Day: 06/23/2015

Nonphotosynthetic pigments could be biosignatures of life on other worlds.

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Some nearby exoplanets in the Milky Way. How will we know if there is life on planets outside of our solar system?

To find life in the universe, it helps to know what it might look like. If there are organisms on other planets that do not rely wholly on photosynthesis — as some on Earth do not — how might those worlds appear from light-years away?

That’s among the questions University of Washington doctoral student Edward Schwieterman and astronomer Victoria Meadows of the UW-based, interdisciplinary Virtual Planetary Laboratory sought to answer in research published in May in the journal Astrobiology.

Using computer simulations, the researchers found that if organisms with nonphotosynthetic pigments — those that process light for tasks other than energy production — cover enough of a distant planet’s surface, their spectral signal could be strong enough to be detected by powerful future telescopes now being designed. The knowledge could add a new perspective to the hunt for life beyond Earth.

Such organisms ‘will produce reflectance, or brightness, signatures different than those of land vegetation like trees,’ said lead author Schwieterman. ‘This could push us to broaden our conception of what surface biosignatures might look like’ on an exoplanet, or world beyond our solar system.

He said the research grew from a meeting with co-author Charles Cockell of the UK Centre for Astrobiology in 2012. Schwieterman sought a topic for a research rotation in the UW Astrobiology program in which students do work outside their main field of study.

‘I was interested in doing biology in the lab and linking it to remotely detectable biosignatures, which are indications there is life on a planet based on observations that could be made from a space-based telescope or large ground-based telescope,’ Schwieterman said.

There had already been literature about looking for something akin to Earth’s vegetation ‘red edge’ as a possible biosignature on exoplanets, he said. The red edge — caused by oxygen-producing organisms such as trees — is the increase in brightness when you move from the visible wavelength range to the infrared, or light too red to see. It’s why foliage looks bright in infrared photography and is often used to map vegetation cover by Earth-observing satellites.

Schwieterman and Cockell, a University of Edinburgh astrobiologist, decided to look further, and measure the reflectance of earthly organisms with different kinds of pigments. They included those that do not rely on photosynthesis to see what biosignatures they produce and how those might differ from photosynthetic organisms — or indeed from nonliving surface features like rocks and minerals.

Pigments that absorb light are helpful to earthly organisms in ways other than just producing energy. Some protect against the sun’s radiation or have antioxidants to help the organism survive extreme environments such as salt concentrations, high temperatures or acidity. There are even photosynthetic pigments that do not produce oxygen at all.

Schwieterman and Meadows then plugged their results Virtual Planetary Laboratory spectral models — which include the effects of the atmosphere and clouds — to simulate hypothetical planets with surfaces covered to varying degrees with such organisms.

‘With those models we could determine the potential detectability of those signatures,’ he said.

Exoplanets are much too far away to observe in any detail; even near-future telescopes will deliver light from such distant targets condensed to a single pixel. So even a strong signal of nonphotosynthetic pigments would be seen at best only in the ‘disk average,’ or average planetary brightness in the electromagnetic spectrum, Schwieterman said.

‘This broader perspective might allow us to pick up on something we might have missed or offer an additional piece of evidence, in conjunction with a gaseous biosignature like oxygen, for example, that a planet is inhabited,’ Schwieterman said.

The UW-based planetary lab has a growing database of spectra and pigments of nonphotosynthetic organisms and more that is available to the public, and to which data from this project have been added.

Schwieterman said much work remains to catalogue the range of spectral features that life on Earth produces and also to quantify how much of a planetary surface could conceivably be covered with pigmented organisms of any type.

‘We also need to think about what kinds of adaptations might exist on other worlds that don’t exist on Earth — and what that means for the interaction of those possible extraterrestrial organisms with their light environments.’

CDC confirms red eyes at the pool are caused by urine, not chlorine

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Those red eyes you get from swimming aren’t caused by chlorine, according to an official with the Centers for Disease Control and Prevention.

For their annual Healthy Swimming Program, the Centers for Disease Control (CDC) teamed with Water Quality and the Health Council and the National Swimming Pool Foundation to educate Americans about the dangers of pools and how to stay healthy when swimming, Women’s Health reports.

Beach went on to say that the cough you can get from an indoor pool is also caused by the chemical reaction. The chlorine isn’t what causes the irritation in your lungs; it’s pee.

There’s actually been an increase in disease outbreaks from public swimming pools, according to Beach, thanks in large part to those swimming while they have diarrhea. Those with diarrhea don’t even have to defecate in the pool to spread disease, but just have the germs on their body, which is why the CDC encourages swimmers to shower before getting in the pool.

“We have a new parasitic germ that has emerged that’s immune to chlorine,” says Beach. “We’ve got to keep it out of the pool in the first place. We need additional barriers.”

