Publications by authors named "Risso J"

We describe here the first isolation in Argentina of a lactose-fermenting and lysine decarboxylase-negative non-Typhi Salmonella enterica from a blood culture of a patient with systemic lupus erythematosus. The microorganism was identified as S. enterica (score: 2.

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Decompression sickness (DCS) with neurological disorders is the leading cause of major diving accidents treated in hyperbaric chambers. Exposure to high levels of CO during diving is a safety concern for occupational groups at risk of DCS. However, the effects of prior exposure to CO have never been evaluated.

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Decompression sickness (DCS) with neurological disorders includes an inappropriate inflammatory response which degenerates slowly, even after the disappearance of the bubbles. There is high inter-individual variability in terms of the occurrence of DCS that could have been mastered by the selection and then the breeding of DCS-resistant rats. We hypothesized the selection of single-nucleotide polymorphisms (SNPs) linked to autoimmunity operated upon a generation of a DCS-resistant strain of rats.

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Article Synopsis
  • The microbial community in urban areas is heavily influenced by human activities, particularly through sewage systems, which serve as reservoirs for bacteria and antimicrobial resistance (AMR) genes.
  • The study reveals that different urban water sources like creeks and sewage exhibit unique microbial profiles, with higher human bacteria levels linked to increased AMR genes, specifically beta-lactamases.
  • An alarming rise in carbapenem-resistant infections and the spread of a particular strain of Klebsiella pneumoniae from hospitals to the urban environment emphasizes the urgent need to understand and monitor these changes for public health and urban resilience.
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Climbers and aviators are exposed to severe hypoxia at high altitudes, whereas divers are exposed to hyperoxia at depth. The aim of this study was to report changes in the adenosinergic system induced by exposure to extreme oxygen partial pressures. At high altitudes, the increased adenosine concentration contributes to brain protection against hypoxia through various mechanisms such as stimulation of glycogenolysis for ATP production, reduction in neuronal energy requirements, enhancement in 2,3-bisphosphoglycerate production, and increase in cerebral blood flow secondary to vasodilation of cerebral arteries.

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Article Synopsis
  • Decompression sickness (DCS) alters the cecal metabolome in rats, leading to significant neurological disorders, while a strain of DCS-resistant rats shows distinct metabolomic profiles without hyperbaric exposure.
  • The study aims to analyze the cecal metabolomes of diving and non-diving rats to identify physiological responses to diving stressors, examining a total of 35 diver rats and 21 non-exposed rats with controlled diets of soy and maize.
  • Findings indicate changes in the cecal metabolome of diving rats, including reduced levels of IL-1β and GPX activity, with specific metabolites linked to bile acid metabolism, energy pathways, and inflammation regulation, suggesting an adaptation to oxidative stress management.
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Diagnosing diaphragm dysfunction in the absence of complete paralysis remains difficult. The aim of the present study was to assess the normal values of the thickness and the inspiratory thickening of both hemidiaphragms as measured by ultrasonography in healthy volunteers while in a seated position. Healthy volunteers with a normal pulmonary function test were recruited.

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On one side, decompression sickness (DCS) with neurological disorders lead to a reshuffle of the fecal metabolome from rat caecum. On the other side, there is high inter-individual variability in terms of occurrence of DCS. One could wonder whether the fecal metabolome could be linked to the DCS-susceptibility.

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Purpose: Long static or intense dynamic apnoea-like high-altitude exposure is inducing hypoxia. Adenosine is known to participate to the adaptive response to hypoxia leading to the control of heart rate, blood pressure and vasodilation. Extracellular adenosine level is controlled through the equilibrative nucleoside transporter 1 (ENT-1) and the enzyme adenosine deaminase (ADA).

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Massive bubble formation after diving can lead to decompression sickness (DCS), which can result in neurological disorders. We demonstrated that hydrogen production from intestinal fermentation could exacerbate DCS in rats fed with a standard diet. The aim of this study is to identify a fecal metabolomic signature that may result from the effects of a provocative hyperbaric exposure.

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The Río de la Plata estuary drains the second largest river basin of South America. The occurrence of frequent cyanobacterial blooms of the Microcystis and Dolichospermum complex in the Uruguayan coast are associated with high flows of Uruguay River due to rainy years. In summer 2019, a massive cyanobacterial bloom reached up to the Uruguayan Atlantic coast.

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The prevention, prognosis and resolution of decompression sickness (DCS) are not satisfactory. The etiology of DCS has highlighted thrombotic and inflammatory phenomena that could cause severe neurological disorders or even death. Given the immunomodulatory effects described for minocycline, an antibiotic in widespread use, we have decided to explore its effects in an experimental model for decompression sickness.

