Heparan Sulfate Organizes Neuronal Synapses through Neurexin Partnerships.

Synapses are fundamental units of communication in the brain. The prototypical synapse-organizing complex neurexin-neuroligin mediates synapse development and function and is central to a shared genetic risk pathway in autism and schizophrenia. Neurexin's role in synapse development is thought to be mediated purely by its protein domains, but we reveal a requirement for a rare glycan modification. Mice lacking heparan sulfate (HS) on neurexin-1 show reduced survival, as well as structural and functional deficits at central synapses. HS directly binds postsynaptic partners neuroligins and LRRTMs, revealing a dual binding mode involving intrinsic glycan and protein domains for canonical synapse-organizing complexes. Neurexin HS chains also bind novel ligands, potentially expanding the neurexin interactome to hundreds of HS-binding proteins. Because HS structure is heterogeneous, our findings indicate an additional dimension to neurexin diversity, provide a molecular basis for fine-tuning synaptic function, and open therapeutic directions targeting glycan-binding motifs critical for brain development.

Haploinsufficiency of GABAA receptor-associated Clptm1 enhances phasic and tonic inhibitory neurotransmission, suppresses excitatory synaptic plasticity, and impairs memory.

The mechanisms utilized by neurons to regulate the efficacy of phasic and tonic inhibition and their impacts on synaptic plasticity and behavior are incompletely understood. Cleft lip and palate transmembrane protein 1 (Clptm1) is a membrane-spanning protein that interacts with multiple γ-aminobutyric acid type A receptor (GABAAR) subunits, trapping them in the endoplasmic reticulum and Golgi network. Overexpression and knockdown studies suggest that Clptm1 modulates GABAAR-mediated phasic inhibition and tonic inhibition as well as activity-induced inhibitory synaptic homeostasis in cultured hippocampal neurons. To investigate the role of Clptm1 in the modulation of GABAARs in vivo, we generated Clptm1 knockout mice. Here, we show that genetic knockout of Clptm1 elevated phasic and tonic inhibitory transmission in both male and female heterozygous mice. Although basal excitatory synaptic transmission was not affected, Clptm1 haploinsufficiency significantly blocked high-frequency stimulation induced long-term potentiation in hippocampal CA3-CA1 synapses. In the hippocampus-dependent contextual fear conditioning behavior task, both male and female Clptm1 heterozygous knockout mice exhibited impairment in contextual fear memory. In addition, LTP and contextual fear memory were rescued by application of L-655,708, a negative allosteric modulator of the extrasynaptic GABAAR α5 subunit. These results suggest that haploinsufficiency of Clptm1 contributes to cognitive deficits through altered synaptic transmission and plasticity by elevation of inhibitory neurotransmission, with tonic inhibition playing a major role.Significance Statement The CLPTM1 gene was originally identified as disrupted in a family with cleft lip and palate. At the molecular level, Clptm1 interacts with multiple GABAA receptor subunits to limit their surface expression. Here, we generated Clptm1 knockout mice to uncover its functions in vivo. Clptm1 not only limited hippocampal inhibitory phasic and tonic transmission, it was required for excitatory synaptic plasticity and hippocampus-dependent cognitive function. A modulator of extrasynaptic GABAA receptors rescued the deficits in plasticity and behavior in Clptm1 heterozygous knockout mice, indicating the importance of tonic inhibition. These findings reveal a role for Clptm1 in balancing inhibitory strength and raise the possibility that disruptions of Clptm1 function may contribute to synaptic and cognitive deficits in neurological diseases.

Neurexin-ß Mediates the Synaptogenic Activity of Amyloid Precursor Protein.

