No Effects of Short-Term vs. Long-Term Blood Storage on Mortality after Transfusion


Randomized, controlled trials have suggested that the transfusion of blood after prolonged storage does not increase the risk of adverse outcomes among patients, although most of these trials were restricted to high-risk populations and were not powered to detect small but clinically important differences in mortality. As a result, a study published in the New England Journal of Medicine (2016; 375:1937-1945) was performed to determine whether the duration of blood storage would have an effect on mortality after transfusion in a general population of hospitalized patients.


In this pragmatic, randomized, controlled trial conducted at six hospitals in four countries, patients who required a red-cell transfusion were randomly assigned to receive blood that had been stored for the shortest duration (short-term storage group) or the longest duration (long-term storage group) in a 1:2 ratio. Only patients with type A or O blood were included in the primary analysis, since pilot data suggested that the goal of achieving a difference in the mean duration of blood storage of at least 10 days would not be possible with other blood types. Written informed consent was waived because all the patients received treatment consistent with the current standard of care. The primary outcome was in-hospital mortality, which was estimated by means of a logistic-regression model after adjustment for study center and patient blood type.


From April 2012 through October 2015, a total of 31,497 patients underwent randomization. Of these patients, 6761 who did not meet all the enrollment criteria were excluded after randomization. The primary analysis included 20,858 patients with type A or O blood. Of these patients, 6,936 were assigned to the short-term storage group and 13,922 to the long-term storage group. The mean storage duration was 13.0 days in the short-term storage group and 23.6 days in the long-term storage group. There were 634 deaths (9.1%) in the short-term storage group and 1213 (8.7%) in the long-term storage group (odds ratio, 1.05 P=0.34). When the analysis was expanded to include the 24,736 patients with any blood type, the results were similar, with rates of death of 9.1% and 8.8%, respectively (odds ratio, 1.04, P=0.38). Additional results were consistent in three prespecified high-risk subgroups (patients undergoing cardiovascular surgery, those admitted to intensive care, and those with cancer).


According to the authors, among patients in a general hospital population, there was no significant difference in the rate of death among those who underwent transfusion with the freshest available blood and those who underwent transfusion according to the standard practice of transfusing the oldest available blood.


Statin Use and Risk of Rheumatoid Arthritis


Statins have antiinflammatory/immunomodulatory effects that may be useful in preventing rheumatoid arthritis (RA), but previous observational studies about the risk of RA with statin use yielded conflicting results. As a result, a study published in Arthritis and Rheumatology (27 October 2016) was performed to determine whether high-intensity statin treatment is associated with reduced risk of RA.


The study used data from the UK Clinical Practice Research Datalink. For the analysis, the authors performed a nested case-control analysis in a population-based cohort of patients who began receiving statins between 1997 and 2009 and were followed up until a first diagnosis of RA, death, end of registration with the physician’s practice, or end of January 2011. For each case of RA, age-, gender-, and calendar year-matched controls were randomly selected from risk sets. The hazard ratio (HR) of incident RA was estimated in the highest quintile of duration-weighted average statin intensity compared to the lowest, using conditional logistic regression. Models were adjusted for smoking status, total cholesterol level, obesity, history of cardiovascular disease, coexistent autoimmune disease, hypothyroidism, and persistence with treatment.


The research cohort included 528,654 new users of statins, with 1,357 new cases of RA occurring during a mean follow-up of 3.3 years, for an incidence rate of 7.9 per 10,000 person-years. Cases were more likely to be smokers, to have other autoimmune diseases, and to have had lower total cholesterol levels at baseline. Research showed that the incidence of RA was lower in the highest statin intensity quintile (adjusted HR 0.77 [95% confidence interval 0.63-0.95]) in comparison to the lowest quintile.


The authors concluded that in this large population-based study, high-intensity statin treatment was associated with a reduced risk of RA in comparison to low-intensity statin treatment.


FDA Research Helps to Speed Development of Zika Virus Vaccines and Therapeutics


The recent spread of the Zika virus and its association with increased rates of neurological disorders and complex congenital syndromes, such as microcephaly in babies and Guillain-Barre Syndrome in adults, has created an urgent need for animal models to examine the virus’ pathology. Better understanding the impact and long-term effects of the Zika virus infection in mice may be useful in efforts to find ways to combat it in a human population. A new mouse model developed by scientists at the U.S. Food and Drug Administration may help in exploring the potential activity of Zika virus vaccines and therapeutics. Published in PLoS Pathogens (17 November 2017), is the description of a neonatal mouse model that provides a platform for potentially improving and expediting studies to understand the causes and effects (pathology) of the Zika virus.


