Large earthquakes often do not occur on a simple planar fault but involve rupture of multiple geometrically complex faults. The 2016 Mw 7.8 Kaikoura earthquake, New Zealand, involved the rupture of at least 21 faults, propagating from southwest to northeast for about 180 km. Here we combine space geodesy and seismology techniques to study subsurface fault geometry, slip distribution, and the kinematics of the rupture. Our finite‐fault slip model indicates that the fault motion changes from predominantly right‐lateral slip near the epicenter to transpressional slip in the northeast with a maximum coseismic surface displacement of about 10 m near the intersection between the Kekerengu and Papatea faults. Teleseismic back projection imaging shows that rupture speed was overall slow (1.4 km/s) but faster on individual fault segments (approximately 2 km/s) and that the conjugate, oblique‐reverse, north striking faults released the largest high‐frequency energy. We show that the linking Conway‐Charwell faults aided in propagation of rupture across the step over from the Humps fault zone to the Hope fault. Fault slip cascaded along the Jordan Thrust, Kekerengu, and Needles faults, causing stress perturbations that activated two major conjugate faults, the Hundalee and Papatea faults. Our results shed important light on the study of earthquakes and seismic hazard evaluation in geometrically complex fault systems.

The 2015 Mw 7.8 Nepal‐Gorkha earthquake with casualties of over 9000 people was the most devastating disaster to strike Nepal since the 1934 Nepal‐Bihar earthquake. Its rupture process was imaged by teleseismic back projections (BP) of seismograms recorded by three, large regional networks in Australia, North America, and Europe. The source images of all three arrays reveal a unilateral eastward rupture; however, the propagation directions and speeds differ significantly between the arrays. To understand the spatial uncertainties of the BP analyses, we analyze four moderate size aftershocks recorded by all three arrays exactly as had been conducted for the main shock. The apparent source locations inferred from BPs are systematically biased from the catalog locations, as a result of a slowness error caused by three‐dimensional Earth structures. We introduce a physics‐based slowness correction that successfully mitigates the source location discrepancies among the arrays. Our calibrated BPs are found to be mutually consistent and reveal a unilateral rupture propagating eastward at a speed of 2.7 km/s, localized in a relatively narrow and deep swath along the downdip edge of the locked Himalayan thrust zone. We find that the 2015 Gorkha earthquake was a localized rupture that failed to break the entire Himalayan décollement to the surface, which can be regarded as an intermediate event during the interseismic period of larger Himalayan ruptures that break the whole seismogenic zone width. Thus, our physics‐based slowness correction is an important technical improvement of BP, mitigating spatial uncertainties and improving the robustness of single and multiarray studies.

Combining space-based geodetic and array seismology observations can provide detailed information about earthquake ruptures in remote regions. Here we use Landsat-8 imagery and ALOS-2 and Sentinel-1 radar interferometry data combined with data from the European seismology network to describe the source of the December 7, 2015, Mw7.2 Murghab (Tajikistan) earthquake. The earthquake reactivated a ∼79 km-long section of the Sarez-Karakul Fault, a NE oriented sinistral, trans-tensional fault in northern Pamir. Pixel offset data delineate the geometry of the surface break and line of sight ground shifts from two descending and three ascending interferograms constrain the fault dip and slip solution. Two right-stepping, NE-striking segments connected by a more easterly oriented segment, subvertical or steeply dipping to the west were involved. The solution shows two main patches of slip with up to 3.5 m of left lateral slip on the southern and central fault segments. The northern segment has a left-lateral and normal oblique slip of up to a meter. Back-projection of high-frequency seismic waves

