Warren Pearlson, Target’s Director of Business Development, will be attending the Bio International Convention in San Francisco, June 6th-9th. Please let us know if you plan to attend. We welcome the opportunity to meet with you.
Praying Mantis – James Farley Photography
Praying Mantis (a baby, not even an inch long), hunting for food (insects) on Dahlia blossoms, at dusk mid-week this week. Make sure to hit the zoom on your viewer, to see more detail. James shot this magnificent photo on his Canon 5D Mark III with 100mm Macro f2.8 lens at f11.
Praying Mantis Baby ©JFarley Photography 2016
ON TARGET is the newsletter of Target Health Inc., a NYC – based, full – service, contract research organization (eCRO), providing strategic planning, regulatory affairs, clinical research, data management, biostatistics, medical writing and software services to the pharmaceutical and device industries, including the paperless clinical trial.
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
How Much Do You Know About Shingles?
Shingles is a disease caused by the varicella-zoster 1) ___, the same virus that causes chickenpox. After an attack of chickenpox, the virus lies dormant in the nerve tissue. As people get older, it is possible for the virus to reappear in the form of shingles.
Almost 1 out of every 3 people in the United States will develop shingles, also known as zoster or herpes zoster, in their lifetime. There are an estimated 1 million cases of shingles each year in this country. Anyone who has recovered from 2) ___ may develop shingles; even children can get shingles. However the risk of shingles increases as you get older. About half of all cases occur in men and women 60 years old or older. People who develop shingles typically have only one episode in their lifetime. However, a person can have a second or even a third episode. Some people have a greater risk of getting shingles. This includes people who:
have medical conditions that keep their immune systems from working properly, such as certain 3) ___ like leukemia and lymphoma, and human immunodeficiency virus (HIV), and
receive immunosuppressive drugs, such as steroids and drugs that are given after organ transplantation.
Shingles is caused by the varicella 4) ___ virus (VZV), the same virus that causes chickenpox. After a person recovers from chickenpox, the virus stays dormant (inactive) in the body. For reasons that are not fully known, the virus can reactivate years later, causing shingles. Shingles is not caused by the same virus that causes genital herpes, a sexually transmitted disease. Shingles is a painful 5) ___ that develops on one side of the face or body. The rash forms blisters that typically scab over in 7 to 10 days and clears up within 2 to 4 weeks. Before the rash develops, people often have pain, itching, or tingling in the area where the rash will develop. This may happen anywhere from 1 to 5 days before the rash appears. Most commonly, the rash occurs in a single stripe around either the left or the 6) ___ side of the body. In other cases, the rash occurs on one side of the face. In rare cases (usually among people with weakened immune systems), the rash may be more widespread and look similar to a chickenpox rash. Shingles can affect the eye and cause loss of vision. Other symptoms of shingles can include: fever, headache, chills, upset 7) ___.
If a rash develops, it should be diagnosed by a 8) ___ , who can start treatment right away, if it is shingles. There is no cure for shingles, but how bad an attack it will be and how long it will last can be much reduced if antiviral medication is taken right away. These medicines include acyclovir, valacyclovir, or famcyclovir. If you are age 60 or older speak to your physician about getting vaccinated against this virus.
Shingles causes a painful, blistering skin rash that can last 2 to 4 weeks. For some people, the pain can last for months or even years after the rash goes away. This pain is called postherpetic neuralgia or PHN. The pain from PHN may be severe and debilitating, but it usually resolves in a few weeks. PHN occurs rarely among people under 40 years of age but can occur in up to a third of untreated people who are 60 years of age and older. People have described 9) ___ from shingles as excruciating, aching, burning, stabbing, and shock-like. It has been compared to the pain of childbirth or kidney stones. This pain may also lead to depression, anxiety, difficulty concentrating, loss of appetite, and weight loss. Shingles can interfere with activities of daily living like dressing, bathing, eating, cooking, shopping, and travel. Shingles can lead to eye complications that can result in vision loss.
