Salmon Corn Cakes with Ginger & Dill


It has taken a lot of trial and error, to arrive at this delicious recipe for salmon/corn cakes. And I am happy to share it. The flavors are now, balanced so well, that you get a magnificent mouthful of satisfaction, with the first bite. Not only are these “o-oh so-o“ good, but they are really easy to make, if you take the time to buy all of the ingredients. ©Joyce Hays, Target Health Inc.



A dollop of homemade tartar sauce and you’re in for a real treat. ©Joyce Hays, Target Health Inc.



I made a big batch, but by the end of the weekend they were gone. These salmon/corn cakes are good for dinner, lunch, brunch and snacks. I served them for dinner, Friday night with roasted red, oregano/garlic potato cubes and Brussels sprouts halves, roasted with garlic and aged balsamic vinegar. We started the meal with Hall cabernet sauvignon and cruditees instead of a salad and warm (right out of the oven) home-made corn bread. As you may know, the recipe theme, following Labor Day, has been this season’s superb sweet corn, harvested from local farms. I still have a few more sweet corn recipes, as we enter October. ©Joyce Hays, Target Health Inc.





2 thick salmon fillets (remove any bones and skin)

1 Tablespoon ginger puree

1 Tablespoon lemongrass paste

4 large cloves of garlic, thinly sliced

1 teaspoon turmeric

1/2 cup fresh dill, chopped well

1/2 teaspoon ground coriander

1 teaspoon cardamom

4 fresh ears corn, all kernels scraped off

2 large eggs beaten

2/3 cup fresh cilantro, chopped

1 pinch chili flakes (or cayenne)

1 Tablespoon fish sauce

1 Tablespoon low-sodium soy/tamari sauce

Zest of 1/2 fresh lime

Juice of 1/2 lime

Coconut oil (or ghee) for shallow-frying


Panko to roll the cakes in, before cooking


Get the best fresh ingredients. ©Joyce Hays, Target Health Inc.





Dice one of the salmon fillets, and blend the other to a paste using a food processor. You want to keep some of the salmon in the form of small chunks, to enhance the texture.

Combine all the salmon in a medium bowl. Add the remaining ingredients, and mix well. Marinate this mixture for one hour in the fridge.

You could make rice while you’re waiting and/or a green salad.

When you’re ready to eat, heat the coconut oil in a frying pan. Shape the fish mixture into small patties (I just rolled some into a ball in my hands and then squashed it, slightly, in the pan). But first, roll each salmon/corn cake in the Panko, before cooking.



Rolling the fish cakes in Panko before cooking. ©Joyce Hays, Target Health Inc.



Consider putting a loose (not tight) lid on your pan while the salmon/corn cakes are cooking. Once in a while, you’ll get a corn kernel popping right out of the pan, and you don’t want it to hit you in the eye.



Cook first one side ©Joyce Hays, Target Health Inc.



and then, the other, for about 2 to 3 minutes on each side, depending on how thick your fish cakes are. Lovely smell while cooking. ©Joyce Hays, Target Health Inc.



Fry for a couple of minutes on each side. I bought sushi-grade salmon and cooked it about 2 minutes on each side. If you make your salmon/corn cakes thick, then cook 3 minutes on each side. They should be golden and springy, when done.

Garnish with fresh dill or cilantro. Serve tartar sauce at the table.

Or you could use my previously published whipped white sauce for fish: (it also makes a good veggie dip)

1 container plain Greek yogurt

8 oz. creamy goat cheese (creamy not crumbly), this is optional.

2-3 Polish pickles chopped well

2 large garlic cloves, squeezed

2 Tablespoons Kraft mayo

In a small or medium bowl, whip all of the above ingredients, very well, by hand and serve on the table with the salmon/corn cakes.


Make your favorite rice (boil in chicken broth not water), like jasmine and serve the salmon/corn cakes on top of a mound of rice. You could also serve a fennel pear grape salad, tossed with some toasted sesame seeds, a few flaked almonds and a lemon or lime dressing, garnished with a pinch of fresh coconut shreds. If you serve this in August-October, add fresh figs, cut in quarters.



Naturally, a chilled white wine would be perfect with the salmon/corn cakes; however, if you’re feeling like a red, this Hall cabernet sauvignon is the only red we know of, that goes well with fish. ©Joyce Hays, Target Health Inc.



We were too sad to go out this weekend. The funeral service for one of our most beloved employees, Kuo Ping Yu was on Saturday. Among many, many others, Target Health employees attended. The setting was lovely. His family is especially beautiful, but this occasion was profoundly sad for us.


Farewell, dear KP Yu; you will be greatly missed. You are in our hearts forever.


September 22, 2016

University of California, Irvine

By adding highly accurate radiocarbon dating of soil to standard Earth system models, environmental scientists have learned a dirty little secret: The ground will absorb far less atmospheric carbon dioxide this century than previously thought.



The UCI-led study found that soil integrates carbon far slower than thought, meaning the amount it’s capable of absorbing from the atmosphere this century is much less than predicted by current Earth system models.
Credit: Steve Zylius / UCI



By adding highly accurate radiocarbon dating of soil to standard Earth system models, environmental scientists from the University of California, Irvine and other institutions have learned a dirty little secret: The ground will absorb far less atmospheric carbon dioxide this century than previously thought.

Researchers used carbon-14 data from 157 sample sites around the world to determine that current soil carbon is about 3,100 years old — rather than the 450 years stipulated by many Earth system models.

“This work indicates that soils have a weaker capacity to soak up carbon than we have been assuming over the past few decades,” said UCI Chancellor’s Professor of Earth system science James Randerson, senior author of a new study on the subject to be published in the journal Science. “It means we have to be even more proactive in finding ways to cut emissions of fossil fuels to limit the magnitude and impacts of climate warming.”

