Identification of a Novel Streptomyces sp. Strain HU2014 Showing Growth Promotion and Biocontrol Effect Against Rhizoctonia spp. in Wheat.

Wheat sharp eyespot is a serious disease caused by the phytopathogens Rhizoctonia cerealis and R. solani. Some species in the genus Streptomyces have been identified as potential biocontrol agents against phytopathogens. In this investigation, the physiological, biochemical, phylogenetic, and genomic characteristics of strain HU2014 indicate that it is a novel Streptomyces sp. most closely related to Streptomyces albireticuli. Strain HU2014 exhibited strong antifungal activity against R. cerealis G11 and R. solani YL-3. Ultraperformance liquid chromatography-mass spectrometry on the four extracts from the extracellular filtrate of strain HU2014 identified 10 chemical constituents in the Natural Products Atlas with high match levels (more than 90%). In an antifungal efficiency test on wheat sharp eyespot, two extracts significantly reduced the lesion areas on bean leaves infected by R. solani YL-3. The drenching of wheat in pots with spore suspension of strain HU2014 demonstrated a control efficiency of 65.1% against R. cerealis G11 (compared with 66.9% when treated by a 30% hymexazol aqueous solution). Additionally, in vitro and pot experiments demonstrated that strain HU2014 can produce indoleacetic acid, siderophores, extracellular enzymes, and solubilized phosphate, and it can promote plant growth. We conclude that strain HU2014 could be a valuable microbial resource for growth promotion of wheat and biological control of wheat sharp eyespot.

Regulation of G6PD acetylation by SIRT2 and KAT9 modulates NADPH homeostasis and cell survival during oxidative stress.

Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme in the pentose phosphate pathway (PPP) and plays an essential role in the oxidative stress response by producing NADPH, the main intracellular reductant. G6PD deficiency is the most common human enzyme defect, affecting more than 400 million people worldwide. Here, we show that G6PD is negatively regulated by acetylation on lysine 403 (K403), an evolutionarily conserved residue. The K403 acetylated G6PD is incapable of forming active dimers and displays a complete loss of activity. Knockdown of G6PD sensitizes cells to oxidative stress, and re-expression of wild-type G6PD, but not the K403 acetylation mimetic mutant, rescues cells from oxidative injury. Moreover, we show that cells sense extracellular oxidative stimuli to decrease G6PD acetylation in a SIRT2-dependent manner. The SIRT2-mediated deacetylation and activation of G6PD stimulates PPP to supply cytosolic NADPH to counteract oxidative damage and protect mouse erythrocytes. We also identified KAT9/ELP3 as a potential acetyltransferase of G6PD. Our study uncovers a previously unknown mechanism by which acetylation negatively regulates G6PD activity to maintain cellular NADPH homeostasis during oxidative stress.

The Relationship between Japanese Encephalitis and Environmental Factors in China Explored Using National Surveillance Data.

Japanese encephalitis (JE) is a serious public health issue. This study was undertaken to better understand the relationship between JE distribution and environmental factors in China. JE data from 2005 to 2010 were retrieved from National Notifiable Disease Report System. ArcGIS, remote sensing techniques, and R software was used to exhibit and explore the relationship between JE distribution and environmental factors. Our results indicated that JE cases were mostly concentrated in warm-temperate, semitropical and tropical zones with annual precipitation > 400 mm; Broad-leaved evergreen forest, shrubs, paddy field, irrigated land, dryland, evergreen coniferous forest, and shrubland were risk factors for JE occurrence, and the former five were risk factors for counties with high JE incidence. These findings will inform the effective allocation of limited health resources such as intensive vaccination, surveillance and training in areas with high environmental risk factors.

Identification and control of a poliomyelitis outbreak in Xinjiang, China.

