Biomedical subjects

J M Oliver

Publications and source records attributed to J M Oliver.

At least 37 records · Page 2Linked to original sources

PubMed2000

Tricuspid insufficiency and interatrial septum rupture: a cause of persistent systemic hypoxemia after blunt chest trauma.

The case of a 45-year-old man with severe tricuspid insufficiency and interatrial septum rupture caused by a car accident is described. The patient had a rupture of the anterior papillary muscle of the tricuspid valve and right-to-left shunt through an interatrial defect with severe hypoxemia that was difficult to distinguish from that caused by pulmonary damage. Transesophageal echocardiography was extremely useful for early diagnosis.

Echocardiography, Transesophageal↗

PubMed2000

Negative regulation of FcepsilonRI signaling by FcgammaRII costimulation in human blood basophils.

BACKGROUND: Signaling through the antigen receptors of human B and T cells and the high-affinity IgE receptor FcepsilonRI of rodent mast cells is decreased by cross-linking these receptors to the low-affinity IgG receptor FcgammaRII. The inhibition is thought to involve the tyrosine phosphorylation of immunoreceptor tyrosine-based inhibitory motifs (ITIMs) in the FcgammaRIIB cytoplasmic tail, creating binding sites for SH2-containing protein (Src homology domain containing protein tyrosine phosphatase 1 and 2 [SHP-1, SHP-2]) and/or lipid (SH2 domain-containing polyphosphatidyl-inositol 5-phosphatase) phosphatases that oppose activating signals from the costimulated antigen receptors. OBJECTIVE: In human basophils and mast cells FcepsilonRI signaling generates mediators and cytokines responsible for allergic inflammation. We proposed to determine whether FcepsilonRI signaling is inhibited by FcgammaRII costimulation in human basophils and to explore the underlying mechanism as an approach to improving the treatment of allergic inflammation. METHODS: FcgammaR expression on human basophils was examined using flow cytometry and RT-PCR analysis. FcgammaRII/FcepsilonRI costimulation was typically accomplished by priming cells with anti-dinitrophenol (DNP) IgE and anti-DNP IgG and stimulating with DNP-BSA. Phosphatases were identified by Western blotting, and their partitioning between membrane and cytosol was determined by cell fractionation. Biotinylated synthetic peptides and phosphopeptides corresponding to the FcgammaRIIB ITIM sequence were used for adsorption assays. RESULTS: We report that peripheral blood basophils express FcgammaRII (in both the ITIM-containing FcgammaRIIB and the immunoreceptor tyrosine-based activation motif-containing FcgammaRIIA forms) and that costimulating FcgammaRII and FcepsilonRI inhibits basophil FcepsilonRI-mediated histamine release, IL-4 production, and Ca(2+) mobilization. The inhibition of basophil FcepsilonRI signaling by FcgammaRII/FcepsilonRI costimulation is linked to a significant decrease in Syk tyrosine phosphorylation. Human basophils express all 3 SH2-containing phosphatases. CONCLUSIONS: Evidence that FcgammaRII/FcepsilonRI costimulation induces SHP-1 translocation from the cytosolic to membrane fractions of basophils and that biotinylated synthetic peptides corresponding to the phosphorylated FcgammaRIIB ITIM sequence specifically recruit SHP-1 from basophil lysates particularly implicates this protein phosphatase in the negative regulation of FcepsilonRI signaling by costimulated FcgammaRII.

Basophils↗

PubMed1999

Laminin and beta1 integrins are crucial for normal mammary gland development in the mouse.

