Spin dephasing in n-typed GaAs quantum wells in the presence of high magnetic fields in Voigt configuration

We perform a many-body study of the spin dephasing due to the D'yakonov-Perel' effect in n-typed GaAs (100) quantum wells under high magnetic fields in the Voigt configuration by constructing and numerically solving the kinetic Bloch equations. We include all the spin conserving scattering such as electron-phonon, the electron-nonmagnetic impurity as well as the electron-electron Coulomb scattering in our theory and investigate how the spin dephasing time (SDT) is affected by the initial spin polarization, impurity, and magnetic field. The dephasing obtained from our theory contains not only that due to the effective spin-flipping scattering first proposed by D'yakonov and Perel' [Zh. Eksp. Teor. Fiz. {\bf 60}, 1954 (1971)[Sov. Phys.-JETP {\bf 38}, 1053 (1971)]], but also the recently proposed many-body dephasing due to the inhomogeneous broadening provided by the DP term [Wu, J. Supercond.:Incorp. Novel Mechanism {\bf 14}, 245 (2001); Wu and Ning, Eur. Phys. J. B {\bf 18}, 373 (2000)]. We are able to investigate the spin dephasing with extra large spin polarization (up to 100 %) which has not been discussed both theoretically and experimentally. A huge anomalous resonance of the SDT for large spin polarizations is predicted under the high magnetic field we used.Comment: 8 pages, Revtex, 7 figures in EPS forma

Double Charge Exchange And Configuration Mixing

The energy dependence of forward pion double charge exchange reactions on light nuclei is studied for both the Ground State transition and the Double-Isobaric-Analog-State transitions. A common characteristic of these double reactions is a resonance-like peak around 50 MeV pion lab energy. This peak arises naturally in a two-step process in the conventional pion-nucleon system with proper handling of nuclear structure and pion distortion. A comparison among the results of different nuclear structure models demonstrates the effects of configuration mixing. The angular distribution is used to fix the single particle wave function.Comment: Added 1 figure (now 8) corrected references and various other change

Treatment of Liver Metastases in Patients with Neuroendocrine Tumors of Gastroesophageal and Pancreatic Origin

Well-to-moderately differentiated neuroendocrine tumors of gastroesophageal and pancreatic origin (GEP-NETs) with liver metastasis are a heterogeneous group of malignancies for which a range of therapeutic options have been employed. Surgical resection of hepatic metastases or hepatic artery embolization may be beneficial in patients with hepatic-predominant metastatic disease. Patients with “carcinoid” syndrome and syndromes associated with functional pancreatic NET (PNET) can be effectively treated with somatostatin analogs. On the other hand, the efficacy of systemic chemotherapy for these patients is limited. A placebo-controlled, double-blind, prospective, and randomized study showed that octreotide LAR improves progression-free survival in patients with advanced midgut functional “carcinoids.” In patients with advanced pancreatic NET, randomized, placebo-controlled studies have recently demonstrated that treatment with the tyrosine kinase inhibitor sunitinib or with mTOR inhibitor everolimus is associated with improved progression-free survival. Based on these studies, octreotide LAR, sunitinib, or everolimus are now considered as first-line therapeutic options in patients with advanced NET. Future studies will likely further define the role of these agents in patients with carcinoid liver metastasis and pancreatic NET liver metastasis

Pressure-temperature phase diagrams of selenium and sulfur in terms of Patashinski model

The pressure - temperature phase diagrams of Se and S are calculated. Both melting and polymorphous phase transition are described in the frames of statistical Patashinski model. The results are in good agreement with experimental data of Brazhkin et. al.Comment: 3 eps figures, will appear in Physica A, mail to first author [email protected]

Structural and functional abnormities of amygdala and prefrontal cortex in major depressive disorder with suicide attempts

