Glaciers and ice sheets are renowned for their abrasive power, yet little is known of the mechanochemical reactions which are initiated by abrasion
in these environments and their effect on ...subglacial biogeochemistry. Here, we use sedimentary rocks representative of different subglacial
environments and from a previously glaciated terrain, along with subglacial sediments, to investigate the potential for subglacial erosion to
generate H2O2 and to release bio-utilisable organic carbon and nutrients (N, Fe). Samples were crushed using a ball mill,
water was added to rock powders within gastight vials, and samples were incubated in the dark at 4 ∘C. Headspace and water samples were taken
immediately after the addition of water and then again after 5 and 25 h. Samples generated up to
1.5 µmol H2O2 g−1. The total sulfur content, a proxy for the sulfide content, did not correlate with
H2O2 generation, suggesting that the pyrite content was not the sole determinant of net H2O2 production. Other factors
including the presence of carbonates, Fe-driven Fenton reactions and the pH of the solution were also likely to be important in controlling
both the initial rate of production and subsequent rates of destruction of H2O2. Further, we found that erosion can provide previously
unaccounted sources of bio-utilisable energy substrates and nutrients, including up to 880 nmol CH4 g−1,
680 nmol H2 g−1, volatile fatty acids (up to 1.7 µmol acetate g−1) and 8.2 µmolNH4+g-1
to subglacial ecosystems. These results highlight the potentially important role that abrasion plays in providing nutrient and energy sources to
subglacial microbial ecosystems underlain by sedimentary rocks.
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•METH exposure results in hyperthermia and vascular leakage during seizure development.•Vascular leakage is peaking when continuous seizure activity first appears.•Leakage in limbic ...areas of the primary olfactory system indicate it is likely the site of seizuregenesis.•Other vascular dysfunction such as ischemic events in the primary olfactory system likely contribute to seizuregenesis.•Neurodegeneration is focused in the primary olfactory system, particularly the amygdala.
The initial goals of these experiments were to determine: 1) if blood-brain barrier (BBB) breakdown was a cause or an effect of METH-induced seizures; 2) all the brain regions where BBB is disrupted as seizures progress; and 3) the correlations between body temperature and vascular leakage and neurodegeneration. A fourth objective was added after initial experimentation to determine if sub-strain differences existed in adult male C57 B6 J (Jackson laboratories, JAX) versus C57 B6N (Charles River, CR) mice involving their susceptibility to BBB breakdown and seizure severity. With the 1st “maximal” intensity myoclonic-tonic seizure (MCT) varying degrees of IgG infiltration across the BBB (≤1 mm2) were prominent in olfactory system (OS) associated regions and in thalamus, hypothalamus and neocortex. IgG infiltration areas in the OS-associated regions of the bed nucleus of the stria terminalis, septum and more medial amygdala nuclei, and the hypothalamus were increased significantly by the time continuous behavioral seizures (CBS) developed. Mice receiving METH that had body temperatures of ≥40 °C had IgG infiltration along with MCT or CBS but peak body temperatures above 40 °C did not significantly increase IgG infiltration. Neurodegeneration seen at ≥6 h was restricted to the OS in both JAX and CR mice and was most prominent in the posteromedial cortical amygdaloid nucleus. Neurodegeneration in the anterior septum (tenia tecta) was seen only in the JAX mice. We hypothesize that METH-induced hypertension and hyperthermia lead to BBB breakdown and other vascular dysfunctions in the OS brain regions resulting in OS hyperexcitation. Excitation of the OS neural network then leads to the development of seizures. These seizures in turn exacerbate the energy depletions and the reactive oxygen stress produced by hyperthermia further damaging the BBB and vascular function. These events form a recurrent cycle that results in ever increasing seizure activity and neurotoxicity.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
Our previous studies have raised the possibility that altered blood glucose levels may influence and/or be predictive of methamphetamine (METH) neurotoxicity. This study evaluated the effects of ...exogenous glucose and corticosterone (CORT) pretreatment alone or in combination with METH on blood glucose levels and the neural and vascular toxicity produced. METH exposure consisted of four sequential injections of 5, 7.5, 10, and 10 mg/kg (2 h between injections) D‐METH. The three groups given METH in combination with saline, glucose (METH+Glucose), or CORT (METH+CORT) had significantly higher glucose levels compared to the corresponding treatment groups without METH except at 3 h after the last injection. At this last time point, the METH and METH+Glucose groups had lower levels than the non‐METH groups, while the METH+CORT group did not. CORT alone or glucose alone did not significantly increase blood glucose. Mortality rates for the METH+CORT (40%) and METH+Glucose (44%) groups were substantially higher than the METH (< 10%) group. Additionally, METH+CORT significantly increased neurodegeneration above the other three METH treatment groups (≈ 2.5‐fold in the parietal cortex). Thus, maintaining elevated levels of glucose during METH exposure increases lethality and may exacerbate neurodegeneration. Neuroinflammation, specifically microglial activation, was associated with degenerating neurons in the parietal cortex and thalamus after METH exposure. The activated microglia in the parietal cortex were surrounding vasculature in most cases and the extent of microglial activation was exacerbated by CORT pretreatment. Our findings show that acute CORT exposure and elevated blood glucose levels can exacerbate METH‐induced vascular damage, neuroinflammation, neurodegeneration and lethality.
