Biomedical subjects

L M Wang

Publications and source records attributed to L M Wang.

At least 55 records · Page 3Linked to original sources

PubMed1998

Continuous flumazenil infusion in preventing complications arising from severe benzodiazepine intoxication.

A prospective, randomly controlled study was conducted to test the effect of continuous flumazenil infusion in preventing complications arising from severe benzodiazepine (BZ) intoxication. Patients who were believed to be suffering benzodiazepine intoxication and whose Glasgow Coma Scale (GCS) score was below 10 were enrolled after showing a clear-cut response to flumazenil 0.5 or 1 mg (an improvement by 4 or more on the GCS). The patients were consecutively enrolled and randomized into two groups: a continuous infusion group (CI, n = 50) who were immediately given flumazenil 0.5 mg/h for 5 hours, and a control group (CIN, n = 50). Age, sex, incidence of underlying disease, GCS score at several time points, and complication rate were compared in the two groups. Although the CI group had a higher GCS score at most time points, the complication rate did not significantly differ between the two groups (14 of 36 in the CI group v 12 of 38 in the CIN group, P = .684). A greater incidence of underlying disease and an older age seemed to contribute to the higher complication rates in both groups. Several patients (in both groups) resedated into deeper coma after showing an initial response to flumazenil or after the cessation of flumazenil infusion. For severe BZ intoxication, treatment with flumazenil infusion should still be considered skeptically and should not be recommended as routine management BZ-intoxicated patients with an underlying disease, an older age, and resedation into a deep comatose state after showing an initial response to flumazenil should be treated in an intensive care unit.

Adult↗

PubMed1998

ErbB tyrosine kinases and the two neuregulin families constitute a ligand-receptor network.

The recently isolated second family of neuregulins, NRG2, shares its primary receptors, ErbB-3 and ErbB-4, and induction of mammary cell differentiation with NRG1 isoforms, suggesting functional redundancy of the two growth factor families. To address this possibility, we analyzed receptor specificity of NRGs by using an engineered cellular system. The activity of isoform-specific but partly overlapping patterns of specificities that collectively activate all eight ligand-stimulatable ErbB dimers was revealed. Specifically, NRG2-alpha [corrected], like NRG1-beta [corrected], emerges as a narrow-specificity ligand, whereas NRG2-beta [corrected] is a pan-ErbB ligand that binds with different affinities to all receptor combinations, including those containing ErbB-1, but excluding homodimers of ErbB-2. The latter protein, however, displayed cooperativity with the direct NRG receptors. Apparently, signaling by all NRGs is funneled through the mitogen-activated protein kinase (MAPK). However, the duration and potency of MAPK activation depend on the identity of the stimulatory ligand-receptor ternary complex. We conclude that the NRG-ErbB network represents a complex and nonredundant machinery developed for fine-tuning of signal transduction.

Calcium-Calmodulin-Dependent Protein Kinases↗

PubMed1998

Pulmonary edema induced by angiotensin I in rats.

This study was performed to demonstrate an experimental procedure of pulmonary edema induced by angiotensin I (AT I) in rats and to elucidate the mechanism of hemodynamic pulmonary edema. In the previous pilot study, 20 microg/kg of AT I was found to be an adequate dose for inducing pulmonary edema. To elucidate the mechanism of AT I pulmonary edema and protective measures against it, we observed the effects of captopril (CAP, 5 and 10 mg/kg), an angiotensin converting enzyme inhibitor; losartan (LOS, 10 mg/kg), an angiotensin II (AT II)-receptor antagonist; and phentolamine (PHE, 10 mg/kg), an alpha-adrenergic receptor blocker, on AT I-induced pulmonary edema in rats. Similarly, we also observed the effects of CAP (10 and 20 mg/kg) on pulmonary edema induced by 25 microg/kg of adrenaline (ADR) in rats. The development of AT I-induced pulmonary edema was significantly suppressed by CAP and LOS, but was unaffected by PHE. In contrast, the development of ADR-induced pulmonary edema was not suppressed by CAP. These results suggest that AT I-induced pulmonary edema is developed via the AT II and a specific AT II-receptor, without the indirect action of adrenaline.

Adrenergic alpha-Antagonists↗

PubMed1998

Recombinant heregulin-Pseudomonas exotoxin fusion proteins: interactions with the heregulin receptors and antitumor activity in vivo.

