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Like any other turbomachinery, it is essential that the hydraulic behavior and performance of mixed-flow pumps are evaluated way in advance prior to manufacturing. Pump performance relies heavily on the proper design of the intake structure. Intake structures should be accurately designed in order to minimize and avoid unnecessary swirl and vortex formations. Ensuring the optimum performance condition as well as predicting how a particular intake structure affects the efficiency of the pump often requires either physical model studies or theoretical evaluations. Unfortunately, physical models are costly, time-consuming, and site-specific. Conversely, design and performance predictions using a theoretical approach merely gives performance values or parameters, which are usually unable to determine the root cause of poor pump performance. This study evaluates the viability of using Computational Fluid Dynamics (CFD) as an alternative tool for pump designers and engineers in evaluating pump performance. A procedure for conducting CFD simulations to verify pump characteristics such as head, efficiency, and flow as an aid for preliminary pump design is presented. Afterwards, a multiphase simulation using the VOF approach is applied to compare the fluid dynamics between four different pump intake structures. A full-sized CFD model of the pump sump complete with the pump’s active components was used for the intake structure analysis in order to avoid scaling issues encountered during the reduced-scale physical model test. The results provided a clear illustration of the hydraulic phenomena and characteristic curves of the pump. A performance drop in terms of reduction in TDH was predicted across the various intake structure designs. The CFD simulation of intake structure provided a clear insight on the varying degree of swirl, flow circulation, and effect on pump efficiency between all four cases.

Pump intake structure design is one area where physical models still remain as the only acceptable method that can provide reliable engineering results. Ensuring the amount of turbulence, entrained air vortices, and swirl are kept within acceptable limits requires site-specific, expensive, and time-consuming physical model studies. This study aims to investigate the viability of Computational Fluid Dynamics (CFD) as an alternative tool for pump intake design thus reducing the need for extensive physical experiments. In this study, a transient multiphase simulation of a 530 mm wide rectangular intake sump housing a 116 m3/h pump is presented. The flow conditions, vortex formation and inlet swirl are compared to an existing 1:10 reduced scaled physical model test. For the baseline test, the predicted surface and submerged vortices agreed well with those observed in the physical model. Both the physical model test and the numerical model showed that the initial geometry of the pump sump is unacceptable as per ANSI/HI 9.8 criteria. Strong type 2 to type 3 submerged vortices were observed at the floor of the pump and behind the pump. Consequently, numerical simulations of proposed sump design modification are further investigated. Two CFD models with different fillet-splitter designs are evaluated and compared based on the vortex formation and swirl. In the study, it was seen that a trident-shaped splitter design was able to prevent flow separation and vortex suppression as compared to a cross-baffle design based on ANSI/HI 9.8. CFD results for the cross-baffle design showed that backwall and floor vortices were still present and additional turbulence was observed due to the cross-flow caused by the geometry. Conversely, CFD results for the trident-shaped fillet-splitter design showed stable flow and minimized the floor and wall vortices previously observed in the first two models.

