Interactions between cadmium and lead with acidic soils: Experimental evidence of similar adsorption patterns for a wide range of metal concentrations and the implications of metal migration

The importance of high- and low-affinity surface sites for cadmium and lead adsorption in typical European and Asian soils was investigated. Adsorption experiments on surface and deep horizons of acidic brown (Vosges, France) and red loess soils (Hunan, China) were performed at 25 ◦C as a function of the pH (3.5–8) and a large range of metal concentrations in solution (10−9–10−4 mol l−1). We studied the adsorption kinetics using a Cd2+-selective electrode and desorption experiments as a function of the solid/solution ratio and pH. At a constant solution pH, all samples exhibited similar maximal adsorption capacities (4.0 ± 0.5 µmol/g Cd and 20 ± 2 µmol/g Pb). A constant slope of adsorbed–dissolved concentration dependence was valid over 5 orders of magnitude of metal concentrations. Universal Langmuir and Freundlich equations and the SCM formalism described the adsorption isotherms and the pH-dependent adsorption edge over very broad ranges of metal concentrations, indicating no high- or low-affinity sites for metal binding at the soil surface under these experimental conditions. At pH 5, Cd and Pb did not compete, in accordance with the SCM. The metal adsorption ability exceeded the value for soil protection by two orders of magnitude, but only critical load guarantees soil protection since metal toxicity depends on metal availability

Investigation of polymorphisms in schizophrenia relevant genes

Schizophrenia is a severe, debilitating, and complex disease. It is characterized by delusions, hallucinations, disorganized speech, and grossly disorganized or catatonic behavior. As a complex disease, schizophrenia is thought to be caused by many genes. In addition the etiology is thought to be heterogeneous across the population of persons suffering from schizophrenia. In an attempt to dissect the heterogeneity of the disease, and investigate the role of candidate genes associated with schizophrenia, several studies were completed. The first was a case only association study of neurocognition and COMT, a candidate gene for schizophrenia. This is the largest study of its kind to date. The second study addresses the possibility of predisposition due to differential expression of candidate genes. In this study expression of another candidate gene PRODH was assessed. Together these studies aimed at investigating the polymorphisms of candidate genes for schizophrenia

Pharmacokinetics of epinephrine in patients with septic shock: modelization and interaction with endogenous neurohormonal status

Introduction In septic patients, an unpredictable response to epinephrine may be due to pharmacodynamic factors or to non-linear pharmacokinetics. The purpose of this study was to investigate the pharmacokinetics of epinephrine and its determinants in patients with septic shock. Methods Thirty-eight consecutive adult patients with septic shock were prospectively recruited immediately before epinephrine infusion. A baseline blood sample (C0) was taken to assess endogenous epinephrine, norepinephrine, renin, aldosterone, and plasma cortisol levels before epinephrine infusion. At a fixed cumulative epinephrine dose adjusted to body weight and under steady-state infusion, a second blood sample (C1) was taken to assess epinephrine and norepinephrine concentrations. Data were analyzed using the nonlinear mixed effect modeling software program NONMEM. Results Plasma epinephrine concentrations ranged from 4.4 to 540 nmol/L at steady-state infusion (range 0.1 to 7 mg/hr; 0.026 to 1.67 μg/kg/min). A one-compartment model adequately described the data. Only body weight (BW) and New Simplified Acute Physiologic Score (SAPSII) at intensive care unit admission significantly influenced epinephrine clearance: CL (L/hr) = 127 × (BW/70)0.60 × (SAPS II/50)-0.67. The corresponding half-life was 3.5 minutes. Endogenous norepinephrine plasma concentration significantly decreased during epinephrine infusion (median (range) 8.8 (1 – 56.7) at C0 vs. 4.5 (0.3 – 38.9) nmol/L at C1, P < 0.001). Conclusions Epinephrine pharmacokinetics is linear in septic shock patients, without any saturation at high doses. Basal neurohormonal status does not influence epinephrine pharmacokinetics. Exogenous epinephrine may alter the endogenous norepinephrine metabolism in septic patients

Genotyping Accuracy for Whole-Genome Amplification of DNA from Buccal Epithelial Cells

We compared the accuracy of genotyping for DNA extracted from lymphocytes to that of DNA amplified from buccal epithelial cells. Amplification was via a rolling circle/phi29 DNA polymerase commercial kit. Paired buccal and lymphocyte DNA samples were available from 30 individuals. All samples were genotyped for 12 SNPs, 5 microsatellites and 2 VNTRs. The accuracy of genotyping (no-call proportions, reproducibility, and concordance) was similar for DNA from lymphocytes in comparison to amplified DNA from buccal samples. If used with caution, these data suggest that rolling-circle whole-genome amplification can be used to increase the DNA mass available for large-scale genotyping projects based on DNA from buccal cells