In addition to its role in Alzheimer's disease, amyloid precursor protein (APP) has physiological roles in synapse development and function. APP induces presynaptic differentiation when presented to axons, but the mechanism is unknown. Here we show that APP binds neurexin to mediate this synaptogenic activity. APP specifically binds ß not α neurexins modulated by splice site 4. Binding to neurexin heparan sulfate glycan and LNS protein domains is required for high-affinity interaction and for full-length APP to recruit axonal neurexin. The synaptogenic activity of APP is abolished by triple knockdown of neurexins in hippocampal neurons pooled from male and female rats. Based on these and previous results, our model is that a dendritic-axonal trans dimer of full-length APP binds to axonal neurexin-ß to promote synaptic differentiation and function. Furthermore, soluble sAPPs also bind neurexin-ß and inhibit its interaction with neuroligin-1, raising the possibility that disruption of neurexin function by altered levels of full-length APP and its cleavage products may contribute to early synaptic deficits in Alzheimer's disease.SIGNIFICANCE STATEMENT The prevailing model for the basis of Alzheimer's disease is the amyloid cascade triggered by altered cleavage of amyloid precursor protein (APP). APP also has physiological roles at the synapse, but the molecular basis for its synaptic functions is not well understood. Here, we show that APP binds the presynaptic organizing protein neurexin-ß and that neurexin is essential for the synaptogenic activity of APP. Furthermore, soluble APP forms generated by APP cleavage also bind neurexin-ß and can block interaction with transmembrane synaptogenic ligands of neurexin. These findings reveal a role for neurexin-APP interaction in synapse development and raise the possibility that disruptions of neurexin function may contribute to synaptic and cognitive deficits in the critical early stage of Alzheimer's disease.

Metagenomic Evidence for Cobamide Producers Driving Prokaryotic Co-occurrence Associations and Potential Function in Wastewater Treatment Plants.

Cobamides are required by most organisms but are only produced by specific prokaryotic taxa. These commonly shared cofactors play significant roles in shaping the microbial community and ecosystem function. Wastewater treatment plants (WWTPs) are the world's most common biotechnological systems; knowledge about sharing of cobamides among microorganisms is predicted to be important to decipher the complex microbial relationships in these systems. Herein, we explored prokaryotic potential cobamide producers in global WWTP systems based on metagenomic analyses. A set of 8253 metagenome-assembled genomes (MAGs) were recovered and 1276 (15.5%) of them were identified as cobamide producers, which could potentially be used for the practical biological manipulation of WWTP systems. Moreover, 8090 of the total recovered MAGs (98.0%) contained at least one enzyme family dependent on cobamides, indicating the sharing of cobamides among microbial members in WWTP systems. Importantly, our results showed that the relative abundance and number of cobamide producers improved the complexity of microbial co-occurrence networks and most nitrogen, sulfur, and phosphorus cycling gene abundances, indicating the significance of cobamides in microbial ecology and their potential function in WWTP systems. These findings enhance the knowledge of cobamide producers and their functions in WWTP systems, which has important implications for improving the efficiency of microbial wastewater treatment processes.

The link between the gut microbiome, inflammation, and Parkinson's disease.

As our society ages, the growing number of people with Parkinson's disease (PD) puts tremendous pressure on our society. Currently, there is no effective treatment for PD, so there is an urgent need to find new treatment options. In recent years, increasing studies have shown a strong link between gut microbes and PD. In this review, recent advances in research on gut microbes in PD patients were summarized. Increased potential pro-inflammatory microbes and decreased potential anti-inflammatory microbes are prominent features of gut microbiota in PD patients. These changes may lead to an increase in pro-inflammatory substances (such as lipopolysaccharide and H2S) and a decrease in anti-inflammatory substances (such as short-chain fatty acids) to promote inflammation in the gut. This gut microbiota-mediated inflammation will lead to pathological α-synuclein accumulation in the gut, and the inflammation and α-synuclein can spread to the brain via the microbiota-gut-brain axis, thereby promoting neuroinflammation, apoptosis of dopaminergic neurons, and ultimately the development of PD. This review also showed that therapies based on gut microbiota may have a bright future for PD. However, more research and new approaches are still needed to clarify the causal relationship between gut microbes and PD and to determine whether therapies based on gut microbiota are effective in PD patients. KEY POINTS: • There is a strong association between gut microbes and PD. • Inflammation mediated by gut microbes may promote the development of PD. • Therapies based on the gut microbiome provide a promising strategy for PD prevention.

Relic DNA effects on the estimates of bacterial community composition and taxa dynamics in soil.

