Formation of magnetic impurities and pair-breaking effect in a superfluid Fermi gas

We theoretically investigate a possible idea to introduce magnetic impurities to a superfluid Fermi gas. In the presence of population imbalance ($N_\uparrow>N_\downarrow$, where $N_\sigma$ is the number of Fermi atoms with pseudospin $\sigma=\uparrow,\downarrow$), we show that nonmagnetic potential scatterers embedded in the system are magnetized in the sense that some of excess $\uparrow$-spin atoms are localized around them. They destroy the superfluid order parameter around them, as in the case of magnetic impurity effect discussed in the superconductivity literature. This pair-breaking effect naturally leads to localized excited states below the superfluid excitation gap. To confirm our idea in a simply manner, we treat an attractive Fermi Hubbard model within the mean-field theory at T=0. We self-consistently determine superfluid properties around a nonmagnetic impurity, such as the superfluid order parameter, local population imbalance, as well as single-particle density of states, in the presence of population imbalance. Since the competition between superconductivity and magnetism is one of the most fundamental problems in condensed matter physics, our results would be useful for the study of this important issue in cold Fermi gases.Comment: 27 pages, 14 figure

Superfluid density and condensate fraction in the BCS-BEC crossover regime at finite temperatures

The superfluid density is a fundamental quantity describing the response to a rotation as well as in two-fluid collisional hydrodynamics. We present extensive calculations of the superfluid density \rho_s in the BCS-BEC crossover regime of a uniform superfluid Fermi gas at finite temperatures. We include strong-coupling or fluctuation effects on these quantities within a Gaussian approximation. We also incorporate the same fluctuation effects into the BCS single-particle excitations described by the superfluid order parameter \Delta and Fermi chemical potential \mu, using the Nozi\`eres and Schmitt-Rink (NSR) approximation. This treatment is shown to be necessary for consistent treatment of \rho_s over the entire BCS-BEC crossover. We also calculate the condensate fraction N_c as a function of the temperature, a quantity which is quite different from the superfluid density \rho_s. We show that the mean-field expression for the condensate fraction N_c is a good approximation even in the strong-coupling BEC regime. Our numerical results show how \rho_s and N_c depend on temperature, from the weak-coupling BCS region to the BEC region of tightly-bound Cooper pair molecules. In a companion paper by the authors (cond-mat/0609187), we derive an equivalent expression for \rho_s from the thermodynamic potential, which exhibits the role of the pairing fluctuations in a more explicit manner.Comment: 32 pages, 12 figure

A case of unilateral adrenal medullary hyperplasia.

We report a case of unilateral hyperplasia of the adrenal medulla. The patient showed clinical features suggestive of pheochromocytoma. Removal of the hyperplastic adrenal gland resulted in complete disappearance of all prior symptoms, decrease of the plasma and urinary catecolamine levels and no high uptake in [133I] metaiodobenzylguanidine scintigraphy. A histological study revealed diffuse hyperplasia of the adrenal medulla. Up to now, there are relatively few reports of adrenal medullary hyperplasia in English literatures.</p

Angiotensin II Type 1 Receptor Blockers Reduce Urinary Angiotensinogen Excretion and the Levels of Urinary Markers of Oxidative Stress and Inflammation in Patients with Type 2 Diabetic Nephropathy

