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A study in the Journal of the American Academy of Child and Adolescent Psychiatry (JAACAP), published by Elsevier, finds that Wraparound Care Coordination (Wraparound), which has been adopted in states and jurisdictions across the country to help meet the needs of children and adolescents with serious emotional and behavioral disorders, produces more positive outcomes for youth when compared to more common service approaches.
Moreover, Wraparound may hold the potential for reducing disparities in outcomes for youth of color, which has long been found in mental health services.
A team of researchers, led by Jonathan Olson, PhD, at the University of Washington Department of Psychiatry and Behavioral Sciences, Seattle, WA, USA, conducted a meta-analysis of 17 controlled studies, and their results, published between 1996 and 2019 in order to compare the effects of Wraparound to regular services in youth with SED (serious emotional disorders).
“For many years, public systems have used Wraparound because it makes sense and provides families with the kind of compassionate approach, something that all families say they want and need,” said Dr. Eric Bruns, Professor of Psychiatry and senior author on the research team. “Now we have clear results that support what many have seen in their own local systems of care: that Wraparound is more effective and cost-effective than traditional services.”
Significant effects in favor of Wraparound across a range of important youth outcomes were found — including reduced out-of-home placements and improved mental health functioning and school outcomes. The study also found significantly lower overall care costs for youth in Wraparound care, due to less spending on costly out-of-home placements. Across the 17 studies, Wraparound effects were more positive for samples with higher proportions of youth of color.
“Wraparound lives up to principles we want to uphold — for example, being youth- and family-driven, strengths-based and using a team of people with a blank checkbook to ‘do whatever it takes’ to meet the needs of the youth and family,” added Dr. Bruns. “While many states have taken Wraparound to scale, others have been more hesitant, saying it wasn’t ‘evidence-based.’ This study should help address those concerns.”
Wraparound was established in the 1980s as an alternative to service delivery strategies that kept youth and family services in fragmented siloes, driven by professionals and often relying on costly institution-based care rather than investing in community supports. Instead, Wraparound invests in a care coordinator with a low caseload who convenes a team that includes the family, friends and members of the wider community, as well as service and support providers.
Dr. Olson also points out, however, that the study additionally reinforced how important it is to implement high-quality Wraparound services that are true to the model: “Unfortunately, many studies were conducted before there were measures of fidelity, or measures of ‘doing Wraparound right,'” he said. “However, for studies that did measure fidelity, we saw more positive outcomes for youth and families who received care that was of high-quality and closely adhered to Wraparound principles.”
The potential for Wraparound to better meet the needs of youth of color was an unexpected finding, concluded Dr. Bruns, but perhaps not surprising: “We need to remember that in all these studies, Wraparound was compared to more traditional services delivered in mental health, child welfare and juvenile justice.
“There is a long history of research showing disparities in access and outcomes for youth of color and their families. It may be that by allowing for more youth and family voice and choice, and teams that include family, friends, and community members, Wraparound helps reduce those disparities. However, such questions were not the explicit focus of these studies. We need to investigate the issue of what may address disparities with greater rigor.”
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University of Virginia School of Medicine researchers have developed a noninvasive way to remove faulty brain circuits that could allow doctors to treat debilitating neurological diseases without the need for conventional brain surgery.
The UVA team, together with colleagues at Stanford University, indicate that the approach, if successfully translated to the operating room, could revolutionize the treatment of some of the most challenging and complex neurological diseases, including epilepsy, movement disorders and more. The approach uses low-intensity focused ultrasound waves combined with microbubbles to briefly penetrate the brain’s natural defenses and allow the targeted delivery of a neurotoxin. This neurotoxin kills the culprit brain cells while sparing other healthy cells and preserving the surrounding brain architecture.
“This novel surgical strategy has the potential to supplant existing neurosurgical procedures used for the treatment of neurological disorders that don’t respond to medication,” said researcher Kevin S. Lee, PhD, of UVA’s Departments of Neuroscience and Neurosurgery and the Center for Brain Immunology and Glia (BIG). “This unique approach eliminates the diseased brain cells, spares adjacent healthy cells and achieves these outcomes without even having to cut into the scalp.”