Through photosynthesis, plants absorb CO2 from the air. When trees and vegetation die and decay, they become part of the soil, effectively locking carbon on or beneath Earth’s surface — keeping it out of the atmosphere, where it contributes to global warming. In their study, the researchers showed that since this process unfolds over millennia versus decades or centuries, we should expect less of this land carbon sequestration in the 21st century than suggested by current Earth system models.

“A substantial amount of the greenhouse gas that we thought was being taken up and stored in the soil is actually going to stay in the atmosphere,” said study co-author Steven Allison, UCI associate professor of ecology & evolutionary biology and Earth system science.

In recent years, scientists have used highly complex, computer-based Earth system models — compilations of code integrating data on the planet’s oceans, land surfaces, ice masses, atmosphere and biological systems — to draw conclusions about potential future changes in regional and global temperatures, drought, sea levels and other phenomena.

The models don’t explicitly provide the age of carbon in soils, but lead author Yujie He, a UCI postdoctoral scholar when the study was conducted, said that she and her colleagues figured out a way to improve them through simplification and the addition of dating methods well-established in the scientific community.

“Radiocarbon is an excellent tool for understanding soil dynamics,” He said. “Our study demonstrated that by working to reduce the complexity of Earth system models and combining observational data, we could get them to reveal surprising findings.”

The authors said that adding more carbon to that which has been in the ground for thousands of years is problematic given the pace at which Earth seems capable of integrating it.

“If we waited 300, 400, 1,000 years, then that carbon — we think — would go into the soil. But that’s not going to help us in dealing with climate change, which is happening now,” Allison said. “You have to do a lot of risk assessment to say, well, what’s the actual cost of just waiting for that sequestration, and what policies should we implement to avoid that possible cost? That’s outside the realm of our actual work here, but what we can say is that the problems of carbon emission and climate change are worse than what we expected previously.”

Story Source:

The above post is reprinted from materials provided byUniversity of California, Irvine. Note: Content may be edited for style and length.

Journal Reference:

  1. Yujie He et al. Radiocarbon constraints imply reduced carbon uptake by soils during the 21st century. Science, September 2016 DOI: 10.1126/science.aad4273


Source: University of California, Irvine. “Soil will absorb less atmospheric carbon than expected this century, study finds.” ScienceDaily. ScienceDaily, 22 September 2016. <>.

Gene-regulating RNA molecules could help treat early-stage breast cancer tumors before they spread

September 21, 2016

Massachusetts Institute of Technology

A new gene therapy technique being developed is showing promise as a way to prevent breast cancer tumors from metastasizing. The treatment uses microRNAs — small noncoding RNA molecules that regulate gene expression — to control metastasis.



Breast cancer graphic (stock image).
Credit: © designer491 / Fotolia



The spread of malignant cells around the body, known as metastasis, is the leading cause of mortality in women with breast cancer.

Now, a new gene therapy technique being developed by researchers at MIT is showing promise as a way to prevent breast cancer tumors from metastasizing.

The treatment, described in a paper published in the journalNature Communications, uses microRNAs — small noncoding RNA molecules that regulate gene expression — to control metastasis.

The therapy could be used alongside chemotherapy to treat early-stage breast cancer tumors before they spread, according to Natalie Artzi, a principal research scientist at MIT’s Institute for Medical Engineering and Science (IMES) and an assistant professor of medicine at Brigham and Women’s Hospital, who led the research in collaboration with Noam Shomron, an assistant professor on the faculty of medicine at Tel-Aviv University in Israel.

“The idea is that if the cancer is diagnosed early enough, then in addition to treating the primary tumor [with chemotherapy], one could also treat with specific microRNAs, in order to prevent the spread of cancer cells that cause metastasis,” Artzi says.

The regulation of gene expression by microRNAs is known to be important in preventing the spread of cancer cells. Recent studies by the Shomron team in Tel-Aviv have shown that disruption of this regulation, for example by genetic variants known as single nucleotide polymorphisms (SNPs), can have a significant impact on gene expression levels and lead to an increase in the risk of cancer.

To identify the specific microRNAs that play a role in breast cancer progression and could therefore potentially be used to suppress metastasis, the research teams first carried out an extensive bioinformatics analysis.

They compared three datasets: one for known SNPs; a second for sites at which microRNAs bind to the genome; and a third for breast cancer-related genes known to be associated with the movement of cells.

This analysis revealed a variant, or SNP, known as rs1071738, which influences metastasis. They found that this SNP disrupts binding of two microRNAs, miR-96 and miR-182. This disruption in turn prevents the two microRNAs from controlling the expression of a protein called Palladin.

Previous research has shown that Palladin plays a key role in the migration of breast cancer cells, and their subsequent invasion of otherwise healthy organs.

When the researchers carried out in vitro experiments in cells, they found that applying miR-96 and miR-182 decreased the expression of Palladin levels, in turn reducing the ability of breast cancer cells to migrate and invade other tissue.

“Previous research had discussed the role of Palladin in controlling migration and invasion (of cancer cells), but no one had tried to use microRNAs to silence those specific targets and prevent metastasis,” Artzi says. “In this way we were able to pinpoint the critical role of these microRNAs in stopping the spread of breast cancer.”

The researchers then developed a method to deliver engineered microRNAs to breast cancer tumors. They embedded nanoparticles containing the microRNAs into a hydrogel scaffold, which they then implanted into mice.

They found that this allowed efficient and precise delivery of the microRNAs to a target breast cancer tumor site. The treatment resulted in a dramatic reduction in breast cancer metastasis, says Artzi.

“We can locally change the cells in order to prevent metastasis from occurring,” she says.

