The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Hirotaka Onoe - One of the best experts on this subject based on the ideXlab platform.
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in vivo expression of cyclooxygenase 1 in activated microglia and macrophages during neuroinflammation visualized by pet with 11c Ketoprofen methyl ester
The Journal of Nuclear Medicine, 2011Co-Authors: Miho Shukuri, Misato Takashimahirano, Keiko Tokuda, Tadayuki Takashima, Kiyoshi Matsumura, Masaaki Suzuki, Osamu Inoue, Hirotaka OnoeAbstract:Cyclooxygenase (COX)-1 and -2 are prostanoid-synthesizing enzymes that play important roles in the regulation of neuroinflammation and in the development of neurodegenerative disorders. However, the specific functions of these isoforms are still unclear. We recently developed 11 C-labeled Ketoprofen methyl ester as a PET probe that targets the COXs for imaging neuroinflammation, though its responsible isoform is yet to be determined. In the present study, we performed ex vivo and in vivo imaging studies with 11 C-Ketoprofen methyl ester and determined the contributions of the COX isoforms during the neuroinflammatory process. Methods: To identify the COX isoform responsible for 11 C-Ketoprofen methyl ester in the brain, we examined the ex vivo autoradiography of 11C-Ketoprofen methyl ester using COX-deficient mice. Time-dependent changes in accumulation of 11C-Ketoprofen methyl ester during the neuroinflammatory process were evaluated by PET in rats with hemispheric neuroinflammation induced by intrastriatal injection of lipopolysaccharide or quinolinic acid. In both rat models, cell-type specificity of COX isoform expression during neuroinflammation was identified immunohistochemically. Results: Ex vivo autoradiographic analysis of COX-deficient mice revealed a significant reduction of 11 C-Ketoprofen methyl ester accumulation only in COX-1–deficient mice, not COX-2–deficient mice. PET of rats after intrastriatal injection of lipopolysaccharide showed a significant increase in accumulation of 11 C-Ketoprofen methyl ester in the inflamed area. This increase was evident at the early phase of 6 h, peaked at day 1, and then returned to basal levels by day 7. In addition, immunohistochemical analysis revealed that the population of activated microglia and macrophages was elevated at the early phase with COX-1 expression but not COX-2. A significant increase in 11 C-Ketoprofen methyl ester accumulation was also observed at day 1 after intrastriatal injection of quinolinic acid, with increased COX-1–expressing activated microglia and macrophages. Conclusion: We have identified 11 C-Ketoprofen methyl ester as a COX-1–selective PET probe, and using this, we have also demonstrated a time-dependent expression of COX-1 in activated microglia and macrophages during the neuroinflammatory process in the living brain. Thus, COX-1 may play a crucial role in
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in vivo expression of cyclooxygenase 1 in activated microglia and macrophages during neuroinflammation visualized by pet with 11c Ketoprofen methyl ester
The Journal of Nuclear Medicine, 2011Co-Authors: Miho Shukuri, Misato Takashimahirano, Keiko Tokuda, Tadayuki Takashima, Kiyoshi Matsumura, Masaaki Suzuki, Osamu Inoue, Hisashi Doi, Yasuyoshi Watanabe, Hirotaka OnoeAbstract:Cyclooxygenase (COX)-1 and -2 are prostanoid-synthesizing enzymes that play important roles in the regulation of neuroinflammation and in the development of neurodegenerative disorders. However, the specific functions of these isoforms are still unclear. We recently developed 11C-labeled Ketoprofen methyl ester as a PET probe that targets the COXs for imaging neuroinflammation, though its responsible isoform is yet to be determined. In the present study, we performed ex vivo and in vivo imaging studies with 11C-Ketoprofen methyl ester and determined the contributions of the COX isoforms during the neuroinflammatory process. Methods: To identify the COX isoform responsible for 11C-Ketoprofen methyl ester in the brain, we examined the ex vivo autoradiography of 11C-Ketoprofen methyl ester using COX-deficient mice. Time-dependent changes in accumulation of 11C-Ketoprofen methyl ester during the neuroinflammatory process were evaluated by PET in rats with hemispheric neuroinflammation induced by intrastriatal