Investigating the effect of rotational degree of freedom on a circular cylinder at low reynolds number in cross flow

Numerical simulations of Vortex-Induced Vibrations (VIV) of a circular cylinder in cross flow with a rotational degree of freedom about its axis have been carried out by means of a finite-volume method. The study is performed in two dimensions at a Reynolds number of Re D = 100, based on the free stream velocity and the diameter, D, of the cylinder. The effect of the rotational degree of freedom on the cylinder's lift and drag forces are compared with the baseline simulation results of flow around a stationary cylinder. The introduction of a rotational degree of freedom (d.o.f) is observed to cause the lift and drag forces to change. Also, the pattern of vortex shedding behind the cylinder is found to drastically change when the cylinder is allowed to rotate

A comparative study of immersed-boundary interpolation methods for a flow around a stationary cylinder at low Reynolds number

The accuracy and computational efficiency of various interpolation methods for the implementation of non grid-confirming boundaries is assessed. The aim of the research is to select an interpolation method that is both efficient and sufficiently accurate to be used in the simulation of vortex induced vibration of the flow around a deformable cylinder. Results are presented of an immersed boundary implementation in which the velocities near nonconfirming boundaries were interpolated in the normal direction to the walls. The flow field is solved on a Cartesian grid using a finite volume method with a staggered variable arrangement. The Strouhal number and Drag coefficient for various cases are reported. The results show a good agreement with the literature. Also, the drag coefficient and Strouhal number results for five different interpolation methods were compared it was shown that for a stationary cylinder at low Reynolds number, the interpolation method could affect the drag coefficient by a maximum 2% and the Strouhal number by maximum of 3%. In addition, the bi-liner interpolation method took about 2% more computational time per vortex shedding cycle in companion to the other methods

Decoding gas-solid interaction effects on adsorption isotherm shape: II. Polar adsorptives

A unique set of 6 polar adsorptives of relatively large dipole moment and of increasing kinetic diameter were used to probe pore volumes available and their mechanism of adsorption on a well-characterized microporous carbon. Multiple adsorption isotherm measurements were made and repeatable results with relatively small standard deviations in amount adsorbed at low relative pressures were obtained. Inconsistencies were observed between calculated Gurvitsch volumes. Sources of these were analysed and identified as contributions from one or more of: (a) molecular sieve effects; (b) molecular packing effects, and; (c) 2D molecular structure formation due to hydrogen bonding. These inconsistencies were further studied by comparison with pore volumes derived via the Dubinin-Radushkevich (DR) equation. Qualitative analyses of the micropore filling processes were proposed, and substantiated by complementary DR analyses. Although most of the isotherms showed Type I character, recasting the relative pressure axis in logarithmic format highlighted clear differences as contributions from fluid-fluid and fluid-solid interactions during pore filling. Overall, the adsorptives were classified into three groups: (a) polar adsorptives with primarily specific interactions adsorbing as a condensation process over a relatively narrow relative pressure range in a medium and late pressure range (iso-PrOH, MeOH, 2-methyl, 2-butanol, H2O); (b) polar adsorptives with potential for non-specific interactions adsorbing as a condensation process over a relatively narrow pressure range in a medium pressure range (pyridine, iso-PrOH, 2-methyl, 2- butanol); and, (c) halogenated adsorptives adsorbing with an S-shaped uptake extending over a broad relative pressure (dichloromethane)

The effects of phenoxodiol on the cell cycle of prostate cancer cell lines

Background: Prostate cancer is associated with a poor survival rate. The ability of cancer cells to evade apoptosis and exhibit limitless replication potential allows for progression of cancer from a benign to a metastatic phenotype. The aim of this study was to investigate in vitro the effect of the isoflavone phenoxodiol on the expression of cell cycle genes. Methods: Three prostate cancer cell lines-LNCaP, DU145, and PC3 were cultured in vitro, and then treated with phenoxodiol (10 μM and 30 μM) for 24 and 48 h. The expression of cell cycle genes p21WAF1, c-Myc, Cyclin-D1, and Ki-67 was investigated by Real Time PCR. Results: Here we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21WAF1 in all the cell lines in response to treatment, indicating that activation of p21WAF1 and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation. We found that c-Myc and Cyclin-D1 expression was not consistently altered across all cell lines but Ki-67 signalling expression was decreased in line with the cell cycle arrest. Conclusions: Phenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21WAF1 and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions. These data indicate that phenoxodiol would be effective as a potential future treatment modality for both hormone sensitive and hormone refractory prostate cancer