To increase the effectiveness of the treatment even further, the researchers then added the chemotherapy drug cisplatin to the nanoparticles. This led to a significant reduction in both the growth of the primary tumor, and its metastasis.

“We believe local delivery is much more effective (than systemic treatment), because it gives us a much higher effective dose of the cargo, in this case the two microRNAs and the cisplatin,” she says.

“The research offers the potential for combined experimental therapeutics with traditional chemotherapy in cancer metastasis,” says Julie Teruya-Feldstein, a professor of pathology at Mount Sinai Hospital in New York, who was not involved in the study.

The research team, which also includes MIT post doc Joao Conde and graduate student Nuria Oliva, both from IMES; graduate student Avital Gilam and postdoc Daphna Weissglas-Volkov, from Tel-Aviv University; and Eitan Friedman, an oncogeneticist from Chaim Sheba Medical Center in Israel, now hopes to move on to larger animal studies of the treatment.

“We are very excited about the results so far, and the efficacy seems to be really good. So the next step will be to move on to larger models and then to clinical trials, although there is still a long way to go,” Artzi says.

Story Source:

The above post is reprinted from materials provided byMassachusetts Institute of Technology. The original item was written by Helen Knight. Note: Content may be edited for style and length.

Journal Reference:

  1. Avital Gilam, João Conde, Daphna Weissglas-Volkov, Nuria Oliva, Eitan Friedman, Natalie Artzi, Noam Shomron. Local microRNA delivery targets Palladin and prevents metastatic breast cancer. Nature Communications, 2016; 7: 12868 DOI: 10.1038/ncomms12868


Source: Massachusetts Institute of Technology. “Gene therapy technique may help prevent cancer metastasis: Gene-regulating RNA molecules could help treat early-stage breast cancer tumors before they spread.” ScienceDaily. ScienceDaily, 21 September 2016. <>.

September 20, 2016

Case Western Reserve University

A fungus has been identified as a key factor in the development of Crohn’s disease, an international team of researchers has identified for the first time.



Crohn’s disease is a debilitating inflammatory bowel disease, which causes severe abdominal pain, diarrhea, weight loss, and fatigue.
Credit: © vaakim / Fotolia



A Case Western Reserve University School of Medicine-led team of international researchers has for the first time identified a fungus as a key factor in the development of Crohn’s disease. The researchers also linked a new bacterium to the previous bacteria associated with Crohn’s. The groundbreaking findings, published on September 20th in mBio, could lead to potential new treatments and ultimately, cures for the debilitating inflammatory bowel disease, which causes severe abdominal pain, diarrhea, weight loss, and fatigue.

“We already know that bacteria, in addition to genetic and dietary factors, play a major role in causing Crohn’s disease,” said the study’s senior and corresponding author, Mahmoud A Ghannoum, PhD, professor and director of the Center for Medical Mycology at Case Western Reserve and University Hospitals Cleveland Medical Center “Essentially, patients with Crohn’s have abnormal immune responses to these bacteria, which inhabit the intestines of all people. While most researchers focus their investigations on these bacteria, few have examined the role of fungi, which are also present in everyone’s intestines. Our study adds significant new information to understanding why some people develop Crohn’s disease. Equally important, it can result in a new generation of treatments, including medications and probiotics, which hold the potential for making qualitative and quantitative differences in the lives of people suffering from Crohn’s.”

Both bacteria and fungi are microorganisms — infinitesimal forms of life that can only be seen with a microscope. Fungi are eukaryotes: organism whose cells contain a nucleus; they are closer to humans than bacteria, which are prokaryotes: single-celled forms of life with no nucleus. Collectively, the fungal community that inhabits the human body is known as the mycobiome, while the bacteria are called the bacteriome. (Fungi and bacteria are present throughout the body; previously Ghannoum had found that people harbor between nine and 23 fungal species in their mouths.)

The researchers assessed the mycobiome and bacteriome of patients with Crohn’s disease and their Crohn’s-free first degree relatives in nine families in northern France and Belgium, and in Crohn’s-free individuals from four families living in the same geographic area. Specifically, they analyzed fecal samples of 20 Crohn’s and 28 Crohn’s-free patients from nine families and of 21 Crohn’s-free patients of four families. The researchers found strong fungal-bacterial interactions in those with Crohn’s disease: two bacteria (Escherichia coli and Serratia marcescens) and one fungus (Candida tropicalis) moved in lock step. The presence of all three in the sick family members was significantly higher compared to their healthy relatives, suggesting that the bacteria and fungus interact in the intestines. Additionally, test-tube research by the Ghannoum-led team found that the three work together (with the E. coli cells fusing to the fungal cells and S. marcescens forming a bridge connecting the microbes) to produce a biofilm — a thin, slimy layer of microorganisms found in the body that adheres to, among other sites, a portion of the intestines — which can prompt inflammation that results in the symptoms of Crohn’s disease.

This is first time any fungus has been linked to Crohn’s in humans; previously it was only found in mice with the disease. The study is also the first to include S. marcescens in the Crohn’s-linked bacteriome. Additionally, the researchers found that the presence of beneficial bacteria was significantly lower in the Crohn’s patients, corroborating previous research findings.

“Among hundreds of bacterial and fungal species inhabiting the intestines, it is telling that the three we identified were so highly correlated in Crohn’s patients,” said Ghannoum. “Furthermore, we found strong similarities in what may be called the ‘gut profiles’ of the Crohn’s-affected families, which were strikingly different from the Crohn’s-free families. We have to be careful, though, and not solely attribute Crohn’s disease to the bacterial and fungal makeups of our intestines. For example, we know that family members also share diet and environment to significant degrees. Further research is needed to be even more specific in identifying precipitators and contributors of Crohn’s.”