Objective To demonstrate that the administration of an angiotensin (Ang) II type 1 receptor (AT1R) blocker (ARB) inhibits the vicious cycle of high glucose (HG)-reactive oxygen species (ROS)-angiotensinogen (AGT)-Ang II-AT1R-ROS by suppressing ROSs and inflammation, thus ameliorating diabetic nephropathy (DN). Research Design and Methods Thirteen hypertensive DN patients were administered ARBs, and the following parameters were evaluated before and 16 weeks after the treatment: urinary AGT (UAGT), albumin (albumin-creatinine ratio: ACR), 8-hydroxydeoxyguanosine (8-OHdG), 8-epi-prostaglandin F2α (8-epi-PGF2α), monocyte chemoattractant protein (MCP)-1, interleukin (IL)-6, and IL-10. Results ARB treatment reduced the blood pressure and urinary levels of AGT, ACR, 8-OHdG, 8-epi-PGF2α, MCP-1, and IL-6 but increased the urinary levels of IL-10. The reduction rate of UAGT correlated with the reduction rate of blood pressure; the reduction rates of the urinary ACR, 8-OHdG, 8-epi-PGF2α, MCP-1, and IL-6 levels; and the increase rate of the urinary IL-10 levels. Moreover, subjects who had high UAGT values at baseline exhibited higher reduction rates of urinary albumin excretion. Conclusions ARB-induced blockade of the abovementioned vicious cycle contributes to the renoprotective effects of ARBs in DN. The urinary levels of AGT could represent a predictive factor for reduced ACR in patients receiving ARB treatment

Mechanisms of Copy Number Variation and Hybrid Gene Formation in the KIR Immune Gene Complex

The fine-scale structure of the majority of copy number variation (CNV) regions remains unknown. The killer immunoglobulin receptor (KIR) gene complex exhibits significant CNV. The evolutionary plasticity of the KIRs and their broad biomedical relevance makes it important to understand how these immune receptors evolve. In this paper, we describe haplotype re-arrangement creating novel loci at the KIR complex. We completely sequenced, after fosmid cloning, two rare contracted haplotypes. Evidence of frequent hybrid KIR genes in samples from many populations suggested that re-arrangements may be frequent and selectively advantageous. We propose mechanisms for formation of novel hybrid KIR genes, facilitated by protrusive non-B DNA structures at transposon recombination sites. The heightened propensity to generate novel hybrid KIR receptors may provide a proactive evolutionary measure, to militate against pathogen evasion or subversion. We propose that CNV in KIR is an evolutionary strategy, which KIR typing for disease association must take into account

〔報 文〕 看護職の睡眠に関する疫学研究

Sleep disorders cause work efficiency to deteriorate when workers are sleepy or fall asleep on the job, and shift workers tend to have sleep disorders. The objective of the present study is to clarify the actual status of sleep and lack of rest due to insufficient sleep in nursing professionals who are often engaged in shift work. As of April 2018, a total of 600 subjects including 100 public health nurses, 100 midwives, 300 nurses, and 100 associate nurses, have been randomly selected from members of the Tokyo Nursing Association to be included in a survey of sleep, working environment, lifestyle, stress management, and personal characteristics. The survey was conducted using a self-administered questionnaire sent to subjects by postal mail. Among 346 valid responses, responses from 11 male workers were excluded since the total number was small and responses from 335 female workers were analyzed. The mean age ± standard deviation of the female respondents was 42.0±11.8.Insomnia was defined as one or more complaints of difficulty initiating sleep, difficulty maintaining sleep, or waking up too early. Complaints of insomnia was reported in 23.8％ of respondents and lack of rest due to insufficient sleep was reported in 41.8％ of respondents. The multivariate analysis demonstrated a significant relationship among difficulty initiating sleep and presence or absence of night shifts and stress, and difficulty maintaining sleep and insomnia and stress. It is suggested that getting sufficient sleep, and reducing stress were important

Post-translational Modification of the NKG2D Ligand RAET1G Leads to Cell Surface Expression of a Glycosylphosphatidylinositol-linked Isoform

