Ei Terasawa is dynamic scientist, mentor

When Ei Terasawa first met former WRPRC Director Robert Goy at a scientific conference in Tokyo in early Fall  1972, she had no idea how persistent he could be.

Dr. Goy called her in Japan soon after the conference and invited her to visit the Wisconsin Regional Primate Research Center. An assistant professor at Yokohama City University School of Medicine (YCUSM) at the time, Terasawa remembers the call because it took Goy a while to find her. First, he called the medical school, but it was a Japanese holiday, and a building security guard answered to his call. Despite their language barrier, he finally secured her home telephone number and reached her.

Terasawa wasn’t interested. “I didn’t do anything at first,” she says. ‘I was satisfied where I was.”

Not one to forget a promising scientist, Goy tried again a year later. This time, things had changed and Terasawa decided to take him up on his offer. Her subsequent visit in late 1973 led to an appointment as associate scientist in charge of the WRPRC’s new Neurobiology Unit.

Born and raised in Ihda, Akaho, and Matsumoto, small towns in the Japan Alps, the young Terasawa much admired Marie Curie and wanted to be a physicist. But her father steered her elsewhere, warning his daughter that she would have to be physically very strong, referring to the endless hours Madame Curie spent chemically separating tons of uranium ore.

“My father encouraged me to study biology instead,” Terasawa said. By her senior year in college (University of Tokyo) she was invited to join a brand new laboratory established by a young professor, Masazmi Kawakami, just returned from the U.S. She went on to receive her Ph.D. in medical physiology and completed her post-doctoral training at the University of California-Berkeley and UCLA, under the guidance of Paola S. Timiras and Charles H. Sawyer, respectively. Terasawa then moved back to Japan to teach neurobiology at YCUSM.

Following her return to Japan, however, Terasawa became more aware of certain differences between the way she had done things in California and the way things were done in Japan. By the time Bob Goy called her a second time, she was ripe for a return visit to the States.

Up until this point, Terasawa had been using rats and rabbits to study the control mechanism of gonadotropin secretion, especially the role of the hypothalamus and limbic structures of the brain in reproductive function. At the WRPRC, she began using guinea pigs. She found that neuroendocrine characteristics in female guinea pigs are dissimilar to those in laboratory rodents, but rather similar to those in primates. Subsequently, she and Stan Wiegand, a graduate student in the Neuroscience Training Program,  discovered that neurons in the medial preoptic nucleus (now called the anterior ventral periventricular nucleus, or AVPV), in female rats plays a critical role in cyclic ovulation and positive feedback mechanisms of steroid hormones. These findings have become classics in the literature.

One day, however, Dr. Goy said to her, “This is a primate center, Ei. When are you going to start working with monkeys?” 

Terasawa clearly remembers her first monkey studies. Ironically, one of the earliest things she discovered in monkeys that excited her was never published. She found that reserpine, a drug used to deplete neurotransmitters such as serotonin, dopamine, norepinephrine and epinephrine—important signals for stimulating the preovulatory LH release (and presumably LHRH release) in the rodent brain—does not block the LH surge in rhesus monkeys, indicating that signals for the preovulatory LHRH surge in primates and rodents differ. 

“This observation was eye-opening for me in realizing the importance of studies using the rhesus monkey as a model for the human,” says Terasawa. From there, her lab’s work took off. Terasawa’s first NIH R01 grant, “Hypothalamic Control of Puberty” was awarded in 1977. Her second, “Hypothalamic Control of Gonadotropin Secretion,” would follow shortly thereafter, in 1980. (See Chronology, next page.)

Now a WRPRC senior scientist and UW professor of pediatrics, Dr. Terasawa is never short of ideas. As her research progressed from LHRH studies on the young brain, and then to puberty, her  thoughts eventually turned to the aging brain. “I sort of skipped reproduction and went straight to aging,” she said.  Her newest R01, “Aging of Neuroendocrine Hypothalamus,” was granted in 1999.

After 26 years of research at the Primate Center, Terasawa has extensive collaborations, working with scientists such as Ned Kalin on studies of the amygdala, Anrea Gore on the hypothalamic control mechanism of menopause, and James Thomson on embryonic stem cell transplantation in a rhesus monkey model of  Parkinson’s disease.

Terasawa has never had any regrets about moving to the United States. Although she does not teach as much as she did in Japan, she says, “I love to look after undergraduate and graduate students as well as postdoctoral research fellows. I always tell them their hard work will always pay off. I remind them that they are not working for me, they are working for themselves and for science.” She also acknowledges that for many years she has had excellent trainees and research specialists, such as Kim Keen and Laurelee Luchansky.
 

