Hypoglycemic TCM formulas (Huangqi-Gegen drug pair) have the potential as an Alzheimer's disease.

BACKGROUND: Alzheimer's disease (AD) is a neurological disorder. There is a considerable unmet medical need among those suffering from it. HYPOTHESIS AND PURPOSE: Given the link between type-2 diabetes mellitus (T2DM) and AD, hypoglycemic traditional Chinese medicine formulas (TCMFs) may be a treatment for AD. We investigated the possibility of identifying anti-AD medicines in hypoglycemic TCMFs and presented another option for the screening of AD medications. STUDY DESIGN AND METHODS: Paralysis of the transgenic Caenorhabditis elegans (C. elegans) strain CL4176 (caused by amyloid beta (Aß)1-42 aggregates) was used to evaluate the anti-AD effect. The toxicity and neurodegeneration induced by neuronal expression of Aß in the transgenic C. elegans strain CL2355 were determined using a 5-hydroxytryptamine (5-HT) assay. The transgenic Aß-expressing strain CL 2006 and transgenic tau-expressing strain BR5270 were used to explore the effect of TCMFs on protein expression in C. elegans using ELISAs. Then, network pharmacology was used to determine the mechanism of action. The Traditional Chinese Medicine Inheritance Support System platform was used to investigate prescription patterns, core drugs, and optimum combinations of hypoglycemic TCMFs for AD. RESULTS: Sixteen hypoglycemic TCMFs prolonged the PT50 (half paralysis time) of the CL4176 strain of C. elegans, reduced the percentage of worms paralyzed. The results of network pharmacology showed that prostaglandin-endoperoxide synthase 2 (PTGS2) and acetylcholine esterase (AChE) are main targets of hypoglycemic TCMFs. Enriched pathway analysis showed that the cholinergic receptor-related pathway was the core pathway of hypoglycemic TCMFs. According to the "four qi and five flavors" system of TCM theory, the main pharmacological qualities were "cold" and "sweet." Through the analysis by TCMISS, we found that Huangqi-Gegen drug pair as the significant Chinese herbs of hypoglycemic TCMFs. The Huangqi-Gegen pairing had the most robust therapeutic effect when delivered at a 2:1 (v/v) ratio. It reduced the paralysis caused by 5-HT, decreased protein expression of AChE and PTGS2, and reduced Aß deposition in the brain of the CL2006 strain of C. elegans. CONCLUSIONS: Huangqi-Gegen is a promising treatment of AD, and its mechanism may be induced by suppressing the protein production of AChE and PTGS2, reducing 5-HT intake, and then decreasing Aß deposition.

Intermedin alleviates diabetic vascular calcification by inhibiting GLUT1 through activation of the cAMP/PKA signaling pathway.

BACKGROUND AND AIMS: Vascular calcification (VC) is regarded as an independent risk factor for cardiovascular events in type 2 diabetic patients. Glucose transporter 1 (GLUT1) involves VC. Intermedin/Adrenomedullin-2 (IMD/ADM2) is a cardiovascular protective peptide that can inhibit multiple disease-associated VC. However, the role and mechanism of IMD in diabetic VC remain unclear. Here, we investigated whether IMD inhibits diabetic VC by inhibiting GLUT1. METHODS AND RESULTS: It was found that plasma IMD concentration was significantly decreased in type 2 diabetic patients and in fructose-induced diabetic rats compared with that in controls. Plasma IMD content was inversely correlated with fasting blood glucose level and VC severity. IMD alleviated VC in fructose-induced diabetic rats. Deficiency of Adm2 aggravated and Adm2 overexpression attenuated VC in high-fat diet-induced diabetic mice. In vitro, IMD mitigated high glucose-induced calcification of vascular smooth muscle cells (VSMCs). Mechanistically, IMD reduced advanced glycation end products (AGEs) content and the level of receptor for AGEs (RAGE). IMD decreased glucose transporter 1 (GLUT1) levels. The inhibitory effect of IMD on RAGE protein level was blocked by GLUT1 knockdown. GLUT1 knockdown abolished the effect of IMD on alleviating VSMC calcification. IMD receptor antagonist IMD17-47 and cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) inhibitor H89 abolished the inhibitory effects of IMD on GLUT1 and VSMC calcification. CONCLUSIONS: These findings revealed that IMD exerted its anti-calcification effect by inhibiting GLUT1, providing a novel therapeutic target for diabetic VC.

