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In a previous study from our group, argon has shown to significantly attenuate brain injury, reduce brain inflammation and enhance M 2 microglia/macrophage polarization until 7 days after ischemic stroke. However, the long-term effects of argon have not been reported thus far. In the present study, we analyzed the underlying neuroprotective effects and potential mechanisms of argon, up to 30 days after ischemic stroke. Argon administration with a 3 h delay after stroke onset and 1 h after reperfusion demonstrated long-term neuroprotective effect by preserving the neurons at the ischemic boundary zone 30 days after stroke. Furthermore, the excessive microglia/macrophage activation in rat brain was reduced by argon treatment 30 days after ischemic insult. However, long-lasting neurological improvement was not detectable. More sensorimotor functional measures, age- and disease-related models, as well as further histological and molecular biological analyses will be needed to extend the understanding of argon’s neuroprotective effects and mechanism of action after ischemic stroke.

Retinal ischemia and reperfusion injuries (IRI) permanently affect neuronal tissue and function by apoptosis and inflammation due to the limited regenerative potential of neurons. Recently, evidence emerged that the noble gas Argon exerts protective properties, while lacking any detrimental or adverse effects. We hypothesized that Argon inhalation after IRI would exert antiapoptotic effects in the retina, thereby protecting retinal ganglion cells (RGC) of the rat's eye. IRI was performed on the left eyes of rats (n = 8) with or without inhaled Argon postconditioning (25, 50 and 75 Vol%) for 1 hour immediately or delayed after ischemia (i.e. 1.5 and 3 hours). Retinal tissue was harvested after 24 hours to analyze mRNA and protein expression of Bcl-2, Bax and Caspase-3, NF-κB. Densities of fluorogold-prelabeled RGCs were analyzed 7 days after injury in whole-mounts. Histological tissue samples were prepared for immunohistochemistry and blood was analyzed regarding systemic effects of Argon or IRI. Statistics were performed using One-Way ANOVA. IRI induced RGC loss was reduced by Argon 75 Vol% inhalation and was dose-dependently attenuated by lower concentrations, or by delayed Argon inhalation (1504±300 vs. 2761±257; p<0.001). Moreover, Argon inhibited Bax and Bcl-2 mRNA expression significantly (Bax: 1.64±0.30 vs. 0.78±0.29 and Bcl-2: 2.07±0.29 vs. 0.99±0.22; both p<0.01), as well as caspase-3 cleavage (1.91±0.46 vs. 1.05±0.36; p<0.001). Expression of NF-κB was attenuated significantly. Immunohistochemistry revealed an affection of Müller cells and astrocytes. In addition, IRI induced leukocytosis was reduced significantly after Argon inhalation at 75 Vol%. Immediate and delayed Argon postconditioning protects IRI induced apoptotic loss of RGC in a time- and dose-dependent manner, possibly mediated by the inhibition of NF-κB. Further studies need to evaluate Argon's possible role as a therapeutic option.

Hypothermia is ineffective in 45% of neonates with hypoxic-ischemic encephalopathy. Xenon has additive neuroprotective properties, but is expensive, and its application complicated. Argon gas is cheaper, easier to apply, and also has neuroprotective properties in experimental settings. The aim was to explore the safety of argon ventilation in newborn piglets. Eight newborn piglets (weight 1.4-3.0 kg) were used. Heart rate, blood pressure, regional cerebral saturation, and electrocortical brain activity were measured continuously. All experiments had a 30 min. baseline period, followed by three 60 min. periods of argon ventilation alternated with 30 min argon washout periods. Two animals were ventilated with increasing concentrations of argon (1h 30%, 1 h 50%, and 1 h 80%), two were subjected to 60 min. hypoxia (FiO2 0.08) before commencing 50% argon ventilation, and two animals received hypothermia following hypoxia as well as 50% argon ventilation. Two animals served as home cage controls and were terminated immediately. Argon ventilation did not result in a significant change of heart rate (mean ± s.d. -3.5 ± 3.6 bpm), blood pressure (-0.60 ± 1.11 mmHg), cerebral oxygen saturation (0.3 ± 0.9%), electrocortical brain activity (-0.4 ± 0.7 µV), or blood gas values. Argon ventilation resulted in elevated argon concentrations compared to the home cage controls (34.5, 25.4, and 22.4 vs. 7.3 µl/ml). Ventilation with up to 80% argon during normoxia, and 50% argon after hypoxia did not affect heart rate, blood pressure, cerebral saturation and electrocortical brain activity. Clinical safety studies of argon ventilation in humans seem justified.