Cover Image for this issue: doi. 10.1111/jnc.13819.
This study evaluated exogenous glucose and corticosterone pretreatment to methamphetamine on blood glucose levels and neural/vascular toxicity. Methamphetamine with saline, glucose, or corticosterone had significantly higher glucose levels. Methamphetamine+corticosterone and methamphetamine+glucose mortality rates were substantially higher than methamphetamine. Methamphetamine+corticosterone significantly increased neurodegeneration above other treatments. Neuroinflammation (microglial activation) was associated with degenerating neurons and largely surrounded vasculature after methamphetamine, an effect exacerbated by corticosterone pretreatment. Our findings implicate elevated glucose levels and hyperthermia in methamphetamine‐induced neurotoxicity, neurovascular damage, and lethality.
Cover Image for this issue: doi. 10.1111/jnc.13819.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SAZU, SBCE, SBMB, UL, UM, UPUK
The orbitofrontal cortex (OFC) is essential for decision making, and functional disruptions within the OFC are evident in schizophrenia. Postnatal phencyclidine (PCP) administration in rats is a ...neurodevelopmental manipulation that induces schizophrenia-relevant cognitive impairments. We aimed to determine whether manipulating OFC glutamate cell activity could ameliorate postnatal PCP-induced deficits in decision making.
Male and female Wistar rats (n = 110) were administered saline or PCP on postnatal days 7, 9, and 11. In adulthood, we expressed YFP (yellow fluorescent protein) (control), ChR2 (channelrhodopsin-2) (activation), or eNpHR 3.0 (enhanced halorhodopsin) (inhibition) in glutamate neurons within the ventromedial OFC (vmOFC). Rats were tested on the probabilistic reversal learning task once daily for 20 days while we manipulated the activity of vmOFC glutamate cells. Behavioral performance was analyzed using a Q-learning computational model of reinforcement learning.
Compared with saline-treated rats expressing YFP, PCP-treated rats expressing YFP completed fewer reversals, made fewer win-stay responses, and had lower learning rates. We induced similar performance impairments in saline-treated rats by activating vmOFC glutamate cells (ChR2). Strikingly, PCP-induced performance deficits were ameliorated when the activity of vmOFC glutamate cells was inhibited (halorhodopsin).
Postnatal PCP-induced deficits in decision making are associated with hyperactivity of vmOFC glutamate cells. Thus, normalizing vmOFC activity may represent a potential therapeutic target for decision-making deficits in patients with schizophrenia.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Epiglottitis in the adult can be fatal and should be treated with the same degree of concern and suspicion in respect of airway patency as in children. We present three cases of adult epiglottitis in ...which the airway was lost prior to or during the intervention of an anaesthetist. We suggest that an emphasis on conservative management is distracting and belies the serious nature of this disease.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Brain microglial activations and damage responses are most commonly associated with neurodegeneration or systemic innate immune system activation. Here, we used histological methods to focus on ...microglial responses that are directed towards brain vasculature, previously undescribed, after a neurotoxic exposure to methamphetamine.
Male rats were given doses of methamphetamine that produce pronounced hyperthermia, hypertension, and toxicity. Identification of microglia and microglia-like cells (pericytes and possibly perivascular cells) was done using immunoreactivity to allograft inflammatory factor 1 (Aif1 a.k.a Iba1) and alpha M integrin (Itgam a.k.a. Cd11b) while vasculature endothelium was identified using rat endothelial cell antigen 1 (RECA-1). Regions of neuronal, axonal, and nerve terminal degeneration were determined using Fluoro-Jade C.
