Long term consumption of high fructose and high salt diet did not induce blood pressure elevation in female mice. Is estrogen protective against dietary-induced high blood pressure?

Introduction: High fructose and high salt (HFHS) consumption are linked to hypertension, which is now the leading cause of death worldwide. Results from a previous study showed that the effect of HFHS on blood pressure (BP) is dependent on the concentration and duration of consumption. Sex differences in BP regulation are partially attributed to the effects of sex steroids on key renal sodium transporters.Hypothesis: We hypothesized that HFHS would induce BP elevation in male and female mice, however, females will have higher expression of renal NCC/NKCC during long-term HFHS diet consumption.Methods: Four-week-old male and female CD-1 mice (n= 6/group) were placed in metabolic cages and consumed standard chow and water for seven days, followed by 3months of 4% sodium chloride (NaCl) diet and a drinking solution of 1% NaCl and 20% fructose. Separate mice on the same diet in bins were sacrificed and kidneys extracted at the end of the first week, first and second months, and used for molecular studies.Results: Females expressed higher mRNA levels of NCC and NKCC throughout the study with fold difference of two or higher. Systolic BP averaged weekly and analyzed via ANOVA showed no sex difference in BP from baseline to the third month. Males showed an increase in BP in the third month compared to baseline (123.6 ± 3.6mmHg and 106.3 ± 5.4mmHg, P< 0.5 respectively). There were no sex differences in sodium retention.Conclusion: Females have protection against HFHS induced BP elevation and estrogen may have a protective role

Polymer acceptors based on Y6 derivatives for all-polymer solar cells

No abstract availabl

Multiobjective Reliable Cloud Storage with Its Particle Swarm Optimization Algorithm

Information abounds in all fields of the real life, which is often recorded as digital data in computer systems and treated as a kind of increasingly important resource. Its increasing volume growth causes great difficulties in both storage and analysis. The massive data storage in cloud environments has significant impacts on the quality of service (QoS) of the systems, which is becoming an increasingly challenging problem. In this paper, we propose a multiobjective optimization model for the reliable data storage in clouds through considering both cost and reliability of the storage service simultaneously. In the proposed model, the total cost is analyzed to be composed of storage space occupation cost, data migration cost, and communication cost. According to the analysis of the storage process, the transmission reliability, equipment stability, and software reliability are taken into account in the storage reliability evaluation. To solve the proposed multiobjective model, a Constrained Multiobjective Particle Swarm Optimization (CMPSO) algorithm is designed. At last, experiments are designed to validate the proposed model and its solution PSO algorithm. In the experiments, the proposed model is tested in cooperation with 3 storage strategies. Experimental results show that the proposed model is positive and effective. The experimental results also demonstrate that the proposed model can perform much better in alliance with proper file splitting methods

Effects of estrogen on blood pressure and salt and water excretion during a ten-day Angiotesin ll infusion period in ovariectomized mice

Introduction: Premenopausal women are protected from cardiovascular disease compared to age-matched men. Estrogen (E2) plays important roles in these protective mechanisms.Purpose: Our goal was to determine if E2 reduces angiotensin II (AngII)-induced elevation in blood pressure in ovariectomized (OVX) mice. We also hypothesized that E2 affects renal excretion of water and sodium.Methods: Four-week-old CD-1 OVX mice were placed in metabolic cages for a five-day baseline period followed by implantation of an Alzet osmotic pump containing either vehicle or AngII (1 µg/kg/min) and either a placebo or 0.7mg E2 pellet. Measurements of water intake (WI, ml/day), urine volume (UV, ml/day), and urine sodium excretion (UNaE, μEq/day) were recorded daily in the baseline and ten-day post-implantation periods in three groups of mice: vehicle-placebo (V-P), AngII-placebo (AngII-P), and AngII-E2 (n=4/group). Systolic blood pressure (SBP, mmHg) was determined via the tail-cuff technique.Results: Delta SBP (baseline vs AngII period) was higher in AngII-P but not significantly different from AngII-E2 mice, (33.1±3.5 vs 24.5±4.0, respectively). AngII-E2 mice compared to AngII-P mice had lower WI (4.2±0.02 vs 6.9±0.05, respectively, p<0.001), lower UV (1.3±0.02 vs 2.6±0.03, respectively, p<0.03), and lower UNaE (110.5±20.7 vs 199.7±10.8, respectively, p<0.003).Conclusion: E2 administration reduces WI, UV, and UNaE during a ten-day AngII-infusion in OVX mice. E2 did not significantly reduce SBP. Studies of longer duration are underway to investigate the important E2-induced mechanisms on blood pressure regulation

Reprogramming glioblastoma multiforme cells into neurons by protein kinase inhibitors

