Capillary Endothelial Na+, K+, ATPase Transporter Homeostasis and a New Theory for Migraine Pathophysiology

(Headache 2010;50:459‐478) Background.— Cerebrospinal fluid sodium concentration ([Na⁺]_csf) increases during migraine, but the cause of the increase is not known. Objective.— Analyze biochemical pathways that influence [Na⁺]_csf to identify mechanisms that are consistent with migraine. Method.— We reviewed sodium physiology and biochemistry publications for links to migraine and pain. Results.— Increased capillary endothelial cell (CEC) Na⁺, K⁺, ‐ATPase transporter (NKAT) activity is probably the primary cause of increased [Na⁺]_csf. Physiological fluctuations of all NKAT regulators in blood, many known to be involved in migraine, are monitored by receptors on the luminal wall of brain CECs; signals are then transduced to their abluminal NKATs that alter brain extracellular sodium ([Na⁺]_e) and potassium ([K⁺]_e). Conclusions.— We propose a theoretical mechanism for aura and migraine when NKAT activity shifts outside normal limits: (1) CEC NKAT activity below a lower limit increases [K⁺]_e, facilitates cortical spreading depression, and causes aura; (2) CEC NKAT activity above an upper limit elevates [Na⁺]_e, increases neuronal excitability, and causes migraine; (3) migraine‐without‐aura may arise from CEC NKAT over‐activity without requiring a prior decrease in activity and its consequent spreading depression; (4) migraine triggers disturb, and treatments improve, CEC NKAT homeostasis; (5) CEC NKAT‐induced regulation of neural and vasomotor excitability coordinates vascular and neuronal activities, and includes occasional pathology from CEC NKAT‐induced apoptosis or cerebral infarction.     

Essential Oil Poisoning

Abstract

Alpha-ketoglutaric acid and sodium thiosulfate antagonize the toxic effects of cyanide. The present study was performed to test whether a synergistic effect may occur. The alpha-ketoglutaric acid/sodium thiosulfate solutions were injected intraperitoneally into mice prior to exposure to hydrogen cyanide (HCN) in a dynamic inhalation chamber or preceding an intraperitoneal injection of sodium cyanide (NaCN). All lethal concentration (LCT) and lethal dose (LD) values were determined after a period of 24?h. Alpha-ketoglutaric acid alone provided no protection at 250?mg/kg when challenged with HCN. Sodium thiosulfate 500?mg/kg provided a 5% protection. However, when these doses of alpha-ketoglutaric acid and sodium thiosulfate were combined, protection was increased by 18%. Alpha-ketoglutaric acid (250?mg/kg) and sodium thiosulfate (1000?mg/kg) provided an additional 48% protection against a LCT₈₈ of HCN. A single dose of alpha-ketoglutaric acid (500?mg/kg) and sodium thiosulfate (1000?mg/kg) solutions afforded a 70% increase in survivability of the exposed animals. When mice were injected ip with 100?mg/kg of alpha-ketoglutaric acid 15 min prior to the injection of 5.5?mg/kg (LD₅₀) of NaCN, the lethality was reduced to an LD₃₀. Two hundred?mg/kg alpha-ketoglutaric acid, challenged with the same dose of NaCN, reduced the lethality to 23%. When mice were challenged with 6.0?mg/kg of NaCN (LD₇₀) pretreated with 100?mg/kg of alpha-ketoglutaric acid or 200?mg/kg of sodium thiosulfate, the LD was not altered in the former but reduced to an LD_1S in the latter. At higher doses of sodium thiosulfate (500?mg/kg), an LD₆₀ occurred at 13.6?mg/kg NaCN (2.5 x LD₅₀). Combinations of alpha-ketoglutaric acid and sodium thiosulfate proved to be very effective. Injections in which alpha-ketoglutaric acid and sodium thiosulfate (200 and 500?mg/kg, respectively) were given 15 min prior to NaCN challenges of 26.5?mg/kg (4.8 x LD₅₀) produced an average lethality of 78%. Greater doses of alpha-ketoglutaric acid and sodium thiosulfate were required to provide protection against the lethal effects of inhaled HCN than those of parenteral NaCN. Also, alpha-ketoglutaric acid and sodium thiosulfate are synergistic in their antidotal effects against both HCN and NaCN.     

