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Biomedical subjects

D R Johnson

Publications and source records attributed to D R Johnson.

At least 55 records · Page 3Linked to original sources
PubMed1999

Comparison of outcome between homogeneous and heterogeneous treatment environments in combat-related posttraumatic stress disorder.

This study compared treatment outcome at discharge, and 4, 8, and 12 month follow-up between an inpatient program consisting of a mixture of Vietnam combat veterans with posttraumatic stress disorder (PTSD) and general psychiatric patients (N = 42), and the same program at a later period, consisting of only Vietnam combat veterans with PTSD (N = 33). Veterans rated the homogeneous environment higher in satisfaction, support, order, clarity, and amount of discussion of combat, and lower in hostility, than the heterogeneous condition. However, veterans showed no improvement in condition at 12 month follow-up, with the exception of decreased violence, replicating earlier studies. No differences in outcome were found between homogeneous or heterogeneous treatment environments. This study underscores the enduring nature of chronic posttraumatic stress disorder in the veteran population.

Adult↗
PubMed1999

Susceptibility of group A beta-hemolytic streptococci to thirteen antibiotics: examination of 301 strains isolated in the United States between 1994 and 1997.

BACKGROUND: Because of continuing reports from many countries of increasing resistance of group A streptococci to macrolide antibiotics, we determined the antibiotic susceptibility of recent group A streptococcal isolates from the United States. METHODS: We evaluated 301 Streptococcus pyogenes isolates (245 from patients with uncomplicated pharyngitis and 56 isolates from patients with invasive systemic infections) for susceptibility using the Etest technique. The isolates came from 24 states and the District of Columbia during the years 1994 through 1997. Thirteen antibiotics (azithromycin, ceftriaxone, cephalothin, chloramphenicol, ciprofloxacin, clindamycin, erythromycin, imipenem, levofloxacin, oxacillin, penicillin G, tetracycline and trimethoprim-sulfamethoxazole) were studied. RESULTS: The MIC90 for penicillin was 0.016 microg/ml, which is not significantly different from previous reports. Of the 301 isolates only 2.6% were resistant to a macrolide antibiotic and only 4% were resistant to tetracycline. CONCLUSIONS: These data indicate that antibiotic resistance among recent isolates of group A streptococci (including those from patients with severe infections) currently is not a clinically significant problem in the United States.

Anti-Bacterial Agents↗
PubMed1999

Changes in trabecular bone architecture in women during pregnancy.

OBJECTIVE: To examine the effect of early and late pregnancy on the microarchitecture of maternal cancellous bone. SAMPLE: Transilial bone biopsies were obtained from two groups of pregnant women one group (n = 15) in the first trimester and the other (n = 13) at term. Comparison was made with biopsy and autopsy samples from a group (n = 25) of normal premenopausal nonpregnant women. METHODS: Undecalcified sections were analysed under a low power optical microscope using an automated trabecular analysis system which measures a comprehensive range of structural variables including the bone volume, trabecular number, width, separation and connectivity. RESULTS: In early pregnancy the quantity of cancellous bone fell from a mean relative bone volume of 23.07% (SD 5.49) in nonpregnant controls to 16.72% (SD 3.91) (P < 0.001). This was primarily due to a decline in trabecular thickness from 122.9 microm (SD 10.5) to 97.2 microm (SD 21.8) (P < 0.01) and was accompanied by a loss of trabecular connectivity expressed as a reduction in the trabecular node: terminus ratio from 0.90 (SD 0.71) to 0.38 (SD 0.26) (P < 0.001). By late pregnancy the bone volume had been entirely restored to 23.41% (SD 9.76). This was primarily due to an increase in the number of trabeculae from 73.2 (SD 35.5)/field to 100.3 (SD 33.3) /field (P < 0.05)with an associated reduction in trabecular separation from 431 microm (SD 150) to 315.8 microm (SD 78.5) (P < 0.01). CONCLUSIONS: Pregnancy affects the maternal skeleton by producing a fluctuation in the cancellous bone volume in which early temporary bone loss through trabecular thinning is restored in entirety through the addition of new trabeculae to produce a modestly more complex system of thinner more numerous bars by term.

Adult↗
PubMed1999

Antidepressants augment natural killer cell activity: in vivo and in vitro.

