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Photo:Centers for Disease Control and Prevention

H1N1 An image of the newly identified swine flu virus.

Partly because they can mutate very fast and can mix genes, viruses are turning out to be astonishingly diverse.

The New York Times, May 5, 2009, by Carl Zimmer  —  Evolutionary biology may sometimes seem like an arcane academic pursuit, but just try telling that to Gavin Smith, a virologist at Hong Kong University. For the past week, Dr. Smith and six other experts on influenza in Hong Kong, Arizona, California and Britain have been furiously analyzing the new swine flu to figure out how and when it evolved.

The first viruses from the outbreak were isolated late last month, but Dr. Smith and his colleagues report on their Web site that the most recent common ancestor of the new viruses existed 6 to 11 months ago. “It could just have been going under the radar,” Dr. Smith said.

The current outbreak shows how complex and mysterious the evolution of viruses is. That complexity and mystery are all the more remarkable because a virus is life reduced to its essentials. A human influenza virus, for example, is a protein shell measuring about five-millionths of an inch across, with 10 genes inside. (We have about 20,000.)

Some viruses use DNA, like we do, to encode their genes. Others, like the influenza virus, use single-strand RNA. But viruses all have one thing in common, said Roland Wolkowicz, a molecular virologist at San Diego State University: they all reproduce by disintegrating and then reforming.

A human flu virus, for example, latches onto a cell in the lining of the nose or throat. It manipulates a receptor on the cell so that the cell engulfs it, whereupon the virus’s genes are released from its protein shell. The host cell begins making genes and proteins that spontaneously assemble into new viruses. “No other entity out there is able to do that,” Dr. Wolkowicz said. “To me, this is what defines a virus.”

The sheer number of viruses on Earth is beyond our ability to imagine. “In a small drop of water there are a billion viruses,” Dr. Wolkowicz said. Virologists have estimated that there are a million trillion trillion viruses in the world’s oceans.

Viruses are also turning out to be astonishingly diverse. Shannon Williamson of the J. Craig Venter Institute in Rockville, Md., has been analyzing the genes of ocean viruses. A tank of 100 to 200 liters of sea water may hold 100,000 genetically distinct viruses. “We’re just scratching the surface of virus diversity,” Dr. Williamson said. “I think we’re going to be continually surprised.”

Viruses are diverse because they can mutate very fast and can mix genes. They sometimes pick up genes from their hosts, and they can swap genes with other viruses. Some viruses, including flu viruses, carry out a kind of mixing known as reassortment. If two different flu viruses infect the same cell, the new copies of their genes get jumbled up as new viruses are assembled.

Viruses were probably infecting the earliest primordial microbes. “I believe viruses have been around forever,” Dr. Wolkowicz said.

As new hosts have evolved, some viruses have adapted to them. Birds, for example, became the main host for influenza viruses. Many birds infected with flu viruses do not get sick. The viruses replicate in the gut and are shed with the birds’ droppings.

A quarter of birds typically carry two or more strains of flu at the same time, allowing the viruses to mix their genes into a genetic blur. “Birds are constantly mixing up the constellation of these viruses,” said David Spiro of the J. Craig Venter Institute.

From birds, flu viruses have moved to animals, including pigs, horses and humans. Other viruses, like H.I.V. and SARS, have also managed to jump into our species, but many others have failed. “It’s a very rare event when a virus creates a new epidemic in another species,” said Colin Parrish of Cornell University. In Southeast Asia, for example, a strain of bird flu has killed hundreds of people in recent years, but it cannot seem to move easily from human to human.

Only a few strains of influenza have managed to become true human viruses in the past century. To make the transition, the viruses have to adapt to their new host. Their gene-building enzymes have evolved to run at top speed at human body temperature, for example, which is a few degrees cooler than a bird’s.

Influenza viruses also moved from bird guts to human airways. That shift also required flu viruses to spread in a new way: in the droplets we release in our coughs and sneezes.

“If the virus settles down on the floor, then it’s gone,” said Peter Palese, chairman of microbiology at Mount Sinai School of Medicine. Winter is flu season in the United States, probably because dry air enables the virus-laden droplets to float longer.

Up to a fifth of all Americans become infected each flu season, and 36,000 die. During that time, the flu virus continues to evolve. The surface proteins change shape, allowing the viruses to evade the immune systems and resist antiflu drugs.

Dr. Spiro and his colleagues have also discovered that human flu viruses experience a lot of reassortment each season. “Reassortment may be the major player in generating new seasonal viruses,” Dr. Spiro said.

From time to time, a new kind of flu emerges that causes far more suffering than the typical swarm of seasonal flu viruses. In 1918, for example, the so-called Spanish flu caused an estimated 50 million deaths. In later years, some of the descendants of that strain picked up genes from bird flu viruses.

Sometimes reassortments led to new pandemics. It is possible that reassortment enables flu viruses to escape the immune system so well that they can make people sicker and spread faster to new hosts.

