PubMed Health⌕ Search

Biomedical subjects

R C Schwartz

Publications and source records attributed to R C Schwartz.

At least 37 records · Page 2Linked to original sources

Therapists' differential countertransference reactions toward clients with major depression or borderline personality disorder.

The purpose of this study was to examine psychotherapists' differential countertransference reactions toward either clients diagnosed with either Major Depression or Borderline Personality Disorder. Specifically, psychotherapists' personal perceptions and emotional reactions to these clients were assessed utilizing the Impact Message Inventory and the Stress Appraisal Scale (N = 155). Direct feelings, action tendencies, cognitive attributions, and perceived anxiety were evaluated. Results indicated that clients with Borderline Personality Disorder are perceived as significantly more dominant and hostile, whereas clients with Major Depression were considered significantly more submissive, friendly, and salient. In addition, it was found that as clinicians' years of experience increased, degree of countertransference decreased. These results suggest that countertransference reactions can be measured empirically, that differential countertransference reactions are evoked toward clients manifesting different symptoms, and that awareness of countertransference may be important for positive therapeutic outcome.

Adult↗

The relationship between insight, illness and treatment outcome in schizophrenia.

Lack of awareness of mental disorder in schizophrenia has been increasingly identified by researchers during recent years due to a resurgence of interest in the subject. In addition, better measurement methods have led to more valid and detailed investigations on insight in schizophrenia. Poor insight has been reported as a common phenomenon which may have both nosological and prognostic value. Specifically, due to recent studies indicating that lack of insight in schizophrenia may lead to poor treatment outcome, research focused on this phenomenon could lead to increasingly effective and efficient treatment strategies. However, many past and present studies reporting a correlation between insight and outcome in schizophrenia demonstrate significant theoretical or methodological limitations which may limit the implications and generalization of findings. This article lists and critically analyzes historical and contemporary research focusing on insight, illness, and outcome in schizophrenia. The role of insight is outlined, as are current methods for assessing awareness of mental disorder in schizophrenia. Cumulative research in this area is then reviewed, in terms of hypotheses, methods, conclusions, and limitations. Finally, suggestions for future research in this area are delineated.

Attitude to Health↗

Tumor necrosis factor alpha transcription in macrophages is attenuated by an autocrine factor that preferentially induces NF-kappaB p50.

Macrophages are a major source of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), which are expressed during conditions of inflammation, infection, or injury. We identified an activity secreted by a macrophage tumor cell line that negatively regulates bacterial lipopolysaccharide (LPS)-induced expression of TNF-alpha. This activity, termed TNF-alpha-inhibiting factor (TIF), suppressed the induction of TNF-alpha expression in macrophages, whereas induction of three other proinflammatory cytokines (interleukin-1beta [IL-1beta], IL-6, and monocyte chemoattractant protein 1) was accelerated or enhanced. A similar or identical inhibitory activity was secreted by IC-21 macrophages following LPS stimulation. Inhibition of TNF-alpha expression by macrophage conditioned medium was associated with selective induction of the NF-kappaB p50 subunit. Hyperinduction of p50 occurred with delayed kinetics in LPS-stimulated macrophages but not in fibroblasts. Overexpression of p50 blocked LPS-induced transcription from a TNF-alpha promoter reporter construct, showing that this transcription factor is an inhibitor of the TNF-alpha gene. Repression of the TNF-alpha promoter by TIF required a distal region that includes three NF-kappaB binding sites with preferential affinity for p50 homodimers. Thus, the selective repression of the TNF-alpha promoter by TIF may be explained by the specific binding of inhibitory p50 homodimers. We propose that TIF serves as a negative autocrine signal to attenuate TNF-alpha expression in activated macrophages. TIF is distinct from the known TNF-alpha-inhibiting factors IL-4, IL-10, and transforming growth factor beta and may represent a novel cytokine.

Animals↗

Symptomatology and insight in schizophrenia.

The phenomenon of poor insight of clients with schizophrenia has recently received a great deal of attention; however, the relationship of the symptoms of illness and of poor insight is not fully understood. This study examined the relationship between ratings of symptomatology and ratings of insight deficits for 64 clients with schizophrenia. Symptomatology and insight were evaluated using the Positive and Negative Syndrome Scale. Over-all functioning was evaluated using the Global Assessment of Functioning scale. Ratings on positive symptomatology were significantly related to ratings of poor insight. As ratings of poor insight increased, ratings on severity of positive symptoms, for example, delusions and hallucinations, also increased Implications of this finding are discussed.

Adult↗

Induction of murine CD5 expression by v-H-ras.

