Longitudinal Gut Microbiota Dysbiosis Underlies Olanzapine-Induced Weight Gain.

Olanzapine is one of the most effective medicines available for stabilizing schizophrenia spectrum disorders. However, it has been reported to show the greatest propensity for inducing body weight gain and producing metabolic side effects, which cause a great burden in patients with psychiatric disorders. Since the gut microbiota has a profound impact on the initiation and development of metabolic diseases, we conducted a longitudinal study to explore its role in olanzapine-induced obesity and metabolic abnormalities. Female Sprague-Dawley rats were treated with different doses of olanzapine, and metabolic and inflammatory markers were measured. Olanzapine significantly induced body weight gain (up to a 2.1-fold change), which was accompanied by hepatic inflammation and increased plasma triglyceride levels (up to a 2.9-fold change), as well as gut microbiota dysbiosis. Subsequently, fuzzy c-means clustering was used to characterize three clusters of longitudinal trajectories for microbial fluctuations: (i) genera continuing to increase, (ii) genera continuing to decrease, and (iii) genera temporarily changing. Among them, Enterorhabdus (r = 0.38), Parasutterella (r = 0.43), and Prevotellaceae UCG-001 (r = 0.52) positively correlated with body weight gain. In addition, two MetaCyc metabolic pathways were identified as associated with olanzapine-induced body weight gain, including the superpathway of glucose and xylose degradation and the superpathway of l-threonine biosynthesis. In conclusion, we demonstrate that olanzapine can directly alter the gut microbiota and rapidly induce dysbiosis, which is significantly associated with body weight gain. This may suggest gut microbiota targets in future studies on metabolic abnormalities caused by olanzapine. IMPORTANCE Olanzapine is one of the most effective second-generation antipsychotics for stabilizing schizophrenia spectrum disorders. However, olanzapine has multiple drug-induced metabolic side effects, including weight gain. This study provides insight to the gut microbiota target in olanzapine-induced obesity. Specifically, we explored the longitudinal gut microbiota trajectories of female Sprague-Dawley rats undergoing olanzapine treatment. We showed that olanzapine treatment causes a dynamic alteration of gut microbiota diversity. Additionally, we identified three genera, Parasutterella, Enterorhabdus, and Prevotellaceae UCG-001, that may play an important role in olanzapine-induced obesity. In this case, the supply or removal of specific elements of the gut microbiota may represent a promising avenue for treatment of olanzapine-related metabolic side effects.

Characterizing serum amino acids in schizophrenic patients: Correlations with gut microbes.

Amino acid abnormalities have been suggested to be a key pathophysiological mechanism in schizophrenia (SZ). Recently, gut microbes were found to be critically involved in mental and metabolic diseases. However, the relationship between serum amino acid levels and gut microbes in SZ is rarely studied. Here, we analyzed serum amino acid levels in 76 untreated SZ patients and 79 healthy controls (HC). Serum levels of 10 amino acids were significantly altered in patients with SZ. We further classified the cut-off values for serum arginine, leucine, glutamine, and methionine levels to distinguish SZ patients from controls. These classifiers were shown to be effective in another validation cohort (49 SZ and 48 HC). The correlation between serum amino acids and clinical symptoms and cognitive functions was also analyzed. Arginine, leucine, glutamine, and methionine levels were significantly correlated with clinical symptoms and cognitive impairments in SZ patients. By metagenome shotgun sequencing of fecal samples, we found that patients with SZ with a low level of serum amino acids have higher richness and evenness of the gut microbiota. At the genus level, the abundances of Mitsuokella and Oscillibacter are significantly abnormal. At the mOTU level, 15 mOTUs in the low-level SZ group were significantly different from the HC group. In addition, Mitsuokella multacida was correlated with glutamine and methionine, respectively. Our research revealed that alterations in serum amino acid levels are critically related to changes in gut microbiota composition in SZ patients. These findings may shed light on new strategies for the diagnosis and treatment of SZ.

