Manure replacing synthetic fertilizer improves crop yield sustainability and reduces carbon footprint under winter wheat-summer maize cropping system.

Manure replacing synthetic fertilizer is a viable practice to ensure crop yield and increase soil organic carbon (SOC), but its impact on greenhouse gas (GHG) emissions is inconsistent, thus remains its effect on CF unclear. In this study, a 7-year field experiment was conducted to assess the impact of replacing synthetic fertilizer with manure on crop productivity, SOC sequestration, GHG emissions and crop CF under winter wheat-summer maize cropping system. Five treatments were involved: synthetic nitrogen, phosphorus, and potassium fertilizer (NPK) and 25%, 50%, 75%, and 100% of manure replacing synthetic N (25%M, 50%M, 75%M, and 100%M). Compared with NPK treatment, 25%M and 50%M treatments maintained annual yield (winter wheat plus summer maize) and sustainable yield index (SYI), but 75%M and 100%M treatments significantly decreased annual yield, and 100%M treatment also significantly reduced annual SYI. The SOC content exhibited a significant increasing trend over years in all treatments. After 7 years, SOC storage in manure treatments increased by 3.06-11.82 Mg ha-1 relative to NPK treatment. Manure treatments reduced annual GHG emissions by 14%-60% over NPK treatment. The CF of the cropping system ranged from 0.16 to 0.39 kg CO2 eq kg-1 of grain without considering SOC sequestration, in which the CF of manure treatments lowered by 18%-58% relative to NPK treatment. When SOC sequestration was involved in, the CF varied from -0.39 to 0.37 kg CO2 eq kg-1 of grain, manure treatments significantly reduced the CF by 22%-208% over NPK treatment. It was concluded that replacing 50% of synthetic fertilizer with manure was a sound option for achieving high crop yield and SYI but low CF under the tested cropping system.

Stability of Fe-As composites formed with As(V) and aged ferrihydrite.

During the aging process, ferrihydrite was transformed into mineral mixtures composed of different proportions of ferrihydrite, goethite, lepidocrocite and hematite. Such a transformation may affect the fixed ability of arsenic. In this study, the stability of Fe-As composites formed with As(V) and the minerals aged for 0, 1, 4, 10 and 30 days of ferrihydrite were systematically examined, and the effects of molar of ratios Fe/As were also clarified using kinetic methods combined with multiple spectroscopic techniques. The results indicated that As(V) was rapidly adsorbed on minerals during the initial polymerization process, which delayed both the ferrihydrite conversion and the hematite formation. When the Fe/As molar ratio was 1.875 and 5.66, the As(V) adsorbed by ferrihydrite began to release after 6 hr and 12 hr, respectively. The corresponding release amounts of As(V) were 0.55 g/L and 0.07 g/L, and the adsorption rates were 92.43% and 97.50% at 60 days, respectively. However, the As(V) adsorbed by the transformation products aged for 30 days of ferrihydrite began to release after adsorbed 30 days. The corresponding release amounts of As(V) were 0.25 g/L and 0.03 g/L, and the adsorption rates were 84.23% and 92.18% after adsorbed 60 days, for the Fe/As=1.875 and 5.66, respectively. Overall, the combination of As(V) with ferrihydrite and aged products transformed from a thermodynamically metastable phase to a dynamically stable state within a certain duration. Moreover, the aging process of ferrihydrite reduced the sorption ability of arsenate by iron (hydr)oxide but enhanced the stability of the Fe-As composites.

The contribution of cross-talk between the cell-surface proteins CD36 and CD47-TSP-1 in osteoclast formation and function.

