Premenstrual syndrome(PMS) refers to a group of menstruation-related symptoms that impair daily activity and interpersonal relationship. The therapeutic modality for PMS consists of non-pharmacologic and pharmacologic treatment. Generally, after confirmation of PMS, a set of non-pharmacologic treatments is recommended before pharmacologic treatment. Patients can be benefited from non-pharmacological treatments such as patient education, cognitive therapy, behavioral therapy, and dietary supplementation. Pharmacologic therapy including psychotropic agents, diuretics, and prostaglandin inhibitors may be used, when PMS symptoms are not sufficiently improved after non-pharmacologic treatments, or when symptoms fit the diagnostic criteria of premenstrual dysphoric disorder(PMDD). When treatment fails, hormonal therapy to manipulate menstrual cycle may be considered, and several trials showed improvement of physical and mood symptoms.
Cognitive Therapy ; Dietary Supplements ; Diuretics ; Female ; Humans ; Menstrual Cycle ; Patient Education as Topic ; Premenstrual Syndrome* ; Prostaglandin Antagonists

OBJECTIVETo investigate the effect of prostaglandin D2 receptor antagonists on the airway inflammation in rats with asthma.

METHODSForty male SD rats were randomly divided into four groups: Group A (normal control), Group B (asthma group), Group C (CRTH2 antagonist BAYu3405 treatment group), Group D (DP1 antagonist BWA868C treatment group). Asthma was induced by ovalbumin (OVA) challenge. The rats in each group were sacrificed 24 h after the last challenge of OVA.DP1/CRTH2 receptors on eosinophils (EOS) were measured by radiological binding assay (RBA). The left lungs were used for histological examinations and bronchoalveolar lavage fluid (BALF) was collected from the right lungs. The total cell numbers, EOS absolute count and differential cell counts in BALF were performed. Serum concentrations of IL-4, 5 and IFN-gamma were measured by ELISA.

RESULTSRats in BAYu3405 treatment group showed profoundly decreased infiltrates of EOS and lymphocytes in the wall of bronchus when compared with those of asthma group and BWA868C treatment group. Serum concentrations of IFN-gamma in rats of BAYu3405 treatment group increased, but IL-4 and IL-5 decreased significantly when compared with those in rats of asthma group and BWA868C treatment group (P<0.01), and BALF EOS count was decreased significantly (P<0.01). Peripheral blood EOS count was higher than that in rats of normal control group, but was not significantly different from that in rats of asthma group and BWA868C treatment group. The combining capacity of CRTH2 and DP total combining capacity on EOS in asthma group, BAYu3405 treatment group and BWA868C treatment group were significantly higher than those in Group A (P<0.01). There was no significant difference in DP1 among all the groups (P>0.05).

CONCLUSIONCRTH2, but not DP1 antagonist can effectively ameliorate airway inflammation in rats with asthma.

Animals ; Asthma ; chemically induced ; drug therapy ; pathology ; Bronchi ; immunology ; pathology ; Carbazoles ; pharmacology ; therapeutic use ; Inflammation ; drug therapy ; Male ; Ovalbumin ; Prostaglandin D2 ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, Immunologic ; antagonists & inhibitors ; Receptors, Prostaglandin ; antagonists & inhibitors ; Sulfonamides ; pharmacology ; therapeutic use

BACKGROUND: Prostaglandin inhibitors have been successfully used to inhibit some types of postoperative pain and reduce opioids requirements in others. Antiprostaglandin activity may be ineffective unless the preparations are given at the appropriate time before surgery. This study aimed to determine if the intrarectal administration of acetaminophen immediately before surgery would markedly reduce pain in the postoperative period. METHODS: The children were divided to two groups. Each group was consisted of 15 children. The children in control group were administered intramuscularly glycopyrrolate(0.004 mg/kg) 20 minute. The children in experimental group were administered glycopyrrolate(0.004 mg/kg) intramuscularly and were administered acetaminophen(250 mg) rectally 20 minute before the children were taken to the operating theatre. RESULTS: In the recovery room, the children who had recived acetaminophen were signifcantlly quieter (p<0.01), agitated less(p<0.01) and cried less(p<0.01) painless(p<0.01) than those nonadministered group. There were no obvious differnces between the groups in intra-operative bleeding (as estimated by the surgeon), or in measured blood loss. No postopertive complications become evident. CONCLUSIONS: The preoperative rectal administration of acetaminophen for pain relief after tonsillectomy is safe and effective.
Acetaminophen* ; Administration, Rectal ; Analgesics, Opioid ; Child* ; Dihydroergotamine ; Hemorrhage ; Humans ; Pain, Postoperative* ; Postoperative Period ; Prostaglandin Antagonists ; Recovery Room ; Tonsillectomy*

