Naming the problem that has no name: creating targets for standardized drugs

Many of the most common types of mental health problems that are found in outpatient psychiatric and general medical practices are diffuse, undifferentiated, and amorphous. Before the 1970s this lack of specificity did not conflict with the dominant theories and treatments of the American psychiatric profession or the demands of third party insurers and regulators. However, since that time the legitimacy and solvency of the psychiatric profession has come to depend on the perception that it treats specific disease entities. The establishment of the DSM-III in 1980 provided American psychiatry with many standardized disease entities that could be precisely measured, quantified, and abstracted from their particular contexts. In the late 1980s, these entities became the targets of the new class of psychoactive drugs, the Selective Serotonin Reuptake Inhibitors. Professional, political, economic, and cultural forces that arose in a particular historical era account for the standardization of mental illnesses.     

Introduction: Naming the ineffable

This article does not have an abstract     

Hyperinsulinemic hypoglycemia: effect of epinephrine suppression.

The inhibitory effect of epinephrine on basal and tolbutamide-stimulated insulin release was studied in 5 patients with hyperinsulinemic hypoglycemia. Epinephrine inhibited both basal and tolbutamide-induced insulin release in patients with beta-cell adenoma and hyperplasia, but failed to inhibit insulin release in a patient with beta-cell carcinoma. The inhibition of basal insulin with epinephrine was maximum in patients with beta-cell hyperplasia. This differential inhibitory effect of epinephrine on insulin release may prove to be a useful screening test in the preoperative diagnosis of the nature of the lesion producing hyperinsulinemia.     

Naming dynamic and static actions: neuropsychological evidence.

There has been considerable interest in identifying the neural correlates of action naming, but the bulk of previous work on this topic has utilized static stimuli. Recent research comparing the visual processing of dynamic versus static actions suggests that these two types of stimuli engage largely overlapping neural systems, raising the possibility that the higher-order processing requirements for naming dynamic and static actions might not be very different. To explore this issue in greater depth, we developed the Dynamic Action Naming Test (DANT), which consists of 158 video clips 3-5s in length, for each of which the participant is asked to produce the most appropriate verb. We administered the DANT to 78 brain-damaged patients drawn from our Patient Registry, and to a demographically matched group of 50 normal participants. Out of the 16 patients who performed defectively on the DANT, nearly all (15/16) had damage in the left hemisphere. Lesion analysis indicated that the frontal operculum was the most frequent area of damage in the 15 patients; also, damage to the posterolateral temporal-occipital sector (in and near MT) was specifically related to defective dynamic action naming. Most of the brain-damaged participants (n=71) also received our Static Action Naming Test (SANT), and we found that performances on verb items that were common across the DANT and SANT were highly correlated (R=.91). Moreover, patients who failed the DANT almost invariably also failed the SANT. These findings lend further support to the hypothesis that there is considerable commonality in the neural systems underlying the use of verbs to orally name dynamic and static actions, a conclusion that is in turn compatible with the concept of "representational momentum". Our results also contribute more generally to the rapidly growing field of research on embodied cognition.     

Brave little yeast, please guide us to thebes: sphingolipid function in S. cerevisiae

Sphingolipids typically cover the exoplasmic leaflet of the plasma membrane of eukaryotic cells. They differ from the more abundant glycerophospholipids in that they contain ceramide instead of diacylglycerol as a hydrophobic anchor. Why did nature choose to invent this complex class of lipids, and why do eukaryotic cells follow elaborate remodelling pathways in order to generate dozens to hundreds of different molecular species of sphingolipid, depending on cell type? Yeast may, once again, serve as a model to dissect sphingolipid function at various levels. Almost the complete pathway for sphingolipid synthesis in yeast has been uncovered during the past two decades. More recently, key enzymes in sphingolipid degradation and signalling have been identified. Together with a wealth of genetic data obtained from the characterization of various suppressor mutants, this information now allows for an unprecedented analysis of sphingolipid function in this organism. This overview summarizes recent data on sphingolipid function in cell signalling, their role in the heat-stress response and Ca(2+) homeostasis, and addresses their function in transport of glycosylphosphatidylinositol-anchored proteins.