Since the worst worldwide pandemic ever recorded &#x2014; the 1918 Spanish influenza outbreak that killed more than 20 million people &#x2014; we have achieved significant advances in understanding the influenza virus. However, the fear of such a pandemic remains strong. For example, in 1997, when a lethal influenza variant afflicted eight people in Hong Kong, contributing to the death of six, officials feared the next wave had begun. They managed to solve the problem quickly, however, by destroying all of the poultry in Hong Kong[1].

Sung-Hun Bae

Byong-Seok Choi

Structure of Influenza A Virus Promoter and its Implications for Viral RNA Synthesis

About 130 years ago, Giulio Bizozzero, then in Pavia, made a seminal observation [1]. He divided the tissues of the vertebrate body into three categories: those that divide constantly (labile), such as blood and skin, those that never divide, such as striated muscle and brain (perennial), and those that normally do not divide but can do so if injured (stable). As a consequence, diseases that perturb cell division, such as cancer, affect labile tissues, while degenerative diseases affect perennial tissues where repair is inefficient. Epithelia and blood possess a reservoir of cells that divide and maintain a progenitor pool throughout life (the stem cells) whereas striated muscle and brain were supposed not to contain stem cells. Furthermore, stem cells were supposed to generate only the cells of the tissue where they belong.

Giulio Cossu

Back from the Tip of the Nose

According to government figures, total health care spending in the U.S. in 1999 was $1.316 trillion. The government projects an increase in health care costs to $2.176 trillion by 2008. If we project this growth rate to 2020, health care costs will reach $4.009 trillion. Today, people often spend more health care dollars during the last year of their lives than in all previous years combined. Medical treatment in the last few years of life is usually very expensive and often futile. With the baby-boom generation now moving through middle age, the prescription for the U.S. health care system will be disastrous unless we learn how to keep people healthier longer. This dramatic increase in health care costs leaves us with only one acceptable alternative to rationed health care or financial ruin &#x2014; to discover interventions that make people functionally younger, healthier, and less susceptible to debilitating, age-related diseases.

Stephen R. Spindler

Reversing the Negative Genomic Effects of Aging with Short-Term Calorie Restriction

Obesity is approaching epidemic proportions in the western industrialized world, and is also becoming a major problem among young people in eastern and developing countries [1,2,3]. Unfortunately, excess fat or adipose tissue is associated with a wide array of health problems, including increased incidence of type II diabetes, cardiovascular disease, hypertension, sleep apnea, and skeletomuscular problems [4,5,6]. Obesity is the second leading cause of death from &#x201C;unnecessary&#x201D; causes in the U.S. (after smoking), and costs individuals and society billions of dollars worldwide to treat. Despite common wisdom that &#x201C;one just needs to eat less and exercise more&#x201D; and a multi-billion-dollar diet industry, epidemiological data indicate that the incidence of obesity will continue to rise. This alarming trend is, in part, due to the unprecedented availability of energy-dense foods and an increasingly sedentary lifestyle. These environmental factors may be complicated in some individuals by an unfavorable genetic predisposition. Pharmaceutical companies lead active research programs to identify drugs that target weight control centers in the body and which may help individuals control their weight; however, no satisfactory magic bullet to fight obesity has yet come through the pipeline [7,8].

Ormond A. MacDougald

Signaling Pathway Puts the Break on Fat Cell Formation

Massimo Pasqualetti

Filippo M. Rijli

Vitamin A Prevents Inner Ear Defects in Mice with Congenital Homeobox Gene Deficiency

Inheritance of a deafness-causing genotype does not necessarily mean that a person will have profound hearing loss. The presence of a modifying gene can change the effect of the deafness genotype. As an example, mutations found commonly among the deaf are at times found among their normal hearing relatives [1]. The implication is that there are genes or gene products whose interactions allow the normal physiological function of the inner ear despite a mutation that would normally disrupt the process. Deafness is not the first disorder in which modifiers can change the expected outcome, nor will it be the last, but it is very unusual for the outcome to be so dramatically changed.

Edward Wilcox

Saima Riazuddin

Sheikh Riazuddin

Some Deafness-Causing Mutations Can Be Silenced with the Appropriate Gene Partner

Robert Stickgold

Finding the Stuff that Dreams are Made Of

Michel Jacquet

Georges Renault

Sylvie Lallet

Jan De Mey

Albert Goldbeter

Oscillatory Behavior of the Nuclear Localization of the Transcription Factors Msn2 and Msn4 in Response to Stress in Yeast

Anxiety disorders affect some 19 million people in the U.S. alone, costing $46.6 billion, or one third of the nation&#x2019;s total mental health bill in 1990. Benzodiazepine tranquilizers like the prototypic diazepam are among the most widely used anti-anxiety agents. In addition to their anxiolytic action, they also induce sedation and may impair motor coordination, both of which are undesired side effects when they are used as anxiolytics. Not surprisingly, road traffic accidents may be increased for patients on classical benzodiazepines. In addition, these drugs carry the risk of dependence liability. Benzodiazepines augment the action of the inhibitory neurotransmitter g-aminobutyric acid (GABA) at contact points between two nerve cells called synapses, points at which information is transmitted from one nerve cell to the next. Synaptically released GABA binds to postsynaptic GABAA receptors, thus causing an influx of negatively charged chloride ions into the postsynaptic neuron. This leads to a hyperpolarization and thus functional inhibition of the postsynaptic cell. Benzodiazepines bind to a site on the GABAA receptor which is different from the GABA binding site, thus increasing the chloride current. Benzodiazepines like diazepam bind to GABAA receptors containing the &#x3b1; subunits &#x3b1;1, &#x3b1;2, &#x3b1;3, or &#x3b1;5, most likely in abgabg combinations.

Uwe Rudolph

Identification of Molecular Substrate for the Attenuation of Anxiety: A Step Toward the Development of Better Anti-Anxiety Drugs

Natural cytotoxicity receptors (NCRs), expressed by natural killer (NK) cells, trigger NK lysis of tumor and virus-infected cells on interaction with cell-surface ligands of these target cells. We have determined that viral hemagglutinins expressed on the surface of virus-infected cells are involved in the recognition by the NCRs, NKp44 and NKp46. Recognition of tumor cells by the NCRs NKp30 and NKp46 involves heparan sulfate epitopes expressed on the tumor cell membrane. Our studies provide new evidence for the identity of the ligands for NCRs and indicate that a broader definition should be applied to pathological patterns recognized by innate immune receptors. Since nonmicrobial endogenous carbohydrate structures contribute significantly to this recognition, there is an imperative need to develop appropriate tools for the facile sequencing of carbohydrate moieties.

Angel Porgador

Natural Cytotoxicity Receptors: Pattern Recognition and Involvement of Carbohydrates

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