Significance of Creep-Fatigue Interactions in Strctural Integrity Assessment

Creep-fatigue interaction is a special phenomena that have a detrimental effect on the performance of metal parts of components operating at elevated temperatures. This paper deals with the simultaneous interactions between creep and fatigue. The effect of hold time, hold position, temperature and creep ductility on creep-fatigue interaction life and damage modes of several high temperature alloys are presented in detail. The inherent deficiencies and potentially serious consequences of over-or under- design by using the classical Linear Time and Cycle-Fraction rule for predicting structural durability under high temperature creep-fatigue conditions are presented. The potential of a strain based approach in accurately predicting creep-fatigue life for ensuring structural integrity is outlined

Korteweg - de Vries solitons with different co-ordinate stretchings

The differences between the soliton solutions of the K-dV equation for a homogeneous, collisionless plasma, consisting of cold ions and isothermal electrons arising due to the two different sets of stretched co-ordinates have been discussed. In particular, the differences between the amplitudes and the widths of the solitons and their variations with the soliton velocity have been indicated. Further, the experimental implications of these differences and also of the two sets of stretched co-ordinates have been discussed

Toxicity of CdSe Nanoparticles in Caco-2 Cell Cultures

<p>Abstract</p> <p>Background</p> <p>Potential routes of nanomaterial exposure include inhalation, dermal contact, and ingestion. Toxicology of inhalation of ultra-fine particles has been extensively studied; however, risks of nanomaterial exposure via ingestion are currently almost unknown. Using enterocyte-like Caco-2 cells as a small intestine epithelial model, the possible toxicity of CdSe quantum dot (QD) exposure via ingestion was investigated. Effect of simulated gastric fluid treatment on CdSe QD cytotoxicity was also studied.</p> <p>Results</p> <p>Commercially available CdSe QDs, which have a ZnS shell and poly-ethylene glycol (PEG) coating, and in-house prepared surfactant coated CdSe QDs were dosed to Caco-2 cells. Cell viability and attachment were studied after 24 hours of incubation. It was found that cytotoxicity of CdSe QDs was modulated by surface coating, as PEG coated CdSe QDs had less of an effect on Caco-2 cell viability and attachment. Acid treatment increased the toxicity of PEG coated QDs, most likely due to damage or removal of the surface coating and exposure of CdSe core material. Incubation with un-dialyzed in-house prepared CdSe QD preparations, which contained an excess amount of free Cd²⁺, resulted in dramatically reduced cell viability.</p> <p>Conclusion</p> <p>Exposure to CdSe QDs resulted in cultured intestinal cell detachment and death; cytotoxicity depended largely, however, on the QD coating and treatment (e.g. acid treatment, dialysis). Experimental results generally indicated that Caco-2 cell viability correlated with concentration of free Cd²⁺ions present in cell culture medium. Exposure to low (gastric) pH affected cytotoxicity of CdSe QDs, indicating that route of exposure may be an important factor in QD cytotoxicity.</p

Toxicity of CdSe Nanoparticles in Caco-2 Cell Cultures

<p>Abstract</p> <p>Background</p> <p>Potential routes of nanomaterial exposure include inhalation, dermal contact, and ingestion. Toxicology of inhalation of ultra-fine particles has been extensively studied; however, risks of nanomaterial exposure via ingestion are currently almost unknown. Using enterocyte-like Caco-2 cells as a small intestine epithelial model, the possible toxicity of CdSe quantum dot (QD) exposure via ingestion was investigated. Effect of simulated gastric fluid treatment on CdSe QD cytotoxicity was also studied.</p> <p>Results</p> <p>Commercially available CdSe QDs, which have a ZnS shell and poly-ethylene glycol (PEG) coating, and in-house prepared surfactant coated CdSe QDs were dosed to Caco-2 cells. Cell viability and attachment were studied after 24 hours of incubation. It was found that cytotoxicity of CdSe QDs was modulated by surface coating, as PEG coated CdSe QDs had less of an effect on Caco-2 cell viability and attachment. Acid treatment increased the toxicity of PEG coated QDs, most likely due to damage or removal of the surface coating and exposure of CdSe core material. Incubation with un-dialyzed in-house prepared CdSe QD preparations, which contained an excess amount of free Cd²⁺, resulted in dramatically reduced cell viability.</p> <p>Conclusion</p> <p>Exposure to CdSe QDs resulted in cultured intestinal cell detachment and death; cytotoxicity depended largely, however, on the QD coating and treatment (e.g. acid treatment, dialysis). Experimental results generally indicated that Caco-2 cell viability correlated with concentration of free Cd²⁺ions present in cell culture medium. Exposure to low (gastric) pH affected cytotoxicity of CdSe QDs, indicating that route of exposure may be an important factor in QD cytotoxicity.</p

FORMULATION, CHARACTERIZATION AND EVALUATION OF ANTI-INFLAMMATORY AND ANTI-ANGIOGENIC ACTIVITIES OF MEMECYLAENE NANOEMULSION