Abstract Background Reprogramming of cancers into normal-like tissues is an innovative strategy for cancer treatment. Recent reports demonstrate that defined factors can reprogram cancer cells into pluripotent stem cells. Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor in humans. Despite multimodal therapy, the outcome for patients with GBM is still poor. Therefore, developing novel therapeutic strategy is a critical requirement. Methods We have developed a novel reprogramming method that uses a conceptually unique strategy for GBM treatment. We screened a kinase inhibitor library to find which candidate inhibitors under reprogramming condition can reprogram GBM cells into neurons. The induced neurons are identified whether functional and loss of tumorigenicity. Results We have found that mTOR and ROCK kinase inhibitors are sufficient to reprogram GBM cells into neural-like cells and “normal” neurons. The induced neurons expressed neuron-specific proteins, generated action potentials and neurotransmitter receptor-mediated currents. Genome-wide transcriptional analysis showed that the induced neurons had a profile different from GBM cells and were similar to that of control neurons induced by established methods. In vitro and in vivo tumorigenesis assays showed that induced neurons lost their proliferation ability and tumorigenicity. Moreover, reprogramming treatment with ROCK-mTOR inhibitors prevented GBM local recurrence in mice. Conclusion This study indicates that ROCK and mTOR inhibitors-based reprogramming treatment prevents GBM local recurrence. Currently ROCK-mTOR inhibitors are used as anti-tumor drugs in patients, so this reprogramming strategy has significant potential to move rapidly toward clinical trials

Effects of high salt diet on blood pressure and the renal handling of sodium

Introduction: The association between elevated dietary salt consumption and high blood pressure is well known. Hypertension carries elevated risk for stroke, cardiovascular disease, liver disease, and nervous disorders. Interestingly, sex differences in many areas of pathophysiology. Pre-menopausal women have shown to be protected against hypertension and renal diseases compared to age matched men. It is reasonable to expect that how the kidney handles sodium in presence of high-salt consumption plays a key role in sex differences. The purpose of this study was to determine sex differences in the renal handling of sodium in mice consuming a high-salt diet. We also investigated the effects of high-salt consumption on blood pressure in these mice.Methods: Intact male and female mice (n=6/group) consumed a high-salt (4%, HarlanTeklad) diet for 30 days. Mice were placed individually in metabolic cages where urine could be collected for volume and measurement of Na+ concentration. Urinary Na+ excretion (NAE, mg/day) was determined from daily measurements of urine sodium concentration and urine volume. Sodium intake (Nai, mg/day) was determined from daily food intake of 4% salt diet ad libitum. Blood pressure was measured daily via the tail-cuff method. Expression of key sodium transport proteins in the kidney was measured via real-time quantitative PCR.Results: From the data accumulated during the 30-day period of high salt consumption, female mice showed a significantly lower average of the output-to-input Na+ ratio (NAE/Nai) compared to male mice (53.3 ± 2.7 vs 68.1 ± 1.8, respectively, p<0.0001). Female mice showed lower mean blood pressure (MBP, mmHg) compared to male mice over the 30-day period (78.4 ± 1.0 vs 84.9 ± 1.2 respectively, <0.0005). Molecular expression of the key sodium transporter Na+ -2Cl- -K + (NKCC) in the thick ascending limb was over 5-fold higher in the female kidney.Conclusion: Interestingly, results from this study demonstrated that female mice retained more ingested sodium compared to male mice while on a high-salt diet. Moreover, female mice had lower MBP compared to male mice while on a high-salt diet. We suspect that sex steroids are playing important roles in the renal handling of sodium and in the control of blood pressure. This study suggests that females are protected from deleterious effects of high-salt consumption

Exploratory chandra observation of the ultraluminous quasar SDSS J010013.02+280225.8 at redshift 6.30

We report exploratory Chandra observations of the ultraluminous quasar SDSS J010013.02+280225.8 at redshift 6.30. The quasar is clearly detected by Chandra with a possible component of extended emission.Y.-L.A. thanks the support from NSFC grant Nos. 11273060, 11333008, and State Key Development Program for Basic Research of China (Nos. 2013CB834900 and 2015CB857000). F.W. and X.-B.W. thank the support from the NSFC grants No.11373008 and 11533001, the Strategic Priority Research Program “The Emergence of Cosmological Structures” of the Chinese Academy of Sciences, grant No. XDB09000000, and the National Key Basic Research Program of China 2014CB845700

Tris(2,2′-bipyridine)­nickel(II) hexa­molybdate

The asymmetric unit of the title compound, [Ni(C10H8N2)3][Mo6O19], consists of one complex [(Ni(C10H8N2)3]2+ cation and one Lindqvist-type [Mo6O19]2− polyanion. The Ni2+ ion is in a distorted octa­hedral coordination by six N atoms from three chelating 2,2′-bipyridine ligands. The Lindqvist-type anion exhibits the characteristic Mo—O bond-length distribution, with the shortest bonds being the Mo—O(terminal) bonds [mean = 1.679 (2) Å] and the longest being those to the central O atom [mean = 2.318 (7) Å]. A number of C—H⋯O inter­actions contribute to the crystal packing