Internists, Gastroenterologist (digestive)
23 years of experience

Accepting new patients
CMC Dept of Med Grp. MD
3 Cooper Plz
Rm 104
Camden, NJ 08103
856-757-7732
Locations and availability (10)

Education ?

Medical School Score Rankings
Temple University Physicians (1987)
  • Currently 3 of 4 apples
Top 50%

Awards & Distinctions ?

Associations
American Board of Internal Medicine

Affiliations ?

Dr. Judge is affiliated with 17 hospitals.

Hospital Affilations

Score

Rankings

  • St Francis Hospital
    2500 W 7th St, Wilmington, DE 19805
    • Currently 4 of 4 crosses
    Top 25%
  • Virtua West Jersey Hospital - Marlton
    94 Brick Rd, Marlton, NJ 08053
    • Currently 2 of 4 crosses
  • Cooper University Hospital
    1 Cooper Plz, Camden, NJ 08103
    • Currently 2 of 4 crosses
  • Virtua West Jersey Hospital - Voorhees
    94 Brick Rd, Marlton, NJ 08053
    • Currently 2 of 4 crosses
  • The Memorial Hospital Of Salem County
    310 Woodstown Rd, Salem, NJ 08079
    • Currently 2 of 4 crosses
  • Nyp-Weill Cornell
  • University of Penn Med Center-Presb Med Group
  • Cooper Hospital/U M C
  • Virtua WJ Hospital Marlton
  • Cooper Medical Center
  • St Francis
  • Virtua Health System West Jersey, Voorhees
  • Saint Francis Hospital of Wilmington
  • Hospital of the University of Pennsylvania
  • Virtua WJ Hospital Voorhees
  • Presbyterian Medical Center of the University of Pennsylvania Health System
  • New York Presbyterian Hospital
  • Publications & Research

    Dr. Judge has contributed to 22 publications.
    Title Core Self-evaluations and Job Performance: the Role of the Perceived Work Environment.
    Date January 2010
    Journal The Journal of Applied Psychology
    Excerpt

    Using trait activation theory as a framework, the authors examined the moderating role of two situational variables-perceptions of organizational politics and perceptions of leader effectiveness-on the relationship between core self-evaluations and job performance. Results from two samples (N = 137 and N = 226) indicate that employee perceptions of their work environment moderated the relationship between their core self-evaluations and supervisor ratings of their performance. In particular, those with higher core self-evaluations received higher performance ratings in environments perceived as favorable than in environments perceived as unfavorable.

    Title The Popularity Contest at Work: Who Wins, Why, and What Do They Receive?
    Date March 2009
    Journal The Journal of Applied Psychology
    Excerpt

    In 2 studies, the authors investigated the popularity of employees at work. They tested a model that positioned personality in the form of core self-evaluations and situational position in the form of communication network centrality as antecedents of popularity and interpersonal citizenship and counterproductive work behaviors received from coworkers as outcomes of popularity. Data from 116 employees and 383 coworkers in Study 1 and 139 employees, their significant others, and 808 coworkers in Study 2 generally supported the model. Core self-evaluations and communication network centrality were positively related to popularity, and popular employees reported receiving more citizenship behaviors and fewer counterproductive work behaviors from their coworkers than less popular employees, even controlling for interpersonal liking. (PsycINFO Database Record (c) 2009 APA, all rights reserved).

    Title The Role of Core Self-evaluations in the Coping Process.
    Date March 2009
    Journal The Journal of Applied Psychology
    Excerpt

    In 2 studies, the authors investigated whether core self-evaluations (CSE) serve as an integrative framework for understanding individual differences in coping processes. A meta-analytic review demonstrated that CSEs were associated with fewer perceived stressors, lower strain, less avoidance coping, more problem-solving coping, and were not strongly related to emotion-focused coping. Consistent with the meta-analytic results, a daily diary study demonstrated that individuals with high CSE perceived fewer stressors, experienced less strain after controlling for stressors, and engaged in less avoidance coping. However, both studies demonstrated that emotional stability was uniquely related to the stress and coping process and that emotional stability moderated the relationship between stressors and strain. The discussion focuses on the distinction between depressive self-concept represented by CSE and the anxiety and worry represented by emotional stability. (PsycINFO Database Record (c) 2009 APA, all rights reserved).