Beta-blockade and binding of digoxin to skeletal muscle

Summary. The effect of beta-blockade and a 1-h bicycle exercise test on the digoxin concentration in skeletal muscle (thigh) and serum was studied in 10 healthy men, who had ingested 0·5 mg digoxin daily for 2 weeks. Each subject performed two exercise tests at 100–140 W during maintenance digoxin treatment and 24 h after the latest dose. They rested in the supine position for 2·5 h before the exercise. Sixty minutes before the start of the exercise 0·25 mg/kg b.w. propranolol or saline (control) were injected (single-blind). At the end of the exercise the mean heart rate was 30% lower with beta-blockade (P < 0·001). During exercise the mean skeletal muscle digoxin concentration increased by 29% (P<0·01) in the control situation and by 12% (NS) with beta-blockade. The results indicate that propranolol partly inhibits the exercise-induced increase in skeletal muscle digoxin binding. This might be due to inhibition of a catecholamine-induced stimulation of Na⁺-K⁺ATPase during exercise.     

High-capacity and selective ammonium removal from water using sodium cobalt hexacyanoferrate

A new NH₄⁺ adsorbent with high capacity and selectivity, sodium cobalt(ii) hexacyanoferrate(ii) (NaCoHCF, Na_yCo(ii) [Fe²⁺(CN)₆]_x·zH₂O), was prepared. The adsorption performance was investigated by varying the mixing ratio of [Fe(CN)₆]⁴⁻ to Co²⁺ during synthesis, R_mix. The ammonia capacity was found to be proportional to R_mix, indicating that the NH₄⁺ capacity can be increased by increasing the Na⁺-ion content in NaCoHCF. To conduct a detailed study, we prepared homogeneous nanoparticles by flow synthesis using a micromixer with R_mix = 1.00. Even on the addition of a saline solution (NaCl) with an Na⁺-ion concentration of 9350 mg L⁻¹, the capacity was maintained: q_max = 4.28 mol kg⁻¹. Using Markham–Benton analysis, the selectivity factor, defined by the ratio of equilibrium constants for NH₄⁺ to that for Na⁺, was calculated to be α = 96.2, and 4.36 mol kg⁻¹ was found to be the maximum capacity. The high selectivity of NaCoHCF results in good NH₄⁺-adsorption performance, even from seawater. In comparison with other adsorbents under the same conditions and even for a NH₄Cl solution, NaCoHCF showed the highest capacity. Moreover, the coexisting Na⁺ caused no interference with the adsorption of ammonium by NaCoHCF, whereas the other adsorbents adsorbed ammonia only slightly from the saline solution. We also found that the pores for NH₄⁺ adsorption changed their sizes and shapes after adsorption.

High capacity and selectivity of NH₄ adsorption achieved by the crystal structure optimization.     

Dissimilar Action of Two Cyclic Adenosine-Monophosphate Analogues on the Sodium Current in Intact Rat Papillary Muscle

