Max-Planck-Gesellschaft, November 22, 2008 — Thanks to our ability to learn and to remember, we can perform tasks that other living things can not even dream of. However, we are only just beginning to get the gist of what really goes on in the brain when it learns or forgets something. What we do know is that changes in the contacts between nerve cells play an important role. But can these structural changes account for that well-known phenomenon that it is much easier to re-learn something that was forgotten than to learn something completely new?

Store room for future learning: nerve cells retain many of their newly created connections and if necessary, inactivate only transmission of the information. This makes relearning easier. (Credit: Image: Max Planck Institute of Neurobiology / Hofer)

Scientists at the Max Planck Institute of Neurobiology have been able to show that new cell contacts established during a learning process stay put, even when they are no longer required. The reactivation of this temporarily inactivated “stock of contacts” enables a faster learning of things forgotten.

While an insect still flings itself against the window-pane after dozens of unsuccessful attempts to gain its freedom, our brain is able to learn very complex associations and sequences of movement. This not only helps us to avoid accidents like walking into glass doors, but also enables us to acquire such diverse skills as riding a bicycle, skiing, speaking different languages or playing an instrument. Although a young brain learns more easily, we retain our ability to learn up to an advanced age. For a long time, scientists have been trying to ascertain exactly what happens in the brain while we learn or forget.

Flexible connections:

To learn something, in other words, to successfully process new information, nerve cells make new connections with each other. When faced with an unprecedented piece of information, for which no processing pathway yet exists, filigree appendages begin to grow from the activated nerve cell towards its neighbours. Whenever a special point of contact, called synapse, forms at the end of the appendage, information can be transferred from one cell to the next – and new information is learned. Once the contact breaks down, we forget what we have learned.

The subtle difference between learning and relearning:

Although learning and memory were recently shown to be linked to the changes in brain structure mentioned above, many questions still remain unanswered. What happens, for example, when the brain learns something, forgets it after a while and then has to learn it again later? By way of example, we know from experience that, once we have learned to ride a bicycle, we can easily pick it up again, even if we haven’t practiced for years. In other cases too, “relearning” tends to be easier than starting “from scratch”. Does this subtle difference also have its origins in the structure of the nerve cells?

Scientists at the Max Planck Institute of Neurobiology have now managed to show that there are indeed considerable differences in the number of new cell contacts made – depending on whether a piece of information is new or is being learned second time around. Nerve cells that process visual information, for instance, produced a considerably higher number of new cell contacts if the flow of information from their “own” eye was temporarily blocked. After approximately five days, the nerve cells had rearranged themselves so as to receive and process information from the other eye – the brain had resigned itself to having only one eye at its disposal. Once information flowed freely again from the eye that had been temporarily closed, the nerve cells resumed their original function and now more or less ignored signals from the alternative eye.

“What surprised us most, however, was that the majority of the appendages which developed in response to the information blockade, continued to exist, despite the fact that the blockade was abolished “, project leader Mark Hübener explains. Everything seems to point to the fact that synapses are only disabled, but not physically removed. “Since an experience that has been made may occur again at a later point in time, the brain apparently opts to save a few appendages for a rainy day”, Hübener continues. And true enough, when the same eye was later inactivated again, the nerve cells reorganized themselves much more quickly – because they could make use of the appendages that had stayed in place.

Many of the appendages that develop between nerve cells are thus maintained and facilitate later relearning. This insight is crucial to our understanding of the fundamental processes of learning and memory. And so, even after many years of abstinence, it should be no great problem if we want to have a go at skiing again this winter.

Journal reference:

1. Hofer et al. Experience leaves a lasting structural trace in cortical circuits. Nature, November 12, 2008; DOI: 10.1038/nature07487

ScienceDaily.com, November 23, 2008) — A recent study appearing in the November issue of Journal of American Geriatrics Society revealed that centenarian offspring (children of parents who lived to be at least 97 years old) retain important cardiovascular advantages from their parents compared to a similarly-aged cohort. The study is the first to assess the health of centenarian offspring over time and could be important for future research, as the subjects may be used as a model of healthy aging.

The findings show that centenarian offspring have a 78 percent lower risk for heart attacks, 83 percent lower likelihood of stroke and an 86 percent lower risk of developing diabetes mellitus.