    Title Self-efficacy and Work-related Performance: the Integral Role of Individual Differences.
    Date February 2007
    Journal The Journal of Applied Psychology
    Excerpt

    The present study estimated the unique contribution of self-efficacy to work-related performance controlling for personality (the Big 5 traits), intelligence or general mental ability, and job or task experience. Results, based on a meta-analysis of the relevant literatures, revealed that overall, across all studies and moderator conditions, the contribution of self-efficacy relative to purportedly more distal variables is relatively small. Within moderator categories, there were several cases in which self-efficacy made unique contributions to work-related performance. For example, self-efficacy predicted performance in jobs or tasks of low complexity but not those of medium or high complexity, and self-efficacy predicted performance for task but not job performance. Overall, results suggest that the predictive validity of self-efficacy is attenuated in the presence of individual differences, though this attenuation does depend on the context.

    Title Hostility, Job Attitudes, and Workplace Deviance: Test of a Multilevel Model.
    Date April 2006
    Journal The Journal of Applied Psychology
    Excerpt

    The authors tested a model, inspired by affective events theory (H. M. Weiss & R. Cropanzano, 1996), that examines the dynamic nature of emotions at work, work attitudes, and workplace deviance. Sixty-four employees completed daily surveys over 3 weeks, reporting their mood, job satisfaction, perceived interpersonal treatment, and deviance. Supervisors and significant others also evaluated employees' workplace deviance and trait hostility, respectively. Over half of the total variance in workplace deviance was within-individual, and this intraindividual variance was predicted by momentary hostility, interpersonal justice, and job satisfaction. Moreover, trait hostility moderated the interpersonal justice-state hostility relation such that perceived injustice was more strongly related to state hostility for individuals high in trait hostility.

    Title Colonic Dysplasia and Cancer in Inflammatory Bowel Disease.
    Date January 2003
    Journal Gastrointestinal Endoscopy Clinics of North America
    Excerpt

    Extracolonic malignancies are a relatively rare complication of inflammatory bowel disease. In contrast, colorectal cancer remains a major concern for patients with long-standing UC. The best available evidence suggests that patients with long-standing Crohn's colitis are at similar risk for colorectal cancer as those patients with long-standing UC. In patients with UC, the magnitude of this increased risk appears to be greater in patients with more extensive colonic involvement. It appears that the magnitude of this risk increases with increasing duration of disease, at least in UC. Whether this reflects the increased risk of cancer that occurs with the aging process or a separate phenomena distinct to UC is unclear. To date, the methods available to reduce the risk of cancer are less than optimal. Although surgical procedures eliminate the risk, the mental and physical sequelae of these procedures can be substantial. Surveillance with colonoscopic biopsies is likely effective in reducing although not eliminating the risk of colorectal cancer. Efforts to develop chemopreventative agents and improved surveillance methods remain areas of active investigation.

    Title Evaluation of Polypoid Lesions in Inflammatory Bowel Disease.
    Date January 2003
    Journal Gastrointestinal Endoscopy Clinics of North America
    Excerpt

    This article discusses patients with inflammatory bowel disease (IBD), a group which is at increased risk for colorectal carcinoma based on extent and duration of their disease. Patients with chronic IBD (at least 8-10 years duration) should be screened with colonoscopy every 1 to 2 years with multiple jumbo biopsies every 10 cm through the entire colon. Patients with sporadic adenomas can be followed after complete polypectomy, whereas patients with adenoma-like dysplasia-associated lesion or mass (DALMs) need increased surveillance. Patients with flat dysplasia or non adenoma-like DALMs are at high risk for progression and should undergo colectomy. The patients who have indeterminate lesions can be differentiated based on the endoscopic, histologic, and molecular features of the lesion. Long-term follow-up is necessary to determine the natural history of these lesions.

