Degeneration Locus Research Articles

Genome-Wide Meta-analysis Identifies Risk Loci and Improves Disease Prediction of Age-Related Macular Degeneration

To identify age-related macular degeneration (AMD) risk loci and to establish a polygenic prediction model. Genome-wide association study (GWAS) and polygenic risk score (PRS) construction. We included 64 885 European patients with AMD and 568 740 control participants (with overlapped samples) in the UK Biobank, Genetic Epidemiology Research on Aging (GERA), International AMD Consortium, FinnGen, and published early AMD GWASs in meta-analyses, as well as 733 European patients with AMD and 20 487 control participants from the Canadian Longitudinal Study on Aging (CLSA) and non-Europeans from the UK Biobank and GERA for polygenic risk score validation. A multitrait meta-analysis of GWASs comprised 64 885 patients with AMD and 568 740 control participants; the multitrait approach accounted for sample overlap. We constructed a PRS for AMD based on both previously reported as well as unreported AMD loci. We applied the PRS to nonoverlapping data from the CLSA. We identified several single nucleotide polymorphisms associated with AMD and established a PRS for AMD risk prediction. We identified 63 AMD risk loci alongside the well-established AMD loci CFH and ARMS2, including 9 loci that were not reported in previous GWASs, some of which previously were linked to other eye diseases such as glaucoma (e.g., HIC1). We applied our PRS to nonoverlapping data from the CLSA. A new PRS was constructed using the PRS method, PRS-CS, and significantly improved the prediction accuracy of AMD risk compared with PRSs from previously published datasets. We further showed that even people who carry all the well-known AMD risk alleles at CFH and ARMS2 vary considerably in their AMD risk (ranging from close to 0 in individuals with low PRS to > 50% in individuals with high PRS). Although our PRS was derived in individuals of European ancestry, the PRS shows potential for predicting risk in people of East Asian, South Asian, and Latino ancestry. Our findings improve the knowledge of the genetic architecture of AMD and help achieve better accuracy in AMD prediction. Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Degeneration locus of [formula omitted]-local systems: Conjectures

We introduce a conjecture on the arithmetic sparcity of the degeneration locus of a p-adic local system on a smooth variety over a number field and, modulo the Bombieri–Lang conjecture, show that it follows from a conjecture on the geometry of the level varieties attached to the local system. We present a few applications of our conjecture to classical problems in arithmetic geometry. Eventually, we give some evidences and discuss a few perspectives to attack it, in particular for p-adic local systems arising from geometry.

Elliptical and purely NS superstrata

We analyze the BPS equations in the “superstratum sector” of three-dimensional gauged supergravity. We obtain multi-parameter supersymmetric solutions that include elliptical deformations of the supertubes that underlie standard superstrata. We uplift the three-dimensional solutions to obtain the corresponding six-dimensional geometries. This yields new families of elliptically-deformed, ambi-bolar hyper-Kähler geometries in four dimensions with a non-tri-holomorphic U(1) isometry. We also find a new family of scaling superstrata whose S-dual lives entirely within the NS-sector of supergravity, and will thus be more amenable to exact analysis using string probes. In all these new superstrata, including the scaling ones, if the momentum charge is non-zero we find that the ellipse stays away from the degeneration locus in which the ellipse becomes flat.

Noradrenergic deficits contribute to apathy in Parkinson's disease through the precision of expected outcomes.