In intact papillary muscles from rat we have found with the loose-patch-clamp technique an increase of the fast cardiac sodium current (I_Na⁺) by isoproterenol (ISO). In this study we have tested two membrane permeable analogues of the intracellular second messenger cyclic adenosine-monophosphate (cAMP) to investigate the intracellular pathway: 8-Br-cAMP (50 μM) and the newer developed S_p5,6-Dichloro-1-β-D-ribofuranosylbenzimidazole-3′, 5′-cyclic-monophosphor-othioate (5,6-DCl-cBiMPS, 20 μM). The availability of I_Na⁺ was determined with test pulses to ± 0 mV every 3.5 seconds after 2.5-second conditioning between -130 mV and-50 mV and a holding potential at the resting potential of the cell under examination, and after wash-in of either compound. The peak currents were fit to a Boltzmann equation, and expressed by the maximal attainable current INa⁺_Na,max the mid-point potential V½, and a steepness parameter a. Values are given by mean ± SEM. 8-Br-cAMP showed a significant shift of the availability curve in the hyperpolarized direction (V½= -82 ± 2 mV vs - 66 ± 2 mV, n = 5, P < 0.05) with only minor changes of I⁺_No,max and a. In contrast, 5,6-DCI-cBiMPS had no significant effect on V½ but increased I⁺_Na,max by 8%± 2% versus control (n = 5. P < 0.05). In an intact muscle preparation we have found that 5,6-DCI-cBiMPS has a similar effect as that observed with the β-adrenergic agonist ISO (100 nM), whereas 8-Br-cAMP exhibited a dissimilar action. This indicates, that ihe effects of ISO are transmitted by the cAMP system. On the other hand, 8-Br-cAMP, which is not as permeable and specific an activator of the cAMP dependent proteinkinase, may have other effects on the sodium channel, perhaps mediated through purinergic receptors.     

Clinical review: Practical approach to hyponatraemia and hypernatraemia in critically ill patients

Disturbances in sodium concentration are common in the critically ill patient and associated with increased mortality. The key principle in treatment and prevention is that plasma [Na⁺] (P-[Na⁺]) is determined by external water and cation balances. P-[Na⁺] determines plasma tonicity. An important exception is hyperglycaemia, where P-[Na⁺] may be reduced despite plasma hypertonicity. The patient is first treated to secure airway, breathing and circulation to diminish secondary organ damage. Symptoms are critical when handling a patient with hyponatraemia. Severe symptoms are treated with 2 ml/kg 3% NaCl bolus infusions irrespective of the supposed duration of hyponatraemia. The goal is to reduce cerebral symptoms. The bolus therapy ensures an immediate and controllable rise in P-[Na⁺]. A maximum of three boluses are given (increases P-[Na⁺] about 6 mmol/l). In all patients with hyponatraemia, correction above 10 mmol/l/day must be avoided to reduce the risk of osmotic demyelination. Practical measures for handling a rapid rise in P-[Na⁺] are discussed. The risk of overcorrection is associated with the mechanisms that cause hyponatraemia. Traditional classifications according to volume status are notoriously difficult to handle in clinical practice. Moreover, multiple combined mechanisms are common. More than one mechanism must therefore be considered for safe and lasting correction. Hypernatraemia is less common than hyponatraemia, but implies that the patient is more ill and has a worse prognosis. A practical approach includes treatment of the underlying diseases and restoration of the distorted water and salt balances. Multiple combined mechanisms are common and must be searched for. Importantly, hypernatraemia is not only a matter of water deficit, and treatment of the critically ill patient with an accumulated fluid balance of 20 litres and corresponding weight gain should not comprise more water, but measures to invoke a negative cation balance. Reduction of hypernatraemia/hypertonicity is critical, but should not exceed 12 mmol/l/day in order to reduce the risk of rebounding brain oedema.     

Sodium ion intercalation and multi redox behavior of a Keggin type polyoxometalate during [PMo10V2O40]5− to [PMo10V2O40]27− as a cathode material for Na-ion rechargeable batteries

Recently, the development of cathode materials for Na-ion batteries has gained much attention due to the abundance, low cost, and easy availability of resources. Apart from the usual metal oxides, multi-electron redox materials grabbed attention due to their high energy density and practical capacity with long cycle life. Polyoxometalates (POMs) are inorganic clusters of higher valent metals, and act as electron sponges with multi-electron redox properties. Herein we report a Keggin-type polyoxometalate [PMo₁₀V₂O₄₀]⁵⁻ with Na⁺ and H⁺ counter cations as a cathode material for Na-ion batteries. Further the formation of POM is evidenced by PXRD, FT-IR, flame photometry and XPS studies. In Na-POM, Na⁺ ions in the intercluster cavities provide a better pathway and easy diffusion during the charge/discharge process, and contribute to better electrochemical properties than H-POM. The DFT studies further explore the detailed mechanistic pathway of Na⁺ ions around the clusters in the normal and super-reduced states. Na-POM enables better cycling stability and capacity retention with a specific discharge capacity of 123 mA h g⁻¹ at 0.1C rate at room temperature.