The FDA’s scientists found that neonatal mice of the C57BL/6 mouse strain are susceptible to the Zika virus and develop neurological symptoms 12 days post infection. These mice eventually recover from disease and thus the model provides an opportunity to study the virus’ long-term effects as well as an additional means for early exploration of experimental Zika virus vaccines and therapeutics. This advancement is just one of many research projects the FDA has undertaken as part of the agency’s comprehensive effort to fight the Zika virus. For example, the FDA has invested in initiatives to understand the effectiveness of technologies that reduce pathogens (such as viruses or other microorganisms that can cause disease) in blood, evaluate the impact of red blood cell storage on virus infection, expand the agency’s database of virus-infected samples essential to the development of diagnostic devices, and explore how long the Zika virus persists in body tissues, among other projects.


In addition to advancing research initiatives, the FDA is also working rapidly in a variety of areas to respond to the emerging Zika virus outbreak. The agency’s activities are focused on protecting the safety of our nation’s supply of blood and human cells, tissues and cellular and tissue-based products, encouraging development of diagnostic tests to help clinicians detect and diagnose Zika virus infection, and evaluating the safety and efficacy of any investigational vaccines and therapeutics that are currently in various stages of early development.


Pumpkin/Date Cake with Amaretto & Orange Zest Topping


This new holiday cake recipe overflows with luscious flavors, not the least of which is the Amaretto liqueur. It’s so-o addictive, we could not stop picking at it after we had dessert, because each crumb is replete with yum! ©Joyce Hays, Target Health Inc.



Delicious with or without whipped cream or vanilla ice cream. Here we’re having dessert with a dollop of cool whip. ©Joyce Hays, Target Health Inc.


Ingredients for Cake Layer


3/4 cup butter or canola oil

1 and 1/4 cup brown sugar

2 and 2/4 cups almond flour

2 teaspoons baking powder

1/2 teaspoon baking soda

Pinch salt

2 teaspoons cinnamon

1/4 teaspoon allspice

1/2 teaspoon ground nutmeg, grind your own or use store bought

1/3 cup fresh ginger, grated then chopped very fine

2 Tablespoons Amaretto liqueur

1/2 cup pecans, chopped

5 eggs

2 Tablespoons molasses

One 15-ounce can pumpkin puree


Date Filling Ingredients


4 Tablespoons unsalted butter, melted

3 eggs, beaten

1/4 cup molasses

1/4 cup, golden syrup or organic corn syrup

1/2 teaspoon cardamom

1/4 teaspoon allspice

1/4 teaspoon clove

1/4 teaspoon nutmeg

1/2 teaspoon kosher salt

1 teaspoon orange zest

2 Tablespoons Amaretto liqueur

1/2 teaspoon vanilla extract

1 cup chopped dates (press into the cup)

2 cups pecan halves or pieces (press into the cup)


Glaze Ingredients


1 and 1/4 cups confectioners sugar

2 Tablespoons Amaretto liqueur

1 Tablespoon orange zest





1. Heat oven to 350 degrees.

2. Grease a round 9“ spring-form cake pan

3. Grate the ginger



Grate the fresh ginger. Use the small or medium holes. ©Joyce Hays, Target Health Inc.



4. In a large mixing bowl, on low speed, beat together the butter (or canola oil) and brown sugar until well blended.


Beating together the butter with the brown sugar. ©Joyce Hays, Target Health Inc.



5. Slowly, while beating, add the flour, baking powder, baking soda, salt, spices, ginger, and nuts. Mix well; the batter will be a little crumbly looking.


Just before adding the eggs, the mixture will start to look crumbly. ©Joyce Hays, Target Health Inc.



6. Add the eggs one at a time, scraping the bottom and sides of the bowl after each addition.

7. Stir in the Amaretto, molasses and pumpkin, beating together slowly, so all ingredients are combined well.



After adding the eggs, one at a time, with beaters on, add the pumpkin, molasses and Amaretto. ©Joyce Hays, Target Health Inc.



8. Pour the batter into the greased spring-form cake pan.



With an electric mixer, this recipe is easy. Here, the mixture has been scraped out of the mixing bowl, with a spatula, and poured into the greased spring-form pan. ©Joyce Hays, Target Health Inc.


9. Bake for 30 minutes, or until cake is lightly browned on the edges and the middle springs back when touched.



Into the oven. ©Joyce Hays, Target Health Inc.



10. Remove the bread from the oven and let it cool for 15 minutes before taking it out of the pan(s). Let it cool a bit, then glaze if desired.



Just taken out of the oven. It has risen, but as it cools, it will fall back, making room for the date layer. ©Joyce Hays, Target Health Inc.


11. While the pumpkin cake is baking, make the date filling

12. Chop the dates



Chop the dates. ©Joyce Hays, Target Health Inc.



13. Grate the orange zest


14. In a medium saucepan, whisk together melted butter, eggs, molasses, golden syrup, cardamom, allspice, clove, nutmeg, salt, orange zest, Amaretto, vanilla extract. Cook, stirring, over medium heat until mixture thickens slightly, about 5 minutes. Stir in dates.



