Oscillator Strength of Metallic Carbon Nanotubes

Based on the tight binding method with hopping integral between the nearest-neighbor atoms, an oscillator strength \int_0^{\infty} \d \omega {\rm Re} \sigma (\omega) is discussed for armchair and metallic zigzag carbon nanotubes. The formulae of the oscillator strength are derived for both types of nanotubes and are compared with the result obtained by a linear chain model. In addition, the doping dependence is investigated in the absence of Coulomb interaction. It is shown that the oscillator strength of each carbon nanotube shows qualitatively the same doping dependence, but the fine structure is different due to it's own peculiar band structure. Some relations independent of the radius of the tube are derived, and a useful formula for determining the amount of doping is proposed.Comment: 4 pages, 4 figures, submitted to J. Phys. Soc. Jpn. at June 30, 200

Left ventricular non-compaction: clinical features and cardiovascular magnetic resonance imaging

Background: It is apparent that despite lack of family history, patients with the morphological characteristics of left ventricular non-compaction develop arrhythmias, thrombo-embolism and left ventricular dysfunction. METHODS: Forty two patients, aged 48.7 +/- 2.3 yrs (mean +/- SEM) underwent cardiovascular magnetic resonance (CMR) for the quantification of left ventricular volumes and extent of non-compacted (NC) myocardium. The latter was quantified using planimetry on the two-chamber long axis LV view (NC area). The patients included those referred specifically for CMR to investigate suspected cardiomyopathy, and as such is represents a selected group of patients. RESULTS: At presentation, 50% had dyspnoea, 19% chest pain, 14% palpitations and 5% stroke. Pulmonary embolism had occurred in 7% and brachial artery embolism in 2%. The ECG was abnormal in 81% and atrial fibrillation occurred in 29%. Transthoracic echocardiograms showed features of NC in only 10%. On CMR, patients who presented with dyspnoea had greater left ventricular volumes (both p < 0.0001) and a lower left ventricular ejection fraction (LVEF) (p < 0.0001) than age-matched, healthy controls. In patients without dyspnoea (n = 21), NC area correlated positively with end-diastolic volume (r = 0.52, p = 0.0184) and end-systolic volume (r = 0.56, p = 0.0095), and negatively with EF (r = -0.72, p = 0.0001). CONCLUSION: Left ventricular non-compaction is associated with dysrrhythmias, thromboembolic events, chest pain and LV dysfunction. The inverse correlation between NC area and EF suggests that NC contributes to left ventricular dysfunction

A Comprehensive Resource for Induced Pluripotent Stem Cells from Patients with Primary Tauopathies.

Primary tauopathies are characterized neuropathologically by inclusions containing abnormal forms of the microtubule-associated protein tau (MAPT) and clinically by diverse neuropsychiatric, cognitive, and motor impairments. Autosomal dominant mutations in the MAPT gene cause heterogeneous forms of frontotemporal lobar degeneration with tauopathy (FTLD-Tau). Common and rare variants in the MAPT gene increase the risk for sporadic FTLD-Tau, including progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). We generated a collection of fibroblasts from 140 MAPT mutation/risk variant carriers, PSP, CBD, and cognitively normal controls; 31 induced pluripotent stem cell (iPSC) lines from MAPT mutation carriers, non-carrier family members, and autopsy-confirmed PSP patients; 33 genome engineered iPSCs that were corrected or mutagenized; and forebrain neural progenitor cells (NPCs). Here, we present a resource of fibroblasts, iPSCs, and NPCs with comprehensive clinical histories that can be accessed by the scientific community for disease modeling and development of novel therapeutics for tauopathies

Effect of Stalling after Mismatches on the Error Catastrophe in Nonenzymatic Nucleic Acid Replication

The frequency of errors during genome replication limits the amount of functionally important information that can be passed on from generation to generation. During the origin of life, mutation rates are thought to have been quite high, raising a classic chicken-and-egg paradox: could nonenzymatic replication propagate sequences accurately enough to allow for the emergence of heritable function? Here we show that the theoretical limit on genomic information content may increase substantially as a consequence of dramatically slowed polymerization after mismatches. As a result of postmismatch stalling, accurate copies of a template tend to be completed more rapidly than mutant copies and the accurate copies can therefore begin a second round of replication more quickly. To quantify this effect, we characterized an experimental model of nonenzymatic, template-directed nucleic acid polymerization. We found that most mismatches decrease the rate of primer extension by more than 2 orders of magnitude relative to a matched (Watson-Crick) control. A chemical replication system with this property would be able to propagate sequences long enough to have function. Our study suggests that the emergence of functional sequences during the origin of life would be possible even in the face of the high intrinsic error rates of chemical replication

A combination of right ventricular hypertrabeculation/noncompaction and arrhythmogenic right ventricular cardiomyopathy: a syndrome?

