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Coastal defense structures (e.g., dikes, seawalls) protect vulnerable communities along marine coastlines and estuaries from the physical and chemical influences of adjacent water bodies. These structures are susceptible to overtopping or breaching by tides and waves, with risks amplified by climate change-induced sea-level rise. Repeated inundation by saline water can contaminate freshwater resources and salinize soil, impacting land-use activities, including agricultural productivity. Managed ecosystem-based dike realignment and salt marsh restoration can provide alternatives to traditional coastal adaptation approaches. We assess the changes to soil salinity at a managed dike realignment project prior to the transformation from a diked terrestrial environment to an estuarine environment. Baseline data are compared to conditions following 8-10 months of intermittent flooding at spring tides. Results show that an increase in salinity occurred over the entire site in the shallow subsurface, with the most significant contamination occurring in low-lying areas. Bulk soil electrical conductivity (salinity proxy) measured from geophysical surveys increased from the previous freshwater condition of ∼300 μS/cm to over 6000 μS/cm following <20 flood events, while successive flooding resulted in increased soil moisture as infiltrated floodwater propagated to greater depths. Sediment deposition occurred at high rates, with up to 4 cm of sediment deposited per flood, converting much of the previously cultivated land into tidal mudflats. Deeper sediments and groundwater (i.e., >1.8 m depth) were not impacted over the time scale of this research. This study demonstrates that intermittent shallow flooding can rapidly increase moisture content and soil salinity in surficial sediments and, in turn, adversely impact conditions suitable for agricultural crop production. The realignment zone serves as an engineered analog of coastal flooding, presenting an opportunity to investigate how low-lying coastal environments may experience regular flooding in the future due to sea-level rise and intensifying coastal storms., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

The homogeneous labeling of antibodies and their fragments is a critical step for the generation of robust probes used in immuno-detection applications. To date, numerous chemical, genetic and peptide-based site-specific coupling methods have been developed. Among these methods, co-assembling peptide-tags is one of the most straightforward and versatile solutions. Here, we describe site-specific labeling of nanobodies through the use of two co-associating peptides tags, E3 and K3, originating from the tetramerization domain of p53. These E3 and K3-tags provide a simple and robust method for associating stoichiometric amount of V H H and fluorescent probes, either fluorescent proteins or fluorochromes, at specific positions. As a proof of concept, a nanobody targeting the human epidermal growth factor receptor 2 (HER2), the nano-HER2 was genetically fused to the E3 and associated with different fluorescent K3-derivates. Entities were produced separately in Escherichia coli in soluble forms at high yields and co-assembled in vitro. These molecular probes present high binding specificity on HER2-overexpressing cells in flow-cytometry with relative binding constants in the low nanomolar range and are stable enough to stain HER2-receptor on living cells followed detection using fluorescent confocal microscopy. Altogether, our results demonstrate that the non-covalent conjugation method using these two co-associating peptides can be easily implemented for the modular engineering of molecular probes for cell immuno-staining.

Despite the global interest in green energy alternatives, little attention has focused on the large-scale viability of recycling the ground heat accumulated due to urbanization, industrialization and climate change. Here we show this theoretical heat potential at a multi-continental scale by first leveraging datasets of groundwater temperature and lithology to assess the distribution of subsurface thermal pollution. We then evaluate subsurface heat recycling for three scenarios: a status quo scenario representing present-day accumulated heat, a recycled scenario with ground temperatures returned to background values, and a climate change scenario representing projected warming impacts. Our analyses reveal that over 50% of sites show recyclable underground heat pollution in the status quo, 25% of locations would be feasible for long-term heat recycling for the recycled scenario, and at least 83% for the climate change scenario. Results highlight that subsurface heat recycling warrants consideration in the move to a low-carbon economy in a warmer world., (© 2022. The Author(s).)