Effects of long-term fertilization patterns on bacterial community structure and soil nutrients in dryland of yellow soil.

Understanding the responses of soil bacterial community to long-term fertilization in dryland of yellow soil could provide theoretical basis for establishing scientific fertilization system and cultivating healthy soil. Based on a 25-year long-term fertilization experiment on yellow soil, we collected soil samples from 0-20 cm layer under different fertilization treatments: no fertilization (CK), balanced application of N, P and K fertilizers (NPK), single application of organic fertilizer (M), combined application of constant organic and inorganic fertilizer (MNPK), and 1/2 organic fertilizer instead of 1/2 chemical fertilizer (MNP). Illumina MiSeq high-throughput sequencing technology was used to examine the effects of different fertilization patterns on soil bacterial community structure and soil nutrient content. The main driving factors of soil bacterial community were explored. The results showed that soil pH and organic matter content under treatments with organic fertilizer increased by 11.4%-13.5% and 28.8%-52.0%, respectively, compared to that under NPK treatment. Long-term fertilization did not affect soil bacterial α diversity, but significantly affected soil bacterial ß diversity. Compared with CK and NPK treatment, treatments of M, MNP, and MNPK significantly changed soil bacterial community structure, and increased the relative abundance of Fusobacteria and Anaerobes. Four fertilization treatments increased the relative abundance of Bacteroidetes, and decreased the relative abundance of Actinomyces and Campylobacter, compared to CK. Soil pH was the most important factor affecting soil bacterial community structure. Fertilization-stimulated rare microbial taxa (Pumilomyces and Anaerobes) were more sensitive to changes in different environmental factors and were the main drivers of the formation of community versatility. In conclusion, organic fertilizer improved soil properties and fertility and changed soil bacterial community structure, which are conducive to cultivating healthy soil.

Comprehensive analysis of untargeted metabolomics and lipidomics in girls with central precocious puberty.

Objective: Central precocious puberty (CPP) is a rare condition that causes early sexual development in children. Although the cure is effective, the etiology of central precocious puberty is unclear. Methods: In total, 10 girls with central precocious puberty and same number of age-matched female controls were enrolled. Plasma samples were collected from each participant and subjected to untargeted metabolomics and lipidomics. Student's t-tests were employed to compare the mean of each metabolite and lipid. Furthermore, orthogonal partial least-squares discriminant analysis was conducted and the variable importance in the projection was calculated to identify differentially expressed metabolites or lipids. Subsequent bioinformatics was conducted to investigate the potential function of differentially expressed metabolites and lipids. Results: Fifty-nine differentially expressed metabolites were identified based on the criteria used (variable importance in the projection >1 and a P value < 0.05). Kyoto Encyclopedia Genes and Genome (KEGG) enrichment analysis showed that differentially expressed metabolites were enriched in four pathways: beta-alanine metabolism, histidine metabolism, bile secretion, and steroid hormone biosynthesis. As for the lipidomics, 41 differentially expressed lipids were observed and chain length analysis and lipid saturation analysis yielded similar results. Significant differences between the two groups were only observed in (O-acyl) ω-hydroxy fatty acids (OAHFA). Conclusion: The present study showed that antibiotic overuse, increased meat consumption, and obesity may have potential roles in the development of central precocious puberty in girls. Several metabolites have diagnostic value but further research is required.

Intermedin Alleviates Vascular Calcification in CKD through Sirtuin 3-Mediated Inhibition of Mitochondrial Oxidative Stress.