    Title Extraintestinal Manifestations of Inflammatory Bowel Disease.
    Date December 2002
    Journal Gastroenterology Clinics of North America
    Excerpt

    Numerous extraintestinal diseases have been associated with IBD. The role of the gastrointestinal tract in host response to the foreign antigens present in the gut makes the enteric immune system highly susceptible to any external perturbation to the system. Dysregulation of the enteric immune response results in pathology in various organs outside of the gut. The site-specific manifestations of this immune response are not understood fully. Better understanding of the pathogenesis of IBD and the complex interactions between the gut immune system and the extraintestinal systems would provide insights into the development of many of these extraintestinal manifestations. Much is unknown about the presence of cardiac, pulmonary, and hematologic diseases in patients with IBD. True association or coincidental presence of the diseases in these organ systems with IBD requires better delineation. An important consideration in all patients with IBD presenting with extraintestinal manifestations should be a careful search for medication-related complications.

    Title An Open-label Trial of the Ppar-gamma Ligand Rosiglitazone for Active Ulcerative Colitis.
    Date January 2002
    Journal The American Journal of Gastroenterology
    Excerpt

    OBJECTIVES: Previous research has demonstrated that ligands for the gamma subtype of peroxisome proliferator-activated receptors (PPARs) reduce inflammation in two different murine models of colitis. This study was designed to examine the potential efficacy of rosiglitazone, a ligand for the gamma subtype of PPARs, as a therapy for active ulcerative colitis. METHODS: Fifteen patients with mild to moderately active ulcerative colitis despite therapy with 5-aminosalicylic acid compounds were enrolled in an open-label study of rosiglitazone (4 mg b.i.d. p.o.) for 12 wk. Thirteen of 15 patients were receiving concomitant therapy with corticosteroids and/or immunomodulator medications. Disease activity was measured with the Disease Activity Index. RESULTS: After 12 wk of therapy, four patients (27%) had achieved clinical remission, of whom three (20%) also had an endoscopic remission. Four additional patients (27%) had a clinical response without achieving remission. Two patients were hospitalized with worsened disease activity, and one patient was withdrawn for nephrotic syndrome. CONCLUSIONS: These data suggest that ligands for the gamma subtype of PPARs may represent a novel therapy for ulcerative colitis. A double blind, placebo-controlled, randomized trial is warranted.

    Title Tissue-specific Consequences of the Anti-adenoviral Immune Response: Implications for Cardiac Transplants.
    Date October 1999
    Journal Nature Medicine
    Excerpt

    The immune response to adenoviral vectors can induce inflammation and loss of transgene expression in transfected tissues. This would limit the use of adenovirus-mediated gene transfer in disease states in which long-term gene expression is required. While studying the effect of the anti-adenoviral immune response in transplantation, we found that transgene expression persisted in cardiac isografts transfected with an adenovirus encoding beta-galactosidase. Transfected grafts remained free of inflammation, despite the presence of an immune response to the vector. Thus, adenovirus-mediated gene transfer may have therapeutic value in cardiac transplantation and heart diseases. Furthermore, immunological limitations of adenoviral vectors for gene therapy are not universal for all tissue types.

    Title The Role of Cd80, Cd86, and Ctla4 in Alloimmune Responses and the Induction of Long-term Allograft Survival.
    Date April 1999
    Journal Journal of Immunology (baltimore, Md. : 1950)
    Excerpt

    Blocking the interaction of the CD28 costimulatory receptor with its ligands, CD80 and CD86, inhibits in vivo immune responses, such as allograft rejection, and in some instances induces tolerance. Previously, we found that CTLA4Ig, which blocks the CD28/CTLA-4 (CD152) ligands CD80 and CD86, can be used to induce transplantation tolerance to vascularized allografts. Recent data suggest that an intact CD152-negative signaling pathway is essential for induction of tolerance to nominal Ags. Here, we show that blockade of CD152 using an anti-CD152 mAb at the time of transplantation prevents the induction of long-term allograft survival by agents that target CD80 and CD86. In contrast, CD152 signals are not required for the maintenance of established graft survival. We also report for the first time that blockade of CD86 alone can induce long-term graft survival. This requires that anti-CD86 mAb is given on the day of transplantation and also depends upon an intact CD152 pathway. This result, plus experiments using CD80-deficient mice, suggests a dominant role for CD80 molecules on donor cells as the relevant ligand for CD152. We additionally find that blockade of CD152 at the time of transplantation does not interfere with the effectiveness of anti-CD154 mAbs, suggesting distinct mechanisms for inhibition of graft rejection by blocking the CD28 vs CD154 pathways.

    Title Utility of Adenoviral-mediated Fas Ligand Gene Transfer to Modulate Islet Allograft Survival.
    Date October 1998
    Journal Transplantation
    Excerpt

    BACKGROUND: One of the best-defined mechanisms for the induction of apoptosis involves signaling via the cell surface molecule Fas, after binding of Fas ligand. Expression of Fas ligand is tightly regulated, being expressed primarily by T cells after activation, where it serves as a self-regulatory mechanism for immune responses. Fas ligand has also been found to be expressed constitutively at sites of immune privilege such as the testes and the anterior chamber of the eye. Recently, co-transplantation of Fas ligand-transfected myoblasts in association with islet cell allografts was shown to prolong islet allograft survival but only rarely led to indefinite graft survival. Graft rejection was associated with loss of Fas ligand on the myoblasts, suggesting that direct expression of the transgene on the islets might be more effective. METHODS: A replication-defective adenoviral construct containing murine Fas ligand (Ad/MFL) was prepared by homologous recombination. NIH 3T3 cells, rodent splenocytes, and murine islets were infected with Ad/MFL and examined in vitro for functional murine Fas ligand expression. Survival of Ad/MFL-infected islets was subsequently evaluated in vivo in both syngeneic and allogeneic islet transplantation models. RESULTS: Cell lines and islet allografts transfected with Ad/MFL expressed a functional Fas ligand, capable of inducing apoptosis (confirmed by three distinct assays for DNA fragmentation) in Fas+ targets, but not in Fas- controls. Furthermore, Ad/MFL was able to modify allogeneic immune responses in vitro, as addition of this virus, but not a control adenovirus, significantly reduced proliferation in a mixed lymphocyte reaction. Surprisingly, however, transplantation of islet allografts transfected with Ad/MFL resulted in long-term allograft survival in only 1 of 30 recipients. Moreover, adenoviral-mediated Fas ligand gene transfer was complicated by transient, dose-dependent islet dysfunction, perhaps contributing to the lack of long-term engraftment. CONCLUSION: These data suggest that adenoviral-mediated Fas ligand expression may impair normal islet function in vivo, and indicate that alternative strategies for Fas ligand transgene delivery may be required in this setting.

    Title Adenovirus-mediated Gene Transfer into Cold-preserved Liver Allografts: Survival Pattern and Unresponsiveness Following Transduction with Ctla4ig.
    Date February 1998
    Journal Nature Medicine
    Excerpt

    The immune response of liver transplant recipients was modulated via adenovirus-mediated transduction of the cold-preserved liver with sequences encoding CTLA4Ig. Transplanted allografts demonstrated rapid transient local expression and recombinant protein production shortly after revascularization, resulting in intact liver function, indefinite survival of the recipient, and the development of donor-specific unresponsiveness. Lymphocytic infiltration of the graft was mainly of the T helper 2 (Th2) subset and was not associated with injury to primary cellular targets of the alloimmune response. These findings demonstrate a successful outcome of a feasible and potentially clinically relevant system of gene delivery of sequences encoding proteins capable of inhibiting the alloimmune response.