Membrane proteins (MPs) comprise about one-third of the human proteome, playing critical roles in many physiological processes and associated disorders. Consistently, they represent one of the largest classes of targets for the pharmaceutical industry. Their study at the molecular level is however particularly challenging, resulting in a severe lack of structural and dynamic information that is hindering their detailed functional characterization and the identification of novel potent drug candidates.Magic Angle Spinning (MAS) NMR is a reliable and efficient method for the determination of protein structures and dynamics and for the identification of ligand binding sites and equilibria. MAS-NMR is particularly well suited for MPs since they can be directly analysed in a native-like lipid bilayer environment but used to require aggravating large amounts of isotope enriched material. The frequent toxicity of human MP overexpression in bacterial cultures poses an additional hurdle, resulting in the need for alternative (and often more costly) expression systems. The recent development of very fast (up to 150 kHz) MAS probes has revolutionized the field of biomolecular solid-state NMR enabling higher spectral resolution with significant reduction of the required sample, rendering eukaryotic expression systems cost-effective.Here is presented a set of accessible procedures validated for the production and preparation of eukaryotic MPs for Fast-MAS 1 H-detected NMR analysis. The methodology is illustrated with the human copper uptake protein hCTR1 recombinantly produced and 13 C- 15 N uniformly labeled with the versatile and affordable Pichia pastoris system. Subsequent purification procedures allow the recovery of mg amounts that are then reconstituted into liposome formulations compatible with solid-state NMR handling and analysis., (© 2022. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)

Immunotoxins are emerging candidates for cancer therapeutics. These biomolecules consist of a cell-targeting protein combined to a polypeptide toxin. Associations of both entities can be achieved either chemically by covalent bonds or genetically creating fusion proteins. However, chemical agents can affect the activity and/or stability of the conjugate proteins, and additional purification steps are often required to isolate the final conjugate from unwanted byproducts. As for fusion proteins, they often suffer from low solubility and yield. In this report, we describe a straightforward conjugation process to generate an immunotoxin using coassociating peptides (named K3 and E3), originating from the tetramerization domain of p53. To that end, a nanobody targeting the human epidermal growth factor receptor 2 (nano-HER2) and a protein toxin fragment from Pseudomonas aeruginosa exotoxin A (TOX) were genetically fused to the E3 and K3 peptides. Entities were produced separately in Escherichia coli in soluble forms and at high yields. The nano-HER2 fused to the E3 or K3 helixes (nano-HER2-E3 and nano-HER2-K3) and the coassembled immunotoxins (nano-HER2-K3E3-TOX and nano-HER2-E3K3-TOX) presented binding specificity on HER2-overexpressing cells with relative binding constants in the low nanomolar to picomolar range. Both toxin modules (E3-TOX and K3-TOX) and the combined immunotoxins exhibited similar cytotoxicity levels compared to the toxin alone (TOX). Finally, nano-HER2-K3E3-TOX and nano-HER2-E3K3-TOX evaluated on various breast cancer cells were highly potent and specific to killing HER2-overexpressing breast cancer cells with IC 50 values in the picomolar range. Altogether, we demonstrate that this noncovalent conjugation method using two coassembling peptides can be easily implemented for the modular engineering of immunotoxins targeting different types of cancers.

In the presence of ciprofloxacin (CPFX), free radical adduct formation was demonstrated in rat cerebral microsomes using a spin trap α-(4-pyridyl-1-oxide)-N- tert -butyl-nitrone by electron spin resonance spectroscopy. Active microsomes, dihydronicotinamide-adenine dinucleotide phosphate, and ciprofloxacin were necessary for the formation of a spin trap/radical adduct. Adduct formation increased dose-dependently at 0.5-1 mM CPFX concentration for 180 min, and 0.3-1 mM concentration level for 240 min. The addition of SKF 525A, ZnCl 2 or desferrioxamine to the incubation system caused complete inhibition of the radical formation. However, pretreatment of microsomal system with superoxide dismutase (SOD) did not induce any protective effect. Induction of lipid peroxidation, and depletion of thiol levels by CPFX were also shown in the system. These results strongly suggested that CPFX produces free radical(s) in the cerebral microsomes of rats.