Antibody-mediated blockade of cluster of differentiation 47 (CD47)-thrombospondin-1 (TSP-1) interactions blocks osteoclast formation in vitro and attenuates parathyroid hormone (PTH)-induced hypercalcemia in vivo in mice. Hypercalcemia in this model reflects increased bone resorption. TSP-1 has two cell-associated binding partners, CD47 and CD36. The roles of these two molecules in mediating the effects of TSP1 in osteoclasts are unclear. Osteoclast formation was attenuated but not absent when preosteoclasts isolated from CD47-/- mice were cocultured with WT osteoblasts. Suppressing CD36 in osteoclast progenitors also attenuated osteoclast formation. The hypercalcemic response to a PTH infusion was blunted in CD47-/-/CD36-/- (double knockout (DKO)) female mice but not CD47-/- mice or CD36-/- animals, supporting a role for both CD47 and CD36 in mediating this effect. Consistent with this, DKO osteoclasts had impaired resorptive activity when analyzed in vitro Inhibition of nitric oxide (NO) signaling is known to promote osteoclastogenesis, and TSP-1 suppresses NO production and signaling. An anti-TSP-1 antibody increased NO production in osteoclasts, and the inhibitory effect of anti-TSP-1 on osteoclastogenesis was completely rescued by l-nitroarginine methyl ester (l-NAME), a competitive NO synthase inhibitor. Supportive of an important role for CD36 in mediating the pro-osteoclastogenic effects of TSP-1, engaging CD36 with a synthetic agonist, p907, suppressed NO production in anti-TSP-1-treated cultures, allowing osteoclast maturation to occur. These results establish that CD36 and CD47 both participate in mediating the actions of TSP-1 in osteoclasts and establish a physiologically relevant cross-talk in bone tissue between these two molecules.

The transcription factor T-box 3 regulates colony-stimulating factor 1-dependent Jun dimerization protein 2 expression and plays an important role in osteoclastogenesis.

Colony-stimulating factor 1 (CSF1) is known to promote osteoclast progenitor survival, but its roles in osteoclast differentiation and mature osteoclast function are less well understood. In a microarray screen, Jun dimerization protein 2 (JDP2) was identified as significantly induced by CSF1. Recent reports indicate that JDP2 is required for normal osteoclastogenesis and skeletal metabolism. Because there are no reports on the transcriptional regulation of this gene, the DNA sequence from -2612 to +682 bp (relative to the transcription start site) of the JDP2 gene was cloned, and promoter activity was analyzed. The T box-binding element (TBE) between -191 and -141 bp was identified as the cis-element responsible for CSF1-dependent JDP2 expression. Using degenerate PCR, Tbx3 was identified as the major isoform binding the TBE. Overexpression of Tbx3 induced JDP2 promoter activity, whereas suppressing Tbx3 expression substantially attenuated CSF1-induced transcription. Suppressing Tbx3 in osteoclast precursors reduced JDP2 expression and significantly impaired RANKL/CSF1-induced osteoclastogenesis. A MEK1/2-specific inhibitor was found to block CSF1-induced JDP2 expression. Consistent with these data, JDP2(-/-) mice were found to have increased bone mass. In summary, CSF1 up-regulates JDP2 expression by inducing Tbx3 binding to the JDP2 promoter. The downstream signaling cascade from activated c-Fms involves the MEK1/2-ERK1/2 pathway. Tbx3 plays an important role in osteoclastogenesis at least in part by regulating CSF1-dependent expression of JDP2.

Increasing dietary protein acutely augments intestinal iron transporter expression and significantly increases iron absorption in rats.

Iron (Fe) deficiency is endemic worldwide. Little data are available regarding acute effects of dietary protein on intestinal Fe absorption. The current study evaluated the short-term effects of increasing dietary protein on Fe absorption and expression of genes involved in Fe homeostasis. Sprague Dawley rats (24, female) were randomly assigned to custom-formulated isocaloric diets containing 40, 20 (control), or 5% protein (as percentage of total kilocalories) for 7 d. Whole-body Fe balance studies demonstrated that Fe retention was greater in the 40% group than in the 5% group (30.8 vs. 7.3%; P<0.01). In a separate study utilizing stable iron isotopes, the 40% group absorbed 30% of ingested Fe, while the 20% group absorbed 18% (P=0.005). Whole-genome profiling revealed that increasing dietary protein from 5 to 40% increased duodenal transcript expression of divalent metal transporter 1 (DMT1) 3.2-fold, duodenal cytochrome b (Dcytb) 1.8-fold, and transferrin receptor (TfR) 1.8-fold. Consistent with these findings, DMT1 transcript expression was 4-fold higher in RNA prepared from duodenal mucosa in the 40% group compared to the 20% group (P<0.001). These data suggest that increasing dietary protein increases intestinal Fe absorption in part by up-regulating DMT1, Dcytb, and TfR.

Mitofusin 2 plays a critical role in maintaining the functional integrity of the neuromuscular-skeletal axis.