Contribution of Intrinsic Reactivity of the HIV-1 Envelope Glycoproteins to CD4-Independent Infection and Global Inhibitor Sensitivity

Human immunodeficiency virus (HIV-1) enters cells following sequential activation of the high-potential-energy viral envelope glycoprotein trimer by target cell CD4 and coreceptor. HIV-1 variants differ in their requirements for CD4; viruses that can infect coreceptor-expressing cells that lack CD4 have been generated in the laboratory. These CD4-independent HIV-1 variants are sensitive to neutralization by multiple antibodies that recognize different envelope glycoprotein epitopes. The mechanisms underlying CD4 independence, global sensitivity to neutralization and the association between them are still unclear. By studying HIV-1 variants that differ in requirements for CD4, we investigated the contribution of CD4 binding to virus entry. CD4 engagement exposes the coreceptor-binding site and increases the “intrinsic reactivity” of the envelope glycoproteins; intrinsic reactivity describes the propensity of the envelope glycoproteins to negotiate transitions to lower-energy states upon stimulation. Coreceptor-binding site exposure and increased intrinsic reactivity promote formation/exposure of the HR1 coiled coil on the gp41 transmembrane glycoprotein and allow virus entry upon coreceptor binding. Intrinsic reactivity also dictates the global sensitivity of HIV-1 to perturbations such as exposure to cold and the binding of antibodies and small molecules. Accordingly, CD4 independence of HIV-1 was accompanied by increased susceptibility to inactivation by these factors. We investigated the role of intrinsic reactivity in determining the sensitivity of primary HIV-1 isolates to inhibition. Relative to the more common neutralization-resistant (“Tier 2-like”) viruses, globally sensitive (“Tier 1”) viruses exhibited increased intrinsic reactivity, i.e., were inactivated more efficiently by cold exposure or by a given level of antibody binding to the envelope glycoprotein trimer. Virus sensitivity to neutralization was dictated both by the efficiency of inhibitor/antibody binding to the envelope glycoprotein trimer and by envelope glycoprotein reactivity to the inhibitor/antibody binding event. Quantitative differences in intrinsic reactivity contribute to HIV-1 strain variability in global susceptibility to neutralization and explain the long-observed relationship between increased inhibitor sensitivity and decreased entry requirements for target cell CD4

CD46 Protects against Chronic Obstructive Pulmonary Disease

BACKGROUND: Chronic obstructive pulmonary disease and emphysema develops in 15% of ex-smokers despite sustained quitting, while 10% are free of emphysema or severe lung obstruction. The cause of the incapacity of the immune system to clear the inflammation in the first group remains unclear. METHODS AND FINDINGS: We searched genes that were protecting ex-smokers without emphysema, using microarrays on portions of human lungs surgically removed; we found that loss of lung function in patients with chronic obstructive pulmonary disease and emphysema was associated with a lower expression of CD46 and verified this finding by qRT-PCR and flow cytometry. Also, there was a significant association among decreased CD46(+) cells with decreased CD4(+)T cells, apoptosis mediator CD95 and increased CD8(+)T cells that were protecting patients without emphysema or severe chronic obstructive pulmonary disease. CD46 not only regulates the production of T regulatory cells, which suppresses CD8(+)T cell proliferation, but also the complement cascade by degradation of C3b. These results were replicated in the murine smoking model, which showed increased C5a (produced by C3b) that suppressed IL12 mediated bias to T helper 1 cells and elastin co-precipitation with C3b, suggesting that elastin could be presented as an antigen. Thus, using ELISA from elastin peptides, we verified that 43% of the patients with severe early onset of chronic obstructive pulmonary disease tested positive for IgG to elastin in their serum compared to healthy controls. CONCLUSIONS: These data suggest that higher expression of CD46 in the lungs of ex-smoker protects them from emphysema and chronic obstructive pulmonary disease by clearing the inflammation impeding the proliferation of CD8(+) T cells and necrosis, achieved by production of T regulatory cells and degradation of C3b; restraining the complement cascade favors apoptosis over necrosis, protecting them from autoimmunity and chronic inflammation