BACKGROUND: The last case of infection with wild-type poliovirus indigenous to China was reported in 1994, and China was certified as a poliomyelitis-free region in 2000. In 2011, an outbreak of infection with imported wild-type poliovirus occurred in the province of Xinjiang. METHODS: We conducted an investigation to guide the response to the outbreak, performed sequence analysis of the poliovirus type 1 capsid protein VP1 to determine the source, and carried out serologic and coverage surveys to assess the risk of viral propagation. Surveillance for acute flaccid paralysis was intensified to enhance case ascertainment. RESULTS: Between July 3 and October 9, 2011, investigators identified 21 cases of infection with wild-type poliovirus and 23 clinically compatible cases in southern Xinjiang. Wild-type poliovirus type 1 was isolated from 14 of 673 contacts of patients with acute flaccid paralysis (2.1%) and from 13 of 491 healthy persons who were not in contact with affected persons (2.6%). Sequence analysis implicated an imported wild-type poliovirus that originated in Pakistan as the cause of the outbreak. A public health emergency was declared in Xinjiang after the outbreak was confirmed. Surveillance for acute flaccid paralysis was enhanced, with daily reporting from all public and private hospitals. Five rounds of vaccination with live, attenuated oral poliovirus vaccine (OPV) were conducted among children and adults, and 43 million doses of OPV were administered. Trivalent OPV was used in three rounds, and monovalent OPV type 1 was used in two rounds. The outbreak was stopped 1.5 months after laboratory confirmation of the index case. CONCLUSIONS: The 2011 outbreak in China showed that poliomyelitis-free countries remain at risk for outbreaks while the poliovirus circulates anywhere in the world. Global eradication of poliomyelitis will benefit all countries, even those that are currently free of poliomyelitis.

Regulation of egg quality and lipids metabolism by Zinc Oxide Nanoparticles.

This investigation was designed to explore the effects of Zinc Oxide Nanoparticles (ZnO NP) on egg quality and the mechanism of decreasing of yolk lipids. Different concentration of ZnO NP and ZnSO4 were used to treat hens for 24 weeks. The body weight and egg laying frequency were recorded and analyzed. Albumen height, Haugh unit, and yolk color score were analyzed by an Egg Multi Tester. Breaking strength was determined by an Egg Force Reader. Egg shell thickness was measured using an Egg Shell Thickness Gouge. Shell color was detected by a spectrophotometer. Egg shape index was measured by Egg Form Coefficient Measuring Instrument. Albumen and yolk protein was determined by the Kjeldahl method. Amino acids were determined by an amino acids analyzer. Trace elements Zn, Fe, Cu, and P (mg/kg wet mass) were determined in digested solutions using Inductively Coupled Plasma-Optical Emission Spectrometry. TC and TG were measured using commercial analytical kits. Yolk triglyceride, total cholesterol, pancreatic lipase, and phospholipids were determined by appropriate kits. ß-carotene was determined by spectrophotometry. Lipid metabolism was also investigated with liver, plasma, and ovary samples. ZnO NP did not change the body weight of hens during the treatment period. ZnO NP slowed down egg laying frequency at the beginning of egg laying period but not at later time. ZnO NP did not affect egg protein or water contents, slightly decreased egg physical parameters (12 to 30%) and trace elements (20 to 35%) after 24 weeks treatment. However, yolk lipids content were significantly decreased by ZnO NP (20 to 35%). The mechanism of Zinc oxide nanoparticles decreasing yolk lipids was that they decreased the synthesis of lipids and increased lipid digestion. These data suggested ZnO NP affected egg quality and specifically regulated lipids metabolism in hens through altering the function of hen's ovary and liver.

Association between cardiac changes and stress, and the effect of peroxisome proliferator-activated receptor-γ on stress-induced myocardial injury in mice.