Reassortment also played a big role in the emergence of the current swine flu. Its genes come from several ancestors, which mainly infected pigs.

Scientists first isolated flu viruses from pigs in 1930, and their genetic sequence suggests that they descend from the Spanish flu of 1918. Once pigs picked up the flu from humans, that so-called classic strain was the only one found in pigs for decades. But in the 1970s a swine flu strain emerged in Europe that had some genes from a bird flu strain. A different pig-bird mix arose in the United States.

In the late 1990s, American scientists discovered a triple reassortant that mixed genes from classic swine flu with genes from bird viruses and human viruses. All three viruses – the triple reassortant, and the American and European pig-bird blends – contributed genes to the latest strain.

It is possible that the special biology of pigs helped foster all this mixing. Bird flu and human flu viruses can slip into pig cells, each using different receptors to gain access. “We call the pig a mixing vessel because it can replicate both avian and mammalian influenza virus at the same time,” said Juergen Richt of Kansas State University. “The mixing of these genes can happen much easier in the pig than in any other species.”

Fortunately, the new swine virus seems to behave like seasonal flu in terms of severity, not like the 1918 Spanish flu. “Right now it doesn’t have what it takes to be a killer virus,” Dr. Palese said. But could it? Dr. Palese said it was highly unlikely.

If the swine flu peters out in the next few weeks, virus trackers will still pay close attention to it over the next few months. As flu season ends in the Northern Hemisphere, the virus may be able to thrive in the southern winter or perhaps linger in the tropics, only to return to the north next fall. It will no doubt change along the way as its genes mutate, and it may pick up new genes.

The scientists will be watching that evolutionary journey with a mixture of concern and respect. “Viruses are incredibly adaptable,” Dr. Spiro said. “They have managed to exploit our modern culture and spread around the world.”

Medscape.com, by Martha Kerr, May 5, 2009 (Baltimore, Maryland) – Pediatric infectious diseases specialists and public health experts used the stage of the Pediatric Academic Societies’ annual meeting to update their colleagues on the latest statistics and projections on the H1N1 “swine flu” outbreak.

“I believe that we will see [H1N1 cases] die down over the next month or two, with a reemergence in the fall,” predicted James Cherry, MD, pediatric infectious diseases specialist at the University of California at Los Angeles School of Medicine.

“I’ve lived through 4 shifts of influenza A,” Dr. Cherry told a heavily attended special symposium here. The current strain appears to be more similar to the 1957 strain, when deaths were largely attributed to coinfection with Staphylococcus aureus, than it does to the better recognized 1976 swine influenza outbreak, he said.

“I think we are going to see this strain reemerge in the fall, with MRSA [coinfection]. I believe MRSA will play a major role in morbidity and mortality,” Dr. Cherry warned.

“This is real. This is going to happen. We need vaccines. We should move ahead with vaccine development as fast as possible. Antivirals are not going to manage it,” he said.

The median age of infected patients in this outbreak is 26 years, and the virus primarily infects teens and young adults, he said. “It doesn’t seem to seriously affect anyone over age 50. We don’t know if these individuals have some residual immunity.”

Gail J. Demmler-Harrison, MD, professor of pediatrics at Baylor College of Medicine and Texas Children’s Hospital in Houston, commented that “Dr. Cherry’s adage still holds true: If there is a fever, it is probably influenza. If there are nasal symptoms, then it is likely not.”

There could be exceptions, she cautioned, such as infants with severe gastrointestinal symptoms and apnea, and infants who are immunocompromised may have atypical presentations.

“It is important to obtain a proper specimen of a nasal swab, aspirate or wash…with rapid A/B flu testing at the point of care” in children with fever and flu-like symptoms and close contact with a confirmed or suspected case, Dr. Demmler said. Positive samples should be sent to a laboratory for viral cultures and molecular typing.

Stephen C. Redd, MD, the Centers for Disease Control and Prevention’s Coordinating Center for Infectious Diseases (CDC CCID) influenza team leader, noted that there are no new recommendations for travel. Community mitigation procedures have not been made mandatory.

“Schools should consider closing if there has been a confirmed case among students, or confirmed cases in the neighborhood, but there are no preemptive mandatory regulations for closings or travel restriction,” he emphasized. Mandatory closings are restricted to outbreaks with 1% to 2% or higher mortality, “and that is certainly not the case with this outbreak.”

“This is a rapidly evolving epidemic,” Dr. Redd added. “Susceptibility is widespread, but the severity picture is much less clear than the susceptibility…. Guidance is frequently changing. Stay tuned!”

“Clinicians should recommend early antiviral treatment with oseltamivir (Tamiflu) or zanamivir (Relenza) if the patient is severely ill or is at high risk for complications. Use your clinical judgment to decide whether additional antibacterial therapy is needed,” he said.

“The evidence on the value of induction of secretory IgA or FluMist is unknown,” Dr. Cherry added.