Apathy is a debilitating feature of many neuropsychiatric diseases, that is typically described as a reduction of goal-directed behaviour. Despite its prevalence and prognostic importance, the mechanisms underlying apathy remain controversial. Degeneration of the locus coeruleus-noradrenaline system is known to contribute to motivational deficits, including apathy. In healthy people, noradrenaline has been implicated in signalling the uncertainty of expectations about the environment. We proposed that noradrenergic deficits contribute to apathy by modulating the relative weighting of prior beliefs about action outcomes. We tested this hypothesis in the clinical context of Parkinson's disease, given its associations with apathy and noradrenergic dysfunction. Participants with mild-to-moderate Parkinson's disease (N = 17) completed a randomised double-blind, placebo-controlled, crossover study with 40 mg of the noradrenaline reuptake inhibitor atomoxetine. Prior weighting was inferred from psychophysical analysis of performance in an effort-based visuomotor task, and was confirmed as negatively correlated with apathy. Locus coeruleus integrity was assessed in vivo using magnetisation transfer imaging at ultra-high field 7T. The effect of atomoxetine depended on locus coeruleus integrity: participants with a more degenerate locus coeruleus showed a greater increase in prior weighting on atomoxetine versus placebo. The results indicate a contribution of the noradrenergic system to apathy and potential benefit from noradrenergic treatment of people with Parkinson's disease, subject to stratification according to locus coeruleus integrity. More broadly, these results reconcile emerging predictive processing accounts of the role of noradrenaline in goal-directed behaviour with the clinical symptom of apathy and its potential pharmacological treatment.

Moduli spaces for Lamé functions and Abelian differentials of the second kind

The topology of the moduli space for Lamé functions of degree [Formula: see text] is determined: this is a Riemann surface which consists of two connected components when [Formula: see text]; we find the Euler characteristics and genera of these components. As a corollary we prove a conjecture of Maier on degrees of Cohn’s polynomials. These results are obtained with the help of a geometric description of these Riemann surfaces, as quotients of the moduli spaces for certain singular flat triangles. An application is given to the study of metrics of constant positive curvature with one conic singularity with the angle [Formula: see text] on a torus. We show that the degeneration locus of such metrics is a union of smooth analytic curves and we enumerate these curves.

Space of isospectral periodic tridiagonal matrices

A periodic tridiagonal matrix is a tridiagonal matrix with additional two entries at the corners. We study the space $X_{n,\lambda}$ of Hermitian periodic tridiagonal $n\times n$-matrices with a fixed simple spectrum $\lambda$. Using the discretized Shr\"{o}dinger operator we describe all spectra $\lambda$ for which $X_{n,\lambda}$ is a topological manifold. The space $X_{n,\lambda}$ carries a natural effective action of a compact $(n-1)$-torus. We describe the topology of its orbit space and, in particular, show that whenever the isospectral space is a manifold, its orbit space is homeomorphic to $S^4\times T^{n-3}$. There is a classical dynamical system: the flow of the periodic Toda lattice, acting on $X_{n,\lambda}$. Except for the degenerate locus $X_{n,\lambda}^0$, the Toda lattice exhibits Liouville--Arnold behavior, so that the space $X_{n,\lambda}\setminus X_{n,\lambda}^0$ is fibered into tori. The degenerate locus of the Toda system is described in terms of combinatorial geometry: its structure is encoded in the special cell subdivision of a torus, which is obtained from the regular tiling of the euclidean space by permutohedra. We apply methods of commutative algebra and toric topology to describe the cohomology and equivariant cohomology modules of $X_{n,\lambda}$.

Riemannian metrics on the moduli space of GHMC anti-de Sitter structures

We first extend the construction of the pressure metric to the deformation space of globally hyperbolic maximal Cauchy-compact anti-de Sitter structures. We show that, in contrast with the case of the Hitchin components, the pressure metric is degenerate and we characterize its degenerate locus. We then introduce a nowhere degenerate Riemannian metric adapting the work of Qiongling Li on the $$\mathrm {SL}(3,\mathbb {R})$$ -Hitchin component to this moduli space. We prove that the Fuchsian locus is a totally geodesic copy of Teichmuller space endowed with a multiple of the Weil–Petersson metric.

