Fingermark visualisation on compostable polymers - A comparison among different procedures as an outcome of the 2020 collaborative exercise of the ENFSI Fingerprint Working Group.

In 2020 the Fingerprint Working Group (EFP-WG) of the European Network of Forensic Science Institutes (ENFSI) undertook a collaborative exercise (CE) with the aim of assessing the ability in developing fingermarks on an item constituted of compostable polymers. The test was prepared and managed by the officially established advisory group. The characteristics of the CE are summarised. Different approaches emerged from the outcomes. Multi-Metal Deposition (MMD) was used as reference method for the assessment of the results. It demonstrated to be the more effective and consistent technique for fingermark visualisation on the specific kind of Mater-Bi® compostable polymer used for the test. Alternative techniques, such as Vacuum Metal Deposition (VMD), cyanoacrylate fuming, followed by Basic Yellow 40 dye staining or in its fluorescent forms demonstrated to be effective methods. However, it seems that the operational conditions need to be controlled in order to find the optimal ones. Conversely, data does not support the use of amino acid sensitive techniques.

Fingermark visualisation on thermal paper - A comparison among different procedures as an outcome of the 2018 collaborative exercise of the ENFSI Fingerprint Working Group.

In 2018 the Fingerprint Working Group (EFP-WG) of the European Network of Forensic Science Institutes (ENFSI) undertook a collaborative exercise (CE) with the aim of assessing the ability in developing fingermarks on an item constituted of a thermal layer. The test was prepared and managed by the officially established advisory group. The characteristics of the CE are summarised. Different approaches emerged from the outcomes showing on average valid results. What is evident from data is that the preliminary inspection is highly advisable especially for the thermal side exploiting specific combinations of wavelengths and filters. In general, better performances were achieved by laboratories using multiple processing techniques. Conversely, few laboratories were capable to reach the expected results with only one step process. Finally, data does not support the use of cyanoacrylate, powders, and iodine on this specific substrate.

The 2016 ENFSI Fingerprint Working Group testing programme.

In 2016, the Fingerprint Working Group (EFP-WG) of the European Network of Forensic Science Institutes (ENFSI), officially established an advisory group with the task of organising proficiency tests (PTs), as well as collaborative exercises (CEs) as a way of raising standards within the fingerprint profession. This article will provide an overview of the Visualisation collaborative exercise and the Comparison proficiency test, which were carried out in 2016. Both the exercise and the test were organised and co-funded by the Prevention of and Fight against Crime Programme of the European Union [1-3], Direct Grant "Towards the Vision for European Forensic Science 2020 (TVEFS-2020)" HOME/2013/ISEC/MO/ENFSI/4000005962, work package T3 "Proficiency Tests and Collaborative Exercises for the Fingerprint Domain". The characteristics of the testing programme are summarised, followed by an overview of the knowledge that has been gained, including lessons learnt.

The 2015 ENFSI Fingerprint Working Group testing programme.

As early as 2004, the Fingerprint Working Group (EFP-WG) of the European Network of Forensic Science Institutes (ENFSI) has organised proficiency tests (PT's), as well as collaborative exercises (CE's), as a way of raising standards within the fingerprint profession. This article provides an overview of the three collaborative exercises carried out in 2015. The characteristics of the testing programme are summarised, followed by an overview of the knowledge that has been gained, including depicting what lessons have been learnt.

ENFSI collaborative testing programme for fingermarks: Past experiences and future perspectives.

As early as 2004 the Fingerprint Working Group of the European Network of Forensic Science Institutes (ENFSI) has organised proficiency tests (PT's) as well as collaborative exercises (CE's) as a way of raising standards within the fingerprint profession. Participation in PT's and CE's is a key element in the ISO/IEC accreditation process as they enable laboratories to monitor the quality of their analytical results. On the basis of the European Council Framework Decision 2009/905/JHA, of 30 November 2009, on Accreditation of forensic service providers carrying out laboratory activities[1], from November 15th of 2015, only accredited laboratories are allowed to exchange fingerprint data with other EU countries. This article will provide an overview of the ENFSI collaborative tests for fingermarks in the fields of visualisation, imaging and individualisation. The characteristics of the testing programme are summarised, followed by an overview of the knowledge that has been gained, including lessons learnt. It is hoped that this reflective process can outline the critical issues that should be addressed as well as highlight future opportunities in relation to Monopoly Project 2013, "Proficiency Tests and Collaborative Exercises for the Fingerprint Domain".

Excitotoxic hippocampal membrane breakdown and its inhibition by bilobalide: role of chloride fluxes.

We have previously shown that hypoxia and N-methyl-D-aspartate (NMDA) receptor activation induce breakdown of choline-containing phospholipids in rat hippocampus, a process which is mediated by calcium influx and phospholipase A (2) activation. Bilobalide, a constituent of Ginkgo biloba, inhibited this process in a potent manner (Weichel et al., Naunyn-Schmiedeberg's Arch. Pharmacol. 360, 609-615, 1999). In this study, we used fluorescence microscopy and radioactive flux measurements to show that bilobalide does not interfere with NMDA-induced calcium influx. Instead, bilobalide seems to inhibit NMDA-induced fluxes of chloride ions through ligand-operated chloride channels. In our experiments, substitution of chloride in the superfusion medium fully blocked the effect of NMDA on choline release from hippocampal slices, while the presence of chloride transport inhibitors (furosemide, DIDS) was partially antagonistic. The inhibitory effect of bilobalide and of HA-966, a glycine B receptor antagonist, on NMDA-induced choline release was attenuated in the presence of glycine. The inhibitory effect of bilobalide, but not that of HA-966, was also antagonized by GABA. The inhibitory effect of MK-801, an NMDA channel blocker, on choline release was insensitive to glycine. We conclude from our findings that bilobalide inhibits an NMDA-induced chloride flux through glycine/GABA-operated channels, thereby preventing NMDA-induced breakdown of membrane phospholipids. This effect is expected to contribute to the neuroprotective effects of ginkgo biloba extracts.

