Product Marking and Conformity Assessment of Portland Cements on the Ghanaian Market

Cement bound concrete materials and complementary fittings are requisite ingredients for all civil engineering works. In all these, Portland cement, a basic binding ingredient for the concrete work is the dominant binder. In Ghana, there are various brands of cement on the market. Five major brand products currently in circulation include the Ghana Cement (GHACEM), Western DIAMOND Cement (DIAMOND), CIMAF Cement, DANGOTE Cement and SUPACEM Cement. Increased infrastructural development has placed high demand on cement consumption. Consequently, new products keep emerging in the market. Indeed, a standard measure to provide product marking and evaluations of conformity to standard Class thresholds are required for the desired specification, properties and the performance quality of the cement products. This research therefore sets to ascertain the strength quality of the five cement brands on the Ghanaian market by checking their conformity to C-30 and C-40 standard compressive tests, using their 32.5-R and 42.5-R flagship brands. To achieve this, concrete cubes were moulded with fixed mix ratio of 1:1⅟2:3 and 1:1:2 for C-30 and C-40 respectively. To achieve the desired strength conformity, the slump as well as the coarse and fine aggregate constituents were standardised. The results indicated that the cement brands despite parading same strength thresholds in the market, do not exhibit same strength build-up. There are significant variations in growth of compressive strength over time. It was observed also that conformance threshold within 28 days was not attained for a number of the brands. Indeed, not until 56 days or more some of the brands could not achieve their desired compressive strength thresholds

Liquid phase immunoassay utilizing magnetic marker and high Tc superconducting quantum interference device

We have developed a liquid phase immunoassay system utilizing a magnetic marker and a superconducting quantum interference device (SQUID). In this system, the magnetic marker was used to detect the biological material called antigen. The magnetic marker was designed so as to generate a remanence, and the remanence field of the markers that bound to the antigens was measured with the SQUID. The measurement was performed in a solution that contained both the bound and free (or unbound) markers, i.e., without using the so-called bound/free (BF) separation process. The Brownian rotation of the free markers in the solution was used to distinguish the bound markers from the free ones. Using the system, we conducted the detection of biological material called IgE without BF separation. At present, we could detect the IgE down to 7 pg (or 39 amol

Intense pulsed helium droplet beams

Pulsed (30 - 100 microseconds) nozzle beams have been used to generate helium droplets ( = 10^4-10^5). The dependence of the beam intensity and the mean droplet size on the source stagnation pressure and temperature are studied via mass spectroscopy and laser induced fluorescence of embedded phthalocyanine molecules. In comparison to a cw beam the pulsed source for the same pressure and temperature has a factor of 100 higher flux and the droplet sizes are an order of a magnitude larger.Comment: Accepted by Review of Scientific Instrument

Bipyridinium-bis(carboxylate) Radical Based Materials: X-ray, EPR and Paramagnetic Solid-State NMR Investigations

The zwitterionic 1,1′-bis(4-carboxyphenyl)-4,4′-bipyridinium (bp4pc) has been synthesized and crystals of its hydrated form bp4pc·2H2O and of its protonated reduced form H-bp4pc have been obtained. Upon heating, bp4pc·2H2O undergoes partial dehydration, leading to bp4pc·H2O at 160 °C, together with a color change from yellow (room temperature) to green (140 °C) and finally to brown (160–180 °C). Analysis of bond lengths in the solid state reveals the expected short (d = 1.425 Å) and long (d = 1.485 Å) C–C central bond lengths in the all-radical salt H-bp4pc and bp4pc·2H2O, respectively, whereas the distance of 1.475 Å in bp4pc·H2O does not allow a conclusion to be drawn regarding the presence of radicals in this compound. EPR and solid-state paramagnetic NMR experiments of H-bp4pc and the hydrated zwitterion bp4pc·2H2O at different temperatures, however, show that the color change of the latter upon heating is due to the presence of bipyridinium radicals, the concentration of which, although low, increases with increasing temperature. The nature of the electron donor involved in this thermal-induced electron transfer is not fully understood. Most plausible is the possibility that it is the carboxylate group with an intramolecular electron-transfer process; on the other hand it, cannot be excluded that the electron stems from the water molecule, which decomposes into O2, H+, and e– giving H-bp4pc entities

Sterol Composition of the Indian Green Lipped Mussel Perna virdis

Sterol composition of green lipped mussel Perna virdis was analysed using GCMS. Cholesterol was found to be the dominant sterol (54.162% of the total sterol content). Other sterols such as Cholesta-5,22-dien-3-ol (3β), ergosta-5,22-dien-3-ol (3 β,22E, 24S),  26,26-dimethyl-5,24 (28)-Ergostadien-3β-ol, 26-nor-5cholesten- 3β-ol, stigmasterol and γ sitosterol were also detected. Presence of phytosterols like stigmasterol and γ sitosterol underlines high nutritional potential and food value of this bivalve mollusk

