New testing methodology for the quantification of rock crushability: Compressive crushing value (CCV)

Crushing is a size reduction process that plays a key role in both mineral processing and crushing-screening plant design. Investigations on rock crushability have become an important issue in mining operations and the manufacture of industrial crusher equipment. The main objective of this research is to quantify the crushability of hard rocks based on their mineralogical and mechanical properties. For this purpose, the mineralogical, physical, and mechanical properties of various hard rocks were determined. A new compressive crushing value (CCV) testing methodology was proposed. The results obtained from CCV tests were compared with those from mineralogical inspections, rock strength as well as mechanical aggregate tests. Strong correlations were found between CCV and several rock and aggregate properties such as uniaxial compressive strength (UCS), the brittleness index (S₂₀), and aggregate impact value (AIV). Furthermore, the relationship between the mineralogical properties of the rocks and their CCVs were established. It is concluded that the proposed testing methodology is simple and highly repeatable and could be utilized as a pre-design tool in the design stage of the crushing process for rock quarries.     

CEP152 is a genome maintenance protein disrupted in Seckel syndrome

Functional impairment of DNA damage response pathways leads to increased genomic instability. Here we describe the centrosomal protein CEP152 as a new regulator of genomic integrity and cellular response to DNA damage. Using homozygosity mapping and exome sequencing, we identified CEP152 mutations in Seckel syndrome and showed that impaired CEP152 function leads to accumulation of genomic defects resulting from replicative stress through enhanced activation of ATM signaling and increased H2AX phosphorylation.     

TRIM24 links a non-canonical histone signature to breast cancer

Recognition of modified histone species by distinct structural domains within 'reader' proteins plays a critical role in the regulation of gene expression. Readers that simultaneously recognize histones with multiple marks allow transduction of complex chromatin modification patterns into specific biological outcomes. Here we report that chromatin regulator tripartite motif-containing 24 (TRIM24) functions in humans as a reader of dual histone marks by means of tandem plant homeodomain (PHD) and bromodomain (Bromo) regions. The three-dimensional structure of the PHD-Bromo region of TRIM24 revealed a single functional unit for combinatorial recognition of unmodified H3K4 (that is, histone H3 unmodified at lysine 4, H3K4me0) and acetylated H3K23 (histone H3 acetylated at lysine 23, H3K23ac) within the same histone tail. TRIM24 binds chromatin and oestrogen receptor to activate oestrogen-dependent genes associated with cellular proliferation and tumour development. Aberrant expression of TRIM24 negatively correlates with survival of breast cancer patients. The PHD-Bromo of TRIM24 provides a structural rationale for chromatin activation through a non-canonical histone signature, establishing a new route by which chromatin readers may influence cancer pathogenesis.     

Determination of discontinuities in marble blocks via a nondestructive ultrasonic technique

Miners working in the marble industry have always been interested in identifying structural weaknesses in marble blocks before they are transported to marble processing plants. To achieve this difficult task, several simple methods have been developed among miners but observation-based methods do not consistently provide satisfactory results. A nondestructive method developed for testing concrete could be used for this purpose. In this study, this simple method based on differences in ultrasonic wave propagation in different materials was presented, and the test results performed both in the laboratory and a marble quarry were discussed.     

Labelling of a pyrazole derivative with 131I and investigation of its radiopharmaceutical potential

We investigated the radiolabeling efficiency, in vitro stability, and biodistribution of radioactive iodine (131I)-labeled 4-benzoyl-1-(4-carboxyphenyl)-5-phenyl-1H-pyrazole-3-carboxylic acid (P3CA). A quality-control study of the labeled substance ( 131I-P3CA) was conducted using electrophoresis and radio thin-layer chromatography (RTLC). Biodistribution studies were undertaken in 9 female albino Wistar rats. Rats were killed at various times (15, 60 and 180 min), their organs removed, and percentage of injected dose per gram (ID%/g) values calculated. The labeling yield of P3CA was 97.08%±0.80%. The maximum uptake of 131I-P3CA was seen in the lungs, stomach and spleen at 15 min. The uptake of labeled compound decreased over time in the lungs, whereas that in the stomach decreased. These data suggest that 131I-P3CA had high binding efficiency, high uptake in the lung, and sufficient stability to be used in diagnostic studies.     

Ambra1 regulates autophagy and development of the nervous system

Autophagy is a self-degradative process involved both in basal turnover of cellular components and in response to nutrient starvation or organelle damage in a wide range of eukaryotes. During autophagy, portions of the cytoplasm are sequestered by double-membraned vesicles called autophagosomes, and are degraded after fusion with lysosomes for subsequent recycling. In vertebrates, this process acts as a pro-survival or pro-death mechanism in different physiological and pathological conditions, such as neurodegeneration and cancer; however, the roles of autophagy during embryonic development are still largely uncharacterized. Beclin1 (Becn1; coiled-coil, myosin-like BCL2-interacting protein) is a principal regulator in autophagosome formation, and its deficiency results in early embryonic lethality. Here we show that Ambra1 (activating molecule in Beclin1-regulated autophagy), a large, previously unknown protein bearing a WD40 domain at its amino terminus, regulates autophagy and has a crucial role in embryogenesis. We found that Ambra1 is a positive regulator of the Becn1-dependent programme of autophagy, as revealed by its overexpression and by RNA interference experiments in vitro. Notably, Ambra1 functional deficiency in mouse embryos leads to severe neural tube defects associated with autophagy impairment, accumulation of ubiquitinated proteins, unbalanced cell proliferation and excessive apoptotic cell death. In addition to identifying a new and essential element regulating the autophagy programme, our results provide in vivo evidence supporting the existence of a complex interplay between autophagy, cell growth and cell death required for neural development in mammals.     

A micrococcal nuclease homologue in RNAi effector complexes

RNA interference (RNAi) regulates gene expression by the cleavage of messenger RNA, by mRNA degradation and by preventing protein synthesis. These effects are mediated by a ribonucleoprotein complex known as RISC (RNA-induced silencing complex). We have previously identified four Drosophila components (short interfering RNAs, Argonaute 2 (ref. 2), VIG and FXR) of a RISC enzyme that degrades specific mRNAs in response to a double-stranded-RNA trigger. Here we show that Tudor-SN (tudor staphylococcal nuclease)--a protein containing five staphylococcal/micrococcal nuclease domains and a tudor domain--is a component of the RISC enzyme in Caenorhabditis elegans, Drosophila and mammals. Although Tudor-SN contains non-canonical active-site sequences, we show that purified Tudor-SN exhibits nuclease activity similar to that of other staphylococcal nucleases. Notably, both purified Tudor-SN and RISC are inhibited by a specific competitive inhibitor of micrococcal nuclease. Tudor-SN is the first RISC subunit to be identified that contains a recognizable nuclease domain, and could therefore contribute to the RNA degradation observed in RNAi.