Vascular calcification (VC) is a common pathophysiological process of chronic kidney disease (CKD). Sirtuin 3 (Sirt3), a major NAD+-dependent protein deacetylase predominantly in mitochondria, is involved in the pathogenesis of VC. We previously reported that intermedin (IMD) could protect against VC. In this study, we investigated whether IMD attenuates VC by Sirt3-mediated inhibition of mitochondrial oxidative stress. A rat VC with CKD model was induced by the 5/6 nephrectomy plus vitamin D3. Vascular smooth muscle cell (VSMC) calcification was induced by CaCl2 and ß-glycerophosphate. IMD1-53 treatment attenuated VC in vitro and in vivo, rescued the depressed mitochondrial membrane potential (MMP) level and decreased mitochondrial ROS levels in calcified VSMCs. IMD1-53 treatment recovered the reduced protein level of Sirt3 in calcified rat aortas and VSMCs. Inhibition of VSMC calcification by IMD1-53 disappeared when the cells were Sirt3 absent or pretreated with the Sirt3 inhibitor 3-TYP. Furthermore, 3-TYP pretreatment blocked IMD1-53-mediated restoration of the MMP level and inhibition of mitochondrial oxidative stress in calcified VSMCs. The attenuation of VSMC calcification by IMD1-53 through upregulation of Sirt3 might be achieved through activation of the IMD receptor and post-receptor signaling pathway AMPK, as indicated by pretreatment with an IMD receptor antagonist or AMPK inhibitor blocking the inhibition of VSMC calcification and upregulation of Sirt3 by IMD1-53. AMPK inhibitor treatment reversed the effects of IMD1-53 on restoring the MMP level and inhibiting mitochondrial oxidative stress in calcified VSMCs. In conclusion, IMD attenuates VC by improving mitochondrial function and inhibiting mitochondrial oxidative stress through upregulating Sirt3.

Plasma Level of Elabela in Patients with Coronary Heart Disease and Its Correlation with the Disease Classification.

This study aimed to evaluate the concentration of plasma elabela (ELA) in patients with coronary heart disease (CHD) and its correlation with the disease classification.We enrolled 238 patients diagnosed by coronary angiography as CHD and 86 controls. The CHD group was divided into three subgroups: stable angina (SA), unstable angina (UAP), and acute myocardial infarction (AMI). The plasma levels of ELA were measured in all participants and compared among different groups. The relationship between ELA and CHD classification was analyzed.ELA levels were markedly higher by 10.71% in patients with CHD than in controls (P < 0.05). The concentration of ELA in UAP and AMI subgroups were higher than in controls and SA subgroup. The former difference was significant (P < 0.05), but the latter was not. In addition, the ELA concentration was not correlated with SYNTAX score, left ventricular ejection fraction, and other biochemical variables.The newfound hormone, ELA, significantly increased in patients with UAP and AMI. There is a tendency that ELA levels might be correlated with CHD classification, but not with lesion severity. ELA may play a role in acute coronary syndrome.

Intermedin1-53 attenuates atherosclerotic plaque vulnerability by inhibiting CHOP-mediated apoptosis and inflammasome in macrophages.

Atherosclerotic plaque vulnerability and rupture increase the risk of acute coronary syndromes. Advanced lesion macrophage apoptosis plays important role in the rupture of atherosclerotic plaque, and endoplasmic reticulum stress (ERS) has been proved to be a key mechanism of macrophage apoptosis. Intermedin (IMD) is a regulator of ERS. Here, we investigated whether IMD enhances atherosclerotic plaque stability by inhibiting ERS-CHOP-mediated apoptosis and subsequent inflammasome in macrophages. We studied the effects of IMD on features of plaque vulnerability in hyperlipemia apolipoprotein E-deficient (ApoE-/-) mice. Six-week IMD1-53 infusion significantly reduced atherosclerotic lesion size. Of note, IMD1-53 lowered lesion macrophage content and necrotic core size and increased fibrous cap thickness and vascular smooth muscle cells (VSMCs) content thus reducing overall plaque vulnerability. Immunohistochemical analysis indicated that IMD1-53 administration prevented ERS activation in aortic lesions of ApoE-/- mice, which was further confirmed in oxidized low-density lipoproteins (ox-LDL) induced macrophages. Similar to IMD, taurine (Tau), a non-selective ERS inhibitor significantly reduced atherosclerotic lesion size and plaque vulnerability. Moreover, C/EBP-homologous protein (CHOP), a pro-apoptosis transcription factor involved in ERS, was significantly increased in advanced lesion macrophages, and deficiency of CHOP stabilized atherosclerotic plaques in AopE-/- mice. IMD1-53 decreased CHOP level and apoptosis in vivo and in macrophages treated with ox-LDL. In addition, IMD1-53 infusion ameliorated NLRP3 inflammasome and subsequent proinflammatory cytokines in vivo and in vitro. IMD may attenuate the progression of atherosclerotic lesions and plaque vulnerability by inhibiting ERS-CHOP-mediated macrophage apoptosis, and subsequent NLRP3 triggered inflammation. The inhibitory effect of IMD on ERS-induced macrophages apoptosis was probably mediated by blocking CHOP activation.

