Wisconsin National Primate Research Center
Wisconsin National Primate Research Center
News Article | May 17, 2017
Twice a week, postdoc Phil Auckland leaves the lab at 5:30 p.m. and drives an hour out of Coventry, UK, to a mountain-bike racing track and hills. Here, he finds diversion and distraction from his research programme in a cell-biology lab at the University of Warwick. “It requires so much focus and concentration, doing tricks and jumps, that you are not thinking about anything else,” he says. It helps that Auckland's friends, who hail mainly from his days of professional mountain biking, have all manner of careers. “We don't talk about work — it's a complete escape.” His other hobby, skydiving, also gives him a mental and physical break from lab work. “When you've just thrown yourself out of a plane, work is the last thing that enters your mind.” As Auckland finds with extreme sports, participation in hobbies and activities outside the lab offers important, even crucial, time away from the research environment. Taking breaks, experts say, is key to fighting burn-out, which can easily arise in research careers that require long hours of intense mental activity for weeks or months on end. Although burn-out is not considered a medical diagnosis, researchers have described it as a combination of overwhelming fatigue and loss of motivation caused by chronic stress or frustration. Graduate students and postdocs, who may equate 'working longer' with 'working better', are particularly prone to working themselves into the ground, says Simon Davy, head of the School of Biological Sciences at the Victoria University of Wellington in New Zealand. Davy, who since his days as a PhD student has vowed not to work on Saturdays, says that he sees students slide easily into working seven-day weeks. Some institutions and career-development offices have begun to recognize the importance of addressing mental health in the research workforce. Using an assessment of 12 mental-health symptoms, one team showed in a study published this year that one-third of more than 3,600 doctoral students surveyed in Belgium were at risk of developing mental-health problems, especially depression, as measured by having four or more clinical symptoms ( et al. Res. Policy 46, 868–879; 2017). Fewer than half as many people in comparable highly educated groups were at risk. Burn-out among researchers can lead to more serious issues, such as depression, which should be diagnosed and treated by a professional. But by recognizing work patterns and warning signs of chronic stress in the lab or field, researchers can adjust their routines to avoid reaching the burn-out stage in the first place (see 'Signs of burn-out ahead'). Institutions also need to identify when early-career researchers are hitting a wall, says Kay Guccione, manager of researcher mentoring and coaching at the University of Sheffield, UK. “Your well-being is not only your problem — there is an organizational responsibility as well,” she said in a video chat in March sponsored by Vitae, a researcher-advocacy group in Cambridge, UK. She urges junior researchers to learn about their workplace policies and rights, as well as the institutional resources available should they or their peers need mental-health support. Guccione, who trained as a molecular biologist before switching to researcher development, started the Twitter hashtag #takebreaksmakebreakthroughs as a way to remind herself when it's quitting time, and to set expectations at her institution that graduate students shouldn't work themselves into the ground. An initiative by the Academy of Medical Sciences in London uses #MedSciLife to feature examples of how researchers switch off from work, for example, by taking hikes or acting classes. The type of break doesn't matter. “Knit, play computer games, build chainmail — anything that is completely different from thinking about research questions,” says Guccione. Researchers, she adds, should also pursue an extracurricular activity that gives them a sense of success and worth that is not tied to work. PhD student Juan Pablo Ruiz, who studies blood stem cells in a joint programme between the University of Oxford, UK, and the US National Institutes of Health, founded Labmosphere.com, a website with articles on mental-health struggles experienced by junior researchers. People who are happy and satisfied perform more creatively and productively at work, he notes — an idea that is well supported by research. A 2015 study by a team at the University of Warwick found that workers were 10% more productive after watching a comedy video than a control group that did not watch it — and conversely, people who had experienced a major life shock from a family death or illness in the previous two years, and so reported lower happiness, were 10% less productive ( et al. J. Labor Econ. 33, 789–822; 2015). By boosting overall happiness, taking time off from the job could thus improve one's work, too. Bench scientists should incorporate daily breaks into their routines, says Ben Mead, a PhD candidate in the Harvard-MIT Health Sciences and Technology programme in Cambridge, Massachusetts. He tries to maintain the mindset that graduate training is similar to a marathon, not a short race. As such, he doesn't take lengthy holidays, but takes daily breaks and brief holidays throughout the year. Short breaks should be true time outs from the activity that is dominating a researcher's day and from thinking about any science, says Guccione. A coffee break with labmates while discussing the