Use of certain antiviral drugs during pregnancy not linked with higher risk of major birth defects, study suggests

ScienceDaily (Aug. 31, 2010) — An analysis of data from Denmark finds no associated increased risk of major birth defects for mothers who were exposed during the first trimester of pregnancy to the antiviral drugs acyclovir, valacyclovir, and famciclovir, often used to treat herpes simplex and herpes zoster infections, according to a study in the August 25 issue of JAMA.

The prevalence of herpes simplex is high, and more than 1 percent of susceptible women acquire herpes simplex during the first trimester of pregnancy, with antiviral treatment indicated for a significant number of women in pregnancy. "Although the safety of acyclovir, valacyclovir, and famciclovir in general has been well established, data on the use of these antivirals in early pregnancy are limited," the authors write.

Bjorn Pasternak, M.D., Ph.D., and Anders Hviid, M.Sc., Dr.Med.Sci., of Statens Serum Institut, Copenhagen, Denmark, conducted a registry-based study to assess associations between acyclovir, valacyclovir, and famciclovir use in the first trimester of pregnancy and major birth defects. The study included 837,795 live-born infants in Denmark from January 1996 to September 2008. Participants had no diagnoses of chromosomal aberrations, genetic syndromes, birth defect syndromes with known causes, or congenital viral infections. Nationwide registries were used to ascertain individual-level information on dispensed antiviral drugs, birth defect diagnoses and potential confounders (factors that can influence outcomes).

Among 1,804 pregnancies exposed to acyclovir, valacyclovir, or famciclovir at any time in the first trimester, 40 infants (2.2 percent) had a diagnosis of a major birth defect, compared with 19,920 of 835,991 infants (2.4 percent) among the unexposed pregnancies. Adjusting for several variables, acyclovir, valacyclovir, or famciclovir exposure at any time in the first trimester was not associated with increased risk of major birth defects. First-trimester use of acyclovir, the most commonly prescribed antiviral, was not associated with major birth defects (32 cases among 1,561 exposed [2.0 percent] vs. 2.4 percent in the unexposed). Neither valacyclovir (7 of 229 infants [3.1 percent]) nor famciclovir (1 of 26 infants [3.8 percent]) were associated with major birth defects, although use of famciclovir was uncommon.

Additional analyses revealed no associations between antiviral drug exposure and 13 different subgroups of birth defects, but the number of exposed cases in each subgroup was small.

"Our study, to our knowledge the largest of its kind, found no significant association between first-trimester exposure to antiherpetic antiviral drugs and major birth defects. Consequently, it has immediate clinical implications and may support informed decisions on safety when prescribing antivirals for herpes infections in early pregnancy. Acyclovir is the most extensively documented antiviral and should therefore be the drug of choice in early pregnancy, while data on valacyclovir and famciclovir are still insufficient. Future research on antiherpetic antivirals and mother-child health should include safety studies with regard to spontaneous abortion and preterm birth, and during breastfeeding," the authors conclude.

Editorial: Acyclovir Exposure and Birth Defects -- An Important Advance, But More Are Needed

In an accompanying editorial, James L. Mills, M.D., M.S., and Tonia C. Carter, Ph.D., of the National Institutes of Health, Bethesda, Md., comment on the findings of this study.

"The study by Pasternak and Hviid is helpful in demonstrating the safety of acyclovir in pregnancy, but additional strategies must be developed to resolve the remaining issues. At a time when the health care system in the United States is facing enormous financial challenges, it is important not to ignore any sources of data that could answer critical medical questions."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by JAMA and Archives Journals.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Björn Pasternak, MD, PhD; Anders Hviid, MSc, DrMedSci. Use of Acyclovir, Valacyclovir, and Famciclovir in the First Trimester of Pregnancy and the Risk of Birth Defects. JAMA, 2010;304(8):859-866 DOI: 10.1001/jama.2010.1206

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Shingles vaccine is safe, according to new study

ScienceDaily (Apr. 23, 2012) — The herpes zoster vaccine, also known as the shingles vaccine, is generally safe and well tolerated according to a Vaccine Safety Datalink study of 193,083 adults published online in the Journal of Internal Medicine.

More than 1 million people develop shingles every year in the United States. Shingles is a painful contagious rash caused by the dormant chickenpox virus which can reactivate and replicate, damaging the nerve system. The elderly are especially vulnerable because immunity against the virus that causes shingles declines with age.

The VSD project is a collaborative effort between the Centers for Disease Control and Prevention and integrated care organizations, including Kaiser Permanente. The VSD project monitors immunization safety and addresses the gaps in scientific knowledge about any rare and serious events that occur following immunization.