Story Source:

The above post is reprinted from materials provided by Case Western Reserve University. Note: Content may be edited for style and length.

Journal Reference:

  1. G. Hoarau, P. K. Mukherjee, C. Gower-Rousseau, C. Hager, J. Chandra, M. A. Retuerto, C. Neut, S. Vermeire, J. Clemente, J. F. Colombel, H. Fujioka, D. Poulain, B. Sendid and M. A. Ghannoum. Bacteriome and Mycobiome Interactions Underscore Microbial Dysbiosis in Familial Crohn’s Disease. mBio, September 2016 DOI:10.1128/mBio.01250-16


Source: Case Western Reserve University. “Fungus in humans identified for first time as key factor in Crohn’s disease.” ScienceDaily. ScienceDaily, 20 September 2016. <>.

September 19, 2016

University of Houston

Hydrogen is often considered a fuel for the future, in the form of fuel cells to power electric motors or burned in internal combustion engines. But finding a practical, inexpensive and nontoxic way to produce large amounts of hydrogen gas — especially by splitting water into its component parts, hydrogen and oxygen — has been a challenge.



lllustration shows procedures for growing ternary molybdenum sulfoselenide on the porous foam; b-c, images showing surface roughness of the nickel diselenide foam grown at 600 degrees C; d-e, morphologies of ternary molybdenum sulfoselenide particles on porous foam, grown at 500 degrees C.
Credit: Image courtesy of University of Houston



Hydrogen is often considered a fuel for the future, in the form of fuel cells to power electric motors or burned in internal combustion engines. But finding a practical, inexpensive and nontoxic way to produce large amounts of hydrogen gas — especially by splitting water into its component parts, hydrogen and oxygen — has been a challenge.

A team of researchers from the University of Houston and the California Institute of Technology has reported a more efficient catalyst, using molybdenum sulfoselenide particles on three-dimensional porous nickel diselenide foam to increase catalytic activity.

The foam, made using commercially available nickel foam, significantly improved catalytic performance because it exposed more edge sites, where catalytic activity is higher than it is on flat surfaces, said Zhifeng Ren, MD Anderson Professor of physics at UH.

Ren is lead author of a paper in Nature Communicationsdescribing the discovery. Other researchers involved include Haiqing Zhou, Fang Yu, Jingying Sun, Ran He, Shuo Chen, Jiming Bao and Zhuan Zhu, all of UH, and Yufeng Huang, Robert J. Nielsen and William A. Goddard III of the California Institute of Technology.

“With the massive consumption of fossil fuels and its detrimental impact on the environment, methods of generating clean power are urgent,” the researchers wrote. “Hydrogen is an ideal carrier for renewable energy; however, hydrogen generation is inefficient because of the lack of robust catalysts that are substantially cheaper than platinum.”

Platinum catalysts have the highest efficiency rate for hydrogen evolution, said Ren, who also is a principal investigator at the Texas Center for Superconductivity. But platinum is rare, difficult to extract and too expensive for practical use, he said, and researchers continue to seek less expensive ways to split water into its component parts.

Currently, most hydrogen is produced through steam methane reforming and coal gasification; those methods raise the fuel’s carbon footprint despite the fact that it burns cleanly.

Molybdenum sulfoselenide and similar layered compounds have shown promise as catalysts, but so far no one has boosted their performance to viable levels in bulk form. The researchers say most active catalysis on those layered compounds, known as layered transition-metal dichalcogenides, or LTMDs, takes place at the edges, making the idea of a substrate with a large number of exposed edges more desirable. Also, they wrote, “arranging two different materials into hybrids might lead to synergistic effects that utilize the best properties of each component.”

Their hybrid catalyst is composed of molybdenum sulfoselenide particles with vertically aligned layers on a 3-D porous conductive nickel diselenide scaffold.

Testing determined that the hybrid catalyst required 69 millivolts from an external energy source to achieve a current density of 10 milliamps per square centimeter, which the researchers said is much better than many previously reported tests. In this case, the current “splits” the water, converting it to hydrogen at the cathode. Achieving the necessary current density with lower voltage improves energy conversion efficiency and reduces preparation costs.

A platinum catalyst required 32 millivolts in the testing, but Ren said ongoing testing has reduced the hybrid catalyst requirements to about 40 millivolts, close to the platinum requirements.

Equally important, he said, was the ability to increase current output at a faster rate than the increase in required energy input. The catalyst remained stable after 1,000 cycles at a constant current.

The work will continue as researchers focus on reducing required voltage.

Story Source:

The above post is reprinted from materials provided byUniversity of Houston. The original item was written by Jeannie Kever. Note: Content may be edited for style and length.

Journal Reference:

  1. Haiqing Zhou, Fang Yu, Yufeng Huang, Jingying Sun, Zhuan Zhu, Robert J. Nielsen, Ran He, Jiming Bao, William A. Goddard III, Shuo Chen, Zhifeng Ren. Efficient hydrogen evolution by ternary molybdenum sulfoselenide particles on self-standing porous nickel diselenide foam. Nature Communications, 2016; 7: 12765 DOI:10.1038/ncomms12765


Source: University of Houston. “More efficient way to split water, produce hydrogen.” ScienceDaily. ScienceDaily, 19 September 2016. <>.

Disruptive Innovations (DPharm) Meeting – September 20-21 (Boston)


If you can make it, join us at Disruptive Innovations US (September 20 – 21, 2016), being held at The Fairmont Copley Plaza, Boston. This is the best meeting for those interested in change and getting things to happen. This year, Dr. Jules Mitchel, President of Target Health Inc. will talk about Target Health’s accomplishments in the area of the paperless clinical trial, including highlighting an FDA-cleared product where eSource (Target e*CTR®) was used in the pivotal trial.