Melt the butter © Joyce Hays



To the melted butter add all the other ingredients for the date layer of the pumpkin cake. Stir well ©Joyce Hays, Target Health Inc.



Finally, add the chopped dates and stir well. ©Joyce Hays, Target Health Inc.


15. Pour the date layer, over the prebaked pumpkin cake, then sprinkle pecans over the soft date mixture. Bake for 20 to 30 minutes, or until filling is no longer jiggly and seems set.



With a spatula, scrape every last bit of the date mixture, out of the frying pan and over the top of the now, cooled pumpkin cake. Then press the pecan halves into the soft date layer. ©Joyce Hays, Target Health Inc.



With date layer and pecans added, cake goes into oven for the second time. ©Joyce Hays, Target Health Inc.



16    While cake is baking again, make the glaze: Whisk together all the ingredients, in a small bowl or measuring cup, adding extra liquid until the glaze is smooth and the consistency of molasses.



Mix together the sugar and the Amaretto together, needed for the glaze topping. ©Joyce Hays, Target Health Inc.



17. Remove from oven and cool on a rack for 15 minutes. Run a knife around the edge of pan to loosen cake, then remove the side of the spring-form bake pan.

18. Last, with a spoon, drizzle the sugar/Amaretto topping all over the top of the pumpkin-date cake and let it set. Don’t put cake back into the oven. Let the cake sit with the topping for about 30 minutes, before serving.



After cake has been removed from oven the second time, let it cool for 15 minutes, before you add the glaze. Then with a teaspoon, drizzle the glaze all over the top of the pumpkin-date cake. ©Joyce Hays, Target Health Inc.



Finally, sprinkle the orange zest over the top of the cake and let it sit for another 15 minutes, before you serve it. ©Joyce Hays, Target Health Inc.



19. Serve with vanilla ice cream, cool whip, whipped cream or without anything added.



We ate versions of this pumpkin/date cake all week, while I tried out different ingredients. We had it without pumpkin and the glaze; with a peanut butter topping; with a shortbread crust. Each time we sampled this recipe, for dessert, we gave the rest of cake away. It wasn’t ready to share with our special readers until this past Friday, when I added the Amaretto to the recipe. Hope you enjoy it, we loved doing it and especially the final version. ©Joyce Hays, Target Health Inc.



Trying out a new Italian red. Very good, similar to a cross between a cabernet and a merlot. ©Joyce Hays, Target Health Inc.




From Our Table to Yours !


Bon Appetit!


November 17, 2016

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences

Scientists have established comprehensive maps of the human epigenome, shedding light on how the body regulates which genes are active in which cells. Over the last five years, a worldwide consortium of scientists has established epigenetic maps of 2,100 cell types.



This is a methylated DNA molecule. DNA methylation plays an important role for epigenetic gene regulation in development and cancer.
Credit: Christoph Bock/CeMM



Scientists have established comprehensive maps of the human epigenome, shedding light on how the body regulates which genes are active in which cells. Over the last five years, a worldwide consortium of scientists has established epigenetic maps of 2,100 cell types. Within this coordinated effort, the CeMM Research Center for Molecular Medicine contributed detailed DNA methylation maps of the developing blood, opening up new perspectives for the understanding and treatment of leukemia and immune diseases.

One of the great mysteries in biology is how the many different cell types that make up our bodies are derived from a single cell and from one DNA sequence, or genome. We have learned a lot from studying the human genome, but have only partially unveiled the processes underlying cell determination. The identity of each cell type is largely defined by an instructive layer of molecular annotations on top of the genome — the epigenome — which acts as a blueprint unique to each cell type and developmental stage.

Unlike the genome the epigenome changes as cells develop and in response to changes in the environment. Defects in the factors that read, write, and erase the epigenetic blueprint are involved in many diseases. The comprehensive analysis of the epigenomes of healthy and abnormal cells will facilitate new ways to diagnose and treat various diseases, and ultimately lead to improved health outcomes.

A collection of 41 coordinated papers now published by scientists from across the International Human Epigenome Consortium (IHEC) sheds light on these processes, taking global research in the field of epigenomics a major step forward. These papers represent the most recent work of IHEC member projects from Canada, the European Union, Germany, Japan, Singapore, South Korea, and the United States. Three of these papers have been coordinated by Christoph Bock at CeMM.

The latest study from Christoph Bock’s team, published today in the journal Cell Stem Cell, charts the epigenetic landscape of DNA methylation in human blood. Led by CeMM scientists Matthias Farlik and Florian Halbritter together with Fabian Müller from Max Plank Institute for Informatics, this study highlights the dynamic nature of the epigenome in the development of human blood.