    Title Blockade of Cd40-cd40 Ligand Pathway Induces Tolerance in Murine Contact Hypersensitivity.
    Date February 1998
    Journal European Journal of Immunology
    Excerpt

    Interactions between CD40 on antigen-presenting cells and its ligand (CD40L) on T cells has been implicated in T cell-mediated immune responses. Previously, we have shown that contact hypersensitivity (CHS), a cell-mediated cutaneous immune response in reaction to haptens, could be subclassified based on whether the hapten primed for Th1 or Th2 cytokines in cells isolated from draining lymph nodes. We also found that tolerance to a Th2-priming hapten could be induced only by simultane blockade of the CD40-CD40L and B7-CD28 at the time of sensitization. Here we demonstrate that blockade of CD40-CD40L signaling alone induces long-lasting unresponsiveness to the Th1 hapten 2,4-dinitrofluorobenzene (DNFB), and inhibits antigen-specific T cell proliferation in vitro. We find that CD40-CD40L signaling is required in the sensitization but not elicitation phase of DNFB-induced CHS, as treatment of mice with anti-CD40L monoclonal antibody (mAb) does not affect the response to hapten challenge in previously sensitized and untreated animals. Examination of cytokine production shows that anti-CD40L mAb decreases interferon-gamma production by draining lymph node cells from DNFB-sensitized mice, and reciprocally increases interleukin (IL)-4 production. Consistent with this Th1 to Th2 immune deviation, anti-CD40L mAb prevents the induction of IL-12 mRNA in regional lymph nodes, an event which is normally seen within 12 h following hapten sensitization. In contrast, suppression of CHS by CTLA4Ig decreased the production of all cytokines by draining lymph node cells. Together, these data show that blockade of the CD40-CD40L pathway by itself is sufficient to induce tolerance to DNFB-induced CHS, and that this is associated with blockade of IL-12 induction and Th1 to Th2 immune deviation.

    Title Amelioration of Collagen-induced Arthritis by Cd95 (apo-1/fas)-ligand Gene Transfer.
    Date November 1997
    Journal The Journal of Clinical Investigation
    Excerpt

    Both rheumatoid arthritis and animal models of autoimmune arthritis are characterized by hyperactivation of synovial cells and hyperplasia of the synovial membrane. The activated synovial cells produce inflammatory cytokines and degradative enzymes that lead to destruction of cartilage and bones. Effective treatment of arthritis may require elimination of most or all activated synovial cells. The death factor Fas/Apo-1 and its ligand (FasL) play pivotal roles in maintaining self-tolerance and immune privilege. Fas is expressed constitutively in most tissues, and is dramatically upregulated at the site of inflammation. In both rheumatoid arthritis and animal models of autoimmune arthritis, high levels of Fas are expressed on activated synovial cells and infiltrating leukocytes in the inflamed joints. Unlike Fas, however, the levels of FasL expressed in the arthritic joints are extremely low, and most activated synovial cells survive despite high levels of Fas expression. To upregulate FasL expression in the arthritic joints, we have generated a recombinant replication-defective adenovirus carrying FasL gene; injection of the FasL virus into inflamed joints conferred high levels of FasL expression, induced apoptosis of synovial cells, and ameliorated collagen-induced arthritis in DBA/1 mice. The Fas-ligand virus also inhibited production of interferon-gamma by collagen-specific T cells. Coadministration of Fas-immunoglobulin fusion protein with the Fas-ligand virus prevented these effects, demonstrating the specificity of the Fas-ligand virus. Thus, FasL gene transfer at the site of inflammation effectively ameliorates autoimmune disease.