Growth factor receptors provide unique opportunities for development of targeted anticancer therapy. Members of the type I receptor tyrosine kinase family, including epidermal growth factor (EGF) receptor (EGFR) and ErbB-2/neu, are often overexpressed in various human cancer cells, including breast. Recently, it has been shown that both ErbB-3 and ErbB-4 are receptors for heregulin (HRG)/Neu differentiation factor. Eight chimeric toxins composed of the extracellular and EGF-like domains of four different HRG isoforms and truncated Pseudomonas exotoxin (PE38KDEL) were constructed. The fusion proteins exhibited activity similar to the native HRG in inducing ErbB receptors phosphorylation. The EGF-like domain of HRG13 and HRGbeta2 fused to PE38KDEL showed the highest cytotoxic activity, with a IC50 of < or = 0.001 ng/ml. The alpha isoforms that were fused to PE38KDEL were 100-fold less active than the beta isoforms. The HRG-Pseudomonas exotoxin (PE) toxins show extremely high activity against cells expressing ErbB-4 receptor, alone or together with other members of the ErbB receptor family. Cells that do not express ErbB-4 but express ErbB-3 receptor, together with the ErbB-2 or EGFR, exhibited moderate sensitivity to HRG-PE toxins. HRG-PE toxins have little or no activity against cells expressing EGFR, ErbB-2, or ErbB-3 alone. More than an 80% tumor regression was achieved by intratumor injection of 1 microg of fusion proteins per day for 5 days. Continuous i.p. administration of EGF-like domain of HRGbeta1-PE38KDEL for 7 days via a miniosmotic pump at a dose of 40 microg/kg/day inhibited the growth of ErbB-4 receptor positive but not ErbB-4 receptor negative cell lines in athymic nude mice. We conclude that there is therapeutic potential of HRG-PE toxins in the therapy of cancers overexpressing the ErbB-4 or ErbB-2 plus ErbB-3 receptors.

Animals↗

PubMed1998

Emergency medical resource use in Taipei city.

BACKGROUND: It is a worldwide trend to serve emergency patients at emergency department (EDs) staffed by board-certified emergency physicians (EPs). The question arises as to how many EPs are cost effective? This cannot be answered until utilization of emergency resources in the community is explored, so that appropriate plans for efficient ED use, staffing and training of EPs can be made. METHODS: A prospective randomized chart-review study was conducted from August 1, 1995, until May 31, 1996, in the EDs of eight large hospitals in Taipei City. These included Chung-Hsin Municipal Hospital (CHH), Chung-Shiaw Municipal Hospital (CSH), Ho-Ping Municipal Hospital (HPH), Jen-Ai Municipal (JAH), Mackay Memorial Hospital (MMH), Tri-Service General Hospital (TSGH), Veterans General Hospital-Taipei (VGH-T) and the Yang-Ming Municipal Hospital (YMH). RESULTS: Of 37,889 cases reviewed, the average daily ED census at each hospital was: VGH-T 198; TSGH 148; MMH 224; HPH 62; YMH 84; CHH 41; JAH 102; and CSH 139. At MMH, pediatric patients comprised 38.8% of emergency patients and the elderly comprised 49% of patients of VGH-T. The average age of patients was 56 years in VGH-T and 40 years in other hospitals. There were 71 (11.1%) pediatric patients and 3,087 (1.8%) adult patients taken to hospital by an emergency medical services (EMS) ambulance. A total of 176 pediatric and 2,230 (8.1%) adult patients belonged to triage categories 1 and 2. VGH-T had a much higher percentage of triage 1 and 2 patients (769, 13%) than the other hospitals. A total of 30.7% of pediatric and 17.4% of adult patients were classified as triage 4 (pseudoemergency). Patients requiring advanced life support, referral cases and patients requiring an intensive care unit (ICU) bed accounted for 1.1%, 0.9% and 0.6% of pediatric patients, and 6.8%, 3.4% and 1.8% of adult patients, respectively. These figures increased to 11.1%, 7.7% and 3.5%, respectively, in VGH-T. Among patients requiring ICU admission, 30% of pediatric and 53% of adult patients were not admitted on presentation to the ED. Of 10,099 children and 27,555 adults who were evaluated for case disposition, 651 (6.5%) and 4,061 (14.7%), respectively, were considered for admission. Among these 542 (83.3%) and 2,894 (71.3%), respectively, were admitted. CONCLUSIONS: VGH-T is a favorable training ground for EPs due to its high volume of adult and elderly, advanced life support eligible, ICU and high acuity patients. MMH is an ideal place for training in pediatric emergency medicine. Utilization of the 119 emergency response system is low. The number of patients with high acuity triage in Taipei City is low. However, Taipei City faces a shortage of acute care beds, especially ICU beds.