Diabetic foot ulcers are associated with significant morbidity and mortality, and current treatments are far from optimal. Chronic wounds in diabetes are characterised by impaired angiogenesis, leukocyte function, fibroblast proliferation, and keratinocyte migration and proliferation. : We tested the effect of exposure to argon gas on endothelial cell, fibroblast, macrophage and keratinocyte cell cultures and of a streptozotocin-induced diabetic mouse model. : Exposure to normobaric argon gas promotes multiple steps of the wound healing process. Argon accelerated angiogenesis, associated with upregulation of pro-angiogenic Angiopoietin-1 and vascular endothelial growth factor (VEGF) signalling and . Treatment with argon enhanced expression of transforming growth factor (TGF)-β, early recruitment of macrophages and keratinocyte proliferation. Argon had a pro-survival effect, inducing expression of cytoprotective mediators B-cell lymphoma 2 and heme oxygenase 1. Argon was able to accelerate wound closure in a diabetic mouse model. : Together these findings indicate that argon gas may be a promising candidate for clinical use in treatment of diabetic ulcers.

Numerous death cases due to suffocation in a toxic or oxygen deficient gas atmosphere have been described in the literature, but unfortunately especially cases involving inert gases like helium are often presented without detailed toxicological findings. Observations on two suicides are reported, one by helium and the other by argon inhalation. During autopsies gas samples from the lungs were collected directly into headspace vials by a procedure ensuring minimal loss and dilution. Qualitative gas analyses were performed using headspace gas chromatography–mass spectrometry (HS-GC/MS). For carrier gas the commonly used helium was replaced by hydrogen. Qualitative positive results were obtained in the argon case, but the case involving helium revealed negative findings. The use of HS-GC/MS enables in principle to detect inert gases like argon or helium. However, a number of factors may later influence the results as, e.g. a longer period of time between death and sampling or pre-analytical artefacts during sampling of such highly volatile substances. In absence of analytical data supporting helium exposure, the causes of death in the actual cases were found to be asphyxia and in both cases the manner was suicide.

Introduction Argon at a dosage of 70 % is neuroprotective, when given 1 h after cardiac arrest (CA) in rats. We investigated if a neuroprotective effect of argon would also be observed, when administration was delayed. Methods Twenty-four male Sprague–Dawley rats, weighing between 400 and 500 g were subjected to 7 min of CA and 3 min of cardiopulmonary resuscitation. Animals were randomized to receive either 1 h of 70 % argon ventilation 1 h ( n  = 8) or 3 h ( n  = 8) after return of spontaneous circulation or no argon treatment ( n  = 8). For all animals, a neurological deficit score (NDS) was calculated daily for 7 days following the experiment. On day 8, rats were re-anesthetized and transcardially perfused before brains were harvested for histopathological analyses. Results All animals survived. Control animals exhibited severe neurologic dysfunction at all time points as measured with the NDS. Argon-treated animals showed significant improvements in the NDS through all postoperative days, even when argon administration was delayed for 3 h. This was paralleled by a significant reduction in the neuronal damage index in the neocortex and the hippocampal CA 3/4 region in argon-treated animals, regardless of the timing of argon administration. However, animals of the delayed argon administration group additionally showed significant reductions in the basal ganglia in comparison with control animals. Conclusion Our study demonstrates that a 1-h application of argon provided a significant reduction in histopathological damage, associated with a marked improvement in functional neurologic recovery even when treatment was delayed for 3 h. This is highly significant with regard to clinical situations, where argon treatment cannot be provided timely.

Background The noble gas xenon is considered as a neuroprotective agent, but availability of the gas is limited. Studies on neuroprotection with the abundant noble gases helium and argon demonstrated mixed results, and data regarding neuroprotection after cardiac arrest are scant. We tested the hypothesis that administration of 50 % helium or 50 % argon for 24 h after resuscitation from cardiac arrest improves clinical and histological outcome in our 8 min rat cardiac arrest model. Methods Forty animals had cardiac arrest induced with intravenous potassium/esmolol and were randomized to post-resuscitation ventilation with either helium/oxygen, argon/oxygen or air/oxygen for 24 h. Eight additional animals without cardiac arrest served as reference, these animals were not randomized and not included into the statistical analysis. Primary outcome was assessment of neuronal damage in histology of the region I of hippocampus proper (CA1) from those animals surviving until day 5. Secondary outcome was evaluation of neurobehavior by daily testing of a Neurodeficit Score (NDS), the Tape Removal Test (TRT), a simple vertical pole test (VPT) and the Open Field Test (OFT). Because of the non-parametric distribution of the data, the histological assessments were compared with the Kruskal–Wallis test. Treatment effect in repeated measured assessments was estimated with a linear regression with clustered robust standard errors (SE), where normality is less important. Results Twenty-nine out of 40 rats survived until day 5 with significant initial deficits in neurobehavioral, but rapid improvement within all groups randomized to cardiac arrest. There were no statistical significant differences between groups neither in the histological nor in neurobehavioral assessment. Conclusions The replacement of air with either helium or argon in a 50:50 air/oxygen mixture for 24 h did not improve histological or clinical outcome in rats subjected to 8 min of cardiac arrest.