The speakers have disclosed no relevant financial relationships.

The Pediatric Academic Societies are a consortium of pediatric associations and societies, including the Asian Society for Pediatric Research, the American Society of Pediatric Nephrology, the Association of Pediatric Program Directors, the International Pediatric Hypertension Association, the Pediatric Infectious Diseases Society, and the Programme for Global Paediatric Research.

Pediatric Academic Societies (PAS) 2009 Annual Meeting: Hot Topic Symposium: “H1N1 Influenza A: What the Pediatrician Needs to Know.”

www..Medicinenet.com/MRSA

MRSA stands for methicillin resistant Staphylococcus aureus (S. aureus) bacteria.

This (superbug) highly resistant organism is known for causing skin infections, in addition to many other types of infections. There are other designations in the scientific literature for these bacteria according to where the bacteria are acquired by patients, such as community-acquired MRSA (CA-MRSA), and hospital-acquired MRSA or epidemic MRSA (EMRSA).

Although S. aureus has been causing infections (staph infections) probably as long as the human race has existed, MRSA has a relatively short history. MRSA was first noted in 1961, about two years after the antibiotic methicillin was initially used to treat S. aureus and other infectious bacteria. The resistance to methicillin was due to a penicillin-binding protein coded for by a mobile genetic element termed the methicillin resistant gene (mecA). In recent years, the gene has continued to evolve so that many MRSA strains are currently resistant to several different antibiotics. S. aureus is sometimes termed a “superbug” because of its ability to become resistant to several antibiotics. Unfortunately, MRSA can be found worldwide.

 

MRSA (methicillin resistant Staphylococcus aureus) bacteria causes skin infections with the following signs and symptoms: cellulitis, abscesses, carbuncles, impetigo, styes, and boils. Normal skin tissue doesn’t usually allow MRSA infection to develop. Individuals with depressed immune systems and people with cuts, abrasions, or chronic skin disease are more susceptible to MRSA infection.

 

How is MRSA diagnosed?

 

In 2008, the U.S. Food and Drug Administration (FDA) approved a rapid blood test that can detect the presence of MRSA genetic material in a blood sample in as little as two hours. The test is also able to determine whether the genetic material is from MRSA or from less dangerous Staph bacteria. The test is not recommended for use in monitoring treatment of MRSA infections and should not be used as the only basis for the diagnosis of a MRSA infection.

 

If MRSA is so resistant to many antibiotics, how is it treated or cured?

Fortunately, most MRSA still can be treated by certain specific antibiotics (for example, vancomycin (Vancocin), linezolid (Zyvox), and others). For MRSA carriers, mupirocin antibiotic cream can potentially eliminate MRSA from mucous membrane colonization. A good medical practice is to determine, by microbiological techniques done in a lab, which antibiotic(s) can kill the MRSA and use it alone or, more often, in combination with additional antibiotics to treat the infected patient. Since resistance can change quickly, antibiotic treatments may need to change also. Many people think they are “cured” after a few antibiotic doses and stop taking the medicine. This is a bad decision because the MRSA may still be viable in or on the person and reinfect the person. Also, the surviving MRSA may be exposed to low antibiotic doses when the medicine is stopped too soon; this low dose may allow MRSA enough time to become resistant to the medicine. Consequently, MRSA patients (in fact, all patients) treated with appropriate antibiotics should take the entire course of the antibiotic as directed by their doctor. A note of caution is that, in the last few years, there are reports that a new strain of MRSA has evolved that is resistant to vancomycin (VRSA or vancomycin resistant S. aureus) and other antibiotics. Currently, VRSA is not widespread, but it could be the next “superbug.”

•1.       Mark C. Enright*,,

•2.       D. Ashley Robinson*,

•3.       Gaynor Randle,

•4.       Edward J. Feil*,

•5.       Hajo Grundmann§, and

•6.       Brian G. Spratt

+Author Affiliations

•1.     *Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, United Kingdom; Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, OX3 9DU, United Kingdom; §Division of Microbiology and Infectious Diseases, University Hospital Nottingham, Nottingham, NG7 2UH, United Kingdom; and Department of Infectious Disease Epidemiology, Faculty of Medicine, Imperial College, St. Mary’s Hospital, London W2 1PG, United Kingdom

  • 1. Edited by Christopher T. Walsh, Harvard Medical School, Boston, MA

 

