High resolution angle-resolved photoemission spectroscopy data along the (0,0)-(π,π) nodal direction with significantly improved statistics reveal fine structure in the electron self-energy of the underdoped (La2−xSrx)CuO4 samples in the normal state. Fine structure at energies of (40∼46) meV and (58∼63)meV, and possible fine structure at energies of (23∼29)meV and (75∼85)meV, have been identified. These observations indicate that, in LSCO, more than one bosonic modes are involved in the coupling with electrons.PACS numbers: 74.25.Jb,71.18.+y,74.72.Dn, The recent observation of the electron self-energy renormalization effect in the form of a "kink" in the dispersion has generated considerable interest because it reveals a coupling of the electrons with a collective boson mode of the cuprate superconductors [1]. However, the nature of the bosons involved remains controversial mainly because the previous experiments can only be used to determine an approximate energy of the mode and this energy is close to both the optical phonon [2,3] and the spin resonance [4]. Determining the nature of the mode(s) that couple to the electrons is likely important in understanding the pairing mechanism of superconductivity.In conventional superconductors, identification of the fine structure for the phonon anomalies in the tunnelling spectra has played a decisive role in reaching a consensus on the nature of the bosons involved [5]. The fine structure provides fingerprints for much more stringent comparison with known boson spectra. So far, such fine structure has not been detected in the angleresolved photoemission spectroscopy (ARPES) data. In this Letter we present significantly improved high resolution ARPES data of (La 2−x Sr x )CuO 4 (LSCO) that, for the first time, reveal fine structure in the electron selfenergy, demonstrating the involvement of multiple boson modes in the coupling with electrons.The photoemission measurements were carried out on beamline 10.0.1 at the ALS, using Scienta 2002 and R4000 electron energy analyzers. As high energy resolution and high data statistics are crucial to identify fine structure in the electron self-energy, the experimental conditions were set to compromise between these two conflicting requirements. The measurement is particularly challenging for LSCO system because of the necessity to use a relatively high photon energy (55eV). Different energy resolution between 12 and 20 meV was used for various measurements on different samples, and the angular resolution is 0.3 degree. An example of the high quality of the raw data is shown in Figs. 1a and 1b. Due to space charge problem, the Fermi level calibration has a ±5 meV uncertainty. We mainly present our data on the heavily underdoped LSCO x=0.03 (nonsuperconducting), LSCO x=0.063 (T c =12 K) and LSCO x=0.07 (T c =14 K) samples. These heavily underdoped LSCO samples are best candidates because they exhibit a stronger band renormalization effect above T c [3]; a relatively large magnitude of the real self-energy makes the identification...

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Secretory pore-forming proteins (PFPs) have been identified in organisms from all kingdoms of life. Our studies with the toad species Bombina maxima found an interaction network among aerolysin family PFPs (af-PFPs) and trefoil factors (TFFs). As a toad af-PFP, BmALP1 can be reversibly regulated between active and inactive forms, with its paralog BmALP3 acting as a negative regulator. BmALP1 interacts with BmTFF3 to form a cellular active complex called βγ-CAT. This PFP complex is characterized by acting on endocytic pathways and forming pores on endolysosomes, including stimulating cell macropinocytosis. In addition, cell exocytosis can be induced and/or modulated in the presence of βγ-CAT. Depending on cell contexts and surroundings, these effects can facilitate the toad in material uptake and vesicular transport, while maintaining mucosal barrier function as well as immune defense. Based on experimental evidence, we hereby propose a secretory endolysosome channel (SELC) pathway conducted by a secreted PFP in cell endocytic and exocytic systems, with βγ-CAT being the first example of a SELC protein. With essential roles in cell interactions and environmental adaptations, the proposed SELC protein pathway should be conserved in other living organisms.

Although epidemiological and preclinical studies have shown the preventative effects of n-3 polyunsaturated fatty acids (PUFAs) on breast cancer, inconsistencies still remain in the data and the underlying mechanisms remain unclear. In this study, we identified mammalian target of rapamycin (mTOR) signaling, which plays an essential role in cell proliferation and breast tumorigenesis, as a target of n-3 PUFAs. In breast cancer cell lines, n-3 PUFAs rapidly and efficiently suppress both mTOR complex 1 (mTORC1) and mTORC2 and their downstream signaling, and subsequently inhibit cell proliferation and angiogenesis while promoting apoptosis. Further study indicates that stabilization of the mTOR-raptor complex by n-3 PUFAs may contribute to their inhibitory effect on mTORC1. Importantly, four complementary and well-controlled animal models were utilized to identify the role and molecular target of n-3 PUFAs in the prevention of breast carcinogenesis and progression, namely: (1) chemically induced mammary tumor rats with a high dietary intake of n-3 PUFAs; (2) nude mice implanted with mammary tumor cell lines stably expressing fat-1, a desaturase that catalyzes the conversion of n-6 to n-3 PUFAs and produces n-3 PUFAs endogenously; (3) fat-1 transgenic severe combined immune deficiency mice implanted with breast tumor cells; and (4) the fat-1 transgenic mouse mammary tumor virus-polyoma virus middle T oncogene double-hybrid mice, a model of aggressive breast cancer. In summary, dietary and endogenous n-3 PUFAs abrogate the activity of mTORC1/2 pathways in vitro and in vivo and prevent breast carcinogenesis, tumor growth and metastasis. Taken together, our findings convincingly clarify the causal relationship between n-3 PUFAs and breast cancer prevention and establish mTORC1/2 as a target of n-3 PUFAs.

