Sperm fertilizing egg

Illustration of a human sperm fertilising an egg. The picture shows the size difference between the egg, or ovum, & the spermatozoon. Human spermatozoa are extremely elongated single cells about 65 micrometres long, divided into 3 main regions: a head, neck, & tail. The head, which contains the male nucleus, is about 7 micrometres long. Here, the head appears buried in the follicular cells, which form the corona radia that surrounds the ovum. Beneath the corona radiata is a glycoprotein membrane, the zona pellucida, which the sperm must penetrate to reach the female nucleus. This version on black background. Version on white background is P648 010.

Genetically modified potatoes

 Genetically modified potatoes. Close-up of Amflora potatoes (Solanum tuberosum) with a biohazard symbol. Amflora (also known as EH92-527-1) is a genetically modified potato developed by BASF Plant Science. The Amflora potato plant produces pure amylopectin starch that is processed to waxy potato starch. Amflora was approved for industrial applications in the European Union market on 2nd March 2010.

Over the last few years, potatoes have been losing importance as a food crop. The crop's prospects in the starch and chemical industry, however, have been growing for quite some time. For starch potatoes, taste isn't what's important. Instead, emphasis is placed on the quality and composition of the starch. An optimised starch potato could be making its way to fields in Europe soon. This new potato cultivar is genetically modified.

Only one in four potatoes grown in Europe actually gets eaten by people. Almost half end up being fed to livestock. The remaing one quarter are used as raw material in the production of alcohol and starch.

Potatoes are becoming more and more important as renewable raw materials for the starch industry. The starch produced in potatoes, however, isn't in an ideal form. It's composed of a mixture of two different kinds of starch: amylose and amylopectin. These two kinds of starch have very different properties.

Amylopectin, making up 80 percent of the starch content in potatoes, consists of large, highly-branched molecules. Amylopectin makes starch water soluble and gives it its characteristic stickiness. It is very useful in the food, paper, and chemical industries as paste, glue or as a lubricant.

Amylose is made up of long, chain-like molecules and is used predominantly in the production of films and foils.

Both of these kinds of starch are useful for human nutrition. But for the processing industry, a mixture of different starches is a problem. Industry must separate the two kinds of starch using expensive processes that take a toll on the environment. This is why plant breeders are working hard to develop potatoes that produce only one type of starch. Right now, emphasis has been placed upon developing potatoes containing only amylopectin, due to its diverse applications.

Classical breeding methods have not yet been able to provide an amylose-free potato that has acceptable yield and resistance to pests and diseases. Genetic engineering (Antisense-Strategy), on the other hand, offers a targeted approach to supressing the production of amylose.

Genetically modified amylopectin potatoes have been tested in field trials for several years. In the meantime, applications have been presented to European regulatory authorities for approving the cultivation of these potatoes as a renewable raw material for starch production. Because the post-processing residues would be fed to livestock, a request for the approval of the potatoes as feed has also been submitted. Starch-modified GM potatoes could be growing in European fields soon.

Resistance to pests and diseases

Attempts to confer pest and disease resistance to potatoes using genetic engineering haven't been quite as successful.

Several GM potato cultivars with improved  resistance to viruses and to the potato beetle have been approved in the US and in Canada. In 1999, they were planted on approximately 25,000 hectares. Since then, cultivation of GM potatoes has ceased. The GM potatoes did not prevail, because they were not delivering any economic advantages, and some larger US companies refused to take the GM potatoes for further processing.

Right now, work is being done on potatoes with genetic engineering to confer resistance to  Phytophthora infestans, also known as late blight of potato. Some consider this to be the most dangerous plant disease of all because it can spread extremely rapidly when conditions are warm and moist, leading to devastating losses. The disease is best known for causing the Irish Potato Famine of 1846-1850. Today, the disease is still a major problem. Owing to its flexibility, the disease has been able to survive every management strategy used thus far and has responded with new, adapted forms. Today, the disease is combatted using fungicides and heavy metal treatments. In the meantime, genetic engineers have come up with a promising new strategy. The first field trials with  fungus resistant GM potatoes are already underway. The next few years will show if this new concept is effective.

From: GMO Compass

Gene Therapy

Gene therapy, conceptual image

What is Gene Therapy?

Gene therapy is an experimental technique used in treatment of malfunctioning genes, whereby a deficient or defective gene is replaced by a working gene, so that the body can make the proper enzyme or protein and as a result eliminate the origin of the disease.
Gene therapy is therefore targeted to “genetic metabolic diseases” in which a faulty gene causes an enzyme to be either absent or ineffective in catalyzing a particular metabolic reaction effectively.

There are a number of approaches for correcting defective genes:

The most common approach is inserting a gene into a non-specific location within the genome, replacing a nonfunctional gene.
Through selective reverse mutation, the malformed gene can be repaired to attain its normal role.
Via homologous recombination, the normal gene is exchanged for the abnormal gene
Alteration of the regulation of a particular gene.

How does Gene Therapy work?

To insert the corrected gene into the patient’s targeted cell, a carrier molecule, called a vector must be used. The most common form of vector is a virus which has been genetically modified to contain human DNA within it. The viruses are modified by replacing the deformed gene with the genes encoding for the desired effect. Thus the virus can be used as a 'vehicle' to carry the good genes into the targeted human cell in a pathogenic manner . The target cells are usually a patient’s liver or lung cells, where the viral vector transfers the therapeutic gene into the target cell. The therapeutic gene generates the production of functional proteins and restores the cell to its normal state 

 

The types of viruses used in gene therapy

There are six main types of viruses used as vectors in gene therapy (shown in table below):


1. Retroviruses - A class of viruses that can create double-stranded DNA copies of their RNA genomes. These copies of its genome can be integrated into the chromosomes of host cells. Human immunodeficiency virus (HIV) is a retrovirus.

2. Adenoviruses - A class of viruses with double-stranded DNA genomes that cause respiratory, intestinal, and eye infections in humans. The virus that causes the common cold is an adenovirus. 

3. Adeno-associated viruses - A class of small, single-stranded DNA viruses that can insert their genetic material at a specific site on chromosome 19.

4.Herpes simplex viruses - A class of double-stranded DNA viruses that infect a particular cell type, neurons. Herpes simplex virus type 1 is a common human pathogen that causes cold sores.13

5. Alphaviruses- a single stranded positive sense RNA, particularly used to develop viral vectors for  the Ross-River virus, Sindbis virus, Semliki Forest virus and Venezuelan Equine Encephalitis virus.

6. Vaccina or pox viruses- a large, complex, enveloped virus belonging to the poxvirus family. It has a linear, double-stranded DNA genome of approximately 190 kb in length, which encodes for around 250 genes. Can accept as much as 25kb of foreign DNA making it especially useful in expressing a large gene in gene therapy.
 

Hand holds an aborted human foetus aged 8 weeks

Eight week old foetus. Hand holds an aborted human foetus, eight weeks old. The eighth week of pregnancy represents the end of the formative developmental stage and the embryo becomes a foetus. It is human-like in appearance, with the head large in proportion to the body. Eyes, ears and nose are developing. The limbs are long and bent at the elbows and knees, and the fingers and toes have differentiated. The genital organs develop into male or female at 7 weeks. All major organ systems are formed by the eighth week, but require growth. The umbilical cord is prominent. By eight weeks the foetus is about 3-4cm long (crown-rump length) and weighs under 10 grams.