We have examined the role of integrin-extracellular matrix interactions in the morphogenesis of ductal structures in vivo using the developing mouse mammary gland as a model. At puberty, ductal growth from terminal end buds results in an arborescent network that eventually fills the gland, whereupon the buds shrink in size and become mitotically inactive. End buds are surrounded by a basement membrane, which we show contains laminin-1 and collagen IV. To address the role of cell-matrix interactions in gland development, pellets containing function-perturbing anti-beta1 integrin, anti-alpha6 integrin, and anti-laminin antibodies respectively were implanted into mammary glands at puberty. Blocking beta1 integrins dramatically reduced both the number of end buds per gland and the extent of the mammary ductal network, compared with controls. These effects were specific to the end buds since the rest of the gland architecture remained intact. Reduced development was still apparent after 6 days, but end buds subsequently reappeared, indicating that the inhibition of beta1 integrins was reversible. Similar results were obtained with anti-laminin antibodies. In contrast, no effect on morphogenesis in vivo was seen with anti-alpha6 integrin antibody, suggesting that alpha6 is not the important partner for beta1 in this system. The studies with beta1 integrin were confirmed in a culture model of ductal morphogenesis, where we show that hepatocyte growth factor (HGF)-induced tubulogenesis is dependent on functional beta1 integrins. Thus integrins and HGF cooperate to regulate ductal morphogenesis. We propose that both laminin and beta1 integrins are required to permit cellular traction through the stromal matrix and are therefore essential for maintaining end bud structure and function in normal pubertal mammary gland development.

Animals↗

PubMed1999

Lyn dissociation from phosphorylated Fc epsilon RI subunits: a new regulatory step in the Fc epsilon RI signaling cascade revealed by studies of Fc epsilon RI dimer signaling activity.

Cross-linking the heterotrimeric (alpha beta gamma 2) IgE receptor, Fc epsilon RI, of mast cells activates two tyrosine kinases: Lyn, which phosphorylates beta and gamma subunit immunoreceptor tyrosine-based activation motifs, and Syk, which binds gamma-phospho-immunoreceptor tyrosine-based activation motifs and initiates cellular responses. We studied three Fc epsilon RI-dimerizing mAbs that maintain similar dispersed distributions over the surface of RBL-2H3 mast cells but elicit very different signaling responses. Specifically, mAb H10 receptor dimers induce very little inositol 1,4,5-trisphosphate synthesis, Ca2+ mobilization, secretion, spreading, ruffling, and actin plaque assembly, whereas dimers generated with the other anti-Fc epsilon RI mAbs induce responses that are only modestly lower than that to multivalent Ag. H10 receptor dimers activate Lyn and support Fc epsilon RI beta and gamma subunit phosphorylation but are poor Syk activators compared with Ag and the other anti-Fc epsilon RI mAbs. H10 receptor dimers have two other distinguishing features. First, they induce stable complexes between activated Lyn and receptor subunits. Second, the predominant Lyn-binding phospho-beta isoform found in mAb H10-treated cells is a less tyrosine phosphorylated, more electrophoretically mobile species than the predominant isoform in Ag-treated cells that does not coprecipitate with Lyn. These studies implicate Lyn dissociation from highly phosphorylated receptor subunits as a new regulatory step in the Fc epsilon RI signaling cascade required for Syk activation and signal progression.

Animals↗

PubMed1999

The hope construct, will, and ways: their relations with self-efficacy, optimism, and general well-being.

This investigation (N = 204) examined (a) the relations between the hope construct (Snyder, Harris et al., 1991; Snyder, Irving, & Anderson, 1991) and its two essential components, "will" and "ways," and the related constructs of self-efficacy and optimism; and (b) the ability of hope, self-efficacy, and optimism to predict general well-being. Maximum-likelihood factor analysis recovered will, ways, self-efficacy, and optimism as generally distinct and independent entities. Results of multiple regression analyses predicting well-being indicated that (a) hope taken as a whole predicts unique variance independent of self-efficacy and optimism, (b) will predicts unique variance independent of self-efficacy, and (c) ways predicts unique variance independent of optimism. Overall, findings suggest that will, ways, self-efficacy, and optimism are related but not identical constructs.

Adolescent↗

PubMed1999

Syk deficiency in nonreleaser basophils.