PURPOSE: As increased level of prostaglandin has been identified in the bony lesions of Langerhans cell histiocytosis (LCH), we speculated that indomethacin, a potent prostaglandin inhibitor, may be effective for patients with LCH. METHODS: Retrospective review of 8 children with LCH (male 7, female 1) treated with indomethacin at Seoul National University Children's Hospital from September 1999 to February 2001 was done. The dose of indomethacin ranged from 1.8 to 2.8 mg/kg/day in two divided doses. RESULTS: Four patients with single bony lesion had a complete response to treatment. Among them one patient was treated with indomethacin after fourth relapse. Two patients with multiple bony lesions seemed to have partial response to treatment with indomethacin initially but showed disease progression later. Two patients with extraosseous lesion did not respond, but skull lesions were resolved after treatment. No serious toxicities of indomethacin treatment were observed. CONCLUSION: Indomethacin seems to be a very convenient and useful therapy for LCH involving single bony lesion. The mechanism how the LCH imporves in response to indomethacin has to be elucidated. Whether it has a specific role in slowing disease progression or we are seeing merely a spontaneous remission has to be studied in large scale.
Child ; Disease Progression ; Female ; Histiocytosis, Langerhans-Cell* ; Humans ; Indomethacin* ; Prostaglandin Antagonists ; Recurrence ; Remission, Spontaneous ; Retrospective Studies ; Seoul ; Skull

To investigate the effect of a microsomal prostaglandin E synthase-1 (mPGES-1) inhibitor MK886 on cell cycle of the human acute myeloid leukemia HL-60 cells. HL-60 cells were treated with different concentration of MK886 (10, 25, 50 µmol/L) for 24 h. Flow cytometry, Western blot and ELISA were used to measure cell cycle, cyclin D1, mPGES-1, PGE(2), Akt, P-Akt and C-MYC. The results indicated that after treated with MK886, the percentage of HL-60 cells decreased in G(0)/G(1) phase and increased in S phase, and expressions of mPGES-1, cyclin D1, P-Akt and C-MYC and synthesis of PGE(2) decreased significantly. It is concluded that MK886 can arrest HL-60 cells in G(0)/G(1) phase, the mechanism of which is possibly associated to inhibition of mPGES-1 expression, reduction of PGE(2) synthesis, suppression of Akt phosphorylation and C-MYC expression, down-regulation of cyclin D1 expression.
Cell Cycle ; drug effects ; HL-60 Cells ; Humans ; Indoles ; pharmacology ; Intramolecular Oxidoreductases ; antagonists & inhibitors ; Leukemia ; metabolism ; pathology ; Prostaglandin-E Synthases

A 59-year-old female patient with rheumatoid arthritis showed hypokalemic metabolic alkalosis, normotensive hyperreninemic hyperaldosteronism and high urinary prostaglandin level. She was thought to have Bartter's syndrome. But, her kidney biopsy specimen showed chronic interstitial nephritis. She have used acetaminophen containing analgesics for recent three years. So we thought her disease was caused by drug. But, in this case, clinical manifestations are correspond with Bartter's syndrome and we have witnessed a successful respond to kalium replacement, angiotensin converting enzyme inhibitor, prostaglandin inhibitor and spironolactone administration.
Acetaminophen ; Alkalosis ; Analgesics ; Arthritis, Rheumatoid* ; Bartter Syndrome ; Biopsy ; Female ; Glycogen Storage Disease Type VI ; Humans ; Hyperaldosteronism ; Kidney ; Middle Aged ; Nephritis, Interstitial* ; Peptidyl-Dipeptidase A ; Prostaglandin Antagonists ; Spironolactone

