It is not chordoma, so treatment is possible, go get a sample to test what it is

China Daily/Asia News Network
Wednesday, Jun 06, 2012

CHINA – Li Hongfang, of the remote Tianchao village in Qian county of Xianyang, Northwest China’s Shaanxi province, has seven tumors on her face that scare people away.
The nightmare started for the 40-year-old woman in 2001, when she noticed a fingernail-sized lump on her forehead. She ignored it as it was not itchy or painful. But its increasingly worrisome appearance finally became urgent, and Li sought help at an infirmary in the county, with 300 yuan (S$61) and two bags of wheat in hand.
The scans produced no results. The doctor suggested she go to a large hospital in Xi’an, capital city of the province, for further tests. Li refused because she feared a hefty cost, a decision that she regrets.
After enduring the pain for another four years, during which she lost her husband to a cerebral hemorrhage in 2005, Li sold all her valuables for several thousand yuan, to get surgery in Xi’an. But things did not turn out well.
The doctors, after another examination, diagnosed the seven facial tumors as chordoma, a kind of bone cancer, and it would cost at least 600,000 yuan for the surgery.
Li didn’t understand how big the sum was, but she knew such a number was way beyond what she could afford. She received no government subsidies because she did not participated in China’s rural cooperative medical care system.
The only other option she had was to see more doctors in big cities and try a variety of medicines, which meant she had to commute to Xianyang, 50 kilometers away, and Xi’an, 70 kilometers.
For a widow with two sons to raise, it was a huge hardship. Her savings soon ran out, and the debt-ridded Li sometimes could only beg on the streets for her treatment, which was 700 yuan at a time.
She gained some comfort from her second husband, Guo Yingping, by 2009, who shared her 10-square-meter shed. Guo makes a living by building houses in nearby villages, and he spends all his wages, about 80 yuan per day, on his wife’s treatment.
Her two sons, 17 and 14, left the village to work despite her objections.
But her tumors are getting worse, covering the entire right side of her face and growing down to her breast. She also lost much of her hair.
Li, in spite of all those setbacks, said she would stay positive.
“I don’t want my sons to lose their mother early like I did, so I have to be tough.”
She hopes her sons can go back to school after she is cured.
Several students from home and abroad visited Li in April and wrote about her on Weibo, China’s Twitter-like service, which was forwarded by thousands who sent text messages to encourage Li and called for help from the public.
WASHINGTON: A newly approved drug has shown promise in keeping two rare variations of skin cancer at bay, according to research published in the New England Journal of Medicine on Wednesday.
The drug, Erivedge (vismodegib), is made by Genentech, a US subsidiary of the Swiss drug giant Roche, and was approved by the US Food and Drug Administration in January after an expedited review.
It aims to treat basal cell carcinoma, which is the most common form of skin cancer in the world but which is rarely deadly. Basal cell carcinoma accounts for 80 percent of non-melanoma cancers and some two million new cases in the US each year.
The journal published two studies that show how it helped some patients with two unusual variations of basal cell carcinoma: metastatic basal cell carcinoma and Gorlin syndrome, also known as Basal Cell Nevus Syndrome.
There is no other treatment for Gorlin syndrome, which strikes one in 50,000 people and involves the constant growth of tumours, which are often not deadly but can cause scarring and require frequent surgeries.
Subjects with Gorlin syndrome who took vismodegib developed an average of two new tumours per year, compared with 29 new tumours in subjects taking a placebo, the study said.
When it came to people whose basal cell carcinoma had spread, the study showed 30 percent of 33 patients with metastatic basal cell carcinoma responded to treatment, meaning their tumours shrank.
Forty-three percent of 63 subjects with locally advanced basal cell carcinoma responded in kind.
The phase II study showed a median progression-free survival time of 9.5 months, but overall survival rates have not yet been established.
“It is a landmark day for patients with basal cell carcinoma and all those involved in their care — the greatest advance in therapy yet seen for this disease,” said an accompanying editorial by John Lear, consultant dermatologist at Manchester Royal Infirmary in Britain.
However, he pointed out the high rate of adverse effects, including loss of taste, hair loss and muscle cramps, which led to a high rate of people dropping out of the study early.
“Side effects are considerable and frequent, resulting in high rates of drug discontinuation, and these rates will probably be even higher in clinical practice,” Lear said.
More study is needed to determine how long the drug may work to ward off cancer, what populations it may best serve, and when it should be optimally administered, he added.