Depressed mood has been associated with reduced natural killer cell activity (NKCA). Further, amelioration of depressive symptoms by pharmacotherapy has resulted in augmented NKCA. Serotonin, an indoleamine implicated in the pathophysiology of affective disorders, enhances NKCA in vitro and lymphocytes possess serotonin transporters and receptors. The present study evaluated NKCA in depressed outpatients before and during treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine (Prozac(R)). Further, the SSRIs, fluoxetine and paroxetine (Paxil(R)), were also incubated in vitro with lymphoid cells to evaluate possible direct effects of SSRIs on NKCA. Depressed outpatients were administered fluoxetine (20 mg/day) for 4 weeks. NKCA and severity of depression were evaluated at weeks 0, 1, 2, and 4. Serum concentrations of fluoxetine and norfluoxetine were obtained as well. Mononuclear cells obtained from nonpatient volunteers were incubated with pharmacologic concentrations of fluoxetine or paroxetine and NKCA measured with a standard chromium release assay. Fluoxetine treatment resulted in decreased symptoms of depression and increased serum concentrations of fluoxetine and norfluoxetine. Further, fluoxetine treatment was associated with augmented NKCA in a subgroup of depressed outpatients exhibiting low NKCA at baseline. Fluoxetine had no effect on NKCA in depressed individuals exhibiting high NKCA at baseline. Incubation of mononuclear cells with fluoxetine and paroxetine augmented NKCA in vitro. The enhancing effects of antidepressants on NKCA in vivo and in vitro indicate a possible direct drug interaction with lymphoid cells during pharmacotherapy, suggesting that pharmacologic treatment of depression may result in enhanced immune competence as indexed by enhanced NKCA and that NKCA could be pharmacologically augmented with antidepressants in individuals with compromised immune function.

Adult↗
PubMed1999

Testosterone and men's depression: the role of social behavior.

Medical research suggests that testosterone has positive effects on mood (thereby reducing the chances of depression), and social science research finds testosterone to be related to antisocial behavior, risk behavior, unemployment and low paying jobs, and being unmarried--factors known to be positively related to depression. Analysis of a sample of 4,393 men finds a parabolic model best fits the data. The relationship between testosterone and depression is inverse for men with below average testosterone and direct for those with above average testosterone. The relationship disappears for those with above average testosterone when controls for antisocial and risk behaviors and the absence of protective factors such as marriage and steady employment are in the equation. The relationship is unchanged for those with below average testosterone. The results help explain the difference between medical and social research findings. Mechanisms accounting for the findings are explored.

Adult↗
PubMed1998

Interferon induction of TAP1: the phosphatase SHP-1 regulates crossover between the IFN-alpha/beta and the IFN-gamma signal-transduction pathways.

Interferon (IFN)-gamma and IFN-alpha/beta induction of the transporter associated with antigen processing-1 (TAP1) promoter was compared in HeLa cells and endothelial cells (ECs). In HeLa cells, IFN-gamma acts through Stat1alpha/Stat1alpha homodimers binding to the gamma activating sequence (GAS) and IFN-alpha/beta acts through Stat1/Stat2/p48 binding to the IFN-stimulated response element (ISRE). In ECs, however, IFN-gamma and IFN-alpha/beta act through both the GAS and ISRE. The basis of the IFN signaling crossover in ECs was investigated. HeLa and ECs contain similar ratios of Stat1alpha to Stat2 proteins, and IFN-alpha/beta also activates the same Janus kinases (JAKs) (Jak1 and tyrosine kinase (Tyk) 2 but not Jak2). However, IFN-alpha/beta activates more Stat1alpha than does IFN-gamma in ECs, whereas the reverse occurs in HeLa, and expression of the IFN-alpha/beta receptor-associated phosphatase SHP-1 is much lower in ECs than HeLa cells. Overexpression of SHP-1 in ECs blocks IFN-alpha/beta signaling through GAS, and expression of a dominan negative SHP-1 in HeLa cells permits IFN-alpha/ss signaling through GAS, demonstrating a role for SHP-1 in regulating crossovers between the IFN-alpha/beta and IFN-gamma signaling pathways.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Interferon enhances tumor necrosis factor-induced vascular cell adhesion molecule 1 (CD106) expression in human endothelial cells by an interferon-related factor 1-dependent pathway.

