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Biomedical subjects

J M Weiss

Publications and source records attributed to J M Weiss.

At least 73 records · Page 4Linked to original sources
PubMed1998

Possible role of coagulation factor XIII in the pathogenesis of venous leg ulcers.

BACKGROUND: Aim of this placebo-controlled clinical study was to examine the expression pattern of coagulation factor XIIIa in patients with chronic venous leg ulcers and the impact of a 10 day topical factor XIII treatment on ulcer healing, leg ulcer size and radius reduction. PATIENTS AND METHODS: 24 patients were stratified into two groups, each consisting of 12 patients, with leg ulcers > 1.000 mm2, or < 1.000 mm2. Four patients of each study group were assigned to the control group (n = 8). All leg ulcers were treated by topical application of non-adhering dressings and compression therapy. Patients of the treatment group (n = 16) were treated by additional topical treatment off factor XIII twice daily for ten days. Immunohistochemical staining of leg ulcer specimens before and after treatment (day 10) was performed in all patients. RESULTS: The immunohistochemical staining of factor XIIIa in all specimens before and after therapy showed no significant increase in the expression of factor XIIIa. Comparison of the leg ulcer size, radius and daily radius reduction in the treatment and control group showed no significant differences in values of patients with leg ulcers > 1.000 mm2. However, a decreased leg ulcer size and radius was found in patients of the treatment group with more acute leg ulcers < 1.000 mm2 in contrast to patients with larger leg ulcers (daily ulcer radius reduction from day 0-10; 0.31 mm versus 0.13 mm, p < 0.015). CONCLUSIONS: These results indicate that locally applied factor XIII promotes especially wound healing of more acute smaller venous leg ulcers. Since immunohistochemical staining of factor XIIIa showed no significant differences before and after therapy, we propose that factor XIII is inactivated rapidly after local application on venous leg ulcers.

Administration, Topical↗
PubMed1998

Further characterization of UVB radiation effects on Langerhans cells: altered expression of the costimulatory molecules B7-1 and B7-2.

We have reported previously that low-dose UVB radiation (UVBR, 50-200 J/m2) perturbs the antigen-presenting cell (APC) function of murine Langerhans cells (LC) by interfering with yet undefined costimulatory signals. In this study, we investigated (1) the effects of UVBR on the expression of the costimulatory molecules B7-1 and B7-2 on murine LC, (2) the functional consequences of defective B7-1 and B7-2 signalling on primary and secondary T-cell responses induced by LC and (3) the mechanism by which UVBR interferes with B7-1 and B7-2 expression. Ultraviolet-B radiation dose-dependently inhibited the culture-induced upregulation of B7-1 and B7-2 on LC from both UVB-susceptible (UVBs, C57BL/6) and UVB-resistant (UVBR, Balb/c) mice and abrogated their capacity to stimulate proliferation of naive alloreactive T cells and of the KLH (keyhole limpet hemocyanin)-specific T helper (Th)1 clone HDK-1. The UVBR-induced suppression of B7-1 and B7-2 on LC and their perturbed APC function were related, because exogenous triggering of the B7/CD28 pathway with a stimulatory monoclonal antibody (mAb) for CD28 to UVB-irradiated LC partially restored T-cell proliferation. Such reconstitution was not observed when the mAb was added to killed LC, indicating that the UVBR-induced suppression of APC function was not due to lethal effects on LC. Conditioned supernatants from UVB-irradiated epidermal cells did not inhibit the functional upregulation of B7-1 and B7-2, suggesting that UVBR inhibits B7-1 and B7-2 upregulation by acting directly on LC and not by altering LC costimulatory function via release of soluble immunosuppressive factors. In conclusion, UVBR distorts the functional expression of B7-1 and B7-2 on LC from both UVBS and UVBR mice, thereby contributing to the failure of UVB-irradiated LC to stimulate resting alloreactive T cells or KLH-specific Th1 cells.