The misconception that chlorine just eliminates all germs upon contact is untrue, and it takes time to properly disinfect for each germ. While chlorine kills most bacteria such as E. Coli in less than a minute, it takes at least 16 minutes to kill Hepatitis A, and the Cryptosporidium parasite can last in the swimming pool for over 10 days.

The CDC says the only way to prevent recreational water illnesses is to keep germs out of the pool in the first place and to practice the following steps for healthy swimming:

PAS: Prophylactic indomethacin not associated with lower risk of BPD, death in preterm infants : CHEST Physician

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VITALS

Key clinical point: Prophylactic indomethacin does not reduce odds of BPD or death in any significant way for preterm infants.

Major finding: Prophylactic indomethacin vs. no prophylactic indomethacin outcomes for BPD (44% vs. 44%), death before 36 weeks postmenstrual age (17% vs. 13%), death or BPD (54% vs. 51%) showed no significant benefit of prophylactic indomethacin.

Data source: Observational study of 8,039 infants (aged < 29 weeks’ gestational age) who were enrolled in the Neonatal Research Network Generic Database from 2008 to 2012.

Prophylactic indomethacin does not have any association with reducing the risk of bronchopulmonary dysplasia (BPD) or death in infants born extremely premature, according to an observational study presented by Dr. Erik Jensen, a neonatologist at the Children’s Hospital of Philadelphia, at the annual meeting of the Pediatric Academic Societies.

“Observational studies consistently show that patent ductus arteriosus [PDA] is a strong risk factor for [BPD] in very preterm infants [but] it remains uncertain whether PDA is a cause, or simply a marker, of increased BPD risk,” said Dr. Jensen. “Data from randomized trials indicate that prophylactic indomethacin reduces the risk of subsequent symptomatic PDA, yet there is no evidence from these studies that prophylactic indomethacin reduces BPD.”

© Fuse/Thinkstock

Infants in the study who received prophylactic indomethacin experienced BPD at a rate of 44%, the exact same as those who did not receive prophylactic indomethacin. The rates of death before 36 weeks postmenstrual age also were not significantly different: 17% in infants receiving prophylactic indomethacin vs. 13% in infants who did not. Death or BPD occurred in 54% of prophylactic indomethacin subjects, and in 51% of infants who did not receive prophylactic indomethacin. An infant was defined as having BPD if they received supplemental oxygen at 36 weeks postmenstrual age.

All subjects in the study were enrolled in the Eunice Kennedy Shriver National Institute of Child Health and Human Development’s Neonatal Research Network generic database between 2008 and 2012, and were less than 29 weeks’ gestational age. The mean age of infants who received prophylactic indomethacin was 25.9 weeks, and the mean age was 26.7 weeks for infants who did not (P < .001). Mean body weight was 777 g for those who received prophylactic indomethacin vs. 912 g for those who did not (P < .001). Males made up 49% of the prophylactic indomethacin cohort and 52% of the other cohort (P < .006).

In total, 8,039 infants were included in the study, with 2,671 receiving prophylactic indomethacin and 5,368 infants who did not receive the drug; of those, commencement of PDA treatment was variable from center to center. PDA treatment after day 1 occurred in 21% of infants who received prophylactic indomethacin, and in 36% of those who did not (P < .001).

Cocktail of common chemicals may trigger cancer: Fifty chemicals the public is exposed to on a daily basis may trigger cancer when combined .

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A global taskforce of 174 scientists from leading research centers across 28 countries studied the link between mixtures of commonly encountered chemicals and the development of cancer. The study selected 85 chemicals not considered carcinogenic to humans and found 50 supported key cancer-related mechanisms at exposures found in the environment today.

A global taskforce of 174 scientists from leading research centres across 28 countries studied the link between mixtures of commonly encountered chemicals and the development of cancer. The study selected 85 chemicals not considered carcinogenic to humans and found 50 supported key cancer-related mechanisms at exposures found in the environment today.

Longstanding concerns about the combined and additive effects of everyday chemicals prompted the organisation Getting To Know Cancer led by Lowe Leroy from Halifax Nova Scotia, to put the team together — pitching what is known about mixtures against the full spectrum of cancer biology for the first time.

Cancer Biologist Dr Hemad Yasaei from Brunel University London contributed his knowledge regarding genes and molecular changes during cancer development. He said: “This research backs up the idea that chemicals not considered harmful by themselves are combining and accumulating in our bodies to trigger cancer and might lie behind the global cancer epidemic we are witnessing. We urgently need to focus more resources to research the effect of low dose exposure to mixtures of chemicals in the food we eat, air we breathe and water we drink.”

Professor Andrew Ward from the Department of Biology and Biochemistry at the University of Bath, who contributed in the area of cancer epigenetics and the environment, said: “A review on this scale, looking at environmental chemicals from the perspective of all the major hallmarks of cancer, is unprecedented.”