DRAM-3 modulates autophagy and promotes cell survival in the absence of glucose

Macroautophagy is a membrane-trafficking process that delivers cytoplasmic constituents to lysosomes for degradation. The process operates under basal conditions as a mechanism to turnover damaged or misfolded proteins and organelles. As a result, it has a major role in preserving cellular integrity and viability. In addition to this basal function, macroautophagy can also be modulated in response to various forms of cellular stress, and the rate and cargoes of macroautophagy can be tailored to facilitate appropriate cellular responses in particular situations. The macroautophagy machinery is regulated by a group of evolutionarily conserved autophagy-related (ATG) proteins and by several other autophagy regulators, which either have tissue-restricted expression or operate in specific contexts. We report here the characterization of a novel autophagy regulator that we have termed DRAM-3 due to its significant homology to damage-regulated autophagy modulator (DRAM-1). DRAM-3 is expressed in a broad spectrum of normal tissues and tumor cells, but different from DRAM-1, DRAM-3 is not induced by p53 or DNA-damaging agents. Immunofluorescence studies revealed that DRAM-3 localizes to lysosomes/autolysosomes, endosomes and the plasma membrane, but not the endoplasmic reticulum, phagophores, autophagosomes or Golgi, indicating significant overlap with DRAM-1 localization and with organelles associated with macroautophagy. In this regard, we further proceed to show that DRAM-3 expression causes accumulation of autophagosomes under basal conditions and enhances autophagic flux. Reciprocally, CRISPR/Cas9-mediated disruption of DRAM-3 impairs autophagic flux confirming that DRAM-3 is a modulator of macroautophagy. As macroautophagy can be cytoprotective under starvation conditions, we also tested whether DRAM-3 could promote survival on nutrient deprivation. This revealed that DRAM-3 can repress cell death and promote long-term clonogenic survival of cells grown in the absence of glucose. Interestingly, however, this effect is macroautophagy-independent. In summary, these findings constitute the primary characterization of DRAM-3 as a modulator of both macroautophagy and cell survival under starvation conditions

Targeting quiescent leukemic stem cells using second generation autophagy inhibitors

In chronic myeloid leukemia (CML), tyrosine kinase inhibitor (TKI) treatment induces autophagy that promotes survival and TKI-resistance in leukemic stem cells (LSCs). In clinical studies hydroxychloroquine (HCQ), the only clinically approved autophagy inhibitor, does not consistently inhibit autophagy in cancer patients, so more potent autophagy inhibitors are needed. We generated a murine model of CML in which autophagic flux can be measured in bone marrow-located LSCs. In parallel, we use cell division tracing, phenotyping of primary CML cells, and a robust xenotransplantation model of human CML, to investigate the effect of Lys05, a highly potent lysosomotropic agent, and PIK-III, a selective inhibitor of VPS34, on the survival and function of LSCs. We demonstrate that long-term haematopoietic stem cells (LT-HSCs: Lin−Sca-1+c-kit+CD48−CD150+) isolated from leukemic mice have higher basal autophagy levels compared with non-leukemic LT-HSCs and more mature leukemic cells. Additionally, we present that while HCQ is ineffective, Lys05-mediated autophagy inhibition reduces LSCs quiescence and drives myeloid cell expansion. Furthermore, Lys05 and PIK-III reduced the number of primary CML LSCs and target xenografted LSCs when used in combination with TKI treatment, providing a strong rationale for clinical use of second generation autophagy inhibitors as a novel treatment for CML patients with LSC persistence

Impaired Autophagy of an Intracellular Pathogen Induced by a Crohn's Disease Associated ATG16L1 Variant

The genetic risk factors predisposing individuals to the development of inflammatory bowel disease are beginning to be deciphered by genome-wide association studies. Surprisingly, these new data point towards a critical role of autophagy in the pathogenesis of Crohn's disease. A single common coding variant in the autophagy protein ATG16L1 predisposes individuals to the development of Crohn's disease: while ATG16L1 encoding threonine at amino acid position 300 (ATG16L1*300T) confers protection, ATG16L1 encoding for alanine instead of threonine (ATG16L1*300A, also known as T300A) mediates risk towards the development of Crohn's disease. Here we report that, in human epithelial cells, the Crohn's disease-associated ATG16L1 coding variant shows impairment in the capture of internalized Salmonella within autophagosomes. Thus, we propose that the association of ATG16L1*300A with increased risk of Crohn's disease is due to impaired bacterial handling and lowered rates of bacterial capture by autophagy