Our body produces billions of blood cells every day, which develop from a few thousand stem cells at the top of a complex hierarchy of blood cells. Using the latest sequencing and epigenome mapping technology, Bock’s team now unraveled a blueprint of blood development that is encoded in the DNA methylation patterns of blood stem cells and their differentiating progeny.

This success was made possible by close international cooperation of European scientists: Blood donations of British volunteers were sorted by cell type by the team of Mattia Frontini at the University of Cambridge. These samples were shipped to Austria, where CeMM scientists performed the epigenome mapping. All data were then processed in Germany at the Max Plank Institute for Informatics and jointly analyzed by scientists at CeMM and at the Max Plank Institute for Informatics.

The result of the combined effort of Bock’s team and many other members of IHEC is a detailed map of the human epigenome, similar to a three-dimensional mountain landscape: The stem cells reside on the mountain top, with valleys of cellular differentiation descending in many directions. As the cells differentiate, they pick one of several epigenetically defined routes and follow it downhill, eventually arriving at one specific valley, corresponding to a specialized cell type. Cells cannot easily escape these valleys, which provides robustness and protection against diseases such cancer.

Two other studies by Christoph Bock’s team were published earlier this year and showcase how researchers are seeking to utilize epigenetic information for medicine. For instance, certain routes of differentiation are jammed in leukemia, such that cells can no longer reach their destination and take wrong turns instead. Surveillance of those cells by epigenetic tests can contribute to a more precise diagnosis of leukemia — clinical tests of this approach are ongoing.

“The epigenetic map of the human blood helps us understand how leukemia develops and which cells drive the disease,” says Christoph Bock. This is relevant to cancer diagnostics and personalized medicine, and it provides a compass for future efforts aiming to reprogram the epigenome of individual cells, for example by erasing critical epigenetic alterations from leukemia cells.

Story Source:

Materials provided by CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences. Note: Content may be edited for style and length.

Journal Reference:

  1. Matthias Farlik, Florian Halbritter, Fabian Müller, Fizzah A. Choudry, Peter Ebert, Johanna Klughammer, Samantha Farrow, Antonella Santoro, Valerio Ciaurro, Anthony Mathur, Rakesh Uppal, Hendrik G. Stunnenberg, Willem H. Ouwehand, Elisa Laurenti, Thomas Lengauer, Mattia Frontini, Christoph Bock. DNA Methylation Dynamics of Human Hematopoietic Stem Cell Differentiation. Cell Stem Cell, 2016; DOI: 10.1016/j.stem.2016.10.019


Source: CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences. “Beyond the DNA: Comprehensive map of the human epigenome completed.” ScienceDaily. ScienceDaily, 17 November 2016. <>.

November 16, 2016

American Geophysical Union

Scientists have discovered a new large valley on Mercury that may be the first evidence of buckling of the planet’s outer silicate shell in response to global contraction. The researchers discovered the valley using a new high-resolution topographic map of part of Mercury’s southern hemisphere created by stereo images from NASA’s MESSENGER spacecraft.



A high-resolution digital elevation model derived from stereo images obtained by NASA’s MESSENGER spacecraft has revealed Mercury’s great valley shown here in this 3D perspective view.
Credit: NASA/Johns Hopkins University Applied Physics Laboratory/Carnegie Institution of Washington/DLR/Smithsonian Institution



Scientists have discovered a new large valley on Mercury that may be the first evidence of buckling of the planet’s outer silicate shell in response to global contraction. The researchers discovered the valley using a new high-resolution topographic map of part of Mercury’s southern hemisphere created by stereo images from NASA’s MESSENGER spacecraft. The findings were reported in a new study published inGeophysical Research Letters, a journal of the American Geophysical Union.

The most likely explanation for Mercury’s Great Valley is buckling of the planet’s lithosphere — its crust and upper mantle — in response to global contraction, according to the study’s authors. Earth’s lithosphere is broken up into many tectonic plates, but Mercury’s lithosphere consists of just one plate. Cooling of Mercury’s interior caused the planet’s single plate to contract and bend. Where contractional forces are greatest, crustal rocks are thrust upward while an emerging valley floor sags downward.

“There are examples of lithospheric buckling on Earth involving both oceanic and continental plates, but this may be the first evidence of lithospheric buckling on Mercury,” said Thomas R. Watters, senior scientist at the Center for Earth and Planetary Studies at the Smithsonian’s National Air and Space Museum in Washington, D.C., and lead author of the new study.

The valley is about 400 kilometers (250 miles) wide with its floor as much as 3 kilometers (2 miles) below the surrounding terrain. The valley is more than 1,000 kilometers (600 miles) long and extends into the Rembrandt basin, one of the largest and youngest impact basins on Mercury.