Distributed Control Design for Balancing the Grid Using Flexible Loads

International audienceInexpensive energy from the wind and the sun comes with unwanted volatility, such as ramps with the setting sun or a gust of wind. Controllable generators manage supply-demand balance of power today, but this is becoming increasingly costly with increasing penetration of renewable energy. It has been argued since the 1980s that consumers should be put in the loop: " demand response " will help to create needed supply-demand balance. However, consumers use power for a reason, and expect that the quality of service (QoS) they receive will lie within reasonable bounds. Moreover, the behavior of some consumers is unpredictable, while the grid operator requires predictable controllable resources to maintain reliability. The goal of this chapter is to describe an emerging science for demand dispatch that will create virtual energy storage from flexible loads. By design, the grid-level services from flexible loads will be as controllable and predictable as a generator or fleet of batteries. Strict bounds on QoS will be maintained in all cases. The potential economic impact of these new resources is enormous. California plans to spend billions of dollars on batteries that will provide only a small fraction of the balancing services that can be obtained using demand dispatch. The potential impact on society is enormous: a sustainable energy future is possible with the right mix of infrastructure and control systems

Alzheimer disease models and human neuropathology: similarities and differences

Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease. Numerous mouse transgenic lines have now succeeded in partially reproducing its lesions: the extracellular deposits of Aβ peptide and the intracellular accumulation of tau protein. Mutated human APP transgenes result in the deposition of Aβ peptide, similar but not identical to the Aβ peptide of human senile plaque. Amyloid angiopathy is common. Besides the deposition of Aβ, axon dystrophy and alteration of dendrites have been observed. All of the mutations cause an increase in Aβ 42 levels, except for the Arctic mutation, which alters the Aβ sequence itself. Overexpressing wild-type APP alone (as in the murine models of human trisomy 21) causes no Aβ deposition in most mouse lines. Doubly (APP × mutated PS1) transgenic mice develop the lesions earlier. Transgenic mice in which BACE1 has been knocked out or overexpressed have been produced, as well as lines with altered expression of neprilysin, the main degrading enzyme of Aβ. The APP transgenic mice have raised new questions concerning the mechanisms of neuronal loss, the accumulation of Aβ in the cell body of the neurons, inflammation and gliosis, and the dendritic alterations. They have allowed some insight to be gained into the kinetics of the changes. The connection between the symptoms, the lesions and the increase in Aβ oligomers has been found to be difficult to unravel. Neurofibrillary tangles are only found in mouse lines that overexpress mutated tau or human tau on a murine tau −/− background. A triply transgenic model (mutated APP, PS1 and tau) recapitulates the alterations seen in AD but its physiological relevance may be discussed. A number of modulators of Aβ or of tau accumulation have been tested. A transgenic model may be analyzed at three levels at least (symptoms, lesions, cause of the disease), and a reading key is proposed to summarize this analysis

The impact of surgical delay on resectability of colorectal cancer: An international prospective cohort study

AIM: The SARS-CoV-2 pandemic has provided a unique opportunity to explore the impact of surgical delays on cancer resectability. This study aimed to compare resectability for colorectal cancer patients undergoing delayed versus non-delayed surgery. METHODS: This was an international prospective cohort study of consecutive colorectal cancer patients with a decision for curative surgery (January-April 2020). Surgical delay was defined as an operation taking place more than 4 weeks after treatment decision, in a patient who did not receive neoadjuvant therapy. A subgroup analysis explored the effects of delay in elective patients only. The impact of longer delays was explored in a sensitivity analysis. The primary outcome was complete resection, defined as curative resection with an R0 margin. RESULTS: Overall, 5453 patients from 304 hospitals in 47 countries were included, of whom 6.6% (358/5453) did not receive their planned operation. Of the 4304 operated patients without neoadjuvant therapy, 40.5% (1744/4304) were delayed beyond 4 weeks. Delayed patients were more likely to be older, men, more comorbid, have higher body mass index and have rectal cancer and early stage disease. Delayed patients had higher unadjusted rates of complete resection (93.7% vs. 91.9%, P = 0.032) and lower rates of emergency surgery (4.5% vs. 22.5%, P < 0.001). After adjustment, delay was not associated with a lower rate of complete resection (OR 1.18, 95% CI 0.90-1.55, P = 0.224), which was consistent in elective patients only (OR 0.94, 95% CI 0.69-1.27, P = 0.672). Longer delays were not associated with poorer outcomes. CONCLUSION: One in 15 colorectal cancer patients did not receive their planned operation during the first wave of COVID-19. Surgical delay did not appear to compromise resectability, raising the hypothesis that any reduction in long-term survival attributable to delays is likely to be due to micro-metastatic disease