The Power of PING
The new approach is called PING, and it has already demonstrated exciting potential in laboratory studies. For instance, one of the promising applications for PING could be for the surgical treatment of epilepsies that do not respond to medication. Approximately a third of patients with epilepsy do not respond to anti-seizure drugs, and surgery can reduce or eliminate seizures for some of them. Lee and his team, along with their collaborators at Stanford, have shown that PING can reduce or eliminate seizures in two research models of epilepsy. The findings raise the possibility of treating epilepsy in a carefully-targeted and noninvasive manner without the need for traditional brain surgery.
Another important potential advantage of PING is that it could encourage the surgical treatment of appropriate patients with epilepsy who are reluctant to undergo conventional invasive or ablative surgery.
In a new scientific paper in the Journal of Neurosurgery, Lee and his collaborators detail the ability of PING to focally eliminate neurons in a brain region, while sparing non-target cells in the same area. In contrast, currently available surgical approaches damage all cells in a treated brain region.
A key advantage of the approach is its incredible precision. PING harnesses the power of magnetic-resonance imaging (MRI) to let scientists peer inside the skull so that they can precisely guide sound waves to open the body’s natural blood-brain barrier exactly where needed. This barrier is designed to keep harmful cells and molecules out of the brain, but it also prevents the delivery of potentially beneficial treatments.
The UVA group’s new paper concludes that PING allows the delivery of a highly targeted neurotoxin, cleanly wiping out problematic neurons, a type of brain cell, without causing collateral damage.
Another key advantage of the precision of this approach is that it can be used on irregularly shaped targets in areas that would be extremely difficult or impossible to reach through regular brain surgery. “If this strategy translates to the clinic,” the researchers write in their new paper, “the noninvasive nature and specificity of the procedure could positively influence both physician referrals for and patient confidence in surgery for medically intractable neurological disorders.”
“Our hope is that the PING strategy will become a key element in the next generation of very precise, noninvasive, neurosurgical approaches to treat major neurological disorders,” said Lee, who is part of the UVA Brain Institute.
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People choose whether to seek or avoid information about their health, finances and personal traits based on how they think it will make them feel, how useful it is, and if it relates to things they think about often, finds a new study by UCL researchers.
Most people fall into one of three ‘information-seeking types’: those that mostly consider the impact of information on their feelings when deciding whether to get informed, those that mostly consider how useful information will be for making decisions, and those that mostly seek information about issues they think about often, according to the findings published in Nature Communications.
Co-lead author Professor Tali Sharot (UCL Psychology & Language Sciences and Max Planck UCL Centre for Computational Psychiatry and Ageing Research) said: “Vast amounts of information are now available to individuals. This includes everything from information about your genetic make-up to information about social issues and the economy. We wanted to find out: how do people decide what they want to know? And why do some people actively seek out information, for example about COVID vaccines, financial inequality and climate change, and others don’t?
“The information people decide to expose themselves to has important consequences for their health, finance and relationships. By better understanding why people choose to get informed, we could develop ways to convince people to educate themselves.”
The researchers conducted five experiments with 543 research participants, to gauge what factors influence information-seeking.
In one of the experiments, participants were asked how much they would like to know about health information, such as whether they had an Alzheimer’s risk gene or a gene conferring a strong immune system. In another experiment, they were asked whether they wanted to see financial information, such as exchange rates or what income percentile they fall into, and in another one, whether they would have liked to learn how their family and friends rated them on traits such as intelligence and laziness.

Having an elevated resting heart rate in old age may be an independent risk factor of dementia, according to a study at Karolinska Institutet in Sweden published in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. Since resting heart rate is easy to measure and can be lowered through exercise or medical treatment, the researchers believe that it may help to identify people with higher dementia risk for early intervention.
The number of people living with dementia is expected to increase to 139 million globally by 2050, from 55 million in 2020, according to the organisation Alzheimer’s Disease International. Currently, there is no cure for dementia, but growing evidence suggests that maintaining a healthy lifestyle and cardiovascular health could help delay the onset of dementia and ease symptoms.
In this study, the researchers examined if resting heart rate in 2,147 individuals 60 years old or older and living in Stockholm could be linked to dementia and cognitive decline independent of other known risk factors, such as cardiovascular disease.