DNA-based analyses have become routine methods in soil microbial research, for their high throughput and resolution in characterizing microbial communities. Yet, concerns arise regarding the interference of relic DNA in estimates of viable bacterial community composition and individual taxa dynamics in soils that recovered from post-gamma irradiation. In this study, different soil samples with varying bacterial diversity but similar soil properties were randomly selected. We split each sample into two parts: one part was treated with propidium monoazide (PMA) before DNA extraction, PMA can bind to relic DNA and inhibit PCR amplification by chemical modification; DNA of the other part was extracted following the same process but without PMA pretreatment. Then, soil bacterial abundance was quantified by quantitative polymerase chain reaction, and bacterial community structure was examined by Illumina metabarcoding sequencing of 16S rRNA gene. The results showed that the higher bacterial richness and evenness were estimated when relic DNA was present. The variation trends of bacterial abundance, alpha diversity, and beta diversity remained the same, as reflected by the significant correlations between PMA-treated and -untreated samples (P < 0.05). Moreover, as the mean abundance increased, the reproducibility of detecting individual taxa dynamics between relic DNA present and absent treatments increased. These findings provide empirical evidence that a more even distribution of species abundance derived from relic DNA would result in the overestimation of richness in the total DNA pools and also have crucial implications for guiding proper application of high-throughput sequencing to estimate bacterial community diversity and taxonomic population dynamic. KEY POINTS: • Relic DNA effects on the bacterial community in sterilized soils were assessed. • More even species abundance distribution in relic DNA overestimates true richness. • The reproducibility of individual taxa dynamics increased with their abundance.

The link between increased Desulfovibrio and disease severity in Parkinson's disease.

Parkinson's disease (PD), a progressive and incurable neurodegenerative disease, has taken a huge economic toll and medical burden on our society. Increasing evidence has shown a strong link between PD and the gut microbiome, but studies on the relationship between the gut microbiome and the severity of PD are limited. In this study, 90 fecal samples were collected from newly diagnosed and untreated patients with PD (n = 47) and matched healthy control subjects (n = 43). The 16S rRNA amplicon and shotgun metagenomic sequencing was performed, aiming to uncover the connection between the gut microbiome and disease severity in PD. The results showed that Desulfovibrio was significantly increased in PD compared to healthy controls and positively correlated with disease severity. The increase in Desulfovibrio was mainly driven by enhanced homogeneous selection and weakened drift. Moreover, through metagenome-assembled genomes (MAGs) analysis, a Desulfovibrio MAG (MAG58) was obtained which was also positively correlated with disease severity. MAG58 possesses a complete assimilatory sulfate reduction pathway and a near-complete dissimilatory sulfate reduction pathway to produce hydrogen sulfide which may influence the development of PD. Based on these results, a potential pathogenic mechanism was presented to illustrate how the increased Desulfovibrio accelerates the development of PD by producing excessive hydrogen sulfide. The present study highlighted the vital role of Desulfovibrio in the development of PD, which may provide a new target for the diagnosis and treatment of PD. KEY POINTS: • The evidence for the link between increased Desulfovibrio and disease severity in PD • A Desulfovibrio MAG was obtained which was correlated with PD • A model was presented to illustrate how increased Desulfovibrio causes PD.

Fluoxetine inhibited the activation of A1 reactive astrocyte in a mouse model of major depressive disorder through astrocytic 5-HT2BR/ß-arrestin2 pathway.