This study was aimed to investigate the effect of stress induced by high-intensity exercises on the cardiovascular system. In the epidemiological investigation, 200 subjects (test group) engaged in special high-intensity exercises, and 97 who lived and worked in the same environment and conditions as those in the test group, but did not participate in the exercises served as controls. In the second part of the study, 50 mice were randomly divided into control group, exhaustive swimming group, white noise group, exhaustive swimming plus white noise group, and pioglitazone intervention group. The results showed that the plasma concentrations of the myocardial injury markers heart fatty acid-binding protein (H-FABP), C-reactive protein (CRP), ß-endorphin (ß-EP) and levels of psychological stress were significantly increased in test group as compared with control group; special high-intensity exercises resulted in a significant elevation of the incidence of cardiac arrhythmias. Animal experiments showed that the plasma levels of corticosterone (CORT) and troponin I (TnI) were raised while the level of SOD was reduced in exhaustive swimming group, white noise group, and exhaustive swimming plus white noise group. The expression levels of PPARγ mRNA and protein were decreased in myocardial tissues in these groups as well. HE staining showed no remarkable change in myocardial tissues in all the groups. Treatment with pioglitazone significantly decreased the plasma levels of TnI and CORT, while increased the level of SOD and the expression levels of PPARγ mRNA and protein. It was concluded that the high-intensity exercises may induce a heavy physical and psychological stress and predispose the subjects to accumulated fatigue and sleep deprivation; high-intensity exercises also increases the incidence of arrhythmias and myocardial injury. PPARγ may be involved in the physical and psychological changes induced by high-intensity exercises.

Fever with thrombocytopenia associated with a novel bunyavirus in China.

BACKGROUND: Heightened surveillance of acute febrile illness in China since 2009 has led to the identification of a severe fever with thrombocytopenia syndrome (SFTS) with an unknown cause. Infection with Anaplasma phagocytophilum has been suggested as a cause, but the pathogen has not been detected in most patients on laboratory testing. METHODS: We obtained blood samples from patients with the case definition of SFTS in six provinces in China. The blood samples were used to isolate the causal pathogen by inoculation of cell culture and for detection of viral RNA on polymerase-chain-reaction assay. The pathogen was characterized on electron microscopy and nucleic acid sequencing. We used enzyme-linked immunosorbent assay, indirect immunofluorescence assay, and neutralization testing to analyze the level of virus-specific antibody in patients' serum samples. RESULTS: We isolated a novel virus, designated SFTS bunyavirus, from patients who presented with fever, thrombocytopenia, leukocytopenia, and multiorgan dysfunction. RNA sequence analysis revealed that the virus was a newly identified member of the genus phlebovirus in the Bunyaviridae family. Electron-microscopical examination revealed virions with the morphologic characteristics of a bunyavirus. The presence of the virus was confirmed in 171 patients with SFTS from six provinces by detection of viral RNA, specific antibodies to the virus in blood, or both. Serologic assays showed a virus-specific immune response in all 35 pairs of serum samples collected from patients during the acute and convalescent phases of the illness. CONCLUSIONS: A novel phlebovirus was identified in patients with a life-threatening illness associated with fever and thrombocytopenia in China. (Funded by the China Mega-Project for Infectious Diseases and others.).

Enhanced surveillance of acute flaccid paralysis following importation of wild poliovirus in Xinjiang Uygur Autonomous Region, China.

BACKGROUND: After being polio free for more than 10 years, an outbreak occurred in China in 2011 in Xinjiang Uygur Autonomous Region (Xinjiang) following the importation of wild poliovirus (WPV) originating from neighboring Pakistan. METHODS: To strengthen acute flaccid paralysis (AFP) surveillance in Xinjiang, "zero case daily reporting" and retrospective searching of AFP cases were initiated after the confirmation of the WPV outbreak. To pinpoint all the polio cases in time, AFP surveillance system was expanded to include persons of all ages in the entire population in Xinjiang. RESULTS: Totally, 578 AFP cases were reported in 2011 in Xinjiang, including 21 WPV cases, 23 clinical compatible polio cases and 534 non-polio AFP cases. Of the 44 polio cases, 27 (61.4%) cases were reported among adults aged 15-53 years. Strengthening AFP surveillance resulted in an increase in the number of non-polio AFP cases in 2011 (148 children < 15 years) compared with 76 cases < 15 years in 2010. The AFP surveillance system in Xinjiang was sensitive enough to detect polio cases, with the AFP incidence of 3.28/100,000 among children < 15 years of age. CONCLUSIONS: Incorporating adult cases into the AFP surveillance system is of potential value to understand the overall characteristics of the epidemic and to guide emergency responses, especially in countries facing WPV outbreak following long-term polio free status. The AFP surveillance system in Xinjiang was satisfactory despite limitations in biological sample collection.

Hepatic steatosis using ultrasound-derived fat fraction: First technical and clinical evaluation.

