Coset Character Identities in Superstring Compactifications

We apply the coset character identities (generalization of Jacobi's abstruse identity) to compact and noncompact Gepner models. In the both cases, we prove that the partition function actually vanishes due to the spacetime supersymmetry. In the case of the compact models and discrete parts of the noncompact models, the partition function includes the expected vanishing factor. But the character identities used to the continuous part of the noncompact models suggest that these models have twice as many supersymmetry as expected. This fact is an evidence for the conjecture that the holographically dual of the string theory on an actually singular Calabi-Yau manifold is a super CONFORMAL field theory. The extra SUSY charges are interpreted as the superconformal S generators.Comment: 23 pages, LaTeX, no figure. v2:corrected typos, added detailed calculations, added references. v3:corrected typo

Noncompact Gepner Models with Discrete Spectra

We investigate a noncompact Gepner model, which is composed of a number of SL(2,R)/U(1) Kazama-Suzuki models and N=2 minimal models. The SL(2,R)/U(1) Kazama-Suzuki model contains the discrete series among the SL(2,R) unitary representations as well as the continuous series. We claim that the discrete series contain the vanishing cohomology and the vanishing cycles of the associated noncompact Calabi-Yau manifold. We calculate the Elliptic genus and the open string Witten indices. In the A_{N-1} ALE models, they actually agree with the vanishing cohomology and the intersection form of the vanishing cycles.Comment: 11 pages, LaTeX, 1 figur

Upregulation of Relaxin after Experimental Subarachnoid Hemorrhage in Rabbits

Background. Although relaxin causes vasodilatation in systemic arteries, little is known about its role in cerebral arteries. We investigated the expression and role of relaxin in basilar arteries after subarachnoid hemorrhage (SAH) in rabbits. Methods. Microarray analysis with rabbit basilar artery RNA was performed. Messenger RNA expression of relaxin-1 and relaxin/insulinlike family peptide receptor 1 (RXFP1) was investigated with quantitative RT-PCR. RXFP1 expression in the basilar artery was investigated with immunohistochemistry. Relaxin concentrations in cerebrospinal fluid (CSF) and serum were investigated with an enzyme-linked immunosorbent assay. Using human brain vascular smooth muscle cells (HBVSMC) preincubated with relaxin, myosin light chain phosphorylation (MLC) was investigated with immunoblotting after endothelin-1 stimulation. Results. After SAH, RXFP1 mRNA and protein were significantly downregulated on day 3, whereas relaxin-1 mRNA was significantly upregulated on day 7. The relaxin concentration in CSF was significantly elevated on days 5 and 7. Pretreatment with relaxin reduced sustained MLC phosphorylation induced by endothelin-1 in HBVSMC. Conclusion. Upregulation of relaxin and downregulation of RXFP1 after SAH may participate in development of cerebral vasospasm. Downregulation of RXFP1 may induce a functional decrease in relaxin activity during vasospasm. Understanding the role of relaxin may provide further insight into the mechanisms of cerebral vasospasm

Surgical treatment for therapy-related pectoral hematoma: report of a case and review of published reports

A 96-year-old man with a rapidly growing right chest wall mass was referred to our department for further treatment. Enhanced chest computed tomography showed a huge pectoral hematoma (12×6 cm) in the right thorax. He was on oral antiplatelet medication, but no abnormalities in clotting ability were detected. Because the hematoma was enlarging and painful, it was evacuated surgically and hemostasis achieved around the pectoral branches of the thoraco-acromial artery. His postoperative course was uneventful with no evidence of subcutaneous fluid retention. Surgical hemostasis and hematoma evacuation of this pectoral hematoma might be effective as one treatment method

Gepner-like Description of a String Theory on a Noncompact Singular Calabi-Yau Manifold

We investigate a Gepner-like superstring model described by a combination of multiple minimal models and an N=2 Liouville theory. This model is thought to be equivalent to the superstring theory on a singular noncompact Calabi-Yau manifold. We construct the modular invariant partition function of this model, and confirm the validity of an appropriate GSO projection. We also calculate the elliptic genus and Witten index of the model. We find that the elliptic genus factorises into a rather trivial factor and a non-trivial one, and the non-trivial one has the information on the positively curved base manifold of the cone.Comment: 22 pages, LaTeX, amsmath package, no figures. Corrected typo