Shingles cannot be passed from one person to another. However, a person with shingles can transmit VZV to others. A person who gets infected with VZV for the first time will develop chickenpox, not 10) ___. Shingles may lead to serious complications involving the eye. Very rarely, shingles can also lead to pneumonia, hearing problems, blindness, brain inflammation (encephalitis) or death. Sources: CDC.gov; NIH.gov; Wikipedia
ANSWERS: 1) virus; 2) chicken pox; 3) cancers; 4) zoster; 5) rash; 6) right; 7) stomach; 8) dermatologist; 9) pain; 10) shingles
Progression of shingles. A cluster of small bumps (1) turns into blisters (2). The blisters fill with lymph, break open (3), crust over (4), and finally disappear. Postherpetic neuralgia can sometimes occur due to nerve damage (5). Source: By Renee Gordon – fda.gov; Public Domain, Wikipedia Commons
Peter Krukenberg (1787-1865)
By Unknown – Public Domain: Wikipedia Commons
Varicella-Zoster Virus (VZV) also called Shingles, has a long recorded history. However, historical accounts often fail to distinguish between the poc marks caused by VZV and those caused by small pox. It was only in the late eighteenth century that William Heberden Senior, established a way to clinically differentiate between the two diseases.
Peter Krukenberg (14 February 1787 – 13 December 1865) was a German pathologist who was a native of Konigslutter. He was son-in-law to anatomist Johann Christian Reil (1759-1813), and grandfather to pathologist Friedrich Ernst Krukenberg (1871-1946) and surgeon Hermann Krukenberg (1863-1935). Krukenberg studied at the Collegium Carolinum in Braunschweig and at the Universities of Gottingen and Berlin. In 1814 he became an associate professor of pathology and therapy at the University of Halle, and from 1822 to 1856 was a full professor of pathology and director of the university clinic. In 1816 Krukenberg founded an ambulatory clinic at Halle. One of his better known assistants was dermatologist Friedrich Wilhelm Felix von Barensprung (1822-1864). It was this assistant, Barensprung, who in 1861 published a paper confirming that the disease, shingles, arose from the dorsal root ganglion. Studying and working with Krukenberg was a great advantage for Barensprung, because the senior physician was a pioneer of scientific knowledge-based medicine and was considered one of the leading clinicians of his era.
Friedrich Wilhelm Felix von Barensprung, (30 March 1822 – 26 August 1864) was a German dermatologist born in Berlin. His father, Friedrich von Barensprung (1779-1841), was mayor of Berlin in 1832-34. In 1843 he obtained his doctorate at Halle an der Saale, then furthered his studies in pathology at Prague, where he was also involved with entomological research. In 1845 he became a clinical assistant to Peter Krukenberg (1788-1865) at Halle, and several years later, founded a private clinic in Halle (1850). In 1853 he was appointed chief physician at the Syphilisklinik at the Berlin Charite, and in 1857 became an associate professor at the University of Berlin. Barensprung is credited as being the first physician to demonstrate a definite link between herpes zoster and a lesion of the dorsal root ganglion. Subsequently, he identified nine varieties of the disorder, of which he classified according to the nerve involved. In 1854, he provided the first description of tinea cruris, a fungal condition that is sometimes referred to as Barensprung’s disease in medical literature. Barensprung was in favor of housing projects for the impoverished, and also advocated the creation of day nurseries and children’s homes. These measures, he reasoned, were an effective means to stop the spread of epidemics such as tuberculosis and scrofulosis (tuberculosis of the lymph nodes, particularly of the neck). Among his written works was Atlas der Hautkrankheiten, an atlas on skin diseases that was edited and published posthumously by Ferdinand von Hebra (1867). In the field of entomology, he was instrumental in the founding of the journal, Berliner Entomologische Zeitschrift, in which he published papers on Hemiptera (a large order of insects that have mouthparts adapted to piercing and sucking and usually two pairs of wings, undergo an incomplete metamorphosis. Examples include cicadas, aphids, planthoppers, leafhoppers, and shield bugs.
