Enhancing bauxite residue properties for plant growth: Gypsum and organic amendment effects on chemical properties of soil and leachate.

Here, we assess the effects of gypsum and local organic waste as amendments to non-weathered, filter-pressed bauxite residue (BR) to improve its properties and support plant growth. In addition, we monitored the leachate quality of the amended BR under progressive leaching that simulated precipitation conditions in Northern Brazil. Free-draining column tests consisting of BR amended with gypsum and organic waste, at 5% and 10% w/w, respectively, were leached for 8 weeks to assess the effects on the chemical composition of BR and the leachates. Adding gypsum to BR reduced the exchangeable sodium (Na) percentage (ESP) from approximately 79%-48%, whereas adding only organic waste had smaller effects on ESP (from ∼79% to âˆ¼ 70%). The mean leachate pH ranged from 8.7 to 9.4 for the gypsum, and organic waste amended BR, while this was 10.3 in the leachate of the unamended BR. The treatments had similar trends of electrical conductivity throughout the experiments and were below 2 dS/cm after 8 weeks, when ∼1.700 mm simulated precipitation had leached. Aluminium (Al), Arsenic (As), and Vanadium (V) concentrations in leachates of BR with gypsum, either alone or in combination with organic waste, were significantly lowered than in leachate of non-amended BR. By contrast, metal concentrations increased if organic waste was added to BR. We conclude that amending BR with gypsum, in combination with organic waste, significantly improves the chemical properties of the solid phase and achieved rehabilitation goals for SAR and EC of the leachates after 8 weeks of leaching. However, despite high leaching rates, rehabilitation goals for pH and ESP were not achieved with gypsum either alone or combined with organic waste.

Exogenous phosphorus treatment facilitates chelation-mediated cadmium detoxification in perennial ryegrass (Lolium perenne L.).

Cadmium (Cd) is an on-going environmental pollutant associated with hindered plant growth. In response, plants possess various strategies to alleviate Cd stress, including reactive oxygen species (ROS) scavenging and chelation-mediated Cd detoxification. The present study examined the Cd defense mechanism of perennial ryegrass (Lolium perenne L.), taking into account the effect of exogenous phosphorus (P) input. It was found that despite triggering antioxidant enzyme activity, Cd stress heightened lipid peroxidation levels. Exogenous P input partially mitigated the lipid peroxidation impact and decreased the levels of superoxide dismutase (SOD), catalase (CAT), and peroxidase (POD) antioxidant enzymes, revealing reduced ROS-scavenging activity. Importantly, notable relationships were determined between the amount of Cd uptake in the root and the amount of non-protein thiols (R2 = 0.914), glutathione (R2 = 0.805) and phytochelatins (R2 = 0.904) in proportion to the amount of exogenous P applied. The levels of amino acids proline and cysteine were also enhanced by exogenous P input showing their influence in alleviating Cd stress. Overall, it is reported that Cd detoxification in ryegrass plants can be stimulated by exogenous P input, which facilitates chelation-mediated Cd detoxification processes.

Biochar improves maize growth by alleviation of nutrient stress in a moderately acidic low-input Nepalese soil.

We studied the role of biochar in improving soil fertility for maize production. The effects of biochar on the alleviation of three potential physical-chemical soil limitations for maize growth were investigated, i.e. water stress, nutrient stress and acid stress. Experiments involved soils with two dosages of biochar (0.5% and 2% w:w), as well as ones without biochar, in combination with four different dosages of NPK fertilizer, water and lime. Biochar was produced from the invasive shrubby weed Eupatorium adenophorum using flame curtain kilns. This is the first study to alleviate one by one the water stress, nutrient stress and acid stress in order to investigate the mechanisms of biochar effects on soil fertility. Biochar addition increased soil moisture, potassium (K) and plant available phosphorous (P-AL), which all showed significant positive relationship (p<0.001) with above ground biomass of maize. However, biochar was much more effective at abundant soil watering (+311% biomass) than at water-starved conditions (+67% biomass), indicating that biochar did increase soil moisture, but that this was not the main reason for the positive biomass growth effects. Biochar addition did have a stronger effect under nutrient-stressed conditions (+363%) than under abundant nutrient application (+132%). Biochar amendment increased soil pH, but liming and pH had no effect on maize dry biomass, so acidity stress alleviation was not the mechanism of biochar effects on soil fertility. In conclusion, the alleviation of nutrient stress was the probably the main factor contributing to the increased maize biomass production upon biochar addition to this moderately acidic Inceptisol.

Molecular interrogation of hypothalamic organization reveals distinct dopamine neuronal subtypes.