Abstract

Methicillin-resistant Staphylococcus aureus (MRSA) is a major cause of hospital-acquired infections that are becoming increasingly difficult to combat because of emerging resistance to all current antibiotic classes. The evolutionary origins of MRSA are poorly understood, no rational nomenclature exists, and there is no consensus on the number of major MRSA clones or the relatedness of clones described from different countries. We resolve all of these issues and provide a more thorough and precise analysis of the evolution of MRSA clones than has previously been possible. Using multilocus sequence typing and an algorithm, burst, we analyzed an international collection of 912 MRSA and methicillin-susceptible S. aureus (MSSA) isolates. We identified 11 major MRSA clones within five groups of related genotypes. The putative ancestral genotype of each group and the most parsimonious patterns of descent of isolates from each ancestor were inferred by using burst, which, together with analysis of the methicillin resistance genes, established the likely evolutionary origins of each major MRSA clone, the genotype of the original MRSA clone and its MSSA progenitor, and the extent of acquisition and horizontal movement of the methicillin resistance genes. Major MRSA clones have arisen repeatedly from successful epidemic MSSA strains, and isolates with decreased susceptibility to vancomycin, the antibiotic of last resort, are arising from some of these major MRSA clones, highlighting a depressing progression of increasing drug resistance within a small number of ecologically successful S. aureus genotypes.

Methicillin was introduced in 1959 to treat infections caused by penicillin-resistant Staphylococcus aureus. In 1961 there were reports from the United Kingdom of S. aureus isolates that had acquired resistance to methicillin (methicillin-resistant S. aureus, MRSA) (1), and MRSA isolates were soon recovered from other European countries, and later from Japan, Australia, and the United States. MRSA is now a problem in hospitals worldwide and is increasingly recovered from nursing homes and the community (2, 3). The methicillin resistance gene (mecA) encodes a methicillin-resistant penicillin-binding protein that is not present in susceptible strains and is believed to have been acquired from a distantly related species (4). mecA is carried on a mobile genetic element, the staphylococcal cassette chromosome mec (SCCmec), of which four forms have been described that differ in size and genetic composition (5). Many MRSA isolates are multiply resistant and are susceptible only to glycopeptide antibiotics such as vancomycin and investigational drugs. MRSA isolates that have decreased susceptibility to glycopeptides (glycopeptide intermediately susceptible S. aureus, GISA) (6, 7), reported in recent years, are a cause of great public health concern.

Many studies have characterized MRSA isolates from individual hospitals or countries and have identified strains that appear to be well adapted to the hospital environment, are established in several hospitals within a country, or have spread internationally (epidemic MRSA, EMRSA). MRSA isolates are generally characterized by pulsed-field gel electrophoresis, a powerful technique for identifying the relatedness of isolates from recent outbreaks within a hospital, but are not well suited to long-term global epidemiology, which requires a procedure that is highly discriminatory but that indexes variation that accumulates slowly. Multilocus sequence typing (MLST) provides such a procedure and characterizes isolates of bacteria unambiguously by using the sequences of internal fragments of seven housekeeping genes (8, 9). MLST has been developed and validated for S. aureus (10) and provides a discriminatory method that allows related strains recovered in different countries to be readily identified.

The origins of the major MRSA clones are still poorly understood. Kreiswirth et al. (11) proposed that all MRSAs were descended from a single ancestral S. aureus strain that acquired mecA, but more recent studies (12, 13) show that some MRSAs are very divergent, implying that mecA has been transferred between S. aureus lineages. The data from MLST can be used to probe the evolutionary and population biology of bacterial pathogens and to predict ancestral genotypes and patterns of evolutionary descent within groups of related genotypes. We have applied MLST to an international collection of 359 MRSA isolates, which includes examples of the previously described EMRSA and GISA clones, and compare these to a collection of 553 methicillin-susceptible S. aureus (MSSAs). We demonstrate the limited number of major EMRSA genotypes and provide an unambiguous method for characterizing MRSA and GISA clones and a rational nomenclature. We also identify the ancestral MRSA clone and its MSSA ancestor and suggest the evolutionary pathways by which MRSA clones have repeatedly emerged from successful MSSA clones.

How can people prevent MRSA infection?

Not making direct contact with skin, clothing, and any items that come in contact with either MRSA patients or MRSA carriers is the best way to avoid MRSA infection. In many instances, this situation is simply not practical because such infected individuals or carriers are not immediately identifiable. What people can do is to treat and cover (for example, antiseptic cream and a Band-Aid) any skin breaks and use excellent hygiene practices (for example, hand washing with soap after personal contact or toilet use, washing clothes potentially in contact with MRSA patients or carriers, using disposable items when treating MRSA patients). Also available at most stores are antiseptic solutions and wipes to both clean hands and surfaces that may contact MRSA. Pregnant individuals need to consult with their doctors if they are infected or are carriers of MRSA. Although MRSA is not transmitted to infants by breastfeeding, there are a few reports that infants can be infected by their mothers who have MRSA, but this seems to be an infrequent situation. Some pregnant MRSA carriers have been successfully treated with the antibiotic mupirocin cream.

Can people die from MRSA infections?

Yes. Currently available statistics from the Kaiser foundation in 2007 (http://www.kaisernetwork.org/daily_reports/rep_index.cfm?DR_ID=45809) indicate that about 1.2 million hospitalized patients have MRSA, and the mortality rate is estimated to be between 4%-10%. In general, CA-MRSA has far less risk as long as the patient does well with treatment and does not require hospitalization.