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Previous studies have suggested that the circulatory system was involved in the production of circulatory bubbles after diving. This study was designed to research the cardio-vascular function characteristics related to the production of high bubble grades after diving. Thirty trained divers were investigated both at baseline and after a 30-msw SCUBA dive.

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Circulating mitochondrial DNA (mtDNA) is receiving increasing attention as a danger-associated molecular pattern in conditions such as autoimmunity or trauma. In the context of decompression sickness (DCS), the course of which is sometimes erratic, we hypothesize that mtDNA plays a not insignificant role particularly in neurological type accidents. This study is based on the comparison of circulating mtDNA levels in humans presenting with various types of diving accidents, and punctured upon their admission at the hyperbaric facility.

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In its severest forms, decompression sickness (DCS) may extend systemically and/or induce severe neurological deficits, including paralysis or even death. It seems that the sterile and ischemic inflammatory phenomena are consecutive to the reaction of the bubbles with the organism and that the blood platelet activation plays a determinant role in the development of DCS. According to the hypotheses commonly put forward, the bubbles could either activate the platelets by direct contact or be the cause of abrasion of the vascular epithelium, which would expose the basal plate glycogen and then prompt the platelets to activate.

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Xenon (Xe) is considered to be the golden standard neuroprotective gas. However, Xe has a higher molecular weight and lower thermal conductivity and specific heat than those of nitrogen, the main diluent of oxygen in air. These physical characteristics could impair or at least reduce the intrinsic neuroprotective action of Xe by increasing the patient's respiratory workload and body temperature.

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The noble gases xenon (Xe) and helium (He) are known to possess neuroprotective properties. Xe is considered the golden standard neuroprotective gas. However, Xe has a higher molecular weight and lower thermal conductivity and specific heat than those of nitrogen, the main diluent of oxygen (O2) in air, conditions that could impair or at least reduce the intrinsic neuroprotective properties of Xe by increasing the critical care patient's respiratory workload and body temperature.

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According to the OECD statistical base for 2014, anti-depressants will, on average, be distributed at a rate of 62 daily doses per 1,000 inhabitants for the 25 countries surveyed (Health at a glance: Europe 2014; OECD Health Statistics; World Health Organization and OECD Health Statistics, 2014). Divers must be concerned. On another hand, divers are potentially exposed to decompression sickness including coagulation inflammation and ischemia, which can result in neurological lesions or even death.

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Hyperbaric oxygen induced in rats a decrease in striatal dopamine levels. Such decrease could be a result of changes in glutamatergic and GABAergic controls of the dopaminergic neurons into the Substantia Nigra Pars Compacta. The aim of this study was to determine the role of gluatamatergic and Gama-Amino-Butyric-Acid neurotransmissions in this alteration.

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Normobaric oxygen (NBO) and hyperbaric oxygen (HBO) are emerging as a possible co-treatment of acute ischemic stroke. Both have been shown to reduce infarct volume, to improve neurologic outcome, to promote endogenous tissue plasminogen activator-induced thrombolysis and cerebral blood flow, and to improve tissue oxygenation through oxygen diffusion in the ischemic areas, thereby questioning the interest of HBO compared to NBO. In the present study, in order to investigate and compare the oxygen diffusion effects of NBO and HBO on acute ischemic stroke independently of their effects at the vascular level, we used acute brain slices exposed to oxygen and glucose deprivation, an model of brain ischemia that allows investigating the acute effects of NBO (partial pressure of oxygen (pO) = 1 atmospheres absolute (ATA) = 0.

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The occurrence of paroxysmal narcotic episodes including psychotic-like symptoms in divers participating to experimental deep diving programs with various gas mixtures has constituted, beyond the classical symptoms of the high-pressure neurological syndrome, the major limitation for deep diving. With the development of new saturation deep diving programs and experiments by the eastern nations, such as India and China, we believed that it is of interest to examine what could be the ultimate depth that could be reached by saturation human divers. Based on previous data and the critical volume model of inert gas narcosis, we propose that the ultimate depth for saturation diving could be around 1,000 m.

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Recent data have shown that normobaric oxygen (NBO) increases the catalytic and thrombolytic efficiency of recombinant tissue plasminogen activator (rtPA) , and is as efficient as rtPA at restoring cerebral blood flow in rats subjected to thromboembolic brain ischemia. Therefore, in the present study, we studied the effects of hyperbaric oxygen (HBO) (i) on rtPA-induced thrombolysis and (ii) in rats subjected to thromboembolic middle cerebral artery occlusion-induced brain ischemia. HBO increases rtPA-induced thrombolysis to a greater extent than NBO; in addition, HBO treatment of 5-minute duration, but not of 25-minute duration, reduces brain damage and edema .

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