N, P, Si budgets for the Red River Delta (northern Vietnam): how the delta affects river nutrient delivery to the sea

The Red River Delta (RRD) (Vietnam), a region experiencing rapid population growth, industrialization, and economic development, concentrates 54% of the population of the whole Red River watershed in less than 10% of the basin area. Our study aimed at understanding and quantifying the processes by which the delta affects the nutrient fluxes coming from the upstream watershed before they reach the sea. A comprehensive budget of nitrogen (N), phosphorus (P), and silica (Si) fluxes associated with natural and anthropogenic processes in the terrestrial and hydrological system of the delta was established for five sub-basins of the delta for the period 2000–2006, based on official statistical data, available measurements, and our own sampling campaigns and enquiries. The results show that anthropogenic inputs of N and P brought into the delta area are higher than the amounts delivered by the river from the upstream watershed. However, the amounts of these two elements ultimately delivered to the coastal zone from the delta are lower than the amounts carried by the upstream river, showing extremely efficient retention of both the soils and the delta’s drainage network. For Si (taking into account both dissolved and amorphous solid forms), the retention is much lower. High retention of N and P and low retention of Si in the delta area have up to now protected the coastal zone from severe eutrophication problems.     

First identification of Flavobacterium columnare infection in farmed freshwater striped catfish Pangasianodon hypophthalmus

The bacterium Flavobacterium columnare was recovered and identified as the aetiological agent causing freshwater columnaris infection in farmed striped catfish Pangasianodon hypophthalmus (Sauvage) fingerlings that had suffered high mortality rates within commercial hatchery ponds in Vietnam. The gross clinical signs were typical of columnaris-infected fish. Histological examination found numerous Gram-negative, filamentous bacteria present on the skin, muscle and gill tissues of affected fish. The yellow-pigmented bacteria were isolated and identified as F. columnare using primary, biochemical and PCR methods. An experimental immersion-challenge study with 2 strains was also performed. It fulfilled Koch's postulates and showed a median lethal concentration (LC50) of 4.27 × 105 and 1.66 × 106 cfu ml-1 for the F. columnare strains FC-HN and FC-CT, respectively. To the best of our knowledge this is the first report of freshwater columnaris infection in P. hypophthalmus.     

Angiotensin-(1-7) suppresses the number and function of the circulating fibrocytes by upregulating endothelial nitric oxide synthase expression

There is growing evidence suggesting that circulating fibrocytes (CFs) play a pivotal role in tissue repair and fibrosis. In contrast, in recent studies, angiotensin-(1-7) [Ang-(1-7)] has been shown to antagonize fibrosis. The purpose of this study was to examine the direct effect of Ang-(1-7) on CFs. Total mononuclear cells (MNCs) were isolated from peripheral blood by Ficoll density gradient centrifugation. Using laser scanning confocal microscopy, CFs were identified as adherent cells that stained positive for both CD34 and collagen-I. After 14 days of culture, CFs were stimulated with Ang-(1-7) at concentrations of 10 nM, 100 nM, 1 μM or 10 μM, in the absence and presence of pretreatment with A-779, N(G)-nitro-L-arginine methyl ester (L-NAME) or both, for 24, 48 or 72 h. The number of cells, cellular proliferation, and level of apoptosis were determined by hematoxylin and eosin staining, the Cell Counting Kit-8 (CCK8) assay and the annexin V/propidium iodide binding assay, respectively. The collagen content of CFs was measured by the concentration of hydroxyproline, which was detected using the enzymatic digestion method. The expression of endothelial nitric oxide synthase (eNOS) was assayed by western Blot analysis, while nitric oxide (NO) generation was detected using the Griess method. We found that Ang-(1-7) increases apoptosis and eNOS/NO production in CFs. In addition, Ang-(1-7) decreases the number, proliferative capacity and collagen-secretion of CFs in a concentration- and time-dependent manner. These data suggest that Ang-(1-7) suppresses the both the number and function of CFs possibly by increasing eNOS/NO production in the CFs.     

The enhanced antiproliferative response to combined treatment of trichostatin A with raloxifene in MCF-7 breast cancer cells and its relevance to estrogen receptor β expression

Antiestrogen is one type of the endocrine therapeutic agents for estrogen receptor α (ERα)-positive breast cancer. Unfortunately, this treatment alone is insufficient. Here we reported a novel potential anticancer strategy by using histone deacetylase (HDAC) inhibitor to enhance the action of endocrine therapy in ERα-positive breast cancer cell. The well-described HDAC inhibitor, trichostatin A (TSA), and antiestrogen raloxifene were found to, respectively, inhibit E2-induced proliferation of MCF-7 breast cancer cell in a dose-responsive and time-dependent manner. TSA and raloxifene enhanced the antiproliferative activity of each other by promoting cell death via apoptosis and cell cycle arrest. Thus, they displayed better antiproliferative effects in combined treatment than that with either agent alone. The expression level of estrogen receptor β (ERβ) showed a marked increase after TSA or/and raloxifene treatment. Treatments with TSA or/and raloxifene resulting in the up-regulation of ERβ are in accordance with the antiproliferative effects of the two agents. Furthermore, the over-expression of ERβ by adenovirus delivery could inhibit the proliferation of MCF-7 tumor cells and drastically enhanced the antiproliferative effects of TSA and raloxifene. These results demonstrated that the interference of ERβ on the antiproliferative effects of HDAC inhibitor and antiestrogen constitutes a promising approach for breast cancer treatment.     