Adult↗

PubMed1997

Epidermal growth factor and betacellulin mediate signal transduction through co-expressed ErbB2 and ErbB3 receptors.

Interleukin-3 (IL-3)-dependent murine 32D cells do not detectably express epidermal growth factor receptors (EGFRs) and do not proliferate in response to EGF, heregulin (HRG) or other known EGF-like ligands. Here, we report that EGF specifically binds to and can be crosslinked to 32D transfectants co-expressing ErbB2 and ErbB3 (32D.E2/E3), but not to transfectants expressing either ErbB2 or ErbB3 individually. [125I]EGF-crosslinked species detected in 32D. E2/E3 cells were displaced by HRG and betacellulin (BTC) but not by other EGF-like ligands that were analyzed. EGF, BTC and HRG also induced receptor tyrosine phosphorylation, activation of downstream signaling molecules and proliferation of 32D.E2/E3 cells. 32D transfectants were also generated which expressed an ErbB3-EGFR chimera alone (32D.E3-E1) or in combination with ErbB2 (32D. E2/E3-E1). While HRG stimulation of 32D.E3-E1 cells resulted in DNA synthesis and receptor phosphorylation, EGF and BTC were inactive. However, EGF and BTC were as effective as HRG in mediating signaling when ErbB2 was co-expressed with the chimera in the 32D.E2/E3-E1 transfectant. These results provide evidence that ErbB2/ErbB3 binding sites for EGF and BTC are formed by a previously undescribed mechanism that requires co-expression of two distinct receptors. Additional data utilizing MDA MB134 human breast carcinoma cells, which naturally express ErbB2 and ErbB3 in the absence of EGFRs, supported the results obtained employing 32D cells and suggest that EGF and BTC may contribute to the progression of carcinomas that co-express ErbB2 and ErbB3.

Animals↗

PubMed1997

Insulin receptor substrate (IRS) 1 is reduced and IRS-2 is the main docking protein for phosphatidylinositol 3-kinase in adipocytes from subjects with non-insulin-dependent diabetes mellitus.

The large docking protein IRS-1 is a major substrate for the insulin receptor and other tyrosine kinases. It plays a key role in eliciting many of insulin's actions, including binding and activation of phosphatidylinositol (PI) 3-kinase and the subsequent increase in glucose transport. Gene disruption of IRS-1 in mice is associated with an impaired insulin-stimulated glucose disposal in vivo and glucose transport in vitro, but the survival of the animals and residual insulin sensitivity is dependent on the presence of the alternative docking protein IRS-2. We examined the expression and function of IRS-1 and IRS-2 in adipocytes from healthy and diabetic individuals. Cells from subjects with non-insulin-dependent diabetes mellitus (NIDDM), but not with insulin-dependent diabetes mellitus, had an impaired insulin effect and a marked reduction (70 +/- 6%) in the expression of IRS-1 protein, whereas IRS-2 was unchanged. In normal cells, IRS-1 was the main docking protein for the binding and activation of insulin-stimulated PI 3-kinase; IRS-2 was also functional but required a higher insulin concentration for a similar binding and activation of PI 3-kinase. In contrast in NIDDM cells with a low IRS-1 content, IRS-2 became the main docking protein. These findings may provide important reasons for the insulin resistance in NIDDM.

Adipocytes↗

PubMed1997

Jak1 expression is required for mediating interleukin-4-induced tyrosine phosphorylation of insulin receptor substrate and Stat6 signaling molecules.