BACKGROUND: Peripheral blood basophils from 10% to 20% of donors fail to degranulate in response to cross-linking the high-affinity IgE receptor FcepsilonRI. The molecular mechanisms underlying the nonreleaser phenotype have not been established. OBJECTIVES: Our aim was to compare the expression of FcepsilonRI-associated protein tyrosine kinases between nonreleaser and releaser basophils. METHODS: With use of Western blotting we investigated Syk and Lyn protein levels in highly purified basophils from 3 anti-IgE nonreleasers and 2 releasers. RESULTS: We identified 3 healthy nonatopic donors whose nonreleaser basophils express FcepsilonRI normally but fail to express protein for the tyrosine kinase Syk, which is implicated in the initiation of FcepsilonRI-mediated secretion. Protein levels for the tyrosine kinase Lyn are somewhat reduced but not absent in nonreleaser basophils. Levels of Lyn and Syk protein are similar in B cells, eosinophils, and neutrophils from releaser and nonreleaser donors. During these studies one nonreleaser "converted" into a releaser with concomitant basophil Syk expression. CONCLUSION: The absence of detectable Syk could explain the nonreleaser phenotype of basophils from some donors.

Adolescent↗

PubMed1998

MEK and ERK activation in ras-disabled RBL-2H3 mast cells and novel roles for geranylgeranylated and farnesylated proteins in Fc epsilonRI-mediated signaling.

Cross-linking the high affinity IgE receptor Fc epsilonRI of basophils and mast cells activates receptor-associated protein-tyrosine kinases and stimulates a signaling cascade leading to secretion, ruffling, spreading, and cytokine production. Previous evidence that the pan-prenylation inhibitor lovastatin blocks Ag-stimulated Ca2+ influx, secretion, and membrane/cytoskeletal responses implicated isoprenylated proteins in the Fc epsilonRI-coupled signaling cascade but could not distinguish between contributions of C15 (farnesylated) and C20 (geranylgeranylated) species. Here we establish concentrations of lovastatin and the farnesyl-specific inhibitor BZA-5B that inhibit the farnesylation and Ag-induced activation of Ras species in RBL-2H3 cells (H-Ras, K-RasA, and K-RasB). These inhibitors have little effect on tyrosine kinase activation, which initiates Fc epsilonRI signaling. Although Ras is disabled, only lovastatin substantially blocks Raf-1 activation, and neither inhibitor affects mitogen-activated protein kinase kinase/extracellular signal regulated kinase kinase (MEK) or ERK1/ERK2 activation. Thus, the pathway to Fc epsilonRI-mediated MEK/ERK and ERK activation can apparently bypass Ras and Raf-1. Predictably, only lovastatin inhibits Ag-induced ruffling, spreading, and secretion, previously linked to geranylgeranylated Rho and Rab family members. Additionally, only lovastatin inhibits phospholipase Cgamma-mediated inositol (1,4,5) trisphosphate production, sustained Ca2+ influx, and Ca2+-dependent IL-4 production, suggesting novel roles for geranylgeranylated (lovastatin-sensitive, BZA-5B-insensitive) proteins in Fc epsilonRI signal propagation. Remarkably, BZA-5B concentrations too low to inactivate Ras reduce the lag time to Ag-induced Ca2+ stores release and enhance secretion. These results link a non-Ras farnesylated protein(s) to the negative regulation of Ca2+ release from intracellular stores and secretion. We identified no clear role for Ras in Fc epsilonRI-coupled signaling but suggest its involvement in mast cell growth regulation based on the inhibition of cell proliferation by both BZA-5B and lovastatin.

Alkyl and Aryl Transferases↗

PubMed1998

The identification and characterization of umbilical cord blood-derived human basophils.