The murine CD5 surface antigen is a frequent marker on B-lineage cell lines produced from bone marrow infected with retroviruses expressing v-H-ras. Since CD5+ B cells cannot be detected in adult murine bone marrow, either the viral targets of transformation are a minor contaminating population of CD5+ B-lineage cells or the v-H-ras oncogene is inducing the expression of CD5 on B-lineage cells not previously expressing this marker. We have found that v-H-ras can induce the expression of CD5 on two CD5+ pre-B-cell lines established from murine bone marrow. This induction correlates with increased steady-state levels of CD5 mRNA. These results present the possibility that CD5 expression may be modulated by specific signalling as well as early lineage commitment.

Animals↗

Environmental factors and clients' self-disclosure in counseling.

Self-disclosure by clients is regarded as a fundamental component of counseling, with increased self-disclosure being related to positive outcome of treatment; however, scant attention has focused on environmental characteristics that may facilitate self-disclosure among clients. An evaluation of prior research in this area leads to suggestions for studies on environmental factors and self-disclosure.

Counseling↗

Cloning of the murine CD5 promoter and its tissue-specific regulation.

A genomic clone containing 1700 bp of the 5'-flanking region and first exon of the murine CD5 gene was isolated by screening a NIH 3T3 fibroblast genomic library with the previously characterized murine CD5 cDNA. The CD5 5'-flanking region lacks a consensus TATA box but contains Sp1, AP-1, IgH muE2, SV40 enhancer core, CCAAT, TCF2 alpha/PEA3/ets, and C/EBP motifs. Transcription is initiated from multiple sites upstream of an Inr-like sequence. When linked to the CAT reporter gene, the CD5 5'-flanking region was an active promoter in transient transfection assays using the EL4 (T), PD36 (pre-B) and M12 (B) cell lines, but was inactive in NIH 3T3 fibroblasts. This pattern of lymphoid-specific expression reflects the pattern of in vivo CD5 expression. Successive 5' to 3' deletions of the CD5 promoter/CAT reporter construct were transfected into T and B cells revealing a succession of positive and negative regulatory elements until promoter activity was eliminated at position -27. This result identified sequences from -125 to -27 (which contain the Inr, IgH muE2, SV40 enhancer core, and AP-1 sites) as sufficient for tissue-specific promotion. Isolation and characterization of the CD5 promoter represents an initial step in elucidating the control over tissue-specific expression of the murine CD5 gene.

Animals↗

C/EBP-related protein 2 confers lipopolysaccharide-inducible expression of interleukin 6 and monocyte chemoattractant protein 1 to a lymphoblastic cell line.

C/EBP-related proteins 2 and 3 (CRP2 and CRP3) are differentially expressed by P388 lymphoblasts and their derivative P388D1(IL1) macrophages. We have ectopically expressed CRP2, the predominant CRP in macrophages, in P388 lymphoblasts. The expression of CRP2 is sufficient to confer the lipopolysaccharide (LPS)-inducible expression of interleukin 6 and monocyte chemoattractant protein 1 to lymphoblasts, which normally do not display LPS induction of inflammatory cytokines. Consistent with these findings, the expression of CRP2 antisense RNA blocks the LPS induction of IL-6 expression in P388D1(IL1) macrophages. This work clearly establishes the essential role of CRP2 in the induction of cytokine genes by LPS. Additionally, these data add MCP-1 to the list of cytokines showing an involvement of CRP2 in their expression.

Animals↗

Neuromuscular diseases of childhood.

This review covers three areas. First, dramatic progress in the discovery of abnormal loci on certain chromosomes associated with several motor unit diseases eventually will obviate the need for more invasive testing. Second, new information about the natural course of spinal muscular atrophy is beginning to clarify the nature of this disease. Third, changes in the treatment of the acute and chronic polyneuropathies has shortened hospital stays.

Charcot-Marie-Tooth Disease↗

Synergy of IL-7 and v-Ha-ras in the in vitro neoplastic progression of murine pre-B cells.

A recombinant retrovirus expressing IL-7 was superinfected into a murine pre-B cell line previously infected with a retrovirus expressing v-Ha-ras. Populations of cells polyclonal for integration of the IL-7 virus and independent of IL-7 for growth were generated. These cells were highly tumorigenic. Similarly, co-infection of murine bone marrow with retroviruses expressing IL-7 and v-Ha-ras generated a pre-B lymphoid outgrowth that was tumorigenic. While IL-7 and v-Ha-ras expression are not individually sufficient to induce tumorigenicity, their co-expression yields highly tumorigenic pre-B lymphoid cell lines. IL-7 expression may be equivalent to v-myc expression for synergy with v-H-ras in the neoplastic transformation of murine pre-B cells.

3T3 Cells↗

Isolated left main coronary stenosis and mediastinal irradiation.

This report draws an association between mediastinal irradiation and isolated left main coronary artery stenosis. The report highlights two patients who developed selective left main coronary artery stenosis post mediastinal treatment. In the animal model, it has been shown that high serum cholesterol levels at the time of, or soon after, irradiation are necessary to initiate arteriosclerotic plaque formation.

Carcinoma, Squamous Cell↗

Lineage switch macrophages can present antigen.