The DPharm meeting is a TED-style event showcasing innovators from leading Pharma companies and from other industries. The conference highlights the promises and challenges of innovation in advancing drug development and features new models and collaborations to get therapeutics to patients faster. DPharm also features the full spectrum of clinical research options and is dedicated to finding ways for implementation. Finally, DPharm will explore the companies who are being disruptive so we can all gain a better understanding of how novel approaches are impacting the clinical trial ecosystem.


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, and if you like the weekly newsletter, ON TARGET, you’ll love the Blog.


Joyce Hays, Founder and Editor in Chief of On Target

Jules Mitchel, Editor



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Pollution Particles in the Brain Linked to Alzheimer’s Disease


Increased coal fires burned in London, the winter of 1952, causing deadly air pollution.

Photo source: N T Stobbs,



Photo source: Air Pollution in Hong Kong on two different days.

By Tokyoahead at English Wikipedia:



Microscopic analysis has shown, for the first time, tiny magnetic particles from air pollution lodged in human brains. Researchers believe the large volume of magnetite particles found in brain samples suggest a possible link with Alzheimer’s disease. “Air pollution particles linked to Alzheimer’s found in human brain,“ New research has found tiny particles of magnetite – a potentially toxic by-product of traffic pollution – in samples of 1) ___ tissue. The samples, obtained after death, were taken from 29 people from Mexico City and eight people from Manchester England.


Magnetite is formed naturally in small quantities in the body, but the shapes of the naturally formed particles are jagged and irregular, while the particles found in the brain samples were spherical with smooth, fused surfaces. Magnetite may increase oxidative damage – damage caused at the molecular level – to brain cells, especially in the presence of amyloid beta protein, a key protein linked to 2) ___ disease. While it’s worrying to think pollution particles can enter the brain, it’s unclear what role, if any, these particles really have in the development of the disease. The people studied did not have Alzheimer’s disease, although some of the eight people from the UK had a neurodegenerative disease. The researchers have called for more work to be done to establish whether or not 3) ___ particles from air pollution play a role in causing Alzheimer’s disease. Independent experts have reacted with caution, saying this is as yet unknown.


Air pollution levels have fallen significantly in the UK in the last 40 years, but there has not been a corresponding fall in Alzheimer’s cases, possibly making the link between the two harder to determine. The study was carried out by researchers from the University of Lancaster, the University of Oxford, the University of Glasgow, the University of Manchester, the University of Montana and Universidad Nacional Autonoma de Mexico, and published in the Proceedings of the National Academy of Sciences (6 September 2016). The study analyzed brain tissue samples using four types of particle analysis processes. This type of study can show that these specific particles are present in the brains of the people studied, but nothing else. It can’t tell us whether these particles are found in everyone’s brains or just in the brains of people who live in 4) ___ areas, or whether they are more common in people with Alzheimer’s disease. The study took samples of brain tissue from 29 people from Mexico City aged 3 to 85 years, and eight people from Manchester in the UK aged 62 to 92 years, and analyzed the samples using four different scanning and analysis procedures to examine the minerals, shape and composition of nanoparticles found in the frontal 5) ___ of the brains. The researchers looked at the number and size of the particles. They also compared the qualities of the particles found with previously identified naturally occurring magnetite particles, and also with particles found in air samples taken at roadsides in Lancaster. The study found that all of the brain samples contained “abundant“ magnetite particles “that match precisely the high-temperature magnetite nanospheres formed by combustion and/or friction-derived heating, which are prolific in urban, airborne particulate matter“. The concentrations were mainly highest among older people, although some of the samples taken from much younger Mexico City residents were also very high. Mexico City is known to have high levels of 6) ___ pollution. The researchers say they found two types of particles: the jagged types thought to form naturally, and the spherical, smooth type consistent with particles produced by air pollution. These rounded forms also varied in size much more than the smaller naturally occurring variety. The researchers say their results may explain previous research, which found spherical particles of magnetite in the plaques and tangles of protein in brain tissue from people with Alzheimer’s disease. They also point to previous research from Taiwan, which found people living in areas with higher air pollution were more likely to get Alzheimer’s disease. They say theoretically these particles could get from air into the brain via the 7) ___ nerve, which carries information about smell from the nose to the brain. The study concluded that “Because of their combination of ultrafine size, specific brain toxicity, and ubiquity within airborne particulate matter, pollution-derived magnetite nanoparticles might require consideration as a possible Alzheimer’s disease risk factor.“.


The study is quite limited in what it tells us. We know the researchers found particles of magnetite in all the brain samples studied, but as there was no control group – for example, people without neurodegenerative disease in the UK, or people from a less polluted part of Mexico – we don’t know the significance of the finding. And we don’t know whether brains of people with Alzheimer’s disease are more or less likely to contain magnetite 8) ___ than any other brains. It’s important that scientists investigate these findings further to answer some of these questions. Avoiding pollution is sensible for health reasons if you can manage it – for example, by walking away from the edge of a busy road, or cycling through back streets – but it’s not always possible. Although nothing guarantees that you won’t develop Alzheimer’s disease, there are plenty of things you can do to lower your 9) ___ of the condition:


don’t smoke

drink only in moderation

keep physically active

eat a healthy diet

keep an eye on your 10) ___ pressure

stay mentally active



Maher BA, Ahmed IAM, Karloukovski V, et al. Magnetite pollution nanoparticles in the human brain. PNAS. Published online September 6 2016


Reuters video on YouTube: Air pollution and Alzheimer’s Disease

Tiny particles found in brain


TED Athens: Air Pollution Pandemic


ANSWERS: 1) brain; 2) Alzheimer’s; 3) magnetite; 4) polluted; 5) cortex; 6) air; 7) olfactory; 8) particles; 9) risk; 10) blood


Health and Medical History of President Thomas Jefferson


Thomas Jefferson



History reminds us that a Gordian knot entangles the science of medicine and the art of politics at this level of power.