The Jak1, Jak2, Jak3, and Fes tyrosine kinases have been demonstrated to undergo tyrosine phosphorylation in response to interleukin (IL)-4 stimulation in different cell systems. However, it is not clear which, if any, of these kinases are responsible for initiating IL-4-induced tyrosine phosphorylation of intracellular substrates in vivo. In the present study, we have utilized a mutant Jak1-deficient HeLa cell line, E1C3, and its parental Jak1-expressing counterpart, 1D4, to analyze the role of Jak1 in mediating IL-4-induced tyrosine phosphorylation events. IL-4 treatment rapidly induced tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and IRS-2 in 1D4 but not in E1C3 cells. IL-4-mediated tyrosine phosphorylation of Stat6 was pronounced in 1D4 cells, while no IL-4-induced Stat6 phosphorylation was detected in E1C3 cells. IL-4 also induced Stat6 DNA binding activity from lysates of 1D4 but not E1C3 cells utilizing a radiolabeled immunoglobulin heavy chain germline epsilon promotor sequence (Iepsilon) in an electrophoretic mobility shift assay. Reconstitution of Jak1 expression in E1C3 cells restored the ability of IL-4 to induce IRS and Stat6 tyrosine phosphorylation. These results provide evidence that Jak1 expression is required for mediating tyrosine phosphorylation and activation of crucial molecules involved in IL-4 signal transduction.

HeLa Cells↗

PubMed1997

Insulin receptor substrate-2 is the major 170-kDa protein phosphorylated on tyrosine in response to cytokines in murine lymphohemopoietic cells.

Insulin receptor substrate 1 (IRS-1), and its structural relative IRS-2, are both phosphorylated on tyrosine following treatment of cells with interleukin-4 (IL-4) and insulin. We have investigated whether both IRS-1 and IRS-2 are expressed in murine lymphohemopoietic cells. T and B lymphocytes and macrophages from primary cultures expressed only IRS-2, which became phosphorylated on tyrosine following stimulation with both IL-4 and insulin. Likewise, the murine myeloid cell line FD-5 expressed only IRS-2, which was tyrosine phosphorylated in response to IL-4 and insulin, as well as interleukin-3 and granulocyte-macrophage colony stimulating factor. Neither IRS-1 nor IRS-2 were expressed at detectable levels in primary bone marrow mast cells although these cells do respond to IL-4. Moreover, a factor-dependent lymphocyte cell line, CT.4S, which grows continuously in IL-4, did not express detectable levels of IRS-1 or IRS-2. IRS-2 from FD-5 cells stimulated with either IL-4 or insulin bound to glutathione S-transferase fusion proteins of the p85 subunit of phosphoinositol 3'-kinase, Grb2, and Syp, paralleling reported associations of IRS-1 with these molecules and indicating phosphorylation of the corresponding residues on IRS-2.

Adaptor Proteins, Signal Transducing↗

PubMed1997

Intestinal Behçet's disease associated with non-Hodgkin's lymphoma.

A 45-year-old man with intestinal Behçet's disease noticed an enlarged right cervical lymph node, and was diagnosed with diffuse large cell type, non-Hodgkin's lymphoma. The intrapelvic lymph tract was markedly deformed because of recurrent ileocecal ulceration, and conventional lymphoscintigraphy with a common tracer did not abolish the suspicion that lymphoma cells may have invaded the lymph nodes. Dynamic lymphoscintigraphy with a new tracer, 99mtechnetium-diethylene triamine pentaacetic acid-human serum albumin, because of its high detection sensitivity, was very useful for excluding this suspicion, and for determining the clinical stage of lymphoma. Combination induction chemotherapy led to complete remission without any adverse effects, but subsequent supportive therapy with same protocol could not be completed because of progression of the intestinal lesions. Special management for the intestinal lesions, such as bowel rest, may be essential with chemotherapy for patients with intestinal Behçet's disease.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1997

The demonstration of serum interleukin-8 and superoxide dismutase in Adamantiades-Behçet's disease.

Serum interleukin-8 (IL-8) production was measured in 43 Adamantiades-Behçet's disease (A-BD) patients and in 46 healthy volunteers using a sandwich enzyme-linked immunosorbent assay (ELISA). The mean serum IL-8 level of the patients (14.6 +/- 3 pg/ml) was significantly higher than that of controls (10.8 +/- 3 pg/ml, P < 0.05). Since IL-8 is known to have proinflammatory properties, it may play some role in the pathogenesis of A-BD. We also investigated the activity of serum superoxide dismutase (SOD) in the 43 patients with A-BD and in the 46 healthy volunteers. Serum SOD activity was markedly increased in the patients with A-BD (13.1 +/- 3%), especially in active A-BD, compared with that in the healthy volunteers (6.7 +/- 3%, P < 0.01). Our results suggest the involvement of IL-8 and SOD in the pathogenesis of A-BD as seen in other inflammatory diseases.