Supercoset CFT's for String Theories on Non-compact Special Holonomy Manifolds

We study aspects of superstring vacua of non-compact special holonomy manifolds with conical singularities constructed systematically using soluble N = 1 superconformal field theories (SCFT's). It is known that Einstein homogeneous spaces G/H generate Ricci flat manifolds with special holonomies on their cones R_+ x G/H, when they are endowed with appropriate geometrical structures, namely, the Sasaki-Einstein, tri-Sasakian, nearly Kahler, and weak G_2 structures for SU(n), Sp(n), G_2, and Spin(7) holonomies, respectively. Motivated by this fact, we consider the string vacua of the type: R^{d-1,1} x (N = 1 Liouville) x (N=1 supercoset CFT on G/H) where we use the affine Lie algebras of G and H in order to capture the geometry associated to an Einstein homogeneous space G/H. Remarkably, we find the same number of spacetime and worldsheet SUSY's in our ``CFT cone'' construction as expected from the analysis of geometrical cones over G/H in many examples. We also present an analysis on the possible Liouville potential terms (cosmological constant type operators) which provide the marginal deformations resolving the conical singularities.Comment: 60 pages, no figure, 2 tables; v2 typos correcte

A novel ex vivo lung cancer model based on bioengineered rat lungs

Introduction: Two-dimensional cell cultures have contributed substantially to lung cancer research, but 3D cultures are gaining attention as a new, more efficient, and effective research model. A model reproducing the 3D characteristics and tumor microenvironment of the lungs in vivo, including the co-existence of healthy alveolar cells with lung cancer cells, is ideal. Here, we describe the creation of a successful ex vivo lung cancer model based on bioengineered lungs formed by decellularization and recellularization.Methods: Human cancer cells were directly implanted into a bioengineered rat lung, which was created with a decellularized rat lung scaffold reseeded with epithelial cells, endothelial cells and adipose-derived stem cells. Four human lung cancer cell lines (A549, PC-9, H1299, and PC-6) were applied to demonstrate forming cancer nodules on recellularized lungs and histopathological assessment were made among these models. MUC-1 expression analysis, RNA-seq analysis and drug response test were performed to demonstrate the superiority of this cancer model.Results: The morphology and MUC-1 expression of the model were like those of lung cancer in vivo. RNA sequencing revealed an elevated expression of genes related to epithelial-mesenchymal transition, hypoxia, and TNF-α signaling via NF-κB; but suppression of cell cycle-related genes including E2F. Drug response assays showed that gefitinib suppressed PC-9 cell proliferation equally well in the 3D lung cancer model as in 2D culture dishes, albeit over a smaller volume of cells, suggesting that fluctuations in gefitinib resistance genes such as JUN may affect drug sensitivity.Conclusions: A novel ex vivo lung cancer model was closely reproduced the 3D structure and microenvironment of the actual lungs, highlighting its possible use as a platform for lung cancer research and pathophysiological studies

A multi-ethnic meta-analysis identifies novel genes, including ACSL5, associated with amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a devastating progressive motor neuron disease that affects people of all ethnicities. Approximately 90% of ALS cases are sporadic and thought to have multifactorial pathogenesis. To understand the genetics of sporadic ALS, we conducted a genome-wide association study using 1,173 sporadic ALS cases and 8,925 controls in a Japanese population. A combined meta-analysis of our Japanese cohort with individuals of European ancestry revealed a significant association at the ACSL5 locus (top SNP p = 2.97 × 10−8). We validated the association with ACSL5 in a replication study with a Chinese population and an independent Japanese population (1941 ALS cases, 3821 controls; top SNP p = 1.82 × 10−4). In the combined meta-analysis, the intronic ACSL5 SNP rs3736947 showed the strongest association (p = 7.81 × 10−11). Using a gene-based analysis of the full multi-ethnic dataset, we uncovered additional genes significantly associated with ALS: ERGIC1, RAPGEF5, FNBP1, and ATXN3. These results advance our understanding of the genetic basis of sporadic ALS

Review Article : Feudalism or Absolute Monarchism?

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68809/2/10.1177_009770049001600304.pd