Animals↗
PubMed1997

An essential role for CD44 variant isoforms in epidermal Langerhans cell and blood dendritic cell function.

Upon antigen contact, epidermal Langerhans cells (LC) and dendritic cells (DC) leave peripheral organs and home to lymph nodes via the afferent lymphatic vessels and then assemble in the paracortical T cell zone and present antigen to T lymphocytes. Since splice variants of CD44 promote metastasis of certain tumors to lymph nodes, we explored the expression of CD44 proteins on migrating LC and DC. We show that upon antigen contact, LC and DC upregulate pan CD44 epitopes and epitopes encoded by variant exons v4, v5, v6, and v9. Antibodies against CD44 epitopes inhibit the emigration of LC from the epidermis, prevent binding of activated LC and DC to the T cell zones of lymph nodes, and severely inhibit their capacity to induce a delayed type hypersensitivity reaction to a skin hapten in vivo. Our results demonstrate that CD44 splice variant expression is obligatory for the migration and function of LC and DC.

Animals↗
PubMed1996

The cubic ternary complex receptor-occupancy model. III. resurrecting efficacy.

Early work in pharmacology characterized the interaction of receptors and ligands in terms of two parameters, affinity and efficacy, an approach we term the bipartite view. A precise formulation of efficacy only exists for very simple pharmacological models. Here we extend the notion of efficacy to models that incorporate receptor activation and G-protein coupling. Using the cubic ternary complex model, we show that efficacy is not purely a property of the ligand-receptor interaction; it also depends upon the distributional details of the receptor species in the native receptor ensemble. This suggests a distinction between what we call potential efficacy (a vector) and realized efficacy (a scalar). To each receptor species in the native receptor ensemble we assign a part-worth utility; taken together these utilities comprise the potential efficacy vector. Realized efficacy is the expectation of these part-worth utilities with respect to the frequency distribution of receptor species in the native receptor ensemble. In the parlance of statistical decision theory, the binding of a ligand to a receptor ensemble is a random prospect and realized efficacy is the utility of this prospect. We explore the implications that our definition of efficacy has for understanding agonism and in assessing the legitimacy of the bipartite view in pharmacology.

Humans↗
PubMed1996

Susceptibility and resistance of rats to stress-induced decreases in swim-test activity: a selective breeding study.

In this study, selective breeding was used to generate two populations of rats that differed in their susceptibility to showing decreased struggling activity in a swim test after being exposed to uncontrollable electric tail-shock. After five generations of selective breeding, we obtained a population that displayed large decreases in swim-test struggling after shock (swim-test susceptible) and a population that displayed no decrease in struggling after shock (swim-test resistant). Males of this fifth generation from the two selectively-bred populations were then compared for differences in non-swim behavioral measures (home-cage 24-h spontaneous ambulatory activity and food/water intake) and several aspects of brain catecholaminergic activity, including electrophysiological activity of locus coeruleus (LC) neurons, catecholamine/metabolite concentrations in various brain regions, and in vivo tyrosine hydroxylase activity. Interestingly, swim-test resistant rats displayed larger decreases in home-cage ambulatory activity and water intake after exposure to shock than did swim-test susceptible animals. Marked differences were also seen in measures of brain noradrenergic activity. Compared to the susceptible rats, resistant rats showed higher levels of evoked activity of LC neurons, larger shock-induced depletions of norepinephrine (NE) and 3-methoxy-4-hydroxyphenylglycol (MHPG) in the LC, lower in vivo tyrosine hydroxylase (TH) activity in ventral bundle projection areas such as the hypothalamus, and larger amounts of NE in dorsal bundle projection areas. Finally, swim-test resistant rats had much higher concentrations of dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in striatum and nucleus accumbens than susceptible rats. These results appear to be explainable on the basis that differences in swim-test struggling behavior for which the two populations were selectively bred were a consequence of differences in forebrain DA whereas stress-induced differences in other behavioral measures (i.e. spontaneous ambulation and intake) occurred because swim-test resistant animals showed greater disturbance of the LC-NE system after uncontrollable shock.