injection of lipopolysaccharide or quinolinic acid. In both rat models, cell-type specificity of COX isoform expression during neuroinflammation was identified immunohistochemically. Results: Ex vivo autoradiographic analysis of COX-deficient mice revealed a significant reduction of 11C-Ketoprofen methyl ester accumulation only in COX-1–deficient mice, not COX-2–deficient mice. PET of rats after intrastriatal injection of lipopolysaccharide showed a significant increase in accumulation of 11C-Ketoprofen methyl ester in the inflamed area. This increase was evident at the early phase of 6 h, peaked at day 1, and then returned to basal levels by day 7. In addition, immunohistochemical analysis revealed that the population of activated microglia and macrophages was elevated at the early phase with COX-1 expression but not COX-2. A significant increase in 11C-Ketoprofen methyl ester accumulation was also observed at day 1 after intrastriatal injection of quinolinic acid, with increased COX-1–expressing activated microglia and macrophages. Conclusion: We have identified 11C-Ketoprofen methyl ester as a COX-1–selective PET probe, and using this, we have also demonstrated a time-dependent expression of COX-1 in activated microglia and macrophages during the neuroinflammatory process in the living brain. Thus, COX-1 may play a crucial role in the pathology of neuroinflammation and might be a critical target for the diagnosis and therapy of neurodegenerative disorders.
Miho Shukuri - One of the best experts on this subject based on the ideXlab platform.
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in vivo expression of cyclooxygenase 1 in activated microglia and macrophages during neuroinflammation visualized by pet with 11c Ketoprofen methyl ester
The Journal of Nuclear Medicine, 2011Co-Authors: Miho Shukuri, Misato Takashimahirano, Keiko Tokuda, Tadayuki Takashima, Kiyoshi Matsumura, Masaaki Suzuki, Osamu Inoue, Hirotaka OnoeAbstract:Cyclooxygenase (COX)-1 and -2 are prostanoid-synthesizing enzymes that play important roles in the regulation of neuroinflammation and in the development of neurodegenerative disorders. However, the specific functions of these isoforms are still unclear. We recently developed 11 C-labeled Ketoprofen methyl ester as a PET probe that targets the COXs for imaging neuroinflammation, though its responsible isoform is yet to be determined. In the present study, we performed ex vivo and in vivo imaging studies with 11 C-Ketoprofen methyl ester and determined the contributions of the COX isoforms during the neuroinflammatory process. Methods: To identify the COX isoform responsible for 11 C-Ketoprofen methyl ester in the brain, we examined the ex vivo autoradiography of 11C-Ketoprofen methyl ester using COX-deficient mice. Time-dependent changes in accumulation of 11C-Ketoprofen methyl ester during the neuroinflammatory process were evaluated by PET in rats with hemispheric neuroinflammation induced by intrastriatal injection of lipopolysaccharide or quinolinic acid. In both rat models, cell-type specificity of COX isoform expression during neuroinflammation was identified immunohistochemically. Results: Ex vivo autoradiographic analysis of COX-deficient mice revealed a significant reduction of 11 C-Ketoprofen methyl ester accumulation only in COX-1–deficient mice, not COX-2–deficient mice. PET of rats after intrastriatal injection of lipopolysaccharide showed a significant increase in accumulation of 11 C-Ketoprofen methyl ester in the inflamed area. This increase was evident at the early phase of 6 h, peaked at day 1, and then returned to basal levels by day 7. In addition, immunohistochemical analysis revealed that the population of activated microglia and macrophages was elevated at the early phase with COX-1 expression but not COX-2. A significant increase in 11 C-Ketoprofen methyl ester accumulation was also observed at day 1 after intrastriatal injection of quinolinic acid, with increased COX-1–expressing activated microglia and macrophages. Conclusion: We have identified 11 C-Ketoprofen methyl ester as a COX-1–selective PET probe, and using this, we have also demonstrated a time-dependent expression of COX-1 in activated microglia and macrophages during the neuroinflammatory process in the living brain. Thus, COX-1 may play a crucial role in