Inhibition of Notch1-mediated inflammation by intermedin protects against abdominal aortic aneurysm via PI3K/Akt signaling pathway.

The Notch1-mediated inflammatory response participates in the development of abdominal aortic aneurysm (AAA). The vascular endogenous bioactive peptide intermedin (IMD) plays an important role in maintaining vascular homeostasis. However, whether IMD inhibits AAA by inhibiting Notch1-mediated inflammation is unclear. In this study, we found Notch intracellular domain (NICD) and hes1 expression were higher in AAA patients' aortas than in healthy controls. In angiotensin II (AngII)-induced AAA mouse model, IMD treatment significantly reduced AAA incidence and maximal aortic diameter. IMD inhibited AngII-enlarged aortas and -degraded elastic lamina, reduced NICD, hes1 and inflammatory factors expression, decreased infiltration of CD68 positive macrophages and the NOD-like receptor family pyrin domain containing 3 protein level. IMD inhibited lipopolysaccharide-induced macrophage migration in vitro and regulated macrophage polarization. Moreover, IMD overexpression significantly reduced CaCl2-induced AAA incidence and down-regulated NICD and hes1 expression. However, IMD deficiency showed opposite results. Mechanically, IMD treatment significantly decreased cleavage enzyme-a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) level. Pre-incubation with IMD17-47 (IMD receptors blocking peptide) and the phosphatidylinositol 3-kinase/protein kinase b (PI3K/Akt) inhibitor LY294002 reversed ADAM10 level. In conclusion, exogenous and endogenous IMD could inhibit the development of AAA by inhibiting Notch1 signaling-mediated inflammation via reducing ADAM10 through IMD receptor and PI3K/Akt pathway.

STAT3 Promotes Schistosome-Induced Liver Injury by Inflammation, Oxidative Stress, Proliferation, and Apoptosis Signal Pathway.

Schistosomiasis is a parasitic helminth disease that can cause organ lesions leading to health damage. During a schistosome infection, schistosome eggs can flow into the liver along the portal vein. Numerous inflammatory cells gather around the eggs, causing granulomas and fibrosis in the liver. In this process, many molecules are involved in the initiation and regulation of the fibrous scar formation. However, the precise molecular mechanisms responsible for the progression of granuloma formation and fibrosis initiation caused by schistosome infection have not been extensively studied. In this study, C57BL/6 wild-type mice and Stat3flox/flox Alb-Cre mice were infected with cercariae of Schistosoma japonicum Liver injury, effector molecule levels, and RNA transcriptome resequencing of liver tissue were detected at 4, 5, and 6 weeks postinfection. We investigated the role of STAT3 (signal transducer and activator of transcription 3) in Schistosoma-induced liver injury in mice. After 6 weeks postinfection, there was obvious liver fibrosis. A sustained pathological process (inflammation, oxidative stress, proliferation, and apoptosis) occurred in S. japonicum-induced liver fibrosis initiation. Meanwhile, we observed activation of the STAT3 pathway in hepatic injury during S. japonicum infection by RNA transcriptome resequencing. Liver deficiency of phospho-STAT3 alleviated infection-induced liver dysfunction, hepatic granuloma formation, and fibrosis initiation. It also promoted STAT3-dependent apoptosis and reduced liver inflammation, oxidative stress, and proliferation. Our results suggest that STAT3 signal pathway and its mediating inflammation, oxidative stress, proliferation, and apoptosis are involved in S. japonicum-induced liver injury and may be a new potential guideline for the treatment of schistosomiasis.

Intermedin alleviates pathological cardiac remodeling by upregulating klotho.