latest piece of lab equipment, or eating lunch while answering work e-mails or reading a research paper doesn't count. Ruiz's hospital workplace has a waiting room with an aquarium, and he often eats lunch there to gaze at the fish and give his eyes a break from staring at cells under the microscope or at spreadsheet data. It also helps to look at landscapes, a cityscape or an urban river walk. When struggling with a lack of motivation, Mead uses the 'pomodoro' technique to advance his work. The method, named after a tomato-shaped timer that its developer used, sections off tasks into 4 sets of 25-minute intervals, split up by breaks of 3–5 minutes and then punctuated by a longer one of 15–30 minutes. Mead sets his lab timer for 20 minutes of work, then gives himself a 2–3-minute break for social media or another distraction. Lab supervisors recommend structuring the day so that hard, critical-thinking or technically challenging tasks happen during the hours of peak productivity, and easier, more-mindless work is done when focus wanes. Many researchers recognize their daily patterns and dash to the gym when they are drooping, often in the late afternoon. As a university student, Yuxuan Wang found that the best way for her to stick to a weekly exercise routine was by becoming an instructor for kickboxing and step-aerobics classes. She found similar work when she moved to Johns Hopkins University in Baltimore, Maryland, for MD-PhD studies in oncology. “The second I walk in the exercise room, I forget all my experiments that did not work or the paper that got rejected,” says Wang. Weekly breaks can also involve a switch up in research routines rather than time out entirely, and are important for giving scientists the stamina to face intense bouts of research or writing. When Auckland faces a particularly tricky line of experiments in his research on how chromosomes move around the cell, he does experiments in parallel that are easier and likely to yield positive results. “Then I'm not completely demoralized by having months go by without any data,” he says. Even small successes, such as stitching together a needed piece of a DNA probe, can lift his spirits and help him to feel productive. Postdoc Jenna Kropp often has 12-hour days doing multiple, back-to-back in vitro fertilization surgeries at the Wisconsin National Primate Research Center in Madison — work that allows no do-overs. When Kropp knows that such a day is coming, she'll often take the day off beforehand to ride her horse. Time spent outside is the best antidote to stress, she says; she often comes into work by 7 a.m. and leaves lab in the late afternoon to help with daily barn chores. “You have to listen to your body, rather than think, 'I have to be here from this hour to this hour',” she says. The farm chores are mundane, but she still feels that she has accomplished something, she says. Such solitary hobbies are great for letting off steam, but researchers should also make time for socializing outside the lab to get a regular reprieve from research questions. As the sole graduate student starting in her reproductive-physiology programme at the University of Wisconsin–Madison in 2015, Sydney Nguyen knew that she would need to find a group off-campus for socializing. She participated in a roller-derby camp during the summer after her first year, and loved it. She finds support and encouragement from her teammates, both on and off the track, and the sport's aggressive tactics gives her an outlet for frustrations. Practising and perfecting a difficult move lets Nguyen feel successful even if the week's lab work hasn't gone well. Supervisors can support healthy work–life balance by fostering conversations about well-being and by being a good role model. Tammy Steeves, a conservation geneticist at the University of Canterbury in Christchurch, New Zealand, sets clear expectations in her group for taking time off. She encourages supportive lab interactions over competition, and says that this style helps young scientists to admit when they are struggling with balance. Her group has a simple motto: “Everyone here is smart and kind — don't distinguish yourself by being otherwise.” Steeves, who is also a postgraduate coordinator for the School of Biological Sciences at Canterbury, emphasizes to students the importance of managing their well-being and incorporating self-care. She's found that an easy way for international students (and herself) to visit family abroad each year is to tack extra time on to conference travels. She and one of her students reached an agreement this year that he could telecommute temporarily from the United States, where he has family and friends, while analysing and writing up his data. Her mentoring style, she says, helps students to feel comfortable about proposing such arrangements. Many young scientists say that they value efficiency in their work more than total time put in — a key part of self-awareness that prevents burn-out. Wang says that colleagues may find her staring out her fifth-floor window with a cup of tea when she needs to decompress and recall the bigger picture. “I'm working with patient samples, and those are patients with cancer,” she says. Aside from their own mental health and well-being, researchers who take care to avoid burn-out and reset their minds and bodies regularly might see better returns in their data, too. “The science we generate is richer,” says Steeves. “Lots of people come to the science table from different places, and we all need to take care of their well-being to keep them there.”
