Nonlinear waves in counter-current gas–liquid film flow

We investigate the dynamics of a thin laminar liquid film flowing under gravity down the lower wall of an inclined channel when turbulent gas flows above the film. The solution of the full system of equations describing the gas–liquid flow faces serious technical difficulties. However, a number of assumptions allow isolating the gas problem and solving it independently by treating the interface as a solid wall. This permits finding the perturbations to pressure and tangential stresses at the interface imposed by the turbulent gas in closed form. We then analyse the liquid film flow under the influence of these perturbations and derive a hierarchy of model equations describing the dynamics of the interface, i.e. boundary-layer equations, a long-wave model and a weakly nonlinear model, which turns out to be the Kuramoto– Sivashinsky equation with an additional term due to the presence of the turbulent gas. This additional term is dispersive and destabilising (for the counter-current case; stabilizing in the co-current case). We also combine the long-wave approximation with a weighted-residual technique to obtain an integral-boundary-layer approximation that is valid for moderately large values of the Reynolds number. This model is then used for a systematic investigation of the flooding phenomenon observed in various experiments: as the gas flow rate is increased, the initially downward-falling film starts to travel upwards while just before the wave reversal the amplitude of the waves grows rapidly. We confirm the existence of large-amplitude stationary waves by computing periodic travelling waves for the integral-boundary-layer approximation and we corroborate our travelling-wave results by time-dependent computations

Anti-α-glucose-based glycan IgM antibodies predict relapse activity in multiple sclerosis after the first neurological event

Background There is no specific serum-based biomarker for the diagnosis or prognosis of relapsing-remitting multiple sclerosis (RRMS). Objective We investigated whether levels of IgM antibodies to Glc(alpha 1,4) Glc(alpha) (GAGA4) or to a panel of four glucose-based glycans could differentiate MS from other neurological diseases (OND) or predict risk of early relapse following first presentation (FP) of RRMS. Methods Retrospective analysis of 440 sera samples of three cohorts: A) FP-RRMS (n = 44), OND (n = 44); B) FP-RRMS (n = 167), OND (n = 85); and C) FP (n = 100). Anti-GAGA4 IgM levels were measured by enzyme immunoassay in cohort-A and cohort-B. Cohort-C IgM antibodies to glucose-based glycan panel were measured by immunofluorescence. Results FP-RRMS had higher levels of anti-GAGA4 IgM than OND patients (cohort-A, P = 0.01; cohort-B, P = 0.0001). Sensitivity and specificity were 27% and 97% for cohort-A; and 26% and 90% for cohort-B, respectively. In cohort-C, 58 patients experienced early relapse (= 24 months), and 11 did not experience second attack during follow-up. Kaplan-Meier curves demonstrated decrease in time to next relapse for patients positive for the antibody panel (P = 0.02, log rank). Conclusions Serum anti-GAGA4 IgM discerns FP-RRMS patients from OND patients. Higher levels of serum anti-alpha-glucose IgM in FP patients predict imminent early relapse. Multiple Sclerosis 2009; 15: 422-430. http://msj.sagepub.co

Is a super-enhancer greater than the sum of its parts?

The recent back-to-back articles by Hay et al.1 and Shin et al.2 both addressed the important question of how the constituent enhancers of a so-called 'super-enhancer' combine to activate the expression of a target gene. Super-enhancers are collections of closely spaced genomic regions that exhibit hallmarks of enhancers, such as binding by the Mediator complex and acetylation of histone H3 at lysine 27 (H3K27ac)3, 4, 5. As the authors of these articles noted1, 2, there is continuing controversy over whether super-enhancers genuinely represent a new paradigm in transcriptional regulation or whether they may essentially just be clusters of conventional enhancers that together produce a strong transcriptional response6

The effects of pravastatin on the normal human placenta: Lessons from <i>ex-vivo</i> models

<div><p>Introduction</p><p>Research in animal models and preliminary clinical studies in humans support the use of pravastatin for the prevention of preeclampsia. However, its use during pregnancy is still controversial due to limited data about its effect on the human placenta and fetus.</p><p>Methods</p><p>In the present study, human placental cotyledons were perfused in the absence or presence of pravastatin in the maternal reservoir (PraM). In addition, placental explants were treated with pravastatin for 5, 24 and 72 h under normoxia and hypoxia. We monitored the secretion of placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), soluble endoglin (sEng), endothelial nitric oxide synthase (eNOS) expression and activation and the fetal vasoconstriction response to angiotensin-II.</p><p>Results</p><p>The concentrations of PlGF, sFlt-1 and sEng were not significantly altered by pravastatin in PraM cotyledons and in placental explants compared to control. Under hypoxic conditions, pravastatin decreased sFlt-1 concentrations. eNOS expression was significantly increased in PraM cotyledons but not in pravastatin-treated placental explants cultured under normoxia or hypoxia. eNOS phosphorylation was not significantly affected by pravastatin. The feto-placental vascular tone and the fetal vasoconstriction response to angiotensin-II, did not change following exposure of the maternal circulation to pravastatin.</p><p>Conclusion</p><p>We found that pravastatin does not alter the essential physiological functions of the placenta investigated in the study. The relevance of the study lays in the fact that it expands the current knowledge obtained thus far regarding the effect of the drug on the normal human placenta. This data is reassuring and important for clinicians that consider the treatment of high-risk patients with pravastatin, a treatment that exposes some normal pregnancies to the drug.</p></div

Antibodies against Glucan, Chitin, and Saccharomyces cerevisiae Mannan as New Biomarkers of Candida albicans Infection That Complement Tests Based on C. albicans Mannan▿

Antibodies against Saccharomyces cerevisiae mannan (ASCA) and antibodies against synthetic disaccharide fragments of glucans (ALCA) and chitin (ACCA) are biomarkers of Crohn's disease (CD). We previously showed that Candida albicans infection generates ASCA. Here, we explored ALCA and ACCA as possible biomarkers of invasive C. albicans infection (ICI). ASCA, ALCA, ACCA, and Candida mannan antigen and antibody detection tests were performed on 69 sera obtained sequentially from 18 patients with ICIs proven by blood culture, 59 sera from CD patients, 47 sera from hospitalized subjects colonized by Candida species (CZ), and 131 sera from healthy controls (HC). ASCA, ALCA, and ACCA levels in CD and ICI patients were significantly different from those in CZ and HC subjects (P < 0.0001). In ICI patients, these levels increased as infection developed. Using ASCA, ALCA, ACCA, and Platelia Candida tests, 100% of ICIs were detected, with the kinetics of the antibody response depending on the patient during the time course of infection. A large number of sera presented with more than three positive tests. This is the first evidence that the detection of antibodies against chitin and glucans has diagnostic value in fungal infections and that these tests can complement more specific tests. Future trials are necessary to assess the value of these tests in multiparametric analysis, as well as their pathophysiological relevance