Reverse diversity-biomass patterns in grasslands are constrained by climates and stoichiometry along an elevational gradient.

Diversity and biomass play an important role in grassland ecosystem functions. However, diversity and biomass are variable because of their high sensitivity to environmental change in natural ecosystems. How plant diversity, biomass, and driving factors (climates, soils, and plants) in grasslands vary with environmental change remains unclear. We conducted intensive fieldwork (≈1000 km transect) on plant diversity, biomass, and associated drivers (i.e., climates, soils, and plants) to identify the patterns of diversity and biomass along an elevational gradient (50-4000 m) in grasslands of southwest China. Grassland biomass decreased significantly, but grassland diversity increased with increasing elevation. Consequently, a significant reverse pattern between biomass and diversity was detected along an elevational gradient. We also observed that the reverse pattern was primarily driven by the shifts in climates (i.e., temperature and precipitation), leaf stoichiometric traits (i.e., leaf N:P ratio), and soil properties (i.e., soil N content) along the elevational gradient. Our results contradicted previous studies on the positive diversity-biomass relationships, suggesting that previous studies might weaken the effects of climatic factors and plant stoichiometry under environmental change. These findings revealed that the reverse pattern between diversity and biomass in grasslands was shaped by the combined effects (climates, plants, soils) in grasslands, thus providing new insights into the debates and predictions on the diversity and biomass in grasslands under climate change.

Effectiveness of yoga therapy for migraine treatment: A meta-analysis of randomized controlled studies.

INTRODUCTION: Yoga therapy may have some potential in treating migraine, and thus this meta-analysis aims to explore the efficacy of yoga therapy for patients with migraine. METHODS: PubMed, EMbase, Web of science, EBSCO and Cochrane library databases have been systematically searched and we included the randomized controlled trials (RCTs) reporting the efficacy of yoga therapy for migraine patients. The outcomes included. RESULTS: This meta-analysis included six RCTs. The results revealed that compared with control group for migraine, yoga therapy was associated with remarkably decreased pain intensity (SMD = -1.21; 95% CI = -2.17 to -0.25; P = 0.01), headache frequency (SMD = -1.43; 95% CI = -2.23 to -0.64; P = 0.0004), headache duration (SMD = -1.03; 95% CI = -1.85 to -0.21; P = 0.01), HIT-6 score (SMD = -2.28; 95% CI = -3.81 to -0.75; P = 0.003) and MIDAS score (SMD = -0.52; 95% CI = -0.77 to -0.27; P < 0.0001). CONCLUSIONS: Yoga therapy may be effective to treat migraine patients, but it should be recommended with caution because of heterogeneity.

Soil enzyme activity and stoichiometry in secondary grasslands along a climatic gradient of subtropical China.

Soil extracellular enzymes plays key roles in ecosystem carbon (C), nitrogen (N), and phosphorus (P) cycling, and are very sensitive to climatic, plant, and edaphic factors. However, the interactive effects of these factors on soil enzyme activities at large spatial scales remain unclear. Here, we investigated the spatial pattern of the activities of five soil hydrolyzing enzymes [ß-D-cellobiohydrolase (CB), ß-1,4-glucosidase (BG), ß-1,4-N-acetyl-glucosaminidase (NAG), L-leucine aminopeptidase (LAP), and acid phosphatase (AP)], and their C:N:P acquisition ratios in relation to plant inputs and edaphic properties across a 600-km climatic gradient in secondary grasslands of subtropical China. The activities of CB, BG, and NAG decreased while that of LAP increased with the increasing mean annual temperature (MAT). The activities of all enzymes did not significantly vary with the mean annual precipitation (MAP). We found that the activities of BG, NAG, and AP were predominately dependent on plant N contents, while the soil LAP activity was tightly related to soil recalcitrant C and N contents. In contrast, the ecoenzymatic C:nutrient (N and P) acquisition ratios increased with increasing MAP and decreasing MAT, primarily due to the increase in plant input at warmer and wetter sites. In addition to climates, plant C inputs, C use efficiency, soil pH, soil organic C, soil C:P, and N:P ratios explained 79% and 72% of the overall variation in ecoenzymatic C:nutrient and P:N acquisition ratios, respectively. The pattern of ecoenzymatic C:N:P acquisition ratios also revealed unexpected N limitation in subtropical grasslands. Overall, our study highlighted the importance of climate in controlling soil biological C, N, and P acquisition activities through its direct and indirect effects on plant inputs and soil edaphic factors, thereby providing useful information for better understanding and predictions of soil C and nutrient cycling in grassland ecosystems at regional scales.