Cross-linking allergen-specific immunoglobin E on human peripheral blood basophils results in the release of histamine and other inflammatory mediators that initiate allergy and asthma. The signaling pathways leading from IgE binding to mediator release have not been well established, mainly due to the difficulty in obtaining adequate numbers of highly purified basophils. It was the goal of this study to easily obtain Fc epsilonRI-positive human basophils in high yield and purity for studies of signal transduction pathways. We describe an in vitro culture system in which pulsing normal human cord blood leukocytes with interleukin-3 (IL-3) for 3-4 h followed by incubation in medium with fetal bovine serum generates a cell population that is predominately Fc epsilonRI positive between 14 and 28 days of culture. These cells resemble peripheral blood basophils when examined by light and electron microscopy. Like normal blood basophils, they express the integrins, CD11b, CD18, CD29, and CD49d. A majority of the IL-3-pulsed cells also express a marker recognized by the basophil-specific antibody, 2D7. Fc epsilonRI cross-linking results in a time and dose-dependent release of histamine. Fc epsilonRI cross-linking also stimulates protein-tyrosine phosphorylation, thought to be the first event leading to the IgE-mediated activation of peripheral blood basophils. These studies establish cord blood as an accessible source from which basophil-like cells can be developed to examine Fc epsilonRI-mediated signal transduction.

Allergens↗

PubMed1998

Identification of the Fc epsilonRI-activated tyrosine kinases Lyn, Syk, and Zap-70 in human basophils.

BACKGROUND: In human blood basophils, cross-linking the high-affinity IgE receptor Fc epsilonRI with multivalent antigen activates a signaling pathway leading to Ca2+ mobilization, actin polymerization, shape changes, secretion, and cytokine production. METHODS AND RESULTS: The role of tyrosine kinases in human Fc epsilonRI signaling was explored by using human basophils isolated by Percoll gradient centrifugation followed by negative and/or positive selection with antibody-coated magnetic beads. Fc epsilonRI cross-linking of more than 95% pure basophil preparations activates the protein-tyrosine kinases Lyn and Syk, previously linked to Fc epsilonRI-coupled rodent mast cell activation, as well as Zap-70, previously implicated in T-cell receptor signaling, and causes the tyrosine phosphorylation of multiple proteins. The presence of Lyn, Syk, and Zap-70 in basophils was confirmed by Western blotting in lysates of highly purified basophils and independently by confocal fluorescence microscopy in cells labeled simultaneously with kinase-specific antibodies and with the basophil-specific antibody 2D7. Comparable amounts of Lyn and Syk were found in basophils and B cells, whereas T cells appear to have greater amounts of Zap-70 than basophils. The tyrosine kinase inhibitor piceatannol spares IgE-mediated Lyn activation but inhibits IgE-induced Syk and Zap-70 activation as well as overall protein tyrosine phosphorylation and secretion. Overall protein-tyrosine phosphorylation increases steadily over a range of anti-IgE concentrations that are low to optimal for secretion. However, tyrosine phosphorylation continues to increase at high anti-IgE concentrations that elicit very little secretion (the characteristic high-dose inhibition of secretion). CONCLUSIONS: Our data demonstrate the association of anti-IgE-stimulated, protein-tyrosine phosphorylation by a cascade of tyrosine kinases, including Zap-70 as well as Lyn and Syk, with the initiation of Fc epsilonRI-mediated signaling in human basophils.

Basophil Degranulation Test↗

PubMed1998

Calcium-dependent clustering of inositol 1,4,5-trisphosphate receptors.