Recent reports of "lineage switching" from a lymphoid to macrophage phenotype have left unresolved the question of whether such cells are functional macrophages or nonfunctional products of differentiation gone awry. This study demonstrates that several "macrophage-like" cell lines derived from v-Ha-ras-transformed pre-B cells have gained the capacity to effectively present antigen in MHC-restricted fashion. Using an assay involving the cocultivation of putative antigen-presenting cells with chicken ovalbumin (cOVA) and a cOVA-specific T-cell hybridoma, "lineage switch" cell lines were found to present antigen as effectively as macrophage-containing peritoneal exudates. Neither the original pre-B-cell precursors nor B-cell lymphomas derived from them present antigen. Thus, we have demonstrated that these "lineage switch" macrophages are capable of antigen presentation, a mature differentiated function. While gaining macrophage characteristics, these cells have also rearranged their kappa light-chain immunoglobulin locus, suggesting that macrophage differentiation and immunoglobulin rearrangement are not mutually exclusive processes. The existence of both lymphoid and myeloid characteristics in a cell fully capable of antigen presentation suggests greater plasticity in hematopoietic lineage commitment than conventionally thought to be the case.

Animals↗

Use of a modified Transwell culture to quantitate the contribution of non-IL-7 substances to growth of an IL-7-dependent pre-B cell clone.

Clone 3 is a mouse pre-B cell line that cannot grow in standard tissue culture media but is immortalized by coculture with a bone marrow-derived feeder layer. In addition, clone 3 cells can be passaged indefinitely in recombinant interleukin-7 (IL-7) in the absence of a feeder layer if maintained at high cell density. Using monoclonal antibody to IL-7 and Transwells ligated to dialysis membranes, we have examined the relative contributions of IL-7, both endogenous and exogenous, and of "non-IL-7" feeder layer factors to growth promotion of clone 3 cells. There is synergy between feeder layers and exogenous IL-7 that is most marked when the latter is present in suboptimal concentrations. The synergizing activity is not neutralized by antibody to IL-7 and appears to be freely dialyzable. This "non-IL-7" effect is common to two different feeder layers, the one derived from bone marrow (3E) being an IL-7 producer, and the other, 3T3 fibroblasts, making no detectable IL-7. These experiments reveal a substantial contribution of the dialyzable moiety to the total feeder layer effect, and are the first to demonstrate cytokine-dependent low-molecular-weight synergy in a coculture. This demonstration is possible because the synergizing cofactor(s) can cross a semipermeable membrane whereas the cytokine and its neutralizing antibody cannot.

3T3 Cells↗

Tumorigenesis of a v-Ha-ras-expressing pre-B cell line selects for c-myc activation.

Seven tumors independently derived from a v-Ha-ras-expressing pre-B cell line were examined to determine the oncogene activations cooperating with v-Ha-ras in in vivo tumor progression. The pre-B cell line was generated by infection with Moloney murine leukemia virus (MoMuLV) and a MoMuLV-derived recombinant expressing v-Ha-ras. Two of seven tumors possessed a MoMuLV integration immediately upstream and in reverse transcriptional orientation to c-myc. This correlated with a 3-fold increased level of c-myc mRNA. Two other tumors displayed elevated c-myc mRNA levels, although the mechanism of enhanced expression was unclear. Thus the tumor progression of a v-Ha-ras-expressing murine pre-B cell line selects for the activation of c-myc.

Animals↗

Several types of adherent cells elaborate a dialyzable lymphopoietic cofactor (Abelson Growth Promoter).

We have cloned a stromal cell from mouse bone marrow selected on the basis of its ability to promote the growth of an Abelson virus-transformed pre-B cell line. These stromal cells have smooth muscle features, and the ultrafiltrate of stromal cell-conditioned medium has proliferative effects on all feeder layer-responsive mouse pre-B cell lines tested, as well as on normal pre-B cells. One of these low MW substances is a protease-resistant factor with an MW of approximately 450 Da which we designate Abelson Growth Promoter (AGP). AGP was initially characterized as an activity which promotes the growth of Abelson virus-transformed mouse pre-B cells, but it also promotes the growth of a ras-transformed pre-B cell line as a single agent and in synergistic fashion with recombinant interleukin (IL) 7. AGP as a single agent has no effect on normal pre-B cells, which have a brisk response to IL-7. In contrast, transformed pre-B cells display a blunted response to IL-7. We propose that AGP plays a role in normal lymphopoiesis by expanding clones of pre-B cells which have been activated by other stromal cell-derived signals, such as IL-7, and directly promotes the growth of nascently transformed pre-B cells.

Abelson murine leukemia virus↗

Linkage analysis in Marfan syndrome.

We have analysed 40 marker loci on 13 chromosomes for linkage with Marfan syndrome. None of the loci was linked to the Marfan syndrome locus at theta = 0.00. This study provides a basis for an exclusion map and for further collaboration in mapping of the locus.

Alleles↗