In 1888, it was suggested by Dr. James von Bokay that chicken pox and shingles were caused by the same virus. Physicians began to report that cases of shingles were often followed by chickenpox in the younger people who lived with the person with shingles. The idea of an association between the two diseases gained strength when it was shown that lymph from a person with shingles could induce chickenpox in young volunteers. However, it was not until 1953 that Weller and Stoddard isolated virus both from chickenpox and zoster and compared the viruses, that this connection was confirmed: chickenpox and herpes zoster were indeed due to the same virus! This was finally proved by the first isolation of the virus in cell cultures, by the Nobel laureate Thomas Huckle Weller, in 1953.
Until the 1940s the disease was considered benign, and serious complications were thought to be very rare. However, by 1942, it was recognized that shingles was a more serious disease in adults than in children, and that it increased in frequency with advancing age. Further studies during the 1950s on immunosuppressed individuals showed that the disease was not as benign as once thought, and the search for various therapeutic and preventive measures began. By the mid-1960s, several studies identified the gradual reduction in cellular immunity in old age, observing that in a cohort of 1,000 people who lived to the age of 85, approximately 500 (i.e., 50%) would have at least one attack of shingles, and 10 (i.e., 1%) would have at least two attacks. In historical shingles studies, shingles incidence generally increased with age. However, in his 1965 paper, Dr. Hope-Simpson suggested that the peculiar age distribution of zoster may in part reflect the frequency with which the different age groups encounter cases of varicella and because of the ensuing boost to their antibody protection have their attacks of zoster postponed. Lending support to this hypothesis that contact with children with chickenpox boosts adult cell-mediated immunity to help postpone or suppress shingles, a study by Thomas et al. reported that adults in households with children had lower rates of shingles than households without children.
Cholesterol Lowering in Intermediate-Risk Persons without Cardiovascular Disease
Previous trials have shown that the use of statins to lower cholesterol reduces the risk of cardiovascular events among persons without cardiovascular disease. Those trials have involved persons with elevated lipid levels or inflammatory markers and involved mainly white persons. It is unclear whether the benefits of statins can be extended to an intermediate-risk, ethnically diverse population without cardiovascular disease.
As a result, a study published in the New England Journal of Medicine (2016; 374:2021-2031), a clinical trial randomly assigned 12,705 participants in 21 countries who did not have cardiovascular disease and were at intermediate risk to receive rosuvastatin (Crestor) at a dose of 10 mg per day or placebo. The first co-primary outcome was the composite of death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke, and the second co-primary outcome additionally included revascularization, heart failure, and resuscitated cardiac arrest. The median follow-up was 5.6 years.
Results showed that the overall mean low-density lipoprotein cholesterol level was 26.5% lower in the rosuvastatin group than in the placebo group. The first co-primary outcome occurred in 235 participants (3.7%) in the rosuvastatin group and in 304 participants (4.8%) in the placebo group (hazard ratio, 0.76; P=0.002). The results for the second co-primary outcome were consistent with the results for the first (occurring in 277 participants [4.4%] in the rosuvastatin group and in 363 participants [5.7%] in the placebo group; (P<0.001). The results were also consistent in subgroups defined according to cardiovascular risk at baseline, lipid level, C-reactive protein level, blood pressure, and race or ethnic group. In the rosuvastatin group, there was no excess of diabetes or cancers, but there was an excess of cataract surgery (in 3.8% of the participants, vs. 3.1% in the placebo group; P=0.02) and muscle symptoms (in 5.8% of the participants, vs. 4.7% in the placebo group; P=0.005).
According to the authors, treatment with rosuvastatin at a dose of 10 mg per day resulted in a significantly lower risk of cardiovascular events than placebo in an intermediate-risk, ethnically diverse population without cardiovascular disease.
How Differences in Male and Female Brains Emerge
In nematode worms, (known as Caenorhabditis elegans or C. elegans), a small number of neurons are found exclusively in male or female brains. The remaining neurons are found in both genders, although their connection patterns are different in male and female brains. According to new research published online in Nature (4 May 2106), it has been demonstrated how these sexually dimorphic (occurring in either males or females) connections arise in the worm nervous system.
