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Biomedical subjects

William E Ackerman

Publications and source records attributed to William E Ackerman.

15 recordsLinked to original sources
PubMed2006

Efficacy of stellate ganglion blockade for the management of type 1 complex regional pain syndrome.

INTRODUCTION: The purpose of this study was to examine the efficacy of stellate ganglion blockade (SGB) in patients with complex regional pain syndromes (CRPS I) of their hands. METHODS: After IRB approval and patient informed consent, 25 subjects, with a clinical diagnosis of CRPS I of one hand as defined by the International Association for the Study of Pain (IASP) criteria, had three SGB's performed at weekly intervals. Laser Doppler fluxmetric hand perfusion studies were performed on the normal and CRPS I hands pre- and post-SGB therapy. No patient was included in this study if they used tobacco products or any medication or substance that could affect sympathetic function. The appropriate parametric and nonparametric data analyses were performed and a p value <0.05 was used to reject the null hypothesis. RESULTS: Symptom onset of CRPS I until the initiation of SGB therapy ranged between 3 to 34 weeks. Following the SGB series, patient pain relief was as follows: group I, 10/25 (40%) had complete symptom relief; group II, 9/25 (36%) had partial relief and group III, 6/25 (24%) had no relief. The duration of symptoms until SGB therapy was: group I, 4.6 +/- 1.8 weeks, group II, 11.9 +/- 1.6 weeks and group III, 35.8 +/- 27 weeks. Compared with the normal control hand, the skin perfusion in the CRPS I affected hand was greater in group I and decreased in groups II and III. DISCUSSION: The results of our study demonstrate that an inverse relationship exists between hand perfusion and the duration of symptoms of CRPS I. On the other hand, a positive correlation exists between SGB efficacy and how soon SGB therapy is initiated. A duration of symptoms greater than 16 weeks before the initial SGB and/or a decrease in skin perfusion of 22% between the normal and affected hands adversely affects the efficacy of SGB therapy.

Adult↗
PubMed2006

Serum hs-CRP as a useful marker for predicting the efficacy of lumbar epidural steroid injections on pain relief in patients with lumbar disc herniations.

INTRODUCTION: We examined systemic inflammatory serum markers and pain responses to image-guided lumbar epidural steroid injections (LESI) both before and after LESI in patients with lumbar disc herniations with various pathological intervertebral disc changes. METHODS: Sixty male patients were scheduled for LESI every two weeks for three injections. Prior to injection therapy the following laboratory tests were performed: a complete blood count (CBC), high-sensitivity C-reactive protein (hs-CRP), and an erythrocyte sedimentation rate (ESR). Five groups of fifteen patients each were classified according to MRI observation: I) control group, II) disc protrusion, III) disc prolapse, IV) disc extrusion, and V) sequestered disc herniation. LESI were scheduled two weeks apart and were done with fluoroscopy using 40 mg of triamcinolone with 5 ml of preservative-free lidocaine. All patients returned 6 weeks following their initial injection and repeat hs-CRP assays were obtained. RESULTS: No patient in this study had an abnormal CBC or ESR. No patient in the control group had an elevated hs-CRP. The percentage and number of patients in each experimental group with elevated hs-CRP levels were: II) 0% (0/15), III) 20% (3/15), IV) 80% (12/15), and V) 73% (11/15). LESI was more efficacious in the two contained disc herniation groups (II and III). It was found that the higher the hs-CRP levels prior to LESI therapy, the less improvement in pain scores following LESI. DISCUSSION: The results of this study suggest that elevated hs-CRP levels may be useful for objectively evaluating and predicting responses to LESI in those patients with lumbar disc pathology with lower extremity radiculitis.

Adult↗
PubMed2005

Despite transcriptional and functional coordination, cyclooxygenase-2 and microsomal prostaglandin E synthase-1 largely reside in distinct lipid microdomains in WISH epithelial cells.