ANNUAL ABORTION STATISTICS

In 2008, approximately 1.21 million abortions took place in the U.S., down from an estimated 1.29 million in 2002, 1.31 million in 2000 and 1.36 million in 1996. From 1973 through 2008, nearly 50 million legal abortions have occurred in the U.S. (AGI).
In 2008, the highest number of reported abortions occurred in New York (124,867), NYC (89,469), Florida (86,817) and Texas (81,366); the fewest occurred in Wyoming (≤4), South Dakota (848),  North Dakota (1,386), and Idaho (1,481) (CDC).
The 2008 abortion ratios by state ranged from a low of 59 abortions per 1,000 live births in Idaho (Wyoming had too few abortions for reliable tabulation) to a high of 732 abortions per 1,000 live births in NYC (CDC).

The annual number of legal induced abortions in the United States doubled between 1973 and 1979, and peaked in 1990. There was a slow but steady decline through the 1990's. Overall, the number of annual abortions decreased by 3.7% between 2000 and 2008, with temporary spikes in 2002 and 2006. (CDC)

In 1998, the last year for which estimates were made, more than 23% of legal induced abortions were performed in California (CDC).

In 2005, the abortion rate in the United States was higher than recent rates reported for Canada and Western European countries and lower than rates reported for China, Cuba, the majority of Eastern European countries, and certain Newly Independent States of the former Soviet Union (CDC).
Nearly half of pregnancies among American women are unintended; about 4 in 10 of these are terminated by abortion. Twenty-two percent of all U.S. pregnancies end in abortion. (AGI).

WHO HAS ABORTIONS?

In 2008, 84.3% of all abortions were performed on unmarried women (CDC).
Women between the ages of 20-24 obtained 33% of all abortions in 2008; women between 25-29 obtained 24% (CDC).

In 2008, women aged 20-29 years had the highest abortion rates (29.6 abortions per 1,000 women aged 20-24 years and 21.6 abortions per 1,000 women aged 25-29 years) (CDC).

50% of U.S. women obtaining abortions are younger than 25; women aged 20-24 obtain 33% of all U.S. abortions and teenagers obtain 17% (AGI).

In 2008, adolescents under 15 years obtained .05% of all abortions, but had the highest abortion ratio, 821 abortions for every 1,000 live births (CDC).

47% of women who have abortions had at least one previous abortion (AGI).
Black women are more than 4.8 times more likely than non-Hispanic white women to have an abortion, and Hispanic women are 2.7 times as likely (AGI).

37% of women obtaining abortions identify themselves as Protestant, and 28% identify themselves as Catholic (AGI).

At current rates, nearly one-third of American women will have an abortion (AGI).

WHY ARE ABORTIONS PERFORMED?

On average, women give at least 3 reasons for choosing abortion: 3/4 say that having a baby would interfere with work, school or other responsibilities; about 3/4 say they cannot afford a child; and 1/2 say they do not want to be a single parent or are having problems with their husband or partner (AGI).

Mouse foetus

Mouse foetus. Coloured scanning electron micrograph (SEM) of a mouse (Mus sp.) foetus. The embryo has started to develop limb buds (bottom right and left). The head and tail are differentiating and the heart bulge is visible (centre). The embryo attaches to the uterine epithelium about five days after ovulation and the pregnancy lasts for approximately three weeks.

Bat fly

Bat fly. Coloured scanning electron micrograph (SEM) of a bat fly (Nycteribia kolenatii). Bat flies are parasitic spider-like flies that feed on the blood of bats. They do not have eyes or wings and almost never leave the bodies of their hosts. Magnification: x33 when printed 10 centimetres wide.

Giardia lamblia

Giardia lamblia protozoan. Coloured scanning electron micrograph (SEM) of a Giardia lamblia trophozoite, showing the ventral adhesive disk (centre right), which it uses to attach itself to its host. Giardia are single-celled parasites of the intestinal tract. They are most common in tropical regions and have flagella (hair-like structures), which are used for locomotion. This is the trophozoite (active, feeding) life stage of the protozoan. Giardia lamblia is the causative agent of giardiasis, an intestinal disease that causes abdominal pain, diarrhoea and nausea. It is spread through contaminated food and water. Treatment is with antibiotics or antiprotozoal drugs, such as metronidazole.

Malaria vaccine trial disappoints

Malaria vaccine research. Researcher holding a vial containing tissue from the heads of Anopheles sp. mosquitoed bred at a bio-medical research facility. This tissue is filtered to remove the sporozoite stage of the malarial plasmodium parasites found in the insects' salivary glands. The sporozoites are then studies as part of research to develop an anti-malaria vaccine. Photographed at the Pasteur Institute, Paris, France.

WASHINGTON (Reuters) - The numbers were so bad that Dr. Stephen Hoffman did not even want to say them out loud.
"It was a low number," he said. Pressed, he added, "Only a handful." Finally he squeezed the numbers out. "We had five."
Out of 80 volunteers vaccinated with Sanaria's experimental malaria vaccine, only five were protected from infection in the company's first clinical trial.
The Maryland-based company, which opened its doors in 2007, has not given up. But its disappointing results illustrate the uphill battle to develop a vaccine against an infection that kills 800,000 people a year, most of them young African children.
Hoffman gave details about what his team of scientists learned from the trial at a conference of malaria vaccine makers and their backers being held in Washington this week.
Tests in animals suggest that perhaps giving the vaccine intravenously might provide better protection, and Hoffman, founder and chief executive of the small, privately held company, is planning ways to test the idea in people.
"The vaccine was used to immunize 80 volunteers and it was safe and well tolerated," he said in an interview. It did, as expected, stimulate an immune response against the malaria parasite - just not nearly as much as Hoffman had hoped.
Now Sanaria has run out of money from the non-profit PATH Malaria Vaccine Initiative. But Hoffman plans to continue with cash from the U.S. National Institutes of Health and perhaps other government agencies.
"Right now I do need to get a lot more funds," he said.
A malaria vaccine has been the dream of hundreds of experts but has been maddeningly hard to actually develop.
Malaria is caused by a parasite, and making a vaccine against parasites is much harder to do than vaccinating against one-celled organisms like bacteria, or the even simpler viruses.
Plus malaria, which is spread by mosquitoes, has a complicated life cycle, passing from the blood to the liver to other organs.

GETTING CLOSE

GlaxoSmithKline is testing what most experts consider the most promising malaria vaccine, one called RTS,S or Mosquirix.
"We're getting close - we are getting very close," Glaxo's Dr. Joe Cohen said in an interview.
Investigators in seven African countries have enrolled 12,000 children and need just 4,000 more. The first data on safety and efficacy are expected by the end of next year.
In earlier trials, the vaccine appeared to produce a good immune response in African children.
But the goal is set very low - the Malaria Vaccine Initiative is asking only for it to protect 50 percent of the children against severe disease for a year.
"We are looking into the possibility of a next-generation," vaccine," said Cohen. Glaxo has spent about $300 million on Mosquirix, plans to spend about another $100 million and will receive an additional $100 million or so from the non-profit Bill & Melinda Gates Foundation, for a total of $500 million.
Investigators at the conference swapped notes on Tuesday and Wednesday about what the trials have told them so far about trying to vaccinate against the Plasmodium falciparum parasite, which causes most cases of malaria.
And groups presented ideas for new ways to deliver vaccines - such as Pennsylvania-based Inovio Biomedical Corp, which is using its so-called electroporation delivery-DNA vaccine approach to try to make a vaccine against malaria, as well as flu and AIDS vaccines.
Electroporation involves making tiny holes in the skin instead of using a needle to deliver a vaccine.
Dutch biotechnology company Crucell has technology that uses a common cold virus called an adenovirus that can "prime" the immune system and may help get a better response to Glaxo's Mosquirix. Crucell has teamed up with Glaxo to test the two together.
Johnson & Johnson, which already owns nearly 18 percent of Crucell, said this month it planned to buy the Dutch vaccine maker for $2.3 billion.
Then there is the next goal, said Cohen - a vaccine against Plasmodium vivax, the parasite that causes most cases of malaria in Asia.

