Cryogenic setup for trapped ion quantum computing

We report on the design of a cryogenic setup for trapped ion quantum computing containing a segmented surface electrode trap. The heat shield of our cryostat is designed to attenuate alternating magnetic field noise, resulting in 120~dB reduction of 50~Hz noise along the magnetic field axis. We combine this efficient magnetic shielding with high optical access required for single ion addressing as well as for efficient state detection by placing two lenses each with numerical aperture 0.23 inside the inner heat shield. The cryostat design incorporates vibration isolation to avoid decoherence of optical qubits due to the motion of the cryostat. We measure vibrations of the cryostat of less than $\pm$20~nm over 2~s. In addition to the cryogenic apparatus, we describe the setup required for an operation with $^{\mathrm{40}}$Ca$^{\mathrm{+}}$ and $^{\mathrm{88}}$Sr$^{\mathrm{+}}$ ions. The instability of the laser manipulating the optical qubits in $^{\mathrm{40}}$Ca$^{\mathrm{+}}$ is characterized yielding a minimum of its Allan deviation of 2.4$\cdot$10$^{\mathrm{-15}}$ at 0.33~s. To evaluate the performance of the apparatus, we trapped $^{\mathrm{40}}$Ca$^{\mathrm{+}}$ ions, obtaining a heating rate of 2.14(16)~phonons/s and a Gaussian decay of the Ramsey contrast with a 1/e-time of 18.2(8)~ms

On the Ground State of Two Flavor Color Superconductor

The diquark condensate susceptibility in neutral color superconductor at moderate baryon density is calculated in the frame of two flavor Nambu-Jona-Lasinio model. When color chemical potential is introduced to keep charge neutrality, the diquark condensate susceptibility is negative in the directions without diquark condensate in color space, which may be regarded as a signal of the instability of the conventional ground state with only diquark condensate in the color 3 direction.Comment: 4 pages, 2 figure

Quark Potential in a Quark-Meson Plasma

We investigate quark potential by considering meson exchanges in the two flavor Nambu--Jona-Lasinio model at finite temperature and density. There are two kinds of oscillations in the chiral restoration phase, one is the Friedel oscillation due to the sharp quark Fermi surface at high density, and the other is the Yukawa oscillation driven by the complex meson poles at high temperature. The quark-meson plasma is strongly coupled in the temperature region $1\le T/T_c \lesssim 3$ with $T_c$ being the critical temperature of chiral phase transition. The maximum coupling in this region is located at the critical point.Comment: 8 pages and 8 figure

Relation Between Chiral Susceptibility and Solutions of Gap Equation in Nambu--Jona-Lasinio Model

We study the solutions of the gap equation, the thermodynamic potential and the chiral susceptibility in and beyond the chiral limit at finite chemical potential in the Nambu--Jona-Lasinio (NJL) model. We give an explicit relation between the chiral susceptibility and the thermodynamic potential in the NJL model. We find that the chiral susceptibility is a quantity being able to represent the furcation of the solutions of the gap equation and the concavo-convexity of the thermodynamic potential in NJL model. It indicates that the chiral susceptibility can identify the stable state and the possibility of the chiral phase transition in NJL model.Comment: 21 pages, 6 figures, misprints are correcte

Fibrosis in the kidney: is a problem shared a problem halved?

Fibrotic disorders are commonplace, take many forms and can be life-threatening. No better example of this exists than the progressive fibrosis that accompanies all chronic renal disease. Renal fibrosis is a direct consequence of the kidney's limited capacity to regenerate after injury. Renal scarring results in a progressive loss of renal function, ultimately leading to end-stage renal failure and a requirement for dialysis or kidney transplantation

25-Hydroxyvitamin D levels and chronic kidney disease in the AusDiab (Australian Diabetes, Obesity and Lifestyle) study

<p>Abstract</p> <p>Background</p> <p>Low 25-hydroxy vitamin D (25(OH)D) levels have been associated with an increased risk of albuminuria, however an association with glomerular filtration rate (GFR) is not clear. We explored the relationship between 25(OH)D levels and prevalent chronic kidney disease (CKD), albuminuria and impaired GFR, in a national, population-based cohort of Australian adults (AusDiab Study).</p> <p>Methods</p> <p>10,732 adults ≥25 years of age participating in the baseline survey of the AusDiab study (1999–2000) were included. The GFR was estimated using an enzymatic creatinine assay and the CKD-EPI equation, with CKD defined as eGFR <60 ml/min/1.73 m². Albuminuria was defined as a spot urine albumin to creatinine ratio (ACR) of ≥2.5 mg/mmol for men and ≥3.5 for women. Serum 25(OH)D levels of <50 nmol/L were considered vitamin D deficient. The associations between 25(OH)D level, albuminuria and impaired eGFR were estimated using multivariate regression models.</p> <p>Results</p> <p>30.7% of the study population had a 25(OH)D level <50 nmol/L (95% CI 25.6-35.8). 25(OH)D deficiency was significantly associated with an impaired eGFR in the univariate model (OR 1.52, 95% CI 1.07-2.17), but not in the multivariate model (OR 0.95, 95% CI 0.67-1.35). 25(OH)D deficiency was significantly associated with albuminuria in the univariate (OR 2.05, 95% CI 1.58-2.67) and multivariate models (OR 1.54, 95% CI 1.14-2.07).</p> <p>Conclusions</p> <p>Vitamin D deficiency is common in this population, and 25(OH)D levels of <50 nmol/L were independently associated with albuminuria, but not with impaired eGFR. These associations warrant further exploration in prospective and interventional studies.</p