The present study was undertaken to formulate and evaluate the anti-inflammatory, anti-oxidant and anti-angiogenic activities of nanoemulsion of Memecylaene.&nbsp; Memecylaene was isolated from the leaves of Memecylon malabaricum by using various chromatographic methods. An oil-in-water (O/W) nanoemulsion of Memecylaene was formulated by sonication method using sunflower oil (oil phase), Tween 80 (Surfactant) and Ethanol (co-surfactant). The prepared nanoemulsion was characterized for its droplet size, poly dispersity index and zeta potential. Stability studies were performed and the nanoemulsions were subjected to different biological activities. The formulated nanoemulsion had a particle size range of 52.02 nm to 59.47 nm and zeta potential of -1.27 mV. The enhanced activity of Memecylaene, encapsulated in O/W emulsions is evidenced by the inhibition of phospholipase (PLA2) enzyme and H+, K+ -ATPase and thus showing anti-inflammatory and anti-secretagogues effects. The in vitro anti-oxidant activity was evaluated by DPPH radical and Nitric oxide radical scavenging activity. Further, the inhibition of the growth of neo vessels formation in the in-vivo model system of chick chorioallantoic membrane (CAM) assay, which is angiogenesis dependent, was also observed. The above findings would help in understanding the putative potential of Memecylaene-loaded nanoemulsion as a therapeutic agent. Keywords: Anti-angiogenesis, Anti-oxidant, Gastric (H+ K+), Memecylaene, Nanoemulsion, Phospholipase A2 (PLA2)

Uncertainties in Theoretical HeI Emissivities: HII Regions, Primordial Abundance, and Cosmological Recombination

A number of recent works in astronomy and cosmology have relied upon theoretical He I emissivities, but we know of no effort to quantify the uncertainties in the atomic data. We analyze and assign uncertainties to all relevant atomic data, perform Monte Carlo analyses, and report standard deviations in the line emissivities. We consider two sets of errors, which we call "optimistic" and "pessimistic." We also consider three different conditions, corresponding to prototypical Galactic and extragalactic H II regions and the epoch of cosmological recombination. In the extragalactic H II case, the errors we obtain are comparable to or larger than the errors in some recent $Y_p$ calculations, including those derived from CMB observations. We demonstrate a systematic effect on primordial abundance calculations; this effect cannot be reduced by observing a large number of objects. In the cosmological recombination case, the errors are comparable to many of the effects considered in recent calculations.Comment: 5 pages, 3 figures, accepted to MNRAS Letter

Growth, mortality and stock assessment of Arius arius (Hamilton, 1822) from Hooghly-Matlah estuary, West Bengal

The growth, mortality, and stock assessment of Arius arius were estimated based on monthly length-frequency analysis data collected from the Hooghly-Matlah estuary of West Bengal, India from April 2017 to March 2018. The estimated growth parameters were as L∞ = 278 mm, K = 0.97 yr-1, and t0 = -0.0889 years. The different mortality coefficients Z, M, and F were obtained as 5.25 yr-1, 1.79 yr-1, and 3.46 yr-1, respectively. The calculated exploitation ratio (E) was found as 0.66, and the M/K value as 1.845 indicating overexploitation of the fish. The recruitment was found throughout the year with two peaks and the value of Lc was found at 56.00 mm. The estimated virtual population analysis (VPA) indicated that the highest fishing mortality (F) of 3.4499 was observed at the 190-200 mm length class, followed by 3.2393 from the 180-190 mm length class. The fishery was found at the overexploitation level and measures are needed to regulate it for promoting its sustainability

Investigation on Photovoltaic Performance based on Matchstick-Like Cu2S–In2S3Heterostructure Nanocrystals and Polymer

In this paper, we synthesized a novel type II cuprous sulfide (Cu2S)–indium sulfide (In2S3) heterostructure nanocrystals with matchstick-like morphology in pure dodecanethiol. The photovoltaic properties of the heterostructure nanocrystals were investigated based on the blends of the nanocrystals and poly(2-methoxy-5-(2′-ethylhexoxy)-p-phenylenevinylene) (MEH-PPV). In comparison with the photovoltaic properties of the blends of Cu2S or In2S3nanocrystals alone and MEH-PPV, the power conversion efficiency of the hybrid device based on blend of Cu2S–In2S3and MEH-PPV is enhanced by ~3–5 times. This improvement is consistent with the improved exciton dissociation or separation and better charge transport abilities in type II heterostructure nanocrystals

Detection of high levels of mutations involved in anti-malarial drug resistance in Plasmodium falciparum and Plasmodium vivax at a rural hospital in southern Ethiopia

