- Why some pregnancy diets can actually cause complications

- Why Kegels are completely unnecessary, and how they make giving birth more difficult

- Why semen is surprisingly beneficial for a pregnant woman

- The little-known mistakes that most women make, during labor, that cause intense pain

Dayna Martin shares with you the explicit secrets to a healthy, powerful and Sexy Birth!

Author : Dayna Martin
Binding : Kindle Edition
Format : Kindle eBook
PublicationDate : 2012-02-21
ReleaseDate : 2012-02-21

Alex Gorsky, head of the medical device and diagnostics business, will take over as chief executive. Mr. Weldon will remain as chairman.

The news of Mr. Weldon’s retirement comes as Johnson & Johnson has struggled to emerge from a swarm of product recalls, manufacturing lapses and government inquiries that tarnished the name of a company that was once one of the nation’s most trusted household brands. In 2010, the company recalled millions of bottles of liquid children’s Tylenol and other medications, as well as tens of thousands of artificial hips and millions of contact lenses.

Much of the blame for Johnson & Johnson’s stumbles fell on Mr. Weldon, the son of a Broadway stagehand and seamstress who became chief executive in 2002 after spending his entire career at the company. Critics stated the company’s once-vaunted attention to quality slipped under his watch. The company stated in a statement that neither Mr. Weldon nor Mr. Gorsky was available for comment.

There was tiny doubt that Mr. Weldon, 63, was going to retire this year, stated Erik Gordon, who teaches business at the University of Michigan. “I think what he really wanted to do is clean up his image,” Mr. Gordon said. “He didn’t want to leave at a time when it looked like he was being thrown out.”

Plans for Mr. Weldon’s exit became clear in December 2010, when the company promoted Mr. Gorsky and Sheri S. McCoy to vice chairman and vice chairwoman of the executive committee in what was seen as a race to succeed Mr. Weldon. There were other signs that Mr. Weldon planned to step down: over the past year he has sold more than one million shares of Johnson & Johnson stock; the sales earned him almost $69 million.

In 2011, critics of Mr. Weldon, including a group of shareholders, complained of his compensation of about $30 million a year, saying it ignored his troubled leadership.

Mr. Gorsky, who is 51, was considered the favored candidate, stated Les Funtleyder, a portfolio manager who owns the stock at Miller Tabak & Company. Mr. Gorsky is well-known by the company’s investors. “There is a comfort level with him,” Mr. Funtleyder said. Ms. McCoy will continue to lead the pharmaceuticals and consumer groups, the company said, but analysts stated she may leave after having been passed over.

The ascension of Mr. Gorsky, who first joined Johnson & Johnson as a sales representative in 1988, continues the company’s 126-year tradition of hiring leaders from within. The medical devices division generates the largest amount of sales for the company, and it is expected only to grow with the acquisition last year of Synthes, a Swiss-American medical device maker.

“Alex and Sheri are two extraordinary leaders,” Mr. Weldon stated in a statement Tuesday. “The future of Johnson & Johnson is in very capable hands.”

But Mr. Gordon stated the board’s decision to hire another insider showed that it was not serious about changing the corporate culture that had created so many of its problems.

“I think it’s a huge mistake,” he said.

In the wake of the product recalls, Mr. Weldon and the company went on the offensive, initiating a public relations campaign aimed at restoring consumer confidence and revamping quality controls to create a single framework for the company’s drug, medical device and consumer health care divisions.

“From Johnson & Johnson’s perspective, our response to this issue was the most responsible it could possibly be,” Mr. Weldon stated in a telephone interview in 2010.

Even so, Johnson & Johnson has continued to struggle to put its troubles to rest. As recently as last week, the company announced it would recall about a half-million bottles of liquid Infants’ Tylenol because of a faulty dosing system.

Still, Mr. Weldon’s retirement comes as the company shows signs of improving, stated Jeff Jonas, portfolio manager for Gabelli, which owns the stock for investors. “He’s wanted to stay and get through the worst of it,” he said.

Some products are back on the market, Mr. Jonas said, and the company has a well-defined plan with the Food and Drug Administration to bring the plant that was a source of many of the over-the-counter recalls up to federal standards. A drug to treat prostate cancer, to be marketed as Zytiga, was approved by the Food and Drug Administration last year, and the consumer business is recovering.