Glucose plus choline improve passive avoidance behaviour and increase hippocampal acetylcholine release in mice.

The present study tests the effects of glucose and choline, the biosynthetic precursors of acetylcholine, on passive avoidance behaviour and hippocampal acetylcholine release measured by microdialysis in awake mice. Glucose (10 and 30mg/kg) or choline chloride (6-60mg/kg), given by i.p. injection immediately after training, dose-dependently enhanced retention in an inhibitory avoidance task. Combinations of low doses of glucose (10mg/kg) and choline chloride (20mg/kg) which alone were submaximally effective significantly increased retention latencies in a synergistic manner, an effect which was sensitive to atropine (0.5mg/kg). This beneficial effect vanished when higher doses of glucose or choline were combined. Basal hippocampal acetylcholine release in mice habituated to their environment was not affected by administration of glucose and choline. However, when hippocampal acetylcholine release was stimulated either by infusion of scopolamine (0.3microM) or by transferring the mice into a novel environment, the combination of glucose plus choline further increased acetylcholine release to a significant extent. We conclude that low doses of glucose and choline act synergistically to improve memory storage, an effect which is due to facilitation of acetylcholine release. This finding reinforces the view that central cholinergic functions are influenced under certain conditions by dietary intake of precursors.

Serotonergic modulation of hippocampal acetylcholine release after long-term neuronal grafting.

Adult female rats sustained aspirative fimbria-fornix lesions and, 2 weeks later, received intrahippocampal grafts of fetal septal or mixed septal-raphe cell suspensions. Twenty-four months later, the extracellular concentration of hippocampal acetylcholine (ACh) was determined by microdialysis. Basal ACh levels (5-65 fmol/5 microl sham-operated rats) were strongly reduced after lesioning (3-7 fmol/5 microl). In septally transplanted and septal-raphe co-transplanted rats, hippocampal ACh concentrations were restored to near-normal levels (15-25 fmol/5 microl), indicating long-term functional survival of hippocampal transplants. After administration of citalopram (100 microM by infusion) and fenfluramine (20 mg/kg i.p.), the hippocampal ACh efflux was increased by 2- to 3-fold in all groups of rats. The relative increase of ACh was highest in co-transplanted rats, an effect which was possibly due to functional interactions between grafted raphe and septal neurons.

KA-672 inhibits rat brain acetylcholinesterase in vitro but not in vivo.

KA-672, a lipophilic benzopyranone derivative which is currently under development as a cognitive enhancer and antidementia drug, has previously been shown to have facilitatory effects on learning and memory in rats at doses of 0.1-1 mg/kg. We now report that KA-672 inhibited the activity of acetylcholinesterase (AChE), measured in vitro in rat brain cortical homogenate, with an IC50 value of 0.36 microM indicating that KA-672 may improve cognitive functions as a consequence of AChE inhibition. However, when we employed the microdialysis procedure to monitor acetylcholine (ACh) release from rat hippocampus, no effect of KA-672 (0.1-10 mg/kg) was found, indicating a lack of inhibition of brain AChE under in vivo-conditions. [14C]-labelled KA-672 was found to easily penetrate the blood-brain barrier, and an apparent concentration of 0.22 nmol/g brain (equivalent to 0.39 microM tissue concentration) was calculated following an i.p. injection of 1 mg/kg KA-672. However, no labelled substance could be detected in hippocampal microdialysates or in cerebrospinal fluid (CSF) taken from the cisterna magna, indicating that the concentration of KA-672 in brain extracellular fluid must have been below 0.01 microM. We conclude that KA-672 is a potent AChE inhibitor, an activity which, however, does not contribute to its behavioural effects in vivo because the lipophilic drug does not reach sufficient concentrations in the extracellular fluid, apparently due to cellular sequestration.

Bilobalide, a constituent of Ginkgo biloba, inhibits NMDA-induced phospholipase A2 activation and phospholipid breakdown in rat hippocampus.

In rat hippocampal slices superfused with magnesium-free buffer, glutamate (1 mM) caused the release of large amounts of choline due to phospholipid breakdown. This phenomenon was mimicked by N-methyl-D-aspartate (NMDA) in a calcium-sensitive manner and was blocked by NMDA receptor antagonists such as MK-801 and 7-chlorokynurenate. The NMDA-induced release of choline was not caused by activation of phospholipase D but was mediated by phospholipase A2 (PLA2) activation as the release of choline was accompanied by the formation of lyso-phosphatidylcholine (lyso-PC) and glycerophospho-choline (GPCh) and was blocked by 5-[2-(2-carboxyethyl)-4-dodecanoyl-3,5-dimethylpyrrol-1-yl]pentano ic acid, a PLA2 inhibitor. Bilobalide, a constituent of Ginkgo biloba, inhibited the NMDA-induced efflux of choline with an IC50 value of 2.3 microM and also prevented the formation of lyso-PC and GPCh. NMDA also caused a release of choline in vivo when infused into the hippocampus of freely moving rats by retrograde dialysis. Again, the effect was completely inhibited by bilobalide which was administered systemically (20 mg/kg i.p.). Interestingly, convulsions which were observed in the NMDA-treated rats were almost totally suppressed by bilobalide. We conclude that release of choline is a sensitive marker for NMDA-induced phospholipase A2 activation and phospholipid breakdown. Bilobalide inhibited the glutamatergic excitotoxic membrane breakdown both in vitro and in vivo, an effect which may be beneficial in the treatment of brain hypoxia and/or neuronal hyperactivity.