Bears have remarkable senses of smell, but can’t put those scents in odor.
When it comes to detecting odors, bears are reportedly among the best, with more scent receptors per square inch of olfactory epithelium than any other terrestrial vertebrate. Black bears have been observed traveling 18 miles in a straight line to a food source. Grizzlies can reportedly find an elk carcass underwater. Polar bears are able to smell a seal through sea ice.
Humans are way down the smell scale. Our noses are comparatively smallish and unsophisticated. We have about 1.6 inches of scent-detecting olfactory epithelium lining our nasal passages compared to 26 square inches in some dogs. A bear’s brain is one-third the size of a human’s, but the part devoted to smell detection and interpretation is five times larger.
A recent study by neuroscientists at Bates College in Maine reduced the number of basic odor categories that humans can detect to a mere 10. The categorization is similar to the idea that people differentiate just five elemental tastes: sweet, sour, bitter, salty and umami.
To do so, the researchers crunched 30 years of data that profiled 144 distinct odors, then asked human subjects to assess these odors. The sniffers were given a list of 146 words, such as honey, rose and fecal, and asked to rate how well each word described each odor. The scientists were looking to see if the odors could be condensed by word descriptions and patterns.
The end result was the 10 basic odor categories: fragrant, woody/resinous, minty/peppermint, chemical, lemon, fruity (non-citrus), sweet, decayed, pungent and popcorn. For example, reported the Los Angeles Times, specific odors like lavender, soap and cologne all fall into the “fragrant” category while freshly cut grass and mushrooms are “woody/resinous” and kerosene and ammonia are “chemical.”
What qualifies as “popcorn?”
Butter, molasses and fried chicken.
Egyptian mummy heads. Image courtesy of American Exhibitions, Inc.
TB or not TB: that’s really not a question
Tuberculosis is an ancient scourge, but new research by researcher Sebastien Gagneux and colleagues at the Swiss Tropical and Public Health Institute in Basel suggests the disease’s association with humans is much older than previously thought.
TB, according to Gagneux’s findings in Nature Genetics, has been a close and problematic companion of humanity for more than 70,000 years, long before our ancestors even migrated out of Africa.
We have a decidedly distinct and painful relationship with Mycobacterium tuberculosis, the microbe that causes TB. It is an exclusively human pathogen, unable to survive in any other host or reservoir. At the same time, TB has long been exceedingly proficient at killing the very species it needs to survive.
Throughout recorded human history, there are references to its common proclivity to kill, under a variety of names: consumption, phthisis, scrofula, the White Plague. Evidence of deadly TB infections can be found in Neanderthal fossils. It’s estimated that 20 percent of all deaths in Europe during the 19th century were due to TB.
Gagneux’s research suggests that TB’s ability to persist despite its murderous ways may lie with its tendency to go dormant in some hosts, sometimes for decades. By doing so, it ensures that it doesn’t kill every host, which would be problematic in small populations – as was the case among early humans.
Long latency periods make TB hard to control, a fact evidenced by the disease’s continued plaguing of humanity. M. tuberculosis causes 8 to 9 million cases of infection each year, and upwards of 2 million deaths, primarily in Africa, Eastern Europe and the former Soviet Union.
While the specter of drug-resistance is becoming increasingly worrisome, the standard therapy for TB of antibiotics remains largely effective. But it involves a rigorous regimen of treatment that the patient must follow without fail.
“TB can be cured with an antibiotic regimen,” said Richard Garfein, PhD, MPH, professor in the Division of Global Public Health at the UC San Diego School of Medicine. “But the biggest problem care-givers face, especially in developing countries, is making sure patients are compliant with treatment that takes six months or longer to complete.”
Garfein is part of an effort to apply modern technology to an age-old foe. Working with the Verizon Foundation, he is overseeing a pilot program in which TB patients living in San Diego and Tijuana are observed for treatment adherence via videos sent over secure mobile phones. You can read more here.