Mr. Jonas stated the fact that Mr. Weldon plans to step down in April, during the company’s annual meeting, indicates that his departure was not abrupt. “The annual meeting is always a classic time to do the transition,” he said.

Johnson & Johnson’s stock closed at $65.04 Tuesday, having rebounded from a low of $57.50 a share over the last 12 months.

source : feeds.nytimes.com

The statements in that e-mail contrast with those made by the company in recent years about the all-metal hip. Before recalling the device amid rising failure rates in 2010, Johnson & Johnson insisted it was safe and maintained that its internal studies refuted complaints by surgeons and regulators abroad that the device was flawed. The device turned down by the F.D.A. was only sold overseas, but a companion version that was recalled at the same time by Johnson & Johnson was used in 30,000 patients in the United States.

The e-mail at issue was written in August 2009 by a vice president of a Johnson & Johnson subsidiary, DePuy Orthopaedics, just days after the F.D.A. confidentially notified the device maker that it would not approve one version of the hip for sale in this country. In the e-mail, the executive, Pamela Plouhar, explained the reasons for the agency’s decision to three other top executives, including DePuy’s president at the time, David Floyd.

Ms. Plouhar reported that the device had not met F.D.A. approval standards and that a major concern was its high rate of early failure, or “revision,” during clinical trials. She also cautioned that providing the F.D.A. with more data might not change its stance and that it might take years to conduct new studies of the hip, known as the ASR, or articular surface replacement.

“The team’s concern is that given the revision rate in the ASR group that we will still not be able to demonstrate non-inferiority, with additional downside risk,” Ms. Plouhar wrote.

To win approval, a novel medical device like the DePuy hip must be shown to be reasonably safe and effective. One way to prove that is to show that it is at least as effective as, or not inferior to, a traditional hip implant.

In her e-mail, Ms. Plouhar stated there had been “a significant number of revisions in the ASR group” compared with “very few in the control group.”

Many artificial hips last 15 years or more before they wear out and need to be replaced. But by 2008, data from orthopedic databases overseas showed that the ASR was failing at high rates in patients after just a few years. The device also sheds metallic debris as it wears, particles that have damaged tissue in some patients or caused crippling injuries.

A DePuy spokeswoman, Mindy Tinsley, declined to respond to specific questions about the e-mail. In a statement, she stated that the e-mail was “simply a notification to senior management about the F.D.A. feedback as the company appropriately continued to study data” about the implant so that it could make responsible decisions on the behalf of patients.

Last week, Andrew Ekdahl, the current president of DePuy, stated in a statement issued in response to an earlier article in The New York Times that any implication that the F.D.A. had determined there were safety issues with the device was “simply untrue.”

In her 2009 e-mail, Ms. Plouhar referred to complaints about early failures of the ASR from physicians and regulators abroad. Regulators in Australia were then pressuring DePuy to withdraw the artificial hip from the market there or face having it forced off.

“This comes at a time when ASR data from national registries (Australia and UK) is being closely scrutinized because of higher revision rates,” she wrote.

DePuy does not appear to have violated any laws by not publicly releasing the F.D.A. ruling, which was contained in a so-called nonapprovable letter. The F.D.A., as a matter of policy, does not release such decisions, saying that they may contain confidential business information.

But DePuy’s decision not to publicize the agency’s findings to doctors, patients and others while continuing to market the device may undercut its defense in the 5,000 related lawsuits pending against it and could also tarnish its reputation.

source : feeds.nytimes.com

Gang Ren, a materials physicist and electron microscopy expert with Berkeley Lab’s Molecular Foundry, a DOE nanoscience research center, led a study in which the first structural images of CETP interacting with HDLs and LDLs were recorded. The images and structural analyses support the hypothesis that cholesterol is transferred from HDLs to LDLs via a tunnel running through the center of the CETP molecule.