Rabies Virus

Rabies virus. Computer artwork of a rabies (family Rhabdoviridae) virus particle (virion). The virus has a protein coat or capsid, which is made up of helically arranged subunits called capsomeres. Within the coat is the genetic material, which in this virus is single-stranded RNA (ribonucleic acid). Surrounding the protein coat is a lipoprotein envelope studded with surface proteins (pink). The rabies virus is transmitted to man from infected animal bites. Symptoms appear after an incubation period of 10 days to a year and include fever, breathing difficulties, muscle spasms, and hydrophobia.

Tail of a young Nile crocodile

Tail of a young Nile crocodile (Crocodylus niloticus), showing osteoderms (bony scale-like plates). These osteoderms, comprised of the protein keratin, form a protective armour on a crocodile's upper surfaces. These plated, armoured skin areas are shed in patches and replaced as the crocodile grows. This crocodile is a carnivorous predator that inhabits tropical and subtropical areas of Africa, near swamps, lakes and rivers. The young, become independent at the age of two years. Photographed in 2011, at the Pierrelatte crocodile farm (La Ferme aux Crocodiles) in southern France.

Diabetes drug may help fight cancer, but no proof yet

From the REUTERS
A cheap and relatively safe diabetes drug, metformin, might have cancer-fighting properties, according to an international study - but findings fall short of proving it actually can stave off cancer.

Researchers, whose findings were published in the Journal of Clinical Oncology, found that women with diabetes who took the medication had a 25 percent lower risk of developing breast cancer over more than a decade of follow-up.

"Metformin use in postmenopausal women with diabetes was associated with lower incidence of invasive breast cancer," wrote lead researcher Rowan Chlebowski, at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center.

"These results can inform future studies evaluating metformin use in breast cancer management and prevention."

Metformin, also sold under the brand name Glucophage, has been on the market for many years and is generally considered safe, although five to 10 percent of patients experience side effects like nausea and bloating.

It is used by millions of type 2 diabetics every day to help control their blood sugar, and studies have shown it also shrinks lung and breast tumors in mice. Several reports show people taking it for diabetes appear to develop cancer less often.

The new study used data from about 68,000 postmenopausal women who took part in the U.S. government-funded Women's Health Initiative clinical trials.

Over nearly 12 years of observation, there were more than 3,200 new cases of breast cancer among the women.

Every year, 0.42 percent of women without diabetes developed breast cancer, compared to 0.40 percent of diabetics on metformin and 0.47 percent of diabetics taking other drugs.

After taking into account risk factors for breast cancer, the gap between women without diabetes and diabetics on drugs other than metformin vanished. But diabetics on metformin turned out to have a 25 percent lower cancer risk than their diabetes-free peers.

"This is an area of great excitement," said Pamela Goodwin, a breast cancer expert at Mount Sinai Hospital in Toronto, Canada, who wrote an editorial that appeared with the study.

"The evidence is coming together that metformin may actually have a clinically-relevant effect, but none of this is good enough to chance clinical practice just yet."

But she added that while the study is the best of its kind so far, it relies on observations instead of an actual experiment in which women are randomly selected to take metformin or not.

US cancer survivors to rise by a third by 2022

(Reuters) - The number of Americans living with cancer will increase by nearly a third to almost 18 million by 2022, according to a report released on Thursday by the American Cancer Society and the National Cancer Institute.
Researchers found that even though the incidence rates of cancer are decreasing, the number of cancer survivors is on the rise due to a growing - and aging - U.S. population. The incidence of cancer rises dramatically with age.
The report concluded that the expanding population of cancer survivors makes it increasingly important that the medical community understand their unique healthcare needs.
A survey presented last month showed that 94 percent of U.S. primary care doctors were unaware of the long-term side effects of some of the most commonly used chemotherapy drugs, highlighting the difficulties faced by patients after they beat the disease.
"Many survivors, even among those who are cancer free, must cope with the long-term effects of treatment, as well as psychological concerns such as fear of recurrence. As more people survive cancer, it is vital that health care providers are aware of the special needs of cancer patients and caregivers," said Elizabeth R. Ward, national vice president of Intramural Research and senior author of the latest report.
Nearly one-half of American cancer survivors are age 70 or older, while only 5 percent are 40 or younger. The median age of patients at the time of diagnosis is 66.
Almost two-thirds of survivors were diagnosed 5 or more years ago, while 15 percent were diagnosed 20 or more years ago, the report said.
The three most common cancers among men living with the disease are prostate cancer, colorectal cancer and melanoma, according to the report. The most common cancers among women living with cancer were breast cancer, uterine or colorectal cancers.
There are also 58,510 survivors of childhood cancer living in the United States, and 12,060 more children will be diagnosed in 2012.

SOURCE: http://bit.ly/KJGMnA American Cancer Society June 14, 2012.

Breast Cancer in Men

Even though men don't have breasts like women, they do have a small amount of breast tissue. In fact, the "breasts" of an adult man are similar to the breasts of a girl before puberty, and consist of a few ducts surrounded by breast and other tissue. In girls, this tissue grows and develops in response to female hormones, but in men -- who do not secrete the same amounts of these hormones -- this tissue doesn't develop.

However, because it is still breast tissue, men can develop breast cancer. In fact, men get the same types of breast cancers that women do, although cancers involving the milk producing and storing regions of the breast are rare. An estimated 2,190 cases of breast cancer will be diagnosed in men in 2012.

Why Don't I Hear About Breast Cancer in Men as Much as I Hear About Breast Cancer in Women?

Breast cancer in men is uncommon. This is possibly due to their smaller amount of breast tissue and the fact that men produce less hormones such as estrogen that are known to affect breast cancers in women.

In fact, only about 1 in 100 breast cancers affect men and only about 10 men in a million will develop breast cancer.

Which Men Are More Likely to Get Breast Cancer?

It is rare for a man under age 35 to get breast cancer. The likelihood of a man developing breast cancer increases with age. Most male breast cancers are detected between the ages of 60 to 70 years. Other risk factors of male breast cancer include:

Family history of breast cancer in a close female relative.
History of radiation exposure of the chest.
An abnormal enlargement of breasts (called gynecomastia) in response to drug or hormone treatments, or even some infections and poisons.
A rare genetic condition called Klinefelter's syndrome.
Severe liver disease.
Diseases of the testicles such as mumps orchites, a testicular injury, or an undescended testicle.


How Serious Is Breast Cancer in Men?

Doctors used to think that breast cancer in men was a more severe disease than it was in women, but it now seems that for comparably staged breast cancers, men and women have similar outcomes.

The major problem is that breast cancer in men is often diagnosed later than breast cancer in women. This may be because men are less likely to be suspicious of an abnormality in that area. In addition, their small amount of breast tissue is harder to feel -- making it more difficult to catch these cancers early, and allowing tumors to spread more quickly to the surrounding tissues.