– AFP/al

Fun running circles round your enemy?

Kung Fu Panda: Legends of Awesomeness is an American computer-animated television series based on the Kung Fu Panda films. It takes place between the 2 films showing Po’s training to becoming a successful Dragon Warrior. The series was originally set to air on Nickelodeon in 2010, but it was pushed back to 2011 instead. A total of 52 episodes have been produced or ordered.[1] Two special previews were aired on September 19 and October 21, and it premiered on November 7, 2011.[2]
Po and the Furious Five defend the Valley of Peace from villains of different kinds. All the while, Po makes mistakes, learns lessons, learns more about the history of Kung Fu, and meets famous Kung Fu masters like him.
There is no one in the world like me, carry on and fool around with me and I am going to fool around with everybody, you can destroy my business, play tricks with everyone so that girls will not have sex with me until I show you the money, now I will bankrupt you if you still continue, force me to I can even kill everyone involved and nobody dare to do anything to me, I can command the entire army of the entire world, and start a nuclear war anytime, I do not want to start a war, but if this carry on, twist my arm and the world will see my fury. – Contributed by Oogle.

Tarantula in Tinsukia? This species is created and is lethal, no existing mutation of such species

Updated 10:51 PM Jun 05, 2012
GAUHATI (India) – Large biting spiders have sparked panic in remote northeast India, but health authorities fear primitive treatment of the bites’ painful swelling may be more dangerous than the spiders themselves.
Two people died in Tinsukia district after witch doctors used razor blades to drain the wounds. It’s not known if the victims died from spider poison or from the attempted treatment. Local magistrate Kishore Thakuria said the victims were cremated before autopsies could be done.
Another seven bite victims have been treated with antibiotics against infection after they also tried themselves to drain their wounds, said Dr Anil Phapowali at the local Sadiya town hospital.
The hairy spiders were noticed about a month ago across Tinsukia district’s grassy plains and dense jungle forests north of the Brahmaputra River.
Ecologist L.R. Saikia at Assam’s Dibrugarh University said it may be a previously unknown species of tarantula. The spiders are roughly the size of a person’s thumb.
“It looks like a new species. We haven’t been able to identify it,” he said Tuesday. Officials cannot use anti-venom in treating bite victims until the species is identified.
Meanwhile, villagers are keeping lamps on at night and standing guard against spiders entering their mud-and-thatch huts. There are about 100,000 villagers, mostly poor rice farmers, living in the area cut off from roads by the river.
Officials say the spiders are now also showing up south of the Brahmaputra. AP

Because the species is unknown, it is impossible to treat this spider bite, using the wrong antibiotics has consequences, the best is prevention, destroy all the habitats that may support this mutant, by using sulphur to surround your own house or likely places this spider will appear.
– Contributed by Oogle.

Your contributions will be recognised and you will not have to worry as you will have overseas work

Posted: 05 June 2012 1937 hrs
TAIPEI: Taiwan entertainer Makiyo appeared in public for the first time at a charity event on Monday since the conclusion of her cabby assault case in April, reported Taiwan media.
Speaking to the Taiwan media, Makiyo also expressed that her life has taken on a new direction, after she was handed a suspended sentence for her drunken assault on 55-year-old cabby Lin Yu Jun, a little over a month ago.
“I have quit drinking.
“I can’t work in Taiwan for three years (as her work permit had been revoked) … so I’ll just do public service work or charity work for now, exercise, enrich my life and take a good rest,” said Makiyo.
She added that she was now surviving on her savings and had to scrimp and save to get by, spending only about NT$200 (S$8.60) a day on average.
Her appearance at the event raised questions about whether she had been quietly taking on work assignments, despite having her work permit revoked months earlier, due to her involvement in the assault case.
However, her manager explained that Makiyo did not flout any employment laws as she was not paid a dime for her appearance at the charity event.