“Our images show that CETP is a small (53 kilodaltons) banana-shaped asymmetric molecule with a tapered N-terminal domain and a globular C-terminal domain,” Ren says. “We discovered that the CETP’s N-terminal penetrates HDL and its C-terminal interacts with LDL forming a ternary complex. Structure analyses lead us to hypothesize that the interaction may generate molecular forces that twist the terminals, creating pores at both ends of the CETP. These pores connect with central cavities in the CETP to form a tunnel that serves as a conduit for the movement of cholesterol from the HDL.” 

Ren reports the results of this study in a paper in the journal Nature Chemical Biology titled “Structure basis of transfer between lipoproteins by cholesteryl ester transfer protein.” Co-authoring this paper were Lei Zhang, Feng Yan, Shengli Zhang, Dongsheng Lei, M. Arthur Charles, Giorgio Cavigiolio, Michael Oda, Ronald Krauss, Karl Weisgraber, Kerry-Anne Rye, Henry Powna and Xiayang Qiu.

Cardiovascular or heart disease, mainly atherosclerosis, remains the leading cause of death in the United States and throughout the world. Elevated levels of LDL cholesterol and/or reduced levels of HDL cholesterol in human plasma are major risk factors for heart disease. Since CETP activity can reduce HDL-cholesterol concentrations and CETP deficiency is associated with elevated HDL-cholesterol levels, CETP inhibitors have become a highly sought-after pharmacological target for the treatment of heart disease. However, despite this intense clinical interest in CETP, tiny is known concerning the molecular mechanisms of CETP-mediated cholesterol transfersamong lipoproteins, or even how CETP interacts with and binds to lipoproteins.

“It has been very difficult to investigate CETP mechanisms using conventional structural imaging methods because interaction with CETP can modify the size, shape and composition of lipoproteins, especially HDL,” Ren says. “We were successful because we used our optimized negative-staining electron microscopy protocol that grants us to flash-fix the structure and efficiently screen more than 300 samples prepared under different conditions.”

Ren and his colleagues used their optimized negative-staining electron microscopy protocol to image CETP as it interacted with spherical HDL and LDL particles. Image processing techniques yielded three-dimensional reconstructions of CETP and CETP-bound HDL. Molecular dynamic simulations were used to assess CETP molecular mobility and predict the changes that would be associated with cholesterol transfer. CETP antibodies were used to identify the CEPT interaction domains and validate the cholesterol transfer model by inhibiting CETP. This model presents inviting new targets for future CETP inhibitors.

“Our model identifies new interfaces of CETP that interact with HDL and LDL and delineates the mechanism by which the transfer of cholesterol takes place,” Ren says. “This is an important step toward the rational design of next generation CETP inhibitors for treating cardiovascular disease.”

This research was supported in part by the DOE Office of Science, and in part by W. M. Keck foundations, the Chinese Ministry of Education, the National Institutes of Health, and the Tobacco Related Disease Research Program of California.

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It appears that the hormone receptor guanylyl cyclase C (GC-C) — a previously identified tumor suppressor that exists in the intestinal tract — plays a key role in strengthening the body’s intestinal barrier, which helps separate the gut world from the rest of the body, and possibly keeps cancer at bay. Without the receptor, that barrier weakens.

A team led by Scott Waldman, M.D., Ph.D., chair of the Department of Pharmacology and Experimental Therapeutics at Jefferson and director of the Gastrointestinal Cancer Program at Jefferson’s Kimmel Cancer Center, discovered in a pre-clinical study that silencing GC-C in mice compromised the integrity of the intestinal barrier. It granted inflammation to occur and cancer-causing agents to seep out into the body, damaging DNA and forming cancer outside the intestine, including in the liver, lung and lymph nodes.

Conversely, stimulating GC-C in intestines in mice strengthened the intestinal barrier opposing these pathological changes.

A weakened intestinal barrier has been linked to many diseases, like inflammatory bowel disease, asthma and food allergies, but this study provides fresh evidence that GC-C plays a role in the integrity of the intestine. Strengthening it, the team says, could potentially protect people against inflammation and cancer in the rest of the body.

“If the intestinal barrier breaks down, it becomes a portal for stuff in the outside world to leak into the inside world,” stated Dr. Waldman. “When these worlds collide, it can cause many diseases, like inflammation and cancer.”