Previous studies on the antimicrobial activity of cold atmospheric pressure argon plasma showed varying effects against mecA + or mecA - Staphylococcus aureus strains. This observation may have important clinical and epidemiological implications. Here, the antibacterial activity of argon plasma was investigated against 78 genetically different S. aureus strains, stratified by mecA, luk-P, agr1-4, or the cell wall capsule polysaccharide types 5 and 8. kINPen09® served as the plasma source for all experiments. On agar plates, mecA + luk-P - S. aureus strains showed a decreased susceptibility against plasma compared to other S. aureus strains. This study underlines the high complexity of microbial defence against antimicrobial treatment and confirms a previously reported strain-dependent susceptibility of S. aureus to plasma treatment.

Argon has been shown to provide cortical as well as, under certain conditions, subcortical neuroprotection in all models so far (middle cerebral artery occlusion, trauma, neonatal asphyxia, etc.). This has led to the suggestion that argon could be a cost-efficient alternative to xenon, a metabolically inert gas thought to be gold standard in gas pharmacology but whose clinical development suffers its little availability and excessive cost of production. However, whether argon interacts with the thrombolytic agent tissue plasminogen activator, which is the only approved therapy of acute ischemic stroke to date, still remains unknown. This latter point is not trivial since previous data have clearly demonstrated the inhibiting effect of xenon on tPA enzymatic and thrombolytic efficiency and the critical importance of the time at which xenon is administered, during or after ischemia, in order not to block thrombolysis and to obtain neuroprotection. Here, we investigated the effect of argon on tPA enzymatic and thrombolytic efficiency using in vitro methods shown to provide reliable prediction of the in vivo effects of both oxygen and the noble inert gases on tPA-induced thrombolysis. We found that argon has a concentration-dependent dual effect on tPA enzymatic and thrombolytic efficiency. Low and high concentrations of argon of 25 and 75 vol% respectively block and increase tPA enzymatic and thrombolytic efficiency. The possible use of argon at low and high concentrations in the treatment of acute ischemic stroke if given during ischemia or after tPA-induced reperfusion is discussed as regards to its neuroprotectant action and its inhibiting and facilitating effects on tPA-induced thrombolysis. The mechanisms of argon–tPA interactions are also discussed.

Background We describe two cases of recurrent acute angle-closure attack in patients with plateau iris syndrome after cataract extraction. Argon laser peripheral iridoplasty and cataract extraction have been used to reduce the occurrence of acute angle-closure attack in plateau iris syndrome although the risk cannot be completely eliminated. There is no consensus on the long term management of plateau iris syndrome. This is, as far as we know, the first case report of recurrent acute angle-closure attack in plateau iris syndrome after cataract extraction. Case presentation We report two cases of recurrent acute angle-closure attack in 2 Chinese patients with plateau iris syndrome. The first patient was a 69 year-old woman who received bilateral argon laser peripheral iridoplasty and cataract extraction 2 years prior to the latest acute angle-closure with right eye intraocular pressure 48 mmHg. The attack was aborted medically. Peripheral iridotomy was patent and argon laser peripheral iridoplasty marks were mostly at peripheral 2/3 of the iris. Anterior segment optical coherence tomography confirmed bilateral plateau iris configuration. Use of long term pilocarpine or repeated argon laser peripheral iridoplasty to prevent recurrent angle-closure attack was discussed but she opted for observation. The second patient was a 64 year-old man presented with acute angle-closure after cataract extraction despite placement of laser peripheral iridotomy. Plateau iris syndrome was confirmed by anterior segment optical coherence tomography and he received argon laser peripheral iridoplasty. Conclusions Acute angle-closure due to plateau iris syndrome can still occur despite previous cataract extraction and argon laser peripheral iridoplasty. These are the first reported cases of recurrent acute angle-closure attack due to plateau iris syndrome following cataract extraction, with or without previous argon laser peripheral iridoplasty. Repeated treatment with argon laser peripheral iridoplasty or pilocarpine could be considered although the long term efficacy is questionable. Argon laser peripheral iridoplasty should be applied as peripheral as possible so as to open up the drainage angle effectively.