The versatile property of the Keggin type POM is the multi-electron transfer that happens during the switching between [PMo₁₀V₂O₄₀]⁵⁻ to [PMo₁₀V₂O₄₀]²⁷⁻. This tunable behavior makes it unique, efficient material as a cathode for Na-ion batteries.     

Evaluation of point-of-care analyzers’ ability to reduce bias in conductivity-based hematocrit measurement during cardiopulmonary bypass

Most point-of-care testing analyzers use the conductivity method to measure hematocrit (hct). During open-heart surgery, blood-conductivity is influenced by shifts in electrolyte and colloid concentrations caused by infusion media used, and this may lead to considerable bias in the hct measurement. We evaluated to what extent different analyzers correcting for 0, 1, 2, or 3 factors, respectively, compensated for this electrolyte/colloid interference: (1) the conductivity method with no correction (IRMA), (2) with a [Na⁺]-correction (GEM Premier 3000), (3) with a [Na⁺]/[K⁺]-correction (i-STAT), and (4) with a [Na⁺]/[K⁺]-correction in combination with an algorithm that estimates the protein dilution [i-STAT in cardiopulmonary bypass (CPB)-mode]. Bias in hct was measured during three consecutive stages of a CPB procedure: (I) before CPB, (II) start of CPB and (III) after cardioplegia. In order of high to low electrolyte/colloid interference: the analyzer with no correction, [Na⁺]-correction, [Na⁺/]/[K⁺]-correction, and [Na⁺/]/[K⁺]/estimated protein-correction showed a change of bias from stage I to stage III of ?3.9 ± 0.5, ?3.4 ± 0.4, ?2.1 ± 0.5, ?0.3 ± 0.5 %. We conclude that correcting for more parameters (Na⁺, K⁺, estimated protein) gives less bias, but residual bias remains even after [Na⁺/]/[K⁺]/estimated protein-correction. This suggests that a satisfactory algorithm should also correct for other colloidal factors than protein.     

Solvent extraction of rare earths elements from nitrate media in DMDOHEMA/ionic liquid systems: performance and mechanism studies

Extraction of La(iii), Eu(iii) and Fe(iii) was compared in n-dodecane and two ionic liquids (ILs) (1-ethyl-1-butylpiperidinium bis (trifluoromethylsulfonyl)imide [EBPip⁺] [NTf₂⁻] and 1-ethyl-1-octylpiperidinium bis (trifluoromethylsulfonyl)imide [EOPip⁺] [NTf₂⁻]). Using the extractant N,N′-dimethyl-N,N′-dioctylhexylethoxymalonamide (DMDOHEMA), the effect of pH was investigated in detail to recover extraction mechanisms. The use of ILs as the organic solvent instead of n-dodecane, greatly enhances extraction efficiency, and an ionic liquid with a shorter alkyl chain [EBPip⁺] [NTf₂⁻] provides higher extraction than [EOPip⁺] [NTf₂⁻]. The mechanistic study points out that for low nitric acid concentrations ([HNO₃] ≤ 0.01 M), metal is extracted via a cation of the ionic liquids, while for higher nitric acid concentrations ([HNO₃] ≥ 1.0 M), extraction occurs through pure solvation mechanism of DMDOHEMA as in conventional diluents. This latter case is of high interest for applications, as higher extraction can be obtained without any loss of ILs by ion exchange mechanisms.

Extraction of La(iii), Eu(iii) and Fe(iii) was compared in n-dodecane and in two ionic liquids (ILs) [EBPip⁺] [NTf₂⁻] and [EOPip⁺] [NTf₂⁻]. Extraction mechanisms have been investigated as a function of pH.     