What Are the Symptoms of Breast Cancer in Men?

Symptoms of breast cancer in men are very similar to those in women. Most male breast cancers are diagnosed when a man discovers a lump on his chest. However, unlike women, men tend to go to the doctor with more severe symptoms that may include bleeding from the nipple and abnormalities in the skin above the cancer. At that point the cancer may have already spread to the lymph nodes.

From: WEBMD

Herpes Virus

Herpes virus particles. Transmission electron micrograph (TEM) of a cluster of Herpes simplex 1 (HSV-1) virus particles (round) in infected tissue. Each particle consists of a deoxyribonucleic acid (DNA) core (dark purple) surrounded by an icosahedral (20-sided) outer coat (capsid), which is itself surrounded by an envelope. Herpes simplex causes oral herpes (cold sores) and genital herpes in humans. There is no known cure for it and the virus remains in the body for life.

Cheesburger and chips ?

Cheeseburger and chips. Processed foods, such as found, in a cheeseburger are usually low in fibre and high in fats. Too much fatty food in the diet is associated with health risks, including an increased risk of heart disease and strokes.

In one type of cancer, heavier men may live longer

NEW YORK (Reuters Health) - Extra pounds may not be good for your health in general, but heavy men appear more likely to survive a particular form of immune system cancer, a new study finds.
The cancer in question is an aggressive form of non-Hodgkin lymphoma called diffuse large B-cell lymphoma (DLBCL). Non-Hodgkin lymphomas include a large group of cancers that affect the lymphatic system, a part of the immune system.
Some research has linked obesity to a greater risk of developing DLBCL. And in certain other cancers, like breast and colon cancers, obese patients may have a worse prognosis than those who are thinner when they're diagnosed.
"We expected something similar when we started this project," lead researcher Dr. Kenneth Carson, of Washington University School of Medicine in St. Louis, said in an email.
So what the researchers actually found came as a surprise, said Carson, whose findings appear in the Journal of Clinical Oncology.
Of more than 2,500 U.S. veterans with the cancer, men who were obese at diagnosis had only about two-thirds the risk of dying during the study period of normal-weight men -- after considering other factors, like age and overall health.
Out of 625 obese men, 294 -- or 47 percent -- died over the next five years. That compared with 64 percent of 849 men who were normal-weight when they were diagnosed.
Men who were not obese, but overweight, also had a better prognosis than their normal-weight counterparts: a 27 percent lower death risk during the study period.
It's not clear exactly why heavy men with the lymphoma would survive longer.
And Carson stressed that the findings do not mean that men should allow themselves to gain or hang on to excess fat -- especially since obesity may be a risk factor for developing DLBCL in the first place.
"It is important to note that by no means are we trying to discourage weight loss in overweight or obese persons," Carson said.
But figuring out why heavier men with DLBCL have a better outlook could lead to a better understanding of the cancer -- and possibly better treatment for all, according to Carson.
"In my mind," Carson said, "there are two main factors that might explain why overweight and obese patients have improved survival: differences in disease biology or differences in patient responses to chemotherapy."
If obese patients have a tendency to develop DLBCL tumors with a more "favorable" biology, Carson explained, that could give clues to the causes of the lymphoma.
On the other hand, if heavier people respond better to chemotherapy, figuring out why could help improve treatment for patients of all sizes.
It's possible that bigger patients are able to tolerate more-intense chemotherapy before having severe side effects. But, Carson's team notes, other research suggests that in the real world, obese chemotherapy patients may tend to get lower doses relative to their body size.
The American Cancer Society estimates that just over 70,100 Americans will develop some type of non-Hodgkin lymphoma in 2012. DLBCL is the most common form.

Carpenter Ants

Carpenter ants. View of members of a colony of Carpenter ants Camponotus sp., in their nest in a laboratory. At upper left are developing larvae with "minor" workers involved in brood care; large "major" workers take part in foraging. Carpenter ants are notorious destroyers of wood, preferring to chew out their nest in pine trees. Like many other social ants, colonies of Camponotus sp. are self-organising systems which have no leader. But they solve complex problems by individual ants collectively doing simple tasks, such as finding the shortest route to food. This method of group problem solving may help scientists to design future computers, or teamwork in robots.

Does Honey Raise the Glucose Level in the Blood?

Simply put, yes, consuming honey will cause your blood glucose levels to rise. Honey contains carbohydrates, and all carbohydrate-containing foods increase your blood glucose levels. Honey is highly concentrated in carbohydrates, meaning, consuming just a small amount of honey will cause a significant increase in your blood glucose levels.
Carbohydrates
Carbohydrates, unlike proteins and fats, affect your blood glucose levels. Carbohydrates exist in an array of foods including fruits, non-starchy vegetables, starchy vegetables, bread, pasta, rice, breakfast cereal, lentils, beans, nuts and peanut butter, tofu, soy products and milk. Carbohydrates are also found in any food that contains flour -- such as baked goods -- and any food that contains added sugars, such as desserts and candy.


Blood Glucose

After you eat a carbohydrate-containing food such as honey, your body begins to digest it. During the digestion process, the carbohydrates in honey are broken down into sugar molecules. The sugar molecules pass through the lining of your stomach and get absorbed into your bloodstream. This causes your blood sugar levels to rise. When your blood sugar levels rise, your pancreas secretes insulin, a hormone that helps transfer the sugar molecules from your bloodstream to various cells throughout your body.
Sugar
Carbohydrates come in three types: sugar, starch and fiber. Honey is classified as a sugar carbohydrate. Honey -- along with sugars such as granulated sugar, brown sugar, powdered sugar, maple syrup and high-fructose corn syrup -- is considered a fast-acting carbohydrate. This means that honey will cause your blood sugar levels to rise more quickly than complex carbohydrates -- such as whole grains -- will.

Considerations

Carbohydrates -- and the sugar they contain -- provide energy to your cells so that they can perform their functions properly. A healthy diet includes a lot of nutrient-rich carbohydrates such as whole grains, fruits, vegetables and legumes. Honey, and other sugars, do not provide much nutritional value, so use them sparingly. In order to help ensure that your blood glucose levels remain healthy and do not get too high, limit your daily consumption of added sugars to about 6 tsp. if you are a woman and about 9 tsp. if you are a man.

HCG Hormone

The hormone HCG The hormone HCG or beta-HCG (English Human Chorionic Gonadotropin) is a hormone secreted during pregnancy. She has a particular role, and dosage can reveal a multitude of elements, in connection with pregnancy or not.

What is HCG and what is its role?

 The hormone HCG is secreted at the time of implantation, ie when the embryo attaches to the uterine wall, for what would become the placenta.Son role is to maintain the corpus luteum, which is a small formation inside the egg, whose role is to secrete progesterone itself necessary for implantation. Clearly, for the egg is fixed and that the embryo develops, the body needs progesterone, which requires the corpus luteum, itself dependent on the hormone HCG. Its role in pregnancy is therefore essential.

The hormone HCG: a powerful indicator

 This is first HCG hormone that detects pregnancy as it is present in the blood about ten days after fertilization, and in the urine a few days later. It is precisely that it blood and urine tests looking for.

 It then allows to know the exact date of pregnancy by assaying the rate because it varies very precisely during the grossesse.Son assay allows also to ensure the smooth running of pregnancy, because if there is a miscarriage or an ectopic pregnancy, the HCG hormone levels raised the alarm.