Rat basophilic leukemia (RBL-2H3) cells predominantly express the type II receptor for inositol 1,4,5-trisphosphate (InsP3), which operates as an InsP3-gated calcium channel. In these cells, cross-linking the high-affinity immunoglobulin E receptor (FcepsilonR1) leads to activation of phospholipase C gamma isoforms via tyrosine kinase- and phosphatidylinositol 3-kinase-dependent pathways, release of InsP3-sensitive intracellular Ca2+ stores, and a sustained phase of Ca2+ influx. These events are accompanied by a redistribution of type II InsP3 receptors within the endoplasmic reticulum and nuclear envelope, from a diffuse pattern with a few small aggregates in resting cells to large isolated clusters after antigen stimulation. Redistribution of type II InsP3 receptors is also seen after treatment of RBL-2H3 cells with ionomycin or thapsigargin. InsP3 receptor clustering occurs within 5-10 min of stimulus and persists for up to 1 h in the presence of antigen. Receptor clustering is independent of endoplasmic reticulum vesiculation, which occurs only at ionomycin concentrations >1 microM, and maximal clustering responses are dependent on the presence of extracellular calcium. InsP3 receptor aggregation may be a characteristic cellular response to Ca2+-mobilizing ligands, because similar results are seen after activation of phospholipase C-linked G-protein-coupled receptors; cholecystokinin causes type II receptor redistribution in rat pancreatoma AR4-2J cells, and carbachol causes type III receptor redistribution in muscarinic receptor-expressing hamster lung fibroblast E36(M3R) cells. Stimulation of these three cell types leads to a reduction in InsP3 receptor levels only in AR4-2J cells, indicating that receptor clustering does not correlate with receptor down-regulation. The calcium-dependent aggregation of InsP3 receptors may contribute to the previously observed changes in affinity for InsP3 in the presence of elevated Ca2+ and/or may establish discrete regions within refilled stores with varying capacity to release Ca2+ when a subsequent stimulus results in production of InsP3.

Animals↗

PubMed1997

Cooperation between the Fc epsilonR1 and formyl peptide receptor signaling pathways in RBL(FPR) cells: the contribution of receptor-specific Ca2+ mobilization responses.

RBL(FPR) mast cells express the tyrosine kinase-coupled IgE receptor, Fc epsilonR1, and the G-protein-coupled formyl peptide receptor, FPR. Fc epsilonR1 crosslinking causes Ca2+ stores release, Ca2+ influx, Ins(1,4,5)P3 production and secretion. FPR ligation also mobilizes Ca2+, but without measurable Ins(1,4,5)P3 production or secretion. Co-stimulating the FPR and Fc epsilonR1 induces more Ins(1,4,5)P3 production and secretion than Fc epsilonR1 cross-linking alone. Costimulation also produces more rapid and sustained Ca2+ responses than are generated by Fc epsilonR1 activation alone. We identified multiple differences between the FPR- and Fc epsilonR1-coupled Ca2+ responses, including a more rapid Ca2+ spike response to FPR ligation; intracellular Ca2+ stores that are empty following Fc epsilonR1 crosslinking but partially full following FPR activation; a more sustained Ca2+ influx response to Fc epsilonR1 crosslinking; and the immediate inhibition of stimulated Ca2+ influx by FPR antagonists but not by monovalent ligand that terminates Fc epsilonR1 crosslinking. We hypothesize that the interaction of receptor-specific Ca2+ mobilization pathways contributes to the FPR-mediated potentiation of Fc epsilonR1-coupled secretion.

Animals↗

PubMed1997

Relationship of ligand-receptor dynamics to actin polymerization in RBL-2H3 cells transfected with the human formyl peptide receptor.

The human formyl peptide receptor (FPR) expressed in RBL-2H3 transfectants (RBL[FPR]) behaves qualitatively like the FPR expressed by neutrophils except that it causes sustained F-actin accumulation and cell shape change responses on formyl peptide stimulation. These sustained responses were not accounted for by changes in the transfected receptor's ability to interact with ligand or by receptor density. Signal transduction pathways of transfected and neutrophil FPRs are apparently similar. In transfected cells, dissociation of ligand is sensitive to guanine nucleotide, the G protein is pertussis toxin-sensitive, FPR and G protein appear to be precoupled, the F-actin response is stimulated with the same dose-response profile as in neutrophils, and the F-actin accumulation response is directly regulated by the FPR, even long after initial stimulation. Potentially significant differences between neutrophil and transfected FPR were found when receptor processing was measured. In neutrophils, practically 100% of the FPR is converted to forms that dissociate slowly from ligand and are inactive in signal transduction within 2 min of ligand stimulation. By contrast, 20% or more of transfected FPR remains rapidly dissociating even 5 min after stimulation. Although 80% of neutrophil FPR is internalized by 5 min after stimulation, transfected FPR appears to plateau at 50-60% internalized. Because actin responses in neutrophils are regulated by a small number of active receptors, the inefficiency of receptor inactivation in RBL(FPR) transfectants may account for the prolonged F-actin accumulation response.

