Hypercontractivity on the qq-Araki-Woods algebras

Extending a work of Carlen and Lieb, Biane has obtained the optimal hypercontractivity of the $q$-Ornstein-Uhlenbeck semigroup on the $q$-deformation of the free group algebra. In this note, we look for an extension of this result to the type III situation, that is for the $q$-Araki-Woods algebras. We show that hypercontractivity from $L^p$ to $L^2$ can occur if and only if the generator of the deformation is bounded.Comment: 17 page

The distribution of an invasive species, clidemia hirta along roads and trails in Endau Rompin National Park, Malaysia

Invasive species pose a grave threat to many national parks. Construction of roads and trails for tourism may facilitate invasion of alien species. To understand the effect of road and trail construction on invasive species, we established six transects in three land-use types (forest interior and road or trail edges) in Endau Rompin National Park, Johor, Malaysia, where we measured the number of an invasive shrub, Clidemia hirta (Melastomataceae), canopy openness, and soil properties; compared the density of C. hirta between the three land-use types; and finally, identified soil and canopy variables affecting its abundance using generalized linear mixed models. C. hirta was found along the road and trail with density ranging from 0.0 m2 to 33 m2 (average: 3.8 m2), but was not found in the forest interior. Generalized linear mixed models suggested that canopy openness and soil pH negatively affected the density of C. hirta along the road, as did total soil nitrogen along the trail. This suggests that C. hirta was more abundant along dark and nutrient-poor road and trail edges. The construction of narrow roads (2.0–3.8 m) and trails (0.5–2.0 m wide) at our site would be considered a relatively minor disturbance without intensive clear cuts, and C. hirta seemed to prefer habitats with such minor disturbances. In the tropical rainforests, the managers or conservationists of the national park should include consideration of the effects such as minor disturbances have on invasive species

Mekanisme pencairan dana pembiayaan mudharabah dengan agunan cash collateral : studi kasus pada KSPPS Arthamadina Banyuputih-Batang

Koperasi simpan pinjam dan pembiayaan syariah merupakan koperasi yang kegiatan usahanya meliputi pinjaman, simpanan, dan pembiayaan yang pengoprasiannya sesuai dengan perinsip syariah dan juga terdapat kegiatan pengelolaan zakat, infaq/sodakoh, dan wakaf. KSPPS Arthamadina dalam menyalurkan danannya menggunakan akad mudharabah atau akad kerja sama antara shohibul maal dan mudharib, kspps arthamadina juga menyediakan pembiayaan dengan agunan cast collateral untuk mempermudah anggota atau calon anggotanya yang akan mengajukan pembiayaan tetapi tidak mempunyai fix asset. Adapun rumusan masalah yang dalam penelitian ini, adalah bagaimana mekanisme pencairan dana pembiayaan dan apa saja yang dijadikan pertimbangan dalam melakukan pembiayaan dengan agunan cast collateral di KSPPS Arthamadina. Penelitian ini menggunakan metode kualitatif, dengan menggunakan pendekatan deskritif dengan berusaha mengambarkan hasil penelitian yang apa adanya. Teknik pengumpulan data dengan observasi, wawancara, dan dokumentasi. KSPPS Arthamadina adalah tempat yang dijadikan penelitian yang daerah kerjanya di Kabupaten Batang, lebih tepatnya di Jl. Lokojoyo Km. 1 Banyuputih, Batang 51271. Dari hasil penelitian KSPPS Arthamadina belum sepenuhnya menggunakan prinsip syariah dikarenakan di KSPPS Arthamadina masih menggunakan persentase dalam bagi hasilnya. Pembiayaan dengan agunan cast collateral juga diterapkan untuk memberikan kemudahan, kesejahteraan, dan membantu anggotanya yang tidak memiliki agunan fix asset tetapi masih dapat melakukan pembiayaan dengan plafon yang kecil