    Title Immunosuppression Through Blockade of Cd28:b7-mediated Costimulatory Signals.
    Date October 1996
    Journal Immunologic Research
    Excerpt

    It is now well established that T cells require two signals for activation and effector function. The first signal is provided through the T cell receptor for antigen. The best-characterized pathway which provides the second, or costimulatory, signal is through the CD28 receptor on the surface of T cells. In vitro, ligation of the T cell receptor without a second signal induces a long-lived state of anergy in T cells. CD28 has two known ligands, B7-1 and B7-2, expressed on activated antigen-presenting cells. A soluble fusion protein called CTLA4Ig has been produced which binds B7-1 and B7-2 and acts as a competitive inhibitor of CD28. In vitro and in vivo studies with CTLA4Ig demonstrate that it is an extremely effective immunosuppressive agent in models of transplantation and autoimmunity. Mechanistic studies indicate that CTLA4Ig may work by partially inhibiting the expansion of antigen-reactive cells and inducing anergy in the residual population.

    Title The in Vivo Mechanism of Action of Ctla4ig.
    Date August 1996
    Journal Journal of Immunology (baltimore, Md. : 1950)
    Excerpt

    A single dose of CTLA4Ig, an inhibitor of CD28-mediated T cell costimulation, given 2 days after transplantation induces specific unresponsiveness to alloantigens in vivo. However, the mechanisms responsible are unknown. Using pigeon cytochrome c as a model Ag, we monitored the effect of CTLA4Ig on the fate of Ag-reactive T cells in normal mice and on pigeon cytochrome c-specific TCR transgenic cells adoptively transferred into congenic mice. CTLA4Ig significantly inhibits immunization with pigeon cytochrome c. In particular, ELISA and ELISPOT assays indicate an 80 to 90% reduction in Th1 (i.e, IL-2 and IFN-gamma) cytokine production and in the numbers of cytokine-producing cells. Interestingly, despite this profound reduction in cytokine-producing cells, Ag-reactive T cells expand in CTLA4Ig-treated animals, although the degree of expansion is reduced by 50% compared with that in control Ig-treated animals. Thus, loss of Th1 cytokine production in CTLA4Ig-treated animals is not fully explained by the decreased expansion of Ag-specific T cells. These results suggest two mechanisms of action for CTLA4Ig in vivo: inhibition of expansion of Ag-reactive cells and induction of anergy in the residual population.

    Title Suppression of Murine Allergic Contact Dermatitis by Ctla4ig. Tolerance Induction of Th2 Responses Requires Additional Blockade of Cd40-ligand.
    Date August 1996
    Journal Journal of Immunology (baltimore, Md. : 1950)
    Excerpt

    Blockade of costimulation through the B7-CD28 pathway by CTLA4Ig can lead to Ag-specific T cell tolerance. Most models studied to date involve a Th1-dependent response. To investigate whether the tolerizing effects of CTLA4Ig might vary depending upon the cytokine nature of the immune response, we studied its effects on contact hypersensitivity (CHS) in response to two allergens. In BALB/c mice, both 2,4-dinitrofluorobenzene (DNFB) and FITC induce CHS. However, the DNFB response is Th1-predominant, while the FITC response is Th2 predominant. CTLA4Ig treatment during primary sensitization induced long-lasting unresponsiveness to DNFB, with 88% and 76% inhibition of primary (first challenge) and secondary (re-sensitization and re-challenge) CHS, respectively. In contrast, CTLA4Ig inhibited primary CHS to FITC by over 82% but had little effect on secondary CHS. Consistent with its effects on CHS, the suppressive effect of CTLA4Ig on Th2 cells was short-lived in FITC-sensitized mice, while Th1-like cytokine-secreting cells remained reduced in DNFB-sensitized mice, even when the animals were rechallenged with DNFB. The addition of anti-CD40L Ab to CTLA4Ig was able to induce long-lasting unresponsiveness to FITC, indicating the ability of cells mounting this Th2 response to receive costimulatory signals through either pathway. In conclusion, CHS can be mediated by both Th1 and Th2 cells, and the ability of CTLA4Ig to lead to long-standing nonresponsiveness in this model depends on the nature (i.e., cytokine profile) of the immune response.