Estimation of the bidirectional relationship between schizophrenia and inflammatory bowel disease using the mendelian randomization approach.

It has been reported that schizophrenia (SCZ) and inflammatory bowel disease (IBD) are related. However, whether there is a bidirectional interaction between them remains unclear. The aim of this study was to conduct a bidirectional Mendelian randomization (MR) analysis to elucidate the causal relationship between SCZ and IBD and its subtypes, including Crohn's disease (CD) and ulcerative colitis (UC). Single-nucleotide polymorphisms (SNPs) extracted from the summary data of genome-wide association studies were used as genetic instruments. MR was performed using the inverse-variance-weighted method. The MR-Egger and weighted median methods were used for sensitivity analyses. Analysis using 70 SNPs as genetic instruments showed that SCZ was associated with an increased risk of IBD (OR = 1.14, 95% CI: 1.09-1.20, P = 9.21 × 10-8), CD (OR = 1.16, 95% CI: 1.07-1.25, P = 1.42 × 10-4), and UC (OR = 1.14, 95% CI: 1.07-1.21, P = 2.72 × 10-5). The results of the sensitivity analyses were robust and no evidence of pleiotropy was observed. Bidirectional MR analyses showed no causal effects of IBD, CD, or UC on SCZ. This study suggests that SCZ has causal effects on IBD and its subtypes, whereas IBD has no effect on SCZ. Brain-gut axis interactions may help clarify the causal relationship between SCZ and IBD. However, further studies are needed to elucidate the biological mechanisms behind the brain-gut interactions.

Multi-Omics Analysis Reveals Aberrant Gut-Metabolome-Immune Network in Schizophrenia.

Schizophrenia (SCZ) is associated with several immune dysfunctions, including elevated levels of pro-inflammatory cytokines. Microorganisms and their metabolites have been found to regulate the immune system, and that intestinal microbiota is significantly disturbed in schizophrenic patients. To systematically investigate aberrant gut-metabolome-immune network in schizophrenia, we performed an integrative analysis of intestinal microbiota, serum metabolome, and serum inflammatory cytokines in 63 SCZ patients and 57 healthy controls using a multi-omics strategy. Eighteen differentially abundant metabolite clusters were altered in patients displayed higher cytokine levels, with a significant increase in pro-inflammatory metabolites and a significant decrease in anti-inflammatory metabolites (such as oleic acid and linolenic acid). The bacterial co-abundance groups in the gut displayed more numerous and stronger correlations with circulating metabolites than with cytokines. By integrating these data, we identified that certain bacteria might affect inflammatory cytokines by modulating host metabolites, such as amino acids and fatty acids. A random forest model was constructed based on omics data, and seven serum metabolites significantly associated with cytokines and α-diversity of intestinal microbiota were able to accurately distinguish the cases from the controls with an area under the receiver operating characteristic curve of 0.99. Our results indicated aberrant gut-metabolome-immune network in SCZ and gut microbiota may influence immune responses by regulating host metabolic processes. These findings suggest a mechanism by which microbial-derived metabolites regulated inflammatory cytokines and insights into the diagnosis and treatment of mental disorders from the microbial-immune system in the future.

Association between plasma proteome and childhood neurodevelopmental disorders: A two-sample Mendelian randomization analysis.