Professor Francis Martin from Lancaster University who contributed to an examination of how such typical environmental exposures influence dysfunctional metabolism in cancer endorsed this view.

He said: “Despite a rising incidence of many cancers, far too little research has been invested into examining the pivotal role of environmental causative agents. This worldwide team of researchers refocuses our attention on this under-researched area.”

In light of the compelling evidence the taskforce is calling for an increased emphasis on and support for research into low dose exposures to mixtures of environmental chemicals. Current research estimates chemicals could be responsible for as many as one in five cancers. With the human population routinely exposed to thousands of chemicals, the effects need to be better understood to reduce the incidence of cancer globally.

The research will be published in a special series of Oxford University Publishing’s Carcinogenesis journal on Tuesday 23 June (http://carcin.oxfordjournals.org/content/36/Suppl_1). William Goodson III, a senior scientist at the California Pacific Medical Center in San Francisco and lead author of the synthesis said: “We are definitely concerned that we are now starting to see evidence of a wide range of low dose effects that are directly related to carcinogenesis, exerted by chemicals that are unavoidable in the environment.”

Benifits vs Side Effects of Taking Multivitamins

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You aren’t getting enough nutrients needed and are thinking of increasing your vitamin intake, but where do you start? A multivitamin could solve your problem but first let’s take a look at the benefits vs side effects.

Everyone knows how important minerals and vitamins are for the body. The main reason people take multivitamins on a daily basis is that they believe that they are a safe alternative to staying healthy, but this isn’t true. Not everyone’s body needs a multivitamin unless they have some nutrient deficiency.

The Recommended Multivitamin vs. the Multivitamins with Additional Content

The perfect multivitamin contains around 100% of the recommended daily allowance of nutrients that are body needs to operate efficiently. However, if you have a deficiency like say an iron deficiency you may have to take a separate supplement along with the multivitamin.

There are also other types of multivitamins out there that are known as experimental multivitamins, but what’s the difference? Well unlike the regular these contain excess benefits such as phytonutrients and extra antioxidants. But this isn’t a good thing because if you aren’t careful they could cause you to develop cancer based on clinical studies, due to the high dosages. The increased risk of cancer in these products is attributed to the massive vitamin E content. Remember that you should exceed and take dosages above 400 IU; any more than that and you’re taking a gamble with your health.

It Pays to be a Smart Consumer

 Make sure when you take a trip to the market, you read labels and are always cautious when considering purchasing a multivitamin, because of the increased risk of developing cancer. So always research before you buy things you aren’t sure about.

Are Multivitamins a Necessity?

To be honest no. Multivitamins should always be taken with extreme caution and only when you have a good enough reason. And even though reading the label might be considered time-consuming, but do you want to put it in your body without knowing what’s in it?

Source:

http://www.encyclopedia.com/topic/vitamin.aspx

Remote Monitoring, a New Paradigm for Cardiac Implanted Devices? | Medpage Today

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Action Points

  • Patients using remote monitoring of their cardiac implantable electronic devices had fewer hospitalizations, shorter hospital lengths of stay, and lower healthcare utilization costs.
  • Reduced hospitalizations were most likely in patients with heart failure and in patients with atrial fibrillation.
 

Patients who used the remote monitoring (RM) function of their cardiovascular implantable electronic devices (CIEDs) had less healthcare utilization and better survival than those without RM according to a pair of studies.

“For every 100,000 patients years, use of RM is associated with 9,810 fewer hospitalizations, 119,000 fewer days in hospital, and $370,270,000 lower hospital payments,” reported Jonathan Piccini, MD, MHSc, from Duke University, at a late-breaking session at the Heart Rhythm Society’s 36th Annual Scientific Sessions.

 The second study was published concurrently in the Journal of the American College of Cardiology (JACC).

Taken together, the results underscore a new expert consensus statement released this week by the Heart Rhythm Society recommending that RM become standard of care for patients with cardiovascular implantable electronic devices (CIEDs).

Piccini’s nationwide, retrospective study used a large, real-world cohort which included 92,566 patients (average age 72 years) who were implanted with pacemakers (PM), implantable cardioverter-defibrillators (ICDs), or cardiac resynchronization therapy (CRT) devices from any manufacturer.

The cohort, drawn from MarketScan Commercial and Medicare Supplemental (MS) claims databases (2008-2013), included about one-third of the patients, who had RM as well as clinic visits (n=34,259), while two-thirds had no RM and clinic visits only (n=58,307).

PM and ICD patients made up the majority of the group (n=54,520 and n=27,816 respectively), of whom 29% and 49% had RM. Among patients with CRT devices, most (n=9,125) had a CRT pacemaker with a 51% rate of RM, while 1,105 had a CRT pacemaker/defibrillator (CRT-D) and 27% RM rate.