Animals↗
PubMed1996

Influence of corticotropin-releasing hormone on electrophysiological activity of locus coeruleus neurons.

These experiments examined the effects of corticotropin-releasing hormone (CRH) on single-unit electrophysiological activity of locus coeruleus (LC) neurons. As has been reported previously, infusion of CRH into the ventricular system of the brain (i.c.v.) of halothane-anesthetized adult male rats increased spontaneous discharge rate of LC neurons while producing no increase, and possibly a decrease, in sensory-evoked activity. However, when i.c.v. CRH was given to female rats or immature male rats, which had not been studied previously, LC activity was not altered. To attempt to understand this sex and age difference, potential mechanisms by which i.c.v. CRH elevates LC spontaneous activity in adult male rats were examined; in that i.c.v. CRH activates the pituitary-adrenal axis and autonomic nervous system, these response systems were manipulated. Adrenalectomy (with or without corticosterone replacement by pellet) did not affect the ability of i.c.v. CRH to increase LC spontaneous activity in adult male animals, but blockade of sympathetically-mediated autonomic responses, either by chlorisondamine or the beta adrenergic receptor blocker timolol, blocked this increase, indicating that afferent feedback from peripheral autonomic responses was critical for activating LC neurons following i.c.v. CRH. To determine whether CRH neurotransmission might play a role in this feedback pathway, the CRH antagonist alpha-helical CRH (alpha-hCRH) was microinjected into several brain regions including LC prior to i.c.v. CRH. alpha-hCRH microinjected into LC reduced the increase in LC activity caused by i.c.v. CRH; however, blockade of this increase was total when alpha-hCRH was microinjected into the lateral parabrachial nucleus ipsilateral to the LC recording site, suggesting that increased LC activity following i.c.v. CRH is mediated by CRH acting in the parabrachial region. During these studies, it was also observed that microinjection of alpha-hCRH into LC increased LC spontaneous discharge rate; consequently, CRH was microinjected into LC, and produced a dose-dependent decrease in LC spontaneous activity in both male and female rats, which could be blocked by microinjection of alpha-hCRH - these data indicated that the direct influence of CRH on LC neurons is to decrease their spontaneous activity. To reconcile this with the original report that CRH applied to LC neurons increases their activity, one possibility suggested is that the CRH microinjection procedure used in the present study stimulated inhibitory receptors on LC dendrites whereas the original study stimulated excitatory receptors on LC cell bodies. It is concluded that an inhibitory influence of CRH on LC activity is consistent with recent data indicating that decreased LC activity increases anxiety and stress-related responses, but that direct influences of CRH appear rather minor in determining LC neuronal activity in comparison to other inputs to LC such as are seen after i.c.v. CRH infusion.

Adrenalectomy↗
PubMed1996

CD40 is functionally expressed on human keratinocytes.

The CD40/gp39 pathway is known to be an important feature of B/T cell collaboration leading to T cell-dependent activation, proliferation or differentiation of B cells. Additionally, CD40 is involved in the regulation of B cell survival and apoptosis. Recently, CD40 has been shown to be expressed functionally on non-hematopoietic cells, i.e. endothelial cells. Here, we demonstrate that human keratinocytes (KC) cultured in vitro express CD40 constitutively. The surface expression of CD40 is markedly up-regulated following stimulation with interferon (IFN)-gamma, but not with tumor necrosis factor-alpha or interleukin (IL)-1 beta. This process is regulated at the CD40 mRNA level as demonstrated by Northern blot analysis. Furthermore, ligation of CD40 via soluble gp39, the CD40 ligand, enhances intercellular adhesion molecule (ICAM)-1 and Bcl-x up-regulation on IFN-gamma-stimulated KC, but not lymphocyte function-associated antigen (LFA)-3, B7-2, HLA-DR, or Fas expression. The release of IL-8 is also induced following CD40 ligation on KC. In psoriasis, a T cell-mediated inflammatory skin disease, KC have a markedly enhanced expression of CD40. This expression co-localizes with the expression of ICAM-1, Bcl-x, and an influx of CD3+ T cells. These findings suggest a functional role of CD40 on KC in inflammatory skin disorders such as psoriasis and could make a therapeutic intervention by disrupting the CD40/gp39 pathway an approach to consider in these inflammatory skin diseases.