UCLA Press Release

UCLA researchers report a major breakthrough using adult stem cells to treat Parkinson’s disease.

UCLA researchers report a major breakthrough using adult stem cells to treat Parkinson’s disease.

LifeNews.com reports the results were published in the February issue of the Bentham Open Stem Cell Journal. Dr. David Prentice, a fellow with the Family Research Council, says the research features only one patient.

“The gentleman was treated with stem cells into only half of his brain, and he went almost five years (without symptoms),” he explains. “Now his symptoms did start to return after that, and obviously he’d like the other half of his brain treated.”

The patient’s motor skills improved by over 80 percent in the first five years after the procedure. Prentice says he was able to have an active lifestyle. “During that time he was traveling all around the world and living a full life,” he points out.

David Prentice (FRC)No human embryos were killed in the research. “They used the gentleman’s own adult stem cells, so obviously there’s no chance of transplant rejection, no tumors,” Prentice notes, “and of course, adult stem cells really work in patients.”

UCLA researchers will now expand their work to 15 humans.

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Viktor Koen  

The New York Times, May 5, 2009, by John Tierney  —  Imagine that you have ditched your laptop and turned off your smartphone. You are beyond the reach of YouTube, Facebook, e-mail, text messages. You are in a Twitter-free zone, sitting in a taxicab with a copy of “Rapt,” a guide by Winifred Gallagher to the science of paying attention.

The book’s theme, which Ms. Gallagher chose after she learned she had an especially nasty form of cancer, is borrowed from the psychologist William James: “My experience is what I agree to attend to.” You can lead a miserable life by obsessing on problems. You can drive yourself crazy trying to multitask and answer every e-mail message instantly.

Or you can recognize your brain’s finite capacity for processing information, accentuate the positive and achieve the satisfactions of what Ms. Gallagher calls the focused life. It can sound wonderfully appealing, except that as you sit in the cab reading about the science of paying attention, you realize that … you’re not paying attention to a word on the page.

The taxi’s television, which can’t be turned off, is showing a commercial of a guy in a taxi working on a laptop – and as long as he’s jabbering about how his new wireless card has made him so productive during his cab ride, you can’t do anything productive during yours.

Why can’t you concentrate on anything except your desire to shut him up? And even if you flee the cab, is there any realistic refuge anymore from the Age of Distraction?

I put these questions to Ms. Gallagher and to one of the experts in her book, Robert Desimone, a neuroscientist at M.I.T. who has been doing experiments somewhat similar to my taxicab TV experience. He has been tracking the brain waves of macaque monkeys and humans as they stare at video screens looking for certain flashing patterns.

When something bright or novel flashes, it tends to automatically win the competition for the brain’s attention, but that involuntary bottom-up impulse can be voluntarily overridden through a top-down process that Dr. Desimone calls “biased competition.” He and colleagues have found that neurons in the prefrontal cortex – the brain’s planning center – start oscillating in unison and send signals directing the visual cortex to heed something else.

These oscillations, called gamma waves, are created by neurons’ firing on and off at the same time – a feat of neural coordination a bit like getting strangers in one section of a stadium to start clapping in unison, thereby sending a signal that induces people on the other side of the stadium to clap along. But these signals can have trouble getting through in a noisy environment.

“It takes a lot of your prefrontal brain power to force yourself not to process a strong input like a television commercial,” said Dr. Desimone, the director of the McGovern Institute for Brain Research at M.I.T. “If you’re trying to read a book at the same time, you may not have the resources left to focus on the words.”

Now that neuroscientists have identified the brain’s synchronizing mechanism, they’ve started work on therapies to strengthen attention. In the current issue of Nature, researchers from M.I.T., Penn and Stanford report that they directly induced gamma waves in mice by shining pulses of laser light through tiny optical fibers onto genetically engineered neurons. In the current issue of Neuron, Dr. Desimone and colleagues report progress in using this “optogenetic” technique in monkeys.

Ultimately, Dr. Desimone said, it may be possible to improve your attention by using pulses of light to directly synchronize your neurons, a form of direct therapy that could help people with schizophrenia and attention-deficit problems (and might have fewer side effects than drugs). If it could be done with low-wavelength light that penetrates the skull, you could simply put on (or take off) a tiny wirelessly controlled device that would be a bit like a hearing aid.

In the nearer future, neuroscientists might also help you focus by observing your brain activity and providing biofeedback as you practice strengthening your concentration. Researchers have already observed higher levels of synchrony in the brains of people who regularly meditate.

Ms. Gallagher advocates meditation to increase your focus, but she says there are also simpler ways to put the lessons of attention researchers to use. Once she learned how hard it was for the brain to avoid paying attention to sounds, particularly other people’s voices, she began carrying ear plugs with her. When you’re trapped in a noisy subway car or a taxi with a TV that won’t turn off, she says you have to build your own “stimulus shelter.”