The hypothalamus contains the highest diversity of neurons in the brain. Many of these neurons can co-release neurotransmitters and neuropeptides in a use-dependent manner. Investigators have hitherto relied on candidate protein-based tools to correlate behavioral, endocrine and gender traits with hypothalamic neuron identity. Here we map neuronal identities in the hypothalamus by single-cell RNA sequencing. We distinguished 62 neuronal subtypes producing glutamatergic, dopaminergic or GABAergic markers for synaptic neurotransmission and harboring the ability to engage in task-dependent neurotransmitter switching. We identified dopamine neurons that uniquely coexpress the Onecut3 and Nmur2 genes, and placed these in the periventricular nucleus with many synaptic afferents arising from neuromedin S+ neurons of the suprachiasmatic nucleus. These neuroendocrine dopamine cells may contribute to the dopaminergic inhibition of prolactin secretion diurnally, as their neuromedin S+ inputs originate from neurons expressing Per2 and Per3 and their tyrosine hydroxylase phosphorylation is regulated in a circadian fashion. Overall, our catalog of neuronal subclasses provides new understanding of hypothalamic organization and function.

Comparative anatomical distribution of neuronal calcium-binding protein (NECAB) 1 and -2 in rodent and human spinal cord.

Neuronal calcium-binding protein 1 and -2 (NECAB1/2) localize to multiple excitatory neuron populations in the mouse spinal cord. Here, we analyzed rat and human spinal cord, combining in situ hybridization and immunohistochemistry, complementing newly collated data on mouse spinal cord for direct comparisons. Necab1/2 mRNA transcripts showed complementary distribution in rodent's spinal cord. Multiple-labeling fluorescence histochemistry with neuronal phenotypic markers localized NECAB1 to a dense fiber plexus in the dorsal horn, to neurons mainly in superficial layers and to commissural interneurons in both rodent species. NECAB1-positive (+) motor neurons were only found in mice. NECAB1 distribution in the human spinal cord was similar with the addition of NECAB1-like immunoreactivity surrounding myelinated axons. NECAB2 was mainly present in excitatory synaptic boutons in the dorsal horn of all three species, and often in calbindin-D28k(+) neuronal somata. Rodent ependymal cells expressed calbindin-D28k. In humans, they instead were NECAB2(+) and/or calretinin(+). Our results reveal that the association of NECAB2 to excitatory neuronal circuits in the spinal cord is evolutionarily conserved across the mammalian species investigated so far. In contrast, NECAB1 expression is more heterogeneous. Thus, our study suggests that the phenotypic segregation of NECAB1 and -2 to respective excitatory and inhibitory spinal systems can underpin functional modalities in determining the fidelity of synaptic neurotransmission and neuronal responsiveness, and might bear translational relevance to humans.

Effects of calcite and magnesite application to a declining Masson pine forest on strongly acidified soil in Southwestern China.

Liming of strongly acidified soil under a Masson pine (Pinus massoniana Lamb.) forest was studied through a seven-year field manipulation experiment at Tieshanping, Chongqing in Southwestern China. To distinguish between the individual effects of Ca(2+) and Mg(2+) addition, we separately applied calcite (CaCO3) and magnesite (MgCO3), rather than using dolomite [CaMg(CO3)2]. Both calcite and magnesite additions caused a significant increase in pH and a decrease in dissolved inorganic monomeric aluminium (Ali) concentration of soil water. Ecological recovery included increases of herb biomass (both treatments) and Mg content in Masson pine needles (magnesite treatment only). However, the growth rate of Masson pine did not increase under either treatment, possibly because of nutrient imbalance due to phosphorus (P) deficiency or limited observation period. In China, acid deposition in forest ecosystems commonly coincides with large inputs of atmogenic Ca(2+), both enhancing Mg(2+) leaching. Calcite addition may further decrease the Mg(2+) availability in soil water, thereby exacerbating Mg(2+) deficiency in the acidified forest soils of southern and southwestern China. The effect of anthropogenic acidification of naturally acid forest soils on P availability needs further study.

Neuronal calcium-binding proteins 1/2 localize to dorsal root ganglia and excitatory spinal neurons and are regulated by nerve injury.

Neuronal calcium (Ca(2+))-binding proteins 1 and 2 (NECAB1/2) are members of the phylogenetically conserved EF-hand Ca(2+)-binding protein superfamily. To date, NECABs have been explored only to a limited extent and, so far, not at all at the spinal level. Here, we describe the distribution, phenotype, and nerve injury-induced regulation of NECAB1/NECAB2 in mouse dorsal root ganglia (DRGs) and spinal cord. In DRGs, NECAB1/2 are expressed in around 70% of mainly small- and medium-sized neurons. Many colocalize with calcitonin gene-related peptide and isolectin B4, and thus represent nociceptors. NECAB1/2 neurons are much more abundant in DRGs than the Ca(2+)-binding proteins (parvalbumin, calbindin, calretinin, and secretagogin) studied to date. In the spinal cord, the NECAB1/2 distribution is mainly complementary. NECAB1 labels interneurons and a plexus of processes in superficial layers of the dorsal horn, commissural neurons in the intermediate area, and motor neurons in the ventral horn. Using CLARITY, a novel, bilaterally connected neuronal system with dendrites that embrace the dorsal columns like palisades is observed. NECAB2 is present in cell bodies and presynaptic boutons across the spinal cord. In the dorsal horn, most NECAB1/2 neurons are glutamatergic. Both NECAB1/2 are transported into dorsal roots and peripheral nerves. Peripheral nerve injury reduces NECAB2, but not NECAB1, expression in DRG neurons. Our study identifies NECAB1/2 as abundant Ca(2+)-binding proteins in pain-related DRG neurons and a variety of spinal systems, providing molecular markers for known and unknown neuron populations of mechanosensory and pain circuits in the spinal cord.