BACKGROUND: Fluoxetine, a selective serotonin reuptake inhibitor, has been reported to directly bind with 5-HT2B receptor (5-HT2BR), but the precise mechanisms, whereby fluoxetine confers the anti-depressive actions via 5-HT2BR is not fully understood. Although neuroinflammation-induced A1 astrocytes are involved in neurodegenerative diseases, the role of A1 astrocyte in the pathogenesis and treatment of major depressive disorder (MDD) remains unclear. METHODS: Mice were subjected to chronic mild stress (CMS) for 6 weeks and subsequently treated with fluoxetine for 4 weeks. The depressive-like and anxiety-like behaviors and the activation of A1 reactive astrocyte in hippocampus and cortex of mice were measured. Primary astrocytes were stimulated with A1 cocktail (tumor necrosis factor (TNF)-α, interleukin (IL)-1α and C1q), activated (LPS) microglia-conditioned medium (MCM) or IL-6 for 24 h and the expression of A1-special and A2-special markers were determined using RT-qPCR and western blot. The role of 5-HT2BR in the effects of fluoxetine on A1 reactive astrocyte was measured using 5-HT2BR inhibitor and siRNA in vitro and AAVs in vivo. The functions of downstream signaling Gq protein and ß-arrestins in the effects of fluoxetine on the activation of A1 astrocyte were determined using pharmacological inhibitor and genetic knockout, respectively. RESULTS: In this study, we found that fluoxetine inhibited the activation of A1 reactive astrocyte and reduced the abnormal behaviors in CMS mice, as well as ameliorated A1 astrocyte reactivity under three different stimulators in primary astrocytes. We also showed that astrocytic 5-HT2BR was required in the inhibitory effects of fluoxetine on A1 reactive astrocyte in MDD in vivo and in vitro. We further found that the functions of fluoxetine in the activation of A1 astrocyte were independent of either Gq protein or ß-arrestin1 in vitro. ß-arrestin2 pathway was the downstream signaling of astrocytic 5-HT2BR mediated the inhibitory effects of fluoxetine on A1 astrocyte reactivity in primary astrocytes and CMS mice, as well as the improved roles of fluoxetine in behavioral impairments of CMS mice. CONCLUSIONS: These data demonstrate that fluoxetine restricts reactive A1 astrocyte via astrocytic 5-HT2BR/ß-arrestin2 pathway in a mouse model of MDD and provide a novel therapeutic avenue for MDD.

Adenosine A2A receptor antagonism protects against hyperoxia-induced retinal vascular loss via cellular proliferation.

Retinopathy of prematurity (ROP) remains one of the major causes of blindness in children worldwide. While current ROP treatments are mostly disruptive to reduce proliferative neovascularization by targeting the hypoxic phase, protection against early hyperoxia-induced retinal vascular loss represents an effective therapeutic window, but no such therapeutic strategy is available. Built upon our recent demonstration that the protection against oxygen-induced retinopathy by adenosine A2A receptor (A2A R) antagonists is most effective when administered at the hyperoxia (not hypoxic) phase, we here uncovered the cellular mechanism underlying the A2A R-mediated protection against early hyperoxia-induced retinal vascular loss by reversing the inhibition of cellular proliferation via possibly multiple signaling pathways. Specifically, we revealed two distinct stages of the hyperoxia phase with greater cellular proliferation and apoptosis activities and upregulation of adenosine signaling at postnatal 9 day (P9) but reduced cellular activities and adenosine-A2A R signaling at P12. Importantly, the A2A R-mediated protection at P9 was associated with the reversal of hyperoxia-induced inhibition of progenitor cells at the peripheral retina at P9 and of retinal endothelial proliferation at P9 and P12. The critical role of cellular proliferation in the hyperoxia-induced retinal vascular loss was validated by the increased avascular areas by siRNA knockdown of the multiple signaling molecules involved in modulation of cellular proliferation, including activin receptor-like kinase 1, DNA-binding protein inhibitor 1, and vascular endothelial growth factor-A.

Litter nitrogen concentration changes mediate effects of drought and plant species richness on litter decomposition.

Biodiversity loss, exotic plant invasion and climatic change are three important global changes that can affect litter decomposition. These effects may be interactive and these global changes thus need to be considered simultaneously. Here, we assembled herbaceous plant communities with five species richness levels (1, 2, 4, 8 or 16) and subjected them to a drought treatment (no, moderate or intensive drought) that was factorially combined with an invasion treatment (presence or absence of the non-native Symphyotrichum subulatum). We collected litter of these plant communities and let it decompose for 9 months in the plant communities from which it originated. Drought decreased litter decomposition, while invasion by S. subulatum had little impact. Increasing species richness decreased litter decomposition except under intensive drought. A structural equation model showed that drought and species richness affected litter decomposition indirectly through changes in litter nitrogen concentration rather than by altering quantity and diversity of soil meso-fauna or soil physico-chemical properties. The slowed litter decomposition under high species diversity originated from a sampling effect, specifically from low litter nitrogen concentrations in the two dominant species. We conclude that effects on litter decomposition rates that are mediated by changing concentrations of the limiting nutrient in litter need to be considered when predicting effects of global changes such as plant diversity loss.

