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Phase engineering by strains in 2D semiconductors is of great importance for a variety of applications. Here, we present a study of strain induced ferroelectric (FE) transition on bismuth oxyselenide (Bi$_2$O$_2$Se) films, a high-performance (HP) semiconductor for next-generation electronics. Bi$_2$O$_2$Se is non-FE at ambient. Upon a loading force $\gtrsim 400$ nN, piezoelectric force responses exhibit butterfly loops on magnitude and 180$^\textrm{o}$ phase switching. By carefully ruling out extrinsic factors, these features are attributed to a transition to FE phase. The transition is further proved by the appearance of a sharp peak on optical second harmonic generation under an uniaxial strain. Fundamentally, solids with paraelectric at ambient and FE under strains are scarce. FE transition is discussed with the help of first-principle calculations and theoretical simulations. The switching of FE polarization acts as a knob for Schottky barrier engineering at contacts and serves as basis for a memristor with a huge switching ratio of 10$^6$. Our work endows a new degree of freedom to a HP electronic/optoelectronic semiconductor and the integration of FE and HP semiconductivity paving the way for multiple exciting functionalities, including HP neuromorphic computation and bulk piezophotovoltaic., 12 pages, 5 figures

Background Lung adenocarcinoma (LUAD) metastasis significantly reduces patient survival; hence inhibiting the metastatic ability of lung cancer cells will greatly prolong patient survival. Alkaline phosphatase (ALPL), a homodimeric cell surface phosphohydrolase, is reported to play a controversial role in prostate cancer and ovarian cancer cell migration; however, the function of ALPL in LUAD and the related mechanisms remain unclear. Methods TCGA database was used to analysis the expression of ALPL, and further verification was performed in a cohort of 36 LUAD samples by qPCR and western blot. Soft-agar assay, transwell assay and lung metastasis assay were employed to detect the function of ALPL in LUAD progression. The qPCR, luciferase promoter reporter assay and western blot were used to clarify the molecular mechanisms of ALPL in promoting metastasis in LUAD. Results ALPL was downregulated in LUAD, and the disease-free survival rate of patients with low ALPL was significantly reduced. Further studies showed that overexpression of ALPL in LUAD cell lines did not significantly affect cell proliferation, but it did significantly attenuate lung metastasis in a mouse model. ALPL downregulation in LUAD led to a decrease in the amount of phosphorylated (p)-ERK. Because p-ERK promotes the classical c-Myc degradation pathway, the decrease in p-ERK led to the accumulation of c-Myc and therefore to an increase in RhoA transcription, which enhanced LUAD cell metastasis. Conclusion ALPL specially inhibits the metastasis of LUAD cells by affecting the p-ERK/c-Myc/RhoA axis, providing a theoretical basis for the targeted therapy of clinical LUAD.

Metastasis is the main cause of death in colorectal cancer (CRC) patients. However, current treatment options for CRC metastasis are very limited. Lupeol, a triterpene that is widely found in vegetables and fruits, has been reported to possess the cancer-preventive and anti-inflammatory functions. However, the roles of Lupeol in the migration and invasion of colorectal cancer remain unclear. Here, we evaluated the effect of Lupeol treatment on colorectal cancer cell lines, HCT116 and SW620, and delineated its underlying mechanisms. Our results showed that Lupeol induced a dose-dependent inhibition of HCT116 and SW620 cells viability, measured by CCK8 assay. Wound healing and Transwell migration and invasion assays revealed that Lupeol significantly suppressed the migration and invasion of CRC cells. Using laser confocal microscope, we observed that the pseudopods and protrusions of HCT116 and SW620 cells decreased and disrupted after treatment with Lupeol. In addition, the quantitative real-time PCR and Western blotting results showed that Lupeol downregulated the expression of RhoA and RhoC, and their downstream effectors ROCK1, Cofilin, p-MLC, and the associated regulatory protein Cyclin A2. Interestingly, the migration and invasion capacity of CRC cells was reduced after RhoA knockdown. And there were no additional changes in CRC cells with RhoA knockdown to treat with Lupeol. These findings demonstrate that Lupeol can suppress the migration and invasion of colorectal cancer cells by remodeling the actin cytoskeleton via RhoA-ROCK1 pathway inhibition, which may provide an effective anti-metastatic agent for CRC patients.