CSF-1 receptor signalling from endosomes mediates the sustained activation of Erk1/2 and Akt in macrophages

Colony stimulating factor-1 (CSF-1) mediates its pleiotropic effects on macrophages through the CSF-1 receptor (CSF-1R), a receptor tyrosine kinase. Current models of CSF-1 signalling imply that the CSF-1R activates signalling pathways exclusively at the plasma membrane and the subsequent internalisation of the CSF-1R simply facilitates its lysosomal degradation in order to prevent on-going signalling. Here, we sought to establish if the CSF-1R may in fact continue to signal following its internalisation. Erk1/2, Akt and Stat3 activation were abrogated when the internalisation of the CSF-1R was impaired, with the effects on Stat3 distinct from those for Erk1/2 and Akt. Pharmacologic inhibition of the CSF-1R following its internalisation resulted in less sustained Erk1/2 and Akt activity, whereas Stat3 activity was unaffected. Significantly, the suppressive effects of the CSF-1R inhibitor on the up-regulation of gene expression by CSF-1 (e.g. cyclin D1 and Bcl-xL gene expression) were comparable irrespective of whether the inhibitor was added prior to CSF-1 stimulation or following the internalisation of the CSF-1R. Similarly, pharmacologic inhibition of Erk1/2 (or Akt) activity either prior to CSF-1 stimulation or subsequent to CSF-1R internalisation had comparable effects on the regulation of gene expression by CSF-1. Together, our data argue that key signalling responses to CSF-1 depend on the ability of the CSF-1R to signal from endosomes following its internalisation, thus adding an important spatiotemporal aspect to CSF-1R signalling.     

Identifying FGA peptides as nasopharyngeal carcinoma-associated biomarkers by magnetic beads

Early diagnosis and treatment is known to improve prognosis for nasopharyngeal carcinoma (NPC). The study determined the specific peptide profiles by comparing the serum differences between NPC patients and healthy controls, and provided the basis for the diagnostic model and identification of specific biomarkers of NPC. Matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry (MALDI‐TOF‐MS) can be used to detect the molecular mass of peptides. Mass spectra of peptides were generated after extracting and purification of 40 NPC samples in the training set, 21 in the single center validation set and 99 in the multicenter validation set using weak cationic‐exchanger magnetic beads. The spectra were analyzed statistically using FlexAnalysis? and ClinProt? bioinformatics software. The four most significant peaks were selected out to train a genetic algorithm model to diagnose NPC. The diagnostic sensitivity and specificity were 100% and 100% in the training set, 90.5% and 88.9% in the single center validation set, 91.9% and 83.3% in the multicenter validation set, and the false positive rate (FPR) and false negative rate (FNR) were obviously lower in the NPC group (FPR, 16.7%; FNR, 8.1%) than in the other cancer group (FPR, 39%; FNR, 61%), respectively. So, the diagnostic model including four peptides can be suitable for NPC but not for other cancers. FGA peptide fragments identified may serve as tumor‐associated biomarkers for NPC. J. Cell. Biochem. 113: 2268–2278, 2012. © 2012 Wiley Periodicals, Inc.     

Trends in the incidence and outcomes of heart failure in Ontario, Canada: 1997 to 2007

Background:

Heart failure is a leading cause of admission to hospital, but whether the incidence of heart failure is increasing or decreasing is uncertain. We examined temporal trends in the incidence and outcomes of heart failure in Ontario, Canada.

Methods:

Using population-based administrative databases of hospital discharge abstracts and physician health insurance claims, we identified 419 551 incident cases of heart failure in Ontario between Apr. 1, 1997, and Mar. 31, 2008. All patients were classified as either inpatients or outpatients based on the patient’s location at the time of the initial diagnosis. We tracked subsequent outcomes through linked administrative databases.

Results:

The age- and sex-standardized incidence of heart failure decreased 32.7% from 454.7 per 100 000 people in 1997 to 306.1 per 100 000 people in 2007 (p < 0.001). A comparable decrease in incidence occurred in both inpatient and outpatient settings. The greatest relative decrease occurred in patients aged 85 and over. Over the study period, 1-year risk-adjusted mortality decreased from 17.7% in 1997 to 16.2% in 2007 (p = 0.02) for outpatients, with a nonsignificant decrease from 35.7% in 1997 to 33.8% in 2007 (p = 0.1) for inpatients.