<p>Abstract</p> <p>Background</p> <p>In Ethiopia, malaria is caused by <it>Plasmodium falciparum </it>and <it>Plasmodium vivax</it>, and anti-malarial drug resistance is the most pressing problem confronting control of the disease. Since co-infection by both species of parasite is common and sulphadoxine-pyrimethamine (SP) has been intensively used, resistance to these drugs has appeared in both <it>P. falciparum </it>and <it>P. vivax </it>populations. This study was conducted to assess the prevalence of anti-malarial drug resistance in <it>P. falciparum </it>and <it>P. vivax </it>isolates collected at a rural hospital in southern Ethiopia.</p> <p>Methods</p> <p>A total of 1,147 patients with suspected malaria were studied in different months across the period 2007-2009. <it>Plasmodium falciparum dhfr </it>and <it>dhps </it>mutations and <it>P. vivax dhfr </it>polymorphisms associated with resistance to SP, as well as <it>P. falciparum pfcrt </it>and <it>pfmdr1 </it>mutations conferring chloroquine resistance, were assessed.</p> <p>Results</p> <p>PCR-based diagnosis showed that 125 of the 1147 patients had malaria. Of these, 52.8% and 37.6% of cases were due to <it>P. falciparum </it>and <it>P. vivax </it>respectively. A total of 10 cases (8%) showed co-infection by both species and two cases (1.6%) were infected by <it>Plasmodium ovale</it>. <it>Pfdhfr </it>triple mutation and <it>pfdhfr/pfdhps </it>quintuple mutation occurred in 90.8% (95% confidence interval [CI]: 82.2%-95.5%) and 82.9% (95% CI: 72.9%-89.7%) of <it>P. falciparum </it>isolates, respectively. <it>Pfcrt </it>T76 was observed in all cases and <it>pfmdr1 </it>Y86 and <it>pfmdr1 </it>Y1246 in 32.9% (95% CI: 23.4%-44.15%) and 17.1% (95% CI: 10.3-27.1%), respectively. The <it>P. vivax dhfr </it>core mutations, N117 and R58, were present in 98.2% (95% CI: 89.4-99.9%) and 91.2% (95% CI: 80.0-96.7%), respectively.</p> <p>Conclusion</p> <p>Current molecular data show an extraordinarily high frequency of drug-resistance mutations in both <it>P. falciparum </it>and <it>P. vivax </it>in southern Ethiopia. Urgent surveillance of the emergence and spread of resistance is thus called for. The level of resistance indicates the need for implementation of entire population access to the new first-line treatment with artemether-lumefantrine, accompanied by government monitoring to prevent the emergence of resistance to this treatment.</p

A systematic review and meta-analysis of evidence for correlation between molecular markers of parasite resistance and treatment outcome in falciparum malaria

<p>Abstract</p> <p>Background</p> <p>An assessment of the correlation between anti-malarial treatment outcome and molecular markers would improve the early detection and monitoring of drug resistance by <it>Plasmodium falciparum</it>. The purpose of this systematic review was to determine the risk of treatment failure associated with specific polymorphisms in the parasite genome or gene copy number.</p> <p>Methods</p> <p>Clinical studies of non-severe malaria reporting on target genetic markers (SNPs for <it>pfmdr1</it>, <it>pfcrt</it>, <it>dhfr</it>, <it>dhps</it>, gene copy number for <it>pfmdr1</it>) providing complete information on inclusion criteria, outcome, follow up and genotyping, were included. Three investigators independently extracted data from articles. Results were stratified by gene, codon, drug and duration of follow-up. For each study and aggregate data the random effect odds ratio (OR) with 95%CIs was estimated and presented as Forest plots. An OR with a lower 95^thconfidence interval > 1 was considered consistent with a failure being associated to a given gene mutation.</p> <p>Results</p> <p>92 studies were eligible among the selection from computerized search, with information on <it>pfcrt </it>(25/159 studies), <it>pfmdr1 </it>(29/236 studies), <it>dhfr </it>(18/373 studies), <it>dhps </it>(20/195 studies). The risk of therapeutic failure after chloroquine was increased by the presence of <it>pfcrt </it>K76T (Day 28, OR = 7.2 [95%CI: 4.5–11.5]), <it>pfmdr1 </it>N86Y was associated with both chloroquine (Day 28, OR = 1.8 [95%CI: 1.3–2.4]) and amodiaquine failures (OR = 5.4 [95%CI: 2.6–11.3, p < 0.001]). For sulphadoxine-pyrimethamine the <it>dhfr </it>single (S108N) (Day 28, OR = 3.5 [95%CI: 1.9–6.3]) and triple mutants (S108N, N51I, C59R) (Day 28, OR = 3.1 [95%CI: 2.0–4.9]) and <it>dhfr</it>-<it>dhps </it>quintuple mutants (Day 28, OR = 5.2 [95%CI: 3.2–8.8]) also increased the risk of treatment failure. Increased <it>pfmdr1 </it>copy number was correlated with treatment failure following mefloquine (OR = 8.6 [95%CI: 3.3–22.9]).</p> <p>Conclusion</p> <p>When applying the selection procedure for comparative analysis, few studies fulfilled all inclusion criteria compared to the large number of papers identified, but heterogeneity was limited. Genetic molecular markers were related to an increased risk of therapeutic failure. Guidelines are discussed and a checklist for further studies is proposed.</p