The magnetic properties of CsCo2Se2, possessing a ThCr2Si2-structure, are systematically studied by using specific heat, resistivity, and torque measurements. Our results reveal that CsCo2Se2 undergoes a paramagnetic state to antiferromagnetic order at T N ≈ 80 K at zero magnetic field. The T N is nearly independent of the external magnetic field for H ‖ c-axis, and can be suppressed for H ‖ ab-plane below 4 T, above which spin-flop phase transition sets in. At 2 K, the magnetoresistance has a small value of 2.3% for H ‖ c-axis while goes up to 60% for H ‖ ab-plane at 9 T. A hump-like behavior in resistivity was discovered, which was ascribed to a field-induced spin-flop phase transition. The magnetoresistance results suggest that a crossover of spin-flop phase transition occurs at low temperatures in the field range of 2–4 T for H ‖ ab-plane. Furthermore, the magnetic torque results reveal a novel ordered Co spin structure at low temperatures under 6 T for H ‖ ab-plane. Finally, we summarize the magnetic phase diagram of CsCo2Se2 based on resistivity and torque results.

The extremely large magnetoresistance (XMR) observed in many topologically nontrivial and trivial semimetals has attracted much attention in relation to its underlying physical mechanism. In this paper, by combining the band structure and Fermi surface (FS) calculations with the Hall resistivity and de Haas-Van Alphen (dHvA) oscillation measurements, we studied the anisotropy of magnetoresistance (MR) of ReO$_3$ with a simple cubic structure, an "ordinary" nonmagnetic metal considered previously. We found that ReO$_3$ exhibits almost all the characteristics of XMR semimetals: the nearly quadratic field dependence of MR, a field-induced upturn in resistivity followed by a plateau at low temperatures, high mobilities of charge carriers. It was found that for magnetic field \emph{H} applied along the \emph{c} axis, the MR exhibits an unsaturated \emph{H}$^{1.75}$ dependence, which was argued to arise from the complete carrier compensation supported by the Hall resistivity measurements. For \emph{H} applied along the direction of 15$^\circ$ relative to the \emph{c} axis, an unsaturated \emph{H}$^{1.90}$ dependence of MR up to 9.43~$\times$~$10^3$$\%$ at 10~K and 9~T was observed, which was explained by the existence of electron open orbits extending along the $k_{x}$ direction. Two mechanisms responsible for XMR observed usually in the semimetals occur also in the simple metal ReO$_3$ due to its peculiar FS (two closed electron pockets and one open electron pocket), once again indicating that the details of FS topology are a key factor for the observed XMR in materials., 9 pages, 8 figures. arXiv admin note: text overlap with arXiv:2007.04814

A feasible strategy to realize the Majorana fermions is searching for a simple compound with both bulk superconductivity and Dirac surface states. In this paper, we performed calculations of electronic band structure, the Fermi surface and surface states, as well as measured the resistivity, magnetization, specific heat for TlSb compound with a CsCl-type structure. The band structure calculations show that TlSb is a Dirac semimetal when spin-orbit coupling is taken into account. Meanwhile, we first found that TlSb is a type-II superconductor with $T_c$ = 4.38 K, $H_{c1}$(0) = 148 Oe, $H_{c2}$(0) = 1.12 T and $\kappa_{GL}$ = 10.6, and confirmed it to be a moderately coupled s-wave superconductor. Although we can not determine which bands near the Fermi level $E_F$ to be responsible for superconductivity, its coexistence with the topological surface states implies that TlSb compound may be a simple material platform to realize the fault-tolerant quantum computations., Comment: 7 pages, 8 figures

Additional file 1.Additional Table and Figures.

