Semantic Counting from Self-Collages

While recent supervised methods for reference-based object counting continue to improve the performance on benchmark datasets, they have to rely on small datasets due to the cost associated with manually annotating dozens of objects in images. We propose Unsupervised Counter (UnCo), a model that can learn this task without requiring any manual annotations. To this end, we construct "SelfCollages", images with various pasted objects as training samples, that provide a rich learning signal covering arbitrary object types and counts. Our method builds on existing unsupervised representations and segmentation techniques to successfully demonstrate the ability to count objects without manual supervision. Our experiments show that our method not only outperforms simple baselines and generic models such as FasterRCNN, but also matches the performance of supervised counting models in some domains.Comment: 24 pages. Code available at https://github.com/lukasknobel/SelfCollage

Molecular beam epitaxy of the half-Heusler antiferromagnet CuMnSb

We report growth of CuMnSb thin films by molecular beam epitaxy on InAs(001) substrates. The CuMnSb layers are compressively strained (0.6~\text{%}) due to lattice mismatch. The thin films have a $\omega$ full width half max of $7.7^{''}$ according to high resolution X-ray diffraction, and a root mean square roughness of $0.14~\text{nm}$ as determined by atomic force microscopy. Magnetic and electrical properties are found to be consistent with reported values from bulk samples. We find a N\'eel temperature of $62~\text{K}$, a Curie-Weiss temperature of $-65~\text{K}$ and an effective moment of $5.9~\mu_{\text{B}}/\text{f.u.}$. Transport measurements confirm the antiferromagetic transition and show a residual resistivity at $4~\text{K}$ of $35~\mu\Omega\cdot \text{cm}$.Comment: 6 pages, 5 figures, accepted in PR

DNA polymerase zeta is required for proliferation of normal mammalian cells

Unique among translesion synthesis (TLS) DNA polymerases, pol ζ is essential during embryogenesis. To determine whether pol ζ is necessary for proliferation of normal cells, primary mouse fibroblasts were established in which Rev3L could be conditionally inactivated by Cre recombinase. Cells were grown in 2% O2 to prevent oxidative stress-induced senescence. Cells rapidly became senescent or apoptotic and ceased growth within 3–4 population doublings. Within one population doubling following Rev3L deletion, DNA double-strand breaks and chromatid aberrations were found in 30–50% of cells. These breaks were replication dependent, and found in G1 and G2 phase cells. Double-strand breaks were reduced when cells were treated with the reactive oxygen species scavenger N-acetyl-cysteine, but this did not rescue the cell proliferation defect, indicating that several classes of endogenously formed DNA lesions require Rev3L for tolerance or repair. T-antigen immortalization of cells allowed cell growth. In summary, even in the absence of external challenges to DNA, pol ζ is essential for preventing replication-dependent DNA breaks in every division of normal mammalian cells. Loss of pol ζ in slowly proliferating mouse cells in vivo may allow accumulation of chromosomal aberrations that could lead to tumorigenesis. Pol ζ is unique amongst TLS polymerases for its essential role in cell proliferation

Franck-Condon blockade in suspended carbon nanotube quantum dots

Understanding the influence of vibrational motion of the atoms on electronic transitions in molecules constitutes a cornerstone of quantum physics, as epitomized by the Franck-Condon principle of spectroscopy. Recent advances in building molecular-electronics devices and nanoelectromechanical systems open a new arena for studying the interaction between mechanical and electronic degrees of freedom in transport at the single-molecule level. The tunneling of electrons through molecules or suspended quantum dots has been shown to excite vibrational modes, or vibrons. Beyond this effect, theory predicts that strong electron-vibron coupling dramatically suppresses the current flow at low biases, a collective behaviour known as Franck-Condon blockade. Here we show measurements on quantum dots formed in suspended single-wall carbon nanotubes revealing a remarkably large electron-vibron coupling and, due to the high quality and unprecedented tunability of our samples, admit a quantitative analysis of vibron-mediated electronic transport in the regime of strong electron-vibron coupling. This allows us to unambiguously demonstrate the Franck-Condon blockade in a suspended nanostructure. The large observed electron-vibron coupling could ultimately be a key ingredient for the detection of quantized mechanical motion. It also emphasizes the unique potential for nanoelectromechanical device applications based on suspended graphene sheets and carbon nanotubes.Comment: 7 pages, 3 figure

Inhibition of REV3 Expression Induces Persistent DNA Damage and Growth Arrest in Cancer Cells12

REV3 is the catalytic subunit of DNA translesion synthesis polymerase ζ. Inhibition of REV3 expression increases the sensitivity of human cells to a variety of DNA-damaging agents and reduces the formation of resistant cells. Surprisingly, we found that short hairpin RNA-mediated depletion of REV3 per se suppresses colony formation of lung (A549, Calu-3), breast (MCF-7, MDA-MB-231), mesothelioma (IL45 and ZL55), and colon (HCT116 +/-p53) tumor cell lines, whereas control cell lines (AD293, LP9-hTERT) and the normal mesothelial primary culture (SDM104) are less affected. Inhibition of REV3 expression in cancer cells leads to an accumulation of persistent DNA damage as indicated by an increase in phospho-ATM, 53BP1, and phospho-H2AX foci formation, subsequently leading to the activation of the ATM-dependent DNA damage response cascade. REV3 depletion in p53-proficient cancer cell lines results in a G1 arrest and induction of senescence as indicated by the accumulation of p21 and an increase in senescence-associated β-galactosidase activity. In contrast, inhibition of REV3 expression in p53-deficient cells results in growth inhibition and a G2/M arrest. A small fraction of the p53-deficient cancer cells can overcome the G2/M arrest, which results in mitotic slippage and aneuploidy. Our findings reveal that REV3 depletion per se suppresses growth of cancer cell lines from different origin, whereas control cell lines and a mesothelial primary culture were less affected. Thus, our findings indicate that depletion of REV3 not only can amend cisplatin-based cancer therapy but also can be applied for susceptible cancers as a potential monotherapy