This study examined adverse events after the zoster vaccine was administered to 193,083 adults aged 50 and older from Jan. 1, 2007, to Dec. 31, 2008. Vaccination data were retrieved from electronic health records and collected from eight managed care organizations participating in the VSD project.

Researchers found a small increased risk of local reactions from one to seven days after vaccination. These findings corroborate clinical trials of the vaccine in which there was evidence of a minor local reaction at the injection site in the form of redness and pain.

The study found no increased risk for cerebrovascular diseases; cardiovascular diseases; meningitis, encephalitis, and encephalopathy; Ramsay-Hunt syndrome; or Bell's palsy.

"It's good to know there is no serious adverse reaction to the zoster vaccine. The study supports the CDC's Advisory Committee on Immunization Practices' recommendation and reassures the general public that the vaccine is safe," said study lead author Hung Fu Tseng, PhD, MPH, a research scientist with the Kaiser Permanente Southern California Department of Research & Evaluation in Pasadena, Calif.

The herpes zoster vaccine was licensed in 2006, but few people have been vaccinated, national data shows. The ACIP recommends the vaccine for healthy people age 60 years and older. In 2011, the U.S. Food and Drug Administration approved the use of the herpes zoster vaccine in individuals 50 to 59 years of age. The study results provide important safety data for people in this age group as well as adults 60 and older.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Kaiser Permanente.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

H. F. Tseng, A. Liu, L. Sy, S. M. Marcy, B. Fireman, E. Weintraub, J. Baggs, S. Weinmann, R. Baxter, J. Nordin, M. F. Daley, L. Jackson, S. J. Jacobsen. Safety of zoster vaccine in adults from a large managed-care cohort: a Vaccine Safety Datalink study. Journal of Internal Medicine, 2012; 271 (5): 510 DOI: 10.1111/j.1365-2796.2011.02474.x

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Scientists use genetically altered virus to get tumors to tattle on themselves

ScienceDaily (May 12, 2011) — Scientists have used a genetically re-engineered herpes virus that selectively hunts down and infects cancerous tumors and then delivers genetic material that prompts cancers to secrete a biomarker and reveal their presence.

According to a study appearing May 11 in PLoS ONE, published by the Public Library of Science, the novel technology has the potential to vastly improve cancer diagnosis by allowing the disease to be caught at much earlier stages and to monitor the effectiveness of therapy.

Researchers at Cincinnati Children's Hospital Medical Center who conducted the study say the new technique -- developed in preclinical mouse models -- could also be more cost effective and portable than current scanning technologies. This would make it useful for diagnosing cancers in less developed parts of the world.

"Our study represents a proof-of-principle in mice, and there is certainly room for further refinement. If ultimately validated in human trials, it could have implications for people with known cancer risk or who have a history of cancer and high risk of recurrence,'' said Timothy Cripe, M.D., Ph.D., senior investigator on the study and a physician and researcher in the Division of Oncology at Cincinnati Children's.

"Early cancer detection is vital to improve cure rates because cancer stage predicts prognosis, but biomarkers are known for only a few cancer types. We were able to use a reprogrammed herpes virus administered intravenously to deliver genetic information that induces a known blood biomarker for cancer to be secreted by cancer cells," explained Dr. Cripe, who collaborated on the study with first author, Andrew Browne, Ph.D., a fourth-year medical student at the University of Cincinnati (UC) College of Medicine and a recent graduate from UC's Department of Electrical and Computer Engineering.

The researchers engineered a herpes simplex virus mutant they called rQ-M38G, reprogramming its genetic makeup so it bypasses healthy tissues and instead targets rapidly dividing cancer cells for infection. They also genetically armed the virus so it prompts cancer cells to secrete Gaussia luciferase (GLuc).

GLuc is a luminescent, easily detectable protein the researchers used as a universal blood biomarker for cancer cells infected by rQ-M38G. Because rQ-M38G/GLuc might also help shrink cancer, it is part of a new class of agents dubbed "theragnostics" that can simultaneously be used for diagnosis and therapy, Dr. Cripe said.

Initially the researchers tested rQ-M38G on laboratory cell cultures of healthy dormant human skin cells and on rapidly dividing cancer cells. Virus replication and biomarker production were very low in the dormant normal cells. In contrast, virus replication and biomarker production were much higher in tumor cell lines of malignant peripheral nerve sheath tumors, osteosarcoma (bone cancer), rhabdomyosarcoma (muscle cancer) and Ewing sarcoma.

Researchers then tested the virus's detection capabilities in mouse models of these same cancers by injecting rQ-M38G into their tail veins, and for comparison into the tail veins of healthy control mice. Non-tumor bearing mice showed background signals for the virus without significant replications or biomarker production. More than 90 percent of the tumor bearing mice showed significant virus replication and biomarker production.

The technology even worked in some mice with only microscopic amounts of cancer in their kidneys, researchers report. If it were to work as well in humans, the scientists estimate that hidden tumors less than half-inch in diameter might be detectable. Because of the anticipated immune response against the virus and the GLuc protein in humans, further refinements of the technology will likely be needed to be able to use it more than once.

The study is one more example of the expanding research into using reprogrammed HSV as novel methods to treat or diagnose cancer, especially as medicine reaches the limits of modern chemotherapies. Dr. Cripe said this creates an urgent need for new strategies against stubborn metastatic disease. Less than 30 percent of patients with metastatic cancer survive beyond five years, despite the aggressive use of modern combination therapies that include chemotherapy.

Also collaborating on the current study were Jennifer Leddon, Mark Currier, Jon Williams, Jason Frischer, and Margaret Collins all of Cincinnati Children's.

Funding support for the study came from the CancerFree Kids Pediatric Cancer Research Alliance and the National Institutes of Health.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Cincinnati Children's Hospital Medical Center, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

Andrew W. Browne, Jennifer L. Leddon, Mark A. Currier, Jon P. Williams, Jason S. Frischer, Margaret H. Collins, Chong H. Ahn, Timothy P. Cripe. Cancer Screening by Systemic Administration of a Gene Delivery Vector Encoding Tumor-Selective Secretable Biomarker Expression. PLoS ONE, 2011; 6 (5): e19530 DOI: 10.1371/journal.pone.0019530

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

New study alters long-held beliefs about shingles

ScienceDaily (Feb. 1, 2011) — For decades, medical wisdom about shingles has been that it's a once-in-a-lifetime experience. The commonly-held belief is that patients are protected from a recurrence of the herpes zoster virus, which causes shingles, after one episode. But according to a study published in the February issue of Mayo Clinic Proceedings, recurrences of shingles may be significantly more common than doctors have suspected.

"It's been thought that recurrences were limited to people with compromised immune systems, for instance from chemotherapy or bloodborne malignancies, but this is not the case," says lead author Barbara Yawn, M.D., director of research at Olmsted Medical Center in Rochester. "Recurrence was prevalent in the immunocompetent population. We were very surprised by the results."

The research team examined medical records, dating from 1996 to 2001, of nearly 1,700 patients over age 22 who had a documented episode of shingles. The condition causes a specific type of skin rash and severe pain. They then searched area medical records to determine whether those patients had been treated for a second episode at any point, following them up to 12 years (the average follow-up was eight years). The data showed the recurrence rate was over 5 percent, the same rate an age-matched cohort would be expected to experience a first case of shingles. Some patients had experienced as many as three recurrences. "And that's only within eight years," Dr. Yawn notes. "As you continue to follow these patients throughout their lives, it's likely the recurrence rate will be much higher than 5 percent."

The study found that women, who are more likely than men to have shingles, also were more likely to experience a recurrence of the disease. Although the team had suspected that recurrence rates would be higher in older patients, age did not appear to make individuals more susceptible to another round of the disease. Instead, researchers found the most striking determinant for recurrence was patients' pain during the initial episode. Those who had experienced pain lasting more than 30 days after the initial onset of shingles were more likely to face a recurrence, particularly in the first three to four years after the initial episode. This, too, surprised the research team. "We'd thought that suffering a worse case would possibly give patients more resistance to a second occurrence, but our data presented the exact opposite," says Dr. Yawn.

The results suggest that the herpes zoster vaccine, which is known to reduce first-time occurrences of shingles by 50 percent, may help patients avoid a second episode. "Until now, we haven't been able to tell patients their risks of getting zoster a second time," Dr. Yawn says. "This study offers another piece of information for patients and doctors who are discussing the likelihood of recurrence and considering a prevention strategy."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Mayo Clinic.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

B. P. Yawn, P. C. Wollan, M. J. Kurland, J. L. St. Sauver, P. Saddier. Herpes Zoster Recurrences More Frequent Than Previously Reported. Mayo Clinic Proceedings, 2011; 86 (2): 88 DOI: 10.4065/mcp.2010.0618

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Cellular protein hobbles HIV-1

ScienceDaily (Dec. 13, 2010) — A cellular protein called BST-2 had already been known to interfere with the spread of human immunodeficiency virus type 1 (HIV-1), by inhibiting the release of its progeny particles from infected cells. Now a team from McGill University, Montreal, shows that in addition, each progeny virion's ability to cause infection is severely impaired.