Thomas Jefferson was the primary author of the Declaration of Independence. At age 33 he was one of the youngest delegates to the Second Continental Congress beginning in 1775 at the outbreak of the American Revolutionary War where a formal declaration of independence from Britain was overwhelmingly favored. Jefferson chose his words for the Declaration in June 1775 shortly after the war had begun where the idea of Independence from Britain had long since become popular among the colonies. He was also inspired by the Enlightenment ideals of the sanctity of the individual as well as the writings of Locke and Montesquieu.


Jefferson began his childhood education beside the Randolph children with tutors at Tuckahoe. In 1752, he began attending a local school run by a Scottish Presbyterian minister. At age nine, he started studying Latin, Greek, and French; he learned to ride horses and began nature studies. He was taught from 1758 to 1760 by Reverend James Maury near Gordonsville, Virginia, where he studied history, science, and the classics while boarding with Maury’s family. Jefferson entered the College of William & Mary in Williamsburg, Virginia, at age 16, and studied mathematics, metaphysics, and philosophy under Professor William Small, where Small introduced him to the British Empiricists including John Locke, Francis Bacon, and Isaac Newton. Jefferson improved his French, Greek, and his skill at the violin. He graduated, two years after starting, in 1762. He read the law under Professor George Wythe’s tutelage to obtain his law license, while working as a law clerk in Wythe’s office. Jefferson also read a wide variety of English classics and political works and treasured his books. In 1770 his Shadwell home, including a library of 200 volumes inherited from his father, was destroyed by fire. Nevertheless, by 1773 he had replenished his library with 1,250 titles, and in 1814, his collection grew to almost 6,500 volumes. After the British burned the Library of Congress that year, he sold more than 6,000 books to the Library for $23,950. Though he had intended to pay off some of his large debt, he resumed collecting for his personal library, writing to John Adams, “I cannot live without books“.


Jefferson was admitted to the Virginia bar in 1767. At the start of the Revolution Jefferson was a Colonel and named commander of the Albemarle County Militia on September 26, 1775. He was then elected to the Virginia House of Delegates for Albemarle. Jefferson was elected Virginia’s governor for one-year terms in 1779 and 1780. He transferred the state capital from Williamsburg to Richmond, and introduced measures for public education, religious freedom, and revision of inheritance laws. Following victory in the Revolutionary War and a peace treaty with Great Britain in 1783, the United States formed a Congress of the Confederation, to which Jefferson was appointed as a Virginia delegate. Jefferson was sent by the Congress of the Confederation to join Benjamin Franklin and John Adams as ministers in Europe for negotiation of trade agreements with England, Spain, and France. Soon after returning from France, Jefferson accepted Washington’s invitation to serve as Secretary of State. Jefferson had initially expected to return to France, but Washington insisted Jefferson be on his new Cabinet. Pressing issues at this time were the national debt and the permanent location of the capital. In the 1800 presidential election, Jefferson contended once more against Federalist John Adams. Adams’ campaign was weakened by unpopular taxes and vicious Federalist infighting over his actions in the Quasi-War. Republicans pointed to the Alien and Sedition Acts and accused the Federalists of being secret monarchists, while Federalists charged that Jefferson was a godless libertine in thrall to the French. The election was said to be “one of the most acrimonious in the annals of American history“.


From age 19 on, Jefferson had a tendency to develop prolonged incapacitating headaches, usually at 7-8 year intervals, usually correlated with stress or grief, complicated by indecision and deeply buried rage:


Violent headache for two days after behaving awkwardly in front of a girl he fancied (March 1764, age 20);

Six week headache after his mother’s death on March 31, 1776;

Six weeks of headache soon after arriving, unhappy and homesick, as minister to France in 1785;

While overburdened as Secretary of State, headaches recurred when he learned that a friend had become ill, but recovered (April 1790);

About this time he had a second set of headaches, lasting from sunrise to sunset each day for 6 weeks.


Medical historian, John R. Bumgarner MD concludes these were a form of cluster headache, but also believes there was a tension component, as horseback riding offered relief. At age 75 Jefferson wrote: “A periodical headache has afflicted me occasionally, once perhaps in six to eight years for two to three weeks at a time, which seems now to have left me.“


Other Illnesses:


Jefferson was inoculated against smallpox. He himself inoculated his own family — a procedure not to be taken lightly. In late June 1781,

Jefferson (apparently) broke his arm after being thrown from his horse.

Jefferson also broke his wrist in Paris in summer 1785. This seemingly minor event was to cause him grief the remainder of his life. There are three versions of the incident: (1) He was trying to jump a fence while touring Paris with a married woman, (2) He was trying to jump over a kettle, and (3) He fell while walking with an (unidentified) friend. One account described the fracture as compound and poorly treated by the Parisian doctors. The wrist remained swollen, painful, and useless for weeks. Despite taking the waters at Aix-en-Provence, it remained deformed and bothered him the rest of his life.

Jefferson developed severe dysentery (bloody diarrhea) in 1802. He consulted no doctor, feeling that horseback riding helped. (This seemed to be Jefferson’s cure-all therapy.

After performing extensive manual labor at Monticello (his estate) in late summer 1794, Jefferson became almost totally disabled by a back condition for two and a half months. The nature of the problem is not fully known. Repeated bouts of back pain assailed Jefferson after this initial episode, e.g. in 1797.

Jefferson’s back problems, financial troubles, and personal vicissitudes depressed him ca. 1793-1797. He believed his physical health was so poor that death was near.