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in vivo expression of cyclooxygenase 1 in activated microglia and macrophages during neuroinflammation visualized by pet with 11c Ketoprofen methyl ester
The Journal of Nuclear Medicine, 2011Co-Authors: Miho Shukuri, Misato Takashimahirano, Keiko Tokuda, Tadayuki Takashima, Kiyoshi Matsumura, Masaaki Suzuki, Osamu Inoue, Hisashi Doi, Yasuyoshi Watanabe, Hirotaka OnoeAbstract:Cyclooxygenase (COX)-1 and -2 are prostanoid-synthesizing enzymes that play important roles in the regulation of neuroinflammation and in the development of neurodegenerative disorders. However, the specific functions of these isoforms are still unclear. We recently developed 11C-labeled Ketoprofen methyl ester as a PET probe that targets the COXs for imaging neuroinflammation, though its responsible isoform is yet to be determined. In the present study, we performed ex vivo and in vivo imaging studies with 11C-Ketoprofen methyl ester and determined the contributions of the COX isoforms during the neuroinflammatory process. Methods: To identify the COX isoform responsible for 11C-Ketoprofen methyl ester in the brain, we examined the ex vivo autoradiography of 11C-Ketoprofen methyl ester using COX-deficient mice. Time-dependent changes in accumulation of 11C-Ketoprofen methyl ester during the neuroinflammatory process were evaluated by PET in rats with hemispheric neuroinflammation induced by intrastriatal injection of lipopolysaccharide or quinolinic acid. In both rat models, cell-type specificity of COX isoform expression during neuroinflammation was identified immunohistochemically. Results: Ex vivo autoradiographic analysis of COX-deficient mice revealed a significant reduction of 11C-Ketoprofen methyl ester accumulation only in COX-1–deficient mice, not COX-2–deficient mice. PET of rats after intrastriatal injection of lipopolysaccharide showed a significant increase in accumulation of 11C-Ketoprofen methyl ester in the inflamed area. This increase was evident at the early phase of 6 h, peaked at day 1, and then returned to basal levels by day 7. In addition, immunohistochemical analysis revealed that the population of activated microglia and macrophages was elevated at the early phase with COX-1 expression but not COX-2. A significant increase in 11C-Ketoprofen methyl ester accumulation was also observed at day 1 after intrastriatal injection of quinolinic acid, with increased COX-1–expressing activated microglia and macrophages. Conclusion: We have identified 11C-Ketoprofen methyl ester as a COX-1–selective PET probe, and using this, we have also demonstrated a time-dependent expression of COX-1 in activated microglia and macrophages during the neuroinflammatory process in the living brain. Thus, COX-1 may play a crucial role in the pathology of neuroinflammation and might be a critical target for the diagnosis and therapy of neurodegenerative disorders.
R Lange - One of the best experts on this subject based on the ideXlab platform.
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Ketoprofen 25 mg in the symptomatic treatment of episodic tension type headache double blind placebo controlled comparison with acetaminophen 1000 mg
Cephalalgia, 1998Co-Authors: Timothy J Steiner, R LangeAbstract:Therapies in current use for episodic tension-type headache (ETTH) are often unsatisfactory. Few trials have been conducted to demonstrate efficacy of any of them. This multicenter placebo-controlled randomized parallel-groups study compared the analgesic efficacy of single oral doses of Ketoprofen 25 mg and acetaminophen 1000 mg as outpatient treatment of 1 attack of ETTH. Efficacy was assessed by patients as pain relief on a diary-entered 7-point categorical scale. A total of 457 patients treated 348 attacks, 330 of which were evaluable. There were no serious adverse events (AEs); gastrointestinal AEs were most common on all treatments. Total relief from pain after 2 h was recorded by 16% of patients on placebo, 28% on Ketoprofen, and 22% on acetaminophen. Worthwhile effect or total relief (all other responses were regarded as treatment failures) were recorded by 36% on placebo, 70% on Ketoprofen (p <0.001), 61% on acetaminophen (p <0.001). The difference between Ketoprofen and acetaminophen was not sig...
Andrew R Moore - One of the best experts on this subject based on the ideXlab platform.
