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Propolipid

Manufactured by Fresenius
Sourced in Finland, Sweden

Propolipid is a specialized lab equipment product. It is designed for the preparation and handling of lipid-based materials in a laboratory setting. The core function of Propolipid is to facilitate the precise and controlled manipulation of lipid-containing samples.

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4 protocols using propolipid

1

Phase IV Clinical Trial of Anesthetic Agents

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This randomised, open-label, controlled, parallel group, Phase IV clinical drug trial (ClinicalTrials.gov identifier NCT02624401) was conducted at Turku PET Centre, University of Turku, Turku, Finland as a part of ‘The Neural Mechanisms of Anesthesia and Human Consciousness’ project (from January 2016 to March 2017), as predefined in the trial protocol. This study was approved by the Ethics Committee of the Hospital District of Southwest Finland and the Finnish Medicines Agency Fimea (EudraCT 2015-004982-10). This article adheres to the applicable Consolidated Standards of Reporting Trials (CONSORT) guidelines. A detailed description of the study methods and the CONSORT flow diagram have been published earlier.4 (link), 7 (link)
A total of 160 healthy, ASA physical status Class 1 male subjects were randomly allocated to receive one of the following study treatments: dexmedetomidine (Dexdor 100 μg ml−1; Orion Pharma, Espoo, Finland; n=40), propofol (Propolipid 10 mg ml−1; Fresenius Kabi, Uppsala, Sweden; n=40), sevoflurane (Sevoflurane 100%; AbbVie, Espoo, Finland; n=40), S-ketamine (Ketanest-S 25 mg ml−1; Pfizer, Helsinki, Finland; n=20), or saline placebo (n=20). The inclusion criteria have been described earlier.7 (link) In accordance with the Declaration of Helsinki, a written informed consent was obtained from all study subjects.
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2

Niacinamide Tissue Depot Study

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Pigs (70–90 kg) were anesthetized using Zoletil mixture (1 mg/10 kg; Virbac, Denmark) with intravenous supplement of propolipid (Fresenius Kabi, Sweden). Pigs were placed on their side and injected in the neck region with 50 μl of phosphate buffer (10 mM; pH 7.4) supplemented with niacinamide (170 mM; adjusted to isotonic with 85 mM NaCl) or 1-methyl-niacinamide (170 mM). Tissue samples measuring ~2 x 2 cm were excised at 0 min (acute), 2, 5, 15 or 60 min after injection and immediately frozen in 2-methyl-butane. To evaluate whether niacinamide and 1-methyl-niacinamide were entirely confined within the excised tissue, 1 cm thick sections along the four edges of the 0 min (acute) sample were also excised. Following euthanasia by overdose of pentobarbital (Lundbeck, Denmark), tissue samples measuring ~10 x 10 cm were excised and injected to obtain ex vivo 0 min (acute) and 60 min depots.
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3

General Anesthesia Protocol for Surgical Patients

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All patients received a premedication with 3.75 to 7.5 mg midazolam (Dormicum, Basel, Switzerland); the anesthesia scalp EEG group (Study 1) received additional 1 g oral paracetamol (Paracet, Weifa, Oslo, Norway) as well as 10 mg oxycodone sustained release tablet (OxyContin, Dublin, Ireland) for postoperative pain management. propofol (Propolipid, Fresenius Kabi, Uppsala, Sweden) and remifentanil (Ultiva, GlaxoSmithKline, Parma, Italy) were administered by computer-controlled infusion pumps (B Braun Perfusor Space, Melsungen, Germany) using a target-controlled infusion (TCI) program (Schnider for propofol and Minto for remifentanil) in order to achieve plasma concentrations sufficient for anesthesia and analgesia. Prior to start of anesthesia all patients received an infusion of Ringer’s-Acetate (5 ml /kg) to prevent hypotension during anesthesia induction, as well as 3–5 ml 1% lidocaine intravenously to prevent pain during propofol injection. All patients were pre-oxygenated with 100% oxygen and received the non-depolarizing muscle relaxant cisatracurium for intubation (Nimbex, GlaxoSmithKline, Oslo, Norway). After intubation the inspiratory oxygen fraction was reduced to 40%; nitric oxide was not used.
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4

Comparative Cerebral Metabolism in Anesthesia

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This randomised, open-label, controlled, parallel group, phase IV clinical drug trial was conducted at Turku PET Centre, University of Turku, Finland, as a part of 'The Neural Mechanisms of Anaesthesia and Human Consciousness' project. A detailed description of the study methods has been published previously in an article comparing the effects of anaesthetic agents on regional cerebral glucose metabolism. 22 One hundred and sixty healthy, American Society of Anaesthesiologists class I (ASA I) male volunteers were randomised to receive dexmedetomidine (Dexdor 100 μg ml -1 , Orion Pharma, Espoo, Finland; n = 40), propofol (Propolipid 10 mg ml -1 ; Fresenius Kabi, Bad Homburg, Germany; n = 40), sevoflurane (Sevoflurane 100%, Abbvie, North Chicago, Illinois, U.S.A; n = 40), S-ketamine (Ketanest-S 25 mg ml -1 , Pfizer, NY, U.S.A; n = 20) or placebo (Ringer's acetate, n = 20). The inclusion criteria have been described earlier. 22 Written informed consent was obtained from all participants in accordance with the Declaration of Helsinki.
Only male participants were studied because of radiation exposure related to a subsequent PET study. Due to the exploratory nature of the study, a formal power analysis was not considered applicable. Randomisation was performed using balanced permuted block sizes of 16 as previously described. 22
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