Adult↗
PubMed1996

Expression of the adhesion molecules ICAM-1, VCAM-1, and E-selectin and their ligands VLA-4 and LFA-1 in chronic venous leg ulcers.

BACKGROUND: Leukocyte binding to endothelial cells (ECs) is thought to contribute to the pathogenesis of leg ulcers caused by chronic venous insufficiency. In other systems, such binding is mediated by the interaction of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule- (VCAM-1) and E-selectin (on ECs), and leukocyte function-associated antigen-1(LFA-1) and very late activated antigen-4 (VLA-4) (on Leukocytes). OBJECTIVE: Our purpose was to determine whether an increased expression of these adhesion molecules contributes to the pathogenesis of chronic venous insufficiency. METHODS: Twenty-seven biopsy specimens of inflamed dermatoliposclerotic skin adjacent to venous leg ulcers were stained immunohistochemically with monoclonal antibodies against ICAM-1, VCAM-1, LFA-1, VLA-4, and E-selectin. Staining intensity was compared with that of normal skin. RESULTS: Specimens of leg ulcers caused by chronic venous insufficiency showed increased expression of ICAM-1 and VCAM-1 but not of E-selectin on The expression of LFA-1 and VLA-4 on perivascular leukocytes was increased dramatically in comparison to healthy skin. CONCLUSION: Upregulation of ICAM-1 and VCAM-1 on ECs may contribute to the increased adherence and extravasation of LFA-1 and VLA-4-positive leukocytes in chronic venous insufficiency.

Aged↗
PubMed1996

Hormonal ablation of prostatic cancer: effects on prostate morphology, tumor detection, and staging by endorectal coil MR imaging.

OBJECTIVE: The purpose of our study was to evaluate the effect of androgen deprivation therapy on the MR imaging findings of prostate gland anatomy and cancer pathology in men with prostatic cancer treated with hormonal ablation before radical prostatectomy. MATERIALS AND METHODS: Twenty-two patients (mean age, 66 years old) were divided into two groups: in group I (n=10), MR imaging studies were done before and after hormonal treatment; in group II (n=12), MR imaging studies were done only after hormonal treatment. MR imaging was performed on a 1.5 T-scanner (Signa; General Electric Medical Systems, Milwaukee, WI) and included transverse plane phased-array coil T1-weighted images (TR/TE, 600/12), combined endorectal phased-array coil transverse plane T1-weighted images, fast spin-echo T2-weighted (4000/102), and coronal plane fast spin-echo T2-weighted images. Image evaluation was by consensus and included assessment of the gland size, signal intensity, tumor depiction, extracapsular extension, seminal vesicle invasion, and overall staging accuracy (Jewett and Whitmore classification). MR imaging findings were correlated with pathologic findings of step section radical prostatectomy. RESULTS: After hormonal therapy, the volume of the prostate gland showed a mean decrease of 33.5% +/- 19.6% SD (range, 0-64%). Volume reduction in the transition zone (mean 29.2% +/- 22% SD) was less than in the peripheral zone (mean, 55.8% +/- 25.8% SD) (p < .05). On T2-weighted images, the peripheral zone showed homogeneous decreases in signal intensity in 13 of 22 (58%) patients. Compared with pathologic findings, the accuracy of tumor detection by MR imaging was 74% (98 of 132 sites). Tumor presence was overestimated in 32 of 132 (24%) sites. Overall staging accuracy after hormonal ablation was 68% (15 of 22). The positive predictive value and negative predictive value for extracapsular extension were 57% (13 of 23 sites) and 90% (19 of 21 sites), respectively, and for seminal vesicle invasion were 80% (8 of 10 sites) and 97% (33 of 34 sites), respectively. CONCLUSION: As detected by MR imaging, hormonal ablation caused a decrease in size and signal intensity of the prostate gland and seminal vesicles and overestimation of tumor presence and extracapsular extension.

