TO YOUR HEALTH

By Pam Eastlick

TO YOUR HEALTH

By Pam Eastlick

Welcome to The Deep science and technology column where we cover topics from the deep sea to deep space and beyond. Visit our website at www.thedeepradioshow.com

Greetings and welcome to another romp through the annals of science. This week, we’re visiting the medical file and learning more about the stuff that makes us sick. And our first question is, How long has it been since you went to the dentist? As it turns out, not only is it good for your teeth, it’s also good for your heart.

TAKING A BITE OUT OF HEART DISEASE

Scientists have known for quite a while, that a protein associated with inflammation (called CRP) is elevated in people who are at risk for heart disease. But where’s the inflammation coming from? A new research study by Italian and British scientists shows that those sore and painful infected gums may be one place. According to the study, proper dental hygiene should reduce the risk of arteriosclerosis, stroke and heart disease independently of other measures, such as managing cholesterol. The researchers say that something as simple as taking good care of your teeth and gums can greatly reduce your risk of developing several serious diseases.

To reach this conclusion, the scientists examined the carotid arteries of 35 otherwise healthy people (median age 46) with mild to moderate periodontal disease before and after having their periodontal disease treated. One year after treatment, the scientists observed a reduction in oral bacteria, immune inflammation and the thickening of the blood vessels associated with arteriosclerosis.

Because of our vast love of sweets here in America (more on that later), many of us have gum disease. It turns out that the health of our blood vessels could be hanging by the proverbial thread: dental floss.

Have you flossed lately? Researchers have also recently come up with new ways to deal with those pesky disease-causing bacteria. Read on!

POKING HOLES IN THE PROBLEM

We are at constant war with the disease bacteria and though they have no brains to think with; their sheer numbers often overwhelm us. They have other weapons too. For instance, to protect themselves from human defenses, disease-causing bacteria have evolved a cell wall made from a nearly impenetrable tangle of tightly woven strands that has made it difficult for scientists to see what goes on inside these potentially deadly organisms. But that era is now over. Rockefeller University researchers have now figured out how to drill holes through the Kevlar-like hide of gram-positive bacteria without obliterating them, and in doing so, they’ve made it possible to study, from the inside out, most of the known bacteria on the planet.

The work, led by Vincent A. Fischetti, head of the Laboratory of Bacterial Pathogenesis and Immunology, provides, for the first time ever, a look inside the rapidly multiplying and highly contagious Streptococcus pyogenes, the culprit behind a myriad of diseases, including strep throat and rheumatic fever. At a time when organisms are increasingly acquiring “superbug” powers, Fischetti has used the technique to look specifically at a well-known enzyme called sortase A and its distribution inside the cell. Common to all gram-positive bacteria, the enzyme functions by allowing these bacteria to anchor to your cell walls and breach their defenses.

If you can keep the bacteria from attaching to cell walls, they can’t cause infections. So if the researchers can figure out how sortase A works inside the cell, the more ways they can keep the bacteria from attaching. Although the researchers worked with S. pyogenes, the approach could work on any gram-positive bacteria such as methicillin-resistant Staphylococcus aureus, or MRSA, which is increasingly becoming resistant to even our strongest antibiotics.

The technique relies on enzymes produced by viruses, called bacteriophages, which attack only bacteria. Unlike antibiotics, which take time to take effect, phage enzymes strike with blitzkrieg speed, preventing bacteria from mustering a defense. Normally, these enzymes destroy their target, leaving nothing but cellular debris behind. That’s because the pressure inside a bacterium is like a champagne bottle: Once it’s opened, it explodes.

Dr. Fischetti figured out how to poke holes in S. pyogenes while keeping the bacteria intact. These holes provide an entryway for chemicals that fluoresce when they attach to molecules inside the altered bacteria, allowing scientists to visualize, from the inside out, what makes these single-celled powerhouses infectious.

In the past, if scientists wanted to study what goes on inside bacteria, they were largely limited to working with nonpathogenic types whose cell walls could be punctured with established methods. The new technique, however, allows them to directly study pathogenic bacteria and ask specific questions about them.

The research is ongoing and the scientists on the project have already discovered that sortase A is involved not only in the structures of the cell wall, but also in the division process in the bacteria.

Since strep bacteria divide every 20 or 30 minutes under optimal conditions knowing how to stop or slow down the division could be very important. And scientists now have a new awl in their toolbag, to punch some very important holes!