Cardiac remodeling is accompanied by cardiac hypertrophy, fibrosis, dysfunction, and eventually leading to heart failure. Intermedin (IMD), as a paracrine/autocrine peptide, has a protective effect in cardiovascular diseases. In this study, we elucidated the role and the underlying mechanism of IMD in pathological remodeling. Pathological remodeling mouse models were induced by abdominal aorta constriction for 4 weeks or angiotensin II (Ang II) infusion for 2 weeks in wildtype, IMD-overexpression, IMD-knockout and klotho-knockdown mice. Western blot, real-time PCR, histological staining, echocardiography and hemodynamics were used to detect the role of IMD in cardiac remodeling. Cardiac hypertrophy, fibrosis and dysfunction were significantly aggravated in IMD-knockout mice versus wildtype mice, and the expression of klotho was downregulated. Conversely, cardiac remodeling was alleviated in IMD-overexpression mice, and the expression of klotho was upregulated. Hypertension induced by Ang II infusion rather than abdominal aorta constriction was mitigated by IMD. However, the cardioprotective effect of IMD was blocked in klotho-knockdown mice. Similar results were found in cultured neonatal rat cardiomyocytes, which was pretreated with IMD before Ang II stimulation. Mechanistically, IMD inhibited the phosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and the activity of calcineurin to protect against cardiac hypertrophy through upregulating klotho in vivo and in vitro. Furthermore, peroxisome proliferator-activated receptor γ (PPARγ) might mediate IMD upregulating klotho. In conclusion, pathological remodeling may be alleviated by endogenous IMD, which inhibits the expression of calcineurin and p-CaMKII by upregulating klotho via the PPARγ pathway. It suggested that IMD might be a therapeutic target for heart disease.

Intermedin1-53 attenuates aging-associated vascular calcification in rats by upregulating sirtuin 1.

Vascular calcification is a common phenomenon in older adults. Intermedin (IMD) is a cardiovascular bioactive peptide inhibiting vascular calcification. In this study, we aimed to investigate whether IMD1-53 attenuates aging-associated vascular calcification. Vascular calcification was induced by vitamin D3 plus nicotine (VDN) in young and old rats. The calcification in aortas was more severe in old rats treated with VDN than young control rats, and IMD expression was lower. Exogenous administration of IMD1-53 significantly inhibited the calcium deposition in aortas and the osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) in VDN-treated old rats. Moreover, levels of aging-related p16, p21 and ß-galactosidase were all greatly decreased by IMD1-53. These results were further confirmed in rat and human VSMCs in vitro. In addition, IMD-deficient mouse VSMCs showed senescence features coinciding with osteogenic transition as compared with wild-type mouse VSMCs. Mechanistically, IMD1-53 significantly increased the expression of the anti-aging factor sirtuin 1 (sirt1); the inhibitory effects of IMD1-53 on calcification and senescence were blocked by sirt1 knockdown. Furthermore, preincubation with inhibitors of PI3K, AMPK or PKA efficiently blunted the upregulatory effect of IMD1-53 on sirt1. Consequently, IMD1-53 could attenuate aging-associated vascular calcification by upregulating sirt1 via activating PI3K/Akt, AMPK and cAMP/PKA signaling.

Taurine Alleviates Schistosoma-Induced Liver Injury by Inhibiting the TXNIP/NLRP3 Inflammasome Signal Pathway and Pyroptosis.

Schistosomiasis is a parasitic helminth disease that can cause severe inflammatory pathology, leading to organ damage, in humans. During a schistosomal infection, the eggs are trapped in the host liver, and products derived from eggs induce a polarized Th2 cell response, resulting in granuloma formation and eventually fibrosis. Previous studies indicated that the nucleotide-binding oligomerization domain-, leucine-rich repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasome is involved in schistosomiasis-associated liver fibrosis and that taurine could ameliorate hepatic granulomas and fibrosis caused by Schistosoma japonicum infection. Nevertheless, the precise role and molecular mechanism of the NLRP3 inflammasome and the protective effects of taurine in S. japonicum infection have not been extensively studied. In this study, we investigated the role of the NLRP3 inflammasome and the hepatoprotective mechanism of taurine in schistosoma-induced liver injury in mice. NLRP3 deficiency ameliorated S. japonicum-infection-induced hepatosplenomegaly, liver dysfunction, and hepatic granulomas and fibrosis; it also reduced NLRP3-dependent liver pyroptosis. Furthermore, taurine suppressed hepatic thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation in mice with S. japonicum infections, thereby inhibiting the activation of downstream inflammatory mediators such as interleukin-1ß and subsequent pyroptosis. Our results suggest that the TXNIP/NLRP3 inflammasome pathway and mediating pyroptosis are involved in S. japonicum-induced liver injury and may be a potential therapeutic target for schistosomiasis treatment. In addition, taurine may be useful to alleviate or to prevent the occurrence of schistosomiasis-associated liver fibrosis.