News Article | May 25, 2017
MADISON, Wis. -- Zika virus infection passes efficiently from a pregnant monkey to its fetus, spreading inflammatory damage throughout the tissues that support the fetus and the fetus's developing nervous system, and suggesting a wider threat in human pregnancies than generally appreciated. Researchers at the University of Wisconsin-Madison infected four pregnant rhesus macaque monkeys at the Wisconsin National Primate Research Center with a Zika virus dose similar to what would be transferred by a mosquito bite, and found evidence that the virus was present in each monkey's fetus. "That is a very high level -- 100 percent exposure -- of the virus to the fetus along with inflammation and tissue injury in an animal model that mirrors the infection in human pregnancies quite closely," says Ted Golos, a UW-Madison reproductive physiologist and professor of comparative biosciences and obstetrics and gynecology. "It's sobering. If microcephaly is the tip of the iceberg for babies infected in pregnancy, the rest of the iceberg may be bigger than we've imagined." The UW-Madison researchers, along with collaborators at Duke University and the University of California, Davis, published their study of the Zika-infected pregnancies today in the journal PLOS Pathogens. Their work, which was funded by the National Institutes of Health, followed the pregnancies from infection in the first or third trimester, regularly assessing maternal infection and fetal development and examining the extent of infection in the fetus when the pregnancies reached term. Three of the fetuses involved had small heads, but not quite so small relative to normal that they would meet the human standard for diagnosing microcephaly -- the most striking and widely discussed result of Zika infection since Brazilian doctors raised alarm in 2014 of many babies with arrested brain development. The new study did not find abnormal brain development, but the researchers did discover unusual inflammation in the fetal eyes, in the retinas and optic nerves, in pregnancies infected during the first trimester. "Our eyes are basically part of our central nervous system. The optic nerve grows right out from the fetal brain during pregnancy," says Kathleen Antony, a UW-Madison professor of maternal fetal medicine and an author of the study. "So it makes some sense to see this damage in the monkeys and in human pregnancy -- problems such as chorioretinal atrophy or microphthalmia in which the whole eye or parts of the eye just don't grow to the expected size." The similarities between the monkey pregnancies and reported complications in Zika-affected human pregnancies further establish Zika infection in monkeys as a way to study the progression of the infection and associated health problems in people. "There are so many things about Zika infection we can't study as well in pregnant humans -- or fast enough to make a difference for a lot of people who may be infected," says Dawn Dudley, a UW-Madison pathology research scientist and one of the lead authors of the new research with Antony and obstetrics and gynecology graduate student Sydney Nguyen. An animal model opens the door to studying how Zika infection interacts with other infections (like dengue virus), how the effects of early pregnancy infection might be different from later infection, and, according to Dudley, whether quick treatment with some antiviral therapies could manage the damage of what has come to be known as congenital Zika syndrome. "The precise pathway that the virus takes from mom's bloodstream to the fetal bloodstream, across that interface, cannot be studied except in an animal model," says Golos, whose research group found damage from Zika infection in every part of the interface between mother and fetus -- the placenta, amniotic fluid in the womb and the lining of uterus. While the immediate effects may not be as dramatic as microcephaly, "the results we're seeing in monkey pregnancies make us think that, as they grow, more human babies might develop Zika-related disease pathology than is currently appreciated," Golos says. This work was supported by NIH grants R01 AI107157-01A1, R01AI116382-01A1S1, DP2HD075699 and P51 OD011106. This research was conducted in part at a facility constructed with support from Research Facilities Improvement Program grant numbers RR15459-01 and RR020141-01.