Seeing through walls. An experiment shows that when dividing strep bacteria are stripped of their surface proteins (left), they begin to grow back in just minutes. One surface protein, protein M (green), anchors to the spot where sortase A (red) assembles. Before the bacteria finish dividing (right), sortase A has already begun to migrate to the new site of division. (Credit: Image courtesy of Rockefeller University)

If you’re an avid reader of this column (and I know you all are!) you already know that I have issues with MRSA, the superbug mentioned in the last item. And I know all about the division rate because a MRSA infected bite on my side came within millimeters of punching a hole through my plural lining and into my lungs and it happened in less than 48 hours. So, the next article is of personal interest to me!

SHEDDING SOME LIGHT ON THE SUBJECT

Scientists from the New York Institute of Technology have recently demonstrated that two common strains of methicillin-resistant Staphylococcus aureus, (commonly known as MRSA), were virtually eradicated in the laboratory by exposing them to a wavelength of blue light, in a process called photo-irradiation.

Antibiotic-resistant bacterial infections represent an important and increasing public health threat. Penicillin is completely ineffective on 95% of the various strains of Staphylococcus while approximately 40%-50% of S. aureus strains have developed resistance to newer antibiotics like methicillin as well.

The NYIT researchers had previously shown that when you exposed lab-cultured MRSA to blue light with a wavelength of 405-nm, the bugs died. The problem is that 405-nm blue light is in the ultraviolet range. Now they’ve used blue light with a wave length of 470-nm and have discovered that that kills MRSA as well.

The two MRSA populations studied (the US-300 strain of CA-MRSA and the IS-853 strain of HA-MRSA) represent prominent community-acquired and hospital-acquired strains, respectively. The authors reported that the higher the dose of 470-nm blue light, the more bacteria were killed. High-dose photo-irradiation was able to destroy 90.4% of the US-300 colonies and the IS-853 colonies.

Since MRSA lives on surfaces, a blue light bath should kill large numbers of the little buggers. The effectiveness of the blue light treatment also suggests that it could be effective on people as well, particularly in skin infections of the disease.

Perhaps someday soon, every hospital room, examination room, operating room and treatment room will be equipped with blue lights. They could be left on overnight if their light was annoying to people and they could work at destroying MRSA, using mechanisms that wouldn’t lead to further antibiotic resistance. Gives a whole new meaning to “Blue Light Special”, doesn’t it?

And for our last little item, we come to something I’ve long suspected. You just have to look at all the sodas, King Car tea and beer that are everywhere on this island; and then look at island waistlines.

THE SODA CAN AS SMOKING GUN

According to scientists at the Johns Hopkins Bloomberg School of Public Health, when it comes to weight loss, what you drink may be more important than what you eat. Researchers examined the relationship between beverage consumption among adults and weight change and found that weight loss was positively associated with a reduction in liquid calorie consumption and liquid calorie intake had a stronger impact on weight than solid calorie intake.

The researchers discovered that a reduction on calorie intake for both liquids and solids caused weight loss initially but at the six-month follow-up, only reduction in the liquid calories made any difference. Of the seven types of beverages examined, sugar-sweetened beverages were the only beverages significantly associated with weight change.”

Researchers conducted the study using 810 adults aged 25-79 years old. They measured their height and weight at 6, 12 and 18 month intervals. Their dietary intake was measured by calling the participants periodically and asking them about their caloric intake during the previous 24 hours.

Researchers divided beverages into several categories based on their calorie content and nutritional composition. There was sugar-sweetened beverages (regular soft drinks, fruit drinks, fruit punch, or high-calorie beverages sweetened with sugar), diet drinks (diet soda and other “diet” drinks sweetened with artificial sweeteners), milk (whole milk, 2 percent reduced-fat milk, 1 percent low-fat milk, and skim milk), 100 percent juice (100 percent fruit and vegetable juice), coffee and tea with sugar, coffee and tea without sugar and alcoholic beverages. They discovered that sugar-sweetened beverages were the leading source of liquid calories. (Hmm . . . no surprises there!)

Liquid calorie consumption has increased in parallel with the obesity epidemic. Earlier studies by Bloomberg School researchers project that 75 percent of U.S. adults could be overweight or obese by 2015 and have linked the consumption of sugar-sweetened beverages to the obesity epidemic . Obesity affects two-thirds of adults and increases the risk for adverse health conditions such as type 2 diabetes. The researchers recommend limited liquid calorie intake among adults and to reduce sugar-sweetened beverage consumption as a means to accomplish weight loss or avoid excess weight gain.