Local models and global constraints for degeneracies and band crossings

We study topological properties of families of Hamiltonians which may contain degenerate energy levels aka. band crossings. The primary tool are Chern classes, Berry phases and slicing by surfaces. To analyse the degenerate locus of possibly higher order band crossings aka. degeneracies, we add the study of local models. These give more detailed information including that of the local Chern classes and Berry phases. We then give global constraints for the topological invariants in a systematic fashion. The global constraints are more strict when incorporating symmetries such as time reversal symmetries. We also discuss how the results can be used in the study of deformations. This theory of local models and global constraints is then applied to examples which include the Gyroid geometry, which exhibits two Weyl points and two triple crossings and the honeycomb geometry with its two Dirac points.

Rational cuspidal curves on del-Pezzo surfaces

We obtain an explicit formula for the number of rational cuspidal curves of a given degree on a del-Pezzo surface that pass through an appropriate number of generic points of the surface. This enumerative problem is expressed as an Euler class computation on the moduli space of curves. A topological method is employed in computing the contribution of the degenerate locus to this Euler class.

The Congo as topos of dystopic transgression in fin-de-siècle literature

In this essay, I compare the representation of the Congo as a topos of dystopic transgression in Conrad’s Heart of Darkness (1902), and in a lesser-known novel entitled Tropenwee (Tropical agony) by the Dutch author Henri van Booven, published in 1904. The idea of the Congo as a locus of degeneration will be read, not so much as a Conradian theme, but rather, as an idea that had gained wide currency throughout Europe during the fin-de-siècle period. Particular attention will be paid to some of the narrative techniques that shape this idea and the ideological assumptions it conveys. Moreover, I hope to show that degeneration as reflected by the writings under investigation is at once a colonial and anti-colonial theme, and therefore its significance requires moving beyond singular and clear-cut ideological labels.

On Propagation of Sphericity of Real Analytic Hypersurfaces across Levi Degenerate Loci

A connected real analytic hypersurface M⊂Cn+1 whose Levi form is nondegenerate in at least one point—hence at every point of some Zariski-dense open subset—is locally biholomorphic to the model Heisenberg quadric pseudosphere of signature (k,n-k) in one point if and only if, at every other Levi nondegenerate point, it is also locally biholomorphic to some Heisenberg pseudosphere, possibly having a different signature (l,n-l). Up to signature, pseudosphericity then jumps across the Levi degenerate locus and in particular across the nonminimal locus, if there exists any.

Genetic Isolation of Hypothalamic Neurons that Regulate Context-Specific Male Social Behavior.

Nearly all animals engage in a complex assortment of social behaviors that are essential for the survival of the species. In mammals, these behaviors are regulated by sub-nuclei within the hypothalamus, but the specific cell types within these nuclei responsible for coordinating behavior in distinct contexts are only beginning to be resolved. Here, we identify a population of neurons in the ventral premammillary nucleus of the hypothalamus (PMV) that are strongly activated in male intruder mice in response to a larger resident male but that are not responsive to females. Using a combination of molecular and genetic approaches, we demonstrate that these PMV neurons regulate intruder-specific male social behavior and social novelty recognition in a manner dependent on synaptic release of the excitatory neurotransmitter glutamate. These data provide direct evidence for a unique population of neurons that regulate social behaviors in specific contexts.

On nodal Enriques surfaces and quartic double solids

We consider the class of singular double coverings $X \to \PP^3$ ramified in the degeneration locus $D$ of a family of 2-dimensional quadrics. These are precisely the quartic double solids constructed by Artin and Mumford as examples of unirational but nonrational conic bundles. With such quartic surface $D$ one can associate an Enriques surface $S$ which is the factor of the blowup of $D$ by a natural involution acting without fixed points (such Enriques surfaces are known as nodal Enriques surfaces or Reye congruences). We show that the nontrivial part of the derived category of coherent sheaves on this Enriques surface $S$ is equivalent to the nontrivial part of the derived category of a minimal resolution of singularities of $X$.

