Amnesia Patient's Sister Found in Louisiana

A man who awoke in the emergency room at Desert Regional Medical Center in Palm Springs, Calif., last February speaking only Swedish and suffering from a case of global transient amnesia, has a sister living in Louisiana who is stunned by the fate of her long-lost brother.

The hospital has identified the patient as 61-year-old Michael Thomas Boatwright and says that he has been told he has a sister, Michelle Brewer, 59, of Kentwood, La.

"She hasn't talked to him in over 10 years," Brewer's step-daughter, Shannon Coleman, 36, told ABCNews.com. "She seemed like she was really surprised."

Boatwright, 61, was found unconscious in a Motel 6 and was taken by hospital ambulance to the medical center, according to medical center spokesman Rich Ramhoff.

The only things he had on him were a duffel bag of athletic clothes, a backpack, five tennis rackets, two cell phones, some cash, a set of old photos and four forms of identification, including a Florida license and a veteran's card.

But Boatwright had no memory of who he was or how he got there. He did not speak or understand English and didn't even recognize his own face, according to the Desert Sun, which first reported the story. He told hospital officials his name was Johan Elk.

Brewer said her brother had "just disappeared" and she had no way of getting in touch with him after their mother died last year.

"He's always been a wanderer," she told the Sun. "Then he'd come back when he needed some money or something from somebody. Then he'd take off again."

An investigation into his IDs found that Boatwright was likely a 3-D graphic designer who had worked in China and Japan as an English teacher for a decade. He had flown from Hong Kong to Palm Springs just four days before he was found unconscious. The U.S. Navy veteran, who was raised in Miami, first went to Sweden in 1981.

The Sun tracked down Brewer, but hospital spokesman Ramhoff said the hospital has not yet independently confirmed their relationship. But, he said, Boatwright has "shown an interest in trying to reach out to her."

"We did not find any major trauma on him," he said. "The assumption was the cause [of the amnesia] could have been psychological in nature, but nothing physical was found."

Ramhoff said psychiatrists concurred on the diagnosis of transient global amnesia, a sudden, temporary episode of memory loss that cannot be associated with epilepsy or a stroke, or a general "fugue" state, which can be longer in duration.

For the last five months, Boatwright has been staying at the Desert Regional Medical Center's skilled nursing facility, which reached out to the community and found people who spoke Swedish to help translate.

His social worker, Lisa Hunt-Vasquez, has been trying to locate family and friends by working with the media and making calls to the Veteran's Administration, Florida police and other leads.

"She has spent a lot of time calling China and Sweden to find information, but the language barriers and lack of information ran into dead ends," Ramhoff said.

Media around the world took an interest and stories appeared in the Swedish paper Aftonbladet and in the British press. As a result, the Sun received photos of people who looked like Boatwright.

Internet users in Sweden said they recognized him as an American who moved to Sweden in the 1980s.

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WHO Found Getting Higher Risk Cancer in Fukushima Disaster

The World Health Organization states that those who exposed to the worst levels of radiation during the Japanese nuclear disaster in 2011 have a higher risk for getting some certain types of cancer.

In March 2011In a massive earthquake and tsunami hit Japan. The following disaster happened when Fukushima Dai-ichi nuclear power plant was destroyed heavily. Plant's nuclear reactors revealed and adjacent places were polluted, even radiation sent into the surrounding sea.

Although Japanese Government stopped the leakage, many people were affected and died. According to U.N. agency said the most affected were those near the Fukushima Dai-ichi nuclear power plant. Around 110,000 people in the area were moved in March 2011 after caused a meltdown in the plant's nuclear reactors and sent radiation spewing into the surrounding area.

The WHO report says there is a little rate getting cancer among those outside the Fukushima area.

But the agency estimates there is up to a 70 percent increased risk of thyroid cancer among females exposed as infants in the most contaminated area. The risk of leukemia increased by 7 percent for males exposed as infants.

In order to help the Fukushima victims, WTO advocates a wide-aid with Japanese Government. Many Fortune Global 500 Cooperation involve in the project, such as Isabel Marant

, Microsoft and so on. The attempt is to shape a source of energy to concern the victims and do whatever they can do.