[Responses of soil microbial biomass C and P to different long-term fertilization treatments in the yellow paddy soil]. / 黄壤稻田土壤微生物生物量碳磷对长期不同施肥的响应.

To explore the rational fertilization mode to improve the availability of soil phosphorus (P), we analyzed the changes and coupling characteristics of soil carbon (C) and P, microbial biomass C (MBC) and P (MBP) under different fertilization modes with a successive 22-year field experiment in yellow paddy soil. The experiment had 10 treatments, including no fertilization (CK), single application of nitrogen (N), combination of phosphorus and potassium (PK), combination of nitrogen and potassium (NK), combination of nitrogen and phosphorus (NP), combination of nitrogen, phosphorus and potassium (NPK), single application of organic fertilizer (M), and three organic-inorganic fertilizer combinations (1/4M+3/4NP, 0.5MNP, MNPK). The results showed that, compared with CK, the contents of total organic C (TOC), total P (TP), MBC and MBP in N and NK treatments decreased to some extent, while those in PK, NP and NPK treatments increased. Compared with the treatments of no fertilizer and inorganic fertilizer, the contents of TOC, MBC, MBP and MBP/TP ratio in treatments with manure significantly increased, among which M and MPNK treatments showed the strongest enhancement. The treatments with manure had the lowest MBC/MBP ratio, TOC/MBP ratio and MBC/TP ratio, while N treatment had the highest value. MBC, MBP, MBP/TP ratio, MBC/MBP ratio, TOC/MBP ratio and MBC/TP ratio were significantly correlated with TOC and available P, TOC was the direct factor affecting MBC, MBP, and MBP/TP ratio, while available P was the direct factor affecting MBC/MBP ratio, TOC/MBP ratio, MBC/TP ratio. In summary, soil MBP content and the coupling relationship between C and P could effectively distinguish the modes of production with single chemical fertilizer application and manure application, and could be used as biological indices in the evaluation of soil P fertility. Combined application of manure is an effective way to enhance P availability and increase its potential capacity and maintain soil biological health in yellow paddy soil.

Occurrence characteristics of Echinochloa and its response to long-term fertilization in paddy fields of yellow soil.

We studied the characteristics of Echinochloa and its response to variation of rice yield and soil properties under long-term fertilization in paddy field of yellow soil, based on a 23-year long-term fertilization experiment in Scientific Oberving and Experimental Station of Arable Land Conservation and Agricultural Environment (Guizhou), Ministry of Agriculture. The occurrence characteristics of Echinochloa (density, panicle number per plant, totle panicles, seed number per panicle, 1000-seed mass and seed mass per panicle) of ten treatments including CK, N, PK, NK, NP, NPK, 1/4MNP, 1/2MNP, M (manure), MNPK were examined. The results showed that the characteristics of Echinochloa significantly varied with long-term different fertilization. The highest density, panicle number per plant and total panicles of Echinochloa were attained in the MNPK treatment, followed by the 1/4MNP treatment. Compared with the NPK treatment, the density of Echinochloa was significantly decreased in no fertilizer treatment (CK) and unbalanced chemical fertilizer treatments (N, PK, NK, NP). The panicle number per plant significantly increased in organic fertilizer treatments (1/4MNP, 1/2MNP, M, MNPK). Both the density and total panicles of Echinochloa were positively correlated with rice yield. The occurrence characteristics of Echinochloa were positively correlated with soil organic matter, total N, total P, available N, available P and available K. Results from path analysis showed that soil total N had a direct positive effect on panicle number per plant and soil total P content was the main factor affecting the density and total panicles of Echinochloa. Soil available K content was the factor with strongest influence on seed number per panicle and seed mass per panicle. We concluded that the occurrence characteristics of Echinochloa varied with long-term different fertilization. The density, panicle number per plant and total panicles of Echinochloa could be increased with appling cow manure. Soil total P was the direct influencing factor for the variation of density and total panicle of Echinochloa in paddy field of yellow soil.

[Effect of long-term application of NPK fertilizer on maize yield and yellow soil nutrients sustainability in Guizhou, China]. / é•¿æœŸæ°®ç£·é’¾è‚¥é æ–½å¯¹è´µå·žé»„å£¤çŽ‰ç±³äº§é‡å’ŒåœŸå£¤å »åˆ†å¯æŒç»­æ€§çš„å½±å“.