BACKGROUND: Childhood neurodevelopmental disorders, including autism spectrum disorder (ASD), attention-deficit hyperactivity disorder (ADHD), and Tourette syndrome (TS), comprise a major cause of health-related disabilities in children. However, biomarkers towards pathogenesis or novel drug targets are still limited. Our study aims to provide a comprehensive investigation of the causal effects of the plasma proteome on ASD, ADHD, and TS using the two-sample Mendelian Randomization (MR) approach. METHODS: Genetic associations with 2994 plasma proteins were selected as exposures and genome-wide association data of ASD, ADHD, TS were utilized as outcomes. MR analyses were carried out using the inverse-variance weighted method, and the MR-Egger and weighted median methods were used for sensitivity analysis. FINDINGS: Using single-nucleotide polymorphisms as instruments, the study suggested increased levels of MAPKAPK3 (OR: 1.09; 95% CI: 1.05-1.13; P = 1.43 × 10-6) and MRPL33 (OR: 1.07; 95% CI: 1.04-1.11; P = 5.37 × 10-6) were causally associated with a higher risk of ASD, and increased MANBA level was associated with a lower risk of ADHD (OR: 0.91; 95% CI: 0.88-0.95; P = 8.97 × 10-6). The causal associations were robust in sensitivity analysis, leave-one-out analysis and Multivariable MR, and no pleiotropy was observed. No significant risk protein was identified for TS. INTERPRETATION: The study findings support the idea that the MAPK/ERK signaling pathway and mitochondrial dysfunction are involved in the pathogenesis of ASD, while a deficiency in beta-mannosidase might play a role in the development of ADHD. FUNDING: Natural Science Basic Research Program of Shaanxi (2021JQ-390).

Stressful events induce long-term gut microbiota dysbiosis and associated post-traumatic stress symptoms in healthcare workers fighting against COVID-19.

OBJECTIVE: The microbiota-gut-brain axis is a key pathway perturbed by prolonged stressors to produce brain and behavioral disorders. Frontline healthcare workers (FHWs) fighting against COVID-19 typically experience stressful event sequences and manifest some mental symptoms; however, the role of gut microbiota in such stress-induced mental problems remains unclear. We investigated the association between the psychological stress of FHW and gut microbiota. METHODS: We used full-length 16S rRNA gene sequencing to characterize the longitudinal changes in gut microbiota and investigated the impact of microbial changes on FHWs' mental status. RESULTS: Stressful events induced significant depression, anxiety, and stress in FHWs and disrupted the gut microbiome; gut dysbiosis persisted for at least half a year. Different microbes followed discrete trajectories during the half-year of follow-up. Microbes associated with mental health were mainly Faecalibacterium spp. and [Eubacterium] eligens group spp. with anti-inflammatory effects. Of note, the prediction model indicated that low abundance of [Eubacterium] hallii group uncultured bacterium and high abundance of Bacteroides eggerthii at Day 0 (immediately after the two-month frontline work) were significant determinants of the reappearance of post-traumatic stress symptoms in FHWs. LIMITATIONS: The lack of metabolomic evidence and animal experiments result in the unclear mechanism of gut dysbiosis-related stress symptoms. CONCLUSION: The stressful event sequences of fighting against COVID-19 induce characteristic longitudinal changes in gut microbiota, which underlies dynamic mental state changes.

Effect of genetic liability to visceral adiposity on stroke and its subtypes: A Mendelian randomization study.

BACKGROUND: Observational studies have found an association between visceral adiposity and stroke. AIMS: The purpose of this study was to investigate the role and genetic effect of visceral adipose tissue accumulation on stroke and its subtypes. METHODS: In this two-sample Mendelian randomization study, genetic variants (221 single nucleotide polymorphisms; P < 5 × 10-8) using as instrumental variables for Mendelian randomization analysis was obtained from a genome-wide association study of visceral adipose tissue. The outcome datasets for stroke and its subtypes were obtained from the MEGASTROKE consortium (up to 67,162 cases and 453,702 controls). Mendelian randomization standard analysis (inverse variance weighted method) was conducted to investigate the effect of genetic liability to visceral adiposity on stroke and its subtypes. Sensitivity analyses (Mendelian randomization-Egger, weighted median, Mendelian randomization-pleiotropy residual sum and outlier) were also utilized to assess horizontal pleiotropy and remove outliers. Multi-variable Mendelian randomization analysis was employed to adjust potential confounders. RESULTS: In the standard Mendelian randomization analysis, genetically determined visceral adiposity (per 1 SD) was significantly associated with a higher risk of stroke (odds ratio (OR) 1.30; 95% confidence interval (CI) 1.21-1.41, P = 1.48× 10-11), ischemic stroke (OR 1.30; 95% CI 1.20-1.41, P = 4.01 × 10-10) and large artery stroke (OR 1.49; 95% CI 1.22-1.83, P = 1.16 × 10-4). The significant association was also found in sensitivity analysis and multi-variable Mendelian randomization analysis. CONCLUSIONS: Genetic liability to visceral adiposity was significantly associated with an increased risk of stroke, ischemic stroke, and large artery stroke. The effect of genetic susceptibility to visceral adiposity on the stroke warrants further investigation.