NKG2D is an important activating receptor on lymphocytes. In human, it interacts with two groups of ligands: the major histocompatibility complex class I chain-related A/B (MICA/B) family and the UL-16 binding protein (ULBP) family, also known as retinoic acid early transcript (RAET1). MIC proteins are membrane-anchored, but all of the ULBP/RAET1 proteins, except for RAET1E and RAET1G, are glycosylphosphatidylinositol (GPI)-anchored. To address the reason for these differences we studied the association of RAET1G with the membrane. Using epitope-tagged RAET1G protein in conjunction with antibodies to different parts of the molecule and in pulse-chase experiments, we showed that the C terminus of the protein was cleaved soon after protein synthesis. Endoglycosidase H and peptide N-glycosidase treatment and cell surface immunoprecipitation indicated that most of the protein stayed in the endoplasmic reticulum, but some of the cleaved form was modified in the Golgi and transported to the cell surface. We examined the possibility of GPI anchoring of the protein in three ways: (i) Phosphatidylinositol (PI)-specific phospholipase C released the PI-linked form of the protein. (ii) The surface expression pattern of RAET1G decreased in cells defective in GPI anchoring through mutant GPI-amidase. (iii) Site-directed mutagenesis, to disrupt residues predicted to facilitate GPI-anchoring, resulted in diminished surface expression of RAET1G. Thus, a form of RAET1G is GPI-anchored, in line with most other ULBP/RAET1 family proteins. The cytoplasmic tail and transmembrane domains appear to result from gene duplication and frameshift mutation. Together with our previous results, our data suggest that RAET1G is regulated post-translationally to produce a GPI-anchored isoform

Cellular expression, trafficking, and function of two isoforms of human ULBP5/RAET1G

Background: The activating immunoreceptor NKG2D is expressed on Natural Killer (NK) cells and subsets of T cells. NKG2D contributes to anti-tumour and anti-viral immune responses in vitro and in vivo. The ligands for NKG2D in humans are diverse proteins of the MIC and ULBP/RAET families that are upregulated on the surface of virally infected cells and tumours. Two splicing variants of ULBP5/RAET1G have been cloned previously, but not extensively characterised. Methodology/Principal Findings: We pursue a number of approaches to characterise the expression, trafficking, and function of the two isoforms of ULBP5/RAET1G. We show that both transcripts are frequently expressed in cell lines derived from epithelial cancers, and in primary breast cancers. The full-length transcript, RAET1G1, is predicted to encode a molecule with transmembrane and cytoplasmic domains that are unique amongst NKG2D ligands. Using specific anti-RAET1G1 antiserum to stain tissue microarrays we show that RAET1G1 expression is highly restricted in normal tissues. RAET1G1 was expressed at a low level in normal gastrointestinal epithelial cells in a similar pattern to MICA. Both RAET1G1 and MICA showed increased expression in the gut of patients with celiac disease. In contrast to healthy tissues the RAET1G1 antiserum stained a wide variety or different primary tumour sections. Both endogenously expressed and transfected RAET1G1 was mainly found inside the cell, with a minority of the protein reaching the cell surface. Conversely the truncated splicing variant of RAET1G2 was shown to encode a soluble molecule that could be secreted from cells. Secreted RAET1G2 was shown to downregulate NKG2D receptor expression on NK cells and hence may represent a novel tumour immune evasion strategy. Conclusions/Significance: We demonstrate that the expression patterns of ULBP5RAET1G are very similar to the well-characterised NKG2D ligand, MICA. However the two isoforms of ULBP5/RAET1G have very different cellular localisations that are likely to reflect unique functionality

In vitro genetic reconstruction of bacterial transcription initiation by coupled synthesis and detection of RNA polymerase holoenzyme

In vitro reconstitution of a biological complex or process normally involves assembly of multiple individually purified protein components. Here we present a strategy that couples expression and assembly of multiple gene products with functional detection in an in vitro reconstituted protein synthesis system. The strategy potentially allows experimental reconstruction of a multi-component biological complex or process using only DNA templates instead of purified proteins. We applied this strategy to bacterial transcription initiation by co-expressing genes encoding Escherichia coli RNA polymerase subunits and sigma factors in the reconstituted protein synthesis system and by coupling the synthesis and assembly of a functional RNA polymerase holoenzyme with the expression of a reporter gene. Using such a system, we demonstrated sigma-factor-dependent, promoter-specific transcription initiation. Since protein synthesis, complex formation and enzyme catalysis occur in the same in vitro reaction mixture, this reconstruction process resembles natural biosynthetic pathways and avoids time-consuming expression and purification of individual proteins. The strategy can significantly reduce the time normally required by conventional reconstitution methods, allow rapid generation and detection of genetic mutations, and provide an open and designable platform for in vitro study and intervention of complex biological processes