Tumor necrosis factor (TNF) and interleukin 1 are known to initiate endothelial vascular cell adhesion molecule (VCAM)-1 transcription primarily by activating nuclear factor (NF)-kappaB, which translocates to the nucleus. In addition to two NF-kappaB elements found within the minimal cytokine-inducible VCAM-1 promoter, an interferon-related factor (IRF) element (IRF-1) has been identified close to the transcription initiation site, suggesting that cytokines that induce IRF-1 might affect VCAM-1 expression levels. We therefore investigated the effects of interferons (IFNs), which strongly induce IRF-1, on VCAM-1 transcription and expression. We show that IFN-alpha and -gamma enhance TNF-induced VCAM-1 mRNA transcription and protein expression in human endothelial cells. IFN enhancement of TNF-induced expression is also seen using chloramphenicol acetyl transferase reporter genes linked to the minimal cytokine inducible VCAM-1 promoter. Nuclear IRF-1 is the molecular basis of IFN enhancement, because (a) IFN plus TNF-treated cells displayed increased nuclear IRF-1 levels and increased IRF-1 binding to the VCAM-1 promoter, compared with cells treated with TNF alone; (b) kinetics of nuclear IRF-1 levels correlated with VCAM-1 mRNA levels; (c) transfection with an IRF-1 construct substituted for IFN treatment; and (d) transfection with an expression construct encoding IRF-2, a competitive inhibitor of IRF-1, reduced TNF-induced VCAM-1 expression. Our experiments show that IFN amplifies TNF-induced VCAM-1 expression at the transcriptional level by an IRF-1-dependent pathway.

Cell Compartmentation↗
PubMed1998

Arterial and venular endothelial cell costimulation of cytokine secretion by human T cell clones.

Vascular endothelial cell (EC) costimulation of cytokine secretion by T lymphocytes may be important in inflammation and allograft rejection. Venous and arterial iliac endothelial cells (VIEC, AIEC) both costimulate interleukin-2 (IL-2) production by peripheral blood lymphocytes (PBL) or T cell clones stimulated with phytohemagglutinin (PHA). Interferon-gamma (IFN-gamma) production is costimulated in a subset of clones but IL-4 is not. Surprisingly, two T cell clones were reciprocally better costimulated by VIEC or AIEC. EC activation by pretreatment with tumor necrosis factor alpha (TNF-alpha) does not increase T cell costimulation despite large increases in EC cell adhesion molecule expression. Neither VIEC nor AIEC express CTLA4-binding molecules and costimulation is blocked by cyclosporin A, suggesting that CD28 is not involved in EC costimulation of T cells. These data suggest that adult vascular EC costimulate production of IL-2 and IFN-gamma but not IL-4 by mature T cells, that EC costimulation is not increased in inflamed tissues, and that different EC optimally costimulate particular T cells. These findings have implications for the nature of the costimulatory signal(s) provided by EC and may be important in understanding vasculitis or atherosclerosis.

Abatacept↗
PubMed1998

Efficacy of Psychoeducational Group Therapy in reducing symptoms of posttraumatic stress disorder among multiply traumatized women.

OBJECTIVE: The role of group therapy in treatment of posttraumatic stress disorder (PTSD) has been traditionally restricted to issues of self-esteem and interpersonal relationships, rather than primary symptoms of the disorder. In this study, the authors examined the effectiveness of a 16-week trauma-focused, cognitive-behavioral group therapy, named Interactive Psychoeducational Group Therapy, in reducing primary symptoms of PTSD in five groups (N=29) of multiply traumatized women diagnosed with chronic PTSD. METHOD: The authors made assessments at baseline, at 1-month intervals during treatment, at termination, and at 6-month follow-up by using self-report and structured interview measures of PTSD and psychiatric symptoms. The absence of a control group limits the conclusions drawn from the study. RESULTS: At termination, subjects showed significant reductions in all three clusters of PTSD symptoms (i.e., reexperiencing, avoidance, and hyperarousal) and in depressive symptoms; they showed near-significant reductions in general psychiatric and dissociative symptoms, at termination. These improvements were sustained at 6-month follow-up. CONCLUSIONS: The role of group therapy in PTSD treatment should not be prematurely restricted to addressing self-esteem and interpersonal dimensions only. The use of structured, cognitive-behavioral elements within the group format may allow for more targeted treatment of core symptoms of the disorder.

Adult↗
PubMed1998

Rural-urban women's experience of symptoms of depression related to economic hardship.