NHE4 is critical for the renal handling of ammonia in rodents

Ammonia absorption by the medullary thick ascending limb of Henle’s loop (MTALH) is thought to be a critical step in renal ammonia handling and excretion in urine, in which it is the main acid component. Basolateral Na⁺/H⁺ exchangers have been proposed to play a role in ammonia efflux out of MTALH cells, which express 2 exchanger isoforms: Na⁺/H⁺ exchanger 1 (NHE1) and NHE4. Here, we investigated the role of NHE4 in urinary acid excretion and found that NHE4^–/– mice exhibited compensated hyperchloremic metabolic acidosis, together with inappropriate urinary net acid excretion. When challenged with a 7-day HCl load, NHE4^–/– mice were unable to increase their urinary ammonium and net acid excretion and displayed reduced ammonium medulla content compared with wild-type littermates. Both pharmacologic inhibition and genetic disruption of NHE4 caused a marked decrease in ammonia absorption by the MTALH. Finally, dietary induction of metabolic acidosis increased NHE4 mRNA expression in mouse MTALH cells and enhanced renal NHE4 activity in rats, as measured by in vitro microperfusion of MTALH. We therefore conclude that ammonia absorption by the MTALH requires the presence of NHE4 and that lack of NHE4 reduces the ability of MTALH epithelial cells to create the cortico-papillary gradient of NH₃/NH₄⁺ needed to excrete an acid load, contributing to systemic metabolic acidosis.     

Titratable acidity: A Pitts concept revisited

Abstract

Titratable Acidity (TA) in urine can be measured directly or calculated from actual and reference pH, by using the pKa₂ 6,8 for phosphate. In urine, H₂PO₄^? represents the excretion of filtered H₂PO₄^?, filtrated HPO₄^2? being completely reabsorbed by the proximal tubule (the Van Slyke approach). Since excretion of H₂PO₄^? frequently exceeds its glomerular filtration, this approach is considered inadequate by Pitts. He claimed that it is the tubular H⁺ secretion which converts filtered HPO₄^2? to H₂PO₄^?, thereafter excreted in urine. This is only true under conditions of inorganic acid or neutral phosphate loading, when the maximum tubular phosphate reabsorption (TmPi) is overcharged. In controls, H₂PO₄^? excretion is lower than its glomerular filtration, provided that acid-base status is normal and tubular phosphate reabsorption is below the TmPi. The TmPi is lower than its glomerular filtration, provided that acid-base status is normal and tubular phosphate reabsorption is below the TmPi. When the TmPi is exceeded, a portion of HPO₄^2? escapes proximal reabsorption, reaching the distal tubule where its absorption is precluded, while tubular H⁺ secretion converts HPO₄^2? to H₂PO₄^?. In man and dog, the attainment of TmPi is evidenced by a FE% of 20%, and only beyond this limit H₂PO₄^? excretion exceeds glomerular filtration. When FE% is lower than 20%, H₂PO₄^? filtration exceeds excretion, HPO₄^2? being completely reabsorbed at the proximal tubule by NaPi-2a and 2c cotransporters. While Van Slyke's approach is always valid, Pitts’ approach is only valid under loading conditions, when the two processes of H₂PO₄^? excretion overlap each other. NH ^+₄ increases inversely to TA excretion in conditions of acidosis and tP restriction, but is independent of TA in Pi-replete dogs, independently of acidosis.     