Finally, through a mix between the 15th and 17th weeks, the HCG is even a risk indicator trismomie 21! If the rate indicates a risk, amniocentesis may be required to confirm the anomaly, or not.

Early Gut Bacteria Regulate Happiness

UCC scientists have shown that brain levels of serotonin, the 'happy hormone' are regulated by the amount of bacteria in the gut during early life. Their research is being published June 12 in the international psychiatry journal, Molecular Psychiatry.

This research shows that normal adult brain function depends on the presence of gut microbes during development. Serotonin, the major chemical involved in the regulation of mood and emotion, is altered in times of stress, anxiety and depression and most clinically effective antidepressant drugs work by targeting this neurochemical.
Scientists at the Alimentary Pharmabiotic Centre in UCC used a germ-free mouse model to show that the absence of bacteria during early life significantly affected serotonin concentrations in the brain in adulthood. The research also highlighted that the influence is sex dependent, with more marked effects in male compared with female animals. Finally, when the scientists colonized the animals with bacteria prior to adulthood, they found that many of the central nervous system changes, especially those related to serotonin, could not be reversed indicating a permanent imprinting of the effects of absence of gut flora on brain function.
This builds on earlier work, from the Cork group and others, showing that a microbiome-gut-brain axis exists that is essential for maintaining normal health which can affect brain and behavior. The research was carried out by Dr Gerard Clarke, Professor Fergus Shanahan, Professor Ted Dinan and Professor John F Cryan and colleagues at the Alimentary Pharmabiotic Centre in UCC.
"As a neuroscientist these findings are fascinating as they highlight the important role that gut bacteria play in the bidirectional communication between the gut and the brain, and opens up the intriguing opportunity of developing unique microbial-based strategies for treatment for brain disorders," said Professor John F Cryan, senior author on the publication and Head of the Department of Anatomy & Neuroscience at UCC.
This research has multiple health implications as it shows that manipulations of the microbiota (e.g. by antibiotics, diet, or infection) can have profound knock-on effects on brain function. "We're really excited by these findings" said lead author Dr Gerard Clarke. "Although we always believed that the microbiota was essential for our general health, our results also highlight how important our tiny friends are for our mental wellbeing."

Diesel exhausts do cause cancer

Exhaust fumes from diesel engines do cause cancer, a panel of experts working for the World Health Organization says.

It concluded that the exhausts were definitely a cause of lung cancer and may also cause tumours in the bladder.

It based the findings on research in high-risk workers such as miners, railway workers and truck drivers.

However, the panel said everyone should try to reduce their exposure to diesel exhaust fumes.

The International Agency for Research on Cancer, a part of the World Health Organization, had previously labelled diesel exhausts as probably carcinogenic to humans.

IARC has now labelled exhausts as a definite cause of cancer, although it does not compare how risky different carcinogens are. Diesel exhausts are now in the same group as carcinogens ranging from wood chippings to plutonium and sunlight to alcohol.

It is thought people working in at-risk industries have about a 40% increased risk of developing lung cancer.

Dr Christopher Portier, who led the assessment, said: "The scientific evidence was compelling and the Working Group's conclusion was unanimous, diesel engine exhaust causes lung cancer in humans.

"Given the additional health impacts from diesel particulates, exposure to this mixture of chemicals should be reduced worldwide."

The impact on the wider population, which is exposed to diesel fumes at much lower levels and for shorter periods of time, is unknown.

Dr Kurt Straif, also from IARC, said: "For most of the carcinogens when there is high exposure the risk is higher, when there is lower exposure the risk is lower."

There have been considerable efforts to clean up diesel exhausts. Lower sulphur fuel and engines which burn the fuel more efficiently are now in use.

The UK Department of Health said: "We will carefully consider this report. Air pollutants are a significant public health concern, we are looking at this issue as part of our plans to improve public health."

World's first Parkinson's vaccine is trialled

Parkinson's disease. Illustration of the brain, depicting the neurological disorder of Parkinson's disease. A coronal section through the brain is seen, with two elderly figures in a bent posture superimposed. Parkinson's disease is caused by a degeneration of nerve tissue within the basal ganglia (pink areas, at centre) of the brain. As a result, nerve pathways down the spinal cord are altered. Contracted muscle is prevented from relaxing, causing tremor, joint rigidity, and slow movement. Parkinson's disease affects the elderly. It progresses from a slight hand tremor, to an unbalanced, bent-over, shuffling walk. Treatment includes dopamine drugs. There is no cure.

TEN people with Parkinson's disease this week received injections of the first vaccine aimed at combating the condition.

Called PD01A, the drug primes the body's immune system to destroy alpha-synuclein, a protein thought to trigger the disease by accumulating in the brain and disrupting dopamine production.

Affiris, the company in Vienna, Austria, that developed the vaccine, says it is the first treatment to target the cause of the disease. "When it forms clumps in cells, alpha-synuclein disrupts normal levels of dopamine by locking it inside cells that produce it. It is also toxic, killing neurons and their connections," says Mandler Markus, head of preclinical development at the company.

Most existing treatments only ease symptoms by boosting dopamine levels.

In all, 32 people will receive the vaccine in the first trial on humans. The objective is to ensure the vaccine is safe, but researchers will also monitor for signs of improvement in symptoms.

Skin Cancer Large Malignant Tumor

Skin cancer. Large malignant (cancerous) tumour on a patient's foot. This is squamous cell carcinoma, the second most common form of skin cancer.Most cases arise from pre-cancerous lesions known as solar keratoses, which are caused by sun damage.

tick biting the skin

Close-up of a tick biting the skin of the underarm (axilla) in a 70 year old male patient.

Feeding tick. Coloured scanning electron micrograph (SEM) of a tick (Ixodes sp. ) feeding head- down in human skin. Ticks are arachnids which parasitise mammals, birds and reptiles, feeding on their blood. In the feeding process, they cut through the skin with the scissor-like action of their modified mouthparts, and thrust their hypostome (feeding tool) through the lacerated skin, and lock into the surrounding tissues. Ticks can transmit diseases such as relapsing fever and Lyme disease, and their bites may become infected. Magnification: x30 at 6x7cm size.

Man sneezing

Sneeze. High-speed photograph of a jet of droplets erupting from a man's mouth as he sneezes. The sneeze reflex is involuntary and is usually triggered by irritation of the nasal lining, such as occurs during a common cold or influenza (flu). The ejection of fluid helps to cleanse the respiratory tract of dust filtered out of the air, or mucus produced in response to infection. The reflex is exploited by the cold and flu viruses, which uses sneezing as a means of transmission from person to person.

conjunctivitis

Close-up of the red eye (conjunctivitis) in a 78 year old male patient due to an allergy. Conjunctivitis is the inflammation of the membrane covering the eye, causing redness, itching, and sensitivity to light.

 an inflammation of the conjunctiva, the delicate mucous membrane covering the front of the eye & the insides of the eyelids. The conjunctiva becomes red, swollen & may discharge water or pus. Conjunctivitis is caused by bacterial infection, allergy, or by physical or chemical irritants. Bacterial infections respond to antibiotic eye drops. Uncomplicated conjunctivitis is generally not serious & does not usually affect vision.

Shrimp wields strongest club in the world

The snail never saw it coming. One minute it was creeping slowly along the seabed, minding its own business. Then a lightning hammer blow fell, and in an instant its shell was smashed and it was at the mercy of a ruthless predator.