Mendelian randomization analyses reveal novel drug targets for anorexia nervosa.

Among all psychiatric disorders, anorexia nervosa (AN) has the highest mortality rate. However, there is still no pharmacological therapy for AN. The human plasma proteome may be a great cornerstone for the development of new drugs against AN. Here we performed a Mendelian randomization (MR) analysis to identify causal risk proteins for AN. Exposure data were extracted from a large genome-wide association study (GWAS) of 2994 plasma proteins in 3301 subjects of European descent, while outcome data were obtained from another GWAS of AN (16,992 cases and 55,525 controls of European descent). MR analyses were performed using the inverse-variance weighted (IVW) method and other sensitivity analysis methods. Using single nucleotide polymorphisms as instruments, this study suggested that high TXNDC12 levels were associated with a higher risk of AN (IVW Odd's ratio [OR]: 1.12; 95% confidence interval [CI]: 1.08-1.16; P = 2.35 × 10-10), while another protein ADH1B showed the opposite effect (IVW OR: 0.89; 95% CI: 0.85-0.93; P = 2.99 × 10-7). The causal associations were robust in multivariable models, genome-wide significant models, and with additional MR methods. No pleiotropy was observed. Our findings suggest that TXNDC12 was associated with a high risk of AN, while AHD1B was associated with a low risk of AN. They might both have implications in AN by regulating the brain dopamine reward system. In combination with existing knowledge on AN, these proteins may be novel drug targets for AN treatment.

Systems biological assessment of altered cytokine responses to bacteria and fungi reveals impaired immune functionality in schizophrenia.

Evidence suggests that complex interactions between the immune system and brain have important etiological and therapeutic implications in schizophrenia. However, the detailed cellular and molecular basis of immune dysfunction in schizophrenia remains poorly characterized. To better understand the immune changes and molecular pathways, we systemically compared the cytokine responses of peripheral blood mononuclear cells (PBMCs) derived from patients with schizophrenia and controls against bacterial, fungal, and purified microbial ligands, and identified aberrant cytokine response patterns to various pathogens, as well as reduced cytokine production after stimulation with muramyl dipeptide (MDP) in schizophrenia. Subsequently, we performed single-cell RNA sequencing on unstimulated and stimulated PBMCs from patients and controls and revealed widespread suppression of antiviral and inflammatory programs as well as impaired chemokine/cytokine-receptor interaction networks in various immune cell subpopulations of schizophrenic patients after MDP stimulation. Moreover, serum MDP levels were elevated in these patients and correlated with the course of the disease, suggesting increased bacterial translocation along with disease progression. In vitro assays revealed that MDP pretreatment altered the functional response of normal PBMCs to its re-stimulation, which partially recapitulated the impaired immune function in schizophrenia. In conclusion, we delineated the molecular and cellular landscape of impaired immune function in schizophrenia, and proposed a mutual interplay between innate immune impairment, reduced pathogen clearance, increased MDP translocation along schizophrenia development, and blunted innate immune response. These findings provide new insights into the pathogenic mechanisms that drive systemic immune activation, neuroinflammation, and brain abnormalities in schizophrenia.

Mendelian randomization suggests that head circumference, but not birth weight and length, associates with intelligence.