Additionally, the study found that centenarian offspring who were followed in the study were 81 percent less likely to die than the reference group of similarly-aged patients during the follow-up period. The survival rate is evidence that longevity runs in families, and the results reinforce the notion that there may be physiological and genetic reasons that longevity runs in families.

The results are consistent with previous research, which suggested that the avoidance or delay of cardiovascular disease and cardiovascular risk factors, including high blood pressure and diabetes, runs strongly in the families of centenarians, particularly amongst their children.

Dellara F. Terry, co-author of the study, points out that offspring of centenarians maintain these cardiovascular advantages throughout their lives. “These advantages persisted over the several years of the study when they are compared to a similarly-aged group whose parents did not survive to very old age,” Terry said.

Christopher Capozziello for The New York Times
Rita Miller, 65, undergoes dialysis three times a week.

Christopher Capozziello for The New York Times
A SURPRISE Rita Miller learned in 2005 that she had chronic kidney disease.

The New York Times, November 20, 2008, by David Tuller — In February 2005, Rita Miller, a party organizer in Chesapeake, Va., felt exhausted from what she thought was the flu. She was stunned to learn that persistent high blood pressure had caused such severe kidney damage that her body could no longer filter waste products from her blood.

“The doctor walked over to my bed and said, ‘You have kidney failure — your kidneys are like dried-up peas,’ ” recalled Ms. Miller, now 65, who had not been to a doctor or had her blood pressure checked for years.

“The doctor said, ‘Get your family here right away,’ ” she said. “They were telling me I might not make it. I was in shock. I started dialysis the next day.”

Ms. Miller, who has since moved to Connecticut to be with her children, was one of the millions of Americans unaware that they are suffering from chronic kidney disease, which is caused in most cases by uncontrolled hypertension (as in her case) or diabetes, and is often asymptomatic until its later stages. The number of people with the disease — often abbreviated C.K.D. — has been rising at a significant pace, thanks in large part to increased obesity and the aging of the population.

An analysis of federal health data published last November in The Journal of the American Medical Association found that 13 percent of American adults — about 26 million people — have chronic kidney disease, up from 10 percent, or about 20 million people, a decade earlier.

“We’ve had a marked increase in chronic kidney disease in the last 10 years, and that continues with the baby boomers coming into retirement age,” said Dr. Frederick J. Kaskel, director of pediatric nephrology at the Children’s Hospital at Montefiore in the Bronx. “The burden on the health care system is enormous, and it’s going to get worse.

“We won’t have enough units to dialyze these patients.”

Concerned about the emerging picture, federal health officials have started pilot programs to bolster public awareness, increase epidemiologic surveillance and expand efforts to screen those most at risk — people with high blood pressure, diabetes or a family history of kidney disease.

Those people, and those who already have the disease, can often be helped by the same kinds of medicine and lifestyle changes used in hypertension and diabetes. They are urged to quit smoking, lose weight, exercise regularly, restrict their diets and, if necessary, control their blood pressure and diabetes with medication. But such efforts cannot restore kidney function that has been lost.

The trouble is that most people know very little about chronic kidney disease and rarely ask their doctors about kidney function. And many of those who have it feel relatively well until late in the illness, although they may experience nonspecific symptoms like muscle cramps, loss of energy and poor concentration.

“When most people think of kidney disease, they think of dialysis or transplantation,” said Dr. Joseph A. Vassalotti, chief medical officer for the National Kidney Foundation, a major education and advocacy group. “They don’t understand that it encompasses a spectrum, and that the majority of patients are unaware they have the condition.”

Chronic kidney disease progresses over the course of years, with its phases determined according to two criteria: the presence of protein in the urine, known as proteinuria, and how effectively the kidneys are processing waste products.

Patients get dialysis or a kidney transplant only when they are in the final stage of the disease, also known as kidney failure or end-stage renal disease. But the path to kidney failure can take years. “Only a tiny percentage of patients with kidney disease need dialysis,” said Dr. Stephen Fadem, a Houston nephrologist and vice president of the American Association of Kidney Patients.

Chronic kidney disease itself can damage the cardiovascular system and lead to other serious medical conditions, like anemia, vitamin D deficiencies and bone disorders. Patients are far more likely to die from heart disease than to suffer kidney failure.