The role of GC-C outside the gut has remained largely elusive. Dr. Waldman and his team have previously shown its role as a tumor suppressor and biomarker that reveals occult metastases in lymph nodes. They’ve used to it better predict cancer risk, and have even shown a possible correlation with obesity.

Reporting in the Journal of Clinical Investigation, Dr. Waldman colleagues found that silencing GC-C affected appetite in mice, disrupting satiation and inducing obesity. Conversely, mice who expressed the hormone receptor knew when to call it quits at mealtime.

However, its role in intestinal barrier integrity, inflammation, and cancer outside the intestine is new territory in the field.

A new drug containing GC-C is now on the verge of hitting the market, but its intended prescribed purpose is to treat constipation.

This study helps lays the groundwork, Dr. Waldman said, for future pre-clinical and clinical studies investigating GC-C’s capabilities beyond those treatments in humans, including prevention and treatment of inflammatory bowel disease and cancer.

“We’ve shown that when you pull away GC-C in animals, you disrupt the intestinal barrier, putting them at risk for getting inflammatory bowel disease and cancer. And when you treat them with hormones that activate GC-C it helps strengthen the integrity of the intestinal barrier,” Dr. Waldman said. “Now, if you want to prevent inflammation or cancer in humans, then we need to begin thinking about feeding people hormones that activate GC-C to tighten up the barrier.”

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The findings may help explain why risk of drug abuse and addiction increase so dramatically when cocaine use begins during teenage years.

The results were published in the Feb. 14 and Feb. 21 issues of the Journal of Neuroscience.

Researchers including those at Yale have shown that vulnerability to cocaine is much higher in adolescence, when the brain is shifting from an explosive and plastic growth phase to more settled and refined neural connections characteristic of adults. Past studies at Yale have shown that the neurons and their synaptic connections in adolescence change shape when first exposed to cocaine through molecular pathway regulated by the gene integrin beta1, which is crucial to the development of the nervous system of vertebrates.

“This suggests that these structural changes observed are probably protective of the neurocircuitry, an effort of the neuron to protect itself when first exposed to cocaine,” stated Anthony Koleske, professor of molecular biophysics and biochemistry and of neurobiology and senior author of both papers.

In the latest study, Yale researchers report when they knocked out this pathway, mice needed approximately three times less cocaine to induce behavioral changes than mice with an intact pathway.

The research suggests that the relative strength of the integrin beta1 pathway among individuals may explain why some cocaine users end up addicted to the drug while others escape its worst effects, Koleske theorized.

“If you were to become totally desensitized to cocaine, there is no reason to seek the drug,” he said.

Koleske and Jane R. Taylor, professor of psychiatry and psychology and an author of the Feb. 14 paper, are teaming up with other Yale researchers to look for other genes that may play a role in protecting the brain from effects of cocaine and other drugs of abuse.

Shannon Gourley, now of Emory University who worked with Koleske and Taylor, is lead author on the Feb. 14 paper detailing how the structural response to cocaine protects against cocaine sensitivity. Anastasia Oleveska and Michael S. Warren are other Yale authors on this paper. Warren and William D. Bradley of Yale are co-lead authors of the latest Neuroscience paper describing the role for integrin beta 1 in the control of adolescent synapse and dendrite refinement and stability. Yu-Chih Lin, Mark A. Simpson, Charles A. Greer are other Yale-affiliated authors.

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Dan and Tom Heyerman stopped drawing “Pants are Overrated” late in 2011. I noticed.

The Heyermans’ on-line comic strip was about two brothers who know much too much about each other (not surprising, since Dan and Tom are in fact, brothers), who get comfortable by throwing off their office clothes — especially pants — and spend time having wonderfully meaningless, insignificant adventures.

Dan, for example, would fall in love not with a girl but with his Canon camera and try to kiss it on the lens when his brother is not looking. That kind of thing.

The strip was fun — actually pretty good — and then one day, out of the blue, they concocted something that made me gasp. They decided to update Watterson’s “Calvin and Hobbes” strip, by imagining Calvin as a grown-up, 26 years after his being 6. That would make him 32, And in their imaginations, he is married the girl up the block, Susie Derkins, and they now have a tiny girl. Her name is Bacon.