A long-term fertilization field experiment was conducted to investigate the effect of nitrogen (N), phosphorus (P), and potassium (K) fertilizer on maize relative yield, yield-increasing effect and the changes of nutrients in yellow soil in Guizhou Province. Five fertilizer combinations were evaluated, including balanced fertilization (NPK) and nutrient deficiency treatments (N, NK, NP, and PK). The maize relative yield, contribution efficiency of N, P, K fertilizer application, sustainability index of soil N, P, K nutrients, and other indicators were measured. The results revealed that the balanced fertilization (NPK) significantly increased maize yield, and the average yield under each treatment ranked as: NPK>NP>NK>PK>CK. The contribution efficiency and agronomic efficiency of N, P, K fertilizer application was N>P>K. The fertilization dependence was ranked as: combined application of N, P and K>N>P>K. But in the lack of P treatment (NK), the maize relative yield significantly decreased at a speed of 1.4% per year, with the contribution efficiency and fertilization dependence of applied P significantly increasing at a speed of 2.3% per year and 1.4% per year, respectively. Over time, the effect of P fertilizer on maize yield gradually became equal to that of N fertilizer. The pH and soil organic matter content were the lowest in the P-lack treatment (NK), while they were higher in the N-lack treatment (PK). The application of chemical P significantly improved the sustainability index of soil P, but the application of chemical N and K did not significantly change the sustainability index of soil N and K nutrients compared to the N- and K-lack treatments, respectively. In summary, the use of balanced fertilizer application is critical for achieving high maize yield in typical yellow soil regions in Guizhou Province. P and N fertilizers are equally important for improving maize yield, and long-term application of unbalanced chemical fertilizer, especially the lack of P, would not benefit the sustainable use of nutrients in yellow soil.

[Response of Olsen-P to P balance in yellow soil upland of southwestern China under long-term fertilization.] / 长期施肥条件下西南黄壤旱地有效磷对磷盈亏的响应.

Based on a long-term fertilization experiment in Guizhou Province, we explored the relationships between the soil available phosphorus (Olsen-P), soil apparent P balance and P application rate in order to quantify the best application rate of P fertilizer in yellow upland soil of southwestern China. Moreover, the response curve of crop yield to soil Olsen-P was fitted by Mitscherlich equation to determine the critical content of Olsen-P for crop yield. The results showed that the long-term application of P fertilizer could significantly increase the content of soil Olsen-P, and the increasing rates of Olsen-P across different treatments could be mainly explained by the application rate of P fertilizer. Under no-P treatment, the soil P content was in a deficient state for each year, while it displayed a surplus state in the treatments with P fertilizer, and the crop P uptake and P accumulation were found the highest under MNPK treatment. In contrast to single application of chemical fertilizer treatment (NPK), the combined application of organic fertilizer and chemical fertilizer (1/4 M+3/4 NPK, 1/2 M+1/2 NPK) could enhance crop P uptake and improve accumulative P use efficiency. The soil apparent P balance was significantly (P<0.05) correlated with soil Olsen-P. With average P accumulation of 100 kg·hm-2, the soil Olsen-P increased by 16.4, 13.0 , 21.4 , and 5.6 mg·kg-1 in the treatments of MNPK, 1/4 M+3/4 NPK, 1/2 M+1/2 NPK, and NPK, respectively. The result showed that combined application of organic fertilizer and chemical fertilizer could effectively increase the soil Olsen-P content, and the critical value of soil Olsen-P was 22.4 mg·kg-1 in yellow upland soil of southwestern China. The soil P balance and Olsen-P content were significantly (P<0.01) correlated with the annual P application rate. When the amount of average P application was 33.3 kg P·hm-2·a-1, the budgets of soil P balance remained stable, and the application rate of P fertilizer corresponding to the critical value of soil Olsen-P for crop yield was 45.9 kg P·hm-2·a-1. The content of soil Oslen P was mainly affected by the P fertilizer input amount. When the average P application rate was 45.9 kg P·hm-2·a-1, higher crop yield and P fertilizer efficiency would be achieved. When the average P application rate was greater than 45.9 kg P·hm-2·a-1, crop yield showed no response to P fertilizer input, but resulted in a large amount of P surplus in soil, thereby increasing the environmental risk of soil P loss. The long-term application of manure resulted in a higher increase of Olsen-P than the single chemical P ferti-lizer.