Because African-Americans, Latinos and other minority communities suffer disproportionately from hypertension and diabetes, they experience higher rates of kidney disease and kidney failure. Other cases are caused by genetic disorders, autoimmune ailments like systemic lupus erythematosis, prolonged use of certain medications like anti-inflammatory drugs, and a kidney inflammation called glomerulonephritis.

In 2005, more than 485,000 people were living on dialysis or with a transplant, at a total cost of $32 billion. Medicare pays for much of that, because it provides coverage for patients needing dialysis or transplant even if they are not yet 65. In fact, kidney disease and kidney failure account for more than a quarter of Medicare’s annual expenditures.

The National Kidney Foundation, with an annual budget of $85 million, plays a major role in education, policy, research and treatment. The organization provides free screening for adults at risk for kidney disease, publishes a leading journal in the field, lobbies on treatment and policy issues, and conducts extensive public education and outreach.

But it has come under criticism on several fronts, in particular its close financial ties to the pharmaceutical industry. The agency greatly influences clinical care through the development of guidelines to advise doctors on various aspects of the illness. Critics say the guidelines have benefited drug makers, who are major contributors to the foundation.

“These practice guidelines are widely disseminated and heavily influenced by industry, and they come down on the side of recommending higher levels of treatment,” said Dr. Richard Amerling, director of outpatient dialysis at Beth Israel Medical Center in New York.

In 2006, the organization published new guidelines for treating anemia associated with chronic kidney disease. The guidelines were underwritten with support from Amgen, which markets a drug for anemia, and some members of the panel that developed the guidelines had financial ties to the industry.

The kidney foundation guidelines called for raising red blood cell counts to levels higher than those recommended by the Food and Drug Administration, and many nephrologists criticized the guidelines as biased in favor of industry. After new clinical trials suggested that more aggressive treatment could cause an increase in deaths and heart problems, the foundation revised the guidelines.

Ellie Schlam, a spokeswoman for the foundation, said the organization was vigilant “to ensure that no sponsorship funds contributed to the N.K.F.” would influence the content of any guidelines.

The organization has also been criticized by advocates who support financial compensation for organ donors, which the foundation firmly opposes as unethical and unlikely to increase the availability of organs. (In contrast, the American Association of Kidney Patients supports research into how financial incentives would affect organ donation.)

Even the foundation’s classification of chronic kidney disease into five distinct stages, a framework that has been widely accepted, has come under some challenge.

In 2002, the organization published clinical criteria for determining each stage of the disease. But some experts say those guidelines have the effect of overstating the problem by classifying many elderly patients as having the disease when they actually have standard age-related kidney decline. The foundation replies that a reduced kidney function among the elderly should not be accepted as normal just because it is common.

Because of Medicare’s role in paying for dialysis and transplantation, the federal government knows far more about the epidemiology and costs of end-stage renal disease than about chronic kidney disease over all. In recent years, Congress has directed the Centers for Disease Control and Prevention to fill some of these knowledge gaps.

In particular, the centers are seeking to develop a comprehensive surveillance system for the disease, organizing pilot screening projects for people at high risk in California, Florida, Minnesota and New York. The agency is also studying the financial implications of the disease and the cost-effectiveness of various interventions.

The National Kidney Foundation, which has worked closely with the C.D.C. and the National Institutes of Health on initiatives related to chronic kidney disease, has also focused on education and screening, particularly in minority communities. Terri Smith, the urban outreach director at the foundation’s Connecticut affiliate, says she spends a lot of her time going to black churches and community centers to talk about kidney disease, and has been surprised that so few people know anything about it.

“They’re very aware of hypertension and diabetes, but it was a revelation to me that people didn’t get the connection to kidney disease,” she said. “People have no idea they should eat less than a teaspoon of salt a day. I teach them how to read labels; I give them questions they should be asking the doctor.”

In Michigan, the local N.K.F. affiliate reaches out to hair stylists and other salon workers in minority communities, training them in talking to their clients about getting screened. Several years ago, after Mary Hawkins, 61, a nurse who lives in Grand Rapids, received a warning about kidney disease from a masseuse at her local salon, she made an appointment to see her doctor.

Although she did not have kidney disease, she learned that her blood pressure was high. Now she takes three medications to keep it under control, exercises three times a week, takes tai chi classes, no longer smokes and attends a dance class at the same salon.

“I knew kidney disease existed, but I wasn’t in tune with the risk,” she said. “You get so caught up in your own life that the last thing you think about is your health — even though it should be the first thing.”