Cytokine-induced prostaglandin (PG)E(2) synthesis requires increased expression of cyclooxygenase-2 (COX-2) in human WISH epithelial cells. Recently, an inducible downstream PGE synthase (microsomal PGE synthase-1, mPGES-1) has been implicated in this inflammatory pathway. We evaluated cooperation between COX-2 and mPGES-1 as a potential mechanism for induced PGE(2) production in WISH cells. Cytokine stimulation led to increased expression of both enzymes. Selective pharmacological inhibition of these enzymes demonstrated that induced PGE(2) release occurred through a dominant COX-2/mPGES-1 pathway. Unexpectedly, immunofluorescent microscopy revealed that the expression of these enzymes was not tightly coordinated among cells after cytokine challenge. Within cells expressing high levels of both mPGES-1 and COX-2, immunolabeling of high-resolution semithin cryosections revealed that COX-2 and mPGES-1 were largely segregated to distinct regions within continuous intracellular membranes. Using biochemical means, it was further revealed that the majority of mPGES-1 resided within detergent-insoluble membrane fractions, whereas COX-2 was found only in detergent-soluble fractions. We conclude that although mPGES-1 and COX-2 show transcriptional and functional coordination in cytokine-induced PGE(2) synthesis, complementary morphological and biochemical data suggest that a majority of intracellular mPGES-1 and COX-2 are segregated to discrete lipid microdomains in WISH epithelial cells.

Caveolin 1↗
PubMed2005

Modulation of cytokine-induced cyclooxygenase 2 expression by PPARG ligands through NFkappaB signal disruption in human WISH and amnion cells.

Cyclooxygenase (COX) activity increases in the human amnion in the settings of term and idiopathic preterm labor, contributing to the generation of uterotonic prostaglandins (PGs) known to participate in mammalian parturition. Augmented COX activity is highly correlated with increased COX2 (also known as prostaglandin-endoperoxide synthase 2, PTGS2) gene expression. We and others have demonstrated an essential role for nuclear factor kappaB (NFkappaB) in cytokine-driven COX2 expression. Peroxisome proliferator-activated receptor gamma (PPARG), a member of the nuclear hormone receptor superfamily, has been shown to antagonize NFkappaB activation and inflammatory gene expression, including COX2. We hypothesized that PPARG activation might suppress COX2 expression during pregnancy. Using primary amnion and WISH cells, we evaluated the effects of pharmacological (thiazolidinediones) and putative endogenous (15-deoxy-Delta(12,14)-prostaglandin J2, 15d-PGJ2) PPARG ligands on cytokine-induced NFkappaB activation, COX2 expression, and PGE2 production. We observed that COX2 expression and PGE2 production induced by tumor necrosis factor alpha (TNF) were significantly abrogated by 15d-PGJ2. The thiazolidinediones rosiglitazone (ROSI) and troglitazone (TRO) had relatively little effect on cytokine-induced COX2 expression except at high concentrations, at which these agents tended to increase COX2 abundance relative to cells treated with TNF alone. Interestingly, treatment with ROSI, but not TRO, led to augmentation of TNF-stimulated PGE2 production. Mechanistically, we observed that 15d-PGJ2 markedly diminished cytokine-induced activity of the NFkappaB transcription factor, whereas thiazolidinediones had no discernable effect on this system. Our data suggest that pharmacological and endogenous PPARG ligands use both receptor-dependent and -independent mechanisms to influence COX2 expression.

Amnion↗
PubMed2004

Epidermal growth factor and interleukin-1beta utilize divergent signaling pathways to synergistically upregulate cyclooxygenase-2 gene expression in human amnion-derived WISH cells.

In human parturition, uterotonic prostaglandins (PGs) arise predominantly via increased expression of cyclooxygenase-2 (COX-2 [also known as prostaglandin synthase 2]) within intrauterine tissues. Interleukin-1 (IL-1) and epidermal growth factor (EGF), both inducers of COX-2 transcription, are among numerous factors that accumulate within amniotic fluid with advancing gestation. It was previously demonstrated that EGF could potentiate IL-1beta-driven PGE(2) production in amnion and amnion-derived (WISH) cells. To define the mechanism for this observation, we hypothesized that EGF and IL-1beta might exhibit synergism in regulating COX-2 gene expression. In WISH cells, combined treatment with EGF and IL-1beta resulted in a greater-than-additive increase in COX-2 mRNA relative to challenge with either agent independently. Augmentation of IL-1beta-induced transactivation by EGF was not observed in cells harboring reporter plasmids bearing nuclear factor-kappa B (NFkappaB) regulatory elements alone, but was evident when a fragment (-891/ +9) of the COX-2 gene 5'-promoter was present. Both agents transiently activated intermediates of multiple signaling pathways potentially involved in the regulation of COX-2 gene expression. The 26 S proteasome inhibitor, MG-132, selectively abrogated IL-1beta-driven NFkappaB activation and COX-2 mRNA expression. Only pharmacologic blockade of the p38 mitogen-activated protein kinase eliminated COX-2 expression following EGF stimulation. We conclude that EGF and IL-1beta appear to signal through different signaling cascades leading to COX-2 gene expression. IL-1beta employs the NFkappaB pathway predominantly, while the spectrum of EGF signaling is broader and includes p38 kinase. The synergism observed between IL-1beta and EGF does not rely on augmented NFkappaB function, but rather, occurs through differential use of independent response elements within the COX-2 promoter.