References:
Terasawa E, Fernandez DL. Neurobiological mechanisms of the onset of puberty in primates.  Endocrine Review. 22:111-151. 2001. 

Richter TA, Terasawa E. Inhibitory neural mechanisms underlying changes in LHRH release at the onset of puberty in the rhesus monkey. Trends Endocrinol. Metab. 12:353-359. 2001.

Terasawa E. Luteinizing-hormone releasing hormone (LHRH) neurons: Mechanism of pulsatile LHRH release. Vitam. Horm. 63:91-129. 2001.

Terasawa E., Schanhofer WK, Keen KL, Luchansky LL. Intracellular Ca2+ oscillations in luteinizing hormone-releasing hormone (LHRH) cells derived from the embryonic olfactory placode of the rhesus monkey. J. Neurosci. 19: 5898-5909. 1999.

Quanbeck C, Sherwood NJ, Millar RP, Terasawa E. Two populations of luteinizing hormone-releasing hormone neurons in the forebrain of the rhesus macaque during embryonic development. J. Comp. Neurol. 380:293-309. 1997.

Mitsushima D, Hei DL, Terasawa E. g-aminobutyric acid is an inhibitory neurotransmitter restricting the release of luteinizing hormone-releasing hormone before the onset of puberty.  Proc. Natl. Acad. Sci. USA 91: 395-399. 1994.

Watanabe G, Terasawa E. In vivo release of luteinizing hormone releasing hormone increases with puberty in the female rhesus monkey.  Endocrinology. 125: 92-99. 1989.

979-1989: Differential action of progesterone and estrogen on release of LH and LHRH in the rhesus monkey
 

CHRONOLOGY--TERASAWA LAB

In the mid- to late 1970s, the dominant theory in primate neuroendocrine research was that estrogen is the only necessary ovarian steroid for the preovulatory LH surge. The surge was caused by estrogen action on the pituitary rather than on the hypothalamus. Based on her observations in guinea pigs, Dr. Terasawa was not convinced by this theory.

Terasawa examined the role of progesterone in the preovulatory LH surge in rhesus monkeys. She found that progesterone induces an LH surge with a consistent, short peak latency (5-7 hours), and short duration (12-18 hours) in both ovariectomized monkeys with estrogen priming and ovarian intact monkeys during the follicular phase. A series of studies further indicated that progesterone stimulates LH release through hypothalamic neurons, such as neuropeptide Y (NPY) neurons rather than through pituitary gonadotrophs. The progesterone-induced LH surge is blocked by pentobarbital anesthesia; it is also blocked by pituitary stalk section with a Teflon barrier. Progesterone increases single unit activity of the medial basal hypothalamus. Progesterone also increases pulsatile LHRH output in the stalk-median eminence. In contrast, estrogen stimulates both hypothalamic neurons and pituitary gonadotrophs.

These studies led to the hypothesis that the preovulatory increase in progesterone initiates and/or augments the LHRH surge.  “Subsequently, our protocol on the positive feedback effect of progesterone has been commonly used by other investigators and the hypothesis has been supported,”  Terasawa affirms.

1977-Present: The Mechanism Controlling the Onset of Puberty in the Rhesus Monkey—A Major Accomplishment.

For 10 years, Terasawa collected then-scarce physiological and hormonal data on the pubertal process in the female rhesus monkey. Based on these data, she defined the pubertal stage in the rhesus monkey. This became the standard definition for the species. Her findings included:

--Pulsatile LH release increases at the onset of puberty and this increase continues until the time of first ovulation.
--At the onset of puberty, the circadian rhythm of LH release (evening levels are higher than morning levels) becomes prominent.
--The pubertal increase in LH release is not dependent upon the presence of the ovary.
--Lesions of the posterior hypothalamus induce precocious puberty.

Altogether, Terasawa proposed the hypothesis that an increase in LH release, and presumably LHRH release, is the key factor for the onset of puberty and that the removal from neural inhibition triggers the onset of puberty.  Since, in this field, the “gonadostat hypothesis” for the mechanism of the onset of puberty had been dominant for the last 50 years, her hypothesis was not accepted immediately. Nevertheless, at that time she realized the necessity of measuring LHRH directly. So over the next few years Terasawa spent time in developing a push-pull perfusion method. 