Aged↗
PubMed1996

Clinical histochemical and immunohistochemical investigation of the capillary basal membrane in chronic venous insufficiency.

Present investigations regarding the pathogenesis of chronic venous insufficiency (CVI) are focusing on microvascular changes. The aim of our investigation was to examine the correlation between the thickness of pericapillary type IV collagen depositions, basal membrane alterations and transcutaneous oxygen tension (TcPO2) in CVI-patients. Histochemical and immunohistochemical investigation of the capillary basal membrane was performed on 15 biopsies from normal controls, as well as 30 patients with CVI stage I and III (classification by Widmer & Stähelin). In all subjects TcPO2 was measured just prior to biopsy procedures in exactly the same area where the specimen was subsequently excised. The microscopically measured thickness of the collagen IV layer and the basal membrane was increased significantly in patients with CVI. Specimens from normal controls showed a collagen IV layer thinner than 0.1 micron. Patients with CVI stage III revealed strong collagen IV depositions between 0.2 and 0.3 microns. Comparison between TcPO2 and histological findings in the measured ares showed oxygen pressure varying from 62 mmHg (SEM 4.94 mmHg) in normal controls, down to 13 mmHg (SEM 3.39 mmHg) in patients with thick collagen IV layers. Besides an increased collagen IV layer, microvascular thrombosis and a thickened basal membrane have to be considered for impaired capillary perfusion.

Adult↗
PubMed1995

In situ expression of B7 and CD28 receptor families in human malignant melanoma: relevance for T-cell-mediated anti-tumor immunity.

Work in animal models has suggested that interactions of members of the B7 receptor family (e.g., B7-1, B7-2) on tumor cells with their ligands CD28 and CTLA-4 on cytotoxic T cells (CTL) are important for the induction of anti-tumor immunity against malignant melanoma (MM). To determine whether these molecules are of relevance for CTL responses against human MM, we studied the expression of B7-1, B7-2, CD28 and CTLA-4 in primary tumors of MM (PMM), MM metastases (MMM) and benign melanocytic nevi (BMN) by immunohistochemistry (IH) and by reverse transcription polymerase chain reaction (RT-PCR). By RT-PCR, B7-1 and B7-2-specific mRNAs were detected in most PMM, MMM and BMN. These PCR-signals were derived from CD45(+)-infiltrating leukocytes and not from tumor cells since (I) MMM depleted of CD45+ cells contained no B7-1 or B7-2 mRNA; and (2) by IH, B7-1 and B7-2 were found on infiltrating dendritic cells, macrophages and a variable proportion of tumor-infiltrating lymphocytes (TIL) but not on melanoma cells or nevus cells. The important exceptions were 5/5 spontaneously regressing PMM, in which B7-1 and B7-2 were expressed by melanoma cells, that were surrounded by TIL expressing CD28 but not CTLA-4. We conclude that, in PMM, MMM and BMN, the majority of TIL are CD28+ and that B7-1 and B7-2 are expressed by CD45(+)-infiltrating antigen-presenting cells (APC) and TIL, but not by the tumor cells. However, in spontaneously regressing PMM, melanoma cells express B7-1, B7-2 and MHC class-I and -II antigens, particularly in areas with clinical and histological signs of an ongoing anti-tumor response. These data suggest that the absence of B7-1 and B7-2 favors the escape of MM from immunosurveillance, while B7-1, B7-2 expression enhances T-cell-mediated anti-tumor immunity.