She recommends starting your work day concentrating on your most important task for 90 minutes. At that point your prefrontal cortex probably needs a rest, and you can answer e-mail, return phone calls and sip caffeine (which does help attention) before focusing again. But until that first break, don’t get distracted by anything else, because it can take the brain 20 minutes to do the equivalent of rebooting after an interruption. (For more advice, go to nytimes.com/tierneylab.)

“Multitasking is a myth,” Ms. Gallagher said. “You cannot do two things at once. The mechanism of attention is selection: it’s either this or it’s that.” She points to calculations that the typical person’s brain can process 173 billion bits of information over the course of a lifetime.

“People don’t understand that attention is a finite resource, like money,” she said. “Do you want to invest your cognitive cash on endless Twittering or Net surfing or couch potatoing? You’re constantly making choices, and your choices determine your experience, just as William James said.”

During her cancer treatment several years ago, Ms. Gallagher said, she managed to remain relatively cheerful by keeping in mind James’s mantra as well as a line from Milton: “The mind is its own place, and in itself/ Can make a heav’n of hell, a hell of heav’n.”

“When I woke up in the morning,” Ms. Gallagher said, “I’d ask myself: Do you want to lie here paying attention to the very good chance you’ll die and leave your children motherless, or do you want to get up and wash your face and pay attention to your work and your family and your friends? Hell or heaven – it’s your choice.”

Physicians Are Talking About…


The Ponzi Scheme:

U.S. Health Insurance

 
Medscape.com, Spring 2009, by Nancy R. Terry  —  “Healthcare reform cannot wait, it must not wait, and it will not wait another year.” With those words, President Barack Obama, in his first address to a joint session of Congress, rallied Congress and the American people to tackle the “crushing cost of healthcare.” Yet, it remains to be seen whether the President’s reform efforts will target one of the most wasteful sectors of healthcare — the health insurance industry.

Recent postings on Medscape’s Physician Connect (MPC), an all-physician discussion board, deride the excesses of health insurance companies and exhort the need to restructure, if not eliminate, the for-profit health insurance industry.

“Commercial, for-profit health insurance is one of the greatest Ponzi schemes ever foisted on the public,” says a family medicine physician. “The executives are the ones that benefit to the detriment of everyone else. How else does the president of one of the largest insurance companies get to be a billionaire? By being at the top of the pyramid of companies’ and individuals’ premium payments.”

“The single most important factor in the atrociously high cost of healthcare in the United States is the rapacious, money-hungry insurance companies and their fat cat CEOs,” comments an MPC contributor.

“The damage that the insurance companies do is not limited to the salaries of the CEOs,” says another contributor. “They waste the time and resources of healthcare workers, institutions, and patients. They are clearly a negative, wasteful element in healthcare today that needs to be heavily regulated, changed, or eliminated.”

Physicians point to a number of supposedly routine practices of the health insurance companies that cry out for oversight. One MPC participant remarks that health insurance companies increase their premiums even as they decrease coverage. Another discussant notes that insurers typically burden physicians and patients with filing requirements as part of a strategy to delay or deny legitimate claims. According to one contributor, some companies frequently change their coding schemas to avoid paying legitimate claims. “The insurance companies make billions of dollars in profit each year,” says one MPC commentator, “and they do it by limiting care, denying claims, limiting contracts, and limiting reimbursements.”

The practice of systematically denying legitimate reimbursement claims by insurance companies has been the focus of an ongoing investigation by New York Attorney General Andrew Cuomo. In January 2009, Cuomo reached an agreement with UnitedHealth Group, Inc. that the insurer would shut down its controversial Ingenix database and pay $50 million to fund a nonprofit, independent database for the purpose of establishing fair compensation rates. The Ingenix database, which was owned by UnitedHealth, served all the major insurers and, according to The Wall Street Journal, skewed downward the “usual and customary” rates of out-of-network insurance reimbursements through “faulty data collection, poor pooling procedures, and lack of audits, thus forcing customers to pay more out of their own pockets for healthcare.” In February, WellPoint, Inc., the nation’s largest health insurer, agreed to Cuomo’s request to pay $10 million to help fund the new database. WellPoint is the sixth insurance company to make such an agreement with Cuomo’s office. As quoted by New York Daily News, Cuomo commented on the insurers’ use of the Ingenix database, saying, “This is as egregious a situation as I’ve seen, of a virtual monopoly.”

Is health insurance a scam? The 100 MPC postings in response to that question are unanimous in their assertion that the health insurance industry needs reform. Yet, MPC contributors are divided as to the extent and nature of that reform.

“The health insurance system is so profoundly flawed,” says one MPC contributor, “that the only solution is a nonprofit, single-payer healthcare system.” Other MPC contributors contend that a single-payer system would harbor its own set of problems. Comments a psychiatrist, “I would rather have evil insurance companies than absolute power concentrated in a single agency. If you have a complaint about an insurance company, you can complain to the regulators and drop the insurance. If you have a complaint about the government, you are screwed.”