Cinnamaldehyde promotes the defense response in postharvest citrus fruit inoculated with Penicillium digitatum and Geotrichum citri-aurantii.

Induced resistance in harvested fruit and vegetables is a superior strategy to reduce postharvest decay. In the present study, Cinnamaldehyde (CA) was applied to investigate for its induced resistance against Penicillium digitatum and Geotrichum citri-aurantii. The results showed that 5250 mg CA/L wax was effective concentration in inducing the resistance of citrus fruit to green mold and sour rot. Wax+ CA (WCA) reduced significantly green mold and sour rot incidences at different exposure times, with 24 h being the optimal exposure time. The host reactions under infection with different pathogens were similar. During initial exposure, treatment with 5250 mg CA/L wax enhanced significantly the activities of phenylalanine ammonia-lyase (PAL), peroxidase (POD), polyphenol oxidase (PPO), ß-1, 3-glucanase (GLU) and chitinase (CHT) in the presence of direct contact with the pathogen. Simultaneously, WCA induced an increase in total phenolic, flavanone and dihydroflavonol, flavone and flavonol, and lignin contents. Thus, our results suggest that treatment using 5250 mg CA/L wax can be applied early to control diseases by provoking response reactions in citrus fruit.

Differential response of soil CO2 , CH4 , and N2 O emissions to edaphic properties and microbial attributes following afforestation in central China.

Land use change specially affects greenhouse gas (GHG) emissions, and it can act as a sink/source of GHGs. Alterations in edaphic properties and microbial attributes induced by land use change can individually/interactively contribute to GHG emissions, but how they predictably affect soil CO2 , CH4 , and N2 O emissions remain unclear. Here, we investigated the direct and indirect controls of edaphic properties (i.e., dissolved organic carbon [DOC], soil organic C, total nitrogen, C:N ratio, NH4+ -N, NO3- -N, soil temperature [ST], soil moisture [SM], pH, and bulk density [BD]) and microbial attributes (i.e., total phospholipid fatty acids [PLFAs], 18:1ω7c, nitrifying genes [ammonia-oxidizing archaea, ammonia-oxidizing bacteria], and denitrifying genes [nirS, nirK, and nosZ]) over the annual soil CO2 , CH4 , and N2 O emissions from the woodland, shrubland, and abandoned land in subtropical China. Soil CO2 and N2 O emissions were higher in the afforested lands (woodland and shrubland) than in the abandoned land, but the annual cumulative CH4 uptake did not significantly differ among all land use types. The CO2 emission was positively associated with microbial activities (e.g., total PLFAs), while the CH4 uptake was tightly correlated with soil environments (i.e., ST and SM) and chemical properties (i.e., DOC, C:N ratio, and NH4+ -N concentration), but not significantly related to the methanotrophic bacteria (i.e., 18:1ω7c). Whereas, soil N2 O emission was positively associated with nitrifying genes, but negatively correlated with denitrifying genes especially nosZ. Overall, our results suggested that soil CO2 and N2 O emissions were directly dependent on microbial attributes, and soil CH4 uptake was more directly related to edaphic properties rather than microbial attributes. Thus, different patterns of soil CO2 , CH4 , and N2 O emissions and associated controls following land use change provided novel insights into predicting the effects of afforestation on climate change mitigation outcomes.

Asymmetric response of soil methane uptake rate to land degradation and restoration: Data synthesis.

