Psychosomatic symptoms,stress, and modernization: A model

The quantity of research on the effects of stress on disease has increased substantially in recent years, but little effort has been devoted to examining the effects of cultural influences in the stress process. A model is proposed in this paper in which cultural context exerts a modifying influence on the relationship between sociocultural stressors and psychosomatic symptoms, specifically in the context of modernization. In change situations involving increasing modernization there is increased differentiation in systems of social stratification within a community, due to increased potential for upward social mobility. The individuals who are upwardly mobile adopt a particular style of life, involving the acquisition of western consumer goods, as symbolic of their success. Lower class individuals strive to attain this same style of life as a claim to a higher status social identity, but their lower economic condition results in stressful incongruities and higher psychosomatic symptoms. Individuals who are successful in upward mobility are confronted by a different set of stressors that are primarily intrapsychic in nature. Events and circumstances perceived as threats to their self-identity are related to more psychosomatic symptoms. Thus, the meaning of specific stressors changes depending on the sociocultural context of the individual, and this meaning serves as a bridge between environmental circumstances and physiological outcomes. This model receives substantial empirical support in two field studies. Limitations of the model and implications for future research are discussed.Research in St. Lucia was supported by the Connecticut Research Foundation and the University of Connecticut Health Center. Research in the U.S. was supported by Research Grant MH 33943 from the Center for the Study of Minority Group Mental Health, National Institute of Mental Health. Drs. Arthur Kleinman, Lee Badger, H. B. M. Murphy, James Bindon, and Laurence Watkins kindly commented on previous drafts of this paper. Dr. Michael Murphy deserves a special note of gratitude for reading several drafts of the paper and for patiently sitting through several lengthy discussions of it. I alone am responsible for the errors and shortcomings.     

Structural and functional abnormality of ectopic testes in rats

Some males of a mutant strain of King-Holtzman rats exhibit an anomalous heritable defect manifested as either unilateral or bilateral ectopic testes. In the adult, these testes contain seemingly immature Sertoli and Leydig cells, seminiferous tubules greatly reduced in diameter, and exhibit arrested spermatogenesis. Thus, the affected testis is essentially sterile. An inability to produce normal amounts of testosterone and androstenedione by these gonads is probably a reflection of changes that have been effected in their Leydig cells. Thus, this study suggests that abnormal function of the Leydig and Sertoli cells and seminiferous tubule failure in these mutant animals result from the physiologically cryptorchid condition.     

The genera Amblostoma,Lanium, and Stenoglossum (Orchidaceae)

The generaAmblostoma, Lanium, andStenoglossum are discussed, and it is concluded that all three should be included inEpidendrum.Lanium is treated as a section, and new names are proposed for two species whose epithets are preoccupied inEpidendrum: E. macrum (forAmblostoma gracile) andE. stiliferum (forLanium subulatum).     

Culturing Puccinia coronata on a Cell Monolayer of the Avena sativa Coleoptile

A culture of Puccinia coronata on an epidermal cell monolayer dissected from the Avena sativa caleoptile is described. To induce fungal development, infection structure formation had to be induced with a heat treatment. The host cells were fed with 1 % sucrose (or glucose or manitol) to sustain fungal growth. Under these conditions, normal development of hyphae, haustoria with haustorial mother cells and uredospores occurred. Uredospores had normal infectivity.     

Ceramide 1-phosphate, a novel phospholipid in human leukemia (HL-60) cells. Synthesis via ceramide from sphingomyelin

Prior studies demonstrated that conversion of sphingomyelin to ceramide via sphingomyelinase action resulted in the generation of free sphingoid bases and inactivation of protein kinase C in human leukemia (HL-60) cells (Kolesnick, R. N. (1989) J. Biol. Chem. 264, 7617-7623). The present studies define the novel phospholipid ceramide 1-phosphate in these cells and present evidence for formation of this compound by preferential utilization of ceramide derived from spingomyelin. A ceramide 1-phosphate standard, prepared enzymatically via diacylglycerol kinase, was utilized for localization. In cells labeled to equilibrium with 32Pi to label the head group of the molecule, the basal ceramide 1-phosphate level was 30 +/- 2 pmol/10(6) cells. Generation of ceramide via the use of exogenous sphingomyelinase resulted in time- and concentration-dependent formation of ceramide 1-phosphate. As little as 3.8 x 10(-5) units/ml was effective and a 3-fold increase was observed with a maximal concentration of 3.8 x 10(-2) units/ml; ED50 approximately 2 x 10(-4) units/ml. This effect was observed by 5 min and maximal at 30 min. Similarly, in cells labeled with [3H]serine to probe the sphingoid base backbone, the basal level of ceramide 1-phosphate was 39 +/- 5 pmol/10(6) and increased 2.5-fold with sphingomyelinase; ED 50 approximately 5 x 10(-5) units/ml. To determine the source of the phosphate moiety, studies were performed with cells short term labeled with 32Pi and resuspended in medium without radiolabel. Under these conditions, sphingomyelin was virtually unlabeled. Nevertheless, sphingomyelin (3.8 x 10(-2) units/ml) induced a 12-fold increase in radiolabel incorporation, suggesting ceramide 1-phosphate formation occurred via ceramide phosphorylation. This event appeared specific for ceramide derived from sphingomyelin since ceramide from glycosphingolipids was not converted to ceramide 1-phosphate. In sum, these studies demonstrate the novel phospholipid ceramide 1-phosphate in HL-60 cells and suggest the possibility that a path exists from sphingomyelin to ceramide 1-phosphate via the phosphorylation of ceramide.