So . . . are you sitting there reading this with that coke can in your hand or that big bottle of King Car? Do you realize that the King Car bottle contains over a QUARTER CUP of sugar? Do you still wonder why you can’t lose weight?

And if you decided that you really couldn’t stand diet soft drinks back in the day, I suggest you give them a try again. Most diet soft drinks are sweetened with protein sweeteners and guess what? Protein denatures at high temperatures and if you let those soft drink pallets sit out on the dock; they get hot. The protein denatures and the drinks taste AWFUL!

Although there’s been no publicity, the shippers did finally figure this out and as near as I can tell, most of the diet drinks now arrive on Guam with their sweeteners intact. So give the diet drinks another try. You might be surprised. And you’ll probably lose some weight as well!

When it comes to weight loss, what you drink is more important than what you eat!

Cruise on over to the Deep Website at www.thedeepradioshow.com to learn more about your health and many other topics. Enjoy!

GETTING MUDDY (IN MORE WAYS THAN ONE)

By Pam Eastlick

GETTING MUDDY 

(IN MORE WAYS THAN ONE)

By Pam Eastlick

Welcome to The Deep science and technology column where we cover topics from the deep sea to deep space and beyond. Visit our website at www.thedeepradioshow.com

I thought I’d start today with a little news update. Do you remember the mud volcano in Indonesia? Well, let’s take a little trip down memory lane because there’s recent news about Lusi. Keep reading! I wrote this first section two years ago, and the figures on size and people displaced have changed. You’ll get the latest figures in the last section of the article.

THE BACKGROUND

I’ve followed with great interest the saga of the Indonesian mud volcano called Lusi that first erupted near Surabaya, the second largest city in Indonesia three years ago in May of 2006. Mud volcanoes are not unheard of. There are at least 2,000 worldwide including one in the Santa Barbara Channel near Redondo Beach California. But the mud volcano in Indonesia may be one of the few caused by humans.

The viscosity of mud volcanoes is wildly variable. Some look like volcanoes with thick mud flowing from a raised central crater, while others simply look like slowly growing mounds of dirt that are squeezed out of a crack like toothpaste. Others erupt mud that is much thinner and this describes what’s flowing out of the ground in Indonesia. Lusi’s mud is about 70% water and instead of mounding up, is flowing disastrously over the countryside. Since Lusi erupted in May 2006, the soupy mud has covered four square miles to a depth of 16 feet in some places, submerged parts of four villages and displaced about 25,000 people.

When the flow started in May of 2006, Lusi was erupting about a quarter of a million cubic feet of mud every single day. Now, however, the rate has increased to over 5 million cubic feet a day and it shows no sign of stopping anytime soon. In addition, scientists predict that if the underlying mud is drained, the land above it will begin to sag and there may be a dramatic collapse into the empty hole left behind. (Lusi is already sinking and may in fact form that gigantic hole.)

So, what caused Lusi? Lusi erupted from a gas well that was operated by Lapindo Brantas, Inc. one of Indonesia’s biggest oil companies. And we have two interesting opinions about what caused that eruption. On the one hand, we have a statement from Indonesia’s coordinating minister for social welfare, Aburizal Bakrie. He says the volcano is a “natural disaster” unrelated to the drilling activities. Mr. Bakrie stated, “It is not because of the Lapindo drill case but it is because of the quake.” He was referring to an earthquake that occurred two days before the Lusi eruption near the ancient city of Yogyakarta that killed around 6,000 people.

Now that ‘drill case’ he mentions is in response to a finding made by a team led by British scientist Richard Davies, a professor at the University of Durham’s Center for Research into Earth Energy Systems in northeastern England.

That study reported that the kind of drilling done by Lapindo in the geographical regions into which they drilled requires the use of steel casing to support the borehole, to protect against the pressure of fluids such as water, oil or gas.

Mr. Davies reported in a press release; “In the case of Lusi, a pressured limestone rock containing water — a water aquifer — was drilled while the lower part of the borehole was exposed and not protected by casing. As a result, rocks fractured and a mix of mud and water worked its way to the surface. Our research brings us to the conclusion that the incident was most probably the result of drilling.”

So was it drilling or was it the earthquake? Does it make a difference when I tell you that Mr. Aburizal Bakrie, whose job it is to be concerned about social welfare, is one of the wealthiest men in Indonesia and his family firm controls Lapindo Brantas? Apparently that fact made a difference to the president of Indonesia, Susilo Bambang Yudhoyono who ordered Lapindo to pay 3.8 trillion rupiah ($421 million) in compensation and costs related to the mudflow.