In this paper, the magnetic and transport properties were systematically studied for EuAg$_4$As$_2$ single crystals, crystallizing in a centrosymmetric trigonal CaCu$_4$P$_2$ type structure. It was confirmed that two magnetic transitions occur at $\textit{T}$$_{N1}$ = 10 K and $\textit{T}$$_{N2}$ = 15 K, respectively. With the increasing field, the two transitions are noticeably driven to lower temperature. At low temperatures, applying a magnetic field in the $\textit{ab}$ plane induces two successive metamagnetic transitions. For both $\textit{H}$ $\parallel$ $\textit{ab}$ and $\textit{H}$ $\parallel$ $\textit{c}$, EuAg$_4$As$_2$ shows a positive, unexpected large magnetoresistance (up to 202\%) at low fields below 10 K, and a large negative magnetoresistance (up to -78\%) at high fields/intermediate temperatures. Such anomalous field dependence of magnetoresistance may have potential application in the future magnetic sensors. Finally, the magnetic phase diagrams of EuAg$_{4}$As$_{2}$ were constructed for both $\textit{H}$ $\parallel$ $\textit{ab}$ and $\textit{H}$ $\parallel$ $\textit{c}$.

We performed calculations of the electronic band structure and the Fermi surface as well as measured the longitudinal resistivity $\rho_{xx}(T,H)$, Hall resistivity $\rho_{xy}(T,H)$, and magnetic susceptibility as a function of temperature and various magnetic fields for VAs$_2$ with a monoclinic crystal structure. The band structure calculations show that VAs$_2$ is a nodal-line semimetal when spin-orbit coupling is ignored. The emergence of a minimum at around 11 K in $\rho_{xx}(T)$ measured at $H$ = 0 demonstrates that an additional magnetic impurity (V$^{4+}$, $S$ = 1/2) occurs in VAs$_2$ single crystals, evidenced by both the fitting of $\rho_{xx}(T)$ data and the susceptibility measurements. It was found that a large positive magnetoresistance (MR) reaching 649\% at 10 K and 9 T, its nearly quadratic field dependence, and a field-induced up-turn behavior of $\rho_{xx}(T)$ emerge also in VAs$_2$, although MR is not so large due to the existence of additional scattering compared with other topological nontrival/trival semimetals. The observed properties are attributed to a perfect charge-carrier compensation, which is evidenced by both calculations relying on the Fermi surface and the Hall resistivity measurements. These results indicate that the compounds containing V ($3d^3 4s^2$) element as a platform for studying the influence of magnetic impurities to the topological properties., Comment: 8 pages, 5 figures. arXiv admin note: text overlap with arXiv:2007.04814

We performed calculations of the electronic band structure and the Fermi surface as well as measured the longitudinal resistivity ${\ensuremath{\rho}}_{xx}$($T,H$), Hall resistivity ${\ensuremath{\rho}}_{xy}$($T,H$), and quantum oscillations of the magnetization as a function of temperature at various magnetic fields for $\mathrm{Mo}{\mathrm{O}}_{2}$ with a monoclinic crystal structure. The band structure calculations show that $\mathrm{Mo}{\mathrm{O}}_{2}$ is a nodal-line semimetal when spin-orbit coupling is ignored. It was found that a large magnetoresistance reaching $5.03\ifmmode\times\else\texttimes\fi{}{10}^{4}%$ at 2 K and 9 T, its nearly quadratic field dependence, and a field-induced up-turn behavior of ${\ensuremath{\rho}}_{xx}$($T$), the characteristics common for many topologically nontrivial as well as trivial semimetals, emerge also in $\mathrm{Mo}{\mathrm{O}}_{2}$. The observed properties are attributed to a perfect charge-carrier compensation, evidenced by both calculations relying on the Fermi surface topology and the Hall resistivity measurements. Both the observation of negative magnetoresistance for magnetic field along the current direction and the nonzero Berry phase in de Haas--van Alphen measurements indicate that pairs of Weyl points appear in $\mathrm{Mo}{\mathrm{O}}_{2}$, which may be due to the crystal symmetry breaking. These results highlight $\mathrm{Mo}{\mathrm{O}}_{2}$ as a platform for studying the topological properties of oxides.