After suffering the terrifying earthquake tsunami and more horrific Fukushima disaster, all Japanese join in the anti-nuclear and appeal the Japanese government to abolish the application of nuclear. This disaster has impressive on them, and they can't image how soon their hurt will pass away absolutely. Maybe in their time, they will never forget。

Japanese government has it's consideration about forbidding the application of nuclear for the following reasons. Firstly is that nuclear generates electricity up to 80% in the country. Sencondly, nuclear is as a potential weapon to protect it's country safe. Moreover, once who possesses the technology and application of nuclear, you can get more chance in the world. But after this serious disaster, Japenese Government promises strenghten the administration of nuclear.

http://www.officialisabelmarant.org/

listen to people's life and write my own life. happy everyday

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Signs Of Tobacco Smoke Still Found In Non-Smoking Hotel Rooms

Editor's Choice
Academic Journal
Main Category: Smoking / Quit Smoking
Also Included In: Cancer / Oncology
Article Date: 14 May 2013 - 10:00 PDT Current ratings for:
Signs Of Tobacco Smoke Still Found In Non-Smoking Hotel Rooms

Non-smoking hotel rooms with a partial smoking ban do not fully protect guests from harmful exposure to third-hand smoke, according to new research.

The study was conducted by experts from San Diego State University (SDSU) and was published in the journal Tobacco Control.

Georg Matt, professor of psychology at SDSU, said:

"Our findings demonstrate that some non-smoking guest rooms in smoking hotels are as polluted with third-hand smoke as are some smoking rooms. Moreover, non-smoking guests staying in smoking rooms may be exposed to tobacco smoke pollutants at levels found among non-smokers exposed to second-hand smoke."

The surfaces and air quality of rooms in a random sample of low to mid-budget hotels in San Diego were examined. The researchers were looking for traces of tobacco smoke pollution - levels of nicotine and 3-ethenylpyridine (3EP) - referred to as third-hand smoke.

A previous study showed that nicotine in third-hand smoke, the residue from tobacco smoke that clings to essentially all surfaces long after a cigarette has been put out, reacts with the common indoor air pollutant nitrous acid to create dangerous carcinogens.

The sample included 10 hotels with complete smoking bans and 30 with partial smoking bans that had certain rooms designated for non-smokers.

The experts observed a group of non-smokers who spent the night at these hotels. In order to evaluate their exposure to nicotine and NKK, a carcinogen found in tobacco smoke, the subjects were asked to give urine and finger swipe samples.

"Smoking in hotels left a residue of tobacco pollution in both smoking and non-smoking rooms," the authors explained. "Hotels with a partial smoking ban did not protect the occupants of non-smoking rooms from exposure to tobacco pollution."

Surface nicotine and air 3EP were higher in both non-smoking and smoking rooms of hotels with partial bans than in hotels with total smoking bans.

Non-smoking rooms of hotels operating partial bans had surface nicotine levels over two times as high, and air levels of 3EP over 7 times as high, as those of hotels with complete bans.

Rooms where past guests had smoked had surface nicotine levels 35 times higher, and air nicotine levels 22 times greater, than those of rooms in hotels operating a complete smoking ban.

Smoking rooms had notably higher air nicotine levels compared to non-smoking rooms, and the levels were 40% greater in non-smoking rooms of hotels with partial bans than in those with complete bans.

Increased nicotine levels were also found in the hallway surfaces outside smoking rooms, compared to the surfaces outside non-smoking rooms.

Additionally, non-smokers who stayed in hotels with partial bans had higher levels of finger nicotine and urinary cotinine, compared to guests staying in hotels with total bans.

"Urinary NNAL was also significantly higher in those staying in the 10 rooms containing the highest levels of tobacco pollutants," according to the experts.

Matt concluded:

"New hotels should operate total smoking bans to protect not only their guests, but also their employees. In the meantime, guests who wish to protect themselves from exposure to tobacco smoke should avoid hotels that permit smoking and instead stay in completely smoke-free hotels."