Finding neural features of suicide attempts (SA) in major depressive disorder (MDD) may be helpful in preventing suicidal behavior. The ventral and medial prefrontal cortex (PFC), as well as the amygdala form a circuit implicated in emotion regulation and the pathogenesis of MDD. The aim of this study was to identify whether patients with MDD who had a history of SA show structural and functional connectivity abnormalities in the amygdala and PFC relative to MDD patients without a history of SA. We measured gray matter volume in the amygdala and PFC and amygdala-PFC functional connectivity using structural and functional magnetic resonance imaging (MRI) in 158 participants [38 MDD patients with a history of SA, 60 MDD patients without a history of SA, and 60 healthy control (HC)]. MDD patients with a history of SA had decreased gray matter volume in the right and left amygdala (F = 30.270, P = 0.000), ventral/medial/dorsal PFC (F = 15.349, P = 0.000), and diminished functional connectivity between the bilateral amygdala and ventral and medial PFC regions (F = 22.467, P = 0.000), compared with individuals who had MDD without a history of SA, and the HC group. These findings provide evidence that the amygdala and PFC may be closely related to the pathogenesis of suicidal behavior in MDD and implicate the amygdala-ventral/medial PFC circuit as a potential target for suicide intervention

Structural and functional abnormities of amygdala and prefrontal cortex in major depressive disorder with suicide attempts

Finding neural features of suicide attempts (SA) in major depressive disorder (MDD) may be helpful in preventing suicidal behavior. The ventral and medial prefrontal cortex (PFC), as well as the amygdala form a circuit implicated in emotion regulation and the pathogenesis of MDD. The aim of this study was to identify whether patients with MDD who had a history of SA show structural and functional connectivity abnormalities in the amygdala and PFC relative to MDD patients without a history of SA. We measured gray matter volume in the amygdala and PFC and amygdala-PFC functional connectivity using structural and functional magnetic resonance imaging (MRI) in 158 participants [38 MDD patients with a history of SA, 60 MDD patients without a history of SA, and 60 healthy control (HC)]. MDD patients with a history of SA had decreased gray matter volume in the right and left amygdala (F = 30.270, P = 0.000), ventral/medial/dorsal PFC (F = 15.349, P = 0.000), and diminished functional connectivity between the bilateral amygdala and ventral and medial PFC regions (F = 22.467, P = 0.000), compared with individuals who had MDD without a history of SA, and the HC group. These findings provide evidence that the amygdala and PFC may be closely related to the pathogenesis of suicidal behavior in MDD and implicate the amygdala-ventral/medial PFC circuit as a potential target for suicide intervention

The Replicative Consequences of Papillomavirus E2 Protein Binding to the Origin Replication Factor ORC2.

The origin recognition complex (ORC) coordinates a series of events that lead to initiation of DNA strand duplication. As a nuclear double stranded DNA plasmid, the papillomavirus (PV) genome resembles a mini-chromosome in infected cells. To initiate its replication, the viral E2 protein binds to and recruits the E1 DNA helicase at the viral origin. PV genome replication program exhibits three stages: initial amplification from a single genome upon infection to a few copies per cell, a cell cycle linked maintenance phase, and a differentiation dependent late stage where the genome is amplified to thousands of copies. Involvement of ORC or other pre-replication complex (pre-RC) factors has not been described. We report that human PV (HPV) and bovine PV (BPV-1) E2 proteins bind to ORC2, however, ORC2 was not detected at the viral origin. Depletion of ORC2 enhanced PV replication in a transient replication model and in keratinocytes stably maintaining viral episomes, while there was no effect on copy number in a cell line with integrated HPV genomes. Consistent with this, occupancy of E1 and E2 at the viral origin increased following ORC2 silencing. These data imply that ORC2 is not necessary for activation of the PV origin by E1 and E2 but instead suppresses E2 replicative function. Furthermore, we observed that over-expression of HPV E2 decreased ORC2 occupation at two known mammalian origins of replication, suggesting that E2 restricts pre-ORC assembly that could otherwise compete for host replication complexes necessary for viral genome amplification. We infer that the ORC2 complex with E2 restricts viral replication in the maintenance phase of the viral replication program and that elevated levels of E2 that occur during the differentiation dependent amplification stage subvert ORC loading and hence DNA synthesis at cellular origins