The study, which followed the participants for up to 12 years, showed that individuals with a resting heart rate of 80 beats per minute or higher on average had 55 percent higher risk of dementia than those with a heart rate of 60-69 beats per minute. The association remained significant after adjusting for potential confounders such as various cardiovascular diseases. Still, the researchers caution that the result may have been affected by undetected cardiovascular events and the fact that more participants with cardiovascular disease died during the follow-up period and thus didn’t have time to develop dementia.
The study cannot establish a causal relationship, but the researchers offer several plausible explanations for the association, including the effect of underlying cardiovascular diseases and cardiovascular risk factors, stiffened arteries, and imbalance between sympathetic and parasympathetic nerve activities.
“We believe it would be valuable to explore if resting heart rate could identify patients with high dementia risk,” says the study’s leading author Yume Imahori, a researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet. “If we follow such patients’ cognitive function carefully and intervene early, the onset of dementia might be delayed, which can have a substantial impact on their quality of life.”
The study was led by senior lecturer Dr Chengxuan Qiu and the data was derived from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K).
The research was funded by the Swedish Ministry of Health and Social Affairs, the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, the Swedish Foundation for International Cooperation in Research and Higher Education, Karolinska Institutet and the European Union.
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In an effort to predict the future evolutionary maneuvers of SARS-CoV-2, a research team led by investigators at Harvard Medical School has identified several likely mutations that would allow the virus to evade immune defenses, including natural immunity acquired through infection and developed from vaccination as well as antibody-based treatments.
The study, published Dec. 2 in Science as an accelerated publication for immediate release, was designed to gauge how SARS-CoV-2 might evolve as it continues to adapt to its human hosts and in doing so to help public health officials and scientists prepare for future mutations.
Indeed, as the research was nearing publication, a new variant of concern, dubbed omicron, entered the scene and was subsequently found to contain several of the antibody-evading mutations the researchers predicted in the newly published paper. As of Dec. 1, omicron has been identified in 25 countries in Africa, Asia, Australia, Europe, and North and South America, a list that is growing daily.
The researchers caution that the study findings are not directly applicable to omicron because how this specific variant behaves will depend on the interplay among its own unique set of mutations-at least 30 in the viral spike protein — and on how it competes against other active strains circulating in populations around the world. Nonetheless, the researchers said, the study gives important clues about particular areas of concern with omicron, and also serves as a primer on other mutations that might appear in future variants.
“Our findings suggest that great caution is advised with omicron because these mutations have proven quite capable of evading monoclonal antibodies used to treat newly infected patients and antibodies derived from mRNA vaccines,” said study senior author Jonathan Abraham, assistant professor of microbiology in the Blavatnik Institute at HMS and an infectious disease specialist at Brigham and Women’s Hospital. The researchers did not study response to antibodies developed from non-mRNA vaccines.
The longer the virus continues to replicate in humans, Abraham noted, the more likely it is that it will continue to evolve novel mutations that develop new ways to spread in the face of existing natural immunity, vaccines, and treatments. That means that public health efforts to prevent the spread of the virus, including mass vaccinations worldwide as soon as possible, are crucial both to prevent illness and to reduce opportunities for the virus to evolve, Abraham said.

The brain is indeed a target for treating ALS (amyotrophic lateral sclerosis), Northwestern Medicine scientists have discovered. This flips a long-standing belief that the disease starts in the spinal motor neurons and any therapy would need to target the spine as the key focus.
A new Northwestern study shows the degeneration of brain motor neurons (the nerve cells in the brain that control movement of the limbs) is not merely a byproduct of the spinal motor neuron degeneration, as had been previously thought.
“We have discovered that the brain degenerates early in diseases like ALS, sends us warning signals and shows defects very early in the disease,” said lead study author Hande Ozdinler, an associate professor of neurology at Northwestern University Feinberg School of Medicine. “Therefore, we need to repair the brain motor neurons if we want long-term and effective treatment strategies. The brain is important in ALS.”
The paper will be published Dec. 2 in Gene Therapy.
ALS is a swift and fatal neurodegenerative disease that paralyzes its victims.