Objective To investigate the effect of 15-Deoxy-△(12,14)-prostaglandin J2 (15 d-PGJ2) on the expression of macrophage migration inhibitory factor (MIF) and its underlying mechanism in J774A.1. Methods The murine monocyte/macrophage cell line J774A.1 were divided into six groups:lipopolysaccharide (LPS) group,incubated with 1 μg/ml LPS for 1 h;normal control group,incubated with PBS for 1 h;negative control group,incubated with 5 μmol/L 15 d-PGJ2 for 1 h;15 d-PGJ2 group,incubated with 5 μmol/L 15 d-PGJ2 for 1 h followed by 1 μg/ml LPS for 1 h;GW9662 group,incubated with 5 μmol/L 15 d-PGJ2 for 1 h following GW9662 10 μmol/L for 1 h,and then incubated with 1 μg/ml LPS for 1 h;and Vehicle group,control of GW9662,GW9662 was replaced by its solvent DMSO. The expression of MIF was detected via immunofluorescence and agarose gel electrophoresis. RT-qPCR and Western blotting were used to test whether 15 d-PGJ2 could regulate mRNA and protein expression of MIF in J774A.1 upon LPS challenge. The effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) antagonist GW9662 on the regulation of MIF by 15 d-PGJ2 was observed. The effects of 15 d-PGJ2 on the nuclear translocation of PPAR-γ upon LPS challenge were detected via high content screening analysis. Results MIF DNA and protein expressions were detected in J774A.1. MIF mRNA expression was up-regulated (1.75±0.09,P=0.037) when challenged with LPS and 15 d-PGJ2 inhibited its upregulation (0.84±0.08,P=0.026) in J774A.1. The protein level was consistent with the mRNA level. PPAR-γ antagonist GW9662 reversed the effect of 15 d-PGJ2 (mRNA,1.48±0.06,P=0.016;protein,1.28). Furthermore,nuclear translocation of PPAR-γ was regulated by 15 d-PGJ2 in J774A.1 upon LPS challenge(1.39±0.02 vs. 1.01±0.03,P=0.003). Conclusion 15 d-PGJ2 may down-regulate the MIF expression in J774A.1 in a PPAR-γ-dependent manner.
Anilides ; pharmacology ; Animals ; Cell Line ; Intramolecular Oxidoreductases ; metabolism ; Lipopolysaccharides ; Macrophage Migration-Inhibitory Factors ; metabolism ; Mice ; Monocytes ; drug effects ; PPAR gamma ; antagonists & inhibitors ; Prostaglandin D2 ; analogs & derivatives ; pharmacology

Lysophosphatidic acid (LPA) is a bioactive phospholipids and involves in various cellular events, including tumor cell migration. In the present study, we investigated LPA receptor and its transactivation to EGFR for cyclooxygenase-2 (COX-2) expression and cell migration in CAOV-3 ovarian cancer cells. LPA induced COX-2 expression in a dose-dependent manner, and pretreatment of the cells with pharmacological inhibitors of Gi (pertussis toxin), Src (PP2), EGF receptor (EGFR) (AG1478), ERK (PD98059) significantly inhibited LPA- induced COX-2 expression. Consistent to these results, transfection of the cells with selective Src siRNA attenuated COX-2 expression by LPA. LPA stimulated CAOV-3 cell migration that was abrogated by pharmacological inhibitors and antibody of EP2. Higher expression of LPA2 mRNA was observed in CAOV-3 cells, and transfection of the cells with a selective LPA2 siRNA significantly inhibited LPA-induced activation of EGFR and ERK, as well as COX-2 expression. Importantly, LPA2 siRNA also blocked LPA-induced ovarian cancer cell migration. Collectively, our results clearly show the significance of LPA2 and Gi/Src pathway for LPA-induced COX-2 expression and cell migration that could be a promising drug target for ovarian cancer cell metastasis.
Butadienes/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects/*physiology ; Cyclooxygenase 2/*biosynthesis ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism ; Female ; Flavonoids/pharmacology ; GTP-Binding Protein alpha Subunits, Gi-Go/antagonists & inhibitors/*metabolism ; Humans ; Lysophospholipids/pharmacology ; Nitriles/pharmacology ; Ovarian Neoplasms/metabolism/*pathology ; Pertussis Toxin/pharmacology ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Pyrimidines/pharmacology ; Receptor, Epidermal Growth Factor/antagonists & inhibitors/metabolism ; Receptors, Lysophosphatidic Acid/*metabolism ; Receptors, Prostaglandin E/metabolism ; Signal Transduction ; Transcriptional Activation ; Tyrphostins/pharmacology