A severe jaw infection occurred in January 1808. Bumgarner believes this was most likely due to a decayed and infected tooth, but Jefferson’s 1819 statement that he had never lost a tooth to age gives pause.

From “middle age on“ Jefferson required spectacles to read. In his 70s he wore spectacles at night “but not necessarily in the day unless in reading small print“

Jefferson was disabled by “’rheumatism“ in summer 1811. Again, the exact nature of the illness is obscure. It may have been related to his back problems. In 1818 he had his most severe attack of rheumatism ever. It was accompanied by life-threatening constipation. Taking the waters at Warm Springs, VA helped the rheumatism.

In the third week of taking the waters at Warm Springs (1818) Jefferson developed boils on his buttocks. (The 50+ mile ride to the spa plus possibly unsanitary conditions there may have predisposed to the illness.) As may be imagined, his homeward return ride was a trial. Once home, for several weeks he conducted his correspondence lying down. He did not ride a horse for several months. “Jefferson always believed that this experience had greatly injured his health“

Jefferson fell from a broken step at home in 1821 (age 75), fracturing his left arm and wrist. Now both wrists were significantly impaired. He wrote less, even into 1822.

In 1819 (age 75) he was “too feeble to walk much but riding without fatigue six to eight miles per day, and sometimes thirty or forty.“ Comment: This seems like a remarkable dissociation between exercise tolerance while walking and while sitting. Medical speculation: Jefferson may have had spinal stenosis, because these patients are limited in their walking, but may have much better capacity for bicycling and other forms of exercise when seated. Jefferson had a history of back problems.

Jefferson’s strength declined further in winter 1822, but he remained in generally good health. (He dreaded the winters at this age.) He could walk “only [to] reach my garden, and that with sensible fatigue“

In 1819 Jefferson wrote “My hearing is distinct in particular conversation, but confused when several voices cross each other, which unfits me for the society of the table“ (This experience is a classic manifestation of high-frequency hearing loss.) By 1825, however: “This [hearing] dullness of mine causes me to lose much of the conversation of the world and much a stranger to what is passing in it“ It’s possible, that Jefferson’s fondness for shooting as a form of exercise caused the hearing loss.

There are statements (without a description of symptoms) that Jefferson had prostatic enlargement in at least the final year of life.

At age 75 Jefferson wrote: “I have not yet lost a tooth to age“

Asperger Syndrome?  It has been postulated that Jefferson had Asperger Syndrome, a type of autism compatible with high achievement. Distinguishing disease from eccentricity is very difficult 200 years out.

Slept propped up in a bed that was otherwise too short for him. (heard on a tour of Monticello around 1990.)

Jefferson became comatose on July 2, 1826. On the third he awakened and asked, “Is it the fourth?“ He died 50 minutes into the next day, the 50th anniversary of the Declaration of Independence, a few hours before his onetime rival John Adams. Adams’ last words, “Thomas Jefferson still survives“ were mistaken.


Other things about Jefferson:


As he aged, his red hair turned sandy, then white.

He did not use tobacco in any form.

He started the custom of a President shaking hands, rather than bowing, to greet guests.

The following description of Jefferson is a reminder that medical skills in that era were not always restricted to medical people: “He was a gentleman of thirty-two who could calculate an eclipse, survey an estate, tie an artery, plan an edifice, try a cause, break a horse, dance a minuet, and play the violin“

No significant illness as infant or child.


Bumgarner quotes at length from a letter in which Jefferson gave his views on physical fitness. Jefferson encouraged exercise, walking and shooting most of all, observing: “Games played with the ball and others of that nature are too violent for the body.“ Although a dedicated scholar, Jefferson advocated time to exercise even though it meant interrupting study, warning: “Health must not be sacrificed to learning.“ Unfortunately, it appears that Jefferson’s fondness for shooting damaged his hearing.


Writing to a physician in 1819, Jefferson described his health and health habits, including:


Ate little animal meat. Vegetables were his principal diet.

Drank 3 glasses of wine a day, but “halved the effects“ by drinking only the weak wines. Did not drink “ardent wines“ nor “ardent spirits“ in any form. He did consume “malt liqueurs and cider“ as his “table drink.“

Slept from 5 to 8 hours nightly. Always rose with the sun.

Had few chest colds (every 8 to 10 years). Partially ascribed this fact to his habit of bathing his feet in cold water every morning.

Had a fever of longer than 24 hours “not above three or four times in my life.“

Jefferson was no fan of the doctors, to the point where he would look upwards for a buzzard whenever he saw three physicians together. He especially distrusted the practice of bleeding and purging.

But Jefferson was not above practicing medicine himself. His “practice“ included: suturing the wound of a severely bleeding slave, inoculating his family against smallpox, and treating his daughter’s typhoid fever (with Madeira wine). He used the Madeira regimen on dozens of his neighbors as well.

Through his mother’s father, Jefferson could claim descent from King Edward I of England.




Dr. John R. Bumgarner graduated from the Duke University School of Medicine in 1988. He works in Grand Junction, CO and specializes in Radiology and Vascular & Interventional Rad.


1.               Bumgarner, John R. The Health of the Presidents: The 41 United States Presidents Through 1993 from a Physician’s Point of View.

2.               Dallek, Robert. An Unfinished Life: John F. Kennedy 1917-1963.

3.               Hall, Donald (ed.). The Oxford Book of American Literary Anecdotes

4.               Ledgin, Norm. Diagnosing Jefferson: Evidence of a Condition that Guided his Beliefs, Behavior, and Personal Associations.

