Atopic dermatitis is a highly pruritic chronic inflammatory skin disorder affecting 10-20% of children worldwide. Symptoms can persist or begin in adulthood. It is also the most common cause of occupational skin disease in adults. This disease results from an interaction between susceptibility genes, the host's environment, pharmacological abnormalities, skin barrier defects, and immunological factors. New management approaches have evolved from advances in our understanding of the pathobiology of this common skin disorder.

Adverse events associated with dietary supplements are difficult to monitor in the USA, because such products are not registered before sale, and there is little information about their content and safety.

What is the effect of different treatment options for benign prostatic hyperplasia (BPH) on sexual function or dysfunction? With increasing age, sexual dysfunction and BPH become more prevalent. Some treatments for BPH can affect sexual function. Different surgical treatments have different effects on sexual function depending on how much the internal involuntary sphincter is affected. The same is true for medical therapies, each class of drug having a unique affect on sexual function.

Despite great advances in medicine, the common cold continues to be a great burden on society in terms of human suffering and economic losses. Of the several viruses that cause the disease, the role of rhinoviruses is most prominent. About a quarter of all colds are still without proven cause, and the recent discovery of human metapneumovirus suggests that other viruses could remain undiscovered. Research into the inflammatory mechanisms of the common cold has elucidated the complexity of the virus-host relation. Increasing evidence is also available for the central role of viruses in predisposing to complications. New antivirals for the treatment of colds are being developed, but optimum use of these agents would require rapid detection of the specific virus causing the infection. Although vaccines against many respiratory viruses could also become available, the ultimate prevention of the common cold seems to remain a distant aim.

Many trials have been done to compare primary percutaneous transluminal coronary angioplasty (PTCA) with thrombolytic therapy for acute ST-segment elevation myocardial infarction (AMI). Our aim was to look at the combined results of these trials and to ascertain which reperfusion therapy is most effective.

As public awareness of Alzheimer's disease increases, more people are asking for help and advice about memory problems. Memory complaints may be secondary to psychiatric, psychological, and physical conditions and is an almost universal early symptom of dementia. The concept of amnestic mild cognitive impairment attempts to describe those people in whom memory loss is not of such severity to merit a diagnosis of dementia. The importance of this group of people is not just the need to develop interventions which ameliorate individual suffering but that they represent a population at high risk of developing dementia, especially Alzheimer's disease, and are an appropriate target for dementia prevention strategies.

Optic neuritis is a common condition that causes reversible loss of vision. It can be clinically isolated or can arise as one of the manifestations of multiple sclerosis. Occasional cases are due to other causes, and in these instances management can differ radically. The treatment of optic neuritis has been investigated in several trials, the results of which have shown that corticosteroids speed up the recovery of vision without affecting the final visual outcome. Other aspects of management, however, are controversial, and there is uncertainty about when to investigate and when to treat the condition. Here we review the diagnostic features of optic neuritis, its differential diagnosis, and give practical guidance about management of patients. The condition's association with multiple sclerosis will be considered in the light of studies that define the risk for development of multiple sclerosis and with respect to results of trials of disease-modifying drugs in these individuals.

While transfusion-transmissible diseases, including AIDS and viral hepatitis, continue to spread especially in developing countries, the issue of safeguarding the world's blood supply is of paramount importance. China houses more than 20% of the earth's population, and thus its blood supply has the potential to affect the global community. In recent years, Chinese blood centres have tried to improve the nation's blood safety. Although substantial progress has already been made, many daunting difficulties remain. Traditional cultural barriers need to be overcome to successfully mobilise volunteer blood donors. Gaps in information and technology still need to be closed. Insufficiency of economic resources also restrict the blood bank industry. Other developing countries face many of the same challenges as China.

Levodopa is the gold-standard therapy for Parkinson's disease. However, long-term treatment leads to involuntary movements and response fluctuations which add to the complexities of later disease-management. In addition, preclinical evidence suggests that levodopa is toxic to dopaminergic neurons. These problems have led to a move away from levodopa towards initial monotherapy with a dopamine agonist.

Dementia affects about 5% of the elderly population over age 65 years and has an unexplained predominance in women and a low rate in some cultures. Different forms of dementia are now distinguished-Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, and dementia secondary to disease, such as AIDS dementia. However, such nosological boundaries are being re-evaluated because different dementias are believed to have common underlying neuropathology. Neurochemical and neurobiological research has led to advances in understanding causes of dementia, and functional imaging has allowed identification of possible biomarkers; from these, a range of potential treatment approaches have arisen that focus on enhancement of neurotransmitter function, intervention at the level of amyloid production and deposition, and reduction of secondary risk factors such as hypertension, depression, and hypolipidaemia. Molecular diagnostic testing and genetic counselling for families with autosomal dominant early-onset dementia are new developments; however, this approach is not useful for late-onset dementia, in which the identified candidate susceptibility genes have a relatively small effect on risk. While fundamental research works towards new biological treatment strategies, much remains to be done in the area of disease management and the development of appropriate models of long-term care.