The valley is bound by two large fault scarps — steps on the planet’s surface where one side of a fault has moved vertically with respect to the other. Mercury’s contraction caused the fault scarps bounding the Great Valley to become so large they essentially became cliffs. The elevation of the valley floor is far below the terrain surrounding the mountainous faults scarps, which suggests the valley floor was lowered by the same mechanism that formed the scarps themselves, according to the study authors.

“Unlike Earth’s Great Rift Valley in East Africa, Mercury’s Great Valley is not caused by the pulling apart of lithospheric plates due to plate tectonics; it is the result of the global contraction of a shrinking one-plate planet,” Watters said. “Even though you might expect lithospheric buckling on a one-plate planet that is contracting, it is still a surprise when you find that it’s formed a great valley that includes the largest fault scarp and one of the largest impact basins on Mercury.”

Story Source:

Materials provided by American Geophysical Union. Note: Content may be edited for style and length.

Journal Reference:

  1. Thomas R. Watters, Laurent G. J. Montési, Jürgen Oberst, and Frank Preusker. Fault-Bound Valley Associated with the Rembrandt Basin on Mercury. Geophysical Research Letters, 2016; DOI: 10.1002/2016GL070205


Source: American Geophysical Union. “Great valley found on Mercury.” ScienceDaily. ScienceDaily, 16 November 2016. <>.

November 14, 2016

University of California San Diego Health Sciences

By sampling the molecules on cell phones, researchers were able to construct lifestyle sketches for each phone’s owner, including diet, preferred hygiene products, health status and locations visited. This proof-of-concept study could have a number of applications, including criminal profiling, airport screening, medication adherence monitoring, clinical trial participant stratification and environmental exposure studies.



Molecular traces left on cell phones allowed UC San Diego researchers to construct lifestyle sketches of each phone’s owner.
Credit: Amina Bouslimani and Neha Garg



We leave behind trace chemicals, molecules and microbes on every object we touch. By sampling the molecules on cell phones, researchers at University of California San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences were able to construct lifestyle sketches for each phone’s owner, including diet, preferred hygiene products, health status and locations visited. This proof-of-concept study, published November 14 by Proceedings of the National Academy of Sciences, could have a number of applications, including criminal profiling, airport screening, medication adherence monitoring, clinical trial participant stratification and environmental exposure studies.

“You can imagine a scenario where a crime scene investigator comes across a personal object — like a phone, pen or key — without fingerprints or DNA, or with prints or DNA not found in the database. They would have nothing to go on to determine who that belongs to,” said senior author Pieter Dorrestein, PhD, professor in UC San Diego School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences. “So we thought — what if we take advantage of left-behind skin chemistry to tell us what kind of lifestyle this person has?”

In a 2015 study, Dorrestein’s team constructed 3D models to illustrate the molecules and microbes found at hundreds of locations on the bodies of two healthy adult volunteers. Despite a three-day moratorium on personal hygiene products before the samples were collected, the researchers were surprised to find that the most abundant molecular features in the skin swabs still came from hygiene and beauty products, such as sunscreen.

“All of these chemical traces on our bodies can transfer to objects,” Dorrestein said. “So we realized we could probably come up with a profile of a person’s lifestyle based on chemistries we can detect on objects they frequently use.”

Thirty-nine healthy adult volunteers participated in Dorrestein’s latest study. The team swabbed four spots on each person’s cell phone — an object we tend to spend a lot of time touching — and eight spots on each person’s right hand, for a total of nearly 500 samples. Then they used a technique called mass spectrometry to detect molecules from the samples. They identified as many molecules as possible by comparing them to reference structures in the GNPS database, a crowdsourced mass spectrometry knowledge repository and annotation website developed by Dorrestein and co-author Nuno Bandeira, PhD, associate professor at the Jacobs School of Engineering and Skaggs School of Pharmacy and Pharmaceutical Sciences at UC San Diego.

With this information, the researchers developed a personalized lifestyle “read-out” from each phone. Some of the medications they detected on phones included anti-inflammatory and anti-fungal skin creams, hair loss treatments, anti-depressants and eye drops. Food molecules included citrus, caffeine, herbs and spices. Sunscreen ingredients and DEET mosquito repellant were detected on phones even months after they had last been used by the phone owners, suggesting these objects can provide long-term composite lifestyle sketches.

“By analyzing the molecules they’ve left behind on their phones, we could tell if a person is likely female, uses high-end cosmetics, dyes her hair, drinks coffee, prefers beer over wine, likes spicy food, is being treated for depression, wears sunscreen and bug spray — and therefore likely spends a lot of time outdoors — all kinds of things,” said first author Amina Bouslimani, PhD, an assistant project scientist in Dorrestein’s lab. “This is the kind of information that could help an investigator narrow down the search for an object’s owner.”

