102 research outputs found
Lowering the critical temperature with eight-quark interactions
It is shown that eight-quark interactions, which are needed to stabilize the
ground state of the combined three flavor Nambu -- Jona-Lasinio and 't Hooft
Lagrangians, play also an important role in determining the critical
temperature at which transitions occur from the dynamically broken chiral phase
to the symmetric phase.Comment: 4 pages, 2 figure
Spin-one color superconductivity in compact stars?- an analysis within NJL-type models
We present results of a microscopic calculation using NJL-type model of
possible spin-one pairings in two flavor quark matter for applications in
compact star phenomenology. We focus on the color-spin locking phase (CSL) in
which all quarks pair in a symmetric way, in which color and spin states are
locked. The CSL condensate is particularly interesting for compact star
applications since it is flavor symmetric and could easily satisfy charge
neutrality. Moreover, the fact that in this phase all quarks are gapped might
help to suppress the direct Urca process, consistent with cooling models. The
order of magnitude of these small gaps (~1 MeV) will not influence the EoS, but
their also small critical temperatures (T_c ~800 keV) could be relevant in the
late stages neutron star evolution, when the temperature falls below this value
and a CSL quark core could form.Comment: 7 pages, 7 figures, revised version, accepted for the Conference
Proceedings of "Isolated Neutron Stars: from the Interior to the Surface",
London, 24-28. April 200
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
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 with 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
Ferromagnetic Semiconductors: Moving Beyond (Ga,Mn)As
The recent development of MBE techniques for growth of III-V ferromagnetic
semiconductors has created materials with exceptional promise in spintronics,
i.e. electronics that exploit carrier spin polarization. Among the most
carefully studied of these materials is (Ga,Mn)As, in which meticulous
optimization of growth techniques has led to reproducible materials properties
and ferromagnetic transition temperatures well above 150 K. We review progress
in the understanding of this particular material and efforts to address
ferromagnetic semiconductors as a class. We then discuss proposals for how
these materials might find applications in spintronics. Finally, we propose
criteria that can be used to judge the potential utility of newly discovered
ferromagnetic semiconductors, and we suggest guidelines that may be helpful in
shaping the search for the ideal material.Comment: 37 pages, 4 figure
Urinary Aminopeptidase Activities as Early and Predictive Biomarