Editor's note: Science Scan is a roundup of recently published biotechnology-relevant research.

Remember scurvy? pellagra? beriberi? Those once-notorious dietary deficiency diseases are rare now in industrialized parts of the world. But how about rickets? That crippling bone disorder of small children seems to have vanished as well.

In 1907, every other child admitted to Paris hospitals between 6 months and 3 years of age suffered from rickets. Also in 1907, that same statistic applied to New York City hospitals. Ironically, people in both countries referred to rickets as "the English disease." Elsewhere, rickets was known as "the new ailment."

In fact, two sources of vitamin D fight off rickets: calcium-rich foods and sunshine. What then is the present picture of rickets in the Western world?

In its August 2003 issue, the Journal of Clinical Endocrinology & Metabolism, just released online, highlights the need to maintain a healthy diet for infants and children, once breast feeding stops. The article's title: "Nutritional rickets with normal circulating 25-hydroxyvitamin D: A call for re-examining the role of dietary calcium intake in North American infants." Its co-authors are research pediatricians at Yale University School of Medicine.

The paper reports on the medical records of 43 children in New Haven, Conn., who have nutritional rickets. Of this young cohort, 86 percent were African-American, Hispanic or of Middle Eastern descent. More than 93 percent of the children were breast fed, but 15 percent received vitamin D supplementation. The data also showed that 86 percent of the children with available food histories were weaned to diets with minimal dairy content. The average age of developing rickets was 20 months. The paper reported that nearly 50 percent of the children had normal vitamin D status, suggesting that the incidence of calcium-deficiency rickets is much higher than previously thought among North American infants.

"Recent trends indicate," the article's senior author observed, "that the fluid intake of children, once predominantly milk, increasingly consists of soda and fruit juices. Since milk is an excellent source of calcium and vitamin D for children, this trend could be contributing to the high incidence of rickets."

Interferon-Alpha/Beta + p53, If Linked, Explain Their Benefits Against Cervical, Liver Cancers

Two molecules known for their anticancer action may be linked, according to a report published online by Nature, on July 16, 2003. (Its print publication is pending.) The discovery may help explain the beneficial effects of type 1 interferon (IFN-alpha/beta) against cervical and liver cancers.

The co-authors are immunologists at the University of Tokyo. Their paper bears the title "Integration of interferon-a/b signaling to p53 responses in tumor suppression and antiviral defense."

They report that, in cultured cells, type 1 interferon enhances the activity of the tumor suppressor gene p53. When the cell is stressed it can activate its p53 protein reserves and commit suicide. The same mechanism may occur in the cells of cancer patients treated with interferon, the researchers hypothesize.

Interferon is produced naturally by the body in response to viral infection. The team also reports that viral infection boosts p53 levels. Their joint activity may represent a mechanism whereby viruses can indirectly trigger apoptosis - cell death. Common therapeutic drugs often trigger a range of unpleasant side effects. Lower doses of these anticancer agents could be prescribed together with type 1 interferon to produce an effective, less toxic therapy for human cancer patients, the authors speculate.

Cerebral Glad-Not-Sad Drugs, E.g., Prozac, Paxil, Zoloft, Celexa, Pay Serotonin Neuronal Tribute

Mice missing a gene called Lmx1b do not produce the important brain chemical serotonin. An article in Nature Neuroscience, released online Aug. 3, 2003, offers the first evidence that one gene controls development in all cells that produce the neurotransmitter serotonin in the central nervous system. It marks significant progress in understanding this critical nervous system pathway. The journal report bears the title: "Lmx1b is essential for the development of serotonergic neurons." Its co-authors are researchers at Washington University in St. Louis.

While the importance of serotonin in behavior is well known, it is not well understood how the cells that produce this chemical are generated. Elucidating its pathway, the paper's co-authors suggest, may lead to better drug candidates for a number of psychiatric disorders.

Many cells use serotonin to communicate with each other. Some of them are located in the brain; others reside in the spinal cord. It is not clear which gene is responsible for the difference between these two groups. The co-authors have identified one potential candidate gene, Gata3 by name, which appears to be involved in the formation of serotonin cells that connect with the spinal cord but not the brain. Abnormalities in the serotonin pathway can result in a variety of psychiatric disorders, including depression, anxiety and impulsive violence.

Antidepressant medications - typically Prozac, Paxil, Zoloft, Celexa - treat serotonin imbalances. They are all selective reuptake inhibitors of the chemical. Thus regulating its activity in the brain ameliorates mood.

Mutant Enzyme Protects Mice From Diabetes, Obesity, Induced By High-Fat/Carbohydrate Diet

Different mice, from a particular mutant strain, maintain healthy weights and blood sugar levels, even when fed a diet that promotes obesity and diabetes. These rodents are missing genes that produce an enzyme, acetyl-CoA carboxylase 2 (ACC2). To determine how ACC2 affects two such disorders, obesity and Type II diabetes, wild-type (WT) mice and ACC2 mutants were fed a high-fat, high-carbohydrate diet.

Within four months the WT mice became obese and diabetic. In contrast, the mutant mice maintained healthy body weights and blood sugar levels throughout the experiment. These results suggest that ACC2 may play an essential role in controlling the body's fat-burning capabilities.

The research paper in the Proceedings of the National Academy of Sciences (PNAS), dated Aug. 11-15, 2003, is titled "Acetyl-CoA carboxylase 2 mutant mice are protected against obesity and diabetes induced by high-fat/high-carbohydrate diets." Its authors are at Baylor College of Medicine in Houston.