Using this method, developmental changes in LHRH release in the stalk-median eminence (S-ME) were directly measured in prepubertal and pubertal monkeys. As she predicted, LHRH release was low in prepubertal monkeys and an increase in pulsatile LHRH release occurred at the onset of puberty. However, this increase was not due to a decrease in the negative feedback sensitivity to ovarian steroids at the onset of puberty. Further studies with electrical stimulation and NMDA challenge indicated that LHRH neurosecretory neurons are functionally mature before puberty, but that the neuronal systems regulating pulsatile LHRH release may still be immature.

A series of studies indicated that g-aminobutyric acid (GABA) is an inhibitory neurotransmitter responsible for suppressing pulsatile LHRH release before puberty. Again, her lab’s scientific findings:

--GABA release in the S-ME was much higher in prepubertal monkeys than in midpubertal monkeys.
--Bicuculline, a GABAA receptor antagonist, greatly facilitated LHRH release in prepubertal monkeys, while bicuculline at a higher dose only slightly stimulated LHRH release in midpubertal monkeys.
--While GABA infusion did not cause any changes in prepubertal monkeys, GABA suppressed LHRH release in midpubertal monkeys.
--Infusion of an antisense oligo-deoxynucleotide for glutamic acid decarboxylase (GAD) mRNA into the S-ME drastically increased LHRH release in prepubertal monkeys.

--Intermittent infusion of bicuculline into the base of the third ventricle of the sexually immature monkeys resulted in precocious puberty.

These findings showed that the removal of GABA inhibition on LHRH neurons, before facilitatory neural input is established, appears to be the critical factor for the onset of puberty in the non-human primate. Dr. Terasawa’s finding was truly a breakthrough in the field of neurobiology. 

1988-Present: Cellular Mechanisms Controlling the Oscillatory Release of LHRH

The pulsatility of LHRH release is essential for the control of gonadotropin secretion and hence reproductive function. However, the cellular mechanism governing LHRH pulse generation is still unclear, Terasawa explains. 

This is due to the fact that, in primates, approximately 2,000 LHRH neurons are widely scattered in the hypothalamus. Thus, the function of these neurons is difficult to study. Terasawa made significant inroads into solving this problem by establishing a concentrated LHRH neuronal cell culture system. Her culture was derived from the olfactory placode of rhesus monkeys on embryonic day 35-37. She credits guidance from Dr. Philippa Claude on cell cultures as very important to this accomplishment.

Terasawa’s group found that:

--Cultured LHRH neurons release LHRH into media in a pulsatile manner at intervals similar to those in in vivo,
--The presence of extracellular Ca2+ is necessary for LHRH pulsatility and neurosecretion
--Intracellular Ca2+ concentrations in LHRH neurons exhibit spontaneously oscillations
--Intracellular Ca2+ concentrations in LHRH neurons synchronize at intervals similar to LHRH neurosecretion. 

Using the in vivo push-pull perfusion method, Terasawa has found that the pulsatility of LHRH release in the hypothalamus of the rhesus monkey is regulated by input from NPY, and norepinephrine neurons. In addition to LHRH release being pulsatile, the release of NPY and norepinephrine in the stalk-median eminence is also pulsatile, and these pulses of NPY and norepinephrine occur synchronously with LHRH pulses.  Infusion of neuropeptide Y and norepinephrine to the stalk-median eminence stimulates LHRH release, whereas infusion of antagonists to neuropeptide Y and norepinephrine suppresses pulsatile LHRH release.  Moreover, NPY and norepinephrine neurons appear to play a role in mediating the action of steroid hormones.  The steroid-induced LH surge is accompanied by simultaneous changes in the release of these neurotransmitters and LHRH release, and estrogen increases the ability of NPY to stimulate LHRH release 10,000-fold.

Nonhuman primate research contributed to puberty disorder therapies

Ralph Olsen, M.D., spent 47 years practicing pediatrics in Milwaukee and West Bend, Wisconsin, and at West Point Military Academy as Chief of Pediatrics. Nearly 12 years ago, he diagnosed his first case of idiopathic precocious puberty.

While examining a nine-month-old baby girl for a persistent vaginal discharge, he noticed that she also exhibited the enlarged breasts typical of a female baby with idiopathic precocious puberty. (The disorder typically manifests itself as enlarged testicles in a male infant.)

Olsen referred her to endocrinologist Arnold Slyper at the Medical College of Wisconsin, who prescribed a medicine called Lupron (luprolide acetate). Up until the 1980s, physicians did not know they could treat the disorder with drugs that influence hypothalamic control of the pituitary. Olsen acknowledged that, thanks to the basic biological groundwork of researchers like Ernest E. Knobil and colleagues at the University of Pittsburgh and University of Texas-Houston, new treatments are now available. He also noted Ei Terasawa’s contributions to the field, and read her research with renewed interest as his little patient approached her twelfth year.