Sugar and Hypertension : There is no connection, although soy products can reduce the risks of Hypertension

Sugars are carbohydrates. All sugars are composed of carbon (C), hydrogen (H), oxygen (O) in the ratio: C(H2O). But there are many different sugars (for example: glucose, sucrose, lactose, fructose, …, plus more). In addition, sugar as it is commonly used in cooking is not even the pure carbohydrate. It contains other substances that lend various sugars their unique characteristics. Honey, unrefined sugar, “brown sugars”, turbino, … and more. For a lot more info, I direct you to a very readable book: “On Food and Cooking” by Harold McGee (chapter 12) that covers the chemistry and cooking with sugars.
When sugar is heated it begins to lose water (H2O) and carbon dioxide (CO2) but this occurs in stages of a complex series of oxidation (burning) reactions. This process is called “carmelization” and is used by cooks and chefs to bring out special flavors of the oxidation products of carefully decomposed sugars. Various chemical classes of compounds called aldehydes, ketones, carboxylic acids and others are formed — again giving the carmelized sugars their distinctive flavor. Further “cooking” produces more CO2 and H2O and leaves a complex mixture of compounds including some elemental carbon. That carbon is not strictly “ash” since if you continue to heat the carbon it will eventually burn to form CO2. So you can see that the cooking chemistry of sugars is both science and art.
Another method is using up your excess sugar energy by burning up thru exercise, by using a catalyst to quicken the process or simply diluting sugar in your blood with more water. It is therefore possible to increase your water intake tremendously to reduce the sugar intake, diluting the thickness of the blood, what will happen is that you will need to go toilet more often. It is therefore possible used as a method to reduce your sugar level for diabetes, but my advice it should be a method to reduce your medication, not to totally forgo your medication. If a person is not trained in this area, my advice is not to try, unless you are monitored by a doctor. Hypertension risks can be reduced by regularly taking soy products to prevent the harding of by-products in the artery in the old age.

Tuesday, Jun 05, 2012

NEW YORK – Sweet drinks have been linked to a slightly higher risk of developing high blood pressure, but a US study finds that fruit sugar may not be the culprit as found in earlier research.
Researchers followed more than 200,000 men and women for up to 38 years and found that regularly consuming sweetened drinks, either containing sugars or artificially sweetened, was associated with a rise of about 13 per cent in the risk of developing high blood pressure.
Carbonated and cola drinks were most strongly linked to a risk for hypertension, but fruit sugar, or fructose, in drinks did not stand out as a driving factor, the group reported in the Journal of General Internal Medicine.