 The primary outcome of the study was all-cause hospitalizations “because of its nature as a robust endpoint, and because noncardiovascular conditions often precipitate arrhythmias, such as flares of chronic obstructive pulmonary disease and other conditions like pneumonia,” said Piccini.

And even though the RM and non-RM groups were similar in terms of baseline characteristics and follow-up frequency, patients with RM had a significantly lower cumulative incidence of all-cause hospitalization regardless of their device type.

“Following adjustment, use of remote monitoring was associated with an 18% reduction in all-cause hospitalization,” (hazard ratio [HR] 0.82, P<0.001), said Piccini. “And in those patients who were hospitalized, those in the RM group had a 2.8-day lower mean length of stay compared with those without RM (P<0.001).

While the association between lower risk of all-cause hospitalization was “largely preserved across all device types,” the difference between RM and non-RM patients was greatest among those using ICDs and CRT-Ds (HR 0.74 and 0.72 respectively, P<0.001 for both), he reported.

The study also found that RM was associated with an overall 30% reduction in hospitalization costs compared with non-RM — translating to $3,700 less per patient year (P<0.001).

 Again, the magnitude of savings was highest among ICD and CRT-D users (43% and 45%, respectively, P<0.001 for both), he said.

Secondary endpoints of the study included heart failure (HF) hospitalizations in patients with prior HF, 30-day HF rehospitalizations, and stroke hospitalization in patients with prior atrial fibrillation.

For all of these endpoints, RM was associated with a significantly reduced risk of hospitalization and significantly reduced hospitalization costs compared with no RM, reported Piccini.

Since fewer than half of patients in this study used RM, this is “a major opportunity for quality improvement in the U.S. healthcare system,” he commented.

Another study co-authored by Piccini and Niraj Varma, MD, PhD, Cleveland Clinic in Ohio, and published simultaneously in the JACC, struck the message home still further.

 In that study, among 371,217 consecutive patients receiving new CIEDs from one manufacturer (St. Jude Medical, Sylmar, Ca.), RM was associated with improved survival compared with no RM, and the effect increased with greater adherence to RM.

Using four data sources (device implant registration, device RM, postal code sociodemographic data, and the U.S. Social Security Death Master File), the investigators tracked patients’ level of RM adherence and showed that high adherence (defined as weekly maintenance records sent to the server ≥75% of their follow-up time) was associated with significantly better survival compared with no RM (HR 2.10;P<0.001).

Even low adherence (defined as weekly maintenance records sent to the server <75% but more than 0% of their follow-up time) was associated with better survival than no RM (HR: 1.58; P < 0.001).

“Remarkably, only one-quarter of all patients receiving automatic RM-capable CIEDs in this nationwide analysis occupied the high [adherence] category, indicating that the vast majority of recipients do not utilize the full capabilities of their implantable devices,” concluded the authors.

“Clearly it is underutilized,” commented Michael R. Gold, MD, PhD, from the Medical University of South Carolina in Charleston, who was not involved in the research.

 “There were early concerns of medico-legal issues but … I think most physicians you talk to, their impression is that the single biggest reason patients are not remote monitored is that many systems are not compatible with cell phone use, and we’re finding more and more of our patients who only have cell phones, so unless they have a land line they can’t use remote monitoring.”

Reimbursement has also lagged, added Jonathan Kalman,MBBS, PhD, from the Royal Melbourne Hospital, in Melbourne, Australia. “This kind of data can convince providers that they need to pay.”

Commenting on the JACC article, in an accompanying editorial, James V. Freeman, MD, MPH and Leslie Saxon, MD, of the Yale School of Medicine, and Keck School of Medicine of USC, University of Southern California Los Angeles, wrote “research must be conducted to better understand patient- and physician-level impediments to adopting RM and methods to address these barriers”… and “the cardiac implantable device and research communities should continue to investigate ways of optimizing and improving RM.”

Cardiac implantable devices “are in the vanguard of the personal ‘big data’ revolution,” they concluded. “It is imperative that we continue to improve the quality and use of the data they generate to best meet the needs and optimize the outcomes of patients and enable physicians to practice most efficiently.”

Cancer screening Doesn’t Save Lives, Meta-Study Reveals .

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Should we be looking for disease in people who don’t have any symptoms? A large new study indicates the answer is NO.  

Subject to an increasingly expansive disease screening programs, unsuspecting healthy individuals are being transformed into patients every day. Massive ‘awareness raising’ campaigns funded by industries that either cause disease by creating and promoting harmful products, or make profit from the diseases by diagnosing and treating them, dominate mainstream culture, with their tentacles reaching deep into both private and public (i.e. governmental) sectors. Think of KFC’s now defunct “Buckets for the Cure” campaign, or Susan G. Komen’s stamp of approval on a Fracking Drill bit supposed to help find a cure. Or, how about our very own Whitehouse saturating itself with Pink light during Breast Cancer Awareness Month?