This Review is intended to help clinicians, patients, and the public make informed decisions about statin therapy for the prevention of heart attacks and strokes. It explains how the evidence that is available from randomised controlled trials yields reliable information about both the efficacy and safety of statin therapy. In addition, it discusses how claims that statins commonly cause adverse effects reflect a failure to recognise the limitations of other sources of evidence about the effects of treatment. Large-scale evidence from randomised trials shows that statin therapy reduces the risk of major vascular events (ie, coronary deaths or myocardial infarctions, strokes, and coronary revascularisation procedures) by about one-quarter for each mmol/L reduction in LDL cholesterol during each year (after the first) that it continues to be taken. The absolute benefits of statin therapy depend on an individual's absolute risk of occlusive vascular events and the absolute reduction in LDL cholesterol that is achieved. For example, lowering LDL cholesterol by 2 mmol/L (77 mg/dL) with an effective low-cost statin regimen (eg, atorvastatin 40 mg daily, costing about £2 per month) for 5 years in 10 000 patients would typically prevent major vascular events from occurring in about 1000 patients (ie, 10% absolute benefit) with pre-existing occlusive vascular disease (secondary prevention) and in 500 patients (ie, 5% absolute benefit) who are at increased risk but have not yet had a vascular event (primary prevention). Statin therapy has been shown to reduce vascular disease risk during each year it continues to be taken, so larger absolute benefits would accrue with more prolonged therapy, and these benefits persist long term. The only serious adverse events that have been shown to be caused by long-term statin therapy—ie, adverse effects of the statin—are myopathy (defined as muscle pain or weakness combined with large increases in blood concentrations of creatine kinase), new-onset diabetes mellitus, and, probably, haemorrhagic stroke. Typically, treatment of 10 000 patients for 5 years with an effective regimen (eg, atorvastatin 40 mg daily) would cause about 5 cases of myopathy (one of which might progress, if the statin therapy is not stopped, to the more severe condition of rhabdomyolysis), 50–100 new cases of diabetes, and 5–10 haemorrhagic strokes. However, any adverse impact of these side-effects on major vascular events has already been taken into account in the estimates of the absolute benefits. Statin therapy may cause symptomatic adverse events (eg, muscle pain or weakness) in up to about 50–100 patients (ie, 0·5–1·0% absolute harm) per 10 000 treated for 5 years. However, placebo-controlled randomised trials have shown definitively that almost all of the symptomatic adverse events that are attributed to statin therapy in routine practice are not actually caused by it (ie, they represent misattribution). The large-scale evidence available from randomised trials also indicates that it is unlikely that large absolute excesses in other serious adverse events still await discovery. Consequently, any further findings that emerge about the effects of statin therapy would not be expected to alter materially the balance of benefits and harms. It is, therefore, of concern that exaggerated claims about side-effect rates with statin therapy may be responsible for its under-use among individuals at increased risk of cardiovascular events. For, whereas the rare cases of myopathy and any muscle-related symptoms that are attributed to statin therapy generally resolve rapidly when treatment is stopped, the heart attacks or strokes that may occur if statin therapy is stopped unnecessarily can be devastating.

In a follow-up study of patients with type 2 diabetes, mortality benefits in those originally assigned to antihypertensive therapy were evident at the end of follow-up, but in-trial glucose differences did not result in long-term benefits in mortality or macrovascular events. Post-trial follow-up studies involving patients with diabetes have previously shown long-term beneficial effects of earlier periods of intensive glucose control, but not blood-pressure lowering, on a range of outcomes, including mortality and macrovascular events. 1 – 3 The Epidemiology of Diabetes Interventions and Complications (EDIC) study, an extension of the Diabetes Control and Complications Trial (DCCT) involving young patients with type 1 diabetes and no history of cardiovascular disease, hypertension, or hypercholesterolemia, showed a lower risk of macrovascular events, as well as a sustained benefit with respect to microvascular complications, beyond the period of intensive glucose control. 1 The post-intervention follow-up of the . . .

Low-grade serous carcinoma of the ovary or peritoneum is characterised by MAPK pathway aberrations and its reduced sensitivity to chemotherapy relative to high-grade serous carcinoma. We compared the MEK inhibitor trametinib to physician's choice standard of care in patients with recurrent low-grade serous carcinoma. This international, randomised, open-label, multicentre, phase 2/3 trial was done at 84 hospitals in the USA and UK. Eligible patients were aged 18 years or older with recurrent low-grade serous carcinoma and measurable disease, as defined by Response Evaluation Criteria In Solid Tumors version 1.1, had received at least one platinum-based regimen, but not all five standard-of-care drugs, and had received an unlimited number of previous regimens. Patients with serous borderline tumours or tumours containing low-grade serous and high-grade serous carcinoma were excluded. Eligible patients were randomly assigned (1:1) to receive either oral trametinib 2 mg once daily (trametinib group) or one of five standard-of-care treatment options (standard-of-care group): intravenous paclitaxel 80 mg/m2 by body surface area on days 1, 8, and 15 of every 28-day cycle; intravenous pegylated liposomal doxorubicin 40–50 mg/m2 by body surface area once every 4 weeks; intravenous topotecan 4 mg/m2 by body surface area on days 1, 8, and 15 of every 28-day cycle; oral letrozole 2·5 mg once daily; or oral tamoxifen 20 mg twice daily. Randomisation was stratified by geographical region (USA or UK), number of previous regimens (1, 2, or ≥3), performance status (0 or 1), and planned standard-of-care regimen. The primary endpoint was investigator-assessed progression-free survival while receiving randomised therapy, as assessed by imaging at baseline, once every 8 weeks for 15 months, and then once every 3 months thereafter, in the intention-to-treat population. Safety was assessed in patients who received at least one dose of study therapy. This trial is registered with ClinicalTrials.gov, NCT02101788, and is active but not recruiting. Between Feb 27, 2014, and April 10, 2018, 260 patients were enrolled and randomly assigned to the trametinib group (n=130) or the standard-of-care group (n=130). At the primary analysis, there were 217 progression-free survival events (101 [78%] in the trametinib group and 116 [89%] in the standard-of-care group). Median progression-free survival in the trametinib group was 13·0 months (95% CI 9·9–15·0) compared with 7·2 months (5·6–9·9) in the standard-of-care group (hazard ratio 0·48 [95% CI 0·36–0·64]; p<0·0001). The most frequent grade 3 or 4 adverse events in the trametinib group were skin rash (17 [13%] of 128), anaemia (16 [13%]), hypertension (15 [12%]), diarrhoea (13 [10%]), nausea (12 [9%]), and fatigue (ten [8%]). The most frequent grade 3 or 4 adverse events in the standard-of-care group were abdominal pain (22 [17%]), nausea (14 [11%]), anaemia (12 [10%]), and vomiting (ten [8%]). There were no treatment-related deaths. Trametinib represents a new standard-of-care option for patients with recurrent low-grade serous carcinoma. NRG Oncology, Cancer Research UK, Target Ovarian Cancer, and Novartis.