Yihao Wang,1,2,* Dan Hong,1,* Yuqin Qian,3 Xuezi Tu,1 Keke Wang,1 Xianhong Yang,1 Sijia Shao,1 Xinlong Kong,1 Zhefeng Lou,1 Longjin Jin1 1School of Laboratory Medicine and Life Science, Wenzhou Medical University, Zhejiang, People’s Republic of China; 2School of Ophthalmology and Optometry, Wenzhou Medical University, Zhejiang, People’s Republic of China; 3School of the first Clinical Medical Sciences, Wenzhou Medical University, Zhejiang, People’s Republic of China *These authors contributed equally tothis work Background: Lupeol, a triterpene isolated from various herbal plants, possesses an anti-inflammatory function and has been proposed as a candidate for anticancer agents. The purpose of this research was to investigate the effect of lupeol on the viability, apoptosis, cell-cycle distribution, and migration of colorectal cancer cell lines and its molecular mechanism.Methods: Lupeol was assessed for its anticancer effect using two human colorectal cancer cell lines: SW480 and HCT116. These cells were treated with lupeol, and their viability, apoptosis, migration, and cycle distribution were detected by CCK8, flow cytometry, and the transwell method. Quantitative PCR, Western blot, and immunofluorescence were applied to detect the expressions of CTNNB1, TCF4, cMYC, CCND1, CLDN1, and CCNA2.Results: Lupeol suppressed cell viability and migration and induced cellular apoptosis of both cell lines, with increased p53 and decreased Bcl2 protein levels (P

Hypodysfibrinogenemia is the least frequently reported congenital fibrinogen disorder, characterized by both quantity and quality defects of fibrinogen. In this study, we investigated the molecular basis of hypodysfibrinogenemia in a Chinese family. Functional fibrinogen was measured by Clauss method, and the antigenic fibrinogen was measured by immunoturbidimetry assay. All the exons and exon-intron boundaries of fibrinogen genes (FGA, FGB and FGG) were analysed by direct DNA sequencing. To further evaluate its molecular and functional characterizations, fibrinogen was purified from the plasma of propositus, then SDS-PAGE, fibrin polymerization, clot lysis, and electron microscopy scanning were all performed. The propositus showed a slight decrease of immunologic fibrinogen (1.52 g/L) but dramatically reduced functional fibrinogen (0.3 g/L). DNA sequencing revealed a novel heterozygous CCTTTGATG deletion in the exon 8 of FGG, leading to the deletion of Ala289, Phe290, and Asp291 in fibrinogen γ-chain. The polymerization of the fibrinogen from the propositus was markedly impaired, with prolonged lag period and decreased final turbidity. The fibrinogen clottability showed a reduced fraction of participating clot formation. While the clot lysis showed normal. Scanning electron microscopy revealed that the fibers of the propositus were thicker than normal, with larger pores and curlier meshworks. We conclude that γAla289_Asp291del is responsible for the hypodysfibrinogenemia in this case.

We have investigated the X-ray diffraction (XRD) spectra, magnetic susceptibility χ(T) and electrical resistivity with and without magnetic field H, ρ(H, T), of an arc melted MoCx alloy. XRD data suggest that the pristine sample is not in the homogeneity range. Magnetic and electrical transport measurements indicate consistently that the sample become superconducting at around Tc ∼ 5.8 K. Further, the upper critical field (Hc2) is estimated to be 1.6 ± 0.1 Tesla by using empirical formulas.

The critical behavior of ferromagnetic transition is investigated by bulk magnetization measurements for La0.85Co1.68As2 crystal with a ThCr2Si2-type structure, grown by using NaAs as a flux, in which the vacancies on the both La and Co sites exist. The critical exponents [ β = 0.388(3), γ = 1.44(2) and δ = 4.855(9)] with Curie temperature T c = 99.4 K are obtained, whose self-consistency and reliability are verified by the Widom scaling law and the scaling equation. The critical exponents of ferromagnetic transition occurring in La0.85Co1.68As2 belong to the three-dimensional (3D) Heisenberg model, and suggest that the magnetic interaction decays as J ( r ) ∼ r − 4 . 975 with a short range coupling. These results provide helpful information for understanding the mechanism of ferromagnetism emerging in La0.85Co1.68As2 compound.