News Article | May 29, 2017
Zika virus infection passes efficiently from a pregnant monkey to its fetus, spreading inflammatory damage throughout the tissues that support the fetus and the fetus's developing nervous system, and suggesting a wider threat in human pregnancies than generally appreciated. Researchers at the University of Wisconsin-Madison infected four pregnant rhesus macaque monkeys at the Wisconsin National Primate Research Center with a Zika virus dose similar to what would be transferred by a mosquito bite, and found evidence that the virus was present in each monkey's fetus. "That is a very high level -- 100 percent exposure -- of the virus to the fetus along with inflammation and tissue injury in an animal model that mirrors the infection in human pregnancies quite closely," says Ted Golos, a UW-Madison reproductive physiologist and professor of comparative biosciences and obstetrics and gynecology. "It's sobering. If microcephaly is the tip of the iceberg for babies infected in pregnancy, the rest of the iceberg may be bigger than we've imagined." The UW-Madison researchers, along with collaborators at Duke University and the University of California, Davis, published their study of the Zika-infected pregnancies in the journal PLOS Pathogens. Their work, which was funded by the National Institutes of Health, followed the pregnancies from infection in the first or third trimester, regularly assessing maternal infection and fetal development and examining the extent of infection in the fetus when the pregnancies reached term. Three of the fetuses involved had small heads, but not quite so small relative to normal that they would meet the human standard for diagnosing microcephaly -- the most striking and widely discussed result of Zika infection since Brazilian doctors raised alarm in 2014 of many babies with arrested brain development. The new study did not find abnormal brain development, but the researchers did discover unusual inflammation in the fetal eyes, in the retinas and optic nerves, in pregnancies infected during the first trimester. "Our eyes are basically part of our central nervous system. The optic nerve grows right out from the fetal brain during pregnancy," says Kathleen Antony, a UW-Madison professor of maternal fetal medicine and an author of the study. "So it makes some sense to see this damage in the monkeys and in human pregnancy -- problems such as chorioretinal atrophy or microphthalmia in which the whole eye or parts of the eye just don't grow to the expected size." The similarities between the monkey pregnancies and reported complications in Zika-affected human pregnancies further establish Zika infection in monkeys as a way to study the progression of the infection and associated health problems in people. "There are so many things about Zika infection we can't study as well in pregnant humans -- or fast enough to make a difference for a lot of people who may be infected," says Dawn Dudley, a UW-Madison pathology research scientist and one of the lead authors of the new research with Antony and obstetrics and gynecology graduate student Sydney Nguyen. An animal model opens the door to studying how Zika infection interacts with other infections (like dengue virus), how the effects of early pregnancy infection might be different from later infection, and, according to Dudley, whether quick treatment with some antiviral therapies could manage the damage of what has come to be known as congenital Zika syndrome. "The precise pathway that the virus takes from mom's bloodstream to the fetal bloodstream, across that interface, cannot be studied except in an animal model," says Golos, whose research group found damage from Zika infection in every part of the interface between mother and fetus -- the placenta, amniotic fluid in the womb and the lining of uterus. While the immediate effects may not be as dramatic as microcephaly, "the results we're seeing in monkey pregnancies make us think that, as they grow, more human babies might develop Zika-related disease pathology than is currently appreciated," Golos says.
Jegaskanda S.,University of Melbourne |
Weinfurter J.T.,Wisconsin National Primate Research Center |
Weinfurter J.T.,University of Wisconsin - Madison |
Friedrich T.C.,Wisconsin National Primate Research Center |
And 2 more authors.