Aliovalent-doped sodium chromium oxide (Na0.9Cr0.9Sn0.1O2 and Na0.8Cr0.9Sb0.1O2) for sodium-ion battery cathodes with high-voltage characteristics

NaCrO₂ with high rate-capability is an attractive cathode material for sodium-ion batteries (NIBs). However, the amount of reversibly extractable Na⁺ ions is restricted by half, which results in relatively low energy density for practical NIB cathodes. Herein, we describe aliovalent-doped O3–Na_0.9[Cr_0.9Sn_0.1]O₂ (NCSnO) and O3–Na_0.8[Cr_0.9Sb_0.1]O₂ (NCSbO), both of which show high-voltage characteristics that translate to an increase in energy density. In contrast to NaCrO₂, NCSnO and NCSbO can be reversibly charged to 3.80 and 3.95 V, respectively, delivering 0.5 Na⁺ along with Cr^3+/4+ redox alone. The reversible chargeability to Na_0.4[Cr_0.9Sn_0.1]O₂ and Na_0.3[Cr_0.9Sb_0.1]O₂ is not associated with the suppression of Cr⁶⁺ formation. Both compounds show concentrations of Cr⁶⁺ that are higher than that of Na_0.3CrO₂, with an absence of O3′ phases. This implies that aliovalent-doping contributes to a suppression of the Cr⁶⁺ migration into tetrahedral sites in the interslab space, which reduces the possibility of irreversible comproportionation. NCSnO and NCSbO deliver capacities comparable to that of NaCrO₂, but show a higher average discharge voltage (2.94 V for NaCrO₂; 3.14 V for NCSnO; 3.21 V for NCSbO), which leads to a noticeable increase in energy densities. The high-voltage characteristics of NCSnO and NCSbO are also validated via density-functional-theory calculations.

In contrast to O3–NaCrO₂, O3–Na_0.8[Cr_0.9Sb_0.1]O₂ shows reversibility when charged to 3.95 V and high-voltage charge/discharge features, which results in improvement of energy density.     

Aldosterone antagonism studies in the rhesus monkey.

Renal studies in femal rhesus monkeys indicated that 10 micron g was an optimum i.m. sodium-retaining dose of aldosterone. Aldosterone was injected i.m. at dosages of 2.5, 5, 10 and 20 micron g/animal. The 10-micron g dose induced about a 50% reduction in sodium excretion (from 3.7 to 1.7 mEq/6 hr) and was selected as the standard dose for antagonism studies. K excretion and urine volume remained unchanged. Subsequently, the oral antialdosterone activities of spironolactone and canrenone, a delta6 metabolite, were assessed at dosages of 1, 4 and 8 mg/kg. Dose-related increases in the aldosterone-depressed urinary Na/k ratio occurred primarily as a consequence of enhanced sodium excretion. Canrenone possessed antialdosterone potency equal to that of spironolactone. In the absence of exogenous aldosterone, spironolactone (16 mg/kg) was essentially devoid of diuretic activity whereas hydrochlorothiazide (1 mg/kg) induced marked increases in Na (256%) and K (105%) excretion and urine volume (109%).     

Extracellular K+ concentration controls cell surface density of IKr in rabbit hearts and of the HERG channel in human cell lines

Although the modulation of ion channel gating by hormones and drugs has been extensively studied, much less is known about how cell surface ion channel expression levels are regulated. Here, we demonstrate that the cell surface density of both the heterologously expressed K⁺ channel encoded by the human ether-a-go-go–related gene (HERG) and its native counterpart, the rapidly activating delayed rectifier K⁺ channel (I_Kr), in rabbit hearts in vivo is precisely controlled by extracellular K⁺ concentration ([K⁺]_o) within a physiologically relevant range. Reduction of [K⁺]_o led to accelerated internalization and degradation of HERG channels within hours. Confocal analysis revealed colocalization between HERG and ubiquitin during the process of HERG internalization, and overexpression of ubiquitin facilitated HERG degradation under low [K⁺]_o. The HERG channels colocalized with a marker of multivesicular bodies during internalization, and the internalized HERG channels were targeted to lysosomes. Our results provide the first evidence to our knowledge that the cell surface density of a voltage-gated K⁺ channel, HERG, is regulated by a biological factor, extracellular K⁺. Because hypokalemia is known to exacerbate long QT syndrome (LQTS) and Torsades de pointes tachyarrhythmias, our findings provide a potential mechanistic link between hypokalemia and LQTS.     

