Few Correctly Cover Coughs and Sneezes

Before and After XMICROBE™ Antimicrobial Treatment

XMICROBE™ Antimicrobial treated surfaces provide advanced protection against harmful biological contaminants such as: E.coli, Chlorella vulgarus, Salmonella, and just about any other bacteria, fungi, yeast, mold, dust and algae.

XMICROBE™

Long Lasting Germ Protection !

Dry Air Blamed For Flu Outbreaks

MSNBC.com -
By Emily Sohn

It’s one of the hallmarks of winter: The misery of being stuck in bed with the flu. Now, scientists are finally figuring out why the virus hits hardest in the wintertime and why some winters are worse than others.

Blame dry air.

Extremely low humidity levels in winter, according to new research, fuel influenza outbreaks. Particularly dry spells make the problem worse. The discovery might help scientists prepare for epidemics and for the rash of secondary illnesses, like pneumonia, that often slam people once they’re already down.

“It is the first step toward potentially forecasting the risk of influenza outbreaks,” said Jeffrey Shaman, an atmospheric scientist at Oregon State University in Corvallis. “By getting a handle on what’s going on with influenza, we are also getting a handle on the other diseases that really piggy back on influenza.”

To explain why flu and related illnesses strike far more often in the winter than at other times of year, theories have fallen into three categories. One idea is that people spend more time indoors in the winter and schools are in session, so there is more person-to-person contact.

Another theory is that, with less exposure to sunlight, people have lower levels of melatonin and vitamin D, weakening their immune systems and making them more likely to succumb to influenza viruses. Scientists have also hypothesized that temperature and humidity affect how long the virus can last after someone coughs or sneezes.

Previous research has shown that influenza viruses survive longer in air when temperatures are colder and relative humidity is lower. Relative humidity, which appears in many weather reports, describes how close conditions are to the point of forming fog or clouds.

But relative humidity isn’t the best measurement for studying flu outbreaks, Shaman said, because relative humidity varies with temperature. So, there is actually less moisture in the air on a rainy winter day in Seattle than there is on a sunny summer day in the same city.

He thought it would be more useful to look at absolute humidity, which measures exactly how much moisture is in the air, regardless of temperature.

On that scale, Shaman said, winters are usually twice as dry as summers in a place like San Diego and Arizona, four times drier in New York, and up to five times drier in a particularly cold state like Minnesota.

Along with colleagues, he analyzed 31 years of data from around the United States and used a computer model to show that influenza outbreaks were more likely to occur when absolute humidity levels were low. Like a sliding scale, progressively drier air led to progressively higher likelihood that an outbreak would occur, the researchers reported in the journal PLoS Biology. Temperature didn’t play much of a role.

“People had recognized that there was seasonality to this, but nobody has really come up with a unifying explanation,” said Gregory Poland, Director of the Mayo Clinic’s Vaccine Research Group in Rochester, Minn. Humidity, he said, “is likely is part of that unifying explanation.”

Humidity is probably not the only explanation, however, and the weather forecast will probably never serve as a flu forecast. Even in dry conditions, the virus needs to be hanging around, and people need to come into contact to spread it. Still, any insight into what drives epidemics is a step toward saving lives.

When absolute humidity is low, for example, local hospitals could start stockpiling anti-viral medications and other supplies, and they could increase moisture levels in patient rooms.

Humidifying your home could help, too, but moist air alone is not the answer, Shaman said.

“The best defense against influenza remains vaccination. That can’t be stressed enough,” he said. “I would never suggest anyone forgo that to go out and buy a humidifier.”

XMICROBE™ Mode of Action

 

XMICROBE™

Long Lasting Germ Protection !

XMICROBE™ – A Greener Approach to Extended Sanitization

BioShield Services, LLC has developed a technology centered around XMICROBE™ a silicone quaternary ammonium salt microbiostatic agent which provides a durable, long acting, environmental friendly surface protection. While there are no “green” disinfectants, XMICROBE™ supports many of the twelve principles of green chemistry as defined by the United States Environmental Protection Agency (USEPA)1.