Compounds with the A15 structure have attracted extensive attention due to their superconductivity and nontrivial topological band structure. We have successfully grown Nb$_3$Sb single crystals with a A15 structure and systematically measured the longitudinal resistivity, Hall resistivity and quantum oscillations in magnetization. Similar to other topological trivial/nontrivial semimetals, Nb$_3$Sb, exhibits large magnetoresistance (MR) at low temperatures (717$\%$, 2 K and 9 T), unsaturating quadratic field dependence of MR and up-turn behavior in $\rho_{xx}$(\emph{T}) curves under magnetic field, which is considered to result from a perfect hole-electron compensation, as evidenced by the Hall resistivity measurements. The nonzero Berry phase obtained from the de-Hass van Alphen (dHvA) oscillations demonstrates that Nb$_3$Sb is topologically nontrivial. These results indicate that Nb$_{3}$Sb superconductor is also a semimetal with large MR and nontrivial Berry phase, indicating that Nb$_{3}$Sb may be another platform to search for Majorana zero-energy mode., Comment: 5 pages, 5 figures. arXiv admin note: text overlap with arXiv:2007.04814, arXiv:2104.03799

Multiple mechanisms for extremely large magnetoresistance (XMR) found in many topologically nontrivial/trivial semimetals have been theoretically proposed, but experimentally it is unclear which mechanism is responsible in a particular sample. In this article, by the combination of band structure calculations, numerical simulations of magnetoresistance (MR), Hall resistivity and de Haas-van Alphen (dHvA) oscillation measurements, we studied the MR anisotropy of SiP$_{2}$ which is verified to be a topologically trivial, incomplete compensation semimetal. It was found that as magnetic field, $H$, is applied along the $a$ axis, the MR exhibits an unsaturated nearly linear $H$ dependence, which was argued to arise from incomplete carriers compensation. For the $H$ $\parallel$ [101] orientation, an unsaturated nearly quadratic $H$ dependence of MR up to 5.88 $\times$ 10$^{4}$$\%$ (at 1.8 K, 31.2 T) and field-induced up-turn behavior in resistivity were observed, which was suggested due to the existence of hole open orbits extending along the $k_{x}$ direction. Good agreement of the experimental results with the simulations based on the calculated Fermi surface (FS) indicates that the topology of FS plays an important role in its MR., Comment: 9 pages, 8 figures

Metastasis is the main cause of death in colorectal cancer (CRC) patients. However, current treatment options for CRC metastasis are very limited. Lupeol, a triterpene that is widely found in vegetables and fruits, has been reported to possess the cancer-preventive and anti-inflammatory functions. However, the roles of Lupeol in the migration and invasion of colorectal cancer remain unclear. Here, we evaluated the effect of Lupeol treatment on colorectal cancer cell lines, HCT116 and SW620, and delineated its underlying mechanisms. Our results showed that Lupeol induced a dose-dependent inhibition of HCT116 and SW620 cells viability, measured by CCK8 assay. Wound healing and Transwell migration and invasion assays revealed that Lupeol significantly suppressed the migration and invasion of CRC cells. Using laser confocal microscope, we observed that the pseudopods and protrusions of HCT116 and SW620 cells decreased and disrupted after treatment with Lupeol. In addition, the quantitative real-time PCR and Western blotting results showed that Lupeol downregulated the expression of RhoA and RhoC, and their downstream effectors ROCK1, Cofilin, p-MLC, and the associated regulatory protein Cyclin A2. Interestingly, the migration and invasion capacity of CRC cells was reduced after RhoA knockdown. And there were no additional changes in CRC cells with RhoA knockdown to treat with Lupeol. These findings demonstrate that Lupeol can suppress the migration and invasion of colorectal cancer cells by remodeling the actin cytoskeleton via RhoA-ROCK1 pathway inhibition, which may provide an effective anti-metastatic agent for CRC patients.