INTRODUCTION: Birth parameters have long been reported to have a role in human intelligence. However, the causalities reported in previous observational studies were controversial. Our study aims to provide an unbiased investigation of the causal associations between birth parameters and human intelligence using the Mendelian randomization (MR) approach. METHODS: Genetic instrumental variables for MR analyses were extracted from large genome-wide association studies of infant head circumference (N = 10,768), birth length (N = 28,489), and birth weight (N = 321,223). Data for intelligence were obtained from a meta-analysis of genome-wide association studies of 269,867 individuals of the European ancestry. Primary MR analysis was performed using the standard inverse-variance weighted method, and sensitivity analyses were performed using the weighted median, MR-Egger, and MR-PRESSO methods. RESULTS: Using 10 single nucleotide polymorphisms as instrumental variables, we found that 1 standard deviation increase in infant head circumference was associated with 0.14-fold higher scores in intelligence tests (ß = 0.14, 95% confidence interval: 0.09 to 0.18, PIVW =2.05 × 10-9 ). The causal relationship was robust when sensitivity analyses were performed. However, birth length and birth weight had no significant associations with intelligence. CONCLUSION: Our findings suggested infant head circumference, but not birth weight and length were associated with intelligence, which might indicate that brain development rather than general fetal growth was responsible for the development of intelligence.

Causal relationships between genetically determined metabolites and human intelligence: a Mendelian randomization study.

Intelligence predicts important life and health outcomes, but the biological mechanisms underlying differences in intelligence are not yet understood. The use of genetically determined metabotypes (GDMs) to understand the role of genetic and environmental factors, and their interactions, in human complex traits has been recently proposed. However, this strategy has not been applied to human intelligence. Here we implemented a two-sample Mendelian randomization (MR) analysis using GDMs to assess the causal relationships between genetically determined metabolites and human intelligence. The standard inverse-variance weighted (IVW) method was used for the primary MR analysis and three additional MR methods (MR-Egger, weighted median, and MR-PRESSO) were used for sensitivity analyses. Using 25 genetic variants as instrumental variables (IVs), our study found that 5-oxoproline was associated with better performance in human intelligence tests (PIVW = 9.25 × 10-5). The causal relationship was robust when sensitivity analyses were applied (PMR-Egger = 0.0001, PWeighted median = 6.29 × 10-6, PMR-PRESSO = 0.0007), and repeated analysis yielded consistent result (PIVW = 0.0087). Similarly, also dihomo-linoleate (20:2n6) and p-acetamidophenylglucuronide showed robust association with intelligence. Our study provides novel insight by integrating genomics and metabolomics to estimate causal effects of genetically determined metabolites on human intelligence, which help to understanding of the biological mechanisms related to human intelligence.

Pristane promotes anaerobic glycolysis to facilitate proinflammatory activation of macrophages and development of arthritis.

Pristane-induced arthritis (PIA) could be adoptively transferred by splenic T cells in rats, and innate immunity should play critical roles in T cell activation. However, in pre-clinical stage, the activation mechanism of innate cells like macrophages remains unclear. Here we found that PIA was dependent on macrophages since cell depletion alleviated disease severity. Splenic macrophages of PIA rats showed M1 phenotypic shifting. The quantitative proteomics analysis suggested that macrophages initiated metabolic reprogramming with the conversion of aerobic oxidation to glycolysis in response to pristane in vivo. Notably, macrophages treated with pristane showed mitochondrial dysregulation and increased glycolysis flux and enzyme activity. Additionally, TNFα production, strongly associating with the glycolysis enzyme Ldha/Ldhb, could be reduced as glycolysis was inhibited or be enhanced as citrate cycle was blocked. This work provides detailed insights into the molecular mechanisms of pristane-mediated metabolic reprogramming in macrophages and suggests a new therapeutic strategy for arthritic disorders.

Genetically Determined Levels of Serum Metabolites and Risk of Neuroticism: A Mendelian Randomization Study.