The following specifics relate to those principles which apply to the use of XMICROBE™ and are identified using the numbers and headings from the USEPA list:

Prevention:

XMICROBE™ is applied as a spray and generates no excess solutions which must be disposed of. Remaining solution is stable and may be stored for use in the next application.

Designing Safer Chemicals:

Upon application, XMICROBE™ bonds first to the surface and then to itself through its cohesive bonding properties forming a large co-polymer compound. The special bonding abilities of XMICROBE™ can be attributed to its multifunctional bonding receptors. Each bonding site, on the surfaces that are treated or the cell membrane’s receptor proteins, are easily adhered to because XMICROBE™ contains a variety of complimentary binding proteins. The multivariate bonding combinations make XMICROBE™ an excellent combatant for treating surfaces against both Gram positive and Gram negative bacteria, molds, yeast, mildew, and algae. It is extremely effective in destroying Staph, MRSA, E. coli, Salmonella and Influenza A. Once bonded XMICROBE™ immediately begins its assault against microbes using long protein chains which are synthesized from highly reactive, positively charged “R” group amino acids. It is because of the charged “R” group that XMICROBE™ has the ability to bond to a wide diversity of negatively charged, infectious and potentially fast spreading micro organisms. Because the bonds formed between XMICROBE™ and the microbes are covalent bonds the strength of the bond has no dislodgeable residue leaching, off-gassing migration or diffusion of the molecule. Once the bond has been established the length and reactivity of the molecular proteins spikes work quickly and effectively in eliminating the micro organism threat. The methodology is mechanical in nature preventing any creation of resistant strains or toxic residues. Normal cleaning removes any dirt, residue or dead organisms allowing the efficacy of the polymer surface to continue.

Safer Solvents and Auxiliaries:

XMICROBE™ continues to hold its bond even after the annihilation of the micro organism which has a twofold benefit. One, since the covalent bond between XMICROBE™ and the unwanted organism is never compromised, the possibility of latent pieces of microbial DNA being taken up and integrated into a host cell’s genetic code is virtually impossible. Two, due to the positive-to-negative charged bonds, the reactive “R” groups of the proteins are rendered impotent eliminating the possibility of XMICROBE™ rendering to another surface.

Water is the only solvent used for dilution of the XMICROBE™ concentrate to the desired application strength.

Design for Degradation:

The resultant polymer surface is durable and tightly bonded to the surface to which it is applied. Any breakdown material is non-toxic and is removed by normal periodic cleaning. Due to the chemical structure of the ammonium salt the compound renders itself harmless by simple decomposition, leaving behind no harmful residue or lingering byproducts.

Inherently Safer Chemistry for Accident Prevention:

The XMICROBE™ concentrate is classed as a pesticide by USEPA and normal precautionary handling is required. There are no carcinogens in the compound. It is non-flammable, stable under normal conditions and is not subject to hazardous polymerization. In the event of accidental spill, the solution can be deactivated by addition of an anionic surfactant or detergent.

The XMICROBE™ material when used by or according to a certified technician of the Healthier Environment Living Program™ (HELP) provides affordable, long lasting antimicrobial protection. This protection can by monitored and managed through ongoing Indoor Air and Surface Quality testing provided by HELP. View more information on www.HealthierPrograms.com or call 888-558-5254.

Erik J. Waters

Independent Microbiologist

December 2009

XMICROBE™

Long Lasting Germ Protection !

Poison (Chemicals) vs. Mechanical Elimination

Conventional products penetrate living cells and kill by way of poisoning or chemically altering the organism. They are designed to act quickly and dissipate quickly to avoid adverse effects to humans and animals due to their toxic ingredients. (The XMICROBE™ Antimicrobial Does Not) 

Most commercial antimicrobials used for treating building surfaces do a great job of getting a quick kill on bacteria and fungi, although most have a limited spectrum of effectiveness. (XMICROBE™ Antimicrobial Has A Broad Spectrum Of Effectiveness) 

Heavy metal based antimicrobials, such as silver ion may leach into the environment and lose their effectiveness over time. (The XMICROBE™ Antimicrobial Is Water Based That Won’t harm The Environment) 

Here’s The Big Difference… 

XMICROBE™ Antimicrobial takes a totally unique approach. It provides long-term control of growth on treated surfaces because the surface itself is modified to make it antimicrobial active. 