Actins↗

PubMed1997

[Prosthetic endocarditis and splenic abscess caused by Clostridium clostridiformis].

We report the first case of Clostridium clostridiformis endocarditis in a 71 year old man with an aortic prosthetic valve. He was febrile with left upper quadrant pain and left lower lobe infiltrate in chest X ray. The diagnosis was made by gram-positive bacilli grown from three blood cultures. Transthoracic and transesophageal echocardiogram showed a paraaortic abscess. A computed tomographic scan of the abdomen revealed a large splenic abscess. He received penicillin G 4 million units every 4 hours intravenously. A successful percutaneous drainage guided computed tomographic scan was performed. The patient remained febrile and a new computed tomographic scan of the abdomen revealed residual splenic abscess. A splenectomy was performed. The patient defervesced on the second day of surgery and remained afebrile during the remainder of his hospitalization. He has returned for medical follow-up and two years later the patient is asymptomatic.

Abscess↗

PubMed1996

Multiple recurrence of a "sporadic" (non-familial) cardiac myxoma.

This report describes a myxoma with three recurrences, two of them synchronous neoplasms in both atrial chambers, without evidence of familial history or features of the "myxoma complex" (lentiginosis, other non-cardiac myxomas and endocrine overactivity). The patient underwent complete resection of the myxoma with their surrounding tissue 3 times between 1983 and 1992. At the time of writing no other myxoma has been diagnosed in this patient.

Echocardiography↗

PubMed1996

Effect of Ca2+ influx on intracellular free Ca2+ responses in antigen-stimulated RBL-2H3 cells.

We undertake a quantitative investigation of changes in intracellular free Ca2+ concentration ([Ca2+]i) in antigen-stimulated rat basophilic leukemia (RBL-2H3) cells, which include contributions of both Ca2+ store release and Ca2+ influx from the medium. Following Keizer and De Young (J. Keizer and G. De Young. Biophys. J. 61: 649-660, 1992), we develop a highly constrained mathematical model for [Ca2+]i oscillations in RBL-2H3 cells, which includes activation of the inositol trisphosphate receptor (IP3R) by inositol 1,4,5-trisphospate, indirect Ca2+ activation of the IP3R via Ca2+ -dependent activity of phospholipase C-gamma, slow inhibition of the IP3R by cytosolic Ca2+, refilling of Ca2+ stores by a Ca2+ -ATPase (SERCA)-type pump, and a simple representation of the dependence of plasma membrane (PM) fluxes on experimental conditions. Using this full (open cell) model, we simulate [Ca2+]i responses for protocols in which antigen concentration and external Ca2+ are manipulated and compare out calculations with experimental data. In protocol A, cells are stimulated in the presence of external Ca2+, in protocols B and C, cells are stimulated in the absence of external Ca2+, with external Ca2+ later reapplied in protocol C. We are able to reproduce quantitatively the important features of all three protocols, including the dose response of protocol B, the [Ca2+]i response to thapsigargin, and lag time results, and we provide qualitative explanations for the responses derived from our calculations. We also develop a simplified (closed cell) version of the model in which PM fluxes are neglected and total free Ca2+ concentration ([Ca2+]T) is a slowly varying parameter. This permits us to explain in a simple graphical fashion how PM fluxes may influence [Ca2+]i responses in RBH-2H3 cells through modulation of [Ca2+]T.