Increasing levels of atmospheric carbon dioxide leads to ocean acidification, causing significant reductions in the growth of crustose coralline algae. Owing to anthropogenic emissions, atmospheric concentrations of carbon dioxide could almost double between 2006 and 2100 according to business-as-usual carbon dioxide emission scenarios 1 . Because the ocean absorbs carbon dioxide from the atmosphere 2 , 3 , 4 , increasing atmospheric carbon dioxide concentrations will lead to increasing dissolved inorganic carbon and carbon dioxide in surface ocean waters, and hence acidification and lower carbonate saturation states 2 , 5 . As a consequence, it has been suggested that marine calcifying organisms, for example corals, coralline algae, molluscs and foraminifera, will have difficulties producing their skeletons and shells at current rates 6 , 7 , with potentially severe implications for marine ecosystems, including coral reefs 6 , 8 , 9 , 10 , 11 . Here we report a seven-week experiment exploring the effects of ocean acidification on crustose coralline algae, a cosmopolitan group of calcifying algae that is ecologically important in most shallow-water habitats 12 , 13 , 14 . Six outdoor mesocosms were continuously supplied with sea water from the adjacent reef and manipulated to simulate conditions of either ambient or elevated seawater carbon dioxide concentrations. The recruitment rate and growth of crustose coralline algae were severely inhibited in the elevated carbon dioxide mesocosms. Our findings suggest that ocean acidification due to human activities could cause significant change to benthic community structure in shallow-warm-water carbonate ecosystems.

Nine coral survey methods were compared at ten sites in various reef habitats with different levels of coral cover in Kāne'ohe Bay, O'ahu, Hawai'i. Mean estimated coverage at the different sites ranged from less than 10% cover to greater than 90% cover. The methods evaluated include line transects, various visual and photographic belt transects, video transects and visual estimates. At each site 25 m transect lines were laid out and secured. Observers skilled in each method measured coral cover at each site. The time required to run each transect, time required to process data and time to record the results were documented. Cost of hardware and software for each method was also tabulated. Results of this investigation indicate that all of the methods used provide a good first estimate of coral cover on a reef. However, there were differences between the methods in detecting the number of coral species. For example, the classic \"quadrat\" method allows close examination of small and cryptic coral species that are not detected by other methods such as the \"towboard\" surveys. The time, effort and cost involved with each method varied widely, and the suitability of each method for answering particular research questions in various environments was evaluated. Results of this study support the finding of three other comparison method studies conducted at various geographic locations throughout the world. Thus, coral cover measured by different methods can be legitimately combined or compared in many situations. The success of a recent modeling effort based on coral cover data consisting of observations taken in Hawai'i using the different methods supports this conclusion.