The active ingredient in the XMICROBE™ Antimicrobial forms a colorless, odorless, positively charged polymer, which chemically bonds to the treated surface. You could think of it as a layer of electrically charged swords. 

When a microorganism comes in contact with the treated surface, the sword punctures the cell membrane and the electrical charge shocks the cell. Since nothing is transferred to the now dead cell, the anti-microbial doesn’t lose strength and the sword is ready for the next cell to contact it. 

XMICROBE™ Antimicrobial protection continuously fights the growth of microbes. Plus, the XMICROBE™ Antimicrobial protection makes the surfaces in your home easier to clean and keeps them cleaner and fresher between cleanings. 

XMICROBE™ Antimicrobial has undergone extensive independent laboratory testing and has a long 35 year history of safe use. It is registered with the EPA for all applications in which it is used.

XMICROBE™

Long Lasting Germ Protection !

A Look at XMICROBE™

As you can see to the left, XMICROBE™ Antimicrobial works like a bed of nails to draw and impale microbes. 

XMICROBE™ Antimicrobial is an EPA Registered revolutionary product. XMICROBE™ Antimicrobial prevents the growth of an amazingly wide array of bacteria, mold, mildew, algae and yeast.

XMICROBE™ Antimicrobial acts like a bed of microscopic spikes that pierce the cell walls of microbes.

XMICROBE™ Antimicrobial is a totally new approach to providing long lasting anti-microbial protection.

XMICROBE™

Long Lasting Germ Protection !

A Year After Its Emergence, H1N1 Swine Flu Lingers

HealthDay News -
By Amanda Gardner
HealthDay Reporter

A year ago, global alarm over the emergence of an unpredictable new strain of H1N1 pandemic flu was in full swing. Headlines blared that thousands were becoming sick; face masks and hand sanitizers were selling out as soon as they hit store shelves.

So, where is H1N1?

On Thursday, Dr. Margaret Chan, head of the World Health Organization, announced that the virus is still considered pandemic, meaning widespread, although case numbers have ebbed considerably.

Meanwhile in the United States, the U.S. Centers for Disease Control and Prevention noted that, as of May 22, just 1 percent of outpatient visits involved flu.

But, the new H1N1 flu — sometimes called swine flu — long ago pushed aside prior seasonal flu viruses to become the dominant strain. And experts believe it will settle into the regular fall/winter outbreak pattern that people are used to.

This type of major viral shift occurs every few decades with influenza, experts noted.

“What most people are expecting is that [the new H1N1 strain] will supplant the older H1N1 viruses that were the previous seasonal strains and become the seasonal H1N1 virus,” explained Dr. John J. Treanor, professor of medicine and of microbiology and immunology at the University of Rochester Medical Center in New York. “The most likely scenario would be that we would continue to see the descendants of pandemic H1N1 causing seasonal outbreaks of flu, with probably normal timing,” he said.

So H1N1 pandemic flu will — like prior dominant flu strains — probably mount a resurgence this fall and wane again in the spring of next year. That’s the polar opposite of how it first appeared on the scene in the spring of 2009.

Another expert agreed that H1N1 flu may seem to be gone right now, but should not be forgotten.

“I think there’s a perception that the virus has entirely disappeared because we’re not seeing [many] new cases but viruses don’t really go away. They go into hiding,” said Dr. Len Horovitz, a pulmonary specialist with Lenox Hill Hospital in New York City. Often, he said, flu strains are “migrating somewhere where they re-assort [genetically] and reemerge in a different from.”

According to the World Health Organization, H1N1 flu is currently most active in areas of the Caribbean and Southeast Asia, although cases remain relatively low, Agence France-Presse reported. WHO based its announcement Thursday on a report from a 15-member panel of experts. That committee will meet again in July when more data arrives on the progress of flu during the southern hemisphere’s winter season.

Since it first appeared, H1N1 — which had killed 12,000 Americans by the end of March, according to CDC estimates — has distinguished itself from the “regular” flu in several ways.