Land degradation and restoration profoundly affect soil CH4 uptake capacity in terrestrial ecosystems. However, a comprehensive assessment of the response of soil CH4 uptake to land degradation and restoration at global scale is not available. Here, we present a global meta-analysis with a database of 228 observations from 83 studies to investigate the effects of land degradation and restoration on the capacity of soil CH4 uptake. We found that land degradation significantly decreased the capacity of soil CH4 uptake, except the conversion of pasture to cropland where the soil CH4 uptake rate showed no response. In contrast, all types of land restoration significantly increased the capacity of soil CH4 uptake. Interestingly, the response of soil CH4 uptake rate to land degradation and restoration was asymmetric: the increased soil CH4 uptake rate in response to the land restoration was smaller compared to the decrease in CH4 uptake rate induced by the land degradation. The effect of land degradation on soil CH4 uptake rate was not dependent on the time since land use change, but the CH4 sink strength increased with the time since land restoration. The response of soil CH4 uptake rate to both land degradation and restoration was predominantly regulated by changes in the soil water-filled pore space, soil bulk density, and pH, whereas alterations in the substrate quantity and quality had negligible effect. Additionally, the effects of land degradation and restoration on soil CH4 uptake were strongly related to the mean annual precipitation and soil texture. Overall, our results provide novel insights for understanding of how land degradation and restoration can affect the CH4 sink strength of upland soils, and more importantly, our findings are beneficial to take measures to enhance the potential of soil CH4 uptake in response to global land use change.

The dynamic expression of aquaporins 1 and 4 in rats with hydrocephalus induced by subarachnoid haemorrhage.

INTRODUCTION: Hydrocephalus is a common complication of subarachnoid haemorrhage (SAH). As transmembrane water channels, aquaporins 1 and 4 (AQP1 and AQP4) are involved in the pathogenesis of hydrocephalus. We aimed to assess the association between the expressions of AQP1 and AQP4 and the severity and duration of hydrocephalus after SAH. MATERIAL AND METHODS: A double haemorrhage model by injection of autologous blood into the cisterna magna was used to induce SAH in rats. Sham rats received the same procedures, but with the injection of normal saline. The SAH group was divided into the SAH with hydrocephalus group and SAH without hydrocephalus group after identifying hydrocephalus histologically. AQP1 and AQP4 in ventricle regions were detected by immunofluorescence, quantitative polymerase chain reaction (qPCR) and western blot. RESULTS: Hydrocephalus was the most severe at day 3 after SAH. AQP1 and AQP4 mRNA and protein levels increased at day 1 and peaked at day 3. The SAH with hydrocephalus group had a higher expression of AQP1 and AQP4 than the SAH without hydrocephalus group. Higher AQP1 levels were found at the apical and basolateral membrane of the choroid plexus epithelium, while higher AQP4 levels were found in the ependymal cells. A positive correlation between the relative lateral ventricle area and the ratio of AQP1/AQP4 proteins was identified. CONCLUSIONS: AQP1 and AQP4 are remarkably correlated with the severity of hydrocephalus induced by SAH. AQP1 and AQP4 are potential drug targets for developing therapeutic strategies against hydrocephalus.

Anti-seasonal submergence dominates the structure and composition of prokaryotic communities in the riparian zone of the Three Gorges Reservoir, China.

Since the completion of Three Gorges Dam in 2008, a large water-level fluctuation zone with anti-seasonal submergence has formed between the elevations of 145 m and 175 m in the Three Gorges Reservoir in China. In addition to hydrological regime, revegetation has also occurred in this water-level fluctuation zone. However, how the hydrological regime and revegetation regulate soil prokaryotic community remains unclear. Here, we investigated soil prokaryotic community structure, diversity and environmental parameters in different flooding zones from two soil layers (0-10 cm and 10-30 cm) at 6 locations along the water-level fluctuation zone from upstream to downstream. The soil prokaryotic diversity tended to decrease from upstream to downstream, and the alpha diversity was higher in the topsoil than in the deep soil at all sites. Flooding significantly enhanced the prokaryotic diversity compared to the control (i.e., permanent dry zone). The soil prokaryotic composition underwent deterministic processes in the upstream sites and stochastic processes in the downstream sites, with stronger stochastic processes in the topsoil than in the deep soil across all sites and elevations. As expected, the soil pH, moisture, NH4+-N, organic carbon and nitrogen were proven to be determinants of the prokaryotic community composition. Changes in plant traits (plant biomass, richness, and carbon content) after revegetation induced by submergence also played an important role in structuring the prokaryotic community. The prokaryotic community exhibited a shorter average path distance (GD) in the flooding zones compared to the control, with the shortest average degree (avgK) and the lowest levels of stability in the longer periodic inundation zones. Overall, our results suggest that soil properties and plant functional traits are critical controls of the prokaryotic community's ability to develop at regional scales and water submergence can likewise be an important factor for variations in the prokaryotic community composition in riparian zones.