Coral reef ecosystems are presently undergoing decline due to anthropogenic climate change. The chief detrimental factors are increased temperature and increased pCO 2 . The purpose of this study was to evaluate the effect of these two stressors operating independently and in unison on the biological response of common Hawaiian reef corals. Manipulative experiments were performed using five species ( Porites compressa , Pocillopora damicornis , Fungia scutaria , Montipora capitata , and Leptastrea purpurea ) in a continuous-flow mesocosm system under natural sunlight conditions. Corals were grown together as a community under treatments of high temperature (2 °C above normal maximum summer temperature), high pCO 2 (twice present-day conditions), and with both factors acting in unison. Control corals were grown under present-day pCO 2 and at normal summer temperatures. Leptastrea purpurea proved to be an extremely hardy coral. No change in calcification or mortality occurred under treatments of high temperature, high pCO 2 , or combined high temperature–high pCO 2 . The remaining four species showed reduced calcification in the high-temperature treatment. Two species ( L . purpurea and M . capitata ) showed no response to increased pCO 2 . Also, high pCO 2 ameliorated the negative effect of high temperature on the calcification rates of P . damicornis . Mortality was driven primarily by high temperature, with a negative synergistic effect in P . compressa only in the high-pCO 2 –high-temperature treatment. Results support the observation that biological response to temperature and pCO 2 elevation is highly species-specific, so generalizations based on response of a single species might not apply to a diverse and complex coral reef community.

Successful reproduction and survival are crucial to the continuation and resilience of corals globally. As reef waters warm due to climate change, episodic largescale tropical storms are becoming more frequent, drastically altering the near shore water quality for short periods of time. Therefore, it is critical that we understand the effects warming waters, fresh water input, and run-off have on sexual reproduction of coral. To better understand the effects of these near shore stressors on Hawaiian coral, laboratory experiments were conducted at the Institute of Marine Biology to determine the independent effects of suspended sediment concentrations (100 mg l −1 and 200 mg l −1 ), lowered salinity (28‰), and elevated temperature (31 °C) on the successful fertilization, larval survival, and settlement of the scleractinian coral Montipora capitata. In the present study, early developmental stages of coral were exposed to one of three near shore stressors for a period of 24 h and the immediate (fertilization) and latent effects (larval survival and settlement) were observed and measured. Fertilization success and settlement were not affected by any of the treatments; however, larval survival was negatively affected by all of the treatments by 50% or greater ( p  > 0.05). These data show that early life stages of M. capitata may be impacted by near shore stressors associated with warming and more frequent storm events.

Until recently, subtropical Hawai'i escaped the major bleaching events that have devastated many tropical regions, but the continued increases in global long-term mean temperatures and the apparent ending of the Pacific Decadal Oscillation (PDO) cool phase have increased the risk of bleaching events. Climate models and observations predict that bleaching in Hawai'i will occur with increasing frequency and increasing severity over future decades. A freshwater \"kill\" event occurred during July 2014 in the northern part of Kāne'ohe Bay that reduced coral cover by 22.5% in the area directly impacted by flooding. A subsequent major bleaching event during September 2014 caused extensive coral bleaching and mortality throughout the bay and further reduced coral cover in the freshwater kill area by 60.0%. The high temperature bleaching event only caused a 1.0% reduction in live coral throughout the portion of the bay not directly impacted by the freshwater event. Thus, the combined impact of the low salinity event and the thermal bleaching event appears to be more than simply additive. The temperature regime during the September 2014 bleaching event was analogous in duration and intensity to that of the large bleaching event that occurred previously during August 1996, but resulted in a much larger area of bleaching and coral mortality. Apparently seasonal timing as well as duration and magnitude of heating is important. Coral spawning in the dominant coral species occurs early in the summer, so reservoirs of stored lipid in the corals had been depleted by spawning prior to the September 2014 event. Warm months above 27 °C result in lower coral growth and presumably could further decrease lipid reserves, leading to a bleaching event that was more severe than would have happened if the high temperatures occurred earlier in the summer. Hawaiian reef corals decrease skeletal growth at temperatures above 27 °C, so perhaps the \"stress period\" actually started long before the bleaching threshold of 29 °C was reached. Hawai'i is directly influenced by the PDO which may become a factor influencing bleaching events in subtropical Hawai'i in much the same manner as variations in the El Niño Southern Oscillation (ENSO) influences bleaching events at low latitudes in the tropical Pacific. Records show that offshore temperatures measured by satellite will not always predict inshore bleaching because other factors (high cloud cover, high wind and wave action, tidal exchange rate) can limit inshore heating and prevent temperatures in the bay from reaching the bleaching threshold. Low light levels due to cloud cover or high turbidity can also serve to prevent bleaching.