Abatacept↗
PubMed1995

Low-dose UVB radiation perturbs the functional expression of B7.1 and B7.2 co-stimulatory molecules on human Langerhans cells.

In previous studies, we have shown that ultraviolet (UV) B radiation perturbs the APC function of Langerhans cells (LC) by interfering with as-yet unidentified co-stimulatory signals. Recently, B7.1 and B7.2 on APC were shown to deliver important co-stimulatory signals through interaction with their counter receptors CD28 and CTLA-4 on T cells. To determine whether UVB affects the functional expression of B7.1 or B7.2 on LC, B7.1 and B7.2 expression was studied on human LC by multiparameter flow cytometry. Little, if any, B7.1 or B7.2 was detected on LC freshly isolated from skin. However, following 48 h of tissue culture, expression of both B7.1 and B7.2 were markedly up-regulated. To test whether these molecules were functional, primary mixed epidermal cell leukocyte reactions (MECLR) were performed. Blocking monoclonal antibody (mAb) to B7.1 or B7.2 both inhibited the MECLR, with anti-B7.2 being much more effective than anti-B7.1. UVB radiation dose-dependently (100-200 J/m2) suppressed the culture-induced up-regulation of B7.1 and B7.2 on LC. Since LC exposed to the same UVB flux (UVB-LC) failed to stimulate alloreactive T cells in a MECLR, we questioned whether this was related to their inability to provide B7 co-stimulation. Indeed, when effective B7-CD28 signaling was ascertained by adding submitogenic doses of exogenous anti-CD28 mAb to UVB-LC, the proliferative response of alloreactive T cells was restored. We conclude that the suppressive effects of low-dose UVB radiation on the APC function of LC are, at least in part, due to an inhibition of functional B7.1 and B7.2 expression.

Antibodies, Monoclonal↗
PubMed1995

beta-Endorphin enhances the replication of neurotropic human immunodeficiency virus in fetal perivascular microglia.

The effect of an endogenous opiate, beta-endorphin, on the replication of HIV was investigated in brain perivascular microglia. Beta-endorphin enhanced the synthesis of p-24 antigen and transactivation of HIV promoter. Dialysed culture supernatants of endorphin-treated microglia re-activated latent HIV infection. These culture supernatants showed elevated levels of interleukin-1 beta, IL-6 and tumor necrosis factor alpha. Sub-optimal concentration of beta-endorphin potentiated GP-120-induced synthesis of these cytokines. Nalaxone reversed beta-endorphin-induced, but not GP-120-induced, cytokine production and enhanced HIV replication. These results suggest that endogenous opiates may contribute to the progression of AIDS dementia complex.

Cytokines↗
PubMed1995

Pentoxifylline inhibits tumor necrosis factor-alpha (TNF alpha)-induced T-lymphoma cell adhesion to endothelioma cells.

Pentoxifylline, a methylxanthine derivative, has been shown to inhibit T-cell-mediated cutaneous immune response by yet ill-understood mechanisms. Because cell adhesion to endothelial cells is a critical step in the initiation of such immune responses, we analyzed whether pentoxifylline would affect this process. To address this issue, adhesion of mouse T-lymphoma cells (TK-1) to mouse endothelioma cells (eEnd.2), either untreated or stimulated with tumor necrosis factor-alpha (TNF alpha), was studied. Pentoxifylline reduced the ability of endothelioma cells stimulated with different concentrations of TNF alpha, but not of untreated endothelioma cells, to bind T-lymphoma cells in dose-dependent (10(-5)-10(-3) M) fashion. Selective incubation of either endothelioma cells or T-lymphoma cells revealed that pentoxifylline acted exclusively on the endothelioma cells, even when added after TNF alpha stimulation. We questioned whether pentoxifylline suppressed T-lymphoma cell/endothelioma cell interactions by interfering with adhesion molecules expressed by either cell. However, as determined by flow cytometry, pentoxifylline did not alter TNF alpha-induced upregulation of intercellular adhesion molecule-1 or vascular cellular adhesion molecule-1 on endothelioma cells nor did it affect constitutive CD11a, CD18, or alpha 4-integrin expression on T-lymphoma cells, suggesting that rather than affecting quantitative expression of these adhesion molecules, pentoxifylline might modulate their avidity. We conclude that pentoxifylline in therapeutically achievable concentrations is a potent inhibitor of TNF alpha-induced T-lymphoma cell adhesion to endothelioma cells. This finding may account, at least in part, for the recently discovered anti-inflammatory action of pentoxifylline.