OBJECTIVES: To explore the technical and clinical evaluation of ultrasound-derived fat fraction (UDFF) measurement in adult patients in whom fatty liver was suspected. MATERIALS AND METHODS: In this prospective study, 41 participants were initially enrolled in our hospital between October 2022 and December 2022 and received UDFF assessment using Siemens ACUSON Sequoia system equipped with DAX transducer. UDFF measurement was performed three times to obtain UDFF values from each imaging location (V hepatic segment and VIII hepatic segment) per participant, and the depth (skin-to-capsule distance) was automatically measured. The echogenicity of liver tissue in B mode ultrasound (BMUS) was compared to the normal kidney tissue, and fatty liver was graded as mild (Grade 1), moderate (Grade 2), and severe (Grade 3). The median of the acquired overall median UDFF values was used for statistical analysis. All ultrasound examinations were performed by one of two radiologists (with 20 and 10 years of liver ultrasound imaging experience). RESULTS: Finally, UDFF measurement was successfully performed on 38 participants to obtain valid values, including 21 men with a median age of 40.0 years (interquartile range [IQR]: 23.0 - 58.5) and 17 women with a median age of 60.0 years (IQR: 29.5 - 67.0). Fatty liver was diagnosed by BMUS features in 47.4% (18/38) participants. Among all participants, the median UDFF value was 7.0% (IQR: 4.0 - 15.6). A significant difference in UDFF values was found between participants with fatty liver and without fatty liver (U = 7.0, P < 0.001), and UDFF values elevated as the grade of the fatty liver increased (P < 0.001). The median UDFF values from the three UDFF measurements obtained during each ultrasound examination showed excellent agreement (ICC = 0.882 [95% confidence interval: 0.833 - 0.919]). The Spearman correlation of UDFF values in different depths was moderate, with a rs value of 0.546 (P < 0.001). No significant differences in UDFF values were found between V hepatic segment and VIII hepatic segment (U = 684.5, P = 0.697). CONCLUSIONS: UDFF provides a novel non-invasive imaging tool for hepatic steatosis assessment with excellent feasibility.

A glucose-mediated antibiotic resistance metabolic flux from glycolysis, the pyruvate cycle, and glutamate metabolism to purine metabolism.

Introduction: Bacterial metabolic environment influences antibiotic killing efficacy. Thus, a full understanding for the metabolic resistance mechanisms is especially important to combat antibiotic-resistant bacteria. Methods: Isobaric tags for relative and absolute quantification-based proteomics approach was employed to compare proteomes between ceftazidime-resistant and -sensitive Edwarsiella tarda LTB4 (LTB4-RCAZ and LTB4-S, respectively). Results: This analysis suggested the possibility that the ceftazidime resistance mediated by depressed glucose is implemented through an inefficient metabolic flux from glycolysis, the pyruvate cycle, glutamate metabolism to purine metabolism. The inefficient flux was demonstrated by the reduced expression of genes and the decreased activity of enzymes in the four metabolic pathways. However, supplement upstream glucose and downstream guanosine separately restored ceftazidime killing, which not only supports the conclusion that the inefficient metabolic flux is responsible for the resistance, but also provides an effective approach to reverse the resistance. In addition, the present study showed that ceftazidime is bound to pts promoter in E. tarda. Discussion: Our study highlights the way in fully understanding metabolic resistance mechanisms and establishing metabolites-based metabolic reprogramming to combat antibiotic resistance.

Predicting the Activity of Oral Lichen Planus with Glycolysis-related Molecules: A Scikit-learn-based Function.