Animals↗

PubMed1995

Distinct functions of the Fc epsilon R1 gamma and beta subunits in the control of Fc epsilon R1-mediated tyrosine kinase activation and signaling responses in RBL-2H3 mast cells.

In RBL-2H3 rat tumor mast cells, cross-linking the high affinity IgE receptor, Fc epsilon R1, activates the protein-tyrosine kinases Lyn and Syk and initiates a series of responses including protein-tyrosine phosphorylation, inositol 1,4,5-trisphosphate synthesis, Ca2+ mobilization, secretion, membrane ruffling, and actin plaque assembly. The development of chimeric receptors containing cytoplasmic domains of individual subunits of the heterotrimeric (alpha beta gamma 2) Fc epsilon R1 has simplified analyses of early signaling events in RBL-2H3 cells. Here, RBL-2H3 cells were transfected with cDNAs encoding the extracellular and transmembrane domains of the interleukin-2 receptor alpha subunit (the Tac antigen) joined to the C-terminal cytoplasmic domains of the Fc epsilon R1 gamma and beta subunits (TT gamma and TT beta). Both sequences contain tyrosine activation motifs implicated in antigen receptor signal transduction. TT gamma and TT beta are expressed independently of the native Fc epsilon R1, as demonstrated by the ability of Tac cross-linking agents to trigger the clustering and internalization through coated pits of both chimeric receptors without co-clustering the Fc epsilon R1. A full range of signaling activities is induced by TT gamma cross-linking; the TT gamma-induced responses are slower and, except for Lyn activation, smaller than the Fc epsilon R1-induced responses. In striking contrast, TT beta cross-linking elicits no tyrosine phosphorylation or signaling responses, it impairs basal activities measured in secretion and anti-PY (anti-phosphotyrosine antibody) immune complex kinase assays, and it antagonizes Fc epsilon R1-induced Lyn and Syk activation, protein-tyrosine phosphorylation, and signaling responses. We hypothesize that the isolated beta subunit binds a specific kinase or coupling protein(s) required for signaling activity, sequestering it from the signal-transducing gamma subunit. Binding the same kinase or coupling protein to the beta subunit of the intact Fc epsilon R1 may serve instead to present it to the adjacent gamma subunit, resulting in enhanced kinase activation and signaling responses.

Animals↗

PubMed1995

Self-esteem and self-efficacy; perceived parenting and family climate; and depression in university students.

This study examined associations among self-esteem and self-efficacy; perceived unfavorable Parental Rearing Style (perceived PRS) and unfavorable family climate in the family of origin; and depression in undergraduates still in frequent contact with their families (N = 186). Unfavorable perceived PRS and family climate were construed as "affectionless control," in which parents and family provide little affection, but excessive control. Constructs were measured by the Self-Esteem Inventory, the Self-Efficacy Scale, the Child Report of Parental Behavior Inventory, the Family Environment Scale, and the Beck Inventory. Perceived "affectionless control" in both PRS and family climate accounted for about 13% of the variance in self-esteem, self-efficacy, and depression. Neither introversion nor depression mediated the relation between family socialization and self-esteem.

Adolescent↗

PubMed1995

Depressed and anxious moods mediate relations among perceived socialization, self-focused attention, and dysfunctional attitudes.

This study examined three factors that may influence cognitive vulnerability to depression and anxiety: (1) subjects' perceptions of their relationships with their parents and the climate in their family of origin (socialization); (2) self-focused attention (focusing attention inwardly, on the self); and (3) current symptoms of depression and anxiety. Subjects were 173 university undergraduates. Perceptions of unfavorable socialization and public self-consciousness were related to dysfunctional attitudes. However, nearly all these relations disappeared when depression and anxiety were controlled statistically. These results suggest that memories of negative experiences in one's family of origin, self-focused attention, depression and anxiety, and dysfunctional attitudes all may be indicators of latent negative schemas that have been activated, perhaps by recent stress.

Adolescent↗