5.               Montgomery-Massingberd, Hugh (ed). Burke’s Presidential Families of the United States of America

6.               Stern, C. C. Braddock’s Presidential Trivia

7.               Ling and Duff. Pocket Guide to Obstetrics and Gynecology : Principles for Practice

8.               Ostergard et al (ed.). Ostergard’s Urogynecology & Pelvic Floor Dysfunction

9.     , Pubmed

10.            Wikipedia


Extreme Temperatures Could Increase Preterm Birth Risk


A pregnancy is considered full term at between 39 and 40 weeks. Preterm birth occurs before 37 weeks of pregnancy and increases the risk for infant death and long term disability. It is unknown why extremes of hot or cold might influence preterm birth risk.


As a result, a study published in Environmental Health Perspectives (August 2016), assessed whether extreme hot or cold temperatures during pregnancy may increase the risk of preterm birth. The study found that extremes of hot and cold during the first seven weeks of pregnancy were associated with early delivery, and that women exposed to extreme heat for the majority of their pregnancies also were more likely to deliver early. The authors found more consistent associations with early delivery after exposure to extreme heat than to extreme cold weather. They theorized that, during cold spells, people are more likely to seek shelter and so could more easily escape the cold’s effects. But during extreme heatwaves, people are more likely to endure the temperature, particularly when the cost of or access to air conditioning is an impediment. The authors theorize that the stress of temperature extremes could hinder the development of the placenta or alter blood flow to the uterus, both of which could potentially lead to early labor.


To conduct the study, the authors linked electronic medical records from 223,375 births at 12 clinical centers throughout the United States to hourly temperature records for the region surrounding each center. The authors noted that what constitutes a hot or cold temperature varies from person to person and place to place. To compensate for local climate variability and personal susceptibility, the authors evaluated temperatures in the surrounding regions. They defined extreme cold temperatures as below the 10th%ile of average temperatures, and defined extreme heat as above the 90th%ile. The study found that women who experienced extreme cold for the first seven weeks of their pregnancies had a 20% higher risk for delivering before 34 weeks of pregnancy, a 9% increased risk for delivering from 34-36 weeks, and a 3% increased risk for delivering in weeks 37 and 38. Women whose first seven weeks of pregnancy coincided with extreme heatwaves had an 11% increase in risk before 34 weeks, and a 4% increased risk at 37 to 38 weeks. Exposure to extreme heat during weeks 15-21 increased the risk for delivery at 34 weeks and at 34-36 weeks by 18% and for delivery from 37 to 39 weeks by 4%. Hot exposures during weeks 8-14 increased the risk for birth at 37 to 38 weeks by 4%. Overall, exposure to extreme heat for the duration of pregnancy was associated with increases in risk for delivery at 34 weeks and 36-38 weeks by 6 to 21%.


According to the authors, an increase in the number of extreme hot days due to climate change could lead to increases in the preterm birth rate. The authors added that their findings underscore the need for health professionals and policy makers to devise interventions for minimizing pregnant women’s exposure to extreme temperatures. The authors also called for more research to understand how temperature extremes might increase preterm birth risk.


Otulipenia, A New and Rare treatable Inflammatory Disease


Editor’s note: The following shows the exciting intersection of basic research and the pharmaceutical industry. It is time to bring back safe drugs to patients who need them. Remember, we will all be a patient at some time.


Otulipenia is one of several inflammatory diseases that occur when the immune system attacks the host’s own tissues. Inflammation is the body’s natural response to invading bacteria or viruses. The body releases chemicals that cause blood vessels to leak and tissues to swell in order to isolate a foreign substance from further contact with the body’s tissues. Inflammatory diseases affecting the whole body are caused by mutations in genes like OTULIN that are part of a person’s innate immunity (the cells and proteins present at birth that fight infections.   Otulipenia is caused by the malfunction of OTULIN, a single gene on chromosome 5. When functioning properly, OTULIN regulates the development of new blood vessels and mobilization of cells and proteins to fight infection.


According to a publication in the early edition of the Proceedings of the National Academy of Sciences (22 August 2016), a new and rare and sometimes lethal inflammatory disease — otulipenia — that primarily affects young children, has been discovered. Fortunately, anti-inflammatory treatments that ease some of the patients’ symptoms: fever, skin rashes, diarrhea, joint pain and overall failure to grow or thrive, have also been identified.


The results have been amazing and life changing for these children and their families,“ said Daniel Kastner, M.D., Ph.D., co-author and NHGRI scientific director and head of NHGRI’s Inflammatory Disease Section. “We have achieved the important goal of helping these young patients and made progress in understanding the biological pathways and proteins that are important for the regulation of the immune system’s responses.“


For the study, an international network of scientists studying inflammatory diseases identified four children from Pakistani and Turkish families with unexplained skin rashes and inflamed joints. The authors then searched for disease-causing genes usingnext-generation DNA sequencing technology that allows researchers to sequence DNA quickly and economically. Once it was found that the OTULIN gene was abnormal in the sick children, the immune pathways was studied in order to understand the mechanisms of disease and to improve treatment of these patients. When doing this, the authors discovered a problem in the processing of a small protein, ubiquitin, which is critical to the regulation of many other proteins in the body, including immune molecules. In the affected children, the inability to remove the ubiquitin proteins from various molecules resulted in an increased production of chemical messengers that lead to inflammation (inflammatory cytokines).


The authors determined that the children with otulipenia might respond to drugs that turned off tumor necrosis factor, a chemical messenger involved in systemic inflammation. Inflammation subsided in the children who had been treated with anti-tumor necrosis factor drugs (TNF inhibitors). TNF inhibitors are also used to treat chronic inflammatory diseases such as rheumatoid arthritis. This study together with NIH’s 2016 identification of haploinsufficiency of A20 (HA20), suggests a new category of human inflammatory diseases caused by impaired ubiquitination.


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