Dual labeling of vasculature (RECA-1) and microglia (Iba1) showed a strong association of hypertrophied cells surrounding and juxtaposed to vasculature in the septum, medial dorsal hippocampus, piriform cortex, and thalamus. The Iba1 labeling was more pronounced in the cell body while Cd11b more so in the processes of activated microglia. These regions have been previously identified to have vascular leakage after neurotoxic methamphetamine exposure. Dual labeling with Fluoro-Jade C and Iba1 indicated that there was minimal or no evidence of neuronal damage in the septum and hippocampus where many hypertrophied Iba1-labeled cells were found to be associated with vasculature. Although microglial activation around the prominent neurodegeneration was found in the thalamus, there were also many examples of activated microglia associated with vasculature.
The data implicate microglia, and possibly related cell types, in playing a major role in responding to methamphetamine-induced vascular damage, and possibly repair, in the absence of neurodegeneration. Identifying brain regions with hypertrophied/activated microglial-like cells associated with vasculature has the potential for identifying regions of more subtle examples of vascular damage and BBB compromise.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Glacial bulk meltwaters and active-layer groundwaters were sampled from the proglacial zone of Finsterwalderbreen during a single melt season in 1999, in order to determine the geochemical processes ...that maintain high chemical weathering rates in the proglacial zone of this glacier. Results demonstrate that the principle means of solute acquisition is the weathering of highly reactive moraine and fluvial active-layer sediments by supra-permafrost groundwaters. Active-layer groundwater derives from the thaw of the proglacial snowpack, buried ice and glacial bulk meltwaters. Groundwater evolves by sulphide oxidation and carbonate dissolution. Evaporation- and freeze-concentration of groundwater in summer and winter, respectively produce Mg–Ca-sulphate salts on the proglacial surface. Re-dissolution of these salts in early summer produces groundwaters that are supersaturated with respect to calcite.There is a pronounced spatial pattern to the geochemical evolution of groundwater. Close to the main proglacial channel, active layer sediments are flushed diurnally by bulk meltwaters. Here, Mg–Ca-sulphate deposits become exhausted in the early season and geochemical evolution proceeds by a combination of sulphide oxidation and carbonate dissolution. At greater distances from the channel, the dissolution of Mg–Ca-sulphate salts is a major influence and dilution by the bulk meltwaters is relatively minor. The influence of sulphate salt dissolution decreases during the sampling season, as these salts are exhausted and waters become increasingly routed by subsurface flowpaths.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Glaciers and ice sheets host abundant and dynamic communities of
microorganisms on the ice surface (supraglacial environments). Recently, it
has been shown that Streptophyte glacier algae blooming on ...the surface ice
of the south-western coast of the Greenland Ice Sheet are a significant
contributor to the 15-year marked decrease in albedo. Currently, little is
known about the constraints, such as nutrient availability, on this
large-scale algal bloom. In this study, we investigate the relative
abundances of dissolved inorganic and dissolved organic macronutrients (N
and P) in these darkening surface ice environments. Three distinct ice
surfaces, with low, medium and high visible impurity loadings, supraglacial
stream water and cryoconite hole water, were sampled. Our results show a
clear dominance of the organic phase in all ice surface samples containing
low, medium and high visible impurity loadings, with 93 % of the total
dissolved nitrogen and 67 % of the total dissolved phosphorus in the
organic phase. Mean concentrations in low, medium and high visible impurity
surface ice environments are 0.91, 0.62 and 1.0 µM for dissolved inorganic nitrogen (DIN), 5.1, 11 and 14 µM for dissolved organic nitrogen (DON), 0.03, 0.07 and 0.05 µM for dissolved inorganic phosphorus (DIP) and 0.10, 0.15 and 0.12 µM for dissolved organic phosphorus
(DOP), respectively. DON concentrations in all three surface ice samples are
significantly higher than DON concentrations in supraglacial streams and
cryoconite hole water (0 and 0.7 µM, respectively). DOP
concentrations are higher in all three surface ice samples compared to
supraglacial streams and cryoconite hole water (0.07 µM for both).
Dissolved organic carbon (DOC) concentrations increase with the amount of
visible impurities present (low: 83 µM, medium: 173 µM and
high: 242 µM) and are elevated compared to supraglacial streams and
cryoconite hole water (30 and 50 µM, respectively). We
speculate that the architecture of the weathering crust, which impacts on
water flow paths and storage in the melting surface ice and/or the
production of extracellular polymeric substances (EPS), containing both N
and P in conjunction with C, is responsible for the temporary retention of
DON and DOP in the melting surface ice. The unusual presence of measurable DIP
and DIN, principally as NH4+, in the melting surface ice
environments suggests that factors other than macronutrient limitation are
controlling the extent and magnitude of the glacier algae.
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