Journal of Virology | Year: 2013
Emerging influenza viruses pose a serious risk to global human health. Recent studies in ferrets, macaques, and humans suggest that seasonal H1N1 (sH1N1) infection provides some cross-protection against 2009 pandemic influenza viruses (H1N1pdm), but the correlates of cross-protection are poorly understood. Here we show that seasonal infection of influenza-naïve Indian rhesus macaques (Macaca mulatta) with A/Kawasaki/173/2001 (sH1N1) virus induces antibodies capable of binding the hemagglutinin (HA) of both the homologous seasonal virus and the antigenically divergent A/California/04/2009 (H1N1pdm) strain in the absence of detectable H1N1pdm-specific neutralizing antibodies. These influenza virus-specific antibodies activated macaque NK cells to express both CD107a and gamma interferon (IFN-γ) in the presence of HA proteins from either sH1N1 or H1N1pdm viruses. Although influenza virus-specific antibody-dependent cellular cytotoxicity (ADCC)-mediated NK cell activation diminished in titer over time following sH1N1 infection, these cells expanded rapidly within 7 days following H1N1pdm exposure. Furthermore, we found that influenza virus-specific ADCC was present in bronchoalveolar lavage fluid and was able to activate lung NK cells. We concluded that infection with a seasonal influenza virus can induce antibodies that mediate ADCC capable of recognizing divergent influenza virus strains. Cross-reactive ADCC may provide a mechanism for reducing the severity of divergent influenza virus infections © 2013, American Society for Microbiology.
News Article | February 21, 2017
MADISON, Wis. -- Listeria, a common food-borne bacterium, may pose a greater risk of miscarriage in the early stages of pregnancy than appreciated, according to researchers at the University of Wisconsin-Madison School of Veterinary Medicine studying how pathogens affect fetal development and change the outcome of pregnancy. "For many years, listeria has been associated with adverse outcomes in pregnancy, but particularly at the end of pregnancy," says Ted Golos, a UW-Madison reproductive physiologist and professor of comparative biosciences and obstetrics and gynecology. "What wasn't known with much clarity before this study is that it appears it's a severe risk factor in early pregnancy." Golos and his collaborators published their results Feb. 21, 2017 in the journal mBio. According to the Centers for Disease Control, listeria makes about 1,600 Americans sick each year -- a relatively small number, but a group heavy on newborn babies and older adults with undeveloped or weak immune systems. "The problem with this organism is not a huge number of cases. It's that when it is identified, it's associated with severe outcomes," says Charles Czuprynski, a UW-Madison professor of pathobiological sciences and director of the UW-Madison Food Research Institute. Pregnant women are warned to avoid many of the foods -- among them unpasteurized milk and soft cheese, raw sprouts, melon and deli meats not carefully handled -- that can harbor listeria, because the bacterium is known to cause miscarriage and stillbirth, and spur premature labor. Those severe outcomes have resulted in a zero-tolerance regulatory policy for listeria in ready-to-eat foods. But when it occurs, listeria infection in pregnancy may go unnoticed. The few recognizable symptoms are nearly indistinguishable from the discomfort most newly pregnant women feel. "It's striking that mom doesn't get particularly ill from listeria infection, but it has a profound impact on the fetus," says Golos, whose work is funded by the National Institutes of Health. "That's familiar now, because we've been talking about the same difference in Zika virus." Sophia Kathariou, a North Carolina State University professor of food science and microbiology, provided a strain of listeria that caused miscarriage, stillbirth and premature delivery in at least 11 pregnant women in 2000. Four pregnant rhesus macaques at the Wisconsin National Primate Research Center were fed doses of the listeria comparable to what one might encounter in contaminated food. Bryce Wolfe, a UW-Madison graduate student studying cellular and molecular pathology who is lead author of the study, monitored the speed and progression of listeria's spread. "What's particularly striking about the work Bryce did is the detailed information we now have about the organism," Czuprynski says. "The animal ingested it; she tracked it being shed in feces and showing up in the bloodstream. They did ultrasound analysis of the fetus, and could then show events in terms of where the organism was preceding fetal