2-Amino-5-chloro­pyridinium hydrogen succinate

In the title salt, C5H6ClN2 +·C4H5O4 −, the pyridine N atom is protonated. The pyridinium and amino groups associate via a pair of N—H⋯O hydrogen bonds to the carboxyl­ate O atoms of the singly deprotonated succinate anion. The hydrogen succinate anions self-assemble via O—H⋯O hydrogen bonds into chains along the b axis. The crystal structure is further stabilized by additional N—H⋯O hydrogen bonds involving the second amino H atoms, as well as C—H⋯O contacts, forming a three-dimensional network

Bis(2-amino­thia­zolium) succinate succinic acid

In the title compound, 2C3H5N2S+·C4H4O4 2−·C4H6O4, the thia­zolium ring is almost planar, with the maximum deviation from planarity being 0.0056 (8) Å for the C atom carrying the amine substituent. The N atom of the 2-amino­thia­zole mol­ecule is protonated. Both the anion and the acid lie across inversion centres. The crystal packing is consolidated by inter­molecular O—H⋯O, N—H⋯O and C—H⋯O hydrogen bonds. Mol­ecules are stacked down the b axis

4-Amino­pyridinium hydrogen succinate

In the title salt, C5H7N2 +·C4H5O4 −, the asymmetric unit comprises an amino­pyridinium cation and a hydrogen succinate anion as protonation of the aromatic N atom of the 4-amino­pyridine mol­ecule has occurred. The crystal packing is stabilized by inter­molecular O—H⋯O and N—H⋯O hydrogen bonds that lead to a two-dimensional array. Short C—H⋯O contacts are also present

Rats that differentially respond to cocaine differ in their dopaminergic storage capacity of the nucleus accumbens

Cocaine (COC) inhibits the re-uptake of dopamine. However, the dopamine response to COC also depends on dopamine inside storage vesicles. The aim of this study was to investigate whether rats that differentially respond to COC differ in their dopaminergic storage capacity of the nucleus accumbens. Total and vesicular levels of accumbal dopamine as well as accumbal vesicular monoamine transporter-2 levels were established in high (HR) and low responders (LR) to novelty rats. Moreover, the effects of reserpine (RES) on the COC-induced increase of extracellular accumbal dopamine were investigated. HR displayed higher accumbal levels of total and vesicular dopamine than LR. Moreover, HR displayed more accumbal vesicular monoamine transporters-2 than LR. COC increased extracellular accumbal dopamine more strongly in HR than in LR. A low dose of RES prevented the COC-induced increase of accumbal dopamine in LR, but not in HR. A higher dose of RES was required to inhibit the COC-induced increase of accumbal dopamine in HR. These data demonstrate that HR were marked by a larger accumbal dopaminergic storage pool than LR. It is hypothesized that HR are more sensitive to COC than LR, because COC can release more dopamine from accumbal storage vesicles in HR than in LR

Early Presymptomatic and Long-Term Changes of Rest Activity Cycles and Cognitive Behavior in a MPTP-Monkey Model of Parkinson's Disease

It is increasingly recognized that non-motor symptoms are a prominent feature of Parkinson's disease and in the case of cognitive deficits can precede onset of the characteristic motor symptoms. Here, we examine in 4 monkeys chronically treated with low doses of the neurotoxin MPTP the early and long-term alterations of rest-activity rhythms in relationship to the appearance of motor and cognitive symptoms.Behavioral activity recordings as well as motor and cognitive assessments were carried out continuously and in parallel before, during and for several months following MPTP-treatment (12–56 weeks). Cognitive abilities were assessed using a task that is dependent on the functional integrity of the fronto-striatal axis. Rest-activity cycles were monitored continuously using infrared movement detectors of locomotor activity. Motor impairment was evaluated using standardized scales for primates. Results show that MPTP treatment led to an immediate alteration (within one week) of rest-activity cycles and cognitive deficits. Parkinsonian motor deficits only became apparent 3 to 5 weeks after initiating chronic MPTP administration. In three of the four animals studied, clinical scores returned to control levels 5–7 weeks following cessation of MPTP treatment. In contrast, both cognitive deficits and chronobiological alterations persisted for many months. Levodopa treatment led to an improvement of cognitive performance but did not affect rest-activity rhythms in the two cases tested.Present results show that i) changes in the rest activity cycles constituted early detectable consequences of MPTP treatment and, along with cognitive alterations, characterize the presymptomatic stage; ii) following motor recovery there is a long-term persistence of non-motor symptoms that could reflect differential underlying compensatory mechanisms in these domains; iii) the progressive MPTP-monkey model of presymptomatic ongoing parkinsonism offers possibilities for in-depth studies of early non-motor symptoms including sleep alterations and cognitive deficits