PURPOSE: Mitofusin 2 (Mfn2) is one of two mitofusins involved in regulating mitochondrial size, shape and function, including mitophagy, an important cellular mechanism to limit oxidative stress. Reduced expression of Mfn2 has been associated with impaired osteoblast differentiation and function and a reduction in the number of viable osteocytes in bone. We hypothesized that the genetic absence of Mfn2 in these cells would increase their susceptibility to aging-associated metabolic stress, leading to a progressive impairment in skeletal homeostasis over time. METHODS: Mfn2 was selectively deleted in vivo at three different stages of osteoblast lineage commitment by crossing mice in which the Mfn2 gene was floxed with transgenic mice expressing Cre under the control of the promoter for Osterix (OSX), collagen1a1, or DMP1 (Dentin Matrix Acidic Phosphoprotein 1). RESULTS: Mice in which Mfn2 was deleted using DMP1-cre demonstrated a progressive and dramatic decline in bone mineral density (BMD) beginning at 10 weeks of age (n = 5 for each sex and each genotype from age 10 to 20 weeks). By 15 weeks, there was evidence for a functional decline in muscle performance as assessed using a rotarod apparatus (n = 3; 2 males/ 1 female for each genotype), accompanied by a decline in lean body mass. A marked reduction in trabecular bone mass was evident on bone histomorphometry, and biomechanical testing at 25 weeks (k/o: 2 male/1 female, control 2 male/2 female) revealed severely impaired femur strength. Extensive regional myofiber atrophy and degeneration was observed on skeletal muscle histology. Electron microscopy showed progressive disruption of cellular architecture, with disorganized sarcomeres and a bloated mitochondrial reticulum. There was also evidence of neurodegeneration within the ventral horn and roots of the lumbar spinal cord, which was accompanied by myelin loss and myofiber atrophy. Deletion of Mfn2 using OSX-cre or Col1a1-cre did not result in a musculoskeletal phenotype. Where possible, male and female animals were analyzed separately, but small numbers of animals in each group limited statistical power. For other outcomes, where sex was not considered, small sample sizes might still limit the strength of the observation. CONCLUSION: Despite known functional overlap of Mfn1 and Mfn2 in some tissues, and their co-expression in bone, muscle and spinal cord, deletion of Mfn2 using the 8 kB DMP1 promoter uncovered an important non-redundant role for Mfn2 in maintaining the neuromuscular/bone axis.

Effects of different carbon substrates on PAHs fractions and microbial community changes in PAHs-contaminated soils.

Different types of carbon substrates were widely used in soil remediation. However, differences of their impacts and related mechanisms on degradation of polycyclic aromatic hydrocarbons (PAHs) and microbial community structures in contaminated soil still remain unclear. Here, we investigated the effects of corn straw (S), glucose (G), straw combined with glucose (SG), and sodium azide (N, as an abiotic control) on PAHs fractions and bacterial communities in soil. After 70 days' microcosm experiments, total PAHs concentrations were significantly reduced by 30.9%, 19.5% and 44.6% under S, G and SG treatments. Water soluble, acid soluble and residual PAHs under all treatments were significantly decreased after 70 days of incubation, while organically bound PAHs were increased by 11.4%, 22.7% and 36.1% under G, S and SG treatments. Additionally, straw and glucose application increased relative abundance related PAHs-degrading bacteria and the copy numbers of gram-negative (PAHs-RHDα GN) and gram-positive genes (PAHs-RHDα GP) in the contaminated soil. Redundancy analysis (RDA) and Random Forest (RF) indicated that PAHs fractions are crucial factors for biodegradation of PAHs in PAHs-contaminated soils amended with carbon substrates. These suggested that carbon substrates contributed to PAHs conversion from residual PAHs (nonlabile fractions) to organically bound PAHs and thus increased the potential for PAHs conversion to water-soluble and organic acid-soluble PAHs, which were more easy to be utilized by soil microorganisms. This study revealed the new insights of different carbon substrates on degradation and dynamic changes of PAHs fractions and the better potential of combined application of straw and glucose in enhancing degradation of PAHs in PAHs-contaminated soils.

Contradictory tendency of As(V) releasing from Fe-As complexes: Influence of organic and inorganic anions.