Adult↗

PubMed1997

Characterization of the ecdysteroid UDP-glucosyltransferase gene of a single nucleocapsid nucleopolyhedrovirus of Buzura suppressaria.

A putative ecdysteroid UDP-glucosyltransferase (egt) gene was identified in the single nucleocapsid nucleopolyhedrovirus of Buzura suppressaria (BusuNPV). This is the first egt gene to be characterized in a SNPV, suggesting that egt genes are prevalent in nucleopolyhedroviruses and possibly in all baculoviruses. The open reading frame (ORF) of the gene is 1539 nucleotides (nt) long, encoding a putative protein (EGT) of 513 amino acids (aa) with a M of 58922. The 5' noncoding region contains three possible TATA boxes. A polyadenylation signal, AATAAA, was found downstream of the translation stop codon. A putative signal peptide of 16 residues was present at the N-terminus of the EGT. The BusuNPV egt gene has a high degree of nucleotide and amino acid sequence homology to multiple nucleocapsid (M) NPV egt genes, the highest being to the Spodoptera exigua MNPV egt. A phylogenetic tree of eleven known EGTs was constructed using maximum parsimony analysis.

Amino Acid Sequence↗

PubMed1997

Amifostine protects normal tissues from paclitaxel toxicity while cytotoxicity against tumour cells is maintained.

The objectives of this study were to evaluate the protective effects of amifostine against paclitaxel-induced toxicity to normal and malignant human tissues. Haematopoietic progenitor colony assays were used to establish the number of CFU-GEMM and BFU-E colonies after incubation with WR-1065 alone, Amifostine alone, paclitaxel (2.5 or 5 microM) +/- WR-1065 or amifostine. MTT and alkaline elution assays evaluated the in vitro growth inhibitory and DNA damaging effects, respectively, of paclitaxel with or without amifostine against normal human fibroblasts and human non-small cell lung cancer (NSCLC) cells. This combination was also evaluated in vivo using severe combined immune deficient (scid) mouse models of early (non-palpable tumours) and advanced (palpable tumours) human ovarian cancer. Human 2780 ovarian cancer cells were inoculated subcutaneously while paclitaxel and amifostine were administered intraperitoneally. A brief exposure (15 min) to amifostine not only protected human haematopoietic progenitor colonies from paclitaxel toxicity, but stimulated the growth of CFU-GEMM and BFU-E beyond control values. Amifostine protected normal human lung fibroblasts from paclitaxel-induced cytotoxicity and DNA single-strand breaks. However, paclitaxel cytotoxicity and DNA single-strand breaks were actually enhanced by pretreatment with amifostine in the NSCLC model. Importantly, amifostine did not interfere with paclitaxel antitumour activity even with prolonged exposure (24.5 h) of the lung cancer cells to high concentrations (1.2 mM) in vitro or following five repetitive high doses (200 mg/kg) given to scid mice with human ovarian cancer xenografts. Indeed, under certain circumstances, amifostine resulted in sensitisation of tumour cells to paclitaxel. Our results confirm previous reports of the ability of amifostine to protect normal tissues from the toxic effects of chemotherapy drugs and now extend these observations to paclitaxel.

Amifostine↗

PubMed1997

Effects of oren-gedoku-to and unsei-in, Chinese traditional medicines, on interleukin-8 and superoxide dismutase in rats.

This study was conducted to elucidate the mechanisms of action of two Chinese traditional drugs, Oren-gedoku-to and Unsei-in, which have been used for many years in the treatment of inflammatory disorders. In rats with acetic acid-induced inflammation, both drugs reduced interleukin-8 concentrations in the serum. Neither drug significantly affected superoxide dismutase activity in the serum, although Unsei-in increased superoxide dismutase activity in liver after 1 month of administration. Oren-gedoku-to showed no significant effect on liver superoxide dismutase activity. It was considered that these medicines exert their anti-inflammatory effects mainly on the early stages of inflammation, wherein increased capillary permeability and migration of leucocytes occur.

Animals↗

PubMed1997

The IRS-2 gene on murine chromosome 8 encodes a unique signaling adapter for insulin and cytokine action.