Written by Sarah Glynn
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

Visit our smoking / quit smoking section for the latest news on this subject. Thirdhand smoke and exposure in California hotels: non-smoking rooms fail to protect non-smoking hotel guests from tobacco smoke exposure
Georg E Matt, Penelope J E Quintana, Addie L Fortmann, Joy M Zakarian, Vanessa E Galaviz, Dale A Chatfield, Eunha Hoh, Melbourne F Hovell, Carl Winston
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posted by Scott Ewing on 17 May 2013 at 3:49 pm

Secondhand smoke was shown to be a fraud in Federal court in 1998. Only on a technicality was the decision overturned. The findings of the court remain intact. Since SHS was invented our of thin air (sorry for the pun) exactly no one has died from it. Unless you count the innocent smokers being attacked and murdered by being forced outside.But wait, there's more! Now we have Third Hand Smoke. So we have a myth, made from a prior myth.This argument is as thin as a soup made from the shadow of a chicken that starved to death.

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posted by dave copeland on 16 May 2013 at 10:47 am

Years ago people in the smoker’s rights movement joked about third hand smoke. Now, as further proof that our society has become so absurd that satire is nearly impossible, the press is now all abuzz about this new fictitious danger, described as deadly toxic particles that hang out long after the second hand smoke is gone. It started with an article in the once respectable New York Times.

Dr. Jonathan P. Winickoff, evidently desperate for his fifteen minutes of fame, has published a study that, on first glance, appears to bolster this ridiculous claim. “Your nose isn’t lying,” he says. “The stuff is so toxic that your brain is telling you: ’Get away.’”

The article closes with the statement that Third Hand smoke contains polonium-210, “the highly radioactive carcinogen that was used to murder former Russian spy Alexander V. Litvinenko in 2006.” This is yellow journalism at its worst.

Michael McFadden, author of the book Dissecting Antismokers’ Brains sent me some rough calculations about polonium-210. He writes:

“A 30 cig per day smoker gets 1 picocurie per day.

“A typical nonsmoker living or working with smokers would get at most about 1/100th of that per day, more likely only 1/1,000th with good ventilation and/or a more reasonable amount of indoor smoking, so about one femtocurie.

“A child would have to live with a smoker for roughly three trillion days to absorb the dose that killed the Russian.”

And that is for second hand smoke. Since Third Hand Smoke is a fictional construct, we can only base our calculations on assumptions. (These calculations also come from McFadden.) Assuming that 1% of this deadly stuff has been spread on the 10,000 square feet of surface area in a typical 2,000 sq foot house, and also assuming that your method of cleaning is to having your infant lick the kitchen floor clean once a day, the kid would have to lick the floor for one hundred trillion days to accumulate a fatal dose. That comes out to about 274 billion years. The universe is about 13.8 billion years old. The half life of Polonium-210 is a mere 138 days. So in order to ingest a fatal dose, the not only would the floor licker have to keep at it 20 times longer than our universe has existed, we’d also have to completely rewrite the laws of physics to keep the stuff dangerous long enough to do any damage. That wouldn’t even slow down a nicotine nanny, of course – they have quite a bit of experience rewriting the laws of physics!

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posted by Dave Copeland on 15 May 2013 at 6:52 am

When staying in a hotel, I'm always willing to look past the fecal matter, bodily fluids, bacteria, germs and fungus others have left behind. But if there's even a chance I'm being exposed to a contrived, ASH-generated, fear-mongering catch phrase, I will vehemently protest to hotel management!

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'Signs Of Tobacco Smoke Still Found In Non-Smoking Hotel Rooms'

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HER2 Abnormalities Found In Many Advanced Cancers

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Main Category: Cancer / Oncology
Also Included In: Genetics
Article Date: 03 Jun 2013 - 3:00 PDT Current ratings for:
HER2 Abnormalities Found In Many Advanced Cancers

We already know that an over-active HER2 growth factor gene features in breast and gastric cancers. Now a new study reports finding mutations and other abnormalities of the gene in 14 different advanced cancers.

Massimo Cristofanilli, Director of the Jefferson Breast Center at the Kimmel Cancer Center and Thomas Jefferson University Hospital, announced the study results at an oral presentation during the annual meeting of the American Society of Clinical Oncology (ASCO), which is taking place in Chicago until Tuesday.

The gene for human epidermal growth factor receptor 2 (HER2) codes for a protein that promotes the growth of cancer cells. In around 1 in 5 breast cancers, a mutation in the gene causes cancer cells to make too much HER2 protein. The same mutation and the higher protein levels that result, occur in many types of cancer.