The strong ability of ferrihydrite and its aged minerals for fixing arsenate is a key factor in remediating arsenate-polluted environments. It is therefore crucial to clarify the stability of Fe-As complexes and the release conditions for As(V). The As(V) release amount was evaluated and compared in the presence of six representative anions, namely, phosphate, silicate, sulfate, inositol hexaphosphate, citrate, and oxalate. It was found that the As(V) release amount changed with the aging time of ferrihydrite and that this tendency generally followed two rules. These are, longer aging time leads to lower As(V) release (Rule 1), and longer aging time leads to higher As(V) release (Rule 2). Whether Rule 1 or Rule 2 dominated As release depended on the number of surface groups, size of competing anions, and contribution of As(V) re-adsorption. Characterization results using X-ray photoelectron spectroscopy (XPS), Fourier-transform infrared spectroscopy (FTIR), and X-ray diffraction (XRD) provided evidence for the predicted mechanisms of As(V) release under various circumstances. In this work, it was demonstrated that when inorganic anions such as sulfate and silicate are present, ferrihydrite with longer aging time led to decreased As(V) release. When organic anions are present, ferrihydrite with less aging time results in reduced As(V) leaching. For anions such as phosphate, the As(V) release amount in relation to the ferrihydrite aging time depends on the concentration of phosphate ions. Nevertheless, the ligand concentration and As(V) loading rate on ferrihydrite should be simultaneously considered for the rule governing As(V) releasing.

Dominant role of CD47-thrombospondin-1 interactions in myeloma-induced fusion of human dendritic cells: implications for bone disease.

Lytic bone disease in myeloma is characterized by an increase in multinucleate osteoclasts in close proximity to tumor cells. However, the nature of osteoclast precursors and the mechanisms underlying multinuclearity are less understood. Here we show that culture of myeloma cell lines as well as primary myeloma cells with human dendritic cells (DCs) but not monocytes or macrophages leads to spontaneous cell-cell fusion, which then leads to the facile formation of multinucleate bone-resorbing giant cells. Osteoclastogenesis is cell contact dependent, leading to up-regulation of thrombospondin-1 (TSP-1) in DCs. Disruption of CD47-TSP-1 interaction by TSP-1-blocking antibodies or down-regulation of CD47 on tumor cells by RNA interference abrogates tumor-induced osteoclast formation. Blockade of CD47-TSP-1 interactions also inhibits receptor activator for nuclear factor kappaB ligand- and macrophage colony-stimulating factor-induced formation of osteoclasts from human monocytes. Further, TSP-1 blockade attenuates hypercalcemia induced by parathyroid hormone in vivo. These data point to a role for CD47-TSP-1 interactions in regulating cell-fusion events involved in human osteoclast formation. They also suggest that DCs, known to be enriched in myeloma tumors, may be direct precursors for tumor-associated osteoclasts. Disruption of CD47-TSP-1 interactions or preventing the recruitment of DCs to tumors may provide novel approaches to therapy of myeloma bone disease and osteoporosis.

After-effects of straw and straw-derived biochar application on crop growth, yield, and soil properties in wheat (Triticum aestivum L.) -maize (Zea mays L.) rotations: A four-year field experiment.

Research on the after-effects of straw and straw-derived biochar applications on crop growth, yield, and retention of carbon (C) and nitrogen (N) in soil in wheat-maize rotation systems is limited, and has presented inconsistent conclusions. The purpose of this research was to compare the after-effects of straw and straw-derived biochar on wheat (Triticum aestivum L.) and maize (Zea mays L.) growth and yield, and on soil properties. A field experiment was conducted in four consecutive wheat-maize rotation cycles in the Loess Plateau of China under five treatments: CK (control without nitrogen and phosphate fertilizer, straw, or biochar); NP (conventional single application of nitrogen and phosphate chemical fertilizers); SNP (8 t ha-1 wheat straw returned to the field plus fertilizer); B1NP (8 t ha-1 straw-derived biochar plus fertilizer); B2NP (16 t ha-1 straw-derived biochar plus fertilizer). The highest plant height and aboveground biomass for both wheat and maize always occurred with the B2NP treatment for the four study years. Grains per spike/ear and 1000-grain weight for both wheat and maize in B2NP and B1NP were significantly higher than observed for the other treatments. The four-year average wheat yields for NP, SNP, B1NP, and B2NP were 50.5%, 63.1%, 66.3%, and 81.7% greater than for CK, respectively, and the four-year average maize yields were 45.0%, 49.8%, 65.4%, and 72.1% greater than for CK, respectively. The application of straw-derived biochar significantly increased soil organic carbon, total nitrogen, microbial biomass carbon, and nitrogen in the soil surface layer compared with returning straw to the field. Both straw and straw-derived biochar reduced nitrate N leaching. Therefore, using straw-derived biochar to amend soil could be an appropriate practice for sustaining soil fertility and crop yield in wheat-maize rotation systems in the Loess Plateau of China.