"BST-2 may exert a more potent inhibition effect on HIV-1 transmission than previously thought," says coauthor Chen Liang. The research is published in the December Journal of Virology.

BST-2 appears to attenuate infectivity of progeny particles by interfering with their maturation. Normally, during synthesis of new virus particles, a protein called PR55Gag is cleaved into three major structural proteins of HIV. "This cleavage process transforms HIV-1 from an immature and non-infectious virion into a mature and infectious virion," says Chen. The protease inhibitors, drugs given to AIDS patients to contain the disease, block this step. Similarly, BST-2 seems to interfere with this step, because in the study, its presence was associated with accumulation of uncleaved Gag precursor and intermediate products. The mechanism of that interference has yet to be elucidated.

BST-2 (bone marrow stromal cell antigen-2), also known as tetherin, is a cellular protein which has been shown to restrict production of enveloped viruses besides HIV-1, including HIV-2, simian immunodeficiency virus, Kaposi's sarcoma herpes virus, Lassa virus, Marburg virus, and Ebola virus. It interferes with release of new virus particles by anchoring one end of itself in the plasma membrane of the infected cell while the other end becomes inserted into the viral envelope.

Different viruses have evolved various countermeasures. For example, in the case of HIV-1, the viral protein Vpu downregulates BST-2 from the cell surface, removing it from virus budding sites.

"The antiviral function of BST-2 has been extensively studied by a number of groups besides ours," says Chen. "Our hope is that the results of all of these studies can eventually be used to develop a BST-2 based anti-HIV-1 therapy."

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by American Society for Microbiology.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

J. Zhang, C. Liang. BST-2 Diminishes HIV-1 Infectivity. Journal of Virology, 2010; 84 (23): 12336 DOI: 10.1128/JVI.01228-10

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Specific gene linked to cold sore susceptibility, study finds

ScienceDaily (Oct. 28, 2011) — Investigators have identified a human chromosome containing a specific gene associated with susceptibility to herpes simplex labialis (HSL), the common cold sore. Published in The Journal of Infectious Diseases and now available online, the study looks at how several genes may affect the severity of symptoms and frequency of this common infection. The findings, if confirmed, could have implications for the development of new drugs to treat outbreaks.

HSL outbreaks, or cold sores, are skin infections that appear with the reactivation of herpes simplex virus, a virus that infects 70 percent of the U.S. population. Cold sore outbreaks vary in frequency and severity; some people may experience symptoms rarely, only once every 5 to 10 years, while others may experience them once a month or even more frequently. In addition to investigating environmental activating factors (e.g., sunlight) that may play a role in outbreaks, researchers for some time have been looking at the possible role of genetic factors in virus susceptibility and activation.

This study, led by John D. Kriesel, MD, and colleagues from the University of Utah School of Medicine in Salt Lake City and the University of Massachusetts Medical School in Worcester, follows previous studies identifying a region of chromosome 21 as a base for genes possibly linked to cold sore outbreaks. To identify which of six possible genes in this region were associated with the frequency of outbreaks, this latest study used single nucleotide polymorphism genotyping in genome-wide, family-based linkage studies of 618 people from 43 large families. The investigators found a positive link between the frequency of outbreaks, hereditability, and the presence of a specific gene, C21orf91, on chromosome 21.

"While these findings await confirmation in a larger, unrelated population," the study authors note, "these findings could have important implications for the development of new drugs that affect determinants of the cold sore phenotype."

In an accompanying editorial, Anthony L. Cunningham, MD, and David Booth, MD, of the Centre for Virus Research and the Institute of Immunology and Allergy Research at Westmead Millennium Institute and the University of Sydney in Australia, note that if the findings regarding the C21orf91 gene are confirmed, additional research may then begin to determine possible therapeutic applications and whether the same gene also plays a role in recurring genital herpes.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by Infectious Diseases Society of America.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal References:

J. D. Kriesel, B. B. Jones, N. Matsunami, M. K. Patel, C. A. St. Pierre, E. A. Kurt-Jones, R. W. Finberg, M. Leppert, M. R. Hobbs. C21orf91 Genotypes Correlate With Herpes Simplex Labialis (Cold Sore) Frequency: Description of a Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1654 DOI: 10.1093/infdis/jir633A. L. Cunningham, D. Booth. The First Common Cold Sore Susceptibility Gene. Journal of Infectious Diseases, 2011; 204 (11): 1645 DOI: 10.1093/infdis/jir635