[Assessment of accuracy of parents' perception of their 4-36 months old children's picky eating behavior].

OBJECTIVE: To evaluate the accuracy of parents' perception of whether their child is a picky eater and the specific food category the children avoideating according to the food frequency questionnaire. METHODS: This research selected 1 663 infants aged 4-36 months receiving non-diary complimentary food from maternal, infants, nutrition and growth study (MING Study) in 8 Chinese cities in which a combination of systematic cluster random sampling and purposive sampling was used. The general information, dietary status and picky eating status were collected through a self-designed questionnaire from the caregiver of the children. According to the parents' perception, the children were classified into picky/non-picky groups or avoid/non-avoid to a specific food category groups. Mann-Whitney U test was used to compare between the groups. RESULTS: The reported percentage of picky eaters increased from 7.37% in 4-6 months old infants to 36.20% in 25-36 months old infants. Most picky infants in 4-6 months and 7-12 months old infants avoided eating dairy food (25% and 24%); while most picky toddlers aged 13-24 months and 25-36 months avoided eating vegetables (26.92% and 47.46%). The infants aged 4-6 months and 7-12 months who were perceived as picky by their parents took more kinds of food (8 and 19.5 kinds) than those who were not (6 and 18 kinds), while the picky toddlers aged 13-24 months and 25-36 months took fewer kinds of food (28.5 and 34 kinds for picky eaters, 31 and 37 kinds for non-picky eaters). The parents of infants aged 4-6 months judged correctly in every category of food without any statistical significance; the parents of 7-12 months old infants judged correctly only in dairy food and eggs with statistical significance; those of 13-24 months old infants judged correctly in every food category except for vegetables with statistically significant difference in the category of eggs; those of 25-36 months old toddlers misjudged in dairy, beans and grains with no statistically significant difference in every category. CONCLUSION: Parents tend to misjudge their children's picky eating behavior before the first 12 months of the child, and tend to make a more accurate perception after the 12th month.

Review of research on the mechanical properties of the human tooth.

'Bronze teeth' reflect the mechanical properties of natural teeth to a certain extent. Their mechanical properties resemble those of a tough metal, and the gradient of these properties lies in the direction from outside to inside. These attributes confer human teeth with effective mastication ability. Understanding the various mechanical properties of human teeth and dental materials is the basis for the development of restorative materials. In this study, the elastic properties, dynamic mechanical properties (visco-elasticity) and fracture mechanical properties of enamel and dentin were reviewed to provide a more thorough understanding of the mechanical properties of human teeth.

Micromotions and combined damages at the dental implant/bone interface.

Micromotion and fretting damages at the dental implant/bone interface are neglected for the limitation of check methods, but it is particularly important for the initial success of osseointegration and the life time of dental implant. This review article describes the scientific documentation of micromotion and fretting damages on the dental implant/bone interface. The fretting amplitude is less than 30 µm in vitro and the damage in the interface is acceptable. While in vivo, the micromotion's effect is the combination of damage in tissue level and the real biological reaction.

[In vitro anti-tumor effect of methotrexate modified by peptide].

This study is to investigate the anti-tumor effect in vitro of methotrexate modified by LH-RH peptide (LH-RH-MTX). LH-RH receptors highly expressing MCF-7 human breast carcinoma cell line and lowly expressing K562 human erythroleukemia cell line were served as the tested cells. The cell proliferation inhibition rates of LH-RH-MTX were detected by MTT colorimetric assay. The effects of LH-RH-MTX on the cell cycle and apoptosis rates were detected by flow cytometry. The inhibition rate of LH-RH-MTX on MCF-7 cells was much higher than that on K562 cells, and the inhibition rate of LH-RH-MTX on MCF-7 cells was much higher than that of free MTX at the same concentration. The inhibition rate of LH-RH-MTX on rat bone marrow mononuclear cells was less than that of free MTX. The number of MCF-7 cells in S phase increased after administration of LH-RH-MTX. The apoptosis rate of LH-RH-MTX group significantly increased compared with that of the control group and MTX group. The relative expression of LHRHR mRNA of LH-RH-MTX group markedly decreased compared with that of the control group and MTX group. LH-RH-MTX is realizable to reduce drug side effects, increase the therapeutic index and achieve tumor-targeted therapy.