The research team observed that in the worms’ juvenile state, before they reach sexual maturity, their brain connections were in a hybrid, or mixed state, comprised of both male and female arrangements. However, as the worms reached sexual maturity, their brains underwent a pruning process, which got rid of particular connections and led to either male or female patterns. Next, the authors showed that sex-specific wiring in the brain results in dimorphic behavior. They discovered that PHB neurons, chemosensory brain cells that detect chemical cues in the environment such as food, predators or potential mates, work differently in males and females. In males, these neurons proved to be important in recognizing mating cues while in females, the neurons helped them avoid specific taste cues. However, early in development, PHB neurons in males also responded to signals regulating taste, suggesting that even though those neurons are found in all nematodes, in adults, their functions differ as a result of gender-specific wiring in the brain.
For the study, the authors used genetically engineered nematodes to look more carefully at individual connections between brain cells. Results showed that swapping the gender of individual neurons changed wiring patterns and influenced behavioral differences in males and females. Additional experiments helped to identify genes involved in regulating the pruning process during development. The authors discovered that certain transcription factors, which are molecules that help control gene activity, are present in a dimorphic state and may help establish male or female connections in the brain. In future experiments, the authors plan to examine how these molecules target specific connections for pruning.
Draft Guidance – Use of Electronic Health Record Data in Clinical Investigations
FDA has announced the availability of a draft guidance for industry entitled Use of Electronic Health Record Data in Clinical Investigations. The draft guidance is intended to assist sponsors, clinical investigators, contract research organizations (CROs), IRBs, and other interested parties on the use of EHR data in FDA- regulated clinical investigations. In particular, the draft guidance provides recommendations on the following: (1) Deciding whether and how to use EHRs as a source of data in clinical investigations; (2) using EHRs that are interoperable with electronic systems supporting clinical investigations; (3) ensuring the quality and the integrity of EHR data that are collected and used as electronic source data in clinical investigations; and (4) ensuring that the use of EHR data collected and used as electronic source data in clinical investigations meet FDA’s inspection, recordkeeping, and record retention requirements. In an effort to modernize and streamline clinical investigations, the goals of the draft guidance are to facilitate use of EHR data in clinical investigations and to promote the interoperability of EHRs and electronic systems supporting the clinical investigation.
This draft guidance is being issued consistent with FDA’s good guidance practices regulation (21 CFR 10.115). The draft guidance, when finalized, will represent the current thinking of FDA on the use of EHR data in clinical investigations. It does not establish any rights for any person and is not binding on FDA or the public. You can use an alternative approach if it satisfies the requirements of the applicable statutes and regulations. To read the entire Federal Register Notice and to make comments electronically.
Mango & Blueberry, Lemon Poppy Seed Cake
Mangoes are in season now and utterly delicious. In recipes, I’ve been using Champagne Mangos and Indian Saffron Mangoes. They are sweet beyond belief now, compared to mangoes a few months ago. I’ve worked on this recipe for several weeks now, until I got it just right. It went from a frozen mustard colored concoction, to what you see above. Hope you enjoy it! ©Joyce Hays, Target Health Inc.
This cake is as cool and refreshing as it is unbelievably delicious. The good news is, it’s easy to make; and if you do, you’re in for a Memorial Day Mango treat! ©Joyce Hays, Target Health Inc.
1 and 1/2 cups Amaretti biscotti (store-bought)
1 large ripe fresh Mango for cake
1 large ripe Mango for top decoration
1 pint fresh blueberries, well rinsed and dried
3 Tablespoons canned poppy seeds for baking
3 Tablespoons canned marzipan for baking
1 container Tofutti (soy cream cheese), room temperature
2 boxes lemon Jello
2 cups boiling water
whipped topping like Cool Whip, or make your own whipped cream (optional)
A few good ingredients. ©Joyce Hays, Target Health Inc.
Crush the biscotti into small crumbs and put them on the bottom of a spring-form cake pan
This is about 1 and 1/2 cups of the biscotti before crushing it. ©Joyce Hays, Target Health Inc.