Loperamide crystals. Image courtesy of Wellcome Images
The lovely false-colored scanning electron micrograph above by Annie Cavanaugh and David McCarthy depicts lab-induced crystalline loperamide, a drug used to treat diarrhea. Loperamide is an anti-motility medication that works by slowing down the movement of food through the intestine, allowing more time for nutrients and water to be extracted and absorbed back into the body. The remaining material is thus drier and firmer, requiring less frequent trips to the toilet.
Judging from appearances, you’d think the spiky crystalline nature of loperamide might have something to do with its anti-motility ability. (Those pointy ends don’t suggest fast, smooth movements.)
In fact, the action of loperamide is much more complicated. The drug is an opioid receptor antagonist, which works on the mu-opioid receptors in the myenteric plexus, a nerve fiber network in the muscular coat of the large intestine. Loperamide decreases myenteric plexus activity by decreasing the muscle tension of longitudinal smooth muscle while simultaneously boosting the tone of circular smooth muscle in the intestinal wall.
In other words, it slows the sequential intestinal contractions (peristalsis) that push food through that part of the digestive tract.
Treating of diarrhea effectively is a significant medical goal. The condition is a common and problematic symptom of many diseases, including cancer, and, ironically, an adverse side effect of some treatments.
Diarrheal disease is a major public health threat in its own right. According to the World Health Organization, it is the leading cause of malnutrition in children worldwide under five years old and the second leading cause of death for that age group. Each year, diarrhea kills approximately 760,000 children under the age of five.
An abscessed tooth
It makes my teeth hurt
Even with the best of oral hygiene, your mouth is full of microbial activity, with approximately 700 known species enjoying a variety of habitats – teeth, tongue, cheeks, tonsils, the gingival sulcus. That’s not a bad thing in a healthy human oral microbiome. Indeed, various studies indicate some species of oral bacteria provide health benefits elsewhere in the body, such as probiotic resistance to upper respiratory infections.
The flip side, of course, is that poor oral health can translate into poor health overall. Periodontitis, for example, involves the erosion of tissue and bone that support teeth, making it easier for nasty oral pathogens to enter the bloodstream. Some oral microbes have been linked to the formation of atherosclerotic plaque in arteries and the heart, which can lead to heart attacks.
In 2007, a 12-year-old boy named Deamonte Driver died after bacteria from an abscessed tooth spread to his brain. The story attracted widespread media coverage because, apart from being a cautionary tale, it seemed quite rare.
But a new study by Boston researchers, published in the Journal of Endodontics, suggests that preventable tooth infections are not rare, and are in fact sending hundreds of thousands of patients to the emergency rooms each year.
One particular villain is a periapical abscess, which occurs when an untreated dental carie or cavity bores through protective enamel to reach the tip of the tooth’s root. It may result in a host of problems, including fever, malaise and nausea. The tooth is usually a goner, typically removed via a root canal treatment.
The Boston study looked at national patient data from 2000 to 2008, and found that the number of people hospitalized with tooth abscesses increased 40 percent, from 5,757 in 2000 to 8,141 in 2008. Sixty-six of the patients subsequently died.
Abscessed teeth, however, are just part of the problem. In 2012, the Pew Charitable Trusts estimated that preventable dental problems prompted more than 830,000 emergency room visits in 2009, up 16 percent from 2006. Pew researchers estimated that translated into $859.9 million in added health care costs.
Now go brush your teeth.
Cases of Lyme disease, like the ticks that transmit it, are ballooning in some parts of the country.
A recent New Yorker article by Michael Specter, entitled “The Lyme Wars,” recounts in gripping detail the troubling efforts of scientists and doctors to curtail the spread and consequences of Lyme disease.
Lyme disease is spread by tick bite. More specifically, by the bite of ticks http://www.cdc.gov/lyme/transmission/ carrying the bacterium Borrelia burgdorferi. Cases of Lyme disease in San Diego County are exceedingly uncommon, but not unheard of.
In much of the rest of the country, however, Lyme disease is a growing public health problem. In 2009, the Centers for Disease Control and Prevention (CDC) reported 38,000 cases, three times more than in 1991, but most observers believed the actual number was much higher.