Upper motor neuron diseases, such as ALS, hereditary spastic paraplegia and primary lateral sclerosis affect more than 250,000 people a year in the U.S. alone. There is no cure and no effective long-term treatment strategy.
This is the first study to clearly reveal the brain motor neuron degeneration is not a consequence of spinal motor neuron degeneration but is independent of the spinal motor neuron degeneration.
The research also is the first to show that the gene UCHL1 is important for maintaining the health of brain motor neurons that are diseased due to two independent underlying causes. One is the accumulation of badly folded proteins and the other is the accumulation of sticky protein clumps inside the cells. These problems are observed in more than 90% of all ALS cases and also in other cases of upper motor neuron diseases.
“Our findings not only give legitimacy for targeting brain motor neuron health in ALS as a therapeutic intervention, it also reveals the first target gene that can help these neurons be revitalized,” Ozdinler said.
“This has huge clinical implications,” Ozdinler said. “Being able to modulate gene expression in diseased brain motor neurons in upper motor neuron disease patients is mind boggling. Since movement starts in the brain, if we can make the brain motor neurons happy and healthy, if we can boost their health and integrity with directed gene delivery, we may begin to develop personalized treatment options especially for patients with upper motor neuron disease, who currently have no effective treatment options.
Northwestern University scientists have previously identified NU-9, the first compound that eliminates the ongoing degeneration of upper motor neurons that become diseased and are a key contributor to ALS. Now, this study reveals the importance and significance of treating upper motor neurons in ALS and identifies the first genetic target.
The next step is to determine the best dose and the best site of injection with respect to improvement of movement and reduction of disease conditions in at least two different ALS disease models. After preclinical toxicology studies, scientists will move to translate these results into a clinical trial, a process that likely will take several years.
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Materials provided by Northwestern University. Original written by Marla Paul. Note: Content may be edited for style and length.

SARS-CoV-2 causes the pandemic coronavirus disease COVID-19, that is more harmful for elderly people, who show more severe symptoms and are at higher risk of hospitalization and death. A group of Italian and American researchers led by Fabrizio d’Adda di Fagagna now reports that the expression of the cell receptor for the virus, ACE2, which is essential for mediating cell entry of the virus, increases in the lungs of aging mice and humans. They further show that ACE2 expression increases upon telomere shortening or dysfunction — common hallmarks of aging — in cultured human cells and in mice. This increase depends on a DNA damage response elicited by dysfunctional telomeres. The findings published today by EMBO Reports provide one possible molecular explanation for the increased sensitivity of elderly people to SARS-CoV-2.
The reasons for the higher probability of severe symptoms and death in the elderly in response to a SARS-CoV-2 infection remain unclear. ACE2 expression has been positively related to patients’ age, for example in the nasal epithelium, the first point of contact with SARS-CoV-2. Lower ACE2 expression in children relative to adults may explain why COVID-19 is less prevalent in children, and the expression and distribution of the ACE2 receptor may be relevant for the progression and prognosis of COVID-19. The research findings now show that ACE2 protein expression is elevated in aging human and mouse lungs, including in alveolar epithelial type II cells (ATII). In the lungs, ACE2 is mostly found on the surface of ATII cells, and these cells are thus likely the primary target of SARS-CoV-2 infection in the lungs. SARS-CoV-2 mainly spreads via respiratory droplets and the lung is the first target organ of the virus. Indeed, pneumonia is the most common complication seen in COVID-19 patients, at an occurrence of 91%.
In order to reveal the molecular mechanism underlying the upregulation of ACE2 during aging, the researchers turned to in vitro and in vivo models that recapitulate some key aspects of aging. Aging is associated with telomere shortening and damage in a range of tissues in different species, including humans. Telomeres are the regions at the ends of linear chromosomes that are essential to protect chromosome ends from shortening during repeated cell replication cycles, which would result in the loss of crucial genetic information. When telomeres become critically short, they are sensed as DNA breaks and activate DNA damage response pathways. D’Adda di Fagagna working at IFOM in Milan and CNR-IGM in Pavia and colleagues either inhibited the general DNA damage response by targeting ATM, a major enzyme of the DNA damage response pathway, or they inhibited the telomeric DNA damage response specifically using telomeric antisense oligonucleotides (tASO). Both approaches prevent ACE2 gene and protein upregulation following telomere damage in aging cultured cells and in mice. The group also used a cell culture model in which the DNA damage response is activated specifically at telomeres in the absence of telomere shortening, with the same results. These findings indicate that it is the DNA damage response activation, rather than telomeric shortening per se, that is responsible for ACE2 upregulation. Understanding the mechanism of age susceptibility to SARS-CoV-2 infection is important for targeted therapeutic approaches, which might in principle include the use of tASO-mediated inhibition of the telomeric DNA damage response.