Inhibited enzyme activities in soil macroaggregates contribute to enhanced soil carbon sequestration under afforestation in central China.

The fate of soil organic carbon (SOC) sequestered by afforestation is crucial for the mitigation of the anthropogenic climate change but remains largely unclear. This lack of knowledge is particularly true for SOC turnover driven by enzyme activity. Here we measured hydrolase (including ß-glucosidase, α-glucosidase, cellobiohydrolase and xylanase) and oxidase (including polyphenol oxidase and peroxidase) activities in soil aggregates following 30-year afforestation in central China. We also analyzed the relationships of enzyme activities with SOC concentrations, soil C:nitrogen (N) ratios and δ13C values of soil organic pool (removing any carbonates by acid hydrolysis) and stable pool (NaOCl-resistant). Afforestation significantly enhanced soil ß-glucosidase, α-glucosidase and xylanase activities in bulk soil, as well as SOC concentrations in bulk soil and all aggregate fractions compared to those in the open area and cropland. In particular, the woodland increased SOC concentration in >2000 µm macroaggregates by 4.2- and 3.2-fold, compared to the open area and cropland, respectively. Soil hydrolase activities were generally lower but SOC concentrations were higher in >2000 µm macroaggregates compared with those in other aggregate fractions following afforestation. Hydrolase activities were negatively correlated with SOC and C:N ratios in soil aggregate fractions following afforestation. Results of structural equation modeling indicated that the increasingly inhibited hydrolase activities with increasing soil aggregate size indirectly promoted SOC sequestration following afforestation. In addition, both hydrolase and oxidase were positively correlated with δ13C values in the stable pool of the afforested soils, confirming the essential role of enzymes for SOC turnover in soil aggregates following afforestation. Overall, our results highlight the importance of unevenly distributed enzyme activities among soil aggregates in regulating SOC sequestration following afforestation.

The critical role of ABCG1 and PPARγ/LXRα signaling in TLR4 mediates inflammatory responses and lipid accumulation in vascular smooth muscle cells.

Toll-like receptor 4 (TLR4) plays critical roles in vascular inflammation, lipid accumulation and atherosclerosis development. However, the mechanisms underlying these processes are still not well established, especially in vascular smooth muscle cells (VSMCs). ATP-binding cassette transporter G1 (ABCG1) is one of the key genes mediating inflammation and cellular lipid accumulation. The function of TLR4 in regulating the expression of ABCG1 and the underlying molecular mechanisms remain to be elucidated. In this study, we cultured VSMCs from the thoracic aortas of mice and treated the cells with 50 µg/ml oxidized low-density lipoprotein (oxLDL) to activate TLR4 signaling. We observed that activating TLR4 with oxLDL induced inflammatory responses and lipid accumulation in VSMCs. The expression of peroxisome proliferator-activated receptor gamma (PPARγ), liver X receptor alpha (LXRα) and ABCG1 was inhibited by TLR4 activation. However, these effects could be reversed by knocking out TLR4. PPARγ activation by rosiglitazone rescued LXRα and ABCG1 expression and reduced TLR4-induced inflammation and lipid accumulation. Silencing PPARγ expression with a specific small interfering RNA (siRNA) inhibited LXRα and ABCG1 expression and, importantly, enhanced TLR4-induced inflammation and lipid accumulation. In conclusion, ABCG1 expression was down-regulated by TLR4, which induces inflammation and lipid accumulation in VSMCs via PPARγ/LXRα signaling. These findings indicate a novel molecular mechanism underlying TLR4-induced inflammation and lipid accumulation.

PPARγ Inhibits VSMC Proliferation and Migration via Attenuating Oxidative Stress through Upregulating UCP2.