During chronic inflammatory response, mono- cytes/macrophages produce 92-kDa matrix metalloproteinase-9 (MMP-9), which may contribute to their extravasation, migration and tissue remodeling. Activation of peroxisome proliferator- activated factor receptor-gamma (PPAR-gamma) has been shown to inhibit MMP-9 activity. To evaluate whether ox-LDL, a PPAR-gamma activator, inhibits PMA-induced MMP-9 expression and activity, and if so, whether CD36 and PPAR-gamma are involved in this process, we investigated the effect of ox-LDL on MMP-9 expression and activity in PMA-activated human monocytic cell line U937. PMA-induced MMP-9 expression and activity were suppressed by the treatment with ox-LDL (50 micrigram/ml) or PPAR-gamma activators such as troglitazone (5 micrometer), ciglitazone (5 micrometer), and 15d- PGJ2 (1 micrometer) for 24 h. This ox-LDL or PPAR-gamma activator-mediated inhibition of micrometer P-9 activity was diminished by the pre-treatment of cells with a blocking antibody to CD36, or PGF2a (0.3 micrometer), which is a PPAR-gamma inhibitor, as well as overexpression of a dominant-negative form of CD36. Taken together, these results suggest that ox-LDL suppresses PMA-induced MMP-9 expression and activity through CD36-mediated activation of PPAR-gamma.
Antibodies, Blocking/pharmacology ; Antigens, CD36/immunology/*physiology ; Cells, Cultured ; Chromans/pharmacology ; Gelatinase B/antagonists & inhibitors/genetics/*metabolism ; Humans ; Lipoproteins, LDL/pharmacology/*physiology ; Monocytes/drug effects/*enzymology/metabolism ; NF-kappa B/antagonists & inhibitors ; PPAR gamma/*metabolism ; Prostaglandin D2/*analogs & derivatives/pharmacology ; RNA, Messenger/analysis/metabolism ; Research Support, Non-U.S. Gov't ; Tetradecanoylphorbol Acetate/antagonists & inhibitors/pharmacology ; Thiazolidinediones/pharmacology ; Transcription, Genetic/drug effects

PURPOSE: Bartter syndrome is a renal tubular defect in electrolyte transport characterized by hypokalemia, metabolic alkalosis and other clinical signs and symptoms. The aims of this study were to analyze the clinical manifestations and the short- and long-term outcomes of Bartter syndrome. METHODS: We retrospectively reviewed clinical history, laboratory finding of blood and urine, renal ultrasonography, and hearing tests of five patients who were diagnosed and managed with Bartter syndrome at Asan Medical Center from April 1992 to May 2007. We also evaluated height and body weight periodically after institution of therapy. RESULTS: All patients had poor oral intake, failure to thrive and polyuria. Three of them had maternal history of polyhydramnios and premature delivery. The mean age at diagnosis was 11.8 months. All children presented with hypokalemia, metabolic alkalosis, hyperreninemia. Their blood pressures were normal. One patient had nephrocalcinosis on renal ultrasonography and all of them had normal result in hearing tests. After treatment with indomethacin or other prostaglandin inhibitors and potassium supplementation, their clinical features improved with catch-up growth and improvement in the development during long-term follow-up. CONCLUSION: We emphasize that early diagnosis and proper treatment in patient with Bartter syndrome are related to better prognosis.
Alkalosis ; Bartter Syndrome* ; Body Weight ; Child ; Chungcheongnam-do ; Diagnosis ; Early Diagnosis ; Failure to Thrive ; Follow-Up Studies ; Hearing Tests ; Humans ; Hypokalemia ; Indomethacin ; Nephrocalcinosis ; Polyhydramnios ; Polyuria ; Potassium ; Prognosis ; Prostaglandin Antagonists ; Retrospective Studies ; Treatment Outcome ; Ultrasonography