There are limitations, Dorrestein said. First of all, these molecular read-outs provide a general profile of person’s lifestyle, but they are not meant to be a one-to-one match, like a fingerprint. To develop more precise profiles and for this method to be more useful, he said more molecules are needed in the reference database, particularly for the most common foods people eat, clothing materials, carpets, wall paints and anything else people come into contact with. He’d like to see a trace molecule database on the scale of the fingerprint database, but it’s a large-scale effort that no single lab will be able to do alone.

Moving forward, Dorrestein and Bouslimani have already begun extending their study with an additional 80 people and samples from other personal objects, such as wallets and keys. They also hope to soon begin gathering another layer of information from each sample — identities of the many bacteria and other microbes that cover our skin and objects. In a 2010 study, their collaborator and co-author, Rob Knight, PhD, professor in the UC San Diego School of Medicine and Jacobs School of Engineering and director of the Center for Microbiome Innovation at UC San Diego, contributed to a study in which his team found they could usually match a computer keyboard to its owner just based on the unique populations of microbes the person left on it. At that time, they could make the match with a fair amount of accuracy, though not yet precisely enough for use in an investigation.

Beyond forensics, Dorrestein and Bouslimani imagine trace molecular read-outs could also be used in medical and environmental studies. For example, perhaps one day physicians could assess how well a patient is sticking with a medication regimen by monitoring metabolites on his or her skin. Similarly, patients participating in a clinical trial could be divided into subgroups based on how they metabolize the medication under investigation, as revealed by skin metabolites — then the medication could be given only to those patients who can metabolize it appropriately. Skin molecule read-outs might also provide useful information about a person’s exposure to environmental pollutants and chemical hazards, such as in a high-risk workplace or a community living near a potential pollution source.

Story Source:

Materials provided by University of California San Diego Health Sciences. Note: Content may be edited for style and length.

Journal Reference:

  1. Pieter C. Dorrestein et al. Lifestyle chemistries from phones for individual profiling. PNAS, November 2016 DOI: 10.1073/pnas.1610019113


Source: University of California San Diego Health Sciences. “What molecules you leave on your phone reveal about your lifestyle.” ScienceDaily. ScienceDaily, 14 November 2016. <>.

November 10, 2016

Polytechnique Montréal

From stationary to flying qubits at speeds never reached before…. This feat brings us a little closer to the era when information is transmitted via quantum principles.



New research is paving the way to producing quantum communications networks. (stock image)
Credit: © agsandrew / Fotolia



From stationary to flying qubits at speeds never reached before…. This feat, achieved by a team from Polytechnique Montréal and France’s Centre national de la recherche scientifique (CNRS), brings us a little closer to the era when information is transmitted via quantum principles.

A paper titled “High-Fidelity and Ultrafast Initialization of a Hole-Spin Bound to a Te Isoelectronic Centre in ZnSe” was recently published in the journal Physical Review Letters. The creation of a qubit in zinc selenide, a well-known semi-conductor material, made it possible to produce an interface between quantum physics that governs the behaviour of matter on a nanometre scale and the transfer of information at the speed of light, thereby paving the way to producing quantum communications networks.

Classical physics vs. quantum physics

In today’s computers, classical physics rules. Billions of electrons work together to make up an information bit: 0, electrons are absent and 1, electrons are present. In quantum physics, single electrons are instead preferred since they express an amazing attribute: the electron can take the value of 0, 1 or any superposition of these two states. This is the qubit, the quantum equivalent of the classical bit. Qubits provide stunning possibilities for researchers.

An electron revolves around itself, somewhat like a spinning top. That’s the spin. By applying a magnetic field, this spin points up, down, or simultaneously points both up and down to form a qubit. Better still, instead of using an electron, we can use the absence of an electron; this is what physicists call a “hole.” Like its electron cousin, the hole has a spin from which a qubit can be formed. Qubits are intrinsically fragile quantum creature, they therefore need a special environment.

Zinc selenide, tellurium impurities: a world first

Zinc selenide, or ZnSe, is a crystal in which atoms are precisely organized. It is also a semi-conductor into which it is easy to intentionally introduce tellurium impurities, a close relative of selenium in the periodic table, on which holes are trapped, rather like air bubbles in a glass.

This environment protects the hole’s spin — our qubit — and helps maintaining its quantum information accurately for longer periods; it’s the coherence time, the time that physicists the world over are trying to extend by all possible means. The choice of zinc selenide is purposeful, since it may provide the quietest environment of all semiconductor materials.

Polytechnique Montréal and CNRS of France, a team effort

Philippe St-Jean, a doctoral student on Professor Sébastien Francoeur’s team, uses photons generated by a laser to initialize the hole and record quantum information on it. To read it, he excites the hole again with a laser and then collects the emitted photons. The result is a quantum transfer of information between the stationary qubit, encoded in the spin of the hole held captive in the crystal, and the flying qubit — the photon, which of course travels at the speed of light.