And, in fact, it is: Earlier this month, the CDC dramatically revised its estimate of infection, reporting that Lyme disease is 10 times more common than previously thought. The new estimate: At least 300,000 Americans contract the disease each year.
That’s worrisome news because Lyme disease remains a highly problematic and poorly understood ailment. As Specter notes, nearly everything about it – symptoms, diagnosis, prevalence, behavior of the bacterial spirochete after it enters the human body from a tick bite and treatment – is either woefully incomplete or wildly in dispute. It was only recently, for example, that researchers debunked an asserted link between Lyme disease and autism.
Specter’s article, buttressed by the CDC’s new infection numbers, does not paint a particularly encouraging picture. Until 1977, when Lyme disease was definitively described for the first time by a Yale University rheumatologist named Allen Steere, the condition was essentially unknown. Much research obviously remains to be done. There are many more questions than answers.
On the hopeful front, however, there’s this: Researchers in May reported that a vaccine for Lyme disease that is currently in clinical trials appears promising, with significant effectiveness against all of the targeted tick species that carry Borrelia. Success can’t happen fast enough.
The clock is ticking.
A bee delivers both sting and a dose of melittin, the active component in its venom.
Poking holes for good and bad
The active ingredient in bee venom is melittin, a peptide that does its damage by increasing the permeability of cell membranes to ions. In other words, it pokes holes in cells, allowing their contents to leak out.
In small doses, the pore-inducing effects of melittin are temporary. The holes close up. But recent research out of Rice University suggests that at higher concentrations, the pores stabilize and stay open. And at even greater exposures, melittin can cause cell membranes to dissolve altogether.
So add melittin to the list of candidates for a new class of drugs intended to attack and kill bacteria, cancer cells and other targets by lethal puncture. Such drugs don’t exist yet, but their attractiveness is undeniable.
“This strategy of opening holes in the cell membrane is employed by a great number of host-defense antimicrobial peptides, many of which have been discovered over the past 30 years,” says Huey Huang, lead investigator of the Rice study.
“People are interested in using these peptides to fight cancer and other diseases, in part because organisms cannot change the makeup of their membrane, so it would be very difficult for them to develop resistance to such drugs.”
One major hurdle has been figuring out exactly how melittin and similar peptides work. The Rice researchers provide some clues. They created synthetic membrane-enclosed structures similar in size to living cells (dubbed giant unilamellar vesicles or GUVs), filled them with dye, immersed them in solution containing melittin and then filmed the action with time-lapse video.
The peptide, which was labeled with a green fluorescent protein, almost immediately began sticking to GUVs. Within two minutes, so much melittin bound to the outer membrane of the GUVs that their surfaces began to change to accommodate the load. Openings formed and dye began to leak out.
The Rice research advances similar work on-going in lots of places. For example, researchers at Washington University in St. Louis reported earlier this year using nanoparticles filled with bee venom to kill human HIV cells without harming surrounding cells.
Naturally, there’s a flip side to all of this therapeutic experimentation. Toxins like melittin pose an inherent health risk as well. Think MRSA, E. coli and snake venom. They all cause harm by poking holes in cell membranes.
So there’s also a need for a way to sop up these toxins before much damage is done.
Researchers at the UC San Diego Jacobs School of Engineering have created nanosponges capable of removing toxins from the bloodstream. Unlike other anti-toxin platforms that must be custom synthesized to individual toxin types, these sponges absorb a broad class of toxins. You can read more here.
A transmission electron micrograph (false color) depicting a neuron from a patient who suffered from Alzheimer’s disease. The cell nucleus is green, the body of the cell yellow and the surrounding tissue blue. Filaments that form neurofibrillary tangles – a hallmark of AD – are colored red. Image courtesy of Thomas Deerinck, NCMIR
Why don’t we all get Alzheimer’s disease?