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Ketoprofen for episodic tension type headache in adults
Cochrane Database of Systematic Reviews, 2016Co-Authors: Lucy Veys, Sheena Derry, Andrew R MooreAbstract:Background Tension-type headache (TTH) affects about 1 person in 5 worldwide. It is divided into infrequent episodic TTH (fewer than one headache day per month), frequent episodic TTH (2 to 14 headache days per month), and chronic TTH (15 headache days a month or more). Ketoprofen is one of a number of analgesics suggested for acute treatment of headaches in frequent episodic TTH. Objectives To assess the efficacy and safety of Ketoprofen for treatment of episodic TTH in adults compared with placebo or any active comparator. Search methods We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, and the Oxford Pain Relief Database up to May 2016, and also reference lists of relevant published studies and reviews. We sought unpublished studies by asking personal contacts and searching online clinical trial registers and manufacturers' websites. Selection criteria We included randomised, double-blind, placebo-controlled studies (parallel-group or cross-over) using oral Ketoprofen for symptomatic relief of an acute episode of TTH. Studies had to be prospective, with participants aged 18 years or over, and include at least 10 participants per treatment arm. Data collection and analysis Two review authors independently assessed studies for inclusion and extracted data. We used the numbers of participants achieving each outcome to calculate the risk ratio (RR) and number needed to treat for one additional beneficial outcome (NNT) or one additional harmful outcome (NNH) for oral Ketoprofen compared to placebo or an active intervention for a range of outcomes, predominantly those recommended by the International Headache Society (IHS). We assessed the evidence using GRADE and created a 'Summary of findings' table. Main results We included four studies, all of which enrolled adults with frequent episodic TTH. They all specified using the IHS diagnostic criteria and reported mean baseline pain of at least moderate intensity. While 1253 people with TTH participated in these studies, the numbers available for any analysis were lower than this because outcomes were inconsistently reported and because many participants received active comparators. None of the included studies were at low risk of bias across all domains considered, although for most studies and domains this was likely to be due to inadequate reporting rather than poor methods. We judged one study to be at high risk of bias due to small size. Useful information was available only for Ketoprofen 25 mg. For the IHS preferred outcome of being pain-free at two hours the NNT for Ketoprofen 25 mg compared with placebo was 9.0 (95% confidence interval (CI) 4.8 to 72) in two studies (272 participants; low quality evidence). The NNT was 3.7 (95% CI 2.6 to 6.3) for pain-free or mild pain at two hours in two studies (272 participants; moderate quality evidence). Fewer people needed rescue medication with Ketoprofen 25 mg than with placebo, with a number needed to treat to prevent one event (NNTp) of 6.2 (95% CI 4.3 to 11) in three studies (605 participants; moderate quality evidence). The number of participants reporting any adverse event was higher with Ketoprofen 25 mg than placebo (NNH 15, (95% CI 8.7 to 45)) in three studies (651 participants with 66 events; low quality evidence). Most events were of mild to moderate intensity. Ketoprofen 25 mg was not different from paracetamol 1000 mg in two studies with 276 participants for any efficacy outcomes (low to moderate quality evidence); the RR for pain-free at two hours was 1.3 (95% CI 0.9 to 2.0). The number of participants reporting any adverse event was higher with Ketoprofen 25 mg than with paracetamol (NNH 17, 95% CI 8.9 to 130)) in two studies (582 participants, 68 events; low quality evidence). Studies reported no serious adverse events. We judged the quality of the evidence comparing Ketoprofen 25 mg with placebo or paracetamol 1000 mg as moderate to very low. Where evidence was downgraded it was because of the small number of studies and events. Authors' conclusions Ketoprofen 25 mg provided a small benefit compared with placebo in terms of being pain-free at two hours or having mild or no pain at two hours for people with frequent episodic TTH who have an acute headache of moderate or severe intensity. Its use was associated with more people experiencing adverse events. Ketoprofen 25 mg was not superior to paracetamol 1000 mg for any efficacy outcome.
Suparman Suparman - One of the best experts on this subject based on the ideXlab platform.