Selective deletion of the receptor for CSF1, c-fms, in osteoclasts results in a high bone mass phenotype, smaller osteoclasts in vivo and an impaired response to an anabolic PTH regimen.

The receptor for Colony Stimulating Factor 1 (CSF1), c-fms, is highly expressed on mature osteoclasts suggesting a role for this cytokine in regulating the function of these cells. Consistent with this idea, in vitro studies have documented a variety of effects of CSF1 in mature osteoclasts. To better define the role of CSF1 in these cells, we conditionally deleted c-fms in osteoclasts (c-fms-OC-/-) by crossing c-fmsflox/flox mice with mice expressing Cre under the control of the cathepsin K promoter. The c-fms-OC-/- mice were of normal weight and had normal tooth eruption. However, when quantified by DXA, bone mass was significantly higher in the spine and femur of female knock out mice and in the femurs of male knock out mice. MicroCT analyses of femurs showed that female c-fms-OC-/- mice had significantly increased trabecular bone mass with a similar trend in males and both sexes demonstrated significantly increased trabecular number and reduced trabecular spacing. Histomorphometric analysis of the femoral trabecular bone compartment demonstrated a trend towards increased numbers of osteoclasts, +26% in Noc/BPm and +22% in OcS/BS in the k/o animals but this change was not significant. However, when the cellular volume of osteoclasts was quantified, the c-fms-OC-/- cells were found to be significantly smaller than controls. Mature osteoclasts show a marked spreading response when exposed to CSF1 in a non-gradient fashion. However, osteoclasts freshly isolated from c-fms-OC-/- mice had a near complete abrogation of this response. C-fms-OC-/- mice treated with (1-34)hPTH 80 ng/kg/d in single daily subcutaneous doses for 29 days showed an attenuated anabolic response in trabecular bone compared to wild-type animals. Taken together, these data indicate an important non-redundant role for c-fms in regulating mature osteoclast function in vivo.

An Unanticipated Role for Sphingosine Kinase-2 in Bone and in the Anabolic Effect of Parathyroid Hormone.

Sphingosine-1-phosphate (S1P) is an anabolic clastokine. Sphingosine kinase (SPHK) is the rate-limiting enzyme in S1P production and has 2 isoforms. To evaluate the roles of SPHK1 and SPHK2 in bone, we examined the skeletal phenotype of mice with selective deletion of SPHK1 in osteoclasts (SPHK1-Oc-/-) and mice in which the SPHK2 gene was deleted in all tissues (SPHK2-/-). SPHK1-Oc-/- had normal bone mass. By contrast, SPHK2-/- female mice had a 14% lower spinal bone mineral density (BMD; P < 0.01) and males a 22% lower BMD at the same site (P < 0.001). SPHK2-/- and control mice were subsequently treated either with daily parathyroid hormone [PTH](1-34) or vehicle for 29 days. The response to PTH was significantly attenuated in the SPHK2-/-mice. The mean femoral bone volume to total volume fraction (BV/TV) increased by 24.8% in the PTH-treated female control animals vs 10.6% in the vehicle-treated female controls (P < 0.01). In contrast, in the SPHK2-/- female mice the difference in femoral trabecular BV/TV at the end of treatment was not significant (20.5 vs13.3%, PTH vs vehicle, P = NS). The anabolic response to PTH was significantly attenuated in the spine of male SPHK2-/- mice (29.7% vs 23.1%, PTH vs vehicle, in controls, P < 0.05; 26.9% vs 19.5% PTH vs vehicle in SPHK2-/- mice, P = NS). The spine responded normally in the SPHK2-/- female mice. Interestingly, suppression of sclerostin was blunted in the SPHK2-/- mice when those animals were treated with an anabolic PTH regimen. We conclude that SPHK2 has an important role in mediating both normal bone remodeling and the anabolic response to PTH.

Effect of organic amendments on yield-scaled N2O emissions from winter wheat-summer maize cropping systems in Northwest China.