Evaluation of GeneXpert EV assay for the rapid diagnosis of enteroviral meningitis: a systematic review and meta-analysis.

BACKGROUND: GeneXpert enterovirus Assay is a PCR-based assay for Enterovirus meningitis diagnosis. However, there is currently no research about the performance of GeneXpert enterovirus assay in the diagnosis of enterovirus meningitis. Thus, a systematic review and meta-analysis is significant on the topic. METHODS: Embase, Cochrane Library, Web of Science, and PubMed were systematically reviewed with retrieval types. Some criteria were used to filter the studies. Only studies published in English, that made a comparison between GeneXpert enterovirus assay and RT-PCR, and could be formulated in a 2*2 table, were included. The quality of the included studies was evaluated by QUADAS-2. The effect of the GeneXpert enterovirus assay was assessed by the Sensitivity, Specificity, Positive Likelihood Ratio, Negative Likelihood Ratio, Diagnosis Odds Ratio, and summary receiver operating characteristic (SROC) curve. Publication bias and heterogeneity were evaluated by the Deeks' funnel test and Bivariate Box plot respectively. RESULTS: 7 studies were recruited in the analysis. The Pooled Sensitivity was 0.96 [95% CI (0.94-0.97)], Pooled Specificity was 0.99 [95% CI (0.98-0.99)], Positive Likelihood Ratio was 130.46 [95% CI (35.79-475.58)], Negative Likelihood Ratio was 0.04 [95% CI (0.02-0.10)], and Diagnostic Odds Ratio was 3648.23 (95% CI [963.99-13,806.72)]. In SROC Curve, Area Under Curve (AUC) was 0.9980, and Q*= 0.9849. In Deeks' funnel test, the P-value was 0.807 (P > 0.05), indicating no publication bias. The Bivariate Box plot indicated no evident heterogeneity. CONCLUSIONS: The GeneXpert enterovirus assay demonstrated high diagnostic accuracy in diagnosing enterovirus meningitis.

Plant Diversity Enhances Soil Fungal Diversity and Microbial Resistance to Plant Invasion.

Interactions and feedbacks between aboveground and belowground biomes are fundamental in controlling ecosystem functions and stability. However, the relationship between plant diversity and soil microbial diversity is elusive. Moreover, it remains unknown whether plant diversity loss will cause the stability of soil microbial communities to deteriorate. To shed light on these questions, we conducted a pot-based experiment to manipulate the plant richness gradient (1, 2, 4, or 8 species) and plant [Symphyotrichum subulatum (Michx.) G. L. Nesom] invasion status. We found that, in the noninvasion treatment, soil fungal diversity significantly and positively correlated with plant diversity, while the relationship between bacterial and plant diversity was not significant. Under plant invasion conditions, the coupling of plant-fungal alpha diversity relationship was enhanced, but the plant-fungal beta diversity relationship was decoupled. We also found significant positive relationships between plant diversity and soil microbial resistance. The observed positive relationships were determined by turnover (species substitution) and nestedness (species loss) processes for bacterial and fungal communities, respectively. Our study demonstrated that plant diversity enhanced soil fungal diversity and microbial resistance in response to plant invasion. This study expands our knowledge about the aboveground-belowground diversity relationship and the diversity-stability relationship.IMPORTANCE Our study newly showed that plant invasion significantly altered relationships between aboveground and belowground diversity. Specifically, plant richness indirectly promoted soil fungal richness through the increase of soil total carbon (TC) without plant invasion, while plant richness had a direct positive effect on soil fungal richness under plant invasion conditions. Our study highlights the effect of plant diversity on soil fungal diversity, especially under plant invasion conditions, and the plant diversity effect on microbial resistance in response to plant invasion. These novel findings add important knowledge about the aboveground-belowground diversity relationship and the diversity-stability relationship.