BACKGROUND: Neuroticism is a strong predictor for a variety of social and behavioral outcomes, but the etiology is still unknown. Our study aims to provide a comprehensive investigation of causal effects of serum metabolome phenotypes on risk of neuroticism using Mendelian randomization (MR) approaches. METHODS: Genetic associations with 486 metabolic traits were utilized as exposures, and data from a large genome-wide association study of neuroticism were selected as outcome. For MR analysis, we used the standard inverse-variance weighted (IVW) method for primary MR analysis and 3 additional MR methods (MR-Egger, weighted median, and MR pleiotropy residual sum and outlier) for sensitivity analyses. RESULTS: Our study identified 31 metabolites that might have causal effects on neuroticism. Of the 31 metabolites, uric acid and paraxanthine showed robustly significant association with neuroticism in all MR methods. Using single nucleotide polymorphisms as instrumental variables, a 1-SD increase in uric acid was associated with approximately 30% lower risk of neuroticism (OR: 0.77; 95% CI: 0.62-0.95; PIVW = 0.0145), whereas a 1-SD increase in paraxanthine was associated with a 7% higher risk of neuroticism (OR: 1.07; 95% CI: 1.01-1.12; PIVW = .0145). DISCUSSION: Our study suggested an increased level of uric acid was associated with lower risk of neuroticism, whereas paraxanthine showed the contrary effect. Our study provided novel insight by combining metabolomics with genomics to help understand the pathogenesis of neuroticism.

Trends in the incidence and DALYs of schizophrenia at the global, regional and national levels: results from the Global Burden of Disease Study 2017.

AIM: Schizophrenia is a serious health problem worldwide. This systematic analysis aims to quantify the burden of schizophrenia at the global, regional and national levels using the Global Burden of Disease Study 2017 (GBD 2017). METHODS: We collected detailed information on the number of incidence cases, disability-adjusted life years (DALYs) and age-standardised incidence rate (ASIR) and age-standardised rate of DALYs (ASDR) during 1990-2017 from GBD 2017. The estimated annual percentage changes (EAPCs) in the ASIR and in the ASDR were calculated to quantify the temporal trends in the ASIR and ASDR of schizophrenia. RESULTS: Globally there were 1.13 million (95% uncertainty interval [UI] = 1.00 to 1.28) incident schizophrenia cases and 12.66 million (95% UI = 9.48 to 15.56) DALYs due to schizophrenia in 2017. The global ASIR decreased slightly from 1990 to 2017 (EAPC = -0.124, 95% UI = -0.114 to -0.135), while the ASDR was stable. The number of incident cases, DALYs, ASIR and ASDR were higher for males than for females. The incident rate and DALYs rate were highest among those aged 20-29 and 30-54 years, respectively. ASIR and ASDR were highest in East Asia in 2017, at 19.66 (95% UI = 17.72 to 22.00) and 205.23 (95% UI = 153.13 to 253.34), respectively. In 2017, the ASIR was highest in countries with a high-moderate sociodemographic index (SDI) and the ASDR was highest in high-SDI countries. We also found that the EAPC in ASDR was negatively correlated with the ASDR in 1990 (P = 0.001, ρ = -0.23). CONCLUSION: The global burden of schizophrenia remains large and continues to increase, thereby increasing the burden on health-care systems. The reported findings should be useful for resource allocation and health services planning for the increasing numbers of patients with schizophrenia in ageing societies.

Comparative efficacy and acceptability of first-line drugs for the acute treatment of generalized anxiety disorder in adults: A network meta-analysis.