The effect of dairy manure amendments to agricultural soil on the yield-scaled nitrous oxide (N2O) emissions remains unclear. We hypothesize that an optimum ratio of dairy manure to synthetic fertilizers leads to large nitrogen use efficiency (NUE) and small yield-scaled N2O emissions. The aims of this study were to (1) quantify the variations in the crop yields and N2O emissions from winter wheat-summer maize cropping systems in Northwest China, (2) determine the responses of the NUE and yield-scaled N2O emission to the ratio of organic materials to synthetic fertilizers, and (3) evaluate the relationship between the NUE and yield-scaled N2O emissions. Field measurements were conducted within long- and short-term fertilization experiments between the years of 2014 and 2016. Treatments included synthetic fertilizers, synthetic fertilizers plus crop residues, and synthetic fertilizers plus dairy manure at both sites. The annual grain yields and N2O emissions varied from 13.3 to 18.0 Mg ha-1 and from 1.3 to 3.6 kg N ha-1, respectively, across the treatments. The yield-scaled N2O emissions related negatively to the NUE, suggesting that agronomic aims of improving NUE are an effective approach to mitigate N2O emissions. The ratio of organic materials to synthetic fertilizers was not a significant limit on the NUE and yield-scaled N2O emissions. We conclude that organic amendments appeared to play a minor influence on the promotion of the NUE and N2O mitigation.

The anabolic response to parathyroid hormone is augmented in Rac2 knockout mice.

PTH is the only currently available anabolic therapy for osteoporosis. In clinical practice, the skeletal response to PTH varies and because therapy is limited to 2 yr, approaches to maximize the therapeutic response are desirable. Rac2 is a small GTPase that is expressed only in hematopoietic tissue. Rac2(-/-) mice have a slight increase in bone mass and osteoclasts isolated from these animals have reduced basal resorptive activity and reduced chemotaxis. To evaluate the anabolic response to PTH in Rac2(-/-) mice, we treated 18 Rac2(-/-) and 17 control, age-matched wild-type animals once daily for 28 d with 80 ng/g body weight of h(1-34)PTH. Treatment resulted in significantly greater increments in spinal, femur, and total bone density in the Rac2(-/-) as compared with wild-type animals. Microcomputed tomography analysis demonstrated greater increases in trabecular thickness and cortical thickness in the knockout mice. Interestingly, histomorphometric analysis showed an equivalent increase in osteoblast and osteoclast number in response to PTH treatment in both groups of animals. However, as judged by changes in serum markers, the resorptive response to PTH was impaired. Thus, telopeptide of type 1 collagen was 15.9+/-6.9 ng/ml after PTH treatment in the knockout animals and 26.8+/-11.1 ng/ml in the PTH-treated wild-type group. In contrast, serum aminoterminal propeptide of type 1 collagen and osteocalcin were equivalent in both groups. We conclude that, in the genetic absence of Rac2, the anabolic response to PTH is increased. This appears to be due to attenuated resorptive activity of osteoclasts.

Breast cancer-associated gene 3 interacts with Rac1 and augments NF-κB signaling in vitro, but has no effect on RANKL-induced bone resorption in vivo.

Breast cancer-associated gene 3 (BCA3) is a recently identified adaptor protein whose functions are still being defined. BCA3 has been reported to be an important regulator of nuclear factor-κB (NF-κB) signaling. It has also been reported to interact with the small GTPase, Rac1. Consistent with that observation, in the present study, BCA3 was found to interact with nuclear Rac1 in 293 cells and influence NF-κB signaling. Additional experiments revealed that depending on cell type, BCA3 augmented, attenuated or had no effect on NF-κB signaling in vitro. Since canonical NF-κB signaling is a critical downstream target from activated receptor activator of nuclear factor κB (RANK) that is required for mature osteoclast formation and function, BCA3 was selectively overexpressed in osteoclasts in vivo using the cathepsin K promoter and the response to exogenous receptor activator of nuclear factor κB ligand (RANKL) administration was examined. Despite its ability to augment NF-κB signaling in other cells, transgenic animals injected with high-dose RANKL had the same hypercalcemic response as their wild­type littermates. Furthermore, the degree of bone loss induced by a 2-week infusion of low-dose RANKL was the same in both groups. Combined with earlier studies, the data from our study data indicate that BCA3 can affect NF-κB signaling and that BCA3 plays a cell-type dependent role in this process. The significance of the BCA3/NF-κB interaction in vivo in bone remains to be determined.