“She got a shot once a month and it really worked beautifully in allowing her to grow at a normal rate,” Olsen said. “This year, she has reached a nice height and is being taken off the medication.”

Olsen, incidentally, is no stranger to nonhuman primate care. He was the pediatrician contacted by the Milwaukee County Zoo to take care of rare twin orangutans Trick and Treat. The two were born at Henry Vilas Zoo in Madison in the 1970s. They spent several months at the WRPRC before moving to Milwaukee. (Primate Record, Winter, 1975-76, WRPRC).
 
 

WRPRC Research Highlight: From embryo to placenta, gene transfer in primates a success

By Terry Devitt, UW-Madison News and Public Affairs

By successfully inserting a gene from a jellyfish into the fertilized eggs of rhesus monkeys, scientists 
have managed to make transgenic placentas, placentas where the inserted gene functions as it does in the jellyfish. 

Writing Sept. 11 in the Proceedings of the National Academy of Sciences, Thaddeus G. Golos of the Wisconsin Regional Primate Research Center at the University of Wisconsin-Madison, described the successful insertion of a “reporter gene”  into two fertilized rhesus macaque embryos. The gene, which causes jellyfish cells to produce a robust green glow, likewise conferred this activity on the placental cells where it was found. 

“The infants produced here did not carry the gene in their DNA,” Golos says, “but they did carry it and produce large amounts of the transgenic protein within their placentas during pregnancy.” 

In mammals, the placenta develops in the uterus from the embryo during gestation. Its role is to provide nourishment to the developing fetus and to transfer fetal wastes to the maternal circulation. 

This new work, Golos says, will help provide a way to explore the role that individual genes play in pathologies of pregnancy. It promises new insight into such problems in maternal and fetal health as infertility, recurrent spontaneous miscarriage, and fetal growth and low birth weight. 

“These are the most important issues in terms of a healthy pregnancy,” Golos says. “A healthy placenta is a requirement for a healthy fetus. Placental defects and problems are the causes of significant fetal and maternal morbidity and mortality.” 

Because the green-glow gene can be seen in cells, it is a much used “reporter” gene that can tell scientists that it has been effectively delivered to the host cell. 

The work reported today by the Wisconsin group is important because it is the first time a gene that has been transferred into a primate embryo has been shown to be functional throughout development to a successful live birth. It also demonstrates that successful pregnancy is possible when genes foreign to the mother are engineered into the embryos of nonhuman primates. 

The Wisconsin group adapted technology currently in development for human gene therapy by using extensively modified components of the genetic material of HIV as a vector to ferry the gene into the cells of early-stage rhesus monkey embryos. The vector, Golos says, is stripped of disease-causing genes and employs just a small percentage of the HIV genome to trick embryonic cells into accepting the transgene. 

In effect, Golos says, the vector, which was developed by Robert G. Hawley at the American Red Cross Holland Laboratory, is used to “package the transgene into a noninfectious viral particle, and to allow the transgene to be inserted into the genome of the embryo.”

The engineered embryos were then implanted in surrogate rhesus macaque mothers and carried to term. One of the pregnancies resulted in twins, but only one twin survived to term. Twin pregnancies are rare in rhesus monkeys. 

Because rhesus macaques are genetically very close to humans, the work underscores the potential of the rhesus macaque as a model for future studies to establish the safety and effectiveness of human gene and stem cell therapy. The work is just a small step away from making a truly transgenic monkey, where foreign DNA is not only transferred from one species to another but is functional as well. A more immediate consideration, Golos says, is that the accomplishment forms the basis for new experimental insights into placental health and function. 

Last January, a group at the Oregon Regional Primate Research Center reported the birth of a single rhesus monkey carrying transgenic DNA. Although the Oregon monkey carried the foreign DNA, the introduced DNA did not produce the protein that the transgene is supposed to make. 

“This is an important distinction,” Golos says, “since the success of transgenic or gene transfer studies is determined by whether or not the protein is produced.”

Golos notes that the surrogate mothers carrying the engineered embryos developed antibodies to the jellyfish protein at about mid-pregnancy. Despite this immune response, the pregnancies were carried successfully to term, demonstrating that primate embryos with working transgenes are a viable experimental model for exploring how the maternal immune system accepts the fetus, whose genes are, in part, inherited from the father. 