The guide recommends SSRI and SNRI drugs as first-line treatments for generalized anxiety disorder (GAD). Therefore, we aimed to update the evidence using network meta-analysis by comparing the efficacy and acceptability of first-line drugs. The relevant electronic databases were searched for placebo-controlled and head-to-head trials of 11 drugs used for the acute treatment of adults with GAD from 1980 up to January 1, 2019. Data on demographics, clinical, and treatment information were extracted from each eligible study. The primary outcomes were efficacy (quantified as the change in the total score on the Hamilton Anxiety Scale from baseline) and acceptability (quantified as treatment discontinuations due to any cause). Overall, the data on 41 RCTs were sufficient or appropriate for inclusion. In terms of efficacy, all of the drugs except fluoxetine and vortioxetine were more effective than placebo, with the weighted mean difference of the Hamilton Anxiety Scale score ranging between -3.2 (95% credible interval [CrI] = -4.2 to -2.2) for escitalopram and -1·8 (95% CrI = -3.1 to -0.55) for vilazodone. For acceptability, only vilazodone (OR = 1.7, 95% CrI = 1.1 to 2.7) were worse than placebo, others did not show significant differences from placebo. In head-to-head comparisons, vortioxetine showed better acceptability and tolerability but worse efficacy and response rate. In conclusion, most drugs are more effective than placebo, and there are few significant differences between the active drugs and placebo on acceptability. Overall, duloxetine and escitalopram showed better efficacy while vortioxetine showed better acceptability.

Characterization of spectral responses of dissolved organic matter (DOM) for atrazine binding during the sorption process onto black soil.

This study was aim to investigate the interaction between soil-derived dissolved organic matter (DOM) and atrazine as a kind of pesticides during the sorption process onto black soil. According to the experimental data, the adsorption capacity of Soil + DOM, Soil and DOM were 41.80, 31.45 and 9.35 mg kg-1, separately, which indicated that DOM significantly enhanced the adsorption efficiency of atrazine by soil. Data implied that the pseudo-second-order kinetic equation could well explain the adsorption process. The adsorption isotherms (R2 > 0.99) had a satisfactory fit in both Langmuir and Freundlich models. Three-dimensional excitation-emission matrix (3D-EEM), synchronous fluorescence, two-dimensional correlation spectroscopy (2D-COS) and Fourier transform infrared spectroscopy (FT-IR) were selected to analyze the interaction between DOM and atrazine. 3D-EEM showed that humic acid-like substances were the main component of DOM. The fluorescence of DOM samples were gradually quenched with the increased of atrazine concentrations. Synchronous fluorescence spectra showed that static fluorescence quenching was the main quenching process. 2D-COS indicated that the order of the spectral changes were as following: 336 nm > 282 nm. Furthermore, the fluorescence quenching of humic-like fraction occurred earlier than that of protein-like fraction under atrazine surroundings. FT-IR spectra indicated that main compositions of soil DOM include proteins, polysaccharides and humic substances. The findings of this study are significant to reveal DOM played an important role in the environmental fate of pesticides during sorption process onto black soil and also provide more useful information for understanding the interaction between DOM and pesticides by using spectral responses.

[Spatial Variability and Distribution Pattern of Soil Organic Matter in a Mollisol Watershed of China].

Spatial variability of soil organic matter and its distribution pattern are the hot issues of soil scientific research. Selecting Haigouhe watershed as the study area, this paper mainly focused on the spatial variability, distribution pattern and its impact factors of SOM in the surface soil by classical statistics, Geo-statistics and "3S" technology. The results showed that: compared with the other black soil areas, the SOM content in Haigouhe watershed was a little lower, there was a spatial autocorrelation, and a moderate variability. Random factors, such as human activities, cultivation measures and so on, had little impact on the spatial variation, while the structural factors had a dominant function, and there was a remarkable spatial anisotropy of SOM. The SOM content reduced gradually from east to west with the familiar changes of height, so the co-kriging interpolation, selecting elevation as the co-variate, was employed to improve the accuracy. The spatial variability of SOM and its distribution pattern in Haigouhe watershed were greatly affected by topography and land use but weakly influenced by traffic, villages and other social factors. The surrounding environment of the samples would increase the uncertainty of spatial variability and interpolation of SOM and it cannot be ignored in future studies. In summary, it was a significant scientific research to analyze the spatial variability, distribution pattern of SOM and its main impact factors in a mollisol hilly watershed of China.