ACE2 also has a role in the regulation of blood pressure and the balance of fluids and salts and is expressed in other human tissues, for example the heart and kidney. The findings reported here may thus also have broader medical implications beyond COVID-19.
However, further research is needed to establish whether reducing ACE2 expression has beneficial effects on SARS-CoV-2 infection rates and on the severity of COVID-19 symptoms in in vivo models. Further work also needs to be carried out to understand how DNA damage response signaling leads to increased Ace2 gene expression.
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In a comparison of seven different brands, researchers found that most shots give a strong boost, even in mix-and-match combinations.People looking for a booster shot of a Covid-19 vaccine probably don’t need to fret about what brand it is: Many combinations of shots are likely to provide strong protection, according to a large new study.In a comparison of seven different vaccine brands, British researchers found that most of them prompted a strong immune response, with the mRNA shots from Moderna and Pfizer-BioNTech eliciting the largest responses. The study was published on Thursday in The Lancet.“These are welcome data for policymakers,” said Merry Voysey, a statistician at the University of Oxford who was not involved in the study. “The most significant take-home message here is that there are a large number of excellent boosting options for third doses.”It’s too soon for researchers to say much about how well different vaccine boosters will work against the new Omicron variant, which has mutations that may allow it to evade some of the antibodies produced by existing Covid-19 vaccines. Some researchers suspect that people would need a very high level of antibodies to protect against it.All of the study’s 2,878 volunteers initially received two shots of either the AstraZeneca or Pfizer vaccines. (Both of those vaccines are authorized in Britain; shots by Pfizer, Moderna and Johnson & Johnson have been authorized in the United States.)The researchers then tested seven different vaccines as boosters: along with AstraZeneca and Pfizer, they tried three brands that have been authorized in various countries: Johnson & Johnson, Moderna and Novavax. They also tried two shots that have not been authorized anywhere: an mRNA vaccine from CureVac, and a vaccine from Valneva made from inactivated coronaviruses. Finally, some of the volunteers received a meningitis vaccine as a control.After four weeks, the researchers collected blood samples from the volunteers and measured their antibody levels. They also looked for immune cells, known as T cells, that specifically attack other cells infected with the coronavirus.Antibodies and T cell levels increased in people who received a Covid-19 booster shot compared with those who got the meningitis vaccine. The range was quite large, however. People who got the Valneva booster after a Pfizer vaccine saw only a 30 percent increase above the control group. But a Moderna booster produced at least a 1,000 percent increase.The new study also found that boosters increased T cells that recognize the coronavirus. Antibodies may be good at knocking the coronavirus out early in an infection, when the virus is colonizing the nose. But deep in the airway, T cells may provide a second line of defense.The trial did not follow the volunteers to see how well the booster shots actually prevented infection or disease. But in recent months, researchers have shown that measuring antibody levels can be a pretty good way of predicting the effectiveness of a vaccine.Most of the boosters used in the study raised antibodies to a level that would be the equivalent of at least 90 percent protection against infection. And the mRNA vaccines by Pfizer and Moderna produced much higher antibody levels than the other vaccines did.“I would say whatever you had first time around, having an mRNA booster is probably a good idea,” said Eleanor Riley, an immunologist at the University of Edinburgh who was not involved in the new study.Still, other scientists said, most of the other vaccines in the study performed strongly enough that people should feel comfortable getting them as well.The Coronavirus Pandemic: Key Things to KnowCard 1 of 4The Omicron variant.

