The effects of fire on soil nitrogen associated with patches of the actinorhizal shrub Ceanothus cordulatus

Nitrogen is a limiting resource in many temperate forests and nitrogen-fixing plants are usually limited to the early stages of post-disturbance succession. In fire-dependent Sierra Nevada forests, however, Ceanothus cordulatus is relatively abundant even in old-growth forest conditions which are at least partly maintained by fire. We conducted a field experiment to determine if soil beneath Ceanothus patches represent `resource islands' of available N which persist after fire. Nine plots containing discrete patches of Ceanothus, Arctostaphylos patula (manzanita; chosen as a non N-fixing reference species), and bare forest floor were subjected to either a low-intensity (n=3) or high-intensity (n=3) bum treatment, or remained unburned as controls (n=3). Soil temperatures during the bum were monitored by a network of thermocouples placed at the surface of the mineral soil and at ca. 10 cm depths. Soil samples were collected from the organic horizon, 0-10 cm and 15-25 cm depths within each patch type immediately before burning and 2 days, and 6, and 11 months after. Soil moisture, total C and N, and ammonium and nitrate concentrations were determined in the laboratory. Before the burn, Ceanothus patches were significantly enriched in total and inorganic N in the organic horizon relative to the other patch types. A sharp increase in inorganic N was observed in all patch types and depths immediately following burning, but by 6 months after the burn, Ceanothus patches were significantly enriched relative to the surrounding patch types and remained so at months. Resprouting Ceanothus patches will continue to be an important source of a limiting nutrient in this fire-prone ecosystem.     

Sexual health education interventions for young people: a methodological review.

OBJECTIVES--To locate reports of sexual health education interventions for young people, assess the methodological quality of evaluations, identify the subgroup with a methodologically sound design, and assess the evidence with respect to the effectiveness of different approaches to promoting young people''s sexual health. DESIGN--Survey of reports in English by means of electronic databases and hand searches for relevant studies conducted in the developed world since 1982. Papers were reviewed for eight methodological qualities. The evidence on effectiveness generated by studies meeting four core criteria was assessed. Judgments on effectiveness by reviewers and authors were compared. PAPERS--270 papers reporting sexual health interventions. MAIN OUTCOME MEASURE--The methodological quality of evaluations. RESULTS--73 reports of evaluations of sexual health interventions examining the effectiveness of these interventions in changing knowledge, attitudes, or behavioural outcomes were identified, of which 65 were separate outcome evaluations. Of these studies, 45 (69%) lacked random control groups, 44 (68%) failed to present preintervention and 38 (59%) postintervention data, and 26 (40%) omitted to discuss the relevance of loss of data caused by drop outs. Only 12 (18%) of the 65 outcome evaluations were judged to be methodologically sound. Academic reviewers were more likely than authors to judge studies as unclear because of design faults. Only two of the sound evaluations recorded interventions which were effective in showing an impact on young people''s sexual behaviour. CONCLUSIONS--The design of evaluations in sexual health intervention needs to be improved so that reliable evidence of the effectiveness of different approaches to promoting young people''s sexual health may be generated.     

Growth requirements and neoplastic transformation of two types of normal human breast epithelial cells derived from reduction mammoplasty

Summary A chemically defined culture medium was developed to support the growth of two distinctly different types of normal human breast epithelial cells (HBEC) derived from reduction mammoplasty. Type I cells expressed luminal epithelial cell markers and were deficient in gap junctional intercellular communication (GJIC), whereas Type II cells expressed basal epithelial cell markers and were efficient in GJIC. In this study, we examined and compared the growth factor and hormone requirements of these two types of cells and a series of cell lines that were obtained by sequential transfection with SV40 DNA (extended lifespan, nontumorigenic), treatment with 5-bromodeoxyuridine (BrdU)/black light (immortal and weakly tumorigenic), and infection of a virus carrying the neu oncogene (highly tumorigenic). Growth of Type I cells was inhibited by withdrawing epidermal growth factor (EGF), hydrocortisone (HC), or insulin (INS) from the culture media, but was enhanced by fetal bovine serum (FBS) supplementation. Growth of Type II cells was inhibited by withdrawal of EGF, HC, or INS from the media, and was inhibited by FBS supplementation. Withdrawal of human transferrin (HT) or 17β-estradiol (E₂) from the media did not alter the growth of Type I or Type II cells. SV40 transfected Type I cell lines still required EGF, HC, or INS for optimal growth. However, the highly tumorigenic cell line did not show a growth dependence on EGF, HC, or INS but did appear to require HT and 3,3′,5-triiodo-D.L. thyronine (T₃) for optimal growth. In addition, FBS stimulated the growth of these cell lines. Thus, this study shows that Type I HBEC are distinctly different from Type II HBEC in growth response to FBS and that neoplastically transformed Type I cells could become growth factor and hormone independent.     

Association of beta-arrestin with G protein-coupled receptors during clathrin-mediated endocytosis dictates the profile of receptor resensitization.

Resensitization of G protein-coupled receptors (GPCRs) following agonist-mediated desensitization is a necessary step for maintaining physiological responsiveness. However, the molecular mechanisms governing the nature of GPCR resensitization are poorly understood. Here, we examine the role of beta-arrestin in the resensitization of the beta(2) adrenergic receptor (beta(2)AR), known to recycle and resensitize rapidly, and the vasopressin V2 receptor (V2R), known to recycle and resensitize slowly. Upon agonist activation, both receptors recruit beta-arrestin to the plasma membrane and internalize in a beta-arrestin- and clathrin-dependent manner. However, whereas beta-arrestin dissociates from the beta(2)AR at the plasma membrane, it internalizes with the V2R into endosomes. The differential trafficking of beta-arrestin and the ability of these two receptors to dephosphorylate, recycle, and resensitize is completely reversed when the carboxyl-terminal tails of these two receptors are switched. Moreover, the ability of beta-arrestin to remain associated with desensitized GPCRs during clathrin-mediated endocytosis is mediated by a specific cluster of phosphorylated serine residues in the receptor carboxyl-terminal tail. These results demonstrate that the interaction of beta-arrestin with a specific motif in the GPCR carboxyl-terminal tail dictates the rate of receptor dephosphorylation, recycling, and resensitization, and thus provide direct evidence for a novel mechanism by which beta-arrestins regulate the reestablishment of GPCR responsiveness.     

Stage-specific expression of Smad2 and Smad3 during folliculogenesis

Paracrine and autocrine growth factors can affect many different aspects of ovarian follicle development. Many members of the transforming growth factor beta (TGFbeta) family of growth factors and their receptors are expressed in developing follicles. However, the presence and function of the family of the TGFbeta signaling molecules known as Smads have not been evaluated during follicle development. We have demonstrated that two Smad family members that function as mediators for both activin and TGFbeta are expressed in granulosa cells of preantral follicles but not in large antral follicles. Smad2 expression, but not Smad3 expression, returns in luteal cells. Both Smad2 and Smad3 are translocated to the nucleus of granulosa cells in response to treatment with either TGFbeta or activin. However, Smad2 is more responsive to activin stimulation, and Smad3 is more responsive to TGFbeta stimulation. Stage-specific expression and differing ligand sensitivity of signaling molecules may work together to allow different effects of TGFbeta family ligands using the same signaling pathways over the course of follicular development.