“We don’t know what causes the increased risk in artificial- or sugar-sweetened beverages,” said Lisa Cohen, lead author of the study and a researcher at the University of Maryland Medical Center.
“It’s hard to say that from the fructose itself you’re increasing your hypertension risk.”
New York City Mayor Michael Bloomberg last week proposed a ban on large-size sugary sodas, the latest in a string of public health initiatives that include a campaign to cut salt in restaurant meals and packaged foods.
Earlier studies had implicated fructose as a factor related to a risk of high blood pressure, but Cohen noted that those have only taken a snapshot in time and could not determine which came first, the high blood pressure or taste for sweet drinks.
Cohen and her colleagues looked at data from three massive studies, including nearly 224,000 healthcare workers, whose diet and health were tracked for 16 to 38 years. No participants had diagnosed high blood pressure at the start of the study.
Over time, those who drank at least one sugar-sweetened beverage a day had a 13 per cent increased risk of developing hypertension relative to those who only had a sweet drink once a month or less.
Similarly, people who drank at least one artificially-sweetened drink a day had a 14 per cent increased risk of developing hypertension relative to those who had few or none.
To see if it was the fructose that was responsible, researchers also looked at people who had high levels of fructose in their diets from other sources, such as fruits.
Among people who consumed 15 per cent of their calories from fructose sources other than drinks, the risk of developing hypertension was either lower or the same as people who ate very little fructose.
“You would think if fructose were the causative factor, then eating a lot of apples (for example) would also increase your risk of hypertension,” Cohen told Reuters Health.
The “markedly” stronger link between carbonated sweet drinks and increased hypertension risk might be explained by the larger serving sizes associated with sodas, or some other unknown ingredient common to all of them, the researchers said – but further research is needed.

Same risks as IVF(if the egg and sperm is modified) where there is a possibility of creating a mutant and should not be allowed

Updated 12:05 PM Jun 05, 2012
LONDON – Children with three genetic parents could become a reality as the fertility regulator has launched a consultation on changing the rules banning it outside research, according to The Daily Telegraph.
The controversial techniques would allow women with serious inheritable diseases to avoid passing them on to her children.
The conditions, collectively known as mitochondrial disease, can cause severe disability and death.
The Human Fertilisation and Embryology Authority (HFEA) has launched a public consultation on whether the fertility techniques, currently only allowed for research, can be offered to women.
It is thought the consultation was brought forward after British Prime Minister David Cameron expressed his support.
There are two methods under question, one involving the early stage embryo and the other manipulating the egg before it is fertilised.
In the first, the genetic material from the mother is removed from the embryo and placed into another early stage embryo with healthy mitochondria from a donor.
The second does the same thing but before fertilisation so the mother’s genetic material is removed from the egg with the faulty mitochondria and placed into an unaffected donor egg.
Technically the resulting child would have genetic material from three people, but the contribution from the donor is small, experts have said.
But critics have argued this is genetic modification of humans and should not be allowed.
There are around 150 mitochondrial diseases and one in every 5,000 children or 160 every year are affected.
The HFEA will be conducting surveys, meetings and online interactive forums as part of the consultation which will close at the end of the year.
A Department of Health spokesman said: “Moving from laboratory research to clinical use could be a major breakthrough to prevent mitochondrial disease.
“Such a move raises important questions, which is why we have asked the Human Fertilisation and Embryology Authority to conduct a thorough consultation, which includes gathering evidence from experts and seeking views from members of the public.” AGENCIES

Mitochondrial diseases are a group of disorders caused by dysfunctional mitochondria, the organelles that generate energy for the cell. Mitochondria are found in every cell of the human body except red blood cells. Mitochondria convert the energy of food molecules into the ATP that powers most cell functions.
Mitochondrial diseases are often caused by genetics or mutations to the mitochondrial DNA that affect mitochondria function. Mitochondrial diseases take on unique characteristics both because of the way the diseases are often inherited and because mitochondria are so critical to cell function. The subclass of these diseases that have neuromuscular disease symptoms are often called a mitochondrial myopathy.
Mitochondria is vital for cell formation and should not be altered, or it has the effects of “dolly the sheep”, the possibility of creating a mutant, you can modify other DNA but not this, and if this understood you could perfect intro-fertilisation(genetic modification-where there is a possibility of other modifications of DNA), taking away the risks of mutation. Although the risk is very small, as long as there is a risk it should be closely monitored, and perfected before you go ahead to create a life.
– Contributed by Oogle.