For one thing, it has tended to strike harder at children and younger adults than at the elderly, who were the most likely to succumb to previous seasonal flu strains. That could be because older people picked up some immunity in their youth from prior, related H1N1 outbreaks.

And pregnant women, especially, were endangered from the H1N1 strain. In a study published in April in the Journal of the American Medical Association, CDC researchers found that while pregnant women make up about 1 percent of the U.S. population at any given time, during the 2009 H1N1 swine flu outbreak they made up 5 percent of deaths.

Still, compared to prior seasons of “regular” flu, H1N1 actually caused milder disease and fewer deaths overall. (The conventional seasonal flu typically kills about 36,000 Americans every year.) That might remain the case in the near future, experts said, but changes to the H1N1 virus and those most affected could occur over time.

“As H1N1 becomes mature, I would expect that the relative number of hospitalizations between young adults and the elderly will start to change but that’ll mostly be because of decreased number of hospitalizations in young people rather than in increases in the elderly,” Treanor said. “I wouldn’t be surprised if over the next flu seasons the impact on the elderly becomes relatively less.”

Less illness and fewer deaths among the elderly and overall are a good thing, but more mortality among the young means more years of life lost, Treanor pointed out.

One thing is certain — the H1N1 virus is easily passed from one person to another, having swept the globe last year at rapid speed.

“Transmission has been excellent,” said Dr. Scott Lillibridge, assistant dean of the Texas A&M Health Science Center School of Rural Public Health in Houston and executive director of the National Center for Emergency Medical Preparedness and Response.

Meanwhile, the 2010/2011 flu vaccine will definitely include the H1N1 strain, along with two other strains, Treanor said.

“Pandemic or no pandemic, H1N1 will still exist,” WHO spokesman Gregory Haertl told AFP. “If there is no pandemic it means that H1N1 is behaving like a seasonal influenza virus but it is still there. Therefore vaccination against H1N1 is still important, especially for pregnant women, the young and those weakened by other ailments.”

More information

There’s more on H1N1 influenza at the U.S. Centers for Disease Control and Prevention .

SOURCES: John J. Treanor M.D., professor of medicine and of microbiology and immunology, University of Rochester Medical Center, Rochester, N.Y.; Len Horovitz, M.D., pulmonary specialist, Lenox Hill Hospital, New York City; Scott Lillibridge, M.D., assistant dean, Texas A&M Health Science Center School of Rural Public Health, Houston, and executive director, National Center for Emergency Medical Preparedness and Response; Agence France-Presse

Last Updated: June 04, 2010

Copyright © 2010 HealthDay. All rights reserved.

Asthma Linked to Worsened Flu Symptoms

LiveScience.com -

Allergic reactions to pet dander, dust mites and mold may prevent people with allergic asthma from generating a healthy immune response to respiratory viruses such as influenza, a new study finds.

“Our findings imply that the better your asthma is controlled, the more likely you are to have an appropriate response to a virus,” said Dr. Michelle Gill, assistant professor of pediatrics and internal medicine at UT Southwestern Medical Center. “When individuals with asthma come in contact with an allergic trigger and a respiratory virus, the allergen may actually interfere with the immune response to the virus. This interruption in the antiviral response may contribute to exacerbations of asthma that are commonly associated with respiratory viral infections.”

The study involved a small number of participants, however, so more research will be needed to firm up the results. The finding are detailed in the June edition of The Journal of Immunology.

More than half of the 20 million people diagnosed with asthma in the U.S., including 2.5 million children, have been diagnosed with allergic asthma.

Fifty-six people ranging in age from 3 to 35 participated in the study. Twenty-six of the participants suffered from allergic asthma; the remaining 30 made up the control group. Most of the participants were African-American, and the mean age was 15 years in both the asthma and control groups. In addition, those in the asthma group had been diagnosed by a physician and had a positive skin test to at least one indoor allergen.

Researchers first isolated immune cells called dendritic cells from study participants. These cells are found in blood and tissues that are in contact with the environment, such as skin and the linings of the nose and lungs. When they encounter respiratory viruses such as flu, dendritic cells normally produce proteins that help the body mobilize the immune system and overcome the viral infection. When the dendritic cells first encounter an allergic stimulus, however, they are significantly impaired in their ability to produce such antiviral proteins.