Maintaining water balance is a real challenge for amphibians in terrestrial environments. Our previous studies with toad Bombina maxima discovered a pore-forming protein and trefoil factor complex βγ-CAT, which is assembled under tight regulation depending on environmental cues. Here we report an unexpected role for βγ-CAT in toad water maintaining. Deletion of toad skin secretions, in which βγ-CAT is a major component, increased animal mortality under hypertonic stress. βγ-CAT was constitutively expressed in toad osmoregulatory organs, which was inducible under the variation of osmotic conditions. The protein induced and participated in macropinocytosis in vivo and in vitro. During extracellular hyperosmosis, βγ-CAT stimulated macropinocytosis to facilitate water import and enhanced exosomes release, which simultaneously regulated aquaporins distribution. Collectively, these findings uncovered that besides membrane integrated aquaporin, a secretory pore-forming protein can facilitate toad water maintaining via macropinocytosis induction and exocytosis modulation, especially in responses to osmotic stress.

The influence of carbon concentration on the superconductivity ( SC ) in MgCxNi3 has been investigated by measuring the low temperature specific heat combined with first principles electronic structure calculation. It is found that the specific heat coefficient γn = Cen/T of the superconducting sample (x ≈ 1) in normal state is twice that of the non-superconducting one (x ≈ 0.85). The comparison of measured γn and the calculated electronic density of states ( DOS ) shows that the effective mass renormalization changes remarkably as the carbon concentration changes. The large mass renormalization for the superconducting sample and the low Tc( 7K ) indicate that more than one kind of boson mediated electron-electron interactions exist in MgCxNi3.

We report the discovery of superconductivity on high-quality single crystals of transition-metal pnictides WP grown by chemical vapor transport (CVT) method.Bulk superconductivity is observed at T c = 0.84 K under ambient pressure by electrical resistivity and AC magnetic susceptibility measurements. The effects of magnetic field on the superconducting transitions are studied, leading to a large anisotropy parameter around 2 with the in-plane and out-of-plane upper critical fields of 2,∥ =172 Oe and 2,⊥ =85 Oe, respectively. Our finding demonstrates that WP is the first superconductor in 5d transition-metal at ambient pressure in MnP-type, which will help to search for new superconductors in transition-metal pnictides.

BackgroundNon small cell lung cancer (NSCLC) is one of the most common cancers in the world. DHA is known to be capable of suppressing NSCLC cell proliferation and metastasis. However, the mechanisms by which DHA exhibits its antitumor effects are unknown. Here we aimed to identify the effects and mechanisms of DHA and its metabolites on lung cancer cell growth and invasion.MethodsAs measures of cell proliferation and invasion ability, the cell viability and transwell assays were used in vitro. Transgenic mfat-1 mice, which convert ω-6 PUFAs to ω-3 PUFAs, were used to detect the effect of endogenous DHA on tumor transplantation. An LC − MS/MS analysis identified the elevation of several eicosanoid metabolites of DHA. By using qPCR miRNA microarray, online prediction software, luciferase reporter assays and Western blot analysis, we further elucidated the mechanisms.ResultsAddition of exogenous DHA inhibited the growth and invasion in NSCLC cells in vitro. Endogenously produced DHA attenuated LLC-derived tumor growth and metastasis in the transgenic mfat-1 mice. Among the elevation of DHA metabolites, resolvin D1 (RvD1) significantly contributed to the inhibition in cell growth and invasion. MiRNA microarray revealed that the level of miR-138-5p was significantly increased after RvD1 treatment. MiR-138-5p mimics decreased cell viability and invasion; while miR-138-5p inhibitor abolished RvD1-mediated suppression of cell viability and invasion. The expression of FOXC1 was significantly reduced upon overexpression of miR-138-5p while luciferase reporter assay showed that FOXC1 was a direct target of miR-138-5p. In vivo, endogenous DHA by the mfat-1 transgene enhanced miR-138-5p expression and decreased FOXC1 expression. Furthermore, overexpression of FOXC1 reversed the inhibition in cell viability and invasion induced by RvD1 treatment.ConclusionsThese data identified the RvD1/miR-138-5p/FOXC1 pathway as a novel mechanism by DHA and its metabolite, RvD1, and the potential of targeting such pathway as a therapeutic strategy in treating NSCLC.