Amnion↗
PubMed2004

Reciprocal expression of peroxisome proliferator-activated receptor-gamma and cyclooxygenase-2 in human term parturition.

OBJECTIVE: The objective of this study was to test the hypothesis that peroxisome proliferator activated receptor-gamma (PPAR-gamma) is expressed in intrauterine tissues before active term human parturition, and that its repression is associated with up-regulation of cyclooxygenase-2 (COX-2). STUDY DESIGN: Specimens were collected from women with term singleton pregnancies after spontaneous labor or cesarean section before labor, prepared for immunoblot and immunohistochemical analysis, and probed for PPAR-gamma or COX-2. RESULTS: PPAR-gamma expression was prominent in fetal membranes and placenta before active labor. After labor, PPAR-gamma expression was significantly reduced in fetal membranes, but not in placenta. The ratio of COX-2:PPAR-gamma was significantly elevated in fetal membranes with labor. PPAR-gamma immunostaining was prominent in syncytiotrophoblast, extravillous cytotrophoblasts, and cells of the amnion and chorion. COX-2 immunostaining was abundant in the amnion and rare in the placenta. CONCLUSION: PPAR-gamma is highly expressed in term intrauterine tissues. In fetal membranes, PPAR-gamma levels are reduced once active labor commences, coincidental with a relative increase in COX-2 expression.

Adult↗
PubMed2004

Are diagnostic lumbar facet injections influenced by pain of muscular origin?

INTRODUCTION: Nonradicular low back pain can be a difficult entity to accurately diagnose and treat. Facet joints, muscle, ligaments, and fascia have all been reported to be etiologies of acute and chronic low back pain. However, the facet joint as a source of low back pain is controversial. The diagnosis of facet joint pain is made by diagnostic facet joint or median nerve branch injections with a local anesthetic. The purpose of this study was to determine if the results of diagnostic facet joint injections are influenced by the technique used to perform these injections. METHODS: Seventy-five male patients aged 45 years or younger and 18 years or older who were injured while performing heavy work with nonradicular low back pain were included in this study. Diagnostic injection therapy was performed following Institutional Review Board approval and the patient's informed consent. Patients were assigned to one of five groups to receive diagnostic injections in a double-blinded fashion as follows: Group I: facet joint injection with continuous lidocaine administration from the skin to the facet joint as the needle was advanced; Group II: facet joint injection with saline administration from the skin to the facet joint as the needle was advanced; Group III: median nerve branch injection with a lidocaine advancing needle technique; Group IV: median nerve branch injection with saline advancing needle technique; and Group V: injection of the paraspinous muscles with local anesthetic and steroid following noted areas of pain diagnosed with saline injection and radiopaque contrast. After one week, the patients in Groups I to IV who had no pain relief with facet joint or median nerve block injections subsequently received paraspinous muscle injections, while the patients in Group V who had no long-term relief with muscle injections were given facet joint injections. The appropriate parametric and nonparametric tests were performed with statistical significance defined as P < or = 0.05. RESULTS: There were no differences among the groups demographically. The incidence of pain relief was significantly higher in subjects who had a continuous injection of local anesthetic into their musculature than in those individuals who received continuous saline followed by an injection of local anesthetic into their facet joint or median nerve branch. DISCUSSION: The results of this study demonstrated that local anesthetic injections are useful for the diagnosis of nonradicular low back pain but may yield false positive results with respect to lumbar facet pain depending upon the technique utilized.

Journal Article↗