Cocaine abuse induces brain injury and neurodegeneration by a mechanism that has not yet been fully elucidated. Mitochondria play a key role in cell death processes, notably through the opening of the permeability transition pore (PTP). In this work, we examined the involvement of the PTP in cocaine-induced toxicity in PC12 cell lines. We used two different PTP inhibitors -i.e. cyclosporin A (CsA) and metformin-to assess their ability to counteract the cocaine induced effects. We first observed that a 48 h exposure to cocaine strongly sensitized cells to calcium overload, as measured by the calcium retention capacity. CsA and metformin significantly decreased the cocaine-induced PTP opening sensitization. We next showed by confocal microscopy that cocaine induced a permanent PTP opening in intact living cells, a phenomenon characterized by the collapse of the mitochondrial membrane potential and the relocation of the NAD(P)H from the mitochondrial matrix to the cytosol. As expected, a cocaine-induced PTP opening was prevented by PTP inhibitors. Finally, a flow cytometry analysis revealed that cocaine induced cell death while CsA and metformin promoted cell survival. Our results demonstrate that cocaine induces PC12 cell death through a mechanism involving permanent PTP opening., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Obtaining reliable estimates of vertical groundwater flows remains a challenge but is of critical importance to the management of groundwater resources. When large scale land clearing or groundwater extraction occurs, methods based on water table fluctuations or water chemistry are unreliable. As an alternative, a number of methods based on temperature-depth (T-z) profiles are available to provide vertical groundwater flow estimates from which recharge rates may be calculated. However, methods that invoke steady state assumptions have been shown to be inappropriate for sites that have experienced land surface warming. Analytical solutions that account for surface warming are available, but they typically include unrealistic or restrictive assumptions (e.g. no flow initial conditions or linear surface warming). Here, we use a new analytical solution and associated computer program (FAST) that provides flexible initial and boundary conditions to estimate fluxes using T-z profiles from the Willunga Super Science Site, a complex, but densely instrumented groundwater catchment in South Australia. T-z profiles from seven wells (ranging from high elevation to near sea level) were utilised, in addition to mean annual air temperatures at nearby weather stations to estimate boundary conditions, and thermal properties were estimated from down borehole geophysics. Temperature based flux estimates were 5 to 23mmy -1 , which are similar to those estimated using chloride mass balance. This study illustrates that T-z profiles can be studied to estimate recharge in environments where more commonly applied methods fail., (Copyright © 2016 Elsevier B.V. All rights reserved.)

AMP-activated protein kinase (AMPK) and cytosolic brain-type creatine kinase (BCK) cooperate under energy stress to compensate for loss of adenosine triphosphate (ATP) by either stimulating ATP-generating and inhibiting ATP-consuming pathways, or by direct ATP regeneration from phosphocreatine, respectively. Here we report on AMPK-dependent phosphorylation of BCK from different species identified by in vitro screening for AMPK substrates in mouse brain. Mass spectrometry, protein sequencing, and site-directed mutagenesis identified Ser6 as a relevant residue with one site phosphorylated per BCK dimer. Yeast two-hybrid analysis revealed interaction of active AMPK specifically with non-phosphorylated BCK. Pharmacological activation of AMPK mimicking energy stress led to BCK phosphorylation in astrocytes and fibroblasts, as evidenced with a highly specific phospho-Ser6 antibody. BCK phosphorylation at Ser6 did not affect its enzymatic activity, but led to the appearance of the phosphorylated enzyme at the endoplasmic reticulum (ER), close to the ER calcium pump, a location known for muscle-type cytosolic creatine kinase (CK) to support Ca²⁺-pumping., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Ethanol induces brain injury by a mechanism that remains partly unknown. Mitochondria play a key role in cell death processes, notably through the opening of the permeability transition pore (PTP). Here, we tested the effect of ethanol and PTP inhibitors on mitochondrial physiology and cell viability both in vitro and in vivo. Direct addition of ethanol up to 100 mM on isolated mouse brain mitochondria slightly decreased oxygen consumption but did not affect PTP regulation. In comparison, when isolated from ethanol-treated (two doses of 2 g/kg, 2 h apart) 7-day-old mouse pups, brain mitochondria displayed a transient decrease in oxygen consumption but no change in PTP regulation or H2O2 production. Conversely, exposure of primary cultured astrocytes and neurons to 20 mM ethanol for 3 days led to a transient PTP opening in astrocytes without affecting cell viability and to a permanent PTP opening in 10 to 20% neurons with the same percentage of cell death. Ethanol-treated mouse pups displayed a widespread caspase-3 activation in neurons but not in astrocytes and dramatic behavioral alterations. Interestingly, two different PTP inhibitors (namely, cyclosporin A and nortriptyline) prevented both ethanol-induced neuronal death in vivo and ethanol-induced behavioral modifications. We conclude that PTP opening is involved in ethanol-induced neurotoxicity in the mouse.