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PENGARUH PENAMBAHAN SODIUM LAURIL SULFAT (SLS) SEBAGAI SURFAKTAN TERHADAP SIFAT FISIK DAN UJI DISOLUSI TABLET Ketoprofen
'Lembaga Publikasi Ilmiah dan Penerbitan Universitas Muhammadiyah Purwokerto', 2012Co-Authors: Pratama, Adithya Wahyu, Siswanto Agus, Suparman SuparmanAbstract:ABSTRAK Ketoprofen (asam 2-(3-benzoilfenil) propanoat) adalah turunan asam propionat dengan khasiat analgesic, antipiretik, dan antiinflamasi yang cukup baik namun mempunyai kelarutan yang praktis tidak larut dalam air. Penelitian ini bertujuan untuk meningkatkan kecepatan disolusi dan pengaruhnya terhadap sifat fisik tablet Ketoprofen menggunakan Sodium lauril sulfat sebagai surfaktan. Sodium lauril sulfat merupakan surfaktan yang dapat digunakan untuk meningkatkan pembasahan dan laju disolusi. Penelitian ini dilakukan dengan membuat empat formula tablet Ketoprofen dengan konsentrasi Sodium lauril sulfat yang berbeda (0%, 0,5%, 1%, dan 1,5%) sebagai bahan pembasah. Sebagai kontrol digunakan Ketoprofen tanpa penambahan Sodium lauril sulfat. Tablet dibuat dengan metode granulasi basah. Tablet yang dihasilkan diuji sifat fisik (keseragaman bobot, kekerasan, kerapuhan, dan waktu hancur tablet) dan uji disolusi. Uji disolusi dilakukan dengan metode dayung dengan medium disolusi dapar fosfat pH 7,2 dengan kecepatan putar 100 rpm pada suhu 37±0,5ºC selama 60 menit dan parameter uji disolusi yang dipakai adalah Dissolution Efficiency atau DE30 (%). Data yang diperoleh kemudian dianalisis secara statistik menggunakan Analisa Varian (ANOVA) satu jalan dan uji BNT (Beda Nyata Terkecil) pada data yang memiliki perbedaan bermakna dengan tingkat kepercayaan 95%. Hasil penelitian ini menunjukan bahwa penambahan sodium lauril sulfat tidak berpengaruh terhadap uji kekerasan tablet, uji kerapuhan dan uji keseragaman bobot tablet tapi berpengaruh terhadap uji waktu hancur yaitu semakin banyak sodium lauril sulfat yang ditambahkan semakin cepat pula waktu hancurnya, dan laju disolusi tablet semakin besar pula. Persentase Ketoprofen terlarut pada menit ke-30 formula I, II, III, dan IV berturut-turut adalah 14,64% ; 29,66% ; 32,06% ; 35,81%. Kata kunci: sodium lauril sulfat, tablet, Ketoprofen, disolusi. ABSTRACT Ketoprofen (acid 2-(3-benzoilfenil) propanoat) was derivated of propionat acid which has analgesic, antipyretic, and anti-inflammatory with poor solubillity in water. This research allowed to increase the dissolution rate of Ketoprofen tablets and effect on the physical characteristic by adding sodium lauril sulfat as surfactant. Sodium lauryl sulfat is a surfactant that can be used to improve wetting and dissolution rate. This study was done with make four formula of Ketoprofen tablets by different concentration of sodium lauryl sulfat (0%, 0,5%, 1%, and 1,5%) as a wetting agent. Ketoprofen without sodium lauryl sulfat was used as control. The tablets were made by wet granulation method. Tablet produced were tested for the physical characterisation (uniformity of weight, and hardness, friability, and disintegration time tablet) and dissolution test. The dissolution test were done by using pedal method with dissolution buffer of phosphate buffer pH 7,2 with spinning rate of 100 rpm in the temperature 37±0,5ºC for 60 minutes. The parameter used in this research is Dissolution Efficiency or DE30 (%). Data gained then analyzed statistically by using one way Analysis of Variance (ANOVA) and LSD (Least Significant Difference). The result showed the data have signifficant differences at the confidence of 95% The result of this study indicate that the addition of sodium lauryl sulfate had not effects on hardness, fragility and weight uniformity of tablets, but it has effect on the disintegration time. By adding more sodium lauryl sulfat, the disintegration time and the dissolution rate were greater. The percentage of Ketoprofen dissolved after 30th minute, for formula I, II, III and IV respectively were 14,64% ; 29,66% ; 32,06% ; 35,81%. Key words: sodium lauryl sulfate, tablet, Ketoprofen, dissolutio