demise." None of the monkeys showed obvious signs of infection before their pregnancies came to abrupt ends. But in tissue samples taken after each monkey experienced intrauterine fetal death, Wolfe found listeria had invaded the placenta -- the connection between the mother-to-be and the fetus, which usually prevents transmission of bacteria -- as well as the endometrium, the lining of the uterus. "In that region, there's a rich population of specialized immune cells, and it is exquisitely regulated," says Wolfe. "When you introduce a pathogen into the midst of this, it's not very surprising that it's going to cause some sort of adverse outcome disrupting this balance." The researchers believe the inflammation caused by the maternal immune response to the fast-moving listeria also affects the placenta, keeping it from protecting the fetus. "It should be a barrier," Golos says. "But we're hypothesizing that the maternal immune system's attempt to clear the bacteria actually results in collateral damage to the placenta that then allows the bacteria to invade the fetus." The results suggest listeria (and perhaps other pathogens) may be the culprit in some miscarriages that usually go without diagnosed cause, but the bacteria's stealth and speed may still make it hard to control. "There are effective antibiotics available. It is treatable," Wolfe says. "The issue is that because it's asymptomatic, the fetus may be infected by the time anyone realizes the mother was infected." Golos and Wolfe plan to continue work with listeria to better define how the bacterium targets the reproductive tract, its incubation time and the problems it causes leading up to miscarriage. Their goal is to provide basic knowledge about the progression of infection and the maternal immune response to intracellular pathogens in pregnancy, which may help other researchers battling similar dangers such as Zika virus.
News Article | February 21, 2017
Washington, DC - February 21, 2017 -Researchers in Wisconsin have discovered how Listeria monocytogenes, a common foodborne pathogen, travels through the mother's body to fatally attack the placenta and fetus during early pregnancy in a macaque monkey. The study, published this week in mBio®, an open-access journal of the American Society for Microbiology, clarifies why Listeria infection is devastating for many infected pregnant women and their fetuses. The work raises questions about our current understanding of the risk for listeriosis in early pregnancy, and reveals clues that may lead to better screening and interventions during pregnancy. "There was a profound reproductive tract colonization and rapid fetal demise with a first trimester exposure to Listeria," says Ted Golos, professor of reproductive sciences at the School of Veterinary Medicine at the University of Wisconsin--Madison and senior author on the study. "At any time during pregnancy, we wish that we could carefully monitor what's happening in the mom and the fetus following exposure to an infectious agent." (image: scanning electron micrograph of Listeria monocytogenes, Wikimedia Commons) Of course, that is nearly impossible to do in human patients, so Golos and his colleagues at the Wisconsin National Primate Research Center have developed a nonhuman primate model of pregnancy using the cynomolgus macaque--a monkey whose pregnancy, placental and fetal development closely matches that of humans. Listeriosis has been thought to pose the greatest danger to a woman in her third trimester, when it can lead to preterm labor, fetal infection or fetal death. It is the reason pregnant women are cautioned against eating deli meats and milk or soft cheeses that are unpasteurized. "What makes Listeria particularly dangerous is that it can multiply at refrigeration temperatures," says Chuck Czuprynski, director of the Food Research Institute at UW-Madison and project collaborator. Most healthy people can easily clear the bacteria from their systems. Until now, not much was known about Listeria's impact on early pregnancy. The new research raises the possibility that some first trimester miscarriages might be due to an undetected Listeria infection, which often causes no or mild symptoms, like low fever or nausea, in pregnant women. "Obstetricians will tell you that a number of early pregnancy miscarriages are thought to be due to chromosomal problems," says Golos. "But how many may be due to other causes like infections?" His team exposed four pregnant macaques to a moderate dose of Listeria bacteria by tube-feeding them a dollop of tainted whipped cream on days 36-46 of gestation--corresponding to about week 6 or 7 of a