“Scientists can now devise experiments to learn the role of individual genes in human female reproductive health, and maternal and fetal well-being,”  Golos says. 

Co-authors include M.J. Wolfgang, S.G. Eisele, M.A. Browne, M.L. Schotzko, M.A. Garthwaite, M Durning and J.A. Thomson, all of UW-Madison; and A. Ramezani and R.G. Hawley of the American Red Cross. 

The Holland Laboratory is the research and development division of American Red Cross Biomedical Services, supporting the organization's Blood, Tissue and Plasma Services, and the Center for Cellular Therapy.

Reference:
Wolfgang MJ, Eisele SG, Browne MA, Schotzko ML, Garthwaite MA, Durning M, Ramezani A, Hawley RG, Thomson JA, Golos TG. Rhesus monkey placental transgene expression after lentiviral gene transfer into preimplantation embryos. Proc Natl Acad Sci USA. Sep;11;98(19):10728-32. 2001.
 

Just published

Following is a sample listing of recent publications involving WRPRC resources. Abstracts for these and other center publications can be viewed at the National Library of Med-icine’s PubMed Web site at www.ncbi.nlm.nih.gov/PubMed.

Claudia A, Albuquerque SR, Sousa MBC,  Santos HM, Ziegler TE. Behavioral and hormonal analysis of social relationships between oldest females in a wild monogamous group of common marmosets (Callithrix jacchus). International Journal of Primatology. 22(4):631-645. 2001.

Gresl TA, Colman RJ, Roecker EB, Havighurst TC, Huang Z, Allison DB, Bergman RN, Kemnitz JW. Dietary restriction and glucose regulation in aging rhesus monkeys: a follow-up report at 8.5 yr. Am J Physiol Endocrinol Metab. Oct;281(4):E757-65. 2001.

Horton H, Rehrauer W, Meek EC, Shultz MA, Piekarczyk MS, Jing P, Carter DK, Steffen SR, Calore B, Urvater JA, Vogel TU, Wilson NA, Watkins DI. A common rhesus macaque MHC class I molecule which binds a cytotoxic T-lymphocyte epitope in Nef of simian immunodeficiency virus. Immunogenetics. Jul;53(5):423-6. 2001.

Millar R., Lowe S., Conklin D, Pawson A, Maudsley S, Troskie B, Ott,T, Millar M, Lincoln G, Selllar R, Faurholm B, Scobie G, Kuestner R, Terasawa E, and Katz A. A novel mammalian receptor for the evolutionarily conserved type II gonadotropin-releasing hormone. Proc. Nat. Acad. Sci. USA 98:9631-9641. 2001.

Richter TA, Terasawa E. Neural mechanisms underlying the pubertal increase in LHRH release in the rhesus monkey. Trends Endocrinol Metab. Oct;12(8):353-9. 2001.

Smucny DA, Allison DB, Ingram DK, Roth GS, Kemnitz JW, Kohama SG, Lane MA. Changes in blood chemistry and hematology variables during aging in captive rhesus macaques (Macaca mulatta). Primate Aging Database Working group. J Med Primatol. Jun;30(3):161-73. 2001.

Terasawa, E.  Pulse Generation in LHRH Neurons. In: Neuroplasticity, development, and steroid hormone action. Ed: Handa, Hayashi, Terasawa and Kawata. 153-168. 2001.

Terasawa, E. Luteinizing-hormone releasing hormone (LHRH) neurons: Mechanism of pulsatile LHRH release. Vitam. Horm. 63:91-129, 2001.

Terasawa, E., Busser, B.W., Luchansky, L.L., Sherwood, N.M., Jennes, L., Millar, R.P., Glucksman, M.J., and Roberts, J.L. The presence of luteinizing hormone-releasing hormone fragments in the fetal monkey forebrain. J. Comp. Neurol. 439:491-503. 2001.

Wolfgang MJ, Eisele SG, Knowles L, Browne MA, Schotzko ML, Golos TG. Pregnancy and live birth from nonsurgical transfer of in vivo- and in vitro-produced blastocysts in the rhesus monkey. J Med Primatol. Jun;30(3):148-55. 2001.
 

Gleanings

New grants
Ei Terasawa, Ph.D., has received a subcontract grant from the Mount Sinai Medical School, New York, to study estrogen influences on neuroendocrine aging.