Increasing evidence showed that abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) are common event in the pathophysiology of many vascular diseases, including atherosclerosis and restenosis after angioplasty. Among the underlying mechanisms, oxidative stress is one of the principal contributors to the proliferation and migration of VSMCs. Oxidative stress occurs as a result of persistent production of reactive oxygen species (ROS). Recently, the protective effects of peroxisome proliferator-activated receptor γ (PPARγ) against oxidative stress/ROS in other cell types provide new insights to inhibit the suggests that PPARγ may regulate VSMCs function. However, it remains unclear whether activation of PPARγ can attenuate oxidative stress and further inhibit VSMC proliferation and migration. In this study, we therefore investigated the effect of PPARγ on inhibiting VSMC oxidative stress and the capability of proliferation and migration, and the potential role of mitochondrial uncoupling protein 2 (UCP2) in oxidative stress. It was found that platelet derived growth factor-BB (PDGF-BB) induced VSMC proliferation and migration as well as ROS production; PPARγ inhibited PDGF-BB-induced VSMC proliferation, migration and oxidative stress; PPARγ activation upregulated UCP2 expression in VSMCs; PPARγ inhibited PDGF-BB-induced ROS in VSMCs by upregulating UCP2 expression; PPARγ ameliorated injury-induced oxidative stress and intimal hyperplasia (IH) in UCP2-dependent manner. In conclusion, our study provides evidence that activation of PPARγ can attenuate ROS and VSMC proliferation and migration by upregulating UCP2 expression, and thus inhibit IH following carotid injury. These findings suggest PPARγ may represent a prospective target for the prevention and treatment of IH-associated vascular diseases.

SIRT1 improves VSMC functions in atherosclerosis.

Despite advancements in diagnosis and treatment of cardiovascular diseases (CVDs), the morbidity and mortality of CVDs are still rising. Atherosclerosis is a chronic inflammatory disease contributing to multiple CVDs. Considering the complexity and severity of atherosclerosis, it is apparent that exploring the mechanisms of atherosclerotic formation and seeking new therapies for patients with atherosclerosis are required to overcome the heavy burden of CVDs on the quality and length of life of the global population. Vascular smooth muscle cells (VSMCs) play a dominant role in functional and structural changes of the arterial walls in response to atherogenic factors. Therefore, improvement of VSMC functions will slow down the development of atherosclerosis to a large extent. Given its protective performances on regulation of cholesterol metabolism and inflammatory responses, SIRT1 has long been known as an anti-atherosclerosis factor. In this review, we focus on the effects of SIRT1 on VSMC functions and thereby the development of atherosclerosis.

Impaired SIRT1 promotes the migration of vascular smooth muscle cell-derived foam cells.

The formation of fat-laden foam cells, contributing to the fatty streaks of the plaques of atheroma, is the critical early process in atherosclerosis. The previous study demonstrated that vascular smooth muscle cells (VSMCs) contain a much larger burden of the excess cholesterol in comparison with monocyte-derived macrophages in human coronary atherosclerosis, as the main origin of foam cells. It is noteworthy that VSMC-derived foam cells are deposited in subintima but not media, where VSMCs normally deposit in. Therefore, migration from media to intima is an indispensable step for a VSMC to accrue neutral lipids and form foam cell. Whether this migration occurs paralleled with or prior to the formation of foam cell is still unclear. Herein, the present study was designed to test the VSMC migratory capability in the process of foam cell formation induced by oxidized low-density lipoprotein (oxLDL). In conclusion, we provide evidence that oxLDL induces the VSMC-derived foam cells formation with increased migration ability and MMP-9 expression, which were partly attributed to the impaired SIRT1 and enhanced nuclear factor-kappa B (NF-κB) activity. As activation of transient receptor potential vanilloid type 1 (TRPV1) has been reported to have anti-atherosclerotic effects, we investigated its role in oxLDL-treated VSMC migration. It is found that activating TRPV1 by capsaicin inhibits VSMC foam cell formation and the accompanied migration through rescuing the SIRT1 and suppressing NF-κB signaling. The present study provides evidence that SIRT1 may be a promising intervention target of atherosclerosis, and raises the prospect of TRPV1 in prevention and treatment of atherosclerosis.

Association between serum uric acid levels and cerebral white matter lesions in Chinese individuals.