This study compares rural and urban women's experiences of depressive symptoms. Cross-sectional data were used from 623 women 55 years of age and older who were part of a randomly selected community based sample. Theoretical perspectives included individual stress and community context as explanatory factors contributing to differences in the proportion of women who identify having had the experience of symptoms of depression. Results of the analysis using correlation and multiple regression supported the importance of perceptions of financial status. Community type and age were not related to the level of depressive symptoms reported by the women who were interviewed.

Aged↗
PubMed1998

Antistreptolysin O and anti-deoxyribonuclease B titers: normal values for children ages 2 to 12 in the United States.

BACKGROUND: Measurement of antibodies to the extracellular antigens produced by group A streptococci, antistreptolysin O (ASO) and anti-deoxyribonuclease B (anti-DNase B), is often necessary to confirm a clinical diagnosis of a previous group A streptococcal infection, especially in patients suspected of having a nonsuppurative sequel to this infection. Age is among several factors that may influence antibody levels in children. Thus, in contrast to adults, what is considered a normal titer for one age group (infants) is not appropriate for another (older children). Age-related "normal" values for ASO and anti-DNase B are provided in the package inserts of commercially available kits; however, there are no recent comprehensive data to validate such values. OBJECTIVE: Using sera from 1131 children (from 23 states) ages 2 to 12 years, we determined age-specific geometric mean titers (GMT) and upper limits of normal (ULN) of ASO and anti-DNase B. METHODS: ASO and anti-DNase B titers were measured by conventional laboratory methods. RESULTS: Children 7 years of age comprised the largest proportion (14%) of the study population. Approximately two-thirds of the sera were collected during winter and early spring months. For both ASO and anti-DNase B, both GMT values and ULN increased with age. The GMTs for ASO and anti-DNase B for the entire group of subjects were 89 and 112, respectively. The ULN for the entire group for ASO and anti-DNase B were 240 and 640, respectively. CONCLUSION: The age-specific values for GMT and ULN for this group of children from 23 states were slightly higher than previously reported. These values are likely representative of the pediatric population in the United States and should be of clinical value to physicians, epidemiologists, and clinical laboratory personnel.

Age Factors↗
PubMed1998

Tumor necrosis factor is delivered to mitochondria where a tumor necrosis factor-binding protein is localized.

The roles of the known tumor necrosis factor (TNF) receptors (TNFR-I and TNFR-II) and their associated signaling pathways in mediating the diverse actions of TNF remain incompletely defined. We have found that a proportion of exogenous TNF is delivered to mitochondria as well as to lysosomes. Using confocal and immunoelectron microscopy and Western blotting of subcellular fractions, we have identified a 60-kd protein in the inner mitochondrial membrane that is recognized by a monoclonal antibody to TNFR-II. In isolated mitochondria, this protein binds [125I]-TNF. This provides evidence of a mitochondrial binding protein for an extracellular ligand and demonstrates the presence of a pathway capable of delivering TNF from the cell surface to mitochondria. These findings suggest that TNF effects on cells may be due in part to a direct effect on mitochondria.

Adipocytes↗
PubMed1997

Interferon-gamma rapidly increases peptide transporter (TAP) subunit expression and peptide transport capacity in endothelial cells.

Human cytotoxic T lymphocytes (CTL) recognize specific complexes of HLA class I molecules and peptides, which assemble when nascent class I molecules bind peptides transported from the cytoplasm into the endoplasmic reticulum by the heterodimeric transporter associated with antigen processing (TAP). Increased class I molecule expression on the cell surface increases the efficiency of CTL lysis. The kinetics of interferon (IFN)-gamma induction of TAP, peptide transport capacity, and HLA class I molecule expression was determined in endothelial cells, which are targets of CTL following transplantation or viral infection. TAP mRNAs are induced rapidly, increasing 20-fold (TAP1) or 10-fold (TAP2) by 12 h, whereas HLA class I mRNA is induced more slowly, increasing 10-fold in 24 h. TAP1 and TAP2 proteins are also induced rapidly, increasing 10-fold in 24 h, whereas HLA class I heavy chain proteins and surface expression increase more slowly. Peptide transport capacity in endothelial and HeLa cells increases within 6 h of IFN-gamma treatment, suggesting that the IFN-gamma-induced TAP heterodimers are functional. Therefore, the IFN-gamma-induced increase in TAP proteins is accompanied by an increased peptide transport capacity, which may be important in supporting the subsequent rise in HLA class I protein expression.

ATP Binding Cassette Transporter, Subfamily B, Mem↗