Bacon, named for Sir Francis Bacon, an enlightenment scientist, is also 6, Calvin’s age. And Hobbes, of course, is still a working tiger/philosopher, who comes to life for Those Who Believe In Him.

These attempts to reimagine the classics rarely work, because classics are classic. What Bill Watterson did for 10 years was genius. The brothers know it. Plus, their homage was a trespass; loving, yes, but unauthorized, and lord knows what Watterson would think of it. But the thing is, they somehow got close.

They did only two strips, called “Hobbes and Bacon” (see my earlier blog post), which went instantly viral. Sure, some people screamed, “How dare you!” but many more just sighed, “Oh, my … oh yes …” We all miss Calvin. And like bedtime chocolates on your hotel pillow, how could we not gobble up these two tiny sweets, wonderfully called “Bacon.”

Just two. Then, Dan and Tom went back to their brotherly adventures, until last fall, when they decided, like Bill, to retire. They announced the end of “Pants are Overrated” in September, and then, in October, just before disappearing, they gave us two more.

I know, I know. I shouldn’t. They shouldn’t. We shouldn’t look. We should respect our hero Bill. But I am weak. And these two strips made me tear up a little, and think, “Oh my … oh yes.”

And then there is this one, which got to me because I secretly suspect that when Calvin is 80 years old, he will, in some essential way, still be Calvin.

source : www.npr.org

Fruit flies will drink alcohol from fermenting fruit to kill off wasp parasites that can grow inside of them.

As humans, we sometimes pay a price for drinking alcohol — in hangovers, or worse. But if you happen to be a young fruit fly, it turns out that alcohol can be just what the physician ordered.

The pesky tiny fruit flies often show up when apples or bananas are left sitting around for too long on the kitchen counter. Most folks find them annoying, but Todd Schlenke cannot get enough of them.

“I’ve been collecting flies in my backyard for a long time, sort of as a hobby,” states Schlenke, an evolutionary geneticist at Emory University. He studies fruit flies and their mortal enemy: tiny parasitic wasps.

“These tiny wasps lay their eggs in the fly, and if the fly is not able to kill them, the wasps hatch out and eat the flies from the inside out,” Schlenke says. He states since fruit flies lay their eggs on rotting, fermenting fruit, the larvae that hatch can sometimes find themselves swimming in alcohol.

And that, Schlenke says, got him thinking: “I wonder if the alcohol can be used by the flies to protect them from being killed by the wasps.”

Schlenke states the first thing he needed to do was test how well the wasps could hold their liquor. It turns out some wasps cannot even handle inhaling the fumes. No, they do not begin slurring their words and hitting on that adorable firefly at the end of the bar. But close.

“They basically get drunk. They cannot stand upright, and they cannot perform their normal functions, which is to lay a bunch of eggs in fly larvae and try to complete their life cycles,” he says.

That means wasps are less likely to attack flies swimming in boozy fruit juices. But what if a wasp does succeed in laying its eggs inside a young fly? Schlenke found that if the fly larvae drink the alcohol, they can actually kill off the wasps developing inside them.

“And so the next question we asked was: Do flies know that? Do they purposefully consume alcohol once they are infected, in order to kill those wasps living inside of them? So we gave the flies a choice,” he says.

In one half of the Petri dish, a delicious cocktail of baker’s yeast, molasses and 6 percent alcohol. In the other half, the alcohol-free version. Infected flies overwhelmingly chose the booze.

“Essentially the fruit flies are self-medicating,” Schlenke says. “They realize when they are infected, and they are seeking out a substance that helps cure them of that infection. And in this case that substance is alcohol.”

Self-medicating exists all over the animal kingdom. Insects, birds and primates all have been known to eat special plants to rid themselves of parasites or other ailments. But, states Schlenke, this is the only situation that he knows of that has critters using alcohol as a medicine.

Can Drinking Kill Parasites In Humans?

And that raises the question: What about humans? After all, we get our share of parasitic diseases, too — everything from hookworm to malaria. Could alcohol help us get rid of parasites?

We posed the question to Peter Hotez, the dean of the National School of Tropical Medicine at Baylor College of Medicine in Houston. He’s also president of the Sabin Vaccine Institute, which develops vaccines for parasitic infections.

Is there any chance that someone infected with, say, the malaria parasite might find a cure in a night of binge drinking?