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here

Researchers on the trail of a treatment for cancer of the immune system

ScienceDaily (Aug. 22, 2011) — Danish researchers from the University of Copenhagen have become the first in the world to regulate a special receptor or bio-antenna that plays a vital part when the Epstein Barr herpes virus infects us and when this infection appears to be mutating into cancer of the immune system. Using a biochemical blueprint and a tiny bio-molecule the Danish researchers have succeeded in blocking the receptor concerned. This will make it possible to adjust and regulate the memory cells of the immune system.

Infection with Epstein Barr means that the B cells, which are the primary memory cells of the immune system, are hi-jacked.

When the virus has penetrated, researchers observe an excess of a special bio-antenna, a receptor known as EB12, suddenly sprouting from the surface of the B cells. But why they do so remains a mystery.

The receptors are a vital component of the way cells communicate with their surroundings via hormones and other bio-molecules, for example, but in a body consisting of millions of cells and transmitters it can be hard to determine the part each molecule plays.

"It is possible that the large numbers of EB12 receptors could actually be the B cells response to the virus and an attempt to combat the infection. Another possibility is that the EB virus reprogrammes the cell for this explosive growth in the number of EB12 receptors. What we know for certain is that more EB12 receptors assist the B cell infected by the EB virus to multiply more rapidly thus spreading the infection faster," says postdoc Tau Benned-Jensen from the Faculty of Health Sciences, University of Copenhagen.

The Epstein Barr virus can cause cancer

No fewer than 95 per cent of us carry the Epstein Barr Herpes virus.

We often encounter it as kids and it is normally harmless. Are we infected later in life EB virus may cause mononucleosis, and it seems to play a part in some forms of cancer, just as HPV affects the risk of cervical cancer. But we have no drugs to combat the Epstein Barr virus, and no vaccines for it.

"Under normal circumstances our immune systems can keep the EB virus infection in a latent state and a truce or stand-off may arise between the immune system and the virus," explains Mette Rosenkilde, professor of pharmacology at the Department of Neuroscience and Pharmacology, University of Copenhagen.

"We cannot dispense with the infection and we carry it all life long, but to most of us it is harmless. For people whose immune systems do not function due to disease or because they are suppressed by drugs in conjunction with organ transplants it is a very different matter. Now the Epstein Barr virus is suddenly free to reproduce so uninhibitedly and dramatically that it may lead to cancer," says Mette Rosenkilde.

The first step on the road to solving the EB12-puzzle

While researchers know that the B cell EB12 receptors play a part when the cell visits the lymph glands, the immune system's Central Station, we have not yet explained the exact role of the receptor.

So the Danish researchers started by mapping the bio-antenna molecule by molecule and then, as the first in the world, they made a blueprint of a tiny molecule they thought could bind to the B cell EB12 receptor.

"When we know what receptors react to, it tells us more about the part they play," Mette Rosenkilde explains, "and our tiny molecule, a ligand, blocks the EB12 receptor, preventing it from doing its job."

"In time this block may be able to help transplant patients. If we can restrain EB virus reproduction when the immune system is being medically suppressed, we may well be able to avoid cancer," Tau Benned-Jensen says.

"On the other hand the EP virus also appears to play a part in other immune diseases such as autoimmune disease, where the ability to adjust the immune system would be beneficial," says Mette Rosenkilde.

And shortly after the Danish researchers published their article on their ligand, the first articles appeared about natural substances in the body, which activate the EB12 receptor and direct the B cell to specific areas in the lymph glands.

"Our molecule can inhibit the activation of the new substances, and the next step in our research will be experiments to identify even more biochemical dials to twiddle and to help us develop new drugs," Tau-Benned says.

The discovery has just been published in the Journal of Biological Chemistry.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

Story Source:

The above story is reprinted from materials provided by University of Copenhagen.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

T. Benned-Jensen, C. Smethurst, P. J. Holst, K. R. Page, H. Sauls, B. Sivertsen, T. W. Schwartz, A. Blanchard, R. Jepras, M. M. Rosenkilde. Ligand Modulation of the Epstein-Barr Virus-induced Seven-transmembrane Receptor EBI2: IDENTIFICATION OF A POTENT AND EFFICACIOUS INVERSE AGONIST. Journal of Biological Chemistry, 2011; 286 (33): 29292 DOI: 10.1074/jbc.M110.196345

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

View the original article here