human pregnancy. They expected to see some adverse pregnancy outcomes, but they were surprised by how rapidly infection spread to the fetus: by days 7-13 after exposure, all four fetuses had died in the womb. Graduate student Bryce Wolfe tracked the infections in the mothers through blood and fecal sampling and in the fetuses via ultrasound. All of the mothers showed signs of bacterial infection in their bloodstream, but displayed few to no symptoms. When Wolfe examined maternal and fetal tissues for signs of infection, she found that the mothers' immune systems apparently cleared the infections, with very few bacteria showing up in their spleens, livers, and gastrointestinal (GI) lymph nodes. In contrast, Wolfe found high loads of bacteria present in the fetal tissues, amniotic fluid, umbilical cord, placenta, and the decidua, the specialized lining of the pregnant uterus. "We didn't expect to see the bacteria colonize the fetus so quickly, so consistently," says Wolfe, a PhD candidate at UW-Madison and the lead author on the study. "The decidua and the placenta, which make up the maternal-fetal interface, were loaded with bacteria." It appears that the monkey's immune system can protect mom, but not the fetus and that the bacteria target the vulnerable reproductive tissues. In the macaques, Wolfe saw cellular damage to the placenta and the fetal membranes that is often seen in Listeria infections during human pregnancy. Golos hypothesizes that damage to the decidua and placenta could be disrupting the placental barrier meant to keep pathogens out of the womb. Czuprynski says the study raises significant questions about whether Listeria and perhaps other pathogens cause mild infections in mothers that negatively impact pregnancy. The study is the first to track the progress of a pathogen from the GI tract through a pregnant primate's body to the fetus, he notes. "We have reason to believe it mirrors what happens in women." Next, the team will investigate what is happening with the immune cells that survey and protect the maternal-fetal interface. Improving our understanding of what those cells are doing during an infection might lead to better ways to detect and treat the infection to protect the fetus. Again, this takes advantage of the animal model, says Golos. "You can follow the time course of the infection, understand the initiating events, and hopefully devise ways to prevent the damage that leads to a bad pregnancy outcome." The American Society for Microbiology is the largest single life science society, composed of over 48,000 scientists and health professionals. ASM's mission is to promote and advance the microbial sciences. ASM advances the microbial sciences through conferences, publications, certifications and educational opportunities. It enhances laboratory capacity around the globe through training and resources. It provides a network for scientists in academia, industry and clinical settings. Additionally, ASM promotes a deeper understanding of the microbial sciences to diverse audiences.
Seltzer L.J.,University of Wisconsin - Madison |
Ziegler T.E.,Wisconsin National Primate Research Center |
Pollak S.D.,University of Wisconsin - Madison
Proceedings of the Royal Society B: Biological Sciences | Year: 2010
Vocalizations are important components of social behaviour in many vertebrate species, including our own. Less well-understood are the hormonal mechanisms involved in response to vocal cues, and how these systems may influence the course of behavioural evolution. The neurohormone oxytocin (OT) partly governs a number of biological and social processes critical to fitness, such as attachment between mothers and their young, and suppression of the stress response after contact with trusted conspecfics. Rodent studies suggest that OT's release is contingent upon direct tactile contact with such individuals, but we hypothesized that vocalizations might be capable of producing the same effect. To test our hypothesis, we chose human mother-daughter dyads and applied a social stressor to the children, following which we randomly assigned participants into complete contact, speech-only or no-contact conditions. Children receiving a full complement of comfort including physical, vocal and non-verbal contact showed the highest levels of OTand the swiftest return to baseline of a biological marker of stress (salivary cortisol), but a strikingly similar hormonal profile emerged in children comforted solely by their mother's voice. Our results suggest that vocalizations may be as important as touch to the neuroendocrine regulation of social bonding in our species. © 2010 The Royal Society.