In this case, the phrase "hammer blow" is used literally. The peacock mantis shrimp comes equipped with two built-in hammers that can deliver swift and powerful blows, smashing straight through other animals' armour.

But that raises a question. To break through a hard thing, you have to be even harder, or you'll just break yourself. So what is it about the hammer of the peacock mantis shrimp that makes it so tough?

Clubbed to death

Mantis shrimps are not shrimps, though they do belong to the same group. They are, however, aggressive predators. What's more, some mantis shrimps can see circular polarised light, which is used to create 3D movies. The colourful patterns on their bodies reflect polarised light, which may be used as threatening signals.

There are two types of mantis shrimp, with different modifications to their front claws. Some have turned the claws into spears to impale their prey, while others – like the peacock mantis shrimp – have turned them into clubs.

Peacock mantis shrimps can deliver one of the fastest blows in the animal kingdom. Their clubs can move at up to 23 metres per second, and accelerate at over 10,000 gs. That means they can deliver a force of about 700 newtons – equivalent to the weight of a 70-kilogram mass – or even as much as 1500 newtons.

With a weapon like that, it's no surprise they can batter through the shells of molluscs and crabs. Larger peacock mantis shrimps have even been known to smash their way out of fish tanks. What's more, the blows are so powerful they cause cavitation: they create tiny bubbles in the water that instantly implode, delivering even more energy to their victims.

Tough nut

So why don't their clubs break? The shrimps do eventually replace each club when they moult, but not before they have delivered thousands of powerful impacts. David Kisailus at the University of California, Riverside, and his colleagues looked at their structure to find out.

They found that the head of the club is divided into three main layers. The outer impact region is mostly made of a tough mineral called hydroxyapatite, which is also found in bone. The hydroxyapatite is arranged in neat crystals, making for a strong coating.

In the second layer, the hydroxyapatite is less organised. Beneath that is a layer of chitin, the polymer that crustaceans use to make their shells. The three layers differ in how bendy they are, so it's hard for a crack that forms in one layer to extend into the next, so cracks don't spread far. What's more, the chitin is arranged in spirals. That means any cracks in the chitin tend to grow in spiral patterns, which barely weaken the overall structure.

Move over DNA: Six new molecules can carry genes

All of a sudden, DNA has no reason to feel special. For decades it seemed that only a handful of molecules could store genetic information and pass it on. But now synthetic biologists have discovered that six others can pull off the same trick, and there may be many more to find.

The ability to copy information from one molecule to another is fundamental to all life. Organisms pass their genes to their descendants, often with small changes, and as a result life can evolve over the generations. Barring a few exceptions, all known organisms use DNA as the information carrier.

A host of alternative nucleic acids have been made in labs over the years, but no one has made them work like DNA.

This problem has now been cracked. "This unique ability of DNA and RNA to encode information can be implemented in other backbones," says Philipp Holliger of the MRC Laboratory of Molecular Biology in Cambridge, UK.

"Everyone thought we were limited to RNA and DNA," says John Sutherland of the MRC Laboratory of Molecular Biology in Cambridge, UK, who was not involved in the study. "This paper is a game-changer."

Evolving XNA

Holliger's team focused on six XNAs (xeno-nucleic acids). DNA and RNA are made of a sugar, a phosphate and a base. The XNAs had different sugars, and in some of them the sugars are replaced with completely different molecules.

A key hurdle for the team was to create enzymes that could copy a gene from a DNA molecule to an XNA molecule, and other enzymes that could copy it back into DNA.

They started with enzymes that do this in DNA only. Over the years the team made incremental tweaks until they produced enzymes that could work on XNAs.

Once they had created these enzymes, they were able to store information in each of the XNAs, copy it to DNA, and copy it back into a new XNA. In effect, the first XNA passed its information on to the new one – albeit in a roundabout way. "The cycle we have is a bit like a retrovirus, which cycles between RNA and DNA," Holliger says.

This is the first time artificial molecules have been made to pass genes on to their descendants. Because the XNAs can do this, they are capable of evolution.

"The immediate question is whether these XNAs can be introduced into cells," says Farren Isaacs of Yale University in New Haven, Connecticut. Once the XNAs were installed, they could replicate and evolve on their own. "That would be remarkable."

Journal reference: Science DOI: 10.1126/science.1217622

Origin of life

The finding is a proof of principle that life needn't be based on DNA and RNA. Astrobiologists have long suspected as much.

"This is very interesting with respect to the origin of life," says Jack Szostak of Harvard University in Boston, Massachusetts. Nowadays, all life-forms use either DNA or RNA to store genetic information. Many biologists suspect that the first life-forms used RNA, and DNA was adopted later. But we don't know why those two molecules were chosen: are they the best possible storage media, or were they simply the only things available?

Holliger suspects RNA was an opportunistic choice. "Clearly, there is no overwhelming functional imperative to use DNA and RNA," he says. Instead, life may have started with RNA simply because it was made in large quantities on the early Earth.

Most biologists think life on Earth began with RNA because it can both store information and catalyse useful reactions. In his latest experiment, Holliger has now shown that one of his XNA's – 1,5-anhydrohexitol nucleic acid, or HNA – can fold into a 3D shape and bind to specific target molecules. This is the first step in becoming an enzyme. The same thing had previously been done for threose nucleic acid (TNA).

This suggests XNAs might form the basis of life on other planets, where different environments led to different chemistry. "I would be surprised if we find truly extraterrestrial life that was based on DNA and RNA," Holliger says. "There might have been an XNA-world on a different planet."

Mitochondrial disorder treated by targeting nucleus

Mitochondria act like tiny generators inside our cells, but when they go wrong they may trigger a range of diseases. The root of the problem can lie in mutations in the DNA carried within mitochondria, which is distinct from the DNA in the cell's nucleus.

One such mitochondrial disorder is Leber's hereditary optic neuropathy (LHON), a rare cause of vision loss in young adulthood.

In LHON, problems arise with a protein assembly called Complex I, which is encoded in part by the DNA in mitochondria. The dysfunction leads to the death of retinal ganglion cells at the back of the eye.

Using gene therapy to fix glitches in mitochondrial DNA is challenging, not least because the therapy must be delivered to the many mitochondria in each cell. Now Jane Farrar at Trinity College Dublin, Ireland, and her colleagues have demonstrated a workaround. They target the cell's nucleus instead, encouraging it to produce Complex-I-type proteins, which then enter the many mitochondria in the cell. It's not a completely new approach, but the study shows how it can be applied in the eye relatively easily.

Farrar's team mimicked LHON in mice by giving them a drug that inhibits Complex I. Through an injection into the eye, they then used a virus to deliver a gene from yeast (Saccharomyces cerevisiae) into the nucleus of the rodent retinal ganglion cells. The gene, NDI1, codes for a protein that works like mammalian Complex I.

The gene was switched on within the nucleus and the protein it made appeared to compensate for dysfunctional Complex I in the rodent mitochondria.

"In theory the system should rescue Complex I deficiency no matter what mutation was causing the original defect," says Farrar – although there are no guarantees that this kind of treatment will work as well in humans as in mice.

The study expands the possibility of developing a treatment for LHON, says Jean Bennett at the University of Pennsylvania in Philadelphia, who was not involved in the research.

"While there will likely be challenges encountered along the way – including the potential of development of an immune response to the yeast protein – the unequivocal successes in the small animal preclinical studies are encouraging."