This new technique shows that it is possible to create a qubit faster than with all the methods that have been used until now. Indeed, a mere hundred or so picoseconds, or less than a billionth of a second, are sufficient to go from a flying qubit to a static qubit, and vice-versa.

Although this accomplishment bodes well, there remains a lot of work to do before a quantum network can be used to conduct unconditionally secure banking transactions or build a quantum computer able to perform the most complex calculations. That is the daunting task which Sébastien Francoeur’s research team will continue to tackle.

The Natural Sciences and Engineering Research Council of Canada (NSERC) funded the research of Mr. Francoeur and his team.

Story Source:

Materials provided by Polytechnique Montréal. Note: Content may be edited for style and length.

Journal Reference:

  1. P. St-Jean, G. Éthier-Majcher, R. André, S. Francoeur. High-Fidelity and Ultrafast Initialization of a Hole Spin Bound to a Te Isoelectronic Center in ZnSe. Physical Review Letters, 2016; 117 (16) DOI: 10.1103/PhysRevLett.117.167401


Source: Polytechnique Montréal. “Breakthrough in the quantum transfer of information between matter and light.” ScienceDaily. ScienceDaily, 10 November 2016. <>.

UN Panel Discussion on Climate Change and Its Impact on Children’s Health


Target Health Inc. is honored that Jules Mitchel, PhD has been invited to speak at a UN Panel Discussion on “Climate Change and Its Impact on Children’s Health.“ His topic will be “The view from FDA and Biotech World.“ Other presenters will include World Health Organization (WHO) staff, pharmaceutical industry experts and representatives of civil society organizations specializing in climate policy issues. The discussion will consider the issue of climate change and its impact on children’s health and will be followed by an interactive Q&A session with the audience.  This is a free event.


Date: Thursday, November 17, 2016

Time: 2:00 pm – 5:00 pm

Location: UN Church Center

777 United Nations Plaza, 2nd Floor Conference Room

44th Street between First and Second Avenue, New York, NY, 10017.

Please RSVP before November 15

Aaron Etra,

Jules Mitchel,


For more information about Target Health contact Warren Pearlson (212-681-2100 ext. 165). For additional information about software tools for paperless clinical trials, please also feel free to contact Dr. Jules T. Mitchel or Ms. Joyce Hays. The Target Health software tools are designed to partner with both CROs and Sponsors. Please visit the Target Health Website.


Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor



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Bacteria that attempt to grow and divide in the presence of penicillin fail to do so, and instead end up shedding their cell walls. Credit: Shudde – Own work, CC BY-SA 3.0, Wikipedia Commons



Penicillin (PCN or pen) is a group of 1) ___ which include penicillin G (for intravenous use), penicillin V (for oral use), and procaine penicillin and benzathine penicillin (for intramuscular use). Penicillin antibiotics were among the first medications to be effective against many bacterial infections caused by staphylococci and streptococci. Penicillins are still widely used today, though many types of bacteria have developed resistance following extensive use. While 10% of people report that they are allergic to penicillin, realistically, up to 90% of this group may not actually be allergic. Serious allergies only occur in about 0.03% of people.


There are several enhanced penicillin families which are effective against additional bacteria; these include the antistaphylococcal penicillins, aminopenicillins and the antipseudomonal penicillins. They are all derived from Penicillium fungi. While the number of penicillin-resistant 2) ___ is increasing, penicillin can still be used to treat a wide range of infections caused by certain susceptible bacteria, including Streptococci, Staphylococci, Clostridium, and Listeria genera. Common adverse drug reactions (> 1% of people) associated with use of the penicillins include diarrhea, hypersensitivity, nausea, rash, neurotoxicity, urticaria, and superinfection (including candidiasis). Infrequent adverse effects (0.1-1% of people) include fever, vomiting, erythema, dermatitis, angioedema, seizures (especially in people with epilepsy), and pseudomembranous colitis.


Penicillin is a secondary metabolite of certain species of Penicillium and is produced when growth of the 3) ___ is inhibited by stress. It is not produced during active growth. The Penicillium cells are grown using a technique called fed-batch culture, in which the cells are constantly subject to stress, which is required for induction of penicillin production. The biotechnological method of directed evolution has been applied to produce by mutation a large number of Penicillium strains. These techniques include error-prone PCR, DNA shuffling, ITCHY, and strand-overlap PCR. Semisynthetic penicillins are prepared starting from the penicillin nucleus. The discovery of penicillin, one of the world’s first antibiotics, marks a true turning point in human history – when doctors finally had a tool that could completely cure their patients of deadly infectious 4) ___.