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AbstractThe pesticide residues in foods have received increasing attention as one of the most important food safety issues. Therefore, more strict regulations on the maximum residue limits (MRLs) for pesticides in foods have been established in many countries and health organizations, based on the sensitive and reliable analysis methods of pesticide residues. However, the analysis of pesticide residues is a continuing challenge mainly because of the small quantities of analytes as well as the large amounts of interfering substances which can be co-extracted with them, often leading to experimental errors and damage to the analytical instruments. Thus, extensive sample preparation is often required for the pesticide residue analysis for the effective extraction of the analytes and removal of the interferences. This paper focuses on reviewing the recent development in the sample preparation methods for the pesticide residue analysis in foods since 2006. The methods include: liquid-liquid extraction (LLE), supercritical-fluid extraction (SFE), pressurized-liquid extraction (PLE), microwave-assisted extraction (MAE), ultrasound-assisted extraction (UAE), gel permeation chromatography (GPC), solid-phase extraction (SPE), molecularly imprinted polymers (MIPs), matrix solid-phase dispersion (MSPD), solid-phase micro-extraction (SPME), QuEChERS, cloud point extraction (CPE) and liquid phase micro-extraction (LPME), etc. Particularly their advantages, disadvantages and future perspectives will be discussed.

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Purpose Germline variation in solute carrier organic anion (SLCO) genes influences cellular steroid uptake and is associated with prostate cancer (PCa) outcomes. We hypothesized that, due to its steroidal structure, the CYP17A inhibitor abiraterone may undergo SLCO-mediated transport and that SLCO gene variation may influence intracellular abiraterone levels and outcomes. Patients and Methods Steroid and abiraterone levels were measured in serum and tissue from 58 men with localized PCa in a clinical trial of LHRH agonist plus abiraterone acetate plus prednisone for 24 weeks prior to prostatectomy. Germline DNA was genotyped for 13 single nucleotide polymorphisms (SNPS) in 6 SLCO genes. Results Abiraterone levels spanned a broad range (serum median 28ng/ml, 108nM; tissue median 77ng/ml, 271nM) and were correlated (r=0.355, p=0.001). Levels correlated positivey with steroids upstream of CYP17A (pregnenolone, progesterone), and inversely with steroids downstream of CYP17A (DHEA, AED, testosterone). Serum PSA and tumor volumes were higher in men with undetectable vs detectable tissue abiraterone at prostatectomy (median 0.10 vs 0.03ng/dl, p=0.02; 1.28 vs 0.44cc, p=0.09, respectively). SNPs in SLCO2B1 associated with significant differences in tissue abiraterone (rs1789693, p=0.0008; rs12422149, p=0.03) and higher rates of minimal residual disease (tumor volume <0.5cc; rs1789693, 67% vs 27%, p=0.009; rs1077858, 46% vs 0%, p=0.03). LNCaP cells expressing SLCO2B1 showed 2–4 fold higher abiraterone levels compared to vector controls (p<0.05). Conclusions Intraprostatic abiraterone levels and genetic variation in SLCO genes are associated with pathologic responses in high-risk localized PCa. Variation in SLCO genes may serve as predictors of response to abiraterone treatment.

In acute myeloid leukemia (AML) and blast crisis (BC) chronic myeloid leukemia (CML) normal differentiation is impaired. Differentiation of immature stem/progenitor cells is critical for normal blood cell function. MicroRNAs (miRNAs or miRs) are small non-coding RNAs that interfere with gene expression by degrading messenger RNAs (mRNAs) or blocking protein translation. Aberrant miRNA expression is a feature of leukemia and miRNAs also play a significant role in normal hematopoiesis and differentiation. We have identified miRNAs differentially expressed in AML and BC CML and identified a new role for miR-150 in myeloid differentiation. Expression of miR-150 is low or absent in BC CML and AML patient samples and cell lines. We have found that expression of miR-150 in AML cell lines, CD34+ progenitor cells from healthy individuals, and primary BC CML and AML patient samples at levels similar to miR-150 expression in normal bone marrow promotes myeloid differentiation of these cells. MYB is a direct target of miR-150, and we have identified that the observed phenotype is partially mediated by MYB. In AML cell lines, differentiation of miR-150 expressing cells occurs independently of retinoic acid receptor α (RARA) signaling. High-throughput gene expression profiling (GEP) studies of the AML cell lines HL60, PL21, and THP-1 suggest that activation of CEPBA, CEBPE, and cytokines associated with myeloid differentiation in miR-150 expressing cells as compared to control cells contributes to myeloid differentiation. These data suggest that miR-150 promotes myeloid differentiation, a previously uncharacterized role for this miRNA, and that absent or low miR-150 expression contributes to blocked myeloid differentiation in acute leukemia cells.