Alzheimer’s disease afflicts an estimated 5 million Americans, with the number projected to triple by 2050. Currently, no therapy has been shown to slow the progression of the neurodegenerative disease, let alone cure it. The last drug to even temporarily ease symptoms of AD – memantine – was approved a decade ago.
These are worrisome facts that fuel profound questions and concerns, not least among them whether we can afford not to find a remedy.
But the dilemma presents an altogether different question as well: Why don’t we all get Alzheimer’s disease?
The happy reality is that the vast majority of people will never develop the devastating neurological condition. Subhojit Roy, MD, PhD, an associate professor in the departments of Pathology and Neurosciences at the UC San Diego School of Medicine, and colleagues recently proposed an answer in a paper published in the journal Neuron.
As it turns out, every brain cell possesses the ingredients necessary to spark AD, but nature has wisely devised ways to keep the explosive cellular ingredients apart.
“It’s like physically separating gunpowder and match so that the inevitable explosion is avoided,” said Roy, a cell biologist and neuropathologist in the Shiley-Marcos Alzheimer’s Disease Research Center at UC San Diego. “Knowing how the gunpowder and match are separated may give us new insights into possibly stopping the disease.”
The main players are a pair of proteins called APP and BACE-1, both abundant in the brain but largely kept apart from one another. In AD, said Roy, these proteins too often combine with calamitous consequences.
You can read the full news release and watch a video here.
Bologna dropped on a kitchen floor can bear an unsettling resemblance to Petri dishes containing Salmonella bacteria.
Eat. Think. And be wary.
Most folks know the “five-second rule,” an unwritten convention that says if you drop a food item on the floor it may be picked up, dusted off and safely consumed within that designated amount of time.
Apparently this assumes microbes need at least six seconds to make the jump.
In recent years, the scientific integrity of the five-second rule has come under occasional empirical scrutiny.
In 2003, for example, a team of scientists at the University of Illinois at Urbana-Champaign, led by a high school senior Jillian Clarke on a six-week summer internship, investigated the phenomenon. Initially stumped by a lack of working bacteria (they could find no floors on campus with sufficient quantities of indigenous pathogens), the researchers resorted to a controlled experiment in which they coated tiles with a broth of Escherichia coli, a generally harmless intestinal bacteria with the exception of a few strains like E. coli O157:H7 that can cause severe abdominal cramps, diarrhea and vomiting. Clarke and colleagues then dropped Gummy Bears and Fudge Striped cookies on them for specified amounts of time.
They found that large numbers of bacteria did in fact transfer to the fallen food within the five-second limit, but given their earlier, futile efforts to find floors sufficiently rife with pathogens, they concluded that the five-second rule was not incontrovertibly repudiated.
This was a good thing given some of their ancillary findings. In an accompanying survey, Clarke reported that 56 percent of males admitted to invoking the five-second rule, and a whopping 70 percent of females. (It was not determined what percentage of food dropped by women was then given to men.) All of the respondents acknowledged that they were more likely to invoke the five second rule for a piece of candy than for a dropped vegetable.
Clarke’s ground-breaking research was followed up in 2007 by a pair of science majors at Connecticut College who swiped apple slices and Skittles across the floors of the college dining hall and snack bar for predetermined intervals of five, 10, 30 and 60 seconds. They found, oddly enough, that bacteria didn’t transfer in measurable numbers to apples until almost a minute had elapsed. It took microbes almost five minutes to climb aboard Skittles.
But the Connecticut College findings were almost immediately rebuffed by a 2007 Clemson University study by food scientist Paul Dawson and colleagues in which slices of bread and bologna were exposed to various sample surfaces – wood, tile, nylon carpet – coated with Salmonella, a major source of foodborne illness.
Contrary to all earlier findings, Dawson’s team found that pathogenic Salmonella not only have no problem contaminating dropped food, they do it very quickly. Within five seconds, both meat and bread had picked up 150 to 8,000 bacteria. After a minute, the numbers were increased tenfold. Tile and carpet transferred the most microbes.