Almost every woman and some men will encounter hot flushes during their lifetime. Despite the prevalence of the symptoms, the pathophysiology of hot flushes remains unknown. A decline in hormone concentrations might lead to alterations in brain neurotransmitters and to instability in the hypothalamic thermoregulatory setpoint. The most effective treatments for hot flushes include oestrogens and progestagens. However, many women and their physicians are reluctant to accept hormonal treatments. Women want non-pharmacological treatments but unfortunately such treatments are not very effective, and non-hormonal drugs are often associated with adverse effects. Results from recent studies showed that selective serotonin reuptake inhibitors and other similar compounds can safely reduce hot flushes. Moreover, the efficacy of these drugs provides new insight into the pathophysiology of hot flushes. In this critical review, we assess knowledge of the epidemiology, pathophysiology, and treatment of hot flushes.

After identification of the hereditary haemochromatosis gene HFE, and receipt of confirmation that most patients with the condition were homozygous for a single, founder mutation (C282Y), most assumed that C282Y would be a prevalent, highly penetrant mutation in a gene that plays a key part in the regulation of iron absorption and of whole-body iron homoeostasis. With carrier rates of between 10% and 15%, and a homozygote frequency of about one-in-150 in people of northern European descent, C282Y is certainly prevalent. However, it is not highly penetrant. The pronounced variation in phenotype in individuals with the same gene mutation has prompted the search for modifier genes at other loci, and for environmental factors that might affect expression of the condition. Progress in our understanding of how HFE regulates the absorption of dietary iron has been slow, but much can be learnt from the study of the rare instances of haemochromatosis that involve mutations in newly-identified iron-metabolism genes, such as TFR2--a transferrin receptor isoform--and ferroportin1/Ireg1/mtp1--an intestinal iron transporter. The availability of definitive information on penetrance and the identity of genetic modifiers will aid the debate on whether population screening for haemochromatosis should be undertaken or whether alternative strategies should be implemented to improve early detection.

Rising prices of medicines are putting them beyond the reach of many people, even in rich countries. In less-developed countries, millions of individuals do not have access to essential drugs. Drug development is failing to address the major health needs of these countries. The prices of patented medicines usually far exceed the marginal costs of their production; the industry maintains that high prices and patent protection are necessary to compensate for high development costs of innovative products. There is controversy over these claims. Concerns about the harmful effects of the international system of intellectual property rights have led the World Trade Organization to relax the demands placed on least developed countries, and to advocate differential pricing of essential drugs. How these actions will help countries that lack domestic production capacity is unclear. Better access to essential drugs may be achieved through voluntary licensing arrangements between international pharmaceutical companies and manufacturers in developing countries.

Hanahan and Weinberg proposed in 200 that carcinogenesis involves DNA changes that enable cells to:provide their own growth signals, ignore growth-inhibitory signals, avoid apoptosis, replicate without limit, sustain angiogenesis, and invade and proliferate in unnatural locations. The metaplastic cells of Barrett's oesophagus are predisposed to develop these cancer hallmarks.

As our knowledge of Gilles de la Tourette's syndrome increases, so does our appreciation for the pathogenic complexity of this disorder and the challenges associated with its treatment. Advances in the neurosciences have led to new models of pathogenesis, whereas clinical studies have reinvigorated early hypotheses. The interdependent roles of genes and environment in disease formation have yet to be fully elucidated. Results of epidemiological studies have prompted debate on how best to characterise and diagnose this disorder. Absence of ideal anti-tic drugs, combined with knowledge that uncomplicated cases of childhood Tourette's syndrome frequently have a favourable outcome, has led to striking changes in care and treatment of patients. This seminar focuses on these changing views and offers a new perspective on our understanding of the pathogenesis of Tourette's syndrome and on principles for treatment of patients with this disorder.

Preterm delivery and its short-term and long-term sequelae constitute a serious problem in terms of mortality, disability, and cost to society. The incidence of preterm delivery, which has increased in recent years, is associated with various epidemiological and clinical risk factors. Results of randomised controlled trials suggest that attempts to reduce these risk factors by use of drugs are limited by side-effects and poor efficacy. An improved understanding of the physiological pathways that regulate uterine contraction and relaxation in animals and people has, however, helped to define the complex processes that underlie parturition (term and preterm), and has led to new scientific approaches for myometrial modulation. The continuing elucidation of the mechanisms that regulate preterm labour, combined with rigorous clinical assessment, offer hope for future solutions.

Over the past 15 years the causative genes of several inherited muscular dystrophies have been identified. These genes encode sarcolemmal, extracellular matrix, sarcomeric, and nuclear envelope proteins. Although the post-translational processing of muscle proteins has a significant role in their correct assembly and function, these processes have not been shown to be primarily involved in the pathogenesis of muscular dystrophies until recently. In the past 18 months, four different forms of inherited muscular dystrophy in human beings have been associated with mutations in genes encoding for putative glycosyltransferases. Aberrant glycosylation of alpha-dystroglycan, an external membrane protein expressed in muscle, brain, and other tissues, is a common feature in these disorders. alpha-dystroglycan is highly glycosylated, its sugar components varying in different tissues and controlling its interaction with extracellular matrix partners. Disrupted glycosylation of alpha-dystroglycan results in a loss of these interactions, giving rise to both progressive muscle degeneration and abnormal neuronal migration in the brain.