Aerial view of Lusi

IT WAS THE DRILLING

In more of the ongoing Lusi story, in 2008, an international team of petroleum geologists met at Cape Town, South Africa and concluded that Lusi was not a ‘natural’ volcano. She’s man-made.

The 74 scientists considered the evidence presented by four experts in the field and then voted on two scenarios. Forty-two scientists voted that Lusi was triggered when Lapindo Brantas, an Indonesian oil company drilled the gas exploration well called Banjar-Panji-1. Only three scientists voted for the alternative explanation. This hypothesis stated that Luisi’s eruption was triggered by an earthquake that occurred two days earlier with an epicenter located 175 miles from Lusi. Sixteen scientists voted that the evidence was inconclusive and 13 said that a combination of earthquake and drilling were the cause.

There was some pretty strong evidence that the drilling triggered Lusi. The key points presented to support the drilling hypothesis were:

· the earthquake was too small and too far away to have been the trigger.

· the well was being drilled when Lusi erupted and is only 500 feet from the volcano site.

· large amounts of water were pumped into the well the day before the eruption, resulting in pressures the sides of the well couldn’t tolerate.

· the pressure measured in the well after the influx provides strong evidence that the well was leaking and even evidence for the initial eruption at the surface.

One of the speakers, leading geologist Professor Richard Davies of Durham University, UK, commented: “The conference allowed us to present new data on the pressures in the well the day before the eruption and these provide a compelling tape recording of the well as it started to leak. We were particularly grateful to Lapindo, the company involved in the drilling, who were widely applauded at the meeting for their willingness to take part in the discussion.”

Prof Davies added: “I remain convinced that drilling was the cause of the mud volcano. The opinion of the international scientists at the event in South Africa adds further weight to my conviction and the conclusions of many other leading scientists who have studied Lusi.”

Susila Lusiaga a drilling engineer and part of the Indonesian police investigation team said: “There is no question, the pressures in the well went way beyond what it could tolerate – and it triggered the mud volcano.”

Michael Manga, Professor of Earth and Planetary Science at the University of California, Berkeley, said: “The key observation from an earthquake perspective is that there were many much larger and quite a bit closer earthquakes that did not trigger an eruption. The Yogyakarta earthquake was simply too small and too far away to initiate an eruption.”

IT WAS THE EARTHQUAKE

Brave words, guys but it didn’t do any good. In the latest news on Lusi, almost three years to the day from the eruption, Indonesia’s supreme court ruled that it had cleared the government and Lapindo of any wrongdoing related to Lusi’s eruption. The mud has now wiped out 12 villages, killed 13 people and displaced more than 42,000 people in the Sidoarjo district of East Java since it burst from a drilling well operated by the Lapindo company on May 29, 2006.

The company, which is connected to powerful Welfare Minister Aburizal Bakrie, has however agreed to pay millions of dollars in damages to help affected villagers rebuild their lives. However, three years later many victims complain they have received only a fraction of the payout.

In a short statement, court spokesman Nurhadi said judges agreed with earlier rulings in lower courts that cleared the company and the government of neglect related to the disaster.

“The Supreme court has rejected an appeal filed by YLBHI,” he told reporters, referring to the Indonesian Legal Aid Foundation. The YLBHI had argued that the government and Lapindo had failed to prevent the disaster and properly compensate thousands of displaced families.

YLBHI lawyer Zainal Abidin said the supreme court’s judgement was a major blow to the victims, many of whom are now unemployed and live in squalid bamboo shacks awaiting full compensation.

“The judges should have taken into consideration the people’s needs. The court has failed to deliver justice,” he told AFP.

Some 800 hectares (1,977 acres) of villages and fertile farming land now lie beneath the stinking, hot sludge, which continues to spew out of the Lapindo well despite the company’s containment efforts. About 6,000 people have been forced to flee their homes since October as the volcano, dubbed ‘Lusi,’ breaks man-made embankments and devours more land, officials said.

But the people who have lost their homes and are in danger of losing their homes to Lusi don’t have to worry. In a stunning show of compassion, Lapindo Brantas came up with the ultimate solution for them. The company funded a soap opera called “Digging a Hole, Filling a Hole.” Set amidst the misery of the mud, “Digging …” was a love story that reportedly shows the virtues of patience – something in short supply these days.

And in the ultimate news update? “Digging . . . “ was NOT a hit in Indonesian TV. Big surprise, huh?

Cruise on over to the Deep Website at www.thedeepradioshow.com to learn more about taking mud baths and many other topics. Enjoy!