While zinc is an essential trace metal in biology, excess zinc is toxic to organisms. Previous studies have shown that zinc toxicity is associated with disruption of the [4Fe-4S] clusters in various dehydratases in Escherichia coli Here, we report that the intracellular zinc overload in E. coli cells inhibits iron-sulfur cluster biogenesis without affecting the preassembled iron-sulfur clusters in proteins. Among the housekeeping iron-sulfur cluster assembly proteins encoded by the gene cluster iscSUA-hscBA-fdx-iscX in E. coli cells, the scaffold IscU, the iron chaperone IscA, and ferredoxin have strong zinc binding activity in cells, suggesting that intracellular zinc overload inhibits iron-sulfur cluster biogenesis by binding to the iron-sulfur cluster assembly proteins. Mutations of the conserved cysteine residues to serine in IscA, IscU, or ferredoxin completely abolish the zinc binding activity of the proteins, indicating that zinc can compete with iron or iron-sulfur cluster binding in IscA, IscU, and ferredoxin and block iron-sulfur cluster biogenesis. Furthermore, intracellular zinc overload appears to emulate the slow-growth phenotype of the E. coli mutant cells with deletion of the iron-sulfur cluster assembly proteins IscU, IscA, and ferredoxin. Our results suggest that intracellular zinc overload inhibits iron-sulfur cluster biogenesis by targeting the iron-sulfur cluster assembly proteins IscU, IscA, and ferredoxin in E. coli cells.IMPORTANCE Zinc toxicity has been implicated in causing various human diseases. High concentrations of zinc can also inhibit bacterial cell growth. However, the underlying mechanism has not been fully understood. Here, we report that zinc overload in Escherichia coli cells inhibits iron-sulfur cluster biogenesis by targeting specific iron-sulfur cluster assembly proteins. Because iron-sulfur proteins are involved in diverse physiological processes, the zinc-mediated inhibition of iron-sulfur cluster biogenesis could be largely responsible for the zinc-mediated cytotoxicity. Our finding provides new insights on how intracellular zinc overload may inhibit cellular functions in bacteria.

Bismuth oxyselenide (Bi$_2$O$_2$Se) attracts great interest as a potential n-type complement to p-type thermoelectric oxides in practical applications. Previous investigations were generally focused on polycrystals. Here, we performed a study on the thermoelectric properties of Bi$_2$O$_2$Se single crystals. Our samples exhibit electron mobility as high as 250 cm$^2.$V$^{-1}$.s$^{-1}$ and thermal conductivity as low as $2$ W.m$^{-1}$.K$^{-1}$ near room temperature. The maximized figure of merit is yielded to be 0.188 at 390 K, higher than that of polycrystals. Consequently, a rough estimation of the phonon mean free path ($\ell_\textrm{ph}$) from the kinetic model amounts to 12 $\r{A}$ at 390 K and follows a $T^{-1}$ behavior. An extrapolation of $\ell_\textrm{ph}$ to higher temperatures indicates that this system approaches the Ioffe-Regel limit at about 1100 K. In light of the phonon dispersions, we argue that the ultralow $\ell_\textrm{ph}$ is attributed to intense anharmonic phonon-phonon scattering, including Umklapp process and acoustic to optical phonon scattering. Our results suggest that single crystals provide a further improvement of thermoelectric performance of Bi$_2$O$_2$Se., Comment: 6 pages, 4 figures

Metastasis is the main cause of death in colorectal cancer (CRC) patients. However, current treatment options for CRC metastasis are very limited. Lupeol, a triterpene that is widely found in vegetables and fruits, has been reported to possess the cancer-preventive and anti-inflammatory functions. However, the roles of Lupeol in the migration and invasion of colorectal cancer remain unclear. Here, we evaluated the effect of Lupeol treatment on colorectal cancer cell lines, HCT116 and SW620, and delineated its underlying mechanisms. Our results showed that Lupeol induced a dose-dependent inhibition of HCT116 and SW620 cells viability, measured by CCK8 assay. Wound healing and Transwell migration and invasion assays revealed that Lupeol significantly suppressed the migration and invasion of CRC cells. Using laser confocal microscope, we observed that the pseudopods and protrusions of HCT116 and SW620 cells decreased and disrupted after treatment with Lupeol. In addition, the quantitative real-time PCR and Western blotting results showed that Lupeol downregulated the expression of RhoA and RhoC, and their downstream effectors ROCK1, Cofilin, p-MLC, and the associated regulatory protein Cyclin A2. Interestingly, the migration and invasion capacity of CRC cells was reduced after RhoA knockdown. And there were no additional changes in CRC cells with RhoA knockdown to treat with Lupeol. These findings demonstrate that Lupeol can suppress the migration and invasion of colorectal cancer cells by remodeling the actin cytoskeleton via RhoA-ROCK1 pathway inhibition, which may provide an effective anti-metastatic agent for CRC patients.