Application of Direct Renin Inhibition to Chronic Kidney Disease

Chronic kidney disease has serious implications with a high risk for progressive loss of renal function, increased cardiovascular events as well as a substantial financial burden. The renin-angiotensin-aldosterone system (RAAS) is activated in chronic kidney disease, especially in diabetes and hypertension, which are the leading causes of chronic kidney disease. Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) decrease the rate of progression of diabetic and non-diabetic nephropathy and are recommended therapy for chronic kidney disease. Key clinical trials supporting the use of ACE inhibitors and ARBs in chronic kidney disease are discussed. Recent developments in our understanding of RAAS biology and the use of direct renin inhibition are reviewed in the context of their potential impact on the prevention and management of chronic kidney disease. Despite the clinical success of ACE inhibitors and ARBs the rates of mortality and progression to renal failure remain high in these patient populations. ACE inhibitor or ARB monotherapy, in doses commonly used in clinical practice does not result in complete suppression of the RAAS. Aliskiren, a direct renin inhibitor, offers a novel approach to inhibit the RAAS in chronic kidney disease. High dose ARB therapy or combination therapies with ACE inhibitors and ARBs have shown beneficial effects on surrogate markers of chronic kidney disease. Early data based on urinary protein excretion rates as a surrogate marker for renal function suggest a possibly novel role for aliskiren alone or in combination with ARBs in chronic kidney disease

VEGF expression by mesenchymal stem cells contributes to angiogenesis in pancreatic carcinoma

Little is known about the factors that enable the mobilisation of human mesenchymal stem cells (MSC) from the bone marrow into the blood stream and their recruitment to and retention in the tumour. We found specific migration of MSC towards growth factors present in pancreatic tumours, such as PDGF, EGF, VEGF and specific inhibitors Glivec, Erbitux and Avastin interfered with migration. Within a few hours, MSC migrated into spheroids consisting of pancreatic cancer cells, fibroblasts and endothelial cells as measured by time-lapse microscopy. Supernatant from subconfluent MSC increased sprouting of HUVEC due to VEGF production by MSC itself as demonstrated by RT-PCR and ELISA. Only few MSCs were differentiated into endothelial cells in vitro, whereas in vivo differentiation was not observed. Lentiviral GFP-marked MSCs, injected in nude mice xenografted with orthotopic pancreatic tumours, preferentially migrated into the tumours as observed by FACS analysis of green fluorescent cells. By immunofluorescence and intravital microscopic studies, we found the interaction of MSC with the endothelium of blood vessels. Mesenchymal stem cells supported tumour angiogenesis in vivo, that is CD31+ vessel density was increased after the transfer of MSC compared with siVEGF-MSC. Our data demonstrate the migration of MSC toward tumour vessels and suggest a supportive role in angiogenesis

Interactions of Human Endothelial and Multipotent Mesenchymal Stem Cells in Cocultures

Current strategies for tissue engineering of bone rely on the implantation of scaffolds, colonized with human mesenchymal stem cells (hMSC), into a recipient. A major limitation is the lack of blood vessels. One approach to enhance the scaffold vascularisation is to supply the scaffolds with endothelial cells (EC)

HCV genome-wide genetic analyses in context of disease progression and hepatocellular carcinoma

<div><p>Hepatitis C virus (HCV) is a major cause of hepatitis and hepatocellular carcinoma (HCC) world-wide. Most HCV patients have relatively stable disease, but approximately 25% have progressive disease that often terminates in liver failure or HCC. HCV is highly variable genetically, with seven genotypes and multiple subtypes per genotype. This variation affects HCV’s sensitivity to antiviral therapy and has been implicated to contribute to differences in disease. We sequenced the complete viral coding capacity for 107 HCV genotype 1 isolates to determine whether genetic variation between independent HCV isolates is associated with the rate of disease progression or development of HCC. Consensus sequences were determined by sequencing RT-PCR products from serum or plasma. Positions of amino acid conservation, amino acid diversity patterns, selection pressures, and genome-wide patterns of amino acid covariance were assessed in context of the clinical phenotypes. A few positions were found where the amino acid distributions or degree of positive selection differed between in the HCC and cirrhotic sequences. All other assessments of viral genetic variation and HCC failed to yield significant associations. Sequences from patients with slow disease progression were under a greater degree of positive selection than sequences from rapid progressors, but all other analyses comparing HCV from rapid and slow disease progressors were statistically insignificant. The failure to observe distinct sequence differences associated with disease progression or HCC employing methods that previously revealed strong associations with the outcome of interferon α-based therapy implies that variable ability of HCV to modulate interferon responses is not a dominant cause for differential pathology among HCV patients. This lack of significant associations also implies that host and/or environmental factors are the major causes of differential disease presentation in HCV patients.</p></div