Chagas Disease (American Trypanosomiasis)

Assassin bug. Macrophotograph of an assassin or kissing bug (Rhodnius prolixus) feeding on a human. This is a reduviid bug which lives in South and Central America. It feeds on human blood and is the vector of the protozoan parasite Trypanosoma cruzi, which causes Chagas disease. The protozoa are present in the faeces of the bug and are transmitted to humans when they enter wounds on the skin made by the feeding bug. They may also enter via the nose and mouth. T. cruzi migrates to the heart muscles and central nervous system, causing serious inflammation and lesions which may prove fatal if left untreated. 

Chagas disease facts

Chagas disease is an infection caused by a protozoan parasite (Trypanosoma cruzi) that can result in acute inflammatory skin changes (chagomas) and may eventually cause infection and inflammation of many other body tissues, especially those of the heart and intestinal tract.
Chagas disease was first described in 1909 in Brazil.
Chagas disease is caused by a protozoan parasite named Trypanosoma cruzi that is transmitted to humans from the feces of triatomine bugs (kissing bugs).
The parasites usually enter the mammalian (human) host through the bug bite, or breaks in the skin or conjunctiva, replicate in mammalian cells, and may eventually reach other organs through the blood.
Chagas disease may proceed through three phases in an individual: acute, intermediate or indeterminate, and chronic.
Chagas disease symptoms vary widely from no symptoms to severe in the chronic phase.
Acute-phase symptoms of Chagas disease may be swelling and/or redness at the skin infection site (termed chagoma), rash, swollen lymph nodes, fever, head and body aches, fatigue, nausea, vomiting and/or diarrhea, liver and/or spleen enlargement, and the Romaña sign.
Chronic-phase symptoms and signs of Chagas disease may be irregular heartbeats, palpitations, fainting (syncope), cardiomyopathy, congestive heart failure, short of breath (dyspnea), emphysema, stroke, sudden death, chronic abdominal pain, chronic constipation, dilated colon, and difficulty swallowing.
Patient history, physical exam, direct microscopic visualization of the parasites, and detection of antibodies against the parasites are methods used to diagnose Chagas disease.
Treatment with antiparasitic drugs benznidazole (Rochagan, Ragonil) and nifurtimox (Lampit) kill or inhibit T. cruzi parasites.
Chronic-phase patients are usually treated using treatments directed at the specific symptoms or organ damage.
There is no vaccine against Chagas disease parasites for humans, but many experts suggest that elimination of primitive housing and education may prevent most cases of Chagas disease.

What is Chagas disease?

Chagas disease (also termed American trypanosomiasis) is an infection caused by a protozoan parasite (Trypanosoma cruzi) that can result in acute inflammatory skin changes (chagomas) and eventually may cause infection and inflammation of many other body tissues, especially those of the heart and intestinal tract. The disease may have three phases in an individual: acute, with mild or no symptoms that may last weeks to about two months; intermediate or indeterminate phase that has few if any symptoms and may last 10-20 years or longer; and chronic phase that appears after about 20 years, with the more severe symptoms appearing from gradual chronic organ damage (especially to the heart and intestine, although other organs may be affected) with symptoms that usually remain for life. People with Chagas disease seen in the U.S. usually have acquired it while living in a country where the disease is endemic (Mexico, Central and South America). The CDC estimates about 8-11 million people are infected in countries where the disease is endemic.

Whole fetal genome sequenced before birth

The day when you can sequence your baby's genome before it is born might not be too far away. Researchers have reconstructed the genome of a fetus without touching it. Instead, they used both parents' genomes and free-floating fetal DNA, which circulates in the mother's blood.

Several companies already offer non-invasive prenatal tests for diseases caused by having extra copies of chromosomes, such as Down's syndrome, which is also known as trisomy 21 because it involves an extra copy of chromosome 21.

These tests are based on examining the fetal DNA that crosses the placenta, comprising up to 13 per cent of the free-floating DNA in the mother's blood plasma. The ideal screen would detect every genetic disease, some of which are caused by difficult-to-detect mutations.

"If the genome is a book, and a trisomy is an extra chapter, we want to find every typo," says Jay Shendure of the University of Washington in Seattle.

In 2010, researchers used parental genomes and fetal DNA from the mother's blood to map disease-associated mutations in a fetus's genome. Although the method could be used to infer the fetal genotype, it involved sampling the placental tissue, an invasive process that may slightly raise the risk of miscarriage.

Genetic puzzle

In the latest research, Shendure's group sequenced both parents' genomes, using blood from the 18.5-week-pregnant mother and saliva from the father. They then used a technique known as deep sequencing to analyse dozens of samples of fetal DNA from the mother's blood. That left them with an assortment of genetic material.

After working out which parts of the fetal DNA came from the mother and father, it was possible to see which bits were unique to the fetus, and use the information to piece together its genome. The team sequenced the genome again after birth to assess the accuracy of their fetal genome technique. Overall, the genome they pieced together was 98 per cent accurate. The fetus had 44 new mutations of its own, of which the team managed to spot 39.

Shendure says the technology can detect more than 3000 diseases that are caused by mutations in a single gene. However, fetal sequencing faces the same problems as any other genome sequence: researchers are limited in their ability to tell whether any given mutation will actually cause a specific disease. Plus, the rate of falsely predicting a child's chance of having a disease is still far too high to be useful in the clinic, he says.

It may be at least five years before the test reaches the clinic, Shendure says. By then, the price of the technology should have dropped. This sequencing cost about $50,000 to perform.

"The fact that it's still far in the future is good," Shendure adds, considering the legal and ethical complications of parents having the ability to see every disease and trait their child will have before it is born.

Screening finds skin cancer, but does it save lives?

NEW YORK (Reuters Health) - Doctors find a high number of malignant tumors when a state-wide skin cancer screening program is introduced, says a new study.
Based on results from a program in Germany, researchers say 116 people need to be screened for skin cancer and five people need to have a biopsy to find one malignant tumor.
They, however, cannot say whether the screenings actually saved lives.
Still, the numbers reported in the new study are "quite good," said Dr. Alexander Katalinic, one of the study's coauthors, in an email to Reuters Health.
In the United States, the last time the government-backed U.S. Preventive Services Task Force (USPSTF) looked at the screenings in 2009, the group said there was not enough evidence to recommend full-body exams to check for signs of skin cancer in adults. The USPSTF, however, did not recommend against it either.
Dr. Virginia Moyer, the chair of the USPSTF, said the group reviews its guidelines every few years, and as for now its 2009 recommendation stands.
SOME FALSE POSITIVES
For the study, the researchers examined data from the Skin Cancer Research to Provide Evidence for Effectiveness of Screening in Northern Germany (SCREEN) program, which was conducted in the German state of Schleswig-Holstein between 2003 and 2004. (Germany has had a national skin cancer screening program in place since July 2008.)
More than 360,000 people older than 20 years old and living in the state chose to be screened by doctors who went through a special training to identify suspicious skin lesions or moles.
Some people decided to see a dermatologist while others went to a general practitioner who referred them to a dermatologist if they suspected skin cancer.
Overall, about 16,000 people had a biopsy -- about one for every 23 people who were screened. Doctors identified about 3,100 malignant tumors from those biopsies.
The cost for each screening is about $27. A biopsy can run over $100, and the removal of a malignant skin lesion can cost about $800.
The researchers cannot say how many screenings led to an unnecessary biopsy or treatment, because of the program's design. But, Katalinic said "of course there are false positives."
Overall, there were 3,103 malignant skin tumors, and 585 of those were malignant melanomas, the most deadly type.
More than 50 people between the ages of 20 and 49 years old had to have a biopsy to identify one melanoma. That's more than double the 20 biopsies needed to find one in people over 65 years old.
Katalinic said, as an epidemiologist, he thinks the number needed to screen or biopsied should be improved, especially among younger people. There were also 1961 basal cell carcinomas, 392 squamous cell carcinomas and 165 were other types of malignant tumors.