Here’s the crushed Amaretti at the bottom of springform pan. ©Joyce Hays, Target Health Inc.
Put the 2 boxes of lemon Jello into a mixing bowl, with 2 cups boiling water. Stir to combine.
Into a measuring cup, pour 1/2 of the Jello mixture, which is 1 cup of the warm Jello. Set aside, this 1 measuring cup of Jello, and let it reach room temperature.
Set aside 1 cup of the warm Jello mixture. ©Joyce Hays, Target Health Inc.
Peel the mango and put the pieces into a food processor. ©Joyce Hays, Target Health Inc.
Puree the mango pieces in a food processor. ©Joyce Hays, Target Health Inc.
Peel the mango and put the pieces into a food processor.
When you pour the mango puree into the mixing bowl, be sure to use a spatula to scrape every last bit of mango out.
Into the mixing bowl with warm lemon Jello, add the Tofutti and the puree of mango. Turn the beaters on slowly as you add ingredients in. If you don’t have a mixing bowl, it’s easy to beat by hand.
Mixing the ingredients together, slowly. Here the mango puree and Tofutti have been added to the warm Jello. ©Joyce Hays, Target Health Inc.
Add the marzipan while beating.
Beating in the marzipan. ©Joyce Hays, Target Health Inc.
Next, add the poppy seeds and beat in until well mixed.
Beating in the poppy seeds. ©Joyce Hays, Target Health Inc.
Finally, after all the ingredients are well combined in the mixing bowl, slowly pour the Tofutti/Jello contents over the Amaretti crumbs in the spring-form pan. Sometimes, the crumbs stay at the bottom of the pan and sometimes they jump into the mango/Jello mixture. Either way, is fine, since it doesn’t change the flavor one bit.
Now, put the spring-form pan in the fridge for several hours or overnight.
Before you proceed to the final steps, rinse the blueberries well and dry them. Peel the 2nd mango and make long thin mango strips, that can be seen in the very first photo.
Take the spring-form pan out of the fridge and pour the liquid lemon Jello (in the measuring cup) that you left out, over the solidified mixture. Into the liquid lemon Jello, arrange the pieces of fruit. Approximate, the design you want, because the pieces of fruit are going to move around a little. This can’t be helped. Actually, it gives the top of the cake a nice abstract look. Put the cake back in the fridge for several more hours, so the Jello on top can firm up. Or overnight again.
Here the second cup of lemon Jello has just been poured over the previous mixture, left in fridge overnight. ©Joyce Hays, Target Health Inc.
The pieces of mango and blueberries have been added, with a design in mind and have moved around a bit. ©Joyce Hays, Target Health Inc.
To serve, take the sides of the spring-form, off and put the cake with pan bottom on a serving plate. Or do your best to slide a large flat pie server under the Jello cake and move it quickly over to a serving plate. It’s safer not to try to move it.
Serve along with whipped cream or cool whip.
‘Well,’ said Pooh, ‘what I like best,’ and then he had to stop and think. Because although Eating Honey was a very good thing to do, there was a moment just before you began to eat it, which was better than when you were, but he didn’t know what it was called. – A.A Milne
The proof is in the eating. ©Joyce Hays, Target Health Inc.
We had glasses of ice water with this dessert. The Jello cake is sweet and we didn’t want an additional sweet wine or liqueur. We made the right choice, the cake stands on its own.
This is an amazingly delicious cake. You can do this! ©Joyce Hays, Target Health Inc.
We saw a truly intellectually stimulating play, Incognito, by the rising British star, playwright, Nick Payne. We recommend this play highly, if you’re willing to meet it half-way and accept the challenge of deciphering it, as you go. It’s a mind bending mystery, for you to solve. This play is a neuroscientists dream.
We’re proud to say, that Incognito is produced by one of our theater clubs, The Manhattan Theater Club. NYC theater has been filled with excellent work all season. However, our two favorites have medical research embedded in both. The Father, starring the very great Frank Langella, who at 78, brilliantly portrays a man attempting to deal with Alzheimer’s disease. Incognito deals with neuroscience. Both productions, kept us on the edge of our seats. The NY theater season (most of the really good stuff) is basically over by the end of June, so if you can, try to fit this great theater into your schedule. I’ll go out on a limb and predict that Frank Langella will win a Tony for his superb performance in, The Father.