    Title Cloning the Rat Homolog of the Cd28/ctla-4-ligand B7-1: Structural and Functional Analysis.
    Date June 1995
    Journal International Immunology
    Excerpt

    T cell activation involves the delivery of two independent signals to the naive T cell. The first signal occurs with engagement of the TCR. One of the best characterized second signals is ligation of CD28 on the surface of T cells by B7 molecules (B7-1, B7-2) present on the surface of activated antigen presenting cells (APCs). Recent studies have demonstrated that injection of a human fusion protein, CTLA-4-Ig, which in humans binds to both B7-1 and B7-2, prevents cardiac allograft rejection in a rat transplantation model when given 48 h after engraftment. In order to better characterize the role of B7-1 (which is maximally expressed 48 h after activation of APCs) in this model, as well as in models of tumor-induced immune responses, we have cloned the rat homolog of B7-1, and now report on its structure and function. A 1030 bp cDNA containing the entire coding sequence of the rat B7-1 was cloned with a polymerase chain reaction strategy utilizing degenerate primers derived from published murine and human B7-1 sequences. The rat B7-1 coding sequence is 67 and 81% homologous to human and murine B7-1 cDNAs, and the predicted peptide sequence is likewise 57 and 66% identical to the peptide sequences of human and murine B7-1 respectively. The greatest area of identity occurs in the extracellular portion of the molecule, particularly the Ig-C like domain.(ABSTRACT TRUNCATED AT 250 WORDS)

    Title Psoriatic Skin-derived Dendritic Cell Function is Inhibited by Exogenous Il-10. Differential Modulation of B7-1 (cd80) and B7-2 (cd86) Expression.
    Date April 1995
    Journal Journal of Immunology (baltimore, Md. : 1950)
    Excerpt

    Regulation of immune responses depends on interactions between APCs and T cells. Such cellular interactions are mediated by surface molecules including MHC class II Ags (DR) and CD28 ligands B7-1 (CD80) and B7-2 (CD86). Recent evidence indicates that the presence or absence of costimulatory molecules on APCs significantly influences the qualitative and quantitative nature of an immune response. In this report, we analyze two relevant cytokines in skin immunobiology, granulocyte-macrophage (GM)-CSF and IL-10, and demonstrate their effects on cultured dendritic cells obtained from dermis (DDCs) of normal skin and psoriatic lesions. For comparison, the effects on these professional APCs were contrasted with cultured blood-derived monocytes. Normal and psoriatic skin-derived DDCs express high levels of CD86 over CD80, and the overall hierarchy is DR > CD86 > CD80, whereas cultured monocytes express low and equivalent levels of CD80 and CD86. If Ab is added to GM-CSF at the initial period of cultivation, DDCs that emigrate have lower levels of CD86 without any detectable effect on CD80 or DR expression and display a reduced capacity to stimulate either superantigen-driven or alloantigen-responsive T cells. Conversely, by adding GM-CSF to monocytes, CD86 levels are enhanced. When IL-10 was added at the beginning of culture, DDCs had significantly lower levels of CD86, without any effect on CD80 or DR expression, and like anti-GM-CSF-treated cells, these DDCs had approximately a 50% reduction in their T cell-stimulating capacity. In contrast, when monocytes were treated identically with exogenously added IL-10, they retained their relatively low levels of CD80 and CD86 with no detectable change in APC function. Blocking studies of DDC:T cell interaction indicated that CD86 was more important than CD80. Thus, differential expression patterns and functional cytokine responses involving these APC populations may be relevant to skin disorders such as psoriasis, in which discordant patterns of CD28 ligand expression and disordered cytokine networks are present.