Getty Images

The New York Times, November 20, 2008, by Perri Klass MD — The baby didn’t look sick, as he lay in his mother’s arms and looked around the room at the clinic. He wasn’t screaming inconsolably, wasn’t limp and listless. But his mother had told the nurse that he seemed fussy and wasn’t nursing quite as vigorously as usual. And he felt warm to the touch. So the nurse took his temperature: 100.4, less than two degrees above normal.

Pediatricians often need to reassure parents when their toddler or preschooler has a high fever. Yes, we say, your daughter has a temperature of 103, but she looks good; it’s probably just a virus. No need for antibiotics, no need for anything except liquids and an over-the-counter medicine like acetaminophen or ibuprofen.

Yet in this robust baby boy, not quite 2 months old, 100.4 was reason for worry.

Newborns don’t handle infection very well. Their immature immune systems leave them vulnerable to severe infections that can rage out of control. In the worst cases, bacteria get into the bloodstream, from a urinary infection or a skin infection for example, and cause bacterial sepsis. Or even worse, the bacteria leak from the bloodstream through the barrier that is supposed to separate blood and brain, causing meningitis. So if fever occurs in a very young baby, the advice to parents is always to call the doctor right away. But almost two months old is no longer a newborn.

Twenty years ago, when I was in pediatric training, the definition of “very young” was under 3 months. For any fever in that age group, we took samples of blood, urine and spinal fluid and sent them to be cultured for bacteria. While we waited for the results we put the baby in the hospital and treated with intravenous antibiotics.

But in most cases, the aggressive treatment was unnecessary, because the cultures yielded no bacteria. Fortunately, there has been good epidemiologic research in recent years to help predict which babies really need to be hospitalized.

Nowadays, anyone under 1 month old who develops any fever still tends to end up in the hospital. For babies older than 3 months, we now use our clinical judgment: if they appear well, we might order a blood or urine test, but they can go home, as long as we stay in touch with the parents.

Between 1 and 3 months is still a gray zone. And in this case, there were a few other subtle shades of gray, notably the fussiness and reluctance to nurse: after all, an infant with a serious infection has a limited repertory of signals to say, “Hey, Mom, something’s wrong.”

Did his temperature really constitute a fever? As it happened, it fell on the cutoff for “real” fever — 38 degrees Celsius, or 100.4 Fahrenheit.

So age right on the borderline, fever right on the borderline, and story right on the borderline. Here were the doctor’s options:

A. Examine the baby carefully, and if he looks good and the temperature isn’t climbing and the mother seems comfortable and competent, send them home and tell the mother to watch carefully.

B. Get a blood count to check for serious infection, and maybe a urine test to be sure there’s no evidence of a urinary infection. If there’s no evidence of infection on these relatively rapid tests, proceed to A.

C. Send blood and urine to be cultured for bacterial infection, which will take two days. Send the baby home but consider giving him a shot of antibiotics to “cover” him.

D. If the baby looks sick, send him to the emergency room for a spinal tap and a full sepsis workup and admit him to the hospital for intravenous antibiotics while waiting to see if any of the cultures are positive for bacteria.

Each of these responses would have been reasonable and defensible and explainable.

“Pediatricians really wrestle with this issue,” said Dr. William V. Raszka, professor of pediatrics at the University of Vermont College of Medicine and director of the Pediatric Infectious Diseases Service at Vermont Children’s Hospital. He added that “there’s a tremendous amount of conflicting data” about which babies need which tests and treatments.

“The incidence of serious bacterial illness in children who look well between 1 and 3 months of age is really, really low” as long as a urine test is negative, Dr. Raszka said. But on the other hand, if the baby is not completely well, “if mother is sure this is not the normal child, I would be more aggressive in working up the baby.”

In this case, the baby looked pretty good. His fever wasn’t going up; his patient mother was nursing him and he was drinking, while his less patient brother dismantled the exam room. He probably did not have a serious bacterial infection.

We did check a blood count — it looked normal — and we got some urine to be cultured. On the other hand, the mother continued to feel strongly that the baby was not quite “himself.” I couldn’t find anything wrong on his exam, but she knew him better. And because I got my pediatric training in the days when he would have been automatically admitted to the hospital, I’m probably more conservative than younger doctors.