The discovery of 39 K superconductivity in MgB2 and the recent observations of high-T c superconductivity in the high-pressured hydrides motivate ones to search for new superconductors in the compounds containing H or B light element. In this article, we chose the heavier Ge to replace the Si in the ternary borides Mo5SiB2 with the Cr5B3 type tetragonal structure, a relative new group borosilicate superconductors, and prepared Mo5GeB2 polycrystalline sample. By the combination of resistivity, magnetization, and specific heat measurements and band calculations, we determine its superconducting parameters. It was found that Mo5GeB2 is a type II superconductor, with the critical temperature T c = 5.4 K, and the Ginzburg–Landau (GL) parameter k GL (0) = 4.2. The estimated electron-phonon coupling constant λ ph (0.57) and the specific heat jump △ C e l / γ n T c (1.33) demonstrate that Mo5GeB2 is a weak-coupling, single-gap phonon-mediated superconductor. Band calculations reveal that Mo5GeB2 has a similar density of state (DOS) near Fermi energy to that of Mo5SiB2 with the same T c , but smaller than that Mo5PB2 with T c = 9.2 K.

The measurements of magnetization, longitudinal and Hall resistivities are carried out on the intrinsic antiferromagnetic (AFM) topological insulator EuSn 2 As 2. It is confirmed that our EuSn 2 As 2 crystal is a heavily hole doping A-type AFM metal with the Néel temperature T N = 24 K, with a metamagnetic transition from an AFM to a ferromagnetic (FM) phase occurring at a certain critical magnetic field for the different field orientations. Meanwhile, we also find that the carrier concentration does not change with the evolution of magnetic order, indicating that the weak interaction between the localized magnetic moments from Eu 2+ 4f 7 orbits and the electronic states near the Fermi level. Although the quantum anomalous Hall effect (AHE) is not observed in our crystals, it is found that a relatively large negative magnetoresistance (−13%) emerges in the AFM phase, and exhibits an exponential dependence upon magnetic field, whose microscopic origin is waiting to be clarified in future research.

Accumulating evidence supports the notion that epigenetic modifiers are abnormal in carcinogenesis and have a fundamental role in cancer progression. Among these aberrant epigenetic modifiers, the function of histone methyltransferase KMT2A in somatic tumors is not well known. By analyzing KMT2A expression in patient tissues, we demonstrated that KMT2A was overexpressed in colorectal cancer tissues in comparison with adjacent normal tissues and its expression was positively correlated with cancer stages. In KMT2A‐knockdown HCT116 and DLD1 cells, cell invasion and migration were consequently suppressed. In addition, KMT2A depletion effectively suppressed cancer metastasis in vivo. Mechanistically, cathepsin Z (CTSZ) was demonstrated to be an important downstream gene of KMT2A. Further studies showed that p65 could recruit KMT2A on the promoter region of the downstream gene CTSZ and knockdown of p65 could reduce the KMT2A on the promoter of CTSZ. Finally, our present study revealed that KMT2A epigenetically promotes cancer progression by targeting CTSZ, which has specific functions in cancer invasion and metastasis.

Zinc toxicity has been implicated in causing various human diseases. High concentrations of zinc can also inhibit bacterial cell growth. However, the underlying mechanism has not been fully understood. Here, we report that zinc overload in Escherichia coli cells inhibits iron-sulfur cluster biogenesis by targeting specific iron-sulfur cluster assembly proteins. Because iron-sulfur proteins are involved in diverse physiological processes, the zinc-mediated inhibition of iron-sulfur cluster biogenesis could be largely responsible for the zinc-mediated cytotoxicity. Our finding provides new insights on how intracellular zinc overload may inhibit cellular functions in bacteria., While zinc is an essential trace metal in biology, excess zinc is toxic to organisms. Previous studies have shown that zinc toxicity is associated with disruption of the [4Fe-4S] clusters in various dehydratases in Escherichia coli. Here, we report that the intracellular zinc overload in E. coli cells inhibits iron-sulfur cluster biogenesis without affecting the preassembled iron-sulfur clusters in proteins. Among the housekeeping iron-sulfur cluster assembly proteins encoded by the gene cluster iscSUA-hscBA-fdx-iscX in E. coli cells, the scaffold IscU, the iron chaperone IscA, and ferredoxin have strong zinc binding activity in cells, suggesting that intracellular zinc overload inhibits iron-sulfur cluster biogenesis by binding to the iron-sulfur cluster assembly proteins. Mutations of the conserved cysteine residues to serine in IscA, IscU, or ferredoxin completely abolish the zinc binding activity of the proteins, indicating that zinc can compete with iron or iron-sulfur cluster binding in IscA, IscU, and ferredoxin and block iron-sulfur cluster biogenesis. Furthermore, intracellular zinc overload appears to emulate the slow-growth phenotype of the E. coli mutant cells with deletion of the iron-sulfur cluster assembly proteins IscU, IscA, and ferredoxin. Our results suggest that intracellular zinc overload inhibits iron-sulfur cluster biogenesis by targeting the iron-sulfur cluster assembly proteins IscU, IscA, and ferredoxin in E. coli cells. IMPORTANCE Zinc toxicity has been implicated in causing various human diseases. High concentrations of zinc can also inhibit bacterial cell growth. However, the underlying mechanism has not been fully understood. Here, we report that zinc overload in Escherichia coli cells inhibits iron-sulfur cluster biogenesis by targeting specific iron-sulfur cluster assembly proteins. Because iron-sulfur proteins are involved in diverse physiological processes, the zinc-mediated inhibition of iron-sulfur cluster biogenesis could be largely responsible for the zinc-mediated cytotoxicity. Our finding provides new insights on how intracellular zinc overload may inhibit cellular functions in bacteria.