    Title Sucrase-isomaltase Gene Expression Along Crypt-villus Axis of Human Small Intestine is Regulated at Level of Mrna Abundance.
    Date February 1992
    Journal The American Journal of Physiology
    Excerpt

    The mucosal lining of the small intestine is a complex epithelium that is continually renewed by division of a stem cell population located in intestinal crypts, migration of daughter cells along the villus, and, finally, extrusion of senescent cells into the lumen. The majority of cells in both crypt and villus cell compartments are enterocytes that acquire differentiated functions as they migrate out of the crypt. Sucrase-isomaltase (SI) is an enterocyte-specific, brush-border enzyme that has little activity in crypt cells and maximal activity in low and mid villus cells. The mechanism by which enterocytes acquire SI enzymatic activity as they move from crypt to villus is controversial. In this study we examined the distribution of SI mRNA along the crypt-villus axis of human small intestine using isolated epithelial cells and in situ hybridization. A complementary DNA to the 5' portion of the human SI mRNA was amplified and cloned using the polymerase chain reaction. Hybridization analysis of RNA extracted from human intestinal epithelial cells showed that the cloned cDNA recognized a single 6.5-kb mRNA. In situ hybridization of duodenal biopsy specimens was performed using a single-stranded RNA probe derived from this cDNA. This analysis showed that there was little SI mRNA in crypt cells and appearance of mRNA in enterocytes located at the crypt-villus junction. The mRNA levels were maximal in lower and mid villus cells with decreased levels noted in villus tip cells. These results are identical to those previously described in rat intestine and suggest that expression of the SI gene as enterocytes emerge from intestinal crypts is regulated primarily at the level of mRNA accumulation. Study of SI gene regulation may provide a useful model to investigate the mechanisms that regulate enterocyte-specific gene expression and intestinal differentiation.

    Title The Role of Biological Therapy in Inflammatory Bowel Disease.
    Date
    Journal Drugs of Today (barcelona, Spain : 1998)
    Excerpt

    Substantial evidence suggests a central role for TNF-alpha in the pathogenesis of IBD. This molecular observation has been supported by clinical trials with anti-TNF therapies. The most extensively investigated among the various anti-TNF agents is infliximab. Clinical trials to date have demonstrated its efficacy in inducing remission in patients with moderately active, refractory Crohn's disease (CD) and in managing patients with CD complicated by fistulas. One advantage of infliximab is its rapid onset of action. However, as expected with most medications used to treat patients with IBD, the effect of infliximab is of limited duration, with the response lasting 2-3 months in most patients. The efficacy of repeated infusions of infliximab in maintaining remission in patients with inflammatory CD has been demonstrated in one trial to date. The results from the ACCENT I trial should soon be available. Many other important questions regarding the use of infliximab remain unanswered. These include the optimal schedules of infusions, the effect of concomitant therapy with aminosalicylates, immunomodulators and antibiotics, and the timing and indication of using infliximab in the general management algorithm of a patient with CD. Certainly, the efficacy of infliximab in the treatment of ulcerative colitis (UC) remains to be further explored in a controlled fashion, though preliminary uncontrolled data suggests efficacy. As experience with infliximab use accumulates, more data will become available regarding its safety with either short-term or long-term use. A large body of evidence exists regarding the short-term safety of infliximab. The concern of increased risk of hypersensitivity-like reactions with longer interval between treatments will also need to be addressed. The currently available data supports that infliximab is safe and well tolerated. Other anti-TNF therapies will also need to be investigated with the same rigor before widespread use can be advocated. In addition to these agents, advances in molecular engineering techniques have further expanded the array of biologic therapies available to treat IBD. These newer therapies hold promise in targeting specific pathways of the pathogenesis of IBD that may be different from all prior therapies. Certainly, the anti-TNF therapies and others aforementioned have taken the field of IBD into a new and exciting generation, the biological era. (c) 2001 Prous Science. All rights reserved.


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