In the end, we did give him a shot of antibiotics, his cultures went to the lab, and he and his mother went home with a thermometer. The next day he was himself again, his mother reported — less fussy, more alert and happy, nursing well. Nothing grew in his cultures. Maybe he had a mild viral illness, which caused the fever and the fussing, and he fought it off.

From a certain point of view, he was unlucky: he was right on the borderlines of both temperature and age. And from another point of view, he lucked out: 20 years ago, he would have had to spend three days in the hospital.

In either case, the next time he comes into the clinic with fever, he will, I hope, have aged out of the gray zone, out of the high-risk age, and we can concentrate on treating an infection, if we find one, and reassuring his mother that fever by itself is nothing to worry about.

Perri Klass is a professor of journalism and pediatrics at New York University. Her most recent book is the novel “The Mercy Rule.”

Only where the sun doesn’t shine

Aging of the skin is caused by a combination of genetic factors (natural aging) and excessive sun exposure (photoaging). Natural aging appears as fine wrinkles, skin laxity, and sagging; photoaging produces coarse wrinkles. Both processes result, at least in part, from declines in types I and III collagen in the dermis. Topical medications that could restore the youthful appearance of skin are of great interest, and estrogen-containing creams have been suggested as potential candidates in this role. To test this theory, investigators examined the efficacy of topical estradiol on collagen production in 40 postmenopausal women (mean age, 75; range, 65–94).

After 1 week of therapy with topical estradiol, procollagen I and III synthesis and protein expression had increased as much as 3.25-fold in dermal fibroblasts in hip skin unexposed to the sun. Increases in procollagen I and III activity were also observed in 30 age-matched men, but their increases were smaller. Notwithstanding its effect on sun-protected skin, topical estradiol had no effect on collagen production in sun-exposed facial and forearm skin, even though the estradiol penetrated the skin, estrogen receptors were present in equal numbers in photoaged and sun-protected skin, and topical estradiol activated other genes in the skin.

Comment: Given the intense interest in creams that could reverse or prevent aging of the skin, patients will likely ask physicians about topical estrogens for this purpose. These findings showed that topical estradiol did not increase collagen production in the face and other sun-exposed skin. Additional manifestations of photoaging (such as uneven pigmentation and dry skin) might respond to an estrogen cream, but the long-term effects of topical estrogen are unknown, and other topical agents, such as retinoids and moisturizers, can address these problems. Systemic estrogens sometimes produce cutaneous telangiectasias and melasma, and topical formulations might do the same or have systemic effects. Are topical estrogens effective for skin aging? Based on the results of this study, the answer is no.

— Craig A. Elmets, MD

Published in Journal Watch Dermatology November 7, 2008


Women’s Foot Complaints

The most common foot ailments in women are onychomycosis, Morton neuroma, stress fractures, and plantar fasciitis.

A variety of foot conditions plague women more often than men. Many are aggravated by the shoes that women wear but also can be caused by loss of bone density as women age. The most common foot ailments in women are onychomycosis, Morton neuroma, stress fractures, and plantar fasciitis.


A fungal infection of the toenails, onychomycosis most often is caused by dermatophytes (Trichophyton rubrum and T. mentagrophytes) or yeasts and molds, primarily Candida.1 Although diagnosis often is based on the clinician’s judgment, acceptable methods for confirming fungal involvement include use of dermatophyte test medium or a potassium hydroxide test. Onychomycosis results in cosmetically unacceptable nails that are dystrophic, lytic, thick, painful, and discolored. The condition can develop as a consequence of tinea pedis, trauma to the nail, an immunocompromised state, or pedicures (removal of the cuticle creates microtears that allow fungus to enter the nail). Treatment options include debridement, oral or topical antifungal therapies, or permanent removal of the toenail with a chemical or surgical matrixectomy. Simple removal of the toenail without treatment of the fungus will lead to regrowth of the fungal nail. Combination therapy is the most successful approach; for example, results of a 2006 study showed that oral terbinafine plus nail debridement led to higher mycologic cure rates than did treatment with oral terbinafine alone (68% vs. 63%).2


This condition develops from enlargement of the third common digital branch of the medial plantar nerve. Pressure from the corresponding third and fourth metatarsal heads and adjacent deep transverse metatarsal ligament causes pain in the third intermetatarsal space. Burning or sharp, shooting pain to the corresponding toes and the sensation of walking on a pebble or a marble are common complaints. Compressive forces on the forefoot (e.g., from wearing shoes with pointed toes or engaging in certain athletic activities) exacerbate these symptoms. A positive Mulder sign (clicking as the neuroma rubs on the adjacent metatarsal heads) can occur on dorsal-to-plantar or side-to-side compression of the forefoot.3 The diagnosis is best made based on clinical examination or with a diagnostic injection of local anesthetic in the interspace between the metatarsal heads.