New research shows that the first SARS-CoV-2 spike protein a person encounters, be it by vaccination or infection, shapes their subsequent immune response against current and future variants. That is, it imparts different properties that have an impact on the immune system’s ability to protect against variants, and also affects the rate of decay of protection.
The study is published today in Science by a team from Imperial College London and Queen Mary University of London. It is funded by UKRI.
It is known that antibody levels wane over time following infection or vaccination, but the new research shows that an individual’s protective immune responses are also affected by which strain or combination of strains they have been exposed to.
At 23 months into the pandemic, people across the world have very different patterns of immunity to the SARS-CoV-2 virus, based on their exposure. Globally, people have been exposed to the original strain and/or Alpha, Beta, Gamma, Delta variants and now Omicron. In addition, people may be unvaccinated or have had one to three vaccine doses (which are programmed using the spike of the original strain).
Each SARS-CoV-2 variant has different mutations in the spike protein, and the researchers found that these shape the subsequent antibody and T cell responses (the immune repertoire).
Professor Rosemary Boyton, from Imperial’s Department of Infectious Disease, says: “Our first encounter with spike antigen either through infection or vaccination shapes our subsequent pattern of immunity through immune imprinting. Exposure to different spike proteins can result in reduced or enhanced responses to variants further down the line. This has important implications for future proofing vaccine design and dosing strategies.”
The new study looks at ‘immune imprinting’ in healthcare workers after 2 doses of Pfizer vaccine to understand their immune response to infection by variants of concern. It involves detailed, longitudinal follow-up of the ‘Barts COVIDsortium’ healthcare worker cohort of 731 individuals, who have been followed since March 2020.

Scientists around the world have been working in earnest to improve understanding of an increasingly virulent superbug, Clostridium difficile. The highly contagious hospital-acquired pathogen, designated by the Centers for Disease Control and Prevention as one of the five most urgent threats to the U.S. healthcare system, causes more than 500,000 infections and 29,000 deaths each year at a total societal cost exceeding $5 billion.
Biologists at Texas A&M University and Baylor College of Medicine have teamed up in a novel National Institutes of Health-funded systems biology study aimed at tackling the problem at its source — the initial point of infection — in hopes of pinpointing what makes patients susceptible to it in the first place.
Prior studies have shown C. difficile infection to be strongly correlated with a high abundance of secondary bile acids that are toxic to C. difficile in laboratory settings. These small molecules are generated by a healthy gut microbiome from primary bile acids that are synthesized in the liver.
Texas A&M biologist and 2020 Chancellor’s EDGES Fellow Joseph Sorg says scientists have long viewed these small molecules as a key protector in preventing C. difficile infection. The research was first featured by Sorg Laboratory graduate student Andrea Martinez Aguirre in a paper published earlier this fall in the journal PLOS Pathogens with help from Tor Savidge’s group at Baylor College of Medicine.
“Many ongoing efforts are developing probiotic treatment options for C. diff-infected patients — efforts that focus on restoring secondary bile acids to patients,” Sorg said. “Our findings show that these treatments should instead focus on microbes that consume nutrients important for C. diff growth and that secondary bile acids are a red herring for protection.”
As the basis of their study, the team used mice derived germ-free at Baylor College of Medicine that were colonized with a single species of bacteria known to be involved in secondary bile acid generation and strongly correlated with a protective C. difficile environment. As an additional control measure, they selected a mutant mouse strain purchased through the NIH’s Knockout Mouse Project that was bred at Texas A&M and distinct for its inability to synthesize a major class of bile acids, thereby further limiting the secondary bile acid pool.
“Surprisingly, we found that mice colonized with these microbes (C. scindens, C. hiranonis, or C. leptum) protected against C. diff disease but did not produce secondary bile acids,” Sorg said.
Sorg joined the Texas A&M Department of Biology in 2010 and has been working since his postdoctoral days to unlock C. difficile’s basic science, from its physiology to its virulence. He earned his doctorate in microbiology at the University of Chicago in 2006, the same year the C. difficile genome was sequenced, and since has emerged as one of the pioneers of C. difficile study.
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Materials provided by Texas A&M University. Original written by Shana K. Hutchins. Note: Content may be edited for style and length.