PURPOSE/AIM OF THE STUDY: We aimed to evaluate the association between serum uric acid (SUA) levels and cerebral white matter lesions (WMLs) in Chinese individuals. MATERIAL AND METHODS: We prospectively identified patients aged 50 years and older in neurology department from July 2014 to March 2015. Both periventricular WMLs (P-WMLs) and deep WMLs (D-WMLs) were identified on magnetic resonance imanging (MRI) scans and the severity was graded using the Fazekas method. Multivariate logistic regression analyses were performed to examine the association between SUA and WMLs. RESULTS: A total of 480 eligible participants were enrolled in this study. SUA level in severe group was much higher than that in mild group (for P-WMLs: 320.21 ± 79.97 vs. 286.29 ± 70.18, p = 0.000; for D-WMLs: 314.71 ± 74.74 vs. 290.07 ± 74.04, p = 0.031). Subgroup analyses showed that higher SUA level was associated with higher severity of P-WMLs in women, but not in male patients. Multivariate logistic regression analyses showed that SUA was still associated with increased risk of higher severity of P-WMLs (OR = 1.003, 95% = 1.000-1.006), but not D-WMLs. CONCLUSION: Elevated SUA level was independently associated with greater odds of higher severity of P-WMLs, particularly in women.

Telmisartan-induced PPARγ activity attenuates lipid accumulation in VSMCs via induction of autophagy.

Foam cell formation is the hallmark of atherosclerosis. Both telmisartan and autophagy protect against the development of atherosclerosis. However, it has yet to be elucidated whether telmisartan prevents vascular smooth muscle cell (VSMC)-derived foam cell formation. Vascular smooth muscle cells isolated from the thoracic aorta of male C57BL/6J mice were used for this study. To induce foam cell formation, primary VSMCs were incubated in 80 µg/ml oxLDL for 24 h. LC3, beclin-1, PPARγ, AMPK, p-AMPK, mTOR and p-mTOR expression were determined via Western blot. Lipid accumulation was evaluated via oil red O staining and intracellular total cholesterol level measurement. Our study demonstrated that telmisartan dose-dependently increased the expression of beclin-1, the LC3II/LC3I ratio and the quantity of GFP-labeled autophagosomes, displaying a peak effect at 10 µM. In control siRNA-transfected VSMCs, telmisartan (10 µM) decreased lipid droplet accumulation and the total cholesterol level significantly. In contrast, in Atg7 siRNA-transfected VSMCs, telmisartan failed to attenuate lipid accumulation. In addition, telmisartan dose-dependently increased the expression of PPARγ and p-AMPK and decreased the expression of p-mTOR. GW9662 attenuated the telmisartan-induced increase in PPARγ expression, the LC3-II/LC3-I ratio and p-AMPK expression and the telmisartan-induced decrease in p-mTOR expression. Compound C restored mTOR activity and abolished the increase in the LC3-II/LC3-I ratio. Rapamycin significantly reduced p-mTOR expression and increased the LC3-II/LC3-I ratio. In conclusion, this study provides evidence that the chronic pharmacological activation of the PPARγ-mediated autophagy pathway using telmisartan may represent a promising therapeutic strategy for atherosclerosis.

Supramolecular self-assembly of monoend-functionalized methoxy poly(ethylene glycol) and α-cyclodextrin: from micelles to hydrogel.

An effective strategy was developed to fabricate a supramolecular hydrogel with the complexation of α-cyclodextrins (α-CDs) and monoend-functionalized low molecular weight methoxy poly(ethylene glycol) (mPEG, Mn=2000) micelles. Hydrophobic cinnamic acid was immobilized on methoxy poly(ethylene glycol) via L-lysine as linker to prepare amphiphilic mPEG. The monoend-functionalized mPEG self-assembled micelles in aqueous solution. The size and size distribution of the micelles were tested by dynamic laser scattering (DLS). The morphology of the micelles was observed by SEM, TEM and AFM. The critical micelle concentration (CMC) was tested and it was 42.5 mg/L. The monodisperse micelles had core-shell structure and the mean diameter was around 40 nanometers. α-cyclodextrins were added in the suspension of micelles to form supramolecular hydrogel with the polypseudorotaxanes complexation. Hydrophilic drug doxorubicin hydrochloride was used as model drug to study the release profile. The results showed that the hydrogel was a promising carrier for drug delivery.