Neuromas also can be diagnosed with magnetic resonance imaging (MRI), ultrasound, or nerve conduction studies. Other pathologies that can cause similar symptoms are capsulitis, metatarsalgia, avascular necrosis or stress fractures of the metatarsals, soft-tissue tumors, tarsal tunnel syndrome, and plantar plate ruptures. After diagnosis of the neuroma, the patient should be referred to a podiatrist or other foot specialist for evaluation and treatment. Conservative treatments include padding and strapping, orthotic devices, and steroid injections. A less-widely used but successful conservative regimen involves weekly injections of a sclerosing alcohol mixture (a combination of local anesthetic and dehydrated ethyl alcohol). In a 1999 study, 82% of patients who were given weekly sclerosing alcohol injections for 3 to 7 weeks experienced complete relief.4 If conservative therapies are not successful, the neuroma can be excised surgically; however, this will lead to a decrease in sensation in the corresponding digital interspace.


Metatarsal stress fractures commonly affect women during and after the menopausal transition; however, athletes and military recruits also can suffer from the condition. The lesser metatarsals are a common location for stress fractures. Patients complain of persistent pain and swelling in the forefoot and might report recent periods of weight-bearing activity (often involving a particular repetitive motion). Initially, the injury is limited to cortical bone — but, if left untreated, the fracture can extend through the entire bone and even become displaced.5 Although conventional radiographs might be negative for the first 21 days after injury, bone scans or MRIs can reveal the fracture earlier. One study that included 37 female athletes (primarily runners) showed that 47% of stress fractures were identifiable with initial radiographs, whereas 96% were detectable with bone scans.6 Successful conservative treatment consists of compressive bandaging and immobilization (surgical shoe, cam walker boot, or cast). To prevent fracture recurrence, modification of physical activities and shoe gear should be addressed; in addition, treatment for bone density loss, if present, is warranted.


This inflammatory condition of the plantar fascial band (which courses along the plantar aspect of the foot) is one of the most common foot ailments, accounting for 15% of all adult foot complaints.7 Pain often is localized to the medial plantar region of the heel. Patients report pain when they stand after periods of rest (poststatic dyskinesia). Typically, a brief period of walking offers some relief.

Common causes of plantar fasciitis include foot structure, obesity, changes in physical activity, and lack of supportive shoe gear. Plantar fasciitis is best diagnosed clinically, but ultrasound and MRI often are helpful for visualizing changes in the thickness or continuity of the plantar fascial band. Radiographs can reveal the plantar calcaneal spur that often accompanies this condition. Several other conditions that can cause heel pain (i.e., nerve entrapments, bone cysts, calcaneal stress fractures, systemic arthritic conditions, and lumbar spine disorders) should be considered if the patient has an atypical presentation or is not responding to conservative measures.

Conservative therapy renders successful outcomes in most patients and usually should be employed for a minimum of 6 months. The best conservative therapy employs a combination of icing, stretching, nonsteroidal anti-inflammatory drug therapy, padding, strapping, custom molded orthotics, night splints, physical therapy, steroid injections, short-term oral steroid therapy, or immobilization with a cast or cam walker boot. When warranted, surgical treatments for this condition include open or endoscopic plantar fasciotomies. Newer therapies that show promise but are not yet widely used include extracorporeal shockwave therapy,8 cryotherapy, and Topaz coblation (radiofrequency technology).


Several podiatric conditions have higher incidence in women than in men. Early diagnosis of these pathologies can lead to more-focused, successful treatment.

— Mary Ann Bender, DPM

Dr. Bender is a podiatrist and foot surgeon in private practice with J.B. Jenkins and Associates in Chicago, IL. She is also a clinician for the Cook County Community Service rotation at William Scholl College of Podiatric Medicine, Rosalind Franklin University, and serves uninsured and homeless patients at eight clinics and shelters in Chicago.

Published in Journal Watch Women’s Health November 20, 2008