Interpretation:

The incidence of heart failure decreased substantially during the study period. Nevertheless, the prognosis for patients with heart failure remains poor and is associated with high mortality.Heart failure is a leading cause of admission to hospital and is associated with a poor long-term prognosis. In 1996, it was projected that the number of incident hospital admissions for heart failure in Canada would more than double by 2025 because of the aging population and increasing numbers of myocardial infarction survivors.¹ By 2000, patients with heart failure accounted for the second highest number of hospital days in Canada, and the estimated 1-year case-fatality rate, after the first hospital admission, exceeded 35%.^2,3 However, some recent studies suggest that admission and mortality rates for heart failure may actually be falling. It is unclear whether these changes represent lower rates of new incident cases, fewer readmissions, a shift to more outpatient care or improved survival.^4,5We sought to examine temporal trends in the incidence and outcomes of heart failure in Ontario, Canada, in both inpatient and outpatient settings to assess the progress made in reducing the population burden of heart failure and to gain insight into the effectiveness of current preventive and therapeutic strategies.     

Diagnosed hypertension in Canada: incidence, prevalence and associated mortality

Background:

Hypertension is a leading risk factor for cardiovascular diseases. Our objectives were to examine the prevalence and incidence of diagnosed hypertension in Canada and compare mortality among people with and without diagnosed hypertension.

Methods:

We obtained data from linked health administrative databases from each province and territory for adults aged 20 years and older. We used a validated case definition to identify people with hypertension diagnosed between 1998/99 and 2007/08. We excluded pregnant women from the analysis.

Results:

This retrospective population-based study included more than 26 million people. In 2007/08, about 6 million adults (23.0%) were living with diagnosed hypertension and about 418 000 had a new diagnosis. The age-standardized prevalence increased significantly from 12.5% in 1998/99 to 19.6% in 2007/08, and the incidence decreased from 2.7 to 2.4 per 100. Among people aged 60 years and older, the prevalence was higher among women than among men, as was the incidence among people aged 75 years and older. The prevalence and incidence were highest in the Atlantic region. For all age groups, all-cause mortality was higher among adults with diagnosed hypertension than among those without diagnosed hypertension.

Interpretation:

The overall prevalence of diagnosed hypertension in Canada from 1998 to 2008 was high and increasing, whereas the incidence declined during the same period. These findings highlight the need to continue monitoring the effectiveness of efforts for managing hypertension and to enhance public health programs aimed at preventing hypertension.Globally, raised blood pressure is the leading risk factor for death, accounting for about 13% of all deaths,^1,2 and it is the strongest risk factor for lost years of healthy life.¹ Left untreated, hypertension can increase the risk of stroke, coronary artery disease, dementia, heart and kidney failure, and other chronic diseases.^3–6 Managing hypertension through lifestyle modification or the use of antihypertensive medications, or both, can help mitigate these outcomes.⁷ Over the past decades in Canada, mortality associated with cardiovascular diseases has decreased,⁸ partly because of increased awareness and diagnosis of hypertension and better control of blood pressure.^9,10 However, the prevalence of hypertension remains high, and currently there are no mechanisms to track new cases at the national level.To date, information about hypertension in Canada has been mainly obtained by health surveys conducted at the provincial or national levels. Such surveys typically provide prevalence (not incidence) data and include limited data about trends over time.^11–15 National health surveys in Canada are resource intensive, do not include information about people who live in remote areas or institutions, and may underestimate hypertension prevalence because of recall bias and non-response.¹⁶ The use of administrative data that is population-based and routinely collected, such as physician claims and hospital discharge data, allows for a more comprehensive picture of this condition. Other important advantages of using administrative data include the readiness of the data to be analyzed, cost-efficiency, wide geographic coverage and the relatively complete capture of patient contact with the health care system (i.e., less prone to selection bias).Several recent studies in Canada and the United States have established valid methods for using administrative data to identify cases of hypertension.^16–23 In a study conducted in Ontario involving women and men aged 20 years and older, Tu and colleagues found that the prevalence and incidence of diagnosed hypertension were 24.5% in 2005 and 3.2% in 2004, respectively.²⁴ We used the same validated case definition to examine the prevalence and incidence of diagnosed hypertension in Canada from 1998/99 to 2007/08 by age and by province and territory. We also compared all-cause mortality by age and sex among those with and without diagnosed hypertension.     

CXCL9对单个核细胞的趋化作用及其机制探讨

目的 观察趋化因子CXCL9对人外周血单个核细胞的趋化作用,并探讨其对CXCR3受体后信号通路的影响.方法 分离人外周血单个核细胞并进行培养,Transwell小室趋化实验检测不同浓度的趋化因子CXCL9对外周血单个核细胞的趋化作用;Western blot方法检测CXCL9刺激外周血单个核细胞时ERK1/2及PI3K/Akt信号通路的蛋白表达变化,并检测上述通路抑制剂PD98059和Wortmannin处理细胞后,CXCL9对ERK1/2、PI3K/Akt信号通路的影响有无变化.结果 与空白对照组相比,不同浓度的CXCL9刺激对人外周血单个核细胞均有明显的趋化作用,并且CXCL9刺激人外周血单个核细胞能激活ERK1/2及PI3K/Akt信号通路,其关键蛋白ERK1/2及Akt磷酸化水平显著增加;通路特异性抑制剂PD98059和Wortmannin的应用能明显抑制CXCL9对这两条信号通路的激活.结论 CXCL9能趋化人外周血单个核细胞发生迁移,ERK1/2及PI3K/Akt信号通路可能在此过程中发挥重要作用.