Extremely large magnetoresistance (XMR) was recently discovered in many nonmagnetic materials, while its underlying mechanism remains poorly understood due to the complex electronic structure of these materials. Here we report an investigation of the $\ensuremath{\alpha}$-phase ${\mathrm{WP}}_{2}$, a topologically trivial semimetal with monoclinic crystal structure ($C2/m$), which contrasts with the recently discovered robust type-II Weyl semimetal phase in $\ensuremath{\beta}\ensuremath{-}{\mathrm{WP}}_{2}$. We found that $\ensuremath{\alpha}\ensuremath{-}{\mathrm{WP}}_{2}$ exhibits almost all the characteristics of XMR materials: the near-quadratic field dependence of MR, a field-induced up-turn in resistivity followed by a plateau at low temperature, which can be understood by the compensation effect, and high mobility of carriers confirmed by our Hall effect measurements. It was also found that the normalized MRs under different magnetic fields have the same temperature dependence in $\ensuremath{\alpha}\ensuremath{-}{\mathrm{WP}}_{2}$, the Kohler scaling law can describe the MR data in a wide temperature range, and there is no obvious change in the anisotropic parameter $\ensuremath{\gamma}$ value with temperature. The resistance polar diagram has a peanut shape when the field is rotated in the $ac$ plane, which can be understood by the anisotropy of the Fermi surface. These results indicate that both field-induced-gap and temperature-induced Lifshitz transition are not the origin of up-turn in resistivity in the $\ensuremath{\alpha}\ensuremath{-}{\mathrm{WP}}_{2}$ semimetal. Our findings establish $\ensuremath{\alpha}\ensuremath{-}{\mathrm{WP}}_{2}$ as a new reference material for exploring the XMR phenomena.

Wnt signaling pathway plays a major role in the progression of colorectal cancer (CRC). Small molecules which can cut off this signal transduction can be promising anti-cancer drugs for CRC therapy. Therefore, we aimed to investigate the mechanisms of FH535, an inhibitor of the Wnt signaling pathway, on inhibiting proliferation and migration of colorectal cancer cells DLD-1 and SW620. We found that FH535 could significantly suppress the growth of DLD-1 and SW620 cells in a concentration-dependent and time-dependent manner. The results of cell cycle tests showed that FH535 could significantly induce G2/M arrest in colorectal cancer cells. Transwell and Wound-healing assays revealed that FH535 notably inhibited cell migration. Moreover, we found that FH535 down-regulated β-catenin and CyclinA2 expressions while up-regulating Claudin-1 expression at both mRNA and protein levels, which may contribute to the FH535-induced inhibitory effect on proliferation and migration in human colorectal cancer cells. Our study revealed that FH535 inhibited proliferation and migration of colorectal cancer cells by regulating CyclinA2 and Claudin1 gene expression, which enriches regulatory network of FH535 and may contribute to being promising anti-cancer drugs for CRC therapy.