What do these ‘awareness raising’ efforts have in common? They almost all funnel the miseducated masses into fear-driven screening programs that promise to ‘save lives’ by ‘detecting disease early’ instead of focusing on removing and/or lessening the preventable causes of disease. Why not employ real prevention and focus on root cause resolution, which is to say, dietary changes, detoxification, and various modifiable lifestyle factors such as stress reduction — none of which, incidentally, require pharmaceutical intervention. In the case of cancer, the primary focus should be on removing exposure to cancer-causing agents (carcinogens).

But cancer awareness raising campaigns intentionally avoid the term “carcinogen,” as removal of these primary drivers were an irrelevant consideration. The problem is that conventional treatments like chemotherapy and radiation are themselves carcinogenic, and should be avoided in principle by anyone looking to prevent, treat and/or reverse cancer, undermining the cancer industry’s main cash cow for the past half century. Additionally, if you focus on identifying and removing the cause, you can’t get people to throw billions of dollars into fund-raising campaigns by promising a cure that only exists as a possibility in the future, and requires ceaseless cash offerings and supplication to the biotech, pharmaceutical and medical ‘Gods.’

So, have these disease campaigns met their promises?

This all important question is now drawing widespread attention following the publication of study in the International Journal of Epidemiology titled: “Does screening for disease save lives in asymptomatic adults? Systematic review of meta-analyses and randomized trials.”1

As many of our readers who follow our work are already aware, routine mass screening for cancer in healthy populations commonly leads to overdiagnosis (finding lesions that do not cause harm or death), and when not identified as such, overtreatment (a euphemism to what amounts to succumbing to medical abuse).

Screening also leads to a staggering level of false-positives, with the 10 year cumulative rate for women receiving annual x-ray mammography reaching 50%.  Even when false positives are identified, and the patient avoids unnecessary surgery, radiation, or chemotherapy, research shows that the trauma of the false-positive is as severe as a real positive breast cancer diagnosis, for at least six months following the diagnosis.

Overdiagnosis is exceedingly common primarily because of mistakes in cancer classification based on a fundamental, at least half century old misunderstanding of cancer biology. In 2013 the National Cancer Institute commissioned an expert working group to look at present day definitions of screen detected cancers such as ductal carcinoma in situ (DCIS) (‘breast cancer’), high grade intraepithelial neoplasia (HGPIN) (‘prostate cancer’) and thyroid papillary carcinoma (thyroid ‘cancer’), with the shocking conclusion that these should be reclassified as non-cancerous, benign growths of epithelial origin. Yes, after millions in the U.S. over the past few decades had their breasts, prostates, ovaries, and thyroids removed as a ‘precautionary’ approach, now they are being told they  never had cancer to begin with. In other words, they had abnormal tissue growth that would never have progressed to cause harm or death. But these non-malignant lesions or tumors were treated as if they were life-threatening cancers anyway, with patients often losing their breasts or prostates as a result of medical errors that were disingenuously recorded in cancer statistics as ‘life saving’ interventions that ‘detected cancer early,’ resulting in inflating the ‘5-year survival’ rates in a way that appears to show medical progress. These semantical and statistical misrepresentations, are why, absurdly, thecancer industry can announce that they saved over a million lives in the past few decades, when in fact quite the opposite may be true.

As summarized on Science Daily, the new study confirms that despite screening programs picking up millions of new ‘early cancer’ diagnoses disease-specific mortality has not declined significantly as would be expected if these ‘cancers’ were actually non-benign or life threatening”:

“Screening for disease is a key component of modern healthcare. Yet, new surprising new research shows that few currently available screening tests for major diseases where death is a common outcome have documented reductions in disease-specific mortality. Evidence was evaluated on 16 screening tests for 9 major diseases where mortality is a common outcome. The researchers found 45 randomized controlled trials and 98 meta-analyses that evaluated disease-specific or all-cause mortality. Reductions in disease-specific mortality were uncommon and reductions in all-cause mortality were very uncommon.”

Many in the U.S. are still not aware that breast screening for women aged 40-49 and PSA-based prostate screening in healthy men lost their endorsement in 2009 and 2012, respectively, by the U.S. Preventive Task Force (USPSTF), explicitly because of concerns that the psychological and physical harms of overdiagnosis and overtreatment outweighed their benefits in reducing cancer specific mortality.  In fact, prostate screening was associated with increased mortality! Although not discussed by the USPSTF, we have detailed the many ways which which mammography is likely increasing mortality in those undergoing them.