Aims. 3,5,4'-Trihydroxy-trans-stilbene, a natural polyphenolic compound present in wine and grapes and better known as resveratrol, has free radical scavenging properties and is a potent protector against oxidative stress induced by alcohol metabolism. Today, the mechanism by which ethanol exerts its toxicity is still not well understood, but it is generally considered that free radical generation plays an important role in the appearance of structural and functional alterations in cells. The aim of this study was to evaluate the protective action of resveratrol against ethanol-induced brain cell injury. Methods. Primary cultures of rat astrocytes were exposed to ethanol, with or without a pretreatment with resveratrol. We examined the dose-dependent effects of this resveratrol pretreatment on cytotoxicity and genotoxicity induced by ethanol. Cytotoxicity was assessed using the MTT reduction test. Genotoxicity was evidenced using single cell gel electrophoresis. In addition, DNA staining with fluorescent dyes allowed visualization of nuclear damage using confocal microscopy. Results. Cell pretreatment with low concentrations of trans-resveratrol (0.1-10 μM) slowed down cell death and DNA damage induced by ethanol exposure, while higher concentrations (50-100 μM) enhanced these same effects. No protection by cis-resveratrol was observed. Conclusion. Protection offered by trans-resveratrol against ethanol-induced neurotoxicity was only effective for low concentrations of this polyphenol.

The aim of this study was to investigate the possible cytotoxic and oxidative stress inducing effects of ciprofloxacin (CPFX) on primary cultures of rat astrocytes. The cultured cells were incubated with various concentrations of CPFX (0.5-300mg/l), and cytotoxicity was determined by neutral red (NR) and MTT assays. Survival profile of cells was biphasic in NR assay: CPFX did not cause any alteration at any concentration for 7h, whereas < or =50mg/l concentrations induced significant cell proliferation in incubation periods of 24, 48, 72, and 96h. However, cell proliferation gradually decreased at higher concentrations, and 200 and 300mg/l of CPFX exposure was found to be significantly (p<0.05) cytotoxic at all time periods. With MTT assay, no alteration was noted for incubation period of 7h, as observed with NR assay. But, cell viability decreased with approximately > or =50mg/l CPFX exposure in all other time periods. Cell proliferation was only seen in 24h of incubation with 0.5 and 5mg/l CPFX. Vitamin E pretreatment of cell cultures were found to be providing complete protection against cytotoxicity of 300mg/l CPFX in 96h incubation when measured with both NR and MTT assays. The SOD pretreatment was partially protective with NR assay, but no protection was noted when measured with MTT. A significant enhancement of lipid peroxidation was observed with the cytotoxic concentration of the drug, but total glutathione content and catalase activity of cells did not change. The data obtained in this study suggest that, in accordance with our previous results with fibroblast cells, CPFX-induced cytotoxicity is related to oxidative stress. And the biphasic effect of CPFX possibly resulted from the complex dose-dependent relationships between reactive oxygen species, cell proliferation, and cell viability.