But Cristofanilli's results suggest there may be several kinds of gene alteration that can have this effect: not just known mutations but also other irregularities such as amplifications, substitutions, and translocations.

Cancer is essentially a disease of failure to regulate tissue growth. It is when the genes that regulate normal cell growth become altered in some way that the cell becomes cancerous.

Every time a cell divides, the enormous amount of data contained in its genetic material is replicated. When this happens, the chances are that some errors (mutations) will occur. Cells have complex mechanisms to prevent and correct such errors. And even if the faulty cell survives, there is another process, cell suicide or apoptosis, that the body uses to deal with rogue cells.

But if all these error controls fail, then the mutations and alterations survive and are passed on to daughter cells, to sow the seeds of a tumor.

Large-scale mutations occur when a large portion of genetic material is deleted or an extra portion is added. Amplification is when a cell gains many copies of genetic material, usually containing genes known to be cancer-causing. Translocation is when two separate regions become fused.

Small-scale mutations such as point substitutions, deletions and insertions are alterations to the building block units of DNA. For instance, a substitution is a mutation that exchanges two letters of the DNA code, like changing the spelling of a word by swapping around two of its letters.

Small-scale mutations usually affect the expression of a gene and alter the function or stability of the protein it codes for.

There are also other ways genes can change to make cells cancerous, such as when viruses insert bits of their DNA into the genetic material of the host cell, causing, for example, switched off cancer genes to switch on.

In this new study, which examined more than 2,000 tumors, Cristofanilli, a professor of Medical Oncology, and colleagues, found HER2 gene irregularities in 14 different advanced solid tumors.

"No one ever thought that there would be such a variety of genomic alterations in HER2 in this many solid tumors," Cristofanilli says in a statement.

But he says the findings could be good news, "both clinically and scientifically".

It could mean Herceptin and other anti-HER2 cancer therapies that are already in clinical use might help patients with some of these tumors.

From a research point of view, the results add weight to the growing idea of "genome-driven therapy", where the genome profile of the tumor, rather than where it develops, is more important when considering how best to treat the individual patient's cancer.

A number of institutions donated tumor samples for analysis, and their researchers are co-authors of the study. Cristofanilli contributed about 50 breast cancer samples. He discovered that one sample showed one of his patients, who had been diagnosed with triple negative breast cancer, had an HER2 mutation.

"My patient was treated with Herceptin as well as chemotherapy, and derived clinical benefit," says Cristofanilli.

"No one looks for HER2 mutations in this form of breast cancer. To me, this makes the case for the value of genome-driven therapy," he explains.

Foundation Medicine, a cancer diagnostics company in Cambridge, Massachusetts led and paid for the study. They screened 2,223 solid tumor specimens from 20 different advanced cancers, for more than 182 genes alterations known to be linked to cancer.

The results showed HER2 alterations in 14 types of solid tumor. Of these, 29% were esophageal cancer samples, 20% were uterine, 14% were breast, 12% were stomach, and 6% were lung.

They also found large variations in HER2 abnormalities. They found nearly 5% of samples had 116 different abnormalities, including 58% with amplifications, 25% with substitutions, 14% with insertions or deletions, 2% with splice site variants, 2% with translocations, and 5% with more than one alteration. Plus, two of the tumors had both HER2 substitution and amplification.

Cristofanilli says the study "highlights the need to study a broad range of genes at a high level of sensitivity and specificity when searching for novel targets of therapy".

"Widespread use of this approach could provide more treatment options and enable more rapid accrual to ongoing and planned trials of agents targeting pathways under study," he adds.

Another study reported earlier this year found that while some gene alterations may actively drive tumor growth, there may also be some "passenger" alterations that do the opposite and slow cancer down, suggesting cancer may not be a sequence of inevitable accumulation of driver events, but a delicate balance between drivers and passengers.

Written by Catharine Paddock PhD

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'HER2 Abnormalities Found In Many Advanced Cancers'

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Cancer-Suppressing Protein Found To 'Multitask'

Categorie principale : Cancer / oncologie
Egalement inclus dans : genetique
Date de l'article : 13 mai 2013 - 1:00 PDT courants nominaux pour :
Proteine suppresseur du cancer avere ? Multitache ?

