's Mars rover Curiosity through the 545 Martian day, or sol, of the rover's mission on Mars (February 17, 2014).
Numbering of the dots along the line indicate the sol number of each drive. North is up. From Sol 542 to Sol 545, Curiosity had driven a straight line distance of about 151.02 feet (46.03 meters).
The base image from the map is from the High Resolution Imaging Science Experiment Camera (HiRISE) in NASA's Mars Reconnaissance Orbiter.
Image Credit: NASA/JPL-Caltech/Univ. of Arizona
All Images