According to Science Daily, senior author of the new study, professor John Ioannidis stated:

“Our comprehensive overview shows that documented reductions in disease-specific mortality in randomized trials of screening for major diseases are uncommon. Reductions in all-cause mortality are even more uncommon. This overview offers researchers, policy-makers, and health care providers a synthesis of RCT evidence on the potential benefits of screening and we hope that it is timely in the wake of recent controversies.”[emphasis added]

There are vast resources of energy, money, and time put into screening programs. This new meta-analysis should put a pause in the ongoing push to have asymptomatic people subject themselves to unnecessary screening. But the truth is that only we can make these decisions for ourselves. The medical-industrial complex will likely continue to push for these programs regardless of the evidence against them, and the governmental agencies in charge of overseeing them will likely continue to default to a cheerleading instead of regulatory role. We can only hope that our readers continue to educate themselves and make a fully informed choice.

Article References

[1] Nazmus Saquib, Juliann Saquib, and John Ioannidis. Does screening for disease save lives in asymptomatic adults? Systematic review of meta-analyses and randomized trials. International Journal of Epidemiology, 2015 DOI: 10.1093/ije/dyu140

Sexism in science: Did Watson and Crick really steal Rosalind Franklin’s data?

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The race to uncover the structure of DNA reveals fascinating insights into how Franklin’s data was key to the double helix model, but the ‘stealing’ myth stems from Watson’s memoir and attitude rather than facts
Rosalind Franklin in 1950
The wave of protest that followed Sir Tim Hunt’s stupid comments about ‘girls’ in laboratories highlighted many examples of sexism in science. One claim was that during the race to uncover the structure of DNA, Jim Watson and Francis Crick either stole Rosalind Franklin’s data, or ‘forgot’ to credit her. Neither suggestion is true.

Photo 51 taken by Rosalind Franklin and R.G. Gosling

In April 1953, the scientific journal Nature published three back-to-back articles on the structure of DNA, the material our genes are made of. Together, they constituted one of the most important scientific discoveries in history.

The first, purely theoretical, article was written by Watson and Crick from the University of Cambridge. Immediately following this article were two data-rich papers by researchers from King’s College London: one by Maurice Wilkins and two colleagues, the other by Franklin and a PhD student, Ray Gosling.

The model the Cambridge duo put forward did not simply describe the DNA molecule as a double helix. It was extremely precise, based on complex measurements of the angles formed by different chemical bonds, underpinned by some extremely powerful mathematics and based on interpretations that Crick had recently developed as part of his PhD thesis. The historical whodunnit, and the claims of data theft, turn on the origin of those measurements.

The four protagonists would make good characters in a novel – Watson was young, brash, and obsessed with finding the structure of DNA; Crick was brilliant with a magpie mind, and had struck up a friendship with Wilkins, who was shy and diffident. Franklin, an expert in X-ray crystallography, had been recruited to King’s in late 1950. Wilkins expected she would work with him, but the head of the King’s group, John Randall, led her to believe she would be independent.

1959, Boston, Massachusetts, USA -- James Watson and Francis Crick, crackers of the DNA code. Photo taken on occasion of the Massachusetts General Hospital lectures.

From the outset, Franklin and Wilkins simply did not get on. Wilkins was quiet and hated arguments; Franklin was forceful and thrived on intellectual debate. Her friend Norma Sutherland recalled: “Her manner was brusque and at times confrontational – she aroused quite a lot of hostility among the people she talked to, and she seemed quite insensitive to this.”

Watson and Crick’s first foray into trying to crack the structure of DNA took place in 1952. It was a disaster. Their three-stranded, inside-out model was hopelessly wrong and was dismissed at a glance by Franklin. Following complaints from the King’s group that Watson and Crick were treading on their toes, Sir Lawrence Bragg, the head of their lab in Cambridge told them to cease all work on DNA.

However, at the beginning of 1953, a US competitor, Linus Pauling, became interested in the structure of DNA, so Bragg decided to set Watson and Crick on the problem once more.

At the end of January 1953, Watson visited King’s, where Wilkins showed him an X-ray photo that was subsequently used in Franklin’s Nature article. This image, often called ‘Photo 51’, had been made by Raymond Gosling, a PhD student who had originally worked with Wilkins, had then been transferred to Franklin (without Wilkins knowing), and was now once more being supervised by Wilkins, as Franklin prepared to leave the terrible atmosphere at King’s and abandon her work on DNA.
Watson recalled that when he saw the photo – which was far clearer than any other he had seen – ‘my mouth fell open and my pulse began to race.’ According to Watson, photo 51 provided the vital clue to the double helix. But despite the excitement that Watson felt, all the main issues, such as the number of strands and above all the precise chemical organisation of the molecule, remained a mystery. A glance at photo 51 could not shed any light on those details.

What Watson and Crick needed was far more than the idea of a helix – they needed precise observations from X-ray crystallography. Those numbers were unwittingly provided by Franklin herself, included in a brief informal report that was given to Max Perutz of Cambridge University.

In February 1953, Perutz passed the report to Bragg, and thence to Watson and Crick.