OBJECTIVE: Oral lichen planus (OLP) is one of the most common oral mucosa diseases, and is mainly mediated by T lymphocytes. The metabolic reprogramming of activated T cells has been shown to transform from oxidative phosphorylation to aerobic glycolysis. The present study investigated the serum levels of glycolysis-related molecules (lactate dehydrogenase, LDH; pyruvic acid, PA; lactic acid, LAC) in OLP, and the correlation with OLP activity was assessed using the reticular, atrophic and erosive lesion (RAE) scoring system. METHODS: Univariate and multivariate linear regression functions based on scikit-learn were designed to predict the RAE scores in OLP patients, and the performance of these two machine learning functions was compared. RESULTS: The results revealed that the serum levels of PA and LAC were upregulated in erosive OLP (EOLP) patients, when compared to healthy volunteers. Furthermore, the LDH and LAC levels were significantly higher in the EOLP group than in the nonerosive OLP (NEOLP) group. All glycolysis-related molecules were positively correlated to the RAE scores. Among these, LAC had a strong correlation. The univariate function that involved the LAC level and the multivariate function that involved all glycolysis-related molecules presented comparable prediction accuracy and stability, but the latter was more time-consuming. CONCLUSION: It can be concluded that the serum LAC level can be a user-friendly biomarker to monitor the OLP activity, based on the univariate function developed in the present study. The intervention of the glycolytic pathway may provide a potential therapeutic strategy.

Person-to-person transmission of severe fever with thrombocytopenia syndrome bunyavirus through blood contact.

Severe fever with thrombocytopenia syndrome bunyavirus is a newly discovered bunyavirus with high pathogenicity to human. The transmission model has been largely uncharacterized. Investigation on a cluster of severe fever with thrombocytopenia syndrome cases provided evidence of person-to-person transmission through blood contact to the index patient with high serum virus load.

A systematic study of chiral homoprolinols and their derivatives in the catalysis of enantioselective addition of diethylzinc to aldehydes.

Homoprolinol analogs, a class of optically active γ-amino alcohols, were examined systematically in the enantioselective addition reactions of diethylzinc to aldehydes. By comparison of the results catalyzed by these γ-amino alcohols with those by the ß-amino alcohols based on pyrrolidine architecture reported in the literature references, we have observed that the γ-amino alcohols are superior to the corresponding ß-amino alcohols when the nitrogen and the oxygen are unsubstituted. Among the homoprolinols we tested, gave the best results (45-88% yields, 44-81% ee) in the addition reactions. To the best of our knowledge, has been noticed as one of the most efficient γ-amino alcohol catalysts based on pyrrolidine framework.

[Mitochondrial tRNAMet mutation in Chinese Han essential hypertensive individuals].

The objective of the present study was to explore the relationship between mitochondrial tRNAMet mutation and development of essential hypertension in Chinese Han individuals. A total of 990 patients with essential hypertension were involved. The general data (sex, age, body mass index, onset age, and family history) and information on routine blood test, blood biochemical examination, and color Doppler echocardiography of these patients were collected. All subjects under-went venous blood drawing for seperating white blood cells and DNA extraction. Then, mitochondrial tRNAMet was amplified and sequenced after purification. The patients who carried the tRNAMet mutation were taken as the indicative cases and the controls were the patients with essential hypertension who did not carry the mutation. We performed a comparative analysis on the routine blood test, blood biochemical examination, color Doppler echocardiography, and other data between the indicative cases and control cases. Among the 990 essential hypertensive patients, there were 8 who carried the tRNAMet mutation, and 6 mutation sites were confirmed, including A4401G, C4410A, U4418C, A4435G, U4454C, and C4456U. Compared with the control cases, the indicative cases developed essential hypertension at earlier ages. The average levels of high density of lipoprotein cholesterol, left ventricular end diastolic diameter, stroke volume, and cardiac index were higher in the indicative cases than in the controls. While the average levels of hemoglobin and left ventricular ejection fraction were lower in the indicative cases than in the control cases. Among the 8 indicative cases, 5 had maternally inherited hyper-tension; one had paternally inherited hypertension; and two denied any family history of hypertension. These results indicated that the mitochondrial tRNAMet mutations might induce the changes in structure and function, which was involved in the progress of the essential hypertension by disturbing the blood metabolism, the steady-state of the blood cells, and the cardiac structure and function.

[Fifteen-year evolving trends of etiology and prognosis in hospitalized patients with heart failure].