Arbuscular mycorrhizal fungi and plant diversity drive restoration of nitrogen-cycling microbial communities.

Soil microbial communities, key players of many crucial ecosystem functions, are susceptible to environmental disturbances, which might cause the loss of microbial diversity and functions. However, few ecological concepts and practices have been developed for rescuing stressed soil microbial communities. Here, we manipulated an experiment with or without arbuscular mycorrhizal fungi (AMF) inoculation and at three levels (one, three and six species) of plant diversity to disentangle how the AMF and vegetation rescue soil nitrogen (N) -cycling microbial loop from simulated degraded soil ecosystem. Our results showed that AMF inoculation improved the restoration of soil N-cycling microbial communities. This improved restoration was related to the role of AMF in enhancing interactions within the N-cycling microbial loop. Furthermore, increased plant diversity strengthened the role of AMF in rescuing N-cycling microbial communities. Our findings provide novel insights into the roles of AMF and plant diversity in facilitating the rescue of microbial communities in degraded terrestrial ecosystems.

Functional redundancy and specific taxa modulate the contribution of prokaryotic diversity and composition to multifunctionality.

Observational and experimental evidence has revealed the functional importance of microbial diversity. However, the effects of microbial diversity loss on ecosystem functions are not consistent across studies, which are probably tempered by microbial functional redundancy, specific taxa and functions evaluated. Here we conducted diversity manipulation experiments in two independent soils with distinct prokaryotic communities, and investigated how the initial community traits (e.g., distinct functional redundancy and taxonomic composition) modulate the contribution of prokaryotic diversity loss and composition shift to eight ecosystem functions related to soil nutrient cycling. We found that diversity loss impaired three functions (potential nitrification rate, N2 -fixation activity and phosphatase) and multifunctionality only in the communities with low functional redundancy, but all examined functions were unaffected in the communities with high functional redundancy. All significantly affected functions belonged to specialized functions, while the broad function (soil basal respiration) was unaffected. Moreover, prokaryotic composition explained more functional variation than diversity, which was ascribed to the crucial role of specific taxa that influence particular functions. Taken together, this study provides empirical evidence for identifying the mechanism underlying the ecosystem response to changes in microbial community, with implications for improving the prediction of ecosystem process models and managing microbial communities to promote ecosystem services.

Plasmonic optical trapping of nanoparticles using T-shaped copper nanoantennas.

We demonstrate the optical trapping of single dielectric nanoparticles in a microfluidic chamber using a coupled T-shaped copper plasmonic nanoantenna for studying light-matter interaction. The nanoantenna is composed of two identical copper elements separated by a 50 nm gap and each element is designed with two nanoblocks. Our nanoantenna inherits three different advantages compared to previous plasmonic nanoantennas, which are usually made of gold. First, copper is a very promising plasmonic material with its very similar optical properties as gold. Second, copper is comparably cheap, which is compatible with industry-standard fabrication processes and has been widely used in microelectronics. Third, the trapping area of tweezers is expanded due to the intrinsic Fabry-Perot cavity with two parallel surfaces. We present finite element method simulations of the near-field distribution and photothermal effects. And we perform Maxwell stress tensor simulations of optical forces exerted on an individual nanoparticle in the vicinity of the nanoantenna. In addition, we examine how the existence of an oxide layer of cupric oxide and the heat sink substrate influence the optical trapping properties of copper nanoantennas. This work demonstrates that the coupled T-shaped copper nanoantennas are a promising means as optical nanotweezers to trap single nanoparticles in solution, opening up a new route for nanophotonic devices in optical information processing and on-chip biological sensing.

Rapid isolation method of Saccharomyces cerevisiae based on optically induced dielectrophoresis technique for fungal infection diagnosis.