La comprehension de la facon dont une puissante proteine appelee p53 protege contre le developpement du cancer a ete bouleversee par une decouverte par des chercheurs de l'Institut Walter et Eliza Hall.

Plus de la moitie des cancers humains portent des defauts dans le gene p53, et presque tous les autres cancers, avec un gene p53 normal, transporter d'autres defauts qui en quelque sorte portent atteinte a la fonction de la proteine p53. Herite de mutations du gene p53, mettre les gens a un tres haut risque de developper une gamme de cancers.

Fonctions de la proteine p53 sont normalement stimulees par potentiellement cancerigenes des evenements, tels que les dommages a l'ADN de rayonnement ultraviolet (une cause de cancer de la peau), ou la sur-activite des cancerigenes genes.

Mme Liz Valente, Dr Ana Janic et professeur Andreas Strasser de la division de genetique moleculaire du Cancer a l'Institut Walter et Eliza Hall ont ete disseque les processus controles par p53, pour decouvrir comment cette proteine peut supprimer le developpement du cancer. Leurs resultats surprenants sont publies en ligne dans la revue Cell Reports.

Dr Janic a dit que beaucoup de scientifiques croyait que les plus importants processus actives par p53 afin d'empecher la formation de cancer etaient arret cellules avec alteration de l'ADN de se diviser jusqu'a ce que l'ADN pouvait etre repare et rendant les cellules meurent s'ils avaient subi des dommages genetiques irreparable.

? Changements qui rendent les cellules endommagees deviennent longue duree de vie et de diviser de maniere incontrolee sont caracteristiques principales de la formation de cancer ?, a declare le Dr Janic. "Parce que p53 peut controler la survie cellulaire et la division cellulaire, on a suppose que ces deux processus constituaient les fonctions essentielles que p53 utilise pour prevenir le cancer. Le but de notre recherche etait d'examiner si cette hypothese etait correcte".

Mme Valente dit les cellules contre l'equipe qui n'avait pas de p53 avec cellules dans lequel p53 ne pouvait pas regler la survie cellulaire et la division cellulaire. "Dans les 20 dernieres annees qu'il est devenu clair quelles les proteines sont activees par p53 de bloquer la division cellulaire et de promouvoir la mort cellulaire,", a declare Mme Valente. "Nous avons pu supprimer tous ces proteines (appelees p21, Puma et Noxa) de cellules, de desactiver completement la possibilite de la p53 d'arreter la division cellulaire et declencher la mort des cellules. A notre grande surprise, p53 pourrait encore empecher la formation de cancer, meme sans etre en mesure de fabriquer des cellules meurent ou arreter divisant apres des dommages a l'ADN."

Professeur Strasser dit decouverte de l'equipe avait bouleverse la comprehension de la facon dont les fonctions p53. ? Lorsque le p53 suppresseur du cancer fonction a ete decouvert, qu'il etait important de comprendre le fonctionne de cette proteine, ? dit-il. ? Beaucoup de scientifiques avait conclu ce reglement de la division et la mort cellulaire ont ete les roles cles de p53, ? dit-il.

"Nos resultats ont rouvert la question de savoir comment les fonctions de p53. Mon soupcon est que ce n'est pas une proteine mais plusieurs avec de tres nombreuses fonctions critiques qui travaillent ensemble pour prevenir la formation de cancer par coordonner la bonne reparation de l'ADN endommage, plutot que de s'arreter de diviser ou de tuer les cellules. Autres recherches a dechiffrer comment ces processus sont integres sera une etape importante dans la comprehension de la fonction de suppresseur de tumeur p53 fonction. Ces connaissances, a son tour, puis peuvent etre exploitees pour developper des traitements ameliores,"a declare le professeur Strasser.

Article adapte par Medical News Today de communique de presse original. Cliquez sur ? references ? onglet ci-dessus pour la source.
Visitez notre cancer / oncologie section pour les dernieres nouvelles sur ce sujet. La recherche a ete financee par l'Australian National Health et Medical Research Council, la leucemie et Lymphoma Society (Etats-Unis), Cancer Council Victoria, The Lady Tata Memorial Trust, la bourse de Beatriu de Pinos (Union europeenne/Espagne) et le gouvernement de Victoria.
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? Proteine suppresseur du Cancer avere ' multitache ''

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