Two-photon microscopy reveals early rod photoreceptor cell damage in light-exposed mutant mice

Atrophic age-related and juvenile macular degeneration are especially devastating due to lack of an effective cure. Two retinal cell types, photoreceptor cells and the adjacent retinal pigmented epithelium (RPE), reportedly display the earliest pathological changes. Abca4(-/-)Rdh8(-/-) mice, which mimic many features of human retinal degeneration, allowed us to determine the sequence of light-induced events leading to retinal degeneration. Using two-photon microscopy with 3D reconstruction methodology, we observed an initial strong retinoid-derived fluorescence and expansion of Abca4(-/-)Rdh8(-/-) mouse rod cell outer segments accompanied by macrophage infiltration after brief exposure of the retina to bright light. Additionally, light-dependent fluorescent compounds produced in rod outer segments were not transferred to the RPE of mice genetically defective in RPE phagocytosis. Collectively, these findings suggest that for light-induced retinopathies in mice, rod photoreceptors are the primary site of toxic retinoid accumulation and degeneration, followed by secondary changes in the RPE.

Scheme of lines on a family of 2-dimensional quadrics: geometry and derived category

Given a generic family $$Q$$ of 2-dimensional quadrics over a smooth 3-dimensional base $$Y$$ we consider the relative Fano scheme $$M$$ of lines of it. The scheme $$M$$ has a structure of a generically conic bundle $$M \rightarrow X$$ over a double covering $$X \rightarrow Y$$ ramified in the degeneration locus of $$Q \rightarrow Y$$ . The double covering $$X \rightarrow Y$$ is singular in a finite number of points (corresponding to the points $$y \in Y$$ such that the quadric $$Q_y$$ degenerates to a union of two planes), the fibers of $$M$$ over such points are unions of two planes intersecting in a point. The main result of the paper is a construction of a semiorthogonal decomposition for the derived category of coherent sheaves on $$M$$ . This decomposition has three components, the first is the derived category of a small resolution $$X^+$$ of singularities of the double covering $$X \rightarrow Y$$ , the second is a twisted resolution of singularities of $$X$$ (given by the sheaf of even parts of Clifford algebras on $$Y$$ ), and the third is generated by a completely orthogonal exceptional collection.

On the Relation between a Taut Manifold $X$ Modulo $\Delta_X$ and Hyperbolic Modulo $\Delta_X$ Which Is Contained in a Hypersurface of $X$

Let $X$ be a n-dimensional Stein (connected complex) manifold or a compact one whose universal covering is a domain in $\mathbf{C}^n$ or a Stein manifold. Let $\Delta_X$ be the degeneration locus of Kobayashi pseudodistance of $X$ which is contained in a hypersurface $S$ of $X$. Then $X$ is hyperbolic modulo $S$ and taut modulo $S$.

New insights in hepatocellular carcinoma: from bench to bedside.

Hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocyte. The liver is one of the main targets for different metastatic foci, but it represents an important and frequent locus of degeneration in the course of chronic disease. In fact, Hepatocellular carcinoma (HCC) represents the outcome of the natural history of chronic liver diseases, from the condition of fibrosis, to cirrhosis and finally to cancer. HCC is the sixth most common cancer in the world, some 630,000 new cases being diagnosed each year. Furthermore, about the 80% of people with HCC, have seen their clinical history developing from fibrosis, to cirrhosis and finally to cancer. The three main causes of HCC development are represented by HBV, HCV infection and alcoholism. Moreover, metabolic disease [starting from Non Alcoholic Fatty Liver Disease (NAFLD), Non Alcoholic Steatohepatitis (NASH)] and, with reduced frequency, some autoimmune disease may lead to HCC development. An additional rare cause of carcinogenetic degeneration of the liver, especially developed in African and Asian Countries, is represented by aflatoxin B1. The mechanisms by which these etiologic factors may induce HCC development involve a wide range of pathway and molecules, currently under investigation. In summary, the hepatocarcionogenesis results from a multifactorial process leading to the common condition of genetic changes in mature hepatocytes mainly characterized by uncontrolled proliferation and cell death. Advances in understanding the mechanism of action are fundamental for the development of new potential therapies and results primarily from the association of the research activities coming from basic and clinical science. This review article analyzes the current models used in basic research to investigate HCC activity, and the advances obtained from a basic and clinical point of view.