OBJECTIVE: To investigate the etiological and prognostic changes of hospitalized patients with chronic heart failure. METHODS: This retrospective study analyzed 7319 hospitalized patients (male 62.07%) with validated primary discharge diagnosis of chronic heart failure in Chinese PLA General Hospital in Beijing from January 1, 1993 to December 31, 2007. Etiological characteristics, comorbidities and 30-day hospitalized mortality in the following three periods: 1993 - 1997 (n = 1623), 1998 - 2002 (n = 2444), and 2003 - 2007 (n = 3252) were compared. RESULTS: (1) The patient age increased [(56.0 ± 17.5) years, (57.8 ± 17.6) years and (62.7 ± 15.5) years, P < 0.01] and hospital stay time decreased [(31.3 ± 17.4) days, (22.7 ± 14.1) days and (20.1 ± 15.2) days, P < 0.01] from 1993 to 2007. (2) The common causes of heart failure were coronary heart disease, hypertension, rheumatic valvular heart disease and diabetes mellitus. From 1993 - 1998 to 2003 - 2007, the proportion of patients with coronary heart disease, hypertension and diabetes mellitus rose from 37.2%, 23.3% and 12.3% to 46.8%, 46.7% and 21.1%, respectively (all P < 0.05). Meanwhile the proportion of patients with rheumatic valvular heart disease fell from 35.2% to 16.6% (P < 0.05). (3) The main etiologies and comorbidities were atrial fibrillation, myocardial infarction, pneumonia, chronic obstructive pulmonary disease and renal failure. From 1993 - 1998 to 2003 - 2007, atrial fibrillation was the most common cause of heart failure, and the rate of myocardial infarction, pneumonia and renal failure rose from 11.0%, 8.9% and 5.2% to 14.7%, 14.5% and 9.1%, respectively (all P < 0.05) and the rate of COPD fell from 12.9% to 8.4% (P < 0.05). (4) The 30-day hospitalized mortalities in the three periods were 7.0%, 4.5% and 5.1%, respectively, and the mortalities in the 1998 - 2002 and 2003 - 2007 periods were lower than those of in the 1993 - 1998 period (all P < 0.05). The mortality related to coronary heart disease decreased significantly from 1993 to 2007 (9.3%, 5.0% and 3.8% in the three periods, respectively, P < 0.05). CONCLUSIONS: It is demonstrated that the primary diseases causing heart failure were coronary heart disease, hypertension, diabetes mellitus and rheumatic valvular heart disease, and the former three diseases exhibited a upward trend and the later one exhibited a downward trend. Moreover, the proportion of comorbidities in patients with heart failure increased over the study period. The 30-day hospital mortality exhibited a downward trend and decreased significantly in patients with coronary heart disease or myocardial infarction.

In-Situ Growth of Broussonetia-Like NiCo2O4 on Carbon Cloth with Tailored Aqueous Capacitance.

Tailored broussonetia-like NiCo2O4 is grown on carbon cloth using tri-sodium citrate assisted hydrothermal method. The chelating effect of citric ions has been utilized to investigate the morphological and structural evolution of NiCo2O4 on carbon cloth, which have been illustrated by scanning electron microscopy, transmission electron microscopy, and X-ray photoelectron spectra. The results demonstrate that the morphological alteration of NiCo2O4 from single nanowire to broussonetia-like structure has been detected after the addition of tri-sodium citrate. Citric ion plays a crucial role as an electrostatic stabilizer in determining this unique structure. When used as binder-free electrode in aqueous supercapacitors, the broussonetia-like NiCo2O4 electrode exhibits a specific capacitance of 527.9 F g-1 at a current density of 0.5 A g-1. Additionally, an asymmetric supercapacitor is further assembled using NiCo2O4 as the positive electrode and activated carbon as negative electrode. The device exhibits a maximum energy of 26.4 Wh kg-1 at power density of 800 W kg-1. A long-term cycling stability with 82% capacitance retention is maintained after 20,000 cycles at a current density of 5 A g-1, indicating the practical applicability of the tested device.

[Compensation effect of re-watering after different drought stresses on source-sink metabolism during tuber expansion period of potato.] / 马铃薯块茎膨大期不同程度干旱后复水的源库补偿效应.