From Our Table to Yours !
Evidence dates back more than 740 million years
May 25, 2016
University of California – Santa Barbara
A paleobiologist has found evidence of predation in ancient microbial ecosystems dating back more than 740 million years. Using a scanning electron microscope to examine minute fossils, Porter found perfectly circular drill holes that may have been formed by an ancient relation of Vampyrellidae amoebae. These single-celled creatures perforate the walls of their prey and reach inside to consume its cell contents.
Vampires are real, and they’ve been around for millions of years. At least, the amoebae variety has. So suggests new research from UC Santa Barbara paleobiologist Susannah Porter.
Using a scanning electron microscope to examine minute fossils, Porter found perfectly circular drill holes that may have been formed by an ancient relation of Vampyrellidae amoebae. These single-celled creatures perforate the walls of their prey and reach inside to consume its cell contents. Porter’s findings appear in the Proceedings of the Royal Society B.
“To my knowledge these holes are the earliest direct evidence of predation on eukaryotes,” said Porter, an associate professor in UCSB’s Department of Earth Science. Eukaryotes are organisms whose cells contain a nucleus and other organelles such as mitochondria.
“We have a great record of predation on animals going back 550 million years,” she continued, “starting with the very first mineralized shells, which show evidence of drillholes. We had nothing like that for early life — for the time before animals appear. These holes potentially provide a way of looking at predator-prey interactions in very deep time in ancient microbial ecosystems.”
Porter examined fossils from the Chuar Group in the Grand Canyon — once an ancient seabed — that are between 782 and 742 million years old. The holes are about one micrometer (one thousandth of a millimeter) in diameter and occur in seven of the species she identified. The holes are not common in any single one species; in fact, they appear in not more than 10 percent of the specimens.
“I also found evidence of specificity in hole sizes, so different species show different characteristic hole sizes, which is consistent with what we know about modern vampire amoebae and their food preferences,” Porter said. “Different species of amoebae make differently sized holes. The Vampyrellid amoebae make a great modern analog, but because vampirelike feeding behavior is known in a number of different unrelated amoebae, it makes it difficult to pin down exactly who the predator was.”
According to Porter, this evidence may help to address the question of whether predation was one of the driving factors in the diversification of eukaryotes that took place about 800 million years ago.
“If that is true, then if we look at older fossil assemblages — say 1 to 1.6 billion years old — the fossilized eukaryote will show no evidence of predation,” Porter said. “I’m interested in finding out when drilling first appears in the fossil record and whether its intensity changes through time.”
Porter also is interested in seeing whether oxygen played a role in predation levels through time. She noted that the microfossils those organisms attacked were probably phytoplankton living in oxygenated surface waters, but like vampyrellid amoebae today, the predators may have lived in the sediments. She suggests that those phytoplankton made tough-walled cysts — resting structures now preserved as fossils — that sank to the bottom where they were attacked by the amoebae.
“We have evidence that the bottom waters in the Chuar Group in that Grand Canyon basin were relatively deep — 200 meters deep at most — and sometimes became anoxic, meaning they lacked oxygen,” Porter explained.
“I’m interested to know whether the predators only were present and making these drill holes when the bottom waters contained oxygen,” Porter added. “That might tie the diversification of eukaryotes and the appearance of predators to evidence for increasing oxygen levels around 800 million years ago.
“We know from the modern vampire amoebae that at least some of them make resting cysts themselves,” Porter said. “A former student of mine joked we should call these coffins. So one of our motivations is to see if we can find these coffins in the fossil assemblage as well. That’s the next project.”