Signal transduction by insulin and IGF-1, several interleukins (IL-2, IL-4, IL-9, IL-13), interferons, GH, and other cytokines involves IRS proteins, which link the receptors for these factors to signaling molecules with Src homology-2 domains (SH2-proteins). We recently reported the amino acid sequence of murine IRS-2; in order to examine a potential genetic role for this molecule in disease, we isolated the murine IRS-2 gene and compared the expression pattern of IRS-2 against IRS-1. Like IRS-1, IRS-2 is encoded by a single exon. Whereas IRS-1 is located on murine chromosome 1, IRS-2 is located on murine chromosome 8 near the insulin receptor. IRS-2 is expressed together with IRS-1 in many cells and tissues; however, IRS-2 predominates in murine hematopoietic cells where it may be essential for cytokine signaling; IRS-1 predominates in adipocytes and differentiated 3T3-L1 cells where it contributes to the normal insulin response. In 32D cells, IRS-1 and IRS-2 undergo differential tyrosine phosphorylation during insulin or IL-4 stimulation, as assessed indirectly by interaction with various recombinant SH2 domains. Thus, signaling specificity through the IRS proteins may be accomplished by specific expression patterns and distinct phosphorylation patterns during interaction with various activated receptors.

3T3 Cells↗

PubMed1997

Characteristics of tetrahydroprotoberberines on dopamine D1 and D2 receptors in calf striatum.

AIM: To study the characteristics of tetrahydroprotoberberines (THPB) on dopamine D1 and D2 receptors and elucidate their structure-activity relationship. METHODS: Radioligand assay in vitro with a two-site model program analysis. RESULTS: Four THPB with two hydorxyl groups on C2 and C9 or C2 and C10 exhibited RH and RL two binding sites to D1 receptors and guanosine triphosphate regulated the RH binding site of SPD and THPB-132A in competition assay, while eleven THPB including nonhydroxy-THPB, monohydroxy-THPB, and THPB with two hydroxyl groups attaching to C3 and C10 showed one binding site to D1 receptors under the same conditions. However, the tested eleven THPB all manifested one binding site to D2 receptors in competition assay, and the 2-hydroxy-THPB had the most potent affinity for D2 receptors. CONCLUSION: Dihydroxy-THPB with two hydroxyl groups attaching to C2 and C9 or C2 and C10 possess the intrinsic activity of agonist to D1 receptors, while the other THPB do not. The tested eleven THPB all are the antagonists of D2 receptors.

Animals↗

PubMed1997

Effects of tetrahydroprotoberberines on dopamine D2 receptors in ventral tegmental area of rat.

AIM: To compare the actions of tetrahydroprotoberberines (THPB) on dopamine (DA) D2 receptors in the ventral tegmental area (VTA) of rat. METHODS: Extracellular single unit recording technique was used in i.v. gallamine-paralyzed rats. RESULTS: Eleven THPB analogs tested completely attenuated the apomorphine (Apo, 20 micrograms.kg-1)-induced inhibition on VTA DA cell firing activity. The OH group on C2 at THPB was linked with the reversal of Apo-induced inhibition. Their reversal potencies (ED50, microgram.kg-1) for D2 receptors were: THPB-143 (5.6) > SPD (8.5) > Iso (17.0) > THP (33) > THB (48) > THPB-18 (66) > THPB-1 (179) > THPB-19 (408) > THPB-126 (510) > THPB-104 (1019) > THPB-10 (4815). CONCLUSION: Among these 11 THPB, the 2-hydroxyl-THPB (THPB-143) showed the strongest antagonistic action on D2 receptors.

Animals↗

PubMed1997

The anti-inflammatory effects of ketoprofen in animal experiments.

The authors investigated the anti-inflammatory actions of ketoprofen using a battery of tests: in the rat paw oedema test induced by five different inciters, in the capillary permeability test, and in measuring the interleukin-8 (IL-8) production and superoxide dismutase (SOD) activity. The findings in these studies show that ketoprofen inhibits rat paw oedema, suppresses capillary permeability, reduces IL-8 production and increases SOD activity in the acetic-acid-induced inflammatory state. These results would seem to provide a clear rationale for exploring the usefulness of ketoprofen in the treatment of acute and chronic inflammatory diseases.

Acetic Acid↗