Obsessive-Compulsive Disorder After Right Temporal-Lobe Hemorrhage

Back to table of contents Previous article Next article LettersFull AccessObsessive-Compulsive Disorder After Right Temporal-Lobe HemorrhageAbhishek Rai, MBBS, Amit Chopra, M.D., and Piyush Das, M.D.Abhishek RaiSearch for more papers by this author, MBBS, Amit ChopraSearch for more papers by this author, M.D., and Piyush DasSearch for more papers by this author, M.D.Published Online:1 Oct 2011https://doi.org/10.1176/jnp.23.4.jnpe13AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Obsessive-compulsive disorder (OCD) is a psychiatric illness characterized by persistent, intrusive, and senseless thoughts (obsessions) and urges to perform repetitive behaviors (compulsions) that interfere with functioning and/or cause distress. Although OCD secondary to various neurological lesions has been described, cerebral hemorrhage has rarely been associated with OCD. We present the first reported patient; this was a 40-year-old woman who developed OCD that responded successfully to high-dose selective serotonin reuptake inhibitor (SSRI) treatment after right temporal-lobe hemorrhage.Case Report“Mrs. X” was a 40-year-old woman with a medical history significant for frontoparietal hematoma resection during infancy, centroparietal epilepsy (stable on Depakote and levetiracetam), and depression, who presented to psychiatric clinic for gradually worsening obsessions and compulsion to shop (of 7 months' duration), with onset after right temporal-lobe hemorrhage (confirmed by brain imaging). Her depression, previously well controlled on citalopram 20 mg/day, had worsened to a moderately severe depression (Patient Health Questionnaire-9/PHQ-9 Score: 15), and her mild obsessive traits had worsened to distressing obsessions and compulsions to shop, meeting DSM-IV criteria for diagnosis of OCD. The compulsive shopping significantly reduced her anxiety. Other potential causes of her presentation, including worsening of seizure disorder, psychotic disorder, impulse-control disorder, mania, and substance abuse were ruled out. Although a citalopram dose increase to 40 mg daily led to remission of her depression (PHQ-9 score: 3), she continued to endorse compulsions to shop, to the extent that she ended up calling a realtor to buy a house. A gradual increase in citalopram dosage to 80 mg/day led to a 90% improvement in her OCD symptoms, and a further increase, to 100 mg/day, resulted in complete remission at 1-year follow-up. She had regular follow-up with her neurologist in the interim, with no suggestion of worsening of her seizure disorder by high-dose citalopram.DiscussionOCD has been associated with various neurological lesions, including traumatic brain injury, tumors, and infarcts, localized mainly to the frontal cortex and basal ganglia.1 The association of OCD with temporal-lobe epilepsy (TLE) seems strong, as 10%–20% of TLE patients suffer from OCD.2 Our case suggests temporal-lobe hemorrhage as a novel putative cause of OCD. Although there is no known overt locus of neuronal degeneration in OCD, functional-imaging studies suggest an abnormal metabolic activity in orbitofrontal cortex (OFC), anterior cingulate/caudal medial prefrontal cortex, and caudate nucleus.3 The OFC–subcortical circuit, referred to as the “OCD circuit,” projects from OFC to the ventral portion of caudate nucleus. OFC receives both afferent and efferent projections from the temporal lobe,4 which may underlie temporal lobe involvement in causation of OCD. Our patient's response to high-dose SSRI is plausible, considering the fact that serotonin acts on the “OCD circuit” by modulating 5HT3 receptors predominantly present in ventral striatum.5 Besides highlighting a novel mechanism of causation of OCD, we suggest that OCD associated with temporal lobe hemorrhage may be responsive to high-dose SSRI treatment.Dept. of Psychiatry and Psychology Mayo Clinic Rochester, MNCorrespondence: das.[email protected]edu; gen.[email protected]com1. Etcharry-Bouyx F , Dubas F : Obsessive-compulsive disorders associated with focal brain lesions, in: Behaviours and Mood Disorders in Focal Brain Lesions. Edited by Bogousslavsky JCummings J. Cambridge, UK, Cambridge University Press, 2000, pp 304–326Crossref, Google Scholar2. Kaplan PW : Epilepsy and obsessive-compulsive disorder. Dial Clin Neurosci 2010; 12:241–248Medline, Google Scholar3. Graybiel A , Rauch S : Toward a neurobiology of obsessive-compulsive disorder. Neuron 2000; 28:343–347Crossref, Medline, Google Scholar4. Cummings JL : Anatomic and behavioral aspects of frontal-subcortical circuits. Ann N Y Acad Sci 1995; 769:1–13Crossref, Medline, Google Scholar5. Marsden CA : The neuropharmacology of serotonin in central nervous system, in Selective Serotonin Reuptake Inhibitors. Edited by Feighner JPBoyer WF. New York, Wiley, 1991, pp 11–35Google Scholar FiguresReferencesCited byDetailsCited by“Need to Know” or the Strong Urge to Find Names of Unique Entities in Acquired Obsessive-Compulsive DisorderCognitive and Behavioral Neurology, Vol. 32, No. 2Journal of Stroke and Cerebrovascular Diseases, Vol. 28, No. 4Psychiatry and Clinical Psychopharmacology, Vol. 28, No. 3Journal of Neurotrauma, Vol. 32, No. 7Multivariate pattern analysis of DTI reveals differential white matter in individuals with obsessive‐compulsive disorder18 September 2013 | Human Brain Mapping, Vol. 35, No. 6Neuroscience & Biobehavioral Reviews, Vol. 37, No. 3 Volume 23Issue 4 Fall 2011Pages E13-E13 Metrics PDF download History Published online 1 October 2011 Published in print 1 October 2011