Seltzer L.J.,University of Wisconsin - Madison |
Prososki A.R.,University of Wisconsin - Madison |
Ziegler T.E.,Wisconsin National Primate Research Center |
Pollak S.D.,University of Wisconsin - Madison
Evolution and Human Behavior | Year: 2012
Human speech evidently conveys an adaptive advantage, given its apparently rapid dissemination through the ancient world and global use today. As such, speech must be capable of altering human biology in a positive way, possibly through those neuroendocrine mechanisms responsible for strengthening the social bonds between individuals. Indeed, speech between trusted individuals is capable of reducing levels of salivary cortisol, often considered a biomarker of stress, and increasing levels of urinary oxytocin, a hormone involved in the formation and maintenance of positive relationships. It is not clear, however, whether it is the uniquely human grammar, syntax, content and/or choice of words that causes these physiological changes, or whether the prosodic elements of speech, which are present in the vocal cues of many other species, are responsible. In order to tease apart these elements of human communication, we examined the hormonal responses of female children who instant messaged their mothers after undergoing a stressor. We discovered that unlike children interacting with their mothers in person or over the phone, girls who instant messaged did not release oxytocin; instead, these participants showed levels of salivary cortisol as high as control subjects who did not interact with their parents at all. We conclude that the comforting sound of a familiar voice is responsible for the hormonal differences observed and, hence, that similar differences may be seen in other species using vocal cues to communicate. © 2012.
Seltzer L.J.,University of Wisconsin - Madison |
Ziegler T.,Wisconsin National Primate Research Center |
Connolly M.J.,University of Wisconsin - Madison |
Prososki A.R.,University of Wisconsin - Madison |
Pollak S.D.,University of Wisconsin - Madison
Child Development | Year: 2014
Child maltreatment often has a negative impact on the development of social behavior and health. The biobehavioral mechanisms through which these adverse outcomes emerge, however, are not clear. To better understand the ways in which early life adversity affects subsequent social behavior, changes in the neuropeptide oxytocin (OT) in children (n = 73) aged 8.1-11.5 years following a laboratory stressor were examined. Girls with histories of physical abuse have higher levels of urinary OT and lower levels of salivary cortisol following the stressor when compared to controls. Abused and control boys, however, do not differ in their hormonal responses. These data suggest that early adversity may disrupt the development of the stress regulation system in girls by middle childhood. Child Development © 2014 The Society for Research in Child Development, Inc.
Radovick S.,Johns Hopkins University |
Levine J.E.,Wisconsin National Primate Research Center |
Wolfe A.,Johns Hopkins University
Frontiers in Endocrinology | Year: 2012
Reproductive function is regulated by the secretion of luteinizing hormone (LH) and follicle-stimulating hormone from the pituitary and the steroid hormones from the gonads. The dynamic changes in the levels of the reproductive hormones regulate secondary sex char-acteristics, gametogenesis, cellular function, and behavior. Hypothalamic GnRH neurons, with cell bodies located in the basal hypothalamus, represent the final common path-way for neuronally derived signals to the pituitary. As such, they serve as integrators of a dizzying array of signals including sensory inputs mediating information about cir-cadian, seasonal, behavioral, pheromonal, and emotional cues. Additionally, information about peripheral physiological function may also be included in the integrative signal to the GnRH neuron. These signals may communicate information about metabolic status, disease, or infection. Gonadal steroid hormones arguably exert the most important effects on GnRH neuronal function. In both males and females, the gonadal steroid hormones exert negative feedback regulation on axis activity at both the level of the pituitary and the hypothalamus. These negative feedback loops regulate homeostasis of steroid hormone levels. In females, a cyclic reversal of estrogen feedback produces a positive feedback loop at both the hypothalamic and pituitary levels. Central positive feedback results in a dra-matic increase in GnRH secretion (Moenter et al., 1992; Xia et al., 1992; Clarke, 1993; Sisk et al., 2001).This is coupled with an increase in pituitary sensitivity to GnRH (Savoy-Moore et al., 1980;Turzillo et al., 1995), which produces the massive surge in secretion of LH that triggers ovulation. While feedback regulation of the axis in males is in part mediated by estrogen receptors (ER), there is not a clear consensus as to the relative role of ER versus AR signaling in males (Lindzey et al., 1998; Wersinger et al., 1999). Therefore, this review will focus on estrogenic signaling in the female. © 2012 Radovick, Levine and Wolfe.