Crick now had the material he needed to do his calculations. Those numbers, which included the relative distances of the repetitive elements in the DNA molecule, and the dimensions of what is called the monoclinic unit cell – which indicated that the molecule was in two matching parts, running in opposite directions – were decisive.

The report was not confidential, and there is no question that the Cambridge duo acquired the data dishonestly. However, they did not tell anyone at King’s what they were doing, and they did not ask Franklin for permission to interpret her data (something she was particularly prickly about).

Their behaviour was cavalier, to say the least, but there is no evidence that it was driven by sexist disdain: Perutz, Bragg, Watson and Crick would have undoubtedly behaved the same way had the data been produced by Maurice Wilkins.

Ironically, the data provided by Franklin to the MRC were virtually identical to those she presented at a small seminar in King’s in autumn 1951, when Jim Watson was in the audience. Had Watson bothered to take notes during her talk, instead of idly musing about her dress sense and her looks, he would have provided Crick with the vital numerical evidence 15 months before the breakthrough finally came.

By chance, Franklin’s data chimed completely with what Crick had been working on for months: the type of monoclinic unit cell found in DNA was also present in the horse haemoglobin he had been studying for his PhD. This meant that DNA was in two parts or chains, each matching the other. Crick’s expertise explains why he quickly realised the significance of these facts, whereas it took Franklin months to get to the same point.

While Watson and Crick were working feverishly in Cambridge, fearful that Pauling might scoop them, Franklin was finishing up her work on DNA before leaving the lab. The progress she made on her own, increasingly isolated and without the benefit of anyone to exchange ideas with, was simply remarkable.

Franklin’s laboratory notebooks reveal that she initially found it difficult to interpret the outcome of the complex mathematics – like Crick, she was working with nothing more than a slide rule and a pencil – but by 24 February, she had realised that DNA had a double helix structure and that the way the component nucleotides or bases on each strand were connected meant that the two strands were complementary, enabling the molecule to replicate.

Above all, Franklin noted that ‘an infinite variety of nucleotide sequences would be possible to explain the biological specificity of DNA’, thereby showing that she had glimpsed the most decisive secret of DNA: the sequence of bases contains the genetic code.

To prove her point, she would have to convert this insight into a precise, mathematically and chemically rigorous model. She did not get the chance to do this, because Watson and Crick had already crossed the finishing line – the Cambridge duo had rapidly interpreted the double helix structure in terms of precise spatial relationships and chemical bonds, through the construction of a physical model.

In the middle of March 1953, Wilkins and Franklin were invited to Cambridge to see the model, and they immediately agreed it must be right. It was agreed that the model would be published solely as the work of Watson and Crick, while the supporting data would be published by Wilkins and Franklin – separately, of course. On 25 April there was a party at King’s to celebrate the publication of the three articles in Nature. Franklin did not attend. She was now at Birkbeck and had stopped working on DNA.

Franklin died of ovarian cancer in 1958, four years before the Nobel prize was awarded to Watson, Crick and Wilkins for their work on DNA structure. She never learned the full extent to which Watson and Crick had relied on her data to make their model; if she suspected, she did not express any bitterness or frustration, and in subsequent years she became very friendly with Crick and his wife, Odile.

1959, Boston, Massachusetts, USA — James Watson and Francis Crick, crackers of the DNA code. Photo taken on occasion of the Massachusetts General Hospital lectures. Facebook Twitter Pinterest
1959, Boston, Massachusetts, USA: James Watson and Francis Crick, crackers of the DNA code. Photo taken on occasion of the Massachusetts General Hospital lectures. Photograph: Corbis
Our picture of how the structure of DNA was discovered, and the myth about Watson and Crick stealing Franklin’s data, is almost entirely framed by Jim Watson’s powerful and influential memoir, The Double Helix. Watson included frank descriptions of his own appalling attitude towards Franklin, whom he tended to dismiss, even down to calling her ‘Rosy’ in the pages of his book – a nickname she never used (her name was pronounced ‘Ros-lind’). The epilogue to the book, which is often overlooked in criticism of Watson’s attitude to Franklin, contains a generous and fair description by Watson of Franklin’s vital contribution and a recognition of his own failures with respect to her – including using her proper name.

It is clear that, had Franklin lived, the Nobel prize committee ought to have awarded her a Nobel prize, too – her conceptual understanding of the structure of the DNA molecule and its significance was on a par with that of Watson and Crick, while her crystallographic data were as good as, if not better, than those of Wilkins. The simple expedient would have been to award Watson and Crick the prize for Physiology or Medicine, while Franklin and Watkins received the prize for Chemistry.

Whether the committee would have been able to recognise Franklin’s contribution is another matter. As the Tim Hunt affair showed, sexist attitudes are ingrained in science, as in the rest of our culture.