According to experts, it takes fewer than 100 E. coli or 10 Salmonella bacteria to constitute an infectious dose. A later report out of Manchester Metropolitan University found that dropped foods with higher moisture content more easily assumed microbial pathogens than drier comestibles. Sugary foods attracted (and promoted) microbes more than salty foods.
So does the five-second rule have any validity?
Well, given the ubiquity of bacteria in and around us (an estimated 100 billion in your mouth at any moment; 7 billion on a kitchen sponge), there’s some argument to be made that we have evolved sufficient immune defenses to tolerate a microbial dollop to fallen food.
On the other hand, a 2008 University of Arizona study found that 93 percent of examined shoe bottoms bore traces of fecal bacteria.
It may not be a case of worrying about where dropped food has been but rather what’s been walking (and now residing) on that floor.
False-color scanning electron micrograph of artery containing red blood cells.
Blood thicker than oughter
They should. Hypertension, which essentially means blood pressure within arteries is higher than normal, forcing the heart to work harder than normal to push blood through the body’s circulatory system, is a major risk factor stroke, myocardial infarction (heart attacks), heart failure, aneurysms, peripheral arterial disease and a cause of chronic kidney disease.
Even moderate elevation of arterial blood pressure is associated with a shortened life expectancy.
Much is known about how to remedy the situation. Lifestyle changes can do a lot: Maintaining a healthy body weight, getting regular exercise, managing stress, limiting alcohol consumption, not smoking and eating a healthy diet high in fruits and vegetables and low in saturated fats, trans fats, cholesterol and salt.
Much less is known about the fundamental mechanics of hypertension. Indeed, 90 to 95 percent of hypertension cases are categorized as “primary,” meaning there is no obvious underlying cause.
A little bit of hypertension’s mystery, however, may have been stripped away in a new paper by researchers at the UC San Diego School of Medicine, San Diego Supercomputer Center and UC San Diego Moores Cancer Center.
Writing in the journal Bioorganic and Medicinal Chemistry, lead author Igor F. Tsigelny, PhD, and colleagues describe designing new compounds that mimic naturally occurring molecules in the body that regulate blood pressure. The most promising of these may provide the key to controlling hypertension by switching off the signaling pathways that lead to the condition. You can read the whole news release here.
Epithelial cells of the intestine colored by fluorescent proteins. Image courtesy of Hans Clevers, Hubrecht Institute
Showing some guts
On an organ-izational chart, your intestines aren’t likely to draw the same attention as, say, your heart or brain, but they too are marvels of nature and activity. For one thing, much of what constitutes you lives in your gut.
The average human body contains roughly 100 trillion cells, but only one in 10 of those cells is, well, human. The rest are bacteria, viruses and other microorganisms.
A majority of these non-human cells reside in the gut, representing 500 to 1,000 species. For the most part, your gut flora perform valuable services to their host: extracting vitamins, converting foods into energy, generally aiding digestion and keeping nastier bugs at bay. It’s a thankless job, and temporary at that: up to 60 percent of dry fecal matter is composed of excreted bacteria.
Non-human microbes, though, aren’t the only intestinal occupants stuck on the workplace treadmill. While many of the tissues in your body are constantly renewing – you shed an estimated 30,000 to 40,000 skin cells every hour; getting an entirely new skin roughly once a month – no place turns over its employees more rapidly than the lining of your gut.
The epithelial cell lining of the human intestine lasts about a week. These cells begin their brief work lives in deep pits called crypts. As they get older, they are pushed up the sides of tiny projections called villi, which protrude into the intestinal space and multiply exponentially the active surface area of the intestines. Once an epithelial cell has climbed to the top, it dies, detaches and joins the progression of dead bacteria and other biological flotsam on the road to excretion. It’s not much of a career. Neurons, by comparison, can live as long as you do.
Scientists know much about how this process works through clever technologies like the one that produced the image above. Researchers induced stem cells in the intestinal crypts to randomly switch on one of four fluorescent proteins (red, yellow, green or blue) in each newly minted intestinal epithelial cell.
After that, it’s just a matter of tracking and tracing these cells back to their creators.