- Susannah M. Porter. Tiny vampires in ancient seas: evidence for predation via perforation in fossils from the 780–740 million-year-old Chuar Group, Grand Canyon, USA. Proceedings of the Royal Society B: Biological Sciences, 2016; 283 (1831): 20160221 DOI:10.1098/rspb.2016.0221
Source: University of California – Santa Barbara. “Tiny ‘vampires’: Paleobiologist finds evidence of predation in ancient microbial ecosystems: Evidence dates back more than 740 million years.” ScienceDaily. ScienceDaily, 25 May 2016. <www.sciencedaily.com/releases/2016/05/160525161354.htm>.
May 25, 2016
Society for Research in Child Development
A new study analyzing a nationally representative US sample of 19,162 children, has found that frequent residential moves can lead to a decline in academic performance as well as higher rates of emotional and behavioral problems.
America is a mobile society, with most children and their families moving once or more during childhood. Moving can bring new opportunities if families relocate to safer, more comfortable homes, or to communities with better schools. However, previous research has found that more frequent residential moves can lead to stress and disrupt children’s routines, with negative repercussions for healthy development. Now a new study has found that each additional residential move that children experience is associated with a corresponding decline in reading and math scores, as well as less positive social skills and higher rates of emotional and behavioral problems. The study compared children who move frequently with those who don’t move or who move less frequently.
The research was conducted at Boston College and appears in the journalChild Development.
The study analyzed data from a nationally representative U.S. sample of 19,162 children in the Early Childhood Longitudinal Study (Kindergarten Class of 1998-99) who were followed from kindergarten through eighth grade. Researchers sought to determine whether the effects of moving on children accumulated over time or were more salient during specific periods, and whether moving was more disruptive when it occurred in conjunction with changing schools.
They found that moving is differentially harmful for children’s well-being–that is, the effects depend on when the moves occur. “Moves during both early and middle childhood were associated with decreases in children’s social skills and increases in emotional and behavior problems, and these effects lasted for years,” explains Rebekah Levine Coley, professor of applied developmental and educational psychology at Boston College, who led the study.
“In contrast, moves during middle childhood and early adolescence–after children had started school–had shorter-term effects on children’s reading and math skills, and those effects diminished over time,” Coley adds. The study also found that while residential and school mobility was associated with small decreases in children’s functioning, these detriments could accumulate over multiple moves.
The researchers highlight the importance of addressing the myriad social and economic factors that might influence a family’s decision to move, such as changes in mothers’ employment, receipt of public assistance, family structure, or household income. These factors were accounted for in analyses predicting children’s functioning, and results revealed links between moves and children’s cognitive skills, social skills, and emotional and behavior problems, after considering the effects of these social and economic influences on moving residences.
The study also examined the role of moving homes and moving schools, finding that moving schools had unique and slightly stronger associations with children’s cognitive skills above and beyond the effects of just moving homes. Even without changing schools, though, the disruptions in daily routines and contexts caused by moving homes can interrupt children’s focus on their schoolwork and inhibit learning, the study concluded.
The study’s findings suggest that schools may play an important role in exacerbating or stabilizing the lives of children who move. Children might benefit from short-term supports from parents or school personnel after a move to help them retain their focus on academic work, according to the authors. The findings also confirm the importance of stability for children.
“As employment instability and high housing prices continue to destabilize American families, policymakers, school leaders, and teachers must develop strategies to counter the interruptions that home and school moves pose to children’s education and healthy development,” suggests Melissa Kull, formerly a doctoral student at Boston College, now a research scientist at the New York City Department of Health and Mental Hygiene, and the study’s coauthor.
- Rebekah Levine Coley, Melissa Kull. Cumulative, Timing-Specific, and Interactive Models of Residential Mobility and Children’s Cognitive and Psychosocial Skills. Child Development, 2016; DOI:10.1111/cdev.12535
Source: Society for Research in Child Development. “Children’s social, academic functioning is impeded when their families move more often.” ScienceDaily. ScienceDaily, 25 May 2016. <www.sciencedaily.com/releases/2016/05/160525083914.htm>.
10-year project revealed air pollutants accelerate plaque build-up in arteries to the heart
May 24, 2016
University of Washington Health Sciences/UW Medicine
A major, decade-long study of thousands of Americans found that people living in areas with more outdoor pollution — even at lower levels common in the United States — accumulate deposits in the arteries that supply the heart faster than do people living in less polluted areas. The deposits in the coronary arteries accelerate the progression of atherosclerosis, which can contribute to heart disease and heart attacks.