Aims: Ethanol can create progressive neuropathological and functional alterations of neurones. However, the influence of exposure duration is still debated. It is difficult to specify the level of alcohol consumption leading to alcohol-induced brain damage. Moreover, the mechanism of toxicity is assumed to combine direct and metabolically induced effects, although numerous uncertainties remain. Finally, the genotoxic power of ethanol has not fully been investigated in the brain. In the experiment reported herein, primary cultures of neurones were exposed either chronically or acutely to doses of ethanol within the range of blood alcohol levels in intoxicated humans. The impact on the integrity of neurones was assessed by cytotoxicity tests and DNA alterations by single-cell gel electrophoresis (Comet assay) and flow cytometry. Chronic ethanol exposure, even at a low dose, was more harmful to neurones than acute exposure. Both significant reductions in cell viability and DNA alterations were observed in this condition. On the other hand, DNA repair capacities seemed to be preserved as long as the viability measured by specific tests was not affected. Instead, neurones entered a death cell process compatible with apoptosis.

Congenital insensitivity to pain is a rare illness that can cause accidental external and internal injuries in children. When child abuse is suspected, the awareness of this illness can complicate any medicolegal interpretation of findings.Several components are needed to diagnose congenital insensitivity to pain: lack of sensitivity to pain since birth; involvement of the whole body; integrity of osteotendinous reflexes; and other sensitivity processes and negative paraclinical, including histological, examinations.This article describes the case of two siblings examined during an emergency legal procedure at the forensic medicine unit of the Grenobles University Hospital Centre in France. The medico-legal interpretation of facts and examinations must be conservative in case of legal complications and must follow an analysis of the child's and family's medicosocial problems since the child's birth. The family's socioeducational support and the communication of information on this illness should be a priority to avoid any misunderstanding and overrun in the child's management and monitoring.

The nervous system is one of the main targets of ethanol toxicity and it has been suggested that astrocytes might play an important role as their integrity is essential for the normal growth and functioning of neurons. Morphological variations of astrocyte cultures were therefore examined after exposure to various doses of ethanol (0.5, 1 and 2%) for different durations (24, 48, 72 and 96 h). The percentage of cell viability and the cell density were calculated and the changes in astrocyte morphology were assessed by an image analysis system (Samba 2005) allowing the characterization of 5 parameters (perimeter, surface, elongation factor, convexity factor and the form factor) of a great number of cells (over 6500). This was necessary because of the high variability in normal cultured astrocyte morphology. A two-way statistical approach (2-factors ANOVA completed by stepwise discriminant analysis) was adopted to emphasize the differences between control and exposed cells. In such conditions, ethanol treated cells became more elongated, less circular and more concave and did not grow like non-exposed cells. The mean pooled values of these parameters tended to be modified as a function of the dose of ethanol. The relationships between parameters clearly separated the groups as a function of the different doses. Finally no significant difference was observed in cell viability and cell density despite lower scores in the groups exposed to the highest dose of ethanol for the longest time. Our results suggest that ethanol might affect astrocytes in two different but probably complementary ways by modifying the cell shape and by altering normal cell development.