New weapon tested against multi-drug resistant TB

NEW YORK (Reuters Health) - Researchers who tested a novel type of antibiotic against multi-drug-resistant tuberculosis are reporting that nearly half of patients who got the new drug cleared the bacteria from their lung fluid in two months.
The multinational clinical trial of the experimental drug delamanid found that volunteers who received it, along with a standard regimen of other anti-TB medicines, were far more likely to see the bacteria disappear from their sputum than those who got just the older medicines.
That "conversion" of sputum cultures happened much more quickly in patients taking the new drug, according to Lawrence Geiter, a vice president at Otsuka Pharmaceutical Co, which developed delamanid, and an author of the study.
Otsuka also designed and financed the clinical trial, which took place in 17 medical centers across nine countries.
"We saw what we think is a reasonable safety profile," Geiter told Reuters Health in a telephone interview. "(So) this could be the first new class of TB compounds that would be licensed in nearly a half century."
The results, published in the New England Journal of Medicine, are being called "significant but modest" in an accompanying editorial by Drs. Richard Chaisson and Eric Nuermberger of the Johns Hopkins University School of Medicine in Baltimore.
"We've been looking for new chemical classes of drugs for tuberculosis for a while," said Scott G. Franzblau, director of the Institute for Tuberculosis Research at the University of Illinois at Chicago, who was not connected with the study.
He told Reuters Health it's not surprising that a new drug would help against drug-resistant strains.
"That's kind of a given. Any new class of TB drug is expected to work against drug resistant strains because they haven't had a chance to become resistant to it. That's the easier part in making a dent in TB," he said.
"The harder part," Franzblau continued, "is, can you really get a drug that will help you shorten treatment? The preclinical data... in mice suggested that this drug should be able to do that as well as others in its class, one of which is in clinical trial and the other is in a preclinical trial."
Tuberculosis causes about 1.8 million deaths each year and about 440,000 cases worldwide involve bacteria that have learned to resist conventional drugs such as isoniazid and rifampin.
Patients with multi-drug-resistant TB have to take four to six expensive medications, some with significant side effects, for as long as two years at a cost of up to $5,000.
All of the 481 TB patients in the new study received conventional treatment with a drug combination developed by the World Health Organization.
Of the 161 who were also given 100 mg of delamanid twice daily, 45.4 percent had no trace of the TB bacterium in their lung fluid after two months. With a twice-daily dose of 200 mg, given to 160 people, the rate was 41.9 percent. That compares to 29.6 percent among the 160 volunteers given a placebo along with conventional treatment.
Headache, insomnia, and upper abdominal pain affected at least one in five patients getting delamanid. Nausea and vomiting were reported by about a third. But the rate of both side effects wasn't significantly higher than among those receiving placebo.
A more serious concern was the risk of a heart abnormality known as a prolonged QT interval, which stretches out the period between heartbeats.
The researchers found that 13 percent of the patients getting the highest dose of delamanid had a prolonged QT interval, as did 10 percent on the lower dose -- compared to just 3.8 percent in the placebo group.
The problem occurs at the point "when the heart is repolarizing and charging the battery to do the next beat," Geiter said. "If the interval gets really long, much longer than we observed, it's not able to beat again in a functional manner so you start to get fibrillations or arrhythmias" which affect the flow of blood and can cause fainting."
None of the patients had any heart symptoms, however.
"This is something we'll continue to look at," Geiter said.
A longer study that will examine the effect of six months of treatment with delamanid, and follow those patients for 30 months, is underway.

Lupus erythematosus

Systemic lupus erythematosus (SLE) rash on the skin of the face in a male patient, an autoimmune disease where the immune system attacks the body's connective tissue, mainly in the skin, joints and kidneys.

Systemic lupus erythematosus facts

Systemic lupus erythematosus (SLE) is an autoimmune disease.
SLE is characterized by the production of unusual antibodies in the blood.
SLE is eight times more common in women than men.
The cause(s) of SLE is (are) unknown, however, heredity, viruses, ultraviolet light, and drugs all may play some role.
Up to 10% of people with lupus isolated to the skin will develop the systemic form of lupus (SLE).
Eleven criteria help doctors to diagnose SLE.
Treatment of SLE is directed toward decreasing inflammation and/or the level of autoimmune activity.
People with SLE can prevent "flares" of disease by avoiding sun exposure and not abruptly discontinuing medications and monitoring their condition with their doctor.

What is systemic lupus erythematosus? What are the types of lupus?

Lupus is an autoimmune disease characterized by acute and chronic inflammation of various tissues of the body. Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system. The immune system is a complex system within the body that is designed to fight infectious agents, such as bacteria and other foreign microbes. One of the ways that the immune system fights infections is by producing antibodies that bind to the microbes. People with lupus produce abnormal antibodies in their blood that target tissues within their own body rather than foreign infectious agents. These antibodies are referred to as autoantibodies.

Because the antibodies and accompanying cells of inflammation can affect tissues anywhere in the body, lupus has the potential to affect a variety of areas. Sometimes lupus can cause disease of the skin, heart, lungs, kidneys, joints, and/or nervous system. When only the skin is involved, the condition is called lupus dermatitis or cutaneous lupus erythematosus. A form of lupus dermatitis that can be isolated to the skin, without internal disease, is called discoid lupus. When internal organs are involved, the condition is referred to as systemic lupus erythematosus (SLE).

Both discoid lupus and systemic lupus are more common in women than men (about eight times more common). The disease can affect all ages but most commonly begins from 20-45 years of age. Statistics demonstrate that lupus is somewhat more frequent in African Americans and people of Chinese and Japanese descent.


What causes systemic lupus erythematosus? Is lupus hereditary?

The precise reason for the abnormal autoimmunity that causes lupus is not known. Inherited genes, viruses, ultraviolet light, and certain medications may all play some role.

Genetic factors increase the tendency of developing autoimmune diseases, and autoimmune diseases such as lupus, rheumatoid arthritis, and autoimmune thyroid disorders are more common among relatives of people with lupus than the general population. Some scientists believe that the immune system in lupus is more easily stimulated by external factors like viruses or ultraviolet light. Sometimes, symptoms of lupus can be precipitated or aggravated by only a brief period of sun exposure.

It also is known that some women with SLE can experience worsening of their symptoms prior to their menstrual periods. This phenomenon, together with the female predominance of SLE, suggests that female hormones play an important role in the expression of SLE. This hormonal relationship is an active area of ongoing study by scientists.

Research has demonstrated evidence that a key enzyme's failure to dispose of dying cells may contribute the development of SLE. The enzyme, DNase1, normally eliminates what is called "garbage DNA" and other cellular debris by chopping them into tiny fragments for easier disposal. Researchers turned off the DNase1 gene in mice. The mice appeared healthy at birth, but after six to eight months, the majority of mice without DNase1 showed signs of SLE. Thus, a genetic mutation in a gene that could disrupt the body's cellular waste disposal may be involved in the initiation of SLE.