Effects of straw and plastic film mulching on greenhouse gas emissions in Loess Plateau, China: A field study of 2 consecutive wheat-maize rotation cycles.

Mulching practices have long been used to modify the soil temperature and moisture conditions and thus potentially improve crop production in dryland agriculture, but few studies have focused on mulching effects on soil gaseous emissions. We monitored annual greenhouse gas (GHG) emissions under the regime of straw and plastic film mulching using a closed chamber method on a typical winter-wheat (Triticum aestivum L. cv Xiaoyan 22) and summer-maize (Zea mays L. cv Qinlong 11) rotation field over two-year period in the Loess Plateau, northwestern China. The following four field treatments were included: T1 (control, no mulching), T2 (4000kgha-1 wheat straw mulching, covering 100% of soil surface), T3 (half plastic film mulching, covering 50% of soil surface), and T4 (complete plastic film mulching, covering 100% of soil surface). Compared with the control, straw mulching decreased soil temperature and increased soil moisture, whereas plastic film mulching increased both soil temperature and moisture. Accordingly, straw mulching increased annual crop yields over both cycles, while plastic film mulching significantly enhanced annual crop yield over cycle 2. Compared to the no-mulching treatment, all mulching treatments increased soil CO2 emission over both cycles, and straw mulching increased soil CH4 absorption over both cycles, but patterns of soil N2O emissions under straw or film mulching are not consistent. Overall, compared to T1, annual GHG intensity was significantly decreased by 106%, 24% and 26% under T2, T3 and T4 over cycle 1, respectively; and by 20%, 51% and 29% under T2, T3 and T4 over cycle 2, respectively. Considering the additional cost and environmental issues associated with plastic film mulching, the application of straw mulching might achieve a balance between food security and GHG emissions in the Chinese Loess Plateau. However, further research is required to investigate the perennial influence of different mulching applications.

Effects of straw and biochar amendments on aggregate stability, soil organic carbon, and enzyme activities in the Loess Plateau, China.

Soil from the Loess Plateau of China is typically low in organic carbon and generally has poor aggregate stability. Application of organic amendments to these soils could help to increase and sustain soil organic matter levels and thus to enhance soil aggregate stability. A field experiment was carried out to evaluate the effect of the application of wheat straw and wheat straw-derived biochar (pyrolyzed at 350-550 °C) amendments on soil aggregate stability, soil organic carbon (SOC), and enzyme activities in a representative Chinese Loess soil during summer maize and winter wheat growing season from 2013 to 2015. Five treatments were set up as follows: no fertilization (CK), application of inorganic fertilizer (N), wheat straw applied at 8 t ha-1 with inorganic fertilizer (S8), and wheat straw-derived biochar applied at 8 t ha-1 (B8) and 16 t ha-1 (B16) with inorganic fertilizer, respectively. Compared to the N treatment, straw and straw-derived biochar amendments significantly increased SOC (by 33.7-79.6%), microbial biomass carbon (by 18.9-46.5%), and microbial biomass nitrogen (by 8.3-38.2%), while total nitrogen (TN) only increased significantly in the B16 plot (by 24.1%). The 8 t ha-1 straw and biochar applications had no significant effects on soil aggregation, but a significant increase in soil macro-aggregates (>2 mm) (by 105.8%) was observed in the B16 treatment. The concentrations of aggregate-associated SOC increased by 40.4-105.8% in macro-aggregates (>2 mm) under straw and biochar amendments relative to the N treatment. No significant differences in invertase and alkaline phosphatase activity were detected among different treatments. However, urease activity was greater in the biochar treatment than the straw treatment, indicating that biochar amendment improved the transformation of nitrogen in the soil. The carbon pool index and carbon management index were increased with straw and biochar amendments, especially in the B16 treatment. In conclusion, application of carbonized crop residue as biochar, especially at a rate of 16 t ha-1, could be a potential solution to recover the depleted SOC and enhance the formation of macro-aggregates in Loess Plateau soils of China.

Soil aggregation and aggregating agents as affected by long term contrasting management of an Anthrosol.