Hotez states no. “It seems to actually have the opposite impact,” he says, adding that studies of alcoholics show that chronic drinking can make some parasitic infections much worse.

But what about just a tiny alcohol? Can that help?

“The answer, as far as we can tell, is no,” Hotez says. “The closest thing that comes to it is the gin and tonics that were used during the British colonial days to treat malaria. It was not because of the gin — it was because of the tonic, which contained quinine, which had an anti-malarial effect.”

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We’re going back in time now, almost 32,000 years. Scientists in Russia have cultivated a plant from seeds that were buried by squirrels in Ice Age Siberia. The narrow-leafed kampion is blooming again, a small plant with thin green leaves and delicate white flowers. It’s believed to be the oldest plant ever grown from ancient tissue.

One person who believes the research is Grant Zazula. He investigates claims of ancient seeds with the Yukon paleontology program in White Horse, Canada. He joins us now to speak more about this latest discovery. Hi there, Grant.

DR. GRANT ZAZULA: How you doing?

CORNISH: Good. So begin by telling us about sort of the period and the place where these seeds came from and how they have survived all these years.

ZAZULA: During the Ice Age when big continental glaciers covered lots of northern North America and places in Europe, places like Siberia, Alaska and parts of Yukon were never covered by ice sheets, so this was a landscape that was inhabited by woolly mammoths and giant short-faced bears and scimitar cats – you know, these iconic animals of the Ice Age. And so, that part of Siberia that they are working on has this astonishing record of the Ice Age and the life and the environments of the Ice Age.

CORNISH: And apparently squirrels, right? Because I’m reading from the research that these squirrel burrows had perfectly preserved seeds.

ZAZULA: Well, if you have seen the “Ice Age” cartoon movie, like, you know, most children have, you know that tiny squirrel that is running around collecting seeds? It’s kind of the star of the show. And a number of researchers across Siberia and North America here, too, we have been working on these records of Ice Age ground squirrels because they seem to have been these astonishing tiny botanists. What they did during the Ice Age times, 30,000 years ago, they ran around and collected seeds and fruits and leaves and stuff. They carried them underground into their burrows and they used that for hibernation. And the remains of these nests and seeds are buried deeply in the permafrost.

CORNISH: So how exactly did these Russian scientists turn these seeds into an actual flower? And what is novel about the way they did it?

ZAZULA: Well, it’s totally astonishing actually. They first tried actually just growing the seat itself and it never worked. But they recognized within the fruit capsule, the seed capsule, there was viable cells of placenta, which is one of the other reproductive structures within a plant fruit. So, they took that placenta and they immersed it in a growth medium – sort of nutrients and sugars and stuff to help it grow – and sure enough it propagated.

CORNISH: How do we know that this claim is true? I know that you have investigated fake claims of ancient plants before, so what about this one sort of rings true you?

ZAZULA: Well the fact that they were able to radiocarbon date the remains from the nests. So, they did a radiocarbon test and sent it to a reliable lab and it came back 32,000 years, and which is consistent with other nests that are found at those sites. And the fact that they found it frozen, buried within this permafrost and took it immediately back to the lab frozen, there’re sort of the conditions that we can think about to be reliable, I think, have been met. So I think the result is totally legit.

And I think it really pushes the boundaries now, you know, what can we do. And I know there is scientists at the moment that are trying to bring back ancient mammals, extinct mammals, like woolly mammoths. And in Russia, at these same sites…

CORNISH: Really? Could they begin with a squirrel maybe…

ZAZULA: Well, the fact that they could get plants to work is a major step. The whole idea about bringing back woolly mammoths now, you know, it’s all based on the assumption that we can have reproductive cells within mammoth carcasses. ‘Cause in Siberia, you know, every couple of years, they seem to drag a dead woolly mammoth out of the permafrost that is 40,000 years old or something.

And, you know, now that we know that reproductive cells in plants can survive, well, maybe we will find a mammoth carcass that has preserved sperm or eggs. So, that is basically the first indication that this is actually possible, to bring back ancient or extinct life in the permafrost.

CORNISH: Grant Zazula, he works with a Yukon paleontology program in Whitehorse, Canada.

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