Trigeminal nerve impairment is one of the main features of the clinical spectrum observed after trichloroethylene (Tce) exposure. A morphometric study of teased fibres, an analysis of the fatty acid composition of total lipids of the trigeminal trunk, measurements of myelin basic protein (MBP) and of 2'-3'-cyclic nucleotide 3' phosphohydrolase (CNP) activity were used to characterize this lesion. Furthermore, the effects of Tce and of dichloroacetylene (Dca), a breakdown product supposed to be the main cause of the trigeminal neuropathy, were compared under the same experimental conditions. Results showed a significant decrease of the internode length and of the mean fibre diameter in the Dca group whereas these values, although also diminished, were not significantly affected in the Tce group. In the trigeminal nerve, this was associated with a significant (46%) decrease in sigma. (n-6) fatty acid and a 22% decrease in sigma. (n-3) fatty acid contents in the Tce group whereas these decreases were respectively 32% in sigma. (n-6) fatty acid and 27% (significant) in sigma. (n-3) fatty acid contents in the Dca group. In this group, a 64% increase in sigma. Fatty aldehydes was also observed. Finally, Tce or Dca had only a slight effect on the overall profile of fatty acid content in the brain and no significant variation was observed in MBP level and CNP activity. Both compounds can thus induce trigeminal nerve alterations, but with a higher intensity for Dca.

The hypothesis was tested that an acute oxidation deficiency related to potential dietary trigger factors plays a role in the migraine attack. Migraine sufferers (14F and 4M), fulfilling the criteria for migraine with and without aura according to the classification of the International Headache Society, were coadministered oral mephenytoin (100 mg) and debrisoquine (10 mg) during the initial phase of a typical migraine attack. This was repeated during a period without migraine. The hydroxylation of mephenytoin and debrisoquine hydroxylation did not differ during and without the migraine attack. We conclude that hydroxylation, via cytochrome P-450 (2D6, 2C8 and 9), is not reduced during the migraine attack. The results do not support the hypothesis that oxidation deficiency is involved in the pathophysiology of migraine.

Free radical formation from ethanol and acetaldehyde was studied in the presence of a spin-trap and a NADPH generating system with a chemical model, Fenton's reagent, or by enzymatic oxidation of these solvents by rat liver and brain microsomes. The free radicals were detected by electron spin resonance spectroscopy (E.S.R.), using the spin-trapping agent, alpha-(4-pyridyl l-oxide)-N-tertbutyl-nitrone (POBN). Under such conditions, the hydroxyethyl radical derived from ethanol was obtained after both incubation in liver and brain microsomes as well as after exposure to the Fenton system. Enzymatic inhibition and activation showed that the mixed function oxidase system plays an important role in the generation of such a radical, even in the brain. Under all the experimental conditions acetaldehyde could also generate a free radical deriving directly from the parent molecule and modified by enzymatic activation or inhibition. A second, longer lasting radical was also observed in the presence of acetaldehyde. On the basis of a comparative study to a known process causing lipoperoxidation, its lipidic origin was suggested.

Industrial intoxication by trichloroethylene can produce neurological disturbance of the trigeminal nerve. Therefore, among 105 workers exposed to this toxin, we recorded cortical responses after stimulation of the trigeminal nerve (TSEP) and we compared our results with a control group of 52 subjects. We considered the physical examination exploring, the facial sensitivity and reflexes, the levels of urinary metabolites of trichloroethylene and TSEP. We can describe 4 groups of workers: group A, 13 subjects with perturbations of clinical and evoked responses; group B, 27 subjects with normal physical examination though with disturbed TSEP; group C, 6 subjects had an abnormal examination though evoked responses were normal; group D, 59 subjects had normal clinical examination and TSEP. Disturbed TSEP (particularly delayed responses) are found among the older workers with the longest duration of exposure and higher level of exposure. The alteration of TSEP may appear before clinical disturbance. TSEP could represent a useful test for the supervision of the exposed workers and the clinical diagnosis of the trigeminal impairment.