Secretagogin is expressed in sensory CGRP neurons and in spinal cord of mouse and complements other calcium-binding proteins, with a note on rat and human.

BACKGROUND: Secretagogin (Scgn), a member of the EF-hand calcium-binding protein (CaBP) superfamily, has recently been found in subsets of developing and adult neurons. Here, we have analyzed the expression of Scgn in dorsal root ganglia (DRGs) and trigeminal ganglia (TGs), and in spinal cord of mouse at the mRNA and protein levels, and in comparison to the well-known CaBPs, calbindin D-28k, parvalbumin and calretinin. Rat DRGs, TGs and spinal cord, as well as human DRGs and spinal cord were used to reveal phylogenetic variations. RESULTS: We found Scgn mRNA expressed in mouse and human DRGs and in mouse ventral spinal cord. Our immunohistochemical data showed a complementary distribution of Scgn and the three CaBPs in mouse DRG neurons and spinal cord. Scgn was expressed in ~7% of all mouse DRG neuron profiles, mainly small ones and almost exclusively co-localized with calcitonin gene-related peptide (CGRP). This co-localization was also seen in human, but not in rat DRGs. Scgn could be detected in the mouse sciatic nerve and accumulated proximal to its constriction. In mouse spinal cord, Scgn-positive neuronal cell bodies and fibers were found in gray matter, especially in the dorsal horn, with particularly high concentrations of fibers in the superficial laminae, as well as in cell bodies in inner lamina II and in some other laminae. A dense Scgn-positive fiber network and some small cell bodies were also found in the superficial dorsal horn of humans. In the ventral horn, a small number of neurons were Scgn-positive in mouse but not rat, confirming mRNA distribution. Both in mouse and rat, a subset of TG neurons contained Scgn. Dorsal rhizotomy strongly reduced Scgn fiber staining in the dorsal horn. Peripheral axotomy did not clearly affect Scgn expression in DRGs, dorsal horn or ventral horn neurons in mouse. CONCLUSIONS: Scgn is a CaBP expressed in a subpopulation of nociceptive DRG neurons and their processes in the dorsal horn of mouse, human and rat, the former two co-expressing CGRP, as well as in dorsal horn neurons in all three species. Functional implications of these findings include the cellular refinement of sensory information, in particular during the processing of pain.

Hypothalamic mitochondrial dysfunction associated with anorexia in the anx/anx mouse.

The anorectic anx/anx mouse exhibits disturbed feeding behavior and aberrances, including neurodegeneration, in peptidergic neurons in the appetite regulating hypothalamic arcuate nucleus. Poor feeding in infants, as well as neurodegeneration, are common phenotypes in human disorders caused by dysfunction of the mitochondrial oxidative phosphorylation system (OXPHOS). We therefore hypothesized that the anorexia and degenerative phenotypes in the anx/anx mouse could be related to defects in the OXPHOS. In this study, we found reduced efficiency of hypothalamic OXPHOS complex I assembly and activity in the anx/anx mouse. We also recorded signs of increased oxidative stress in anx/anx hypothalamus, possibly as an effect of the decreased hypothalamic levels of fully assembled complex I, that were demonstrated by native Western blots. Furthermore, the Ndufaf1 gene, encoding a complex I assembly factor, was genetically mapped to the anx interval and found to be down-regulated in anx/anx mice. These results suggest that the anorexia and hypothalamic neurodegeneration of the anx/anx mouse are associated with dysfunction of mitochondrial complex I.

The effectiveness and cost-evaluation of manual therapy and physical therapy in patients with sub-acute and chronic non specific neck pain. Rationale and design of a Randomized Controlled Trial (RCT).

BACKGROUND: Manual Therapy applied to patients with non specific neck pain has been investigated several times. In the Netherlands, manual therapy as applied according to the Utrecht School of Manual Therapy (MTU) has not been the subject of a randomized controlled trial. MTU differs in diagnoses and treatment from other forms of manual therapy. METHODS/DESIGN: This is a single blind randomized controlled trial in patients with sub-acute and chronic non specific neck pain. Patients with neck complaints existing for two weeks (minimum) till one year (maximum) will participate in the trial. 180 participants will be recruited in thirteen primary health care centres in the Netherlands.The experimental group will be treated with MTU during a six week period. The control group will be treated with physical therapy (standard care, mainly active exercise therapy), also for a period of six weeks.Primary outcomes are Global Perceived Effect (GPE) and functional status (Neck Disability Index (NDI-DV)). Secondary outcomes are neck pain (Numeric Rating Scale (NRS)), Eurocol, costs and quality of life (SF36). DISCUSSION: This paper presents details on the rationale of MTU, design, methods and operational aspects of the trial. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT00713843.