Advocates of a single-payer system singled out Physicians for a National Health Program as a resource outlining the salient features of a single-payer system. Similarly, several advocates for reorganization of the for-profit insurance system directed readers to Real Health Reform, which proposes, among other healthcare reforms, the restructuring of private health insurance into a regulated utility.

Other contributors less concerned about the overall structure of the industry advocate that health insurance coverage should more closely resemble other types of insurance. “When we protect our house and car, the purpose has traditionally been to provide a safety net if the unforeseen happens to us,” points out an endocrinologist. “Health insurance is not that way. We have come to expect medical insurance to subsidize ordinary expenses, like our prescriptions and our office visits and any number of interventions that are not in themselves financially devastating, the way an auto collision or a home fire would be.” A family medicine physician comments, “Health insurance needs to be made into real insurance that only covers catastrophic events. Then it will be cheaper for everyone.”

Evident throughout the postings is a sense of frustration. One participant comments, “The people are not happy with health insurance, the physicians and allied personnel are not happy with health insurance. What is the government waiting for?”

Some MPC contributors refuse to take a wait-and-see attitude. They advocate that physicians who are disgruntled with the health insurance industry should effectively boycott health insurance.

“We need to immediately stop taking all third-party payments,” says an MPC contributor.

“Bill patients at the time of service,” advises another contributor. “Provide them with the invoice and tell them the truth, the larger truth — that you, the doctor, are not in the business of bandying about with insurance clerks and petty tyrants whose motivation is nothing but to frustrate payment and cost you valuable time and energy, which is duly relegated to patient care.”

“Stop making contracts with HMOs, hospitals, and health insurance,” recommends a neurologist. “Return to cash payment. When other doctors see it works for them the way it has for many, guess what? The yoyos who keep your insurance clerk and billing staff on hold for 2 hours asking for notes and records will be collecting pink slips.”

But the question remains: will the President’s health reform initiative take on the health insurance industry? MPC contributors hope the answer to that question is yes. “Our healthcare system is broken largely due to the insurance companies,” comments an MPC contributor. A urologist agrees, “Only through insurance reform can we begin the process of real healthcare reform.”

Nancy R. Terry, medical writer and editor, Jackson Heights, New York

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Photo by Kathy Keatley Garvey, UC Davis Department of Entomology Honey bee nectaring on button willow.

 

The New York Times, by Leon Kreitzman  —  Gardeners know that plants open and close their flowers at set times during the day. For example, the flowers of catmint open between 6:00 a.m. and 7:00 a.m.; orange hawkweed follows between 7:00 a.m. and 8:00 a.m.; field marigolds open at 9:00 a.m.

In “Philosophia Botanica” (1751), the great taxonomist Carl Linnaeus proposed that it should be possible to plant a floral clock. He noted that two species of daisy, the hawk’s-beard and the hawkbit, opened and closed at their respective times within about a half-hour each day. He suggested planting these daisies along with St. John’s Wort, marigolds, water-lilies and other species in a circle. The rhythmic opening and closing of the plants would be the effective hands of this clock.

Plants have carefully timed routines determined by internally generated rhythms. In 1729, Jean-Jacques d’Ortous de Mairan, a French astronomer, put a Mimosa plant in a cupboard to see what happened when it was kept in the dark. He peeked in at various times, and although the plant was permanently in the dark its leaves still opened and closed rhythmically – it was as though it had its own representation of day and night. The plant’s leaves still drooped during its subjective night and stiffened up during its subjective day. Furthermore, all the leaves moved at the same time. It took another 230 years or so to come up with the term circadian – about a day – to describe these rhythms.

In a similar vein, tobacco plants, stocks and evening primroses release their scent as the sun starts to go down at dusk. These plants attract pollinating moths and night-flying insects. The plants tend to be white or pale. Color vision is difficult under low light, and white best reflects the mainly bluish tinge of evening light.

But plants cannot release their scent in a timely manner simply in response to an environmental cue, like the lowering of the light levels. They need time to produce the oils. To coincide with the appearance of the nocturnal insects, the plant has to anticipate the sunset and produce the scent on a circadian schedule.

Flowers of a given species all produce nectar at about the same time each day, as this increases the chances of cross-pollination. The trick works because pollinators, which in most cases means the honeybee, concentrate foraging on a particular species into a narrow time-window. In effect the honeybee has a daily diary that can include as many as nine appointments – say, 10:00 a.m., lilac; 11:30 a.m., peonies; and so on. The bees’ time-keeping is accurate to about 20 minutes.

The bee can do this because, like the plants and just about every living creature, it has a circadian clock that is reset daily to run in time with the solar cycle. The bee can effectively consult this clock and “check” off the given time and associate this with a particular event.