Phosphorus Sky High and Hidden in Many U.S. Beverages

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Phosphorus levels in the nation’s popular beverages remain largely unknown, putting kidney disease patients at risk, according to a research letter published in the National Kidney Foundation’s American Journal of Kidney Diseases.

The kidneys are critical for keeping phosphorus levels in balance, so anyone with kidney disease is at risk for excess phosphorus in blood and tissues.  Long term elevations in phosphorus can lead to bone and heart disease. High phosphorus intake has been associated with the development of kidney disease and increased mortality in those with kidney disease.

However, the U.S. Food and Drug Administration currently does not require reporting of phosphorus levels on food labels.

“It’s almost impossible to figure out how much phosphorus is in our beverage products,” said Alex Chang, MD, a Clinical Investigator in Nephrology at Geisinger Health System. “Cola products are well-known to contain phosphoric acid, but our analysis found there to be a lot more products out there that have phosphorus additives.”

Forty-six popular beverage products containing phosphorus additives were analyzed for phosphorus content including sodas, lemonades, teas and enhanced waters. The analysis is being used to help inform a study Dr. Chang is conducting on the effects of phosphorus additives on markers of kidney and cardiovascular health.

The independent analysis was compared against values listed in the Nutrition Data System for Research (NDSR), which is commonly used by dietitians.

All products measured had phosphorus content, despite many (35%) having no phosphorus content listed on NDSR. Most, 78%, had phosphorus content higher than that listed in the NDSR. Phosphorus content also varied greatly within the same brand. One popular line of flavored water had phosphorus levels that ranged from 0.9 mg – 261.4 mg per 8 oz., depending on the variety.

According to Dr. Chang, there should be renewed effort to focus on phosphorus additives in the nation’s food supply. Until then, he said, it’s probably best for the nation’s kidney patients to avoid most bottled drinks other than water.

“Patients should avoid products that have ‘phos’ on the ingredients label. However, it can be very difficult to find this information, and it does not give you a great idea for how much phosphorus in the beverage,” Dr. Chang said. “Right now, even with the best nutrition databases, there isn’t a way to adequately plan an individual’s phosphorus intake.”

 

The National Kidney Foundation is the leading organization in the U.S. dedicated to the awareness, prevention and treatment of kidney disease for hundreds of thousands of healthcare professionals, millions of patients and their families, and tens of millions of Americans at risk. For more information, visit www.kidney.org.

Ebola crisis in Guinea ‘has set back malaria fight’

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Bed nets can help prevent malaria (picture taken in Kenya)
Most malaria deaths occur among children living in Africa

The continuing Ebola epidemic in Guinea has set back the country’s fight against malaria, say experts.

They estimate 74,000 cases of malaria went untreated in 2014 because clinics were either closed or patients were too scared to seek help.

They warn that malaria deaths since the Ebola outbreak began will far exceed the number of Ebola deaths in the country – which now stand at 2,444.

Their report is in the Lancet Infectious Diseases journal.

Both Ebola and malaria cause fever. The authors of the Lancet report say fear surrounding the Ebola virus may have stopped patients in Guinea going to see a doctor to get this symptom checked.

‘Extra burden’

Dr Mateusz Plucinski and colleagues analysed how many patients clinics in Guinea were seeing before and during the Ebola epidemic that emerged there in early 2014.

They sampled 60 health facilities in the most Ebola-affected districts and 60 in districts unaffected by Ebola.

And they looked at malaria prescriptions dispensed before and during the epidemic.

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There has been a big Ebola public health campaign across West Africa

Once Ebola hit, outpatient attendances fell dramatically – by nearly half in certain age groups in the worst-affected areas. And the number of treated malaria cases dropped by up to 69%.

At the same time, the rate of “just in case” or presumptive treatment of fever cases with antimalarial drugs in health facilities and by community health workers decreased or did not change.

The US experts warn that malaria deaths will have risen as a result. Meanwhile, Ebola seems to be abating.

According to the World Health Organization (WHO), in the most recent week for which there is data, there were 10 reported cases of Ebola in Guinea. In early 2015, cases were in the hundreds.

But malaria has been a long-standing problem in the region – particularly in the young. WHO estimates suggest it led to around 584,000 deaths globally in 2013. Most occurred among children in Africa.

Dr Franco Pagnoni, from the WHO’s Global Malaria Programme, said untreated malaria cases had placed an additional burden on an already overburdened health system in the Ebola-affected countries.

He said it was important to ensure that Ebola containment and prevention activities were accompanied by efforts to detect, treat and prevent malaria in order to save more lives.

Towards the end of 2014, the World Health Organization recommended mass treatment of malaria irrespective of symptoms in areas heavily affected by Ebola. This happened in Liberia and Sierra Leone, but not Guinea.

Dr Plucinski said: “Malaria control efforts and care delivery must be kept on track during an Ebola epidemic so that progress made in malaria control is not jeopardised and Ebola outbreak response is not impeded.”