Free-radical production during the metabolism of various xenobiotics represents a frequent mechanistic explanation for their toxicity. We tested the hypothesis of production of free radicals from two solvents, diethylether and trichloroethylene (TRI), and from two metabolites of TRI, namely trichloroethanol (TCE) and trichloroacetic acid (TCA). The formation of free radicals was detected by electron spin resonance spectroscopy (ESR), using a spin-trapping agent, alpha-(4-pyridyl-1-oxide)-N-tert-butyl-nitrone (POBN). Two experimental models were used. The first was a chemical model using Fenton's reagent, a mixture of Fe(II)-chelator and H2O2, for which the normal reaction is OH. production, and the second, a preparation from rat liver and brain microsomes containing NADPH and achieving enzymatic oxidation of the solvents. After addition of diethylether, free-radical production was demonstrated under the two experimental conditions. This free radical probably derived from the parent molecule by hydrogen abstraction. TRI and TCE additions to the Fenton system suppressed normal OH. production whereas this production was increased after TCA addition. The addition of TCE to the microsomal preparations was followed by free-radical production which could derive either from the parent molecule or from other sources, e.g. from membrane degradation, with a preference for the first hypothesis because of the characteristics of the signal. This result was not observed after addition of TRI or TCA. In conclusion, these preliminary results confirm the validity of the hypothesis of production of free radicals from diethylether, but they are less consistent for TRI as this production was observed only after addition of TCE; this result is interesting, however, as TCE is considered to play a major role in the toxicity observed after TRI exposure in humans.

24 deep toxic comas with respiratory assistance were studied by brain-stem reflex and BAEP. Laboratory analysis showed several simultaneous toxics (phenobarbital, benzodiazepines, tricyclic antidepressants...). Three groups of patients were defined: Twelve patients with normal BAEP and with relatively preserved brain-stem reflex (oculocephalic and oculovestibular are often disturbed but photomotor is present). Eleven patients with delayed BAEP and with more disturbed brain-stem reflex (photomotor is missing 3 times). In 2 cases (one of which is mentioned above in group B) brain-stem reflex and BAEP disappear and these patients die. Cerebral anoxia is associated here with toxics. Causes of delayed latencies (group B) are discussed (hypothermia, toxics). BAEP seems important in diagnosis and prognosis of toxic coma.

The goal of this study is to appreciate the early and late sequelae caused by Chlorine Gas. 186 exposed patients have been admitted to our unit since 1962-119 had functional respiratory explorations (FRE) with an analysis of blood gases, 79 underwent a study of carbon monoxide transfer. The results are in accordance with the literature for example 25% of the CO transfer test were pathological. 56 occupationally exposed subjects having had at least three acute episodes of exposure have been compared to 197 control subjects (groups were classed in function of age, tobacco intake, and pulmonary antecedent). Chlorine exposure even when frequent has no the influence on the FRE results or the appearance of pulmonary pathology. The pre-existence of a pulmonary disease doesn't affect the prognosis.

Internuclear Ophthalmoplegia (INO), a dysfunction of the medial longitudinal fasciculus, is frequently seen in toxic coma (7 out of 70 cases). INO is most often bilateral and can be associated with different stages of coma. Such an association is a strong argument for the toxic etiology of a coma. But INO has no value in determining the source of intoxication and is no prognostic indicator for the outcome.

Results of a study concerning the trigeminal nerve impairment as the one caused by trichlorethylene chronic intoxication by somatosensory evoked potential reveal three kinds of anomalies: increase of the stimulation voltage, excessive latency delay with morphological anomalies and excessive graph amplitude. These anomalies confirm clinical disturbance (hypoesthesia in the trigeminal area) and open a debate about the real mechanism of the trichlorethylene neurotoxicity.

We report one case of Digoxin intoxication in a child treated with Fab Fragments of Digoxin-Specific antibodies (Fabad), although there was no evidence of early life threatening complications. The efficacy of this treatment, which prevents further complications as well as its safety, represent strong arguments to treat children at the early stage of the intoxication in order to avoid temporary cardiac pacing.

beta-Endorphin was measured in the plasma of control subjects and 12 chronic alcoholics in the acute stage of ethanol intoxication. Naloxone was administered and the level of beta-endorphin was compared before and after treatment. The increased level of beta-endorphin in the intoxicated subjects supports the presence of ethanol interactions with the opioid system, since pituitary secretion does not seem to be involved. Furthermore, the coexistence of high levels of beta-endorphin and an effective naloxone response suggest a possible link between the two.