The compensation effect of re-watering after drought has been widely reported in various crops during different growth stages. It is considered as an important self-regulation mechanism for plants to resist abiotic stresses and also an efficient utilization of limited water resource. In this study, two rounds of re-watering after drought treatments were carried out during tuber expansion period of potato, to investigate the drought threshold of potato and explore the potential mechanisms of compensation effect with source-sink aspect. We used virus-free plantlets of "Atlantic" potato as experimental materials. Four treatments were included: sufficient water supply (W), re-watering after mild drought (D1-W), re-watering after medium drought (D2-W) and re-watering after severe drought (D3-W). The results showed that potato yield exhibited an over-compensation effect after two rounds of D1-W treatment, with water use efficiency and yield being increased by 17.5% and 6.3%, respectively, compared with the sufficient water supply. D2-W treatment had no significant effect on potato yield, but water use efficiency was increased by 8.4%, indicating a near-equivalent compensation effect. On the contrary, D3-W treatment did not show any compensation effect in yield. In addition, leaf chlorophyll content, net photosynthetic rate, and leaf area were all reduced after drought treatment, indicating a reduction in "source" size and activity. After re-watering, D1-W and D2-W treatments showed over-compensation and compensation effects through improving source supply capacity. Meanwhile, re-watering after moderate drought increased the sink activity through significantly enhancing the activities of key enzymes in tubers (sink), thus increased the average weight of tubers. In conclusion, re-watering after moderate drought stress during potato tuber expansion period had compensation and over-compensation effects on both source and sink, and thus could compensate for the drought-induced yield loss and improve water use efficiency.

[Rac1 accelerates endothelial cell senescence induced by hypoxia in vitro].

To investigate the role and mechanism of Rac1 protein in the process of the human umbilical vein endothelial cell (HUVEC) senescence, we used hypoxia as a model for modulating HUVECs entering replicative senescence in vitro. Premature senescence of HUVECs was evidenced by detecting the SA-beta-Gal activity and PAI-1 expression. Meanwhile, cell cycle distribution and cell proliferation rate were investigated by flow cytometry assay and BrdU staining. The results indicated that the HUVECs became enlarged and flattened, both SA-beta-Gal activity and PAI-1 expression increased obviously, while cell proliferation was inhibited and G(1) phase cell cycle arresting occurred when HUVECs were treated with continued hypoxia for 96 h. Accompanied with these changes, the expression of activated Rac1 increased obviously in cells after hypoxia. All these observations suggested that endothelial senescence could be induced by continued hypoxia and it might correlate with the activity of Rac1. To further define the relationship between Rac1 and HUVEC senescence, HUVECs were transiently infected with the constitutively active form of Rac1 (V12Rac1) or dominant negative form of Rac1 (N17Rac1) using retrovirus vector pLNCX-V12Rac1 or pLNCX-N17Rac1. We observed the changes of these three kinds of HUVECs (HUVECs, N17Rac1-HUVECs, V12Rac1-HUVECs) after hypoxia for 48 h and 96 h, the expression and localization of serum response factor (SRF), which is one of the downstream signal molecules of Rac1, were also investigated. The results obtained indicated that after continued hypoxia for 48 h, HUVECs infected by V12Rac1 showed obvious senescence accompanied with SA-beta-Gal activation, PAI-1 expression increase, G(1) phase arrest and cell proliferation inhibition which were similar to HUVECs after continued 96-hour hypoxia treatment, while the senescence of HUVECs infected by N17Rac1 was significantly inhibited even if the cells were exposed to hypoxia for more than 96 h. All the results identified that the activation of Rac1 might accelerate HUVEC senescence induced by hypoxia and that inactivation of Rac1 could partly block the cell senescence. To further investigate the mechanism of HUVEC senescence induced by Rac1, we detected the expression of total SRF (tSRF) and nuclear SRF (nSRF) in these three kinds of HUVECs by immunofluorescent analysis and Western blot assay after hypoxia. The results showed that the expression of nSRF decreased obviously and the nuclear translocation of SRF was inhibited in HUVECs infected by V12Rac1 compared with those in the normal HUVECs. In contrast, the expression of nSRF increased obviously in the HUVECs infected by N17Rac1. These results suggest that activation of Rac1 accelerates endothelial cell senescence and inhibition of Rac1 activity prevents HUVECs from entering senescence induced by hypoxia, while the nuclear translocation of SRF regulated by Rac1 might play an important role in the process of senescence.