When investigators exposed the dendritic cells from the study participants with allergic asthma to influenza, they found that the cells were unable to produce interferon, an immune system protein that plays a key role in fighting off repeated infections of the same virus. Interferon is what makes a person feel run down and tired when fighting viral infections.

The researchers speculate that the immune-suppressing effect of the allergic stimulation of dendritic cells might be related to the high levels of a molecule called IgE normally found in people with allergic asthma. Among the subjects participating in this study, elevated IgE levels were associated with impaired capacity of dendritic cells to produce interferon when exposed to flu.

These findings suggest that when the cold/flu and allergy seasons collide, the immune response in individuals with allergic asthma may worsen their disease.

“These findings imply that allergic triggers associated with exposure to indoor allergens like pet dander and dust mites can potentially render cells deficient in responding to a virus,” Gill said. “It may – although this remains to be proven – also explain why asthmatics who are sensitive to indoor allergens often experience asthma exacerbations when they acquire respiratory viral infections.”

The study was funded primarily by a grant from the Exxon Mobil Corp.

Where Did the Flu Go? It’s Hiding

Livescience.com -

With spring and summer, the flu seems to die out. But it’s just gone into hiding, a new study finds.

The influenza virus is known to evolve rapidly, adapting to new hosts and swapping genes to become more virulent. Researchers wondered if existing flue strains die off each spring, to be replaced each fall by new founding strains from other parts of the world, or if a “hidden chain of sickness” persist over the summer.

A genetic analysis by University of Michigan postdoctoral fellow Trevor Bedford and colleagues reveals that in the United States, not all strains of influenza die off at the end of winter. Some move to South America, and some migrate even farther.

“The prevailing view that has developed over the past three years or so is the out-of-tropics hypothesis, in which the strains that bring about each temperate flu season originate from China and Southeast Asia, where influenza A is less seasonal,” Bedford said.

He and his colleagues tested that hypothesis by analyzing genetic sequences from influenza A (H3N2) viruses collected from patients around the world between 1998 and 2009 and constructing a tree showing relationships among the viruses. The resulting mathematical model accounted for evolutionary processes and rates of migration.

“We found that although China and Southeast Asia play the largest role in the influenza A migration network, temperate regions—particularly the USA—also make important contributions,” Bedford said. Rather than dying off at the end of our flu season, many strains simply move on to more favorable environments.

The results have implications for public health efforts aimed at combating the flu. For example, the new knowledge that influenza frequently migrates out of the U.S. argues for caution in using antivirals, which can promote development of drug-resistant strains. If, as previously thought, those strains died out at the end of the season, they would not be a problem, but their newly-discovered ability to survive and circulate means resistant strains can spread from the U.S. throughout the world. On the flip side, the finding also means that vaccination programs outside of China and Southeast Asia can be effective in curbing influenza’s spread.

In addition, growing knowledge about patterns of flu migration eventually may make it possible to tailor vaccines to particular locations, Bedford said. “We found, for instance, that South America gets almost all of its flu from North America. This would suggest that rather than giving South America the same vaccine that the rest of the world gets, you could construct a vaccine preferentially from the strains that were circulating in North America the previous season. As we gather more data from other regions, this could be done for the entire world.”

The research also can inform disease surveillance, Bedford said.

“By doing this kind of research, we get a clearer idea of where in the world flu is actually coming from. We know that it’s mostly Southeast Asia, but now we see that it can come out of temperate regions as well, so our surveillance needs to become more global.”

Bedford’s coauthors on the paper are postdoctoral fellow Sarah Cobey, professor Peter Beerli of Florida State University, and Mercedes Pascual, who is the Rosemary Grant Collegiate Professor of Ecology and Evolutionary Biology and a Howard Hughes Medical Institute Investigator.

The research was funded by Howard Hughes Medical Institute, the National Institutes of Health and the National Science Foundation. It was detailed online May 27 in the  journal PLoS Pathogens.

Picture Credit: CDC/Cynthia Goldsmith

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