Soil aggregation was studied in a 21-year experiment conducted on an Anthrosol. The soil management regimes consisted of cropland abandonment, bare fallow without vegetation and cropping system. The cropping system was combined with the following nutrient management treatments: control (CONTROL, no nutrient input); nitrogen, phosphorus and potassium (NPK); straw plus NPK (SNPK); and manure (M) plus NPK (MNPK). Compared with the CONTROL treatment, the abandonment treatment significantly increased the formation of large soil macroaggregates (>2 mm) and consequently improved the stability of aggregates in the surface soil layer due to enhancement of hyphal length and of soil organic matter content. However, in response to long-term bare fallow treatment aggregate stability was low, as were the levels of aggregating agents. Long term fertilization significantly redistributed macroaggregates; this could be mainly ascribed to soil organic matter contributing to the formation of 0.5-2 mm classes of aggregates and a decrease in the formation of the >2 mm class of aggregates, especially in the MNPK treatment. Overall, hyphae represented a major aggregating agent in both of the systems tested, while soil organic compounds played significantly different roles in stabilizing aggregates in Anthrosol when the cropping system and the soil management regimes were compared.

Deletion of Rac in Mature Osteoclasts Causes Osteopetrosis, an Age-Dependent Change in Osteoclast Number, and a Reduced Number of Osteoblasts In Vivo.

Rac1 and Rac2 are thought to have important roles in osteoclasts. Therefore, mice with deletion of both Rac1 and Rac2 in mature osteoclasts (DKO) were generated by crossing Rac1(flox/flox) mice with mice expressing Cre in the cathepsin K locus and then mating these animals with Rac2(-/-) mice. DKO mice had markedly impaired tooth eruption. Bone mineral density (BMD) was increased 21% to 33% in 4- to 6-week-old DKO mice at all sites when measured by dual-energy X-ray absorptiometry (DXA) and serum cross-linked C-telopeptide (CTx) was reduced by 52%. The amount of metaphyseal trabecular bone was markedly increased in DKO mice, but the cortices were very thin. Spinal trabecular bone mass was increased. Histomorphometry revealed significant reductions in both osteoclast and osteoblast number and function in 4- to 6-week-old DKO animals. In 14- to 16-week-old animals, osteoclast number was increased, although bone density was further increased. DKO osteoclasts had severely impaired actin ring formation, an impaired ability to generate acid, and reduced resorptive activity in vitro. In addition, their life span ex vivo was reduced. DKO osteoblasts expressed normal differentiation markers except for the expression of osterix, which was reduced. The DKO osteoblasts mineralized normally in vitro, indicating that the in vivo defect in osteoblast function was not cell autonomous. Confocal imaging demonstrated focal disruption of the osteocytic dendritic network in DKO cortical bone. Despite these changes, DKO animals had a normal response to treatment with once-daily parathyroid hormone (PTH). We conclude that Rac1 and Rac2 have critical roles in skeletal metabolism.

The effect of aging on the skeletal response to intermittent treatment with parathyroid hormone.

Little is known about the modifying effects of age on the skeletal response to intermittent treatment with PTH. We therefore compared the response of 63 aged (18 month old) and 61 young-adult (3 month old) C57BL/6 mice to 4 wk of daily sc injections of either vehicle or h(1-34)PTH at a dose of 95 ng/g body weight. The increase in total body bone mineral density (BMD), compared with vehicle-treated animals, was similar in aged and young-adult mice (+5.6 vs. +6.3%). Aged animals demonstrated a greater increase in spinal BMD than their younger counterparts (+12.0 vs. +5.1%, P = 0.01; absolute increment: 57 x 10(-4) vs. 28 x 10(-4) g/cm(2)). Microcomputed tomography analyses in a subset of the vertebrae showed a trend toward higher L5 trabecular bone volume fraction in the PTH-treated aged animals (+40.2 vs. +19.6%). Vertebral histomorphometry demonstrated a greater PTH-induced increase in osteoblast number in aged vs. young-adult animals (694 vs. 396 cells/mm(2)). In contrast, in the femur the PTH-induced increase in BMD tended to be greater in the young-adult than the aged animals, although this did not reach statistical significance (8.1 vs. 4.2%). The numbers of osteoblast progenitors and mineralizing colonies in cultured marrow were unaffected by PTH treatment in either group. We conclude that aging differentially impacts the regional skeletal response to PTH such that the increase in BMD in the spine is augmented, whereas that in the femur is unaffected. Effects on osteoblast progenitor recruitment do not seem to be the basis for these changes.