Mary Schneider, Ph.D., Harlow Center for Biological Psychology, Department of Kinesiology, received 5-year NIH grant, “Fetal alcohol effects in monkeys: Dopamine and behavior.” Co-investigators are UW scientists Andrew Roberts (Psychiatry and Medical Physics), Onofre DeJesus (Medical Physics), Colleen Moore (Psychology), Ann Kelley (Psychiatry), Gary Kraemer (Kinesiology), James Holden (Medical Physics) and Robert Nickles (Medical Physics).

Patent
US6200806: Primate embryonic stem cells. Inventor: Thomson; James A., Madison, WI, issued March 13, 2001 through Wisconsin Alumni Research Foundation.

Honors
Larry Jacobsen, M.L.S., was awarded emeritus status by UW Chancellor John Wiley on Aug. 3. His title is now senior special librarian-emeritus. “I am very happy for this richly deserved recognition for Larry!” says WRPRC Director Joseph Kemnitz. Twenty-five years ago, Jacobsen took over the Primate Center’s Reading Room. The WRPRC Library and Information Service, as it is now named, has since earned a worldwide excellent reputation for its unique primatological collections and its innovative Internet services.

David Watkins, Ph.D., and his staff were honored by the National Institute of Allergy and Infectious Diseases (NIAID) and its Division of AIDS by having their SIV/HIV work placed among the FY 2001 NIAID Top 20 Science Advances and among the Division of AIDS Top 10 Science Advances. Another UW-Madison researcher, Frederick Blattner of the Biotechnology Center, was honored in the Top 20 for his work in sequencing the genes of E. coli pathogens.

In the news
James Thomson, V.M.D., Ph.D., was featured in numerous articles on embryonic stem cell research this year. After President George Bush approved limited federal funding for research on human ES cells, Thomson spoke to the New York Times, Newsweek, and TIME, which featured him on its cover. Others interviewed on the topic included WRPRC and Medical School inves-tigators Dan Kaufman, Ted Golos, Jon Odorico, and Graduate School Associate Dean Tim Mulcahy.

Ted Golos, Ph.D., and colleagues’ Sept. 11 paper in PNAS was covered in BioWorld Today, the Milwaukee Journal-Sentinel, the Wisconsin State Journal, the Capital Times, and the London Daily Telegraph. By successfully inserting a gene from a jellyfish into the fertilized eggs of rhesus monkeys, scientists are closer to being able to use genetic approaches to learn how the placenta functions. The ultimate aim is to explore ways of preventing or treating recurring miscarriages, preclampsia and other problems of pregnancy that may be linked to placental function.

Karen Strier, Ph.D., and her work with muriqui monkeys in Brazil were mentioned in the New York Times article, “Primates barely hanging on,” by Connie Rogers.

Dan Kaufman, M.D., was interviewed by CNN Sept. 4 at the Primate Center for his blood ES cell work.

Retirement and promotion
Joan Scheffler, B.S., MT (ASCP), head of Clinical Pathology Services, retired Aug. 6 after 30 years at the Primate Center. She is succeeded by Stacy Walz, B.S., MT (ASCP), who began working with Joan in 1996 as a student and earned her degree in medical technology from the UW in 1999. Scheffler was a recent recipient of the American Society for Clinical Laboratory Science’s (ASCLS) Keys to the Future award. She also served on the board of directors and as secretary for WISCLS.

New staff
—Carrie Bunger, B.A., Immunology Core, July 1.
—Xuezhu Feng, research assistant, Thomson lab, Sept. 1.
—Matt Fugate, B.S., lab animal tech 1, Aug. 16.
—Kelly Henning, B.S., associate research specialist,  Reproduction Research Services, July 5.
—Tina Johnson, B.S., research specialist, Aug. 1.
Kalin/Shelton lab:
—Becky King, lab animal tech 1,  June 5.
—David Wayne Smith II, B.A., lab animal tech 1, Aug. 24. 
—Sarah Witowski, B.S., research assistant, Thomson lab, July 23.
Watkins lab:
—Candice M. Cullen, research assistant, Sept. 10.
—Elizabeth Dodds, B.S., research specialist, July 5.
—Christopher Fischer, M.S., B.S., research specialist, May 29.
—Scott Paffenroth, program assistant 3, June 17.

Departures
Todd Allen, Ph.D., Watkins Lab, July 16.
Darrel Florence, D.V.M., M.Sc., Animal Services, July 1.
Helen Horton, Ph.D., Watkins Lab, July 20.
Jon Ramsey, Ph.D., Kemnitz Lab, Sept. 1.
Wendy Saltzman, Ph.D., Abbott lab, Aug. 18.