Honeybees really are nature’s little treasures. They are a centimeter or so long, their brains are tiny, and a small set of simple rules can explain the sophisticated social behavior that produces the coordinated activity of a hive. They live by sets of instructions that are familiar to computer programmers as subroutines – do this until the stop code, then into the next subroutine, and so on.

These humble little bees have an innate ability to work out the location of a food source from its position in relation to the sun. They do this even on cloudy days by reading the pattern of the polarization of the light, and pass this information to other bees. In the dark of the hive, they transpose the location of a food source in the horizontal plane through the famous “waggle” dance into communication in the vertical plane of the hive.

Honeybees can tell their sisters how far away the food is up to a distance of about 15 kilometers. For good measure, they can also allow for the fact that the sun moves relative to the hive by about 15 degrees an hour and correct for this when they pass on the information. In other words, they have their own built-in global positioning system and a language that enables them to refer to objects and events that are distant in space or time.

German scientists in the early part of the last century called this ability of bees to learn the time of day when flowers start secreting nectar and visit the flowers at appropriate times Zeitgedächtnis, or time-sense. But the species of flowers in bloom, say, this week, is likely to be replaced by a different species at a different location next week or the week after. The bee needs a flexible, dynamic appointments system that it continually updates, and it has evolved an impressive ability to learn colors, odors, shapes and routes, within a time frame, quickly and accurately.

While the initial dance by a returning scout bee informs her sisters of the location and distance of food plants and the quality of their nectar, bees that visit the food source learn to synchronize their behavior with daily floral rhythms, foraging only when nectar and pollen are at their highest levels. At other times, they remain in the hive, conserving energy that otherwise would be exhausted on non-productive foraging flights.

Although most animals, including humans, cannot sustain long-lasting periods of activity without circadian rhythms, honeybees have developed a marked flexibility in their circadian rhythm that depends on the job they are doing. Whereas a particular circadian determined behavior is usually fixed to a certain phase of the cycle, in honeybees the circadian rhythm is dependent on the job the bee is doing.

Adult worker bees perform a number of tasks in the hive when they are young, like caring for eggs and larvae, and then shift to foraging for nectar and pollen as they age. However, if the hive has a shortage of foragers, some of the young nurse bees will switch jobs and become foragers. The job transition, whether triggered by age or social cues, involves changes in genes in the honeybee brain; some genes turn on, while others turn off.

Young worker bees less than two weeks of age who typically nurse the brood around-the-clock display no circadian rhythms. Older workers (more than three weeks) typically perform foraging activities and have strong circadian rhythms that are needed for the time-compensated sun-compass navigation and timing visits to flowers.

Recent research in Israel has shown that when young worker bees are removed from caring for the brood and placed in individual cages, they rapidly show circadian rhythms in their behavior. Newly emerged bees isolated in individual cages typically show circadian rhythms in locomotor activity when at 3 days to 14 days old, ages at which most bees in the hive perform around-the-clock nursing activities as mentioned above. Older foragers who revert to nursing duties switch back to around-the-clock brood care activity similar to that of young nurses in typical colonies.

The molecular clockwork mechanism that produces the circadian rhythm works by a series of feedback loops in which the proteins produced by several genes feedback to repress their own production. It is a complicated system, but the end result is a near-24-hour cycling in the levels of various proteins that in turn result in the cycling of the secretion of hormones and other substances.

It seems that there is a plasticity, or flexibility, in the organization of this molecular clockwork mechanism in honeybees, and that the social factors that influence division of labor in honeybee colonies are important also for the regulation of this circadian mechanism. As there is mounting evidence for increased pathologies and deterioration in performance when around-the-clock activity is imposed on most animals, including humans, detailed study of the plasticity of the circadian organization in honeybees may provide pointers for ways for us to have our 24/7 cake and eat it.

Honeybees are remarkable not just for the organization of their circadian clockwork. James Gould of Princeton first studied bees as an undergraduate. It was his pioneering study that showed conclusively that Karl von Frisch, who won a Nobel Prize for elucidating the waggle dance, had been right in concluding that the dance was a means of conveying information.

Ironically, an allergy meant that Gould had to stop working directly with the creatures, but his respect for them is enormous. As he has pointed out:

When a human decides whether to recommend a restaurant, taking into account its menus, the tastes of the friend being advised, the cost of the food, the distance to the establishment, the ambience of the dining room, the ease of parking and all the other factors that enter into such a decision, we have little hesitation in attributing conscious decision-making to the calculation. When a small frenetic creature enclosed in an exoskeleton and sprouting supernumerary legs and a sting performs an analogous integration of factors, however, our biases spur us to look for another explanation, different in kind.

We have been exploiting honeybees for thousands of years by systematically robbing them of their honey. The least we can do is take proper care of these wondrous creatures. Instead we are killing them off in their billions through our befouling of their environment. The honeybee brain has only a million or so neurons, several orders of magnitude less than ours. It is a moot point as to whether humans or honeybees make the best use of their neuronal resource.