Inhibition of kidney potassium channels by fluoxetine: In vivo and in vitro studies

In vitro studies have demonstrated that fluoxetine, a commonly used antidepressant drug, can modulate the activity of K⁺ channels. In the present study, we investigated the in vivo effect of acute and sub-chronic treatment of rats with fluoxetine on K⁺ renal transport. Furthermore, OK cells, a kidney epithelial cell line, were used in order to evaluate the in vitro effect of fluoxetine on K⁺ currents. In the sub-chronic study, fluoxetine was administrated daily (10 mg/kg, p.o.) for 15 days to male adult Wistar rats. In the acute study, rats were given increasing doses of fluoxetine (1, 3, 10, 30 and 50 mg/kg, p.o.) for 24 h. Results from the sub-chronic study show that urinary K⁺ content (in mmol/L) was markedly reduced in the fluoxetine-treated animals (fluoxetine: 83 ± 9; control: 131 ± 10; P < 0.001). K⁺ fractional renal excretion (in %) was also significantly lower in the fluoxetine group (fluoxetine: 6 ± 1; control: 13 ± 2; P < 0.001). No significant changes was observed in creatinine clearance and on renal tubular Na⁺,K⁺-ATPase activity. Results obtained from the acute study demonstrate that, after a 24-h administration, fluoxetine produced a dose-dependent decrease in urinary K⁺, with an ED₅₀ (in mg/kg) of 4.2 (2.8; 5.5) and a maximal effect of 62% reduction. In vitro, fluoxetine produced a concentration-dependent inhibition of K⁺ currents in OK cells, with an EC₅₀ of 107 (84.8; 129.5) μM. In conclusion, fluoxetine produces a marked reduction on urinary K⁺ excretion; this effect constitutes an in vivo evidence for the inhibitory action of fluoxetine on kidney epithelial K⁺ channels.     

Superior performance of Na7V4(P2O7)4PO4 in sodium ion batteries

A novel synthetic method has been investigated to fabricate a 1D nanostructure Na₇V₄(P₂O₇)₄PO₄. Mixed polyanion materials with a well-defined 3D framework channel can improve the electrochemical performance of sodium reversible insertion/extraction reactions, and can be especially beneficial for high rate performance and cycling capability. It approaches an initial reversible electrochemical capacity of 92.0 mA h g⁻¹ with a high discharge potential over 3.85 V (vs. Na/Na⁺) and good cycling properties with a capacity retention of 81.4% after 300 cycles at a 0.5C rate in sodium systems. Taking into consideration the superior electrochemical characteristics, the phase-pure composite is considered to have a promising high rate capability as well as being a high capacity electrode material for advanced energy storage applications.

A novel synthetic method has been investigated to fabricate a 1D nanostructure Na₇V₄(P₂O₇)₄PO₄.     

Factors governing the competition between group IA and IB cations for monensin A: a DFT/PCM study

The affinity of monensin A to bind monovalent metal cations was evaluated by means of density functional theory (DFT) combined with polarizable continuum model (PCM) computations. The effect of various factors on complex formation between the monensinate A anion and group IA and IB metal ions was assessed. Competition between Na⁺ taken as a reference and monovalent metal cations was estimated using the Gibbs free energy for substituting the ligand-bound Na⁺ with its rival ions in the process [M⁺-solution] + [Mon⁻Na⁺] → [Mon⁻M⁺] + [Na⁺-solution] (M⁺ = Li⁺, K⁺, Rb⁺, Cs⁺, Cu⁺, Ag⁺ and Au⁺). The calculations revealed that the decrease in size of the cations accompanied by an increase of their accepting ability enhances the metal selectivity towards ligand donor atoms. In the gas-phase the affinity of monensinate A decreases in the order Cu⁺ > Li⁺ > Na⁺ > Au⁺ > Ag⁺ > K⁺ > Rb⁺ > Cs⁺. The complex formation can be manipulated by changing the solvent used. The polyether ionophore selectively binds Na⁺ ions in polar solvents but could become Li⁺ or Cu⁺-selective in low-polarity solvents.