Animals↗
PubMed1995

Prostaglandin E1 inhibits TNF alpha-induced T-cell adhesion to endothelial cells by selective down-modulation of ICAM-1 expression on endothelial cells.

Prostaglandins have been shown to be involved in the suppression of contact hypersensitivity (CHS) by so-far ill understood mechanisms. T-cell migration across the lining of cytokine-activated endothelial cells (EC) is thought to be a central step in the initiation of CHS. The aim of our investigation was therefore to examine whether prostaglandin E1 (PGE1) influences cytokine-induced TK-1 mouse T-cell lymphoma adhesion to eEnd.2 mouse endothelioma cells. Here, we report that PGE1 (10(-12)-10(-8) M) dose-dependently reduced TNF alpha-induced T-cell binding, while TNF alpha-unstimulated adhesion was not affected. To test whether PGE1 acted primarily on T-cells or on EC, they were separately pretreated with PGE1 prior to the adhesion assay. Selective PGE1 pretreatment of eEnd.2, but not of TK-1 dose-dependently inhibited TNF alpha, stimulated T-cell adhesion. Since binding of TK-1 to TNF alpha-treated eEnd.2 is mediated by the interaction of ICAM-1 and VCAM-1 (on EC) with their receptors LFA-1 and VLA-4 (on T-cells), we further investigated whether PGE1 would modulate the expression of these molecules. FACS-analysis revealed PGE1 to inhibit TNF alpha-induced upregulation of ICAM-1, but not of VCAM-1 on EC. Furthermore, constitutive LFA-1 and VLA-4 expression on T-cells was not affected by PGE1. We conclude that PGE1 supresses T-cell adhesion to EC by selectively inhibiting TNF alpha-induced upregulation of ICAM-1 on EC. This may be one mechanism by which prostaglandins suppress immune responses requiring T-cell EC interactions such as contact hypersensitivity in skin.

Alprostadil↗
PubMed1995

Prostate cancer: effect of postbiopsy hemorrhage on interpretation of MR images.

PURPOSE: To assess the frequency of changes in signal intensity after prostatic biopsy and the effect of these changes on the magnetic resonance (MR) imaging staging of prostate cancer. MATERIALS AND METHODS: Seventy-three patients with biopsy-proved prostate cancer were divided into two groups according to time between biopsy and imaging (less than and more than 21 days). The findings at MR imaging were compared with those at pathologic examination. RESULTS: Postbiopsy hemorrhage was detected in 21 of 26 (81%) patients who underwent imaging less than 21 days after biopsy and in 23 of 47 (49%) patients who underwent imaging more than 21 days after biopsy (P < .01). Postbiopsy changes persisted for as long as 4 1/2 months. Less than 21 days after biopsy, there was a tendency to overestimate tumor presence and extracapsular extension. After 21 days, tumor presence was underestimated but the positive predictive value for extracapsular extension was improved. Staging accuracy less than 21 days after biopsy was 46%; this improved to 83% after 21 days (P < .01). CONCLUSION: Staging accuracy is significantly improved when imaging is deferred for 21 days after biopsy.

Biopsy, Needle↗