Long-term exposure to air pollution has been linked to an increased risk of heart disease, but the biological process has not been understood. A major, decade-long study of thousands of Americans found that people living in areas with more outdoor pollution — even at lower levels common in the United States — accumulate deposits in the arteries that supply the heart faster than do people living in less polluted areas.
The study is published May 24 online in The Lancet.
Previous epidemiological studies have shown associations between particle pollution, referred to as particulate matter, and heart disease. It has been unclear, however, how exposure to particulate matter leads to diseases of the cardiovascular system. Earlier studies had been shorter and had depended for their analysis on existing datasets collected for other purposes.
Now, direct evidence from the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a 10-year epidemiological study of more than 6,000 people from six U.S. states, shows that air pollution — even at levels below regulatory standards — accelerates the progression of atherosclerosis. The condition, also called hardening of the arteries, can cause heart attacks. Researchers repeatedly measured calcium deposits in the heart’s arteries by using CT scans. They also assessed each person’s exposure to pollution based on home address.
“The study provides important new information on how pollution affects the main biological process that leads to heart disease,” said Dr. Joel Kaufman, who directs MESA Air and is the lead author of the published paper. He is a University of Washington professor of environmental and occupational health sciences, and also a UW professor of epidemiology, and of medicine.
“The evidence supports worldwide efforts to reduce exposures to ambient air pollutants,” Kaufman said.
He added, “This was the most in-depth study of air pollution exposures ever applied to a large study group specifically designed to examine influences on cardiovascular health.”
The researchers calculated each participant’s exposure to ambient fine particulate matter that is less than 2.5 microns in diameter and too small to be seen by the naked eye. In addition to PM2.5, they also measured exposure to nitrogen oxide and nitrogen dioxide, and black carbon or soot.
The research team collected thousands of air pollution measurements in the study participants’ communities and at their homes. The research team developed and applied computational models that included local information on land use, roadway and traffic volumes, weather conditions, and local sources of air pollution. These models could generate accurate pollution concentrations at each person’s home. Meanwhile, between the years 2000 and 2012, participants visited study clinics several times to undergo CT scanning to determine the amount of calcium deposits in their heart arteries.
Results were strongest for fine particulate matter and the traffic-related pollutant gases called oxides of nitrogen. The study found that for every 5 µg/m3 higher concentration of PM2.5, or 35 parts per billion higher concentration of oxides of nitrogen — about the difference between more and less polluted areas of a U.S. metropolitan area — individuals had a 4 Agatston units/year faster rate of progression of coronary artery calcium scores. This is about a 20 percent acceleration in the rate of these calcium deposits.
“The effects were seen even in the United States where efforts to reduce exposure have been notably successful compared with many other parts of the world,” Kaufman said. Exposures were low when compared to U.S. ambient air quality standards, which permit an annual average PM2.5 concentration of 12 µg/m3. The participants in this MESA-Air study experienced concentrations between 9.2 and 22.6 µg/m3.
In an accompanying editorial in The Lancet, Dr. Bert Brunekreef, a professor at Utrecht University in The Netherlands, and Dr. Barbara Hoffmann, a professor of the University of Düsseldorf in Germany, described the study as “exemplary.” Noting that the results are sobering, they called for decisive action in controlling pollution levels worldwide.
The above post is reprinted from materials provided by University of Washington Health Sciences/UW Medicine. The original item was written by Elizabeth Sharpe. Note: Materials may be edited for content and length.
- Joel D Kaufman et al. Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study. The Lancet, 2016 DOI: 10.1016/S0140-6736(16)00378-0
Source: University of Washington Health Sciences/UW Medicine. “Study shows how air pollution fosters heart disease: 10-year project revealed air pollutants accelerate plaque build-up in arteries to the heart.” ScienceDaily. ScienceDaily, 24 May 2016. <www.sciencedaily.com/releases/2016/05/160524212005.htm>.