Penicillin was discovered in 1928 by Scottish scientist Alexander Fleming. People began using it to treat infections in 1942. As the story goes, Dr. Alexander Fleming, the bacteriologist on duty at St. Mary’s Hospital, returned from a summer vacation in Scotland to find a messy lab bench and a good deal more. Upon examining some colonies of Staphylococcus aureus, Dr. Fleming noted that a mold called Penicillium notatum had contaminated his Petri dishes. After carefully placing the dishes under his microscope, he was amazed to find that the mold prevented the normal growth of the staphylococci. It took Fleming a few more weeks to grow enough of the 5) ___ so that he was able to confirm his findings. There was some factor in the Penicillium mold that not only inhibited the growth of the bacteria but, more importantly, might be harnessed to combat infectious diseases.


Fleming: “When I woke up just after dawn on September 28, 1928, I certainly didn’t plan to revolutionize all medicine by discovering the world’s first antibiotic, or bacteria killer. But I guess that was exactly what I did.“


Fourteen years later, in March 1942, Anne Miller became the first civilian patient to be successfully treated with 6) ___, lying near death at New Haven Hospital in Connecticut, after miscarrying and developing an infection that led to blood poisoning


Actually, Fleming had neither the laboratory resources at St. Mary’s nor the chemistry background to take the next giant steps of isolating the active ingredient of the penicillium mold juice, purifying it, figuring out which germs it was effective against, and how to use it. That task fell to Dr. Howard Florey, a professor of pathology who was director of the Sir William Dunn School of Pathology at 7) ___ University. This landmark work began in 1938 when Florey, who had long been interested in the ways that bacteria and mold naturally kill each other, came across Fleming’s paper on the penicillium mold while leafing through some back issues of The British Journal of Experimental Pathology. Soon after, Florey and his colleagues assembled. They decided to unravel the science beneath what Fleming called penicillium’s “antibacterial action.“ One of Florey’s brightest employees was a biochemist, Dr. Ernst Chain, a Jewish German emmigrant. They produced a series of crude penicillium-mold culture fluid extracts. During the summer of 1940, their experiments centered on a group of 50 mice that they had infected with deadly streptococcus. Half the mice died miserable deaths from overwhelming sepsis. The others, which received penicillin injections, survived. It was at that point that Florey realized that he had enough promising information to test the drug on people. But the problem remained: how to produce enough pure penicillin to treat people. In spite of efforts to increase the yield from the mold cultures, it took 2,000 liters of mold culture fluid to obtain enough pure penicillin to treat a single case of sepsis in a person. Another vital figure in the lab was a biochemist, Dr. Norman Heatley, who used every available container, bottle and bedpan to grow vats of the penicillin mold, suction off the fluid and develop ways to purify the antibiotic. The makeshift mold factory he put together was about as far removed as one could get from the enormous fermentation tanks and sophisticated chemical engineering that characterize modern antibiotic production today.


In the summer of 1941, shortly before the United States entered World War II, Florey and Heatley flew to the United States, where they worked with American scientists in Peoria, Ill., to develop a means of mass producing what became known as the wonder 8) ___. Aware that the fungus Penicillium notatum would never yield enough penicillin to treat people reliably, Florey and Heatley searched for a more productive species. One hot summer day, a laboratory assistant, Mary Hunt, arrived with a cantaloupe that she had picked up at the market and that was covered with a “pretty, golden mold.“ Serendipitously, the mold turned out to be the fungus Penicillium chrysogeum, and it yielded 200 times the amount of penicillin as the species that Fleming had described. Yet even that species required enhancing with mutation-causing X-rays and filtration, ultimately producing 1,000 times as much penicillin as the first batches from Penicillium notatum.


In the WWII, penicillin proved its high worth. Throughout history, the major killer in wars had been 9) ___ rather than battle injuries. In World War I, the death rate from bacterial pneumonia was 18%; in World War II, it fell, to less than 1%. From January to May in 1942, 400 million units of pure penicillin were manufactured. By the end of the war, American pharmaceutical companies were producing 650 billion units a month. Beginning in 1941, after news reporters began to cover the early trials of the antibiotic on people, Fleming was lionized as the discoverer of penicillin. And much to the quiet consternation of Florey, the Oxford group’s contributions were virtually ignored. That problem was partially corrected in 1945, when Fleming, Florey, and Chain – but not Heatley – were awarded the Nobel Prize in Physiology or Medicine. In his acceptance speech, Fleming presciently warned that the overuse of penicillin might lead to bacterial 10) ___. In 1990, Oxford made up for the Nobel committee’s oversight by awarding Heatley the first honorary doctorate of medicine in its 800-year history. Sources: Wikipedia; Dr. Howard Markel; PBS


ANSWERS: 1) antibiotics; 2) bacteria; 3) fungus; 4) diseases; 5) mold; 6) penicillin; 7) Oxford; 8) drug; 9) infection; 10) resistance


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