A volume inequality for quantum Fisher information and the uncertainty principle

Let $A_1,...,A_N$ be complex self-adjoint matrices and let $\rho$ be a density matrix. The Robertson uncertainty principle $$det(Cov_\rho(A_h,A_j)) \geq det(- \frac{i}{2} Tr(\rho [A_h,A_j]))$$ gives a bound for the quantum generalized covariance in terms of the commutators $[A_h,A_j]$. The right side matrix is antisymmetric and therefore the bound is trivial (equal to zero) in the odd case $N=2m+1$. Let $f$ be an arbitrary normalized symmetric operator monotone function and let $_{\rho,f}$ be the associated quantum Fisher information. In this paper we conjecture the inequality $$det (Cov_\rho(A_h,A_j)) \geq det (\frac{f(0)}{2} _{\rho,f})$$ that gives a non-trivial bound for any natural number $N$ using the commutators $i[\rho, A_h]$. The inequality has been proved in the cases $N=1,2$ by the joint efforts of many authors. In this paper we prove the case N=3 for real matrices

New Concepts in Particle Physics from Solution of an Old Problem

Recent ideas on modular localization in local quantum physics are used to clarify the relation between on- and off-shell quantities in particle physics; in particular the relation between on-shell crossing symmetry and off-shell Einstein causality. Among the collateral results of this new nonperturbative approach are profound relations between crossing symmetry of particle physics and Hawking-Unruh like thermal aspects (KMS property, entropy attached to horizons) of quantum matter behind causal horizons, aspects which hitherto were exclusively related with Killing horizons in curved spacetime rather than with localization aspects in Minkowski space particle physics. The scope of this modular framework is amazingly wide and ranges from providing a conceptual basis for the d=1+1 bootstrap-formfactor program for factorizable d=1+1 models to a decomposition theory of QFT's in terms of a finite collection of unitarily equivalent chiral conformal theories placed a specified relative position within a common Hilbert space (in d=1+1 a holographic relation and in higher dimensions more like a scanning). The new framework gives a spacetime interpretation to the Zamolodchikov-Faddeev algebra and explains its thermal aspects.Comment: In this form it will appear in JPA Math Gen, 47 pages tcilate

3D HABITAT COMPLEXITY OF CORAL REEFS IN THE NORTHWESTERN HAWAIIAN ISLANDS IS DRIVEN BY CORAL ASSEMBLAGE STRUCTURE

Corals act as ecosystem engineers by secreting structurally complex calcium carbonate skeletons on the benthic substrate that provide habitat for a diverse array of associated reef organisms. Communities of living corals create large and dynamic benthic structures that directly affect ecological parameters such as habitat provisioning and light availability, thus influencing overall ecosystem function. Despite the important role 3D structural complexity plays in ecosystem biodiversity and productivity, the field of coral ecology has lacked accessibility to practical technology capable of quantifying 3D characteristics of underwater habitats. Advancements in the field of computer vision has led to Structure-from-Motion (SfM) photogrammetry, which provides a simple and cost-effective method for creating high-resolution and spatially accurate 3D reconstructions of natural environments. Integrating SfM approaches into coral reef research and monitoring has provided useful insight into the relationship between 3D habitat complexity and ecological processes. In this study, we examined the relationships among 2D estimates of live coral cover and several metrics of 3D habitat structural complexity among eleven long-term monitoring sites at French Frigate Shoals. Our findings show that coral assemblage structure acts as a significant driver of 3D structural complexity of coral reef habitats at this atoll. This study highlights the importance of diverse and abundant coral assemblages in supporting structurally complex coral reef habitats and provides a framework for future investigations into the ecological role of various coral morphotypes

YY1 haploinsufficiency causes an intellectual disability syndrome featuring transcriptional and chromatin dysfunction