Detection and treatment of melanoma without chemotherapy

A tumor suppressor gene, or anti-oncogene, is a gene that protects a cell from one step on the path to cancer. When this gene is mutated to cause a loss or reduction in its function, the cell can progress to cancer, usually in combination with other genetic changes.
Unlike oncogenes, tumor suppressor genes generally follow the “two-hit hypothesis“, which implies that both alleles that code for a particular protein must be affected before an effect is manifested. This is because if only one allele for the gene is damaged, the second can still produce the correct protein. In other words, mutant tumor suppressors alleles are usually recessive whereas mutant oncogene alleles are typically dominant. The two-hit hypothesis was first proposed by A.G. Knudson for cases of retinoblastoma.[1] Knudson observed that the age of onset of retinoblastoma followed 2nd order kinetics, implying that two independent genetic events were necessary. He recognized that this was consistent with a recessive mutation involving a single gene, but requiring biallelic mutation. Oncogene mutations, in contrast, generally involve a single allele because they are gain-of-function mutations. There are unnoble exceptions to the “two-hit” rule for tumor suppressors, such as certain mutations in the p53 gene product. p53 mutations can function as a “dominant negative”, meaning that a mutated p53 protein can prevent the function of normal protein from the un-mutated allele.[2] Other tumor-suppressor genes that are exceptions to the “two-hit” rule are those that exhibit haploinsufficiency for example PTCH in medulloblastoma. An example of this is the p27Kip1 cell-cycle inhibitor, in which mutation of a single allele causes increased carcinogen susceptibility.[3]
Monday, Jun 04, 2012

CHICAGO – Two new experimental treatments against advanced melanoma have shown promise in keeping the deadly skin cancer at bay, according to research presented in the United States today.
The agents, known as Dabrafenib and Trametinib, are being developed by the British pharmaceutical firm GlaxoSmithKline, and were tested in clinical trials against standard chemotherapy treatments.
The trial on Trametinib included 322 people, of whom 214 took the experimental drug while the rest did standard chemotherapy, researchers said at the American Society of Clinical Oncology meeting in Chicago.

More than 22 per cent of those on Trametinib responded to treatment compared to eight percent in the chemo group.
The Trametinib group also experienced a median 4.8 month period in which the cancer did not advance, and saw their risk of dying from skin cancer diminish by 46 percent compared to the chemo group – 81 percent were still alive after six months of treatment compared to 67 percent in the control group.
The phase III trial was the first to evaluate a treatment against melanoma that inhibits a protein known as MEK, and may help about half of all melanoma patients who have a mutation in the BRAF gene that fuels tumor growth.
“This is the first in a new class of targeted drugs that could benefit patients with melanoma who have BRAF mutations,” said Caroline Robert, head of Dermatology at the Institute Gustave Roussy in Paris, France.
“The findings show that targeting the MEK molecular pathway is a viable strategy for treating many people with the disease,” Robert added.
“Trametinib is likely to become another first-line treatment option for patients with advanced melanoma.” One other therapy on the market, vemurafenib (Zelboraf), is currently approved in the United States and Europe for advanced melanoma.
The second trial involved Dabrafenib, which also targets cancers with the BRAF mutation, and showed a 70 percent lower risk of cancer progression compared to those treated with chemotherapy alone (5.1 months versus 2.7 months.
The phase III trial included 250 participants who had not been treated with any drug prior to enrollment and who had been diagnosed with inoperable melanoma, 187 of whom took the experimental drug while the rest were given standard chemotherapy.
Half of patients in the Dabrafenib group responded to therapy, compared to six percent of patients treated with a chemotherapy treatment known as dacarbazine.
The median time in which the cancer did not progress was 5.1 months in the Dabrafenib group compared to 2.7 months in the control group.
More study is needed to determine the overall survival rate, researchers said.
“These findings represent another advance for melanoma and form the foundation for further studies to evaluate the role of Dabrafenib in combination with other drugs,” said lead investigator Axel Hauschild, a professor of dermatology at University of Kiel in Germany.
According to the US National Cancer Institute, there are about 76,000 new cases of melanoma diagnosed each year in the United States and more than 9,100 deaths.