Saccharomyces cerevisiae(S. cerevisiae) has been classically used as a treatment for diarrhea and diarrhea-related diseases. However, cases of the fungal infections caused by S. cerevisiae have been increasing in the last two decades among immunocompromised patients, while a long time was spent on S. cerevisiae isolation clinically so it was difficult to achieve timely diagnosis the diseases. Here, a novel approach for isolation and selection of S. cerevisiae is proposed by designing a microfluidic chip with an optically induced dielectrophoresis (ODEP) system. S. cerevisiae was isolated from the surroundings by ODEP due to different dielectrophoretic forces. Two special light images were designed and used to block and separate S. cerevisiae, respectively, and several manipulation parameters of ODEP were experimentally optimized to acquire the maximum isolation efficiency of S. cerevisiae. The results on the S. cerevisiae isolation declared that the purity of the S. cerevisiae selected by the method was up to 99.5%±0.05, and the capture efficiency was up to 65.0%±2.5 within 10 min. This work provides a general method to isolate S. cerevisiae as well as other microbial cells with high accuracy and efficiency and paves a road for biological research in which the isolation of high-purity cells is required.

Contrasting patterns and drivers of soil bacterial and fungal diversity across a mountain gradient.

Microbial elevational diversity patterns have been extensively studied, but their shaping mechanisms remain to be explored. Here, we examined soil bacterial and fungal diversity and community compositions across a 3.4 km elevational gradient (consists of five elevations) on Mt. Kilimanjaro located in East Africa. Bacteria and fungi had different diversity patterns across this extensive mountain gradient-bacterial diversity had a U shaped pattern while fungal diversity monotonically decreased. Random forest analysis revealed that pH (12.61% importance) was the most important factor affecting bacterial diversity, whereas mean annual temperature (9.84% importance) had the largest impact on fungal diversity, which was consistent with results obtained from mixed-effects model. Meanwhile, the diversity patterns and drivers of those diversity patterns differ among taxonomic groups (phyla/classes) within bacterial or fungal communities. Taken together, our study demonstrated that bacterial and fungal diversity and community composition responded differently to climate and edaphic properties along an extensive mountain gradient, and suggests that the elevational diversity patterns across microbial groups are determined by distinct environmental variables. These findings enhanced our understanding of the formation and maintenance of microbial diversity along elevation, as well as microbial responses to climate change in montane ecosystems.

Exploring The Psychometric Properties of a Self-Efficacy Scale For High School Students.

In previous studies, researchers have focused on the development and interpretation of measurement tools related to self-efficacy. However, researchers have seldom investigated whether these instruments demonstrate acceptable psychometric properties, including similar item interpretations between subgroups of respondents. The purpose of this study was to explore the extent to which a self-efficacy measure has a consistent interpretation for two self-reported gender subgroups. The researchers utilized Rasch analysis to explore differences in item difficulty between the subgroups. Results suggested differences in item difficulty ordering for certain self-efficacy items. Implications for research and practice are discussed.

Influence of Soil Properties and Aging on Antimony Toxicity for Barley Root Elongation.

The study explored the Sb toxicity by investigating the impacts of 10% and 20% effective concentrations (EC10 and EC20, respectively) of Sb on the inhibition of barley root elongation in 21 Chinese soils with a wide range of physicochemical properties after aging for 3 months. The results demonstrated that various soil properties profoundly influenced the Sb toxicity which was ranged from 201-2506 mg Sb kg-1 to 323-2973 mg Sb kg-1 under EC10 and EC20, respectively. Soil sand fraction was a significant soil factor responsible for elevating Sb bioavailability. The bioavailable Sb concentration accounted for 2.08%-11.94% of total Sb content in all 21 soil samples and the decreased Sb bioavailability in this study was attributed to soil properties including soil clay fraction, amorphous and crystalloid iron, and oxides of manganese and aluminum. The findings would contribute in developing Sb toxicity threshold for establishing standard for Sb regulation in crop production.

Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.

The functions of miR-182-5p in the pathogenesis of diabetic nephropathy (DN) remain largely unclear. Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN. We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target. Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p. The results showed that miR-182-5p was highly expressed in cells isolated from people with DN. In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p. The expression levels of CD2AP mRNA and protein were much lower in the DN group compared with that in the normal group. In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA). Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect. These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.