The results obtained suggest that the metal selectivity of monensin can be modulated by changing the solvents used.     

Different manufacturers of syringes: A new source of variability in blood gas,acid–base balance and related laboratory test?

ObjectiveEvaluate whether four different brands/types of heparin coated syringes can represent a source of variability in blood gas analysis (BGA).Design and methodsBlood was collected from one hundred volunteers into different syringes: Syringe I (lithium heparin and calcium balanced); Syringe II: in-house prepared (sodium heparin); Syringe III: (spray-dried calcium-balanced lithium heparin); Syringe IV (lyophilized electrolyte-balanced lithium heparin).ResultsSignificant differences were as follows: a) Syringe I vs II: pO₂, sO₂, pCO₂^t, cHCO₃^?, ctCO₂, base excess (BE), total hemoglobin (tHb), sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺), glucose (Glu), lactate (Lac), O₂ Hb and p 50; b) Syringe I vs III: pH, pO₂, cHCO₃^?, ctCO₂, BE, Na⁺, Glu, Lac and p 50; c) Syringe I vs IV: pH, pO₂, sO₂, pCO₂^t, BE, Na⁺, K⁺, Ca²⁺, Glu, Lac and O₂ Hb; d) Syringe II vs III: pH, pO₂, sO₂, pCO₂^t, cHCO₃^?, ctCO₂, ctO₂, tHb, Na⁺, K⁺, Ca²⁺, Lac and p 50; e) Syringe II vs IV: pH, pO₂, sO₂, pCO₂^t, cHCO₃^?, ctCO₂, BE, tHb, Na⁺, K⁺, Ca²⁺, Lac, O₂ Hb and p 50; f) Syringe III vs IV: pH, pO₂, sO₂, cHCO₃^?, ctCO₂, ctO₂, BE, Na⁺, K⁺, Ca²⁺, O₂ Hb and p 50.ConclusionThe different manufacturers of syringes can represent new source of variability on BGA.     

Potassium and ventilation during positive and negative work inpatients with chronic obstructive pulmonary disease

In patients with chronic obstructive pulmonary disease (COPD),reduced ventilatory reserves limit exercise tolerance. In these patients, the ventilatoryrequirements of eccentric exercise (negative work, W_neg) are lower thanthose of concentric exercise (positive work, W_pos) at similar workloads.In this study, we investigated the relationship between plasma potassium levels and ventilationduring W_pos and W_neg in these patients. Twelvepatients with stable COPD [mean (SD) FEV₁ 46% (16) of predicted]performed W_pos and W_neg on a cycle ergometer(6 min of exercise; interval ≥1 h) in a randomized order at a constant workload of50% of the individual maximum (positive) work capacity. Minute ventilation (V_E) and arterial plasma potassium concentration ([K⁺]_a) were measured at rest, and at 1-min intervals during exercise and during 3 min ofrecovery. V_E increased less during W_neg thanduring W_pos [6 (range 3–26) vs. 18 (range 8–28) l min^?1; P<0·01]. V_E during W_neg was reduced in proportion to VCO ₂.The increase in [K⁺]_a during W_pos and W_neg [0·45 (range 0·26–0·75) and0·34 (range 0·1–0·97) mM ] did not differsignificantly. V_E was closely correlated with VCO ₂ during both types of exercise. V_E was also closelycorrelated with [K⁺]_a, but the slope of the relationship between[K⁺]_a and V_E was steeper during W_pos than during W_neg [39·1 (range15·2–88·6) vs. 18·3 (range7·2–37·3) l min^?1 mM ^?1; P=0·012]. In contrast, the slope of the relationship betweenVCO ₂ and V_E was similar during bothtypes of exercise [27?8 (range 19·2–37·1) vs. 32·1 (range19·8–48·4)]. Thus, for a given increase in [K⁺]_a, the increase in V_E was significantly less during W_neg. In patients with COPD, potassium did not explain the difference inexercise ventilation between W_neg and W_pos, andmay not play a significant role in the control of breathing during low-intensity exercise.