A combination of ARVC and RV NVM/HVM, which is extremely rare, to our knowledge, is never reported. RV NVM/HVM could be the cause and consequence of ARVC, or RV NVM/HVM and ARVC could be a consequence of a certain undetermined cause. It must be kept in mind, however, that the interaction of NVM/HVM and ARVC could be in part of pathophysiology mechanism of the combination even if as a consequence of an underlying genetic factor

Magnetic Structure and Properties of the S = 5/2 Triangular Antiferromagnet α\alpha-NaFeO2_2

The magnetic properties of $\alpha$-NaFeO$_2$ are studied by neutron diffraction and magnetization measurements. An ordered phase with spins aligned along the b$_hex$ axis exists at low temperatures (T < 4 K). At intermediate temperatures (4 K < T < 11 K), the system passes through an incommensurate ordered phase before transforming into a short range ordered state at higher temperatures that persists up to at least 50 K. Although the short range ordering does not persist to room temperature according to neutron diffraction, the magnetic susceptibility does not follow Curie-Weiss behavior, even up to 320 K. This rich magnetic behavior can be understood qualitatively as a competition between different magnetic exchange interactions that are similar in magnitude. The delicate balance between these interactions makes $\alpha$-NaFeO$_2$ a candidate for more detailed theoretical work to understand magnetic behavior in frustrated magnetic systems.Comment: Submitted to Phys Rev B, 7 pages, 8 figure

Serum uric acid distribution according to SLC22A12 W258X genotype in a cross-sectional study of a general Japanese population

<p>Abstract</p> <p>Background</p> <p>Although <it>SLC22A12 258X </it>allele was found among those with hypouricemia, it was unknown that serum uric acid distribution among those with <it>SLC22A12 258X </it>allele. This study examined serum uric acid (SUA) distribution according to <it>SLC22A12 </it>W258X genotype in a general Japanese population.</p> <p>Methods</p> <p>Subjects were 5,023 health checkup examinees (3,413 males and 1,610 females) aged 35 to 69 years with creatinine < 2.0 mg/dL, who were participants of a cohort study belonging to the Japan Multi-Institutional Collaborative Cohort Study (J-MICC Study). <it>SLC22A12 </it>W258X was genotyped with a polymerase chain reaction with confronting two-pair primers.</p> <p>Results</p> <p>The genotype frequency was 4,793 for <it>WW</it>, 225 for <it>WX</it>, and 5 for <it>XX</it>, which was in Hardy-Weinberg equilibrium (p = 0.164) with <it>X </it>allele 0.023 (95% confidence interval [0.021-0.027]). Mean (range) SUA was 6.2 (2.1-11.4) mg/dL for <it>WW</it>, 3.9 (0.8-7.8) mg/dL for <it>WX</it>, and 0.8 (0.7-0.9) mg/dL for <it>XX </it>among males, and 4.5 (1.9-8.9) mg/dL, 3.3 (2.0-6.5) mg/dL, and 0.60 (0.5-0.7) mg/dL among females, respectively. Six individuals with SUA less than 1.0 mg/dL included two males with <it>XX </it>genotype, one male with <it>WX </it>genotype, and three females with <it>XX </it>genotype. Subjects with <it>WX </it>genotype were 14 (77.8%) of 18 males with a SUA of 1.0-2.9 mg/dL, and 28 (34.6%) of 81 females with the same range of SUA. The corresponding values were 131 (25.1%) of 522 males and 37 (3.5%) of 1,073 females for SUA 3.0-4.9 mg/dL, and 8 (0.4%) of 2,069 males and 5 (1.1%) of 429 females for SUA 5.0-6.9 mg/dL. The <it>X </it>allele effect for SUA less than 3 mg/dL was significantly (p < 0.001) higher in males (OR = 102.5, [33.9-309.8]) than in females (OR = 25.6 [14.4-45.3]).</p> <p>Conclusions</p> <p>Although <it>SLC22A12 </it>W258X was a determining genetic factor on SUA, SUA of those with <it>WX </it>genotype distributed widely from 0.8 mg/dL to 7.8 mg/dL. It indicated that other genetic traits and/or lifestyle affected SUA of those with <it>WX </it>genotype, as well as those with <it>WW </it>genotype.</p

Isolated ventricular noncompaction: a case report

Isolated ventricular noncompaction is an extremely rare cardiomyopathy, not fully clarified