With increasing realization of the extent and consequences of depressive comorbidity in epilepsy, much human and animal research has focussed on its explanation. Recent studies tackle all three explanatory possibilities: that epilepsy leads to depression; that depression contributes to causation of epilepsy; or that shared causal factors or processes lead to both epilepsy and depression. These are not mutually exclusive; all three probably contribute. Animal models have provided many insights into the interplay between epilepsy and depressive-like behaviours, both associations and mechanisms. Notably, experimental stress potently affects epilepsy endpoints, as well as depressive-like behaviour, having actions at multiple relevant biological levels. Current general (nonepilepsy) depression modelling is biopsychosocial in nature, integrating insights from genetics, epidemiology, psychology and neurobiology; and takes a lifespan developmental perspective, as the causation of depression is a multistage process with origins in early life - as is the case for many epilepsies. These perspectives need to be more fully adopted in the epilepsy/depression fi eld.

A prime diffi culty facing all people with epilepsy is dealing with the stigma which is associated with it in almost all societies. Stigma arises from the perception of difference from the norm, particularly powerful when that difference is not understood. This arises from the uniquely human need for predictability, resulting from the ability to think abstractly, and thus to surmise the future. A failure of expectation, or the uncertainty caused by an inability to predict, causes insecurity, or a “fear of the unknown”, which we try to reduce by rejecting its perceived cause. Stigma can be attached to themselves or their epilepsy by the person with epilepsy, as well as by others about them. Such discomfort is accentuated by perceived inconsistency between the familiar and unfamiliar. Discrimination occurs as a result of stigma, causing people with epilepsy to be preoccupied with epilepsy and expending much psychological energy on disclosure anxiety, vigilance and a consequent uncertainty of identity. This can result in lower self-esteem, self-fulfi lling prophecies, self-blame and self-rejection, and ultimately dehumanisation. The most effective means of overcoming stigma is by contact between people with epilepsy and those holding the stigma against them. Such contact must be on an equal status footing, repeated and consistent, require interdependence, be socially approved and enjoyable, contradict the stereotypes held, and be with individuals seen as representative of the out-group as a whole. Hence familiarity, rather than breeding contempt, produces the predictability and consequent comfort and acceptability of the normal.

In this paper, the fundamental assumptions of ethics, values and individual moral agency were reviewed so as to arrive at a position that reconciles the tension between universal moral codes and the contextual influences of different psychiatric professional groups. The moral imperatives that merge from the Nuremburg 'Doctor's trial' and the subsequent allegations of abuses of power by psychiatrists under other authoritarian regimes necessitated the development of universal proclamations of ethical conduct. In light of this tension, the argument that a middle ground of negotiated morality according to basic Hippocratic notions and respect for life can become the foundation of binding moral absolutes in psychiatric ethics. It is neither credible nor possible to assert broader ethical maxims within the psychiatric profession, given the different contexts in which professional groups practice their craft. In conclusion, the empirical studies of the value systems of different psychiatric professions should be elaborated and that these be compared to identify the common ground that might form the basis of a global code of ethics for psychiatry.

No abstract available.

Colorectal cancer is becoming increasingly common in Asian countries and still remains the second leading cause of cancer deaths in the United States. Efforts to prevent colon cancer have targeted early detection through screening and chemoprevention. For the last ten years our laboratory has utilized an in vivo screening assay for the testing of potential cancer preventives for colon cancer. We have conducted investigations on over 150 compounds including many with botanical or herbal origins. As part of our program on natural products we have examined a number of herbal and botanical products in the aberrant crypt foci (ACF) assay including Korean red ginseng powder, green tea catechins, curcumin from the Indian culinary spice, tumeric, compounds from garlic and onion, resveratrol from red grapes, among others. In the ginseng experiments groups of 10 F344 rats were fed ginseng powder at a dose of 0.5 g/kg or 2 mg/kg for 5 weeks. During weeks 2 and 3 rats were injected with 10 mg/kg azoxymethane to induce ACF. Controls (n=10) did not receive azoxymethane (AOM). Rats were killed by CO2 overdose and ACF counted in the rat colon. In 8 week post-initiation experiments ginseng powder inhibited the progression of established ACF, indicating a cytostatic effect. This may be due to an anti-inflammatory effect. There is a body of literature that suggests that compounds in wine, tumeric, and tea inhibit cyclooxygenases, thus reducing prostaglandin-mediated effects on the colon. As colon tumors have been shown to highly express COX-2 protein, and given, that many NSAID drugs also suppress COX-1, it is tempting to speculate that herbal products that inhibit one or both forms of the COX enzyme will be effective agents for the prevention of cancer in man.
Animal ; Anticarcinogenic Agents/*pharmacology ; Colonic Neoplasms/pathology/*prevention & control ; Disease Models, Animal ; Human ; Korea ; *Panax ; Precancerous Conditions/pathology/*prevention & control ; Rats ; Rats, Inbred F344

Cultural Characteristics ; Far East ; Health Promotion ; Humans ; Public Health ; Sleep ; Sleep Wake Disorders ; diagnosis ; therapy

It is standard practice, whenever a researcher finds a new gene, to search databases for genes that have a similar sequence. It is not standard practice, whenever a researcher finds a new gene, to search for genes that have similar expression (co-expression). Failure to perform co-expression searches has lead to incorrect conclusions about the likely function of new genes, and has lead to wasted laboratory attempts to confirm functions incorrectly predicted. We present here the example of Glia Maturation Factor gamma (GMF-gamma). Despite its name, it has not been shown to participate in glia maturation. It is a gene of unknown function that is similar in sequence to GMF-beta. The sequence homology and chromosomal location led to an unsuccessful search for GMF-gamma mutations in glioma. We examined GMF-gamma expression in 1432 human cDNA libraries. Highest expression occurs in phagocytic, antigen-presenting and other hematopoietic cells. We found GMF-gamma mRNA in almost every tissue examined, with expression in nervous tissue no higher than in any other tissue. Our evidence indicates that GMF-gamma participates in phagocytosis in antigen presenting cells. Searches for genes with similar sequences should be supplemented with searches for genes with similar expression to avoid incorrect predictions.
Animals ; Cell Line ; Cloning, Molecular ; DNA, Complementary ; metabolism ; Databases as Topic ; Expressed Sequence Tags ; Gene Expression ; Gene Library ; Glia Maturation Factor ; genetics ; Humans ; RNA, Messenger ; metabolism ; Rats ; Sequence Analysis, DNA

Hematopoietic Stem Cell Transplantation ; Humans ; Multiple Myeloma ; pathology ; therapy ; Neoplasm Staging ; Transplantation, Autologous