Obsessive-Compulsive Disorder After Right Temporal-Lobe Hemorrhage

Back to table of contents Previous article Next article LettersFull AccessObsessive-Compulsive Disorder After Right Temporal-Lobe HemorrhageAbhishek Rai, MBBS, Amit Chopra, M.D., and Piyush Das, M.D.Abhishek RaiSearch for more papers by this author, MBBS, Amit ChopraSearch for more papers by this author, M.D., and Piyush DasSearch for more papers by this author, M.D.Published Online:1 Oct 2011https://doi.org/10.1176/jnp.23.4.jnpe13AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Obsessive-compulsive disorder (OCD) is a psychiatric illness characterized by persistent, intrusive, and senseless thoughts (obsessions) and urges to perform repetitive behaviors (compulsions) that interfere with functioning and/or cause distress. Although OCD secondary to various neurological lesions has been described, cerebral hemorrhage has rarely been associated with OCD. We present the first reported patient; this was a 40-year-old woman who developed OCD that responded successfully to high-dose selective serotonin reuptake inhibitor (SSRI) treatment after right temporal-lobe hemorrhage.Case Report“Mrs. X” was a 40-year-old woman with a medical history significant for frontoparietal hematoma resection during infancy, centroparietal epilepsy (stable on Depakote and levetiracetam), and depression, who presented to psychiatric clinic for gradually worsening obsessions and compulsion to shop (of 7 months' duration), with onset after right temporal-lobe hemorrhage (confirmed by brain imaging). Her depression, previously well controlled on citalopram 20 mg/day, had worsened to a moderately severe depression (Patient Health Questionnaire-9/PHQ-9 Score: 15), and her mild obsessive traits had worsened to distressing obsessions and compulsions to shop, meeting DSM-IV criteria for diagnosis of OCD. The compulsive shopping significantly reduced her anxiety. Other potential causes of her presentation, including worsening of seizure disorder, psychotic disorder, impulse-control disorder, mania, and substance abuse were ruled out. Although a citalopram dose increase to 40 mg daily led to remission of her depression (PHQ-9 score: 3), she continued to endorse compulsions to shop, to the extent that she ended up calling a realtor to buy a house. A gradual increase in citalopram dosage to 80 mg/day led to a 90% improvement in her OCD symptoms, and a further increase, to 100 mg/day, resulted in complete remission at 1-year follow-up. She had regular follow-up with her neurologist in the interim, with no suggestion of worsening of her seizure disorder by high-dose citalopram.DiscussionOCD has been associated with various neurological lesions, including traumatic brain injury, tumors, and infarcts, localized mainly to the frontal cortex and basal ganglia.1 The association of OCD with temporal-lobe epilepsy (TLE) seems strong, as 10%–20% of TLE patients suffer from OCD.2 Our case suggests temporal-lobe hemorrhage as a novel putative cause