Thermoelectric response across the semiconductor-semimetal transition in black phosphorus

In spite of intensive studies on thermoelectricity in metals, little is known about thermoelectric response in semiconductors at low temperature. An even more fascinating and unanswered question is what happens to the Seebeck coefficient when the semiconductor turns to a metal. By precisely tuning the ground state of black phosphorus with pressure from the semiconducting to semimetallic state, we track a systematic evolution of the Seebeck coefficient. Thanks to a manifest correlation between the Seebeck coefficient and resistivity, the Seebeck response in each conduction regime, i.e., intrinsic, saturation, extrinsic, and variable range hopping (VRH) regimes, is identified. In the former two regimes, the Seebeck coefficient behaves in accordance with the present theories, whereas in the later two regimes available theories do not give a satisfactory account for its response. However, by eliminating the extrinsic sample dependence in the resistivity $\rho$ and Seebeck coefficient $S$, the Peltier conductivity $\alpha=S/\rho$ allows to unveil the intrinsic thermoelectric response, revealing vanishing fate for $\alpha$ in the VRH regime. The emerged ionized impurity scattering on entry to the semimetallic state is easily surpassed by electron-electron scattering due to squeezing of screening length accompanied by an increase of carrier density with pressure. In the low temperature limit, a small number of carriers enhances a prefactor of $T$-linear Seebeck coefficient as large as what is observed in prototypical semimetals. A crucial but largely ignored role of carrier scattering in determining the magnitude and sign of the Seebeck coefficient is indicated by the observation that a sign reversal of the $T$-linear prefactor is concomitant with a change in dominant scattering mechanism for carriers.Comment: 13 pages, 16 figure

APC/C – the master controller of origin licensing?

DNA replication must be tightly controlled to prevent initiation of a second round of replication until mitosis is complete. So far, components of the pre-replicative complex (Cdt1, Cdc6 and geminin) were considered key players in this regulation. In a new study, Machida and Dutta have shown that depletion of Emi1 caused cells to replicate their DNA more than once per cell cycle [1]. This effect was dependent on the ability of Emi1 to inhibit the APC/C. In addition to its role in regulating entry into mitosis, oscillation of APC/C activity regulates pre-RC formation: high APC/C activity in late M/G1 allows pre-RC formation and low APC/C activity in S/G2 prevents pre-RC formation for a second time thereby preventing rereplication. Each redundant pathway to prevent rereplication is dependent on regulating one of the pre-RC components, and all of the pathways are co-regulated by Emi1 through the APC/C. In this commentary we discuss how this new role of Emi1 adds to our understanding of the regulation of replication initiation. We also review the literature to analyze whether APC/C has a role in regulating endoreduplication (a normal state of polyploidy in some differentiated cells). Similarly a role of premature APC/C activation in genomic instability of tumors is discussed

A three-finger multisensory hand for dexterous space robotic tasks

The National Space Development Agency of Japan will launch ETS-7 in 1997, as a test bed for next generation space technology of RV&D and space robot. MITI has been developing a three-finger multisensory hand for complex space robotic tasks. The hand can be operated under remote control or autonomously. This paper describes the design and development of the hand and the performance of a breadboard model

Faraday dispersion functions of galaxies

The Faraday dispersion function (FDF), which can be derived from an observed polarization spectrum by Faraday rotation measure synthesis, is a profile of polarized emissions as a function of Faraday depth. We study intrinsic FDFs along sight lines through face-on Milky Way like galaxies by means of a sophisticated galactic model incorporating three-dimensional MHD turbulence, and investigate how much information the FDF intrinsically contains. Since the FDF reflects distributions of thermal and cosmic-ray electrons as well as magnetic fields, it has been expected that the FDF could be a new probe to examine internal structures of galaxies. We, however, find that an intrinsic FDF along a sight line through a galaxy is very complicated, depending significantly on actual configurations of turbulence. We perform 800 realizations of turbulence and find no universal shape of the FDF even if we fix the global parameters of the model. We calculate the probability distribution functions of the standard deviation, skewness, and kurtosis of FDFs and compare them for models with different global parameters. Our models predict that the presence of vertical magnetic fields and the large-scale height of cosmic-ray electrons tend to make the standard deviation relatively large. In contrast, the differences in skewness and kurtosis are relatively less significant.open0

MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor-1.

The oncoprotein transcription factor MYC is a major driver of malignancy and a highly validated but challenging target for the development of anticancer therapies. Novel strategies to inhibit MYC may come from understanding the co-factors it uses to drive pro-tumorigenic gene expression programs, providing their role in MYC activity is understood. Here we interrogate how one MYC co-factor, host cell factor (HCF)-1, contributes to MYC activity in a human Burkitt lymphoma setting. We identify genes connected to mitochondrial function and ribosome biogenesis as direct MYC/HCF-1 targets and demonstrate how modulation of the MYC-HCF-1 interaction influences cell growth, metabolite profiles, global gene expression patterns, and tumor growth in vivo. This work defines HCF-1 as a critical MYC co-factor, places the MYC-HCF-1 interaction in biological context, and highlights HCF-1 as a focal point for development of novel anti-MYC therapies

Use of the index of pulmonary vascular disease for predicting long-term outcome of pulmonary arterial hypertension associated with congenital heart disease

AimsLimited data exist on risk factors for the long-term outcome of pulmonary arterial hypertension (PAH) associated with congenital heart disease (CHD-PAH). We focused on the index of pulmonary vascular disease (IPVD), an assessment system for pulmonary artery pathology specimens. The IPVD classifies pulmonary vascular lesions into four categories based on severity: (1) no intimal thickening, (2) cellular thickening of the intima, (3) fibrous thickening of the intima, and (4) destruction of the tunica media, with the overall grade expressed as an additive mean of these scores. This study aimed to investigate the relationship between IPVD and the long-term outcome of CHD-PAH.MethodsThis retrospective study examined lung pathology images of 764 patients with CHD-PAH aged <20 years whose lung specimens were submitted to the Japanese Research Institute of Pulmonary Vasculature for pulmonary pathological review between 2001 and 2020. Clinical information was collected retrospectively by each attending physician. The primary endpoint was cardiovascular death.ResultsThe 5-year, 10-year, 15-year, and 20-year cardiovascular death-free survival rates for all patients were 92.0%, 90.4%, 87.3%, and 86.1%, respectively. The group with an IPVD of ≥2.0 had significantly poorer survival than the group with an IPVD <2.0 (P = .037). The Cox proportional hazards model adjusted for the presence of congenital anomaly syndromes associated with pulmonary hypertension, and age at lung biopsy showed similar results (hazard ratio 4.46; 95% confidence interval: 1.45–13.73; P = .009).ConclusionsThe IPVD scoring system is useful for predicting the long-term outcome of CHD-PAH. For patients with an IPVD of ≥2.0, treatment strategies, including choosing palliative procedures such as pulmonary artery banding to restrict pulmonary blood flow and postponement of intracardiac repair, should be more carefully considered