Yin and yang 1 (YY1) is a well-known zinc-finger transcription factor with crucial roles in normal development and malignancy. YY1 acts both as a repressor and as an activator of gene expression. We have identified 23 individuals with de novo mutations or deletions of YY1 and phenotypic features that define a syndrome of cognitive impairment, behavioral alterations, intrauterine growth restriction, feeding problems, and various congenital malformations. Our combined clinical and molecular data define "YY1 syndrome" as a haploinsufficiency syndrome. Through immunoprecipitation of YY1-bound chromatin from affected individuals' cells with antibodies recognizing both ends of the protein, we show that YY1 deletions and missense mutations lead to a global loss of YY1 binding with a preferential retention at high-occupancy sites. Finally, we uncover a widespread loss of H3K27 acetylation in particular on the YY1-bound enhancers, underscoring a crucial role for YY1 in enhancer regulation. Collectively, these results define a clinical syndrome caused by haploinsufficiency of YY1 through dysregulation of key transcriptional regulators.Michele Gabriele, Anneke T. Vulto-van Silfhout, Pierre-Luc Germain, Alessandro Vitriolo, Raman Kumar, Evelyn Douglas, Eric Haan, Kenjiro Kosaki, Toshiki Takenouchi, Anita Rauch, Katharina Steindl, Eirik Frengen, Doriana Misceo, Christeen Ramane J. Pedurupillay, Petter Stromme, Jill A. Rosenfeld, Yunru Shao, William J. Craigen, Christian P. Schaaf, David Rodriguez-Buritica, Laura Farach, Jennifer Friedman, Perla Thulin, Scott D. McLean, Kimberly M. Nugent, Jenny Morton, Jillian Nicholl, Joris Andrieux, Asbjørg Stray-Pedersen, Pascal Chambon, Sophie Patrier, Sally A. Lynch, Susanne Kjaergaard, Pernille M. Tørring, Charlotte Brasch-Andersen, Anne Ronan, Arie van Haeringen, Peter J. Anderson, Zöe Powis, Han G. Brunner, Rolph Pfundt, Janneke H.M. Schuurs-Hoeijmakers, Bregje W.M. van Bon, Stefan Lelieveld, Christian Gilissen, Willy M. Nillesen, Lisenka E.L.M. Vissers, Jozef Gecz, David A. Koolen, Giuseppe Testa, Bert B.A. de Vrie

Involvement of mTOR pathway in neurodegeneration in NSF-related developmental and epileptic encephalopathy

Membrane fusion is mediated by soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins. During neurotransmitter exocytosis, SNARE proteins on a synaptic vesicle and the target membrane form a complex, resulting in neurotransmitter release. N-ethylmaleimide-sensitive factor (NSF), a homohexameric ATPase, disassembles the complex, allowing individual SNARE proteins to be recycled. Recently, the association between pathogenic NSF variants and developmental and epileptic encephalopathy (DEE) was reported; however, the molecular pathomechanism of NSF-related DEE remains unclear. Here, three patients with de novo heterozygous NSF variants were presented, of which two were associated with DEE and one with a very mild phenotype. One of the DEE patients also had hypocalcemia from parathyroid hormone deficiency and neuromuscular junction impairment. Using PC12 cells, a neurosecretion model, we show that NSF with DEE-associated variants impaired the recycling of vesicular membrane proteins and vesicle enlargement in response to exocytotic stimulation. In addition, DEE-associated variants caused neurodegenerative change and defective autophagy through overactivation of the mTOR pathway. Treatment with rapamycin, an mTOR inhibitor, or overexpression of wild-type NSF ameliorated these phenotypes. Furthermore, neurons differentiated from patient-derived induced pluripotent stem cells showed neurite degeneration, which was also alleviated by rapamycin treatment or gene correction using genome editing. Protein structure analysis of NSF revealed that DEE-associated variants might disrupt the transmission of the conformational change of NSF monomers and consequently halt the rotation of ATP hydrolysis, indicating a dominant negative mechanism. In conclusion, this study elucidates the pathomechanism underlying NSF-related DEE and identifies a potential therapeutic approach