of OCD. Although there is no known overt locus of neuronal degeneration in OCD, functional-imaging studies suggest an abnormal metabolic activity in orbitofrontal cortex (OFC), anterior cingulate/caudal medial prefrontal cortex, and caudate nucleus.3 The OFC–subcortical circuit, referred to as the “OCD circuit,” projects from OFC to the ventral portion of caudate nucleus. OFC receives both afferent and efferent projections from the temporal lobe,4 which may underlie temporal lobe involvement in causation of OCD. Our patient's response to high-dose SSRI is plausible, considering the fact that serotonin acts on the “OCD circuit” by modulating 5HT3 receptors predominantly present in ventral striatum.5 Besides highlighting a novel mechanism of causation of OCD, we suggest that OCD associated with temporal lobe hemorrhage may be responsive to high-dose SSRI treatment.Dept. of Psychiatry and Psychology Mayo Clinic Rochester, MNCorrespondence: das.[email protected]edu; gen.[email protected]com1. Etcharry-Bouyx F , Dubas F : Obsessive-compulsive disorders associated with focal brain lesions, in: Behaviours and Mood Disorders in Focal Brain Lesions. Edited by Bogousslavsky JCummings J. Cambridge, UK, Cambridge University Press, 2000, pp 304–326Crossref, Google Scholar2. Kaplan PW : Epilepsy and obsessive-compulsive disorder. Dial Clin Neurosci 2010; 12:241–248Medline, Google Scholar3. Graybiel A , Rauch S : Toward a neurobiology of obsessive-compulsive disorder. Neuron 2000; 28:343–347Crossref, Medline, Google Scholar4. Cummings JL : Anatomic and behavioral aspects of frontal-subcortical circuits. Ann N Y Acad Sci 1995; 769:1–13Crossref, Medline, Google Scholar5. Marsden CA : The neuropharmacology of serotonin in central nervous system, in Selective Serotonin Reuptake Inhibitors. Edited by Feighner JPBoyer WF. New York, Wiley, 1991, pp 11–35Google Scholar FiguresReferencesCited byDetailsCited By“Need to Know” or the Strong Urge to Find Names of Unique Entities in Acquired Obsessive-Compulsive DisorderCognitive and Behavioral Neurology, Vol. 32, No. 2Journal of Stroke and Cerebrovascular Diseases, Vol. 28, No. 4Psychiatry and Clinical Psychopharmacology, Vol. 28, No. 3Journal of Neurotrauma, Vol. 32, No. 7Multivariate pattern analysis of DTI reveals differential white matter in individuals with obsessive‐compulsive disorder18 September 2013 | Human Brain Mapping, Vol. 35, No. 6Neuroscience & Biobehavioral Reviews, Vol. 37, No. 3 Volume 23Issue 4 Fall 2011Pages E13-E13 Metrics PDF download History Published online 1 October 2011 Published in print 1 October 2011

Finiteness of Subfamilies of Calabi-Yau N-Folds over Curves with Maximal Length of Yukawa-Coupling

We give a simplified and more algebraic proof of the finiteness of the families of Calabi-Yau n-folds with non-vanishing of Yukawa-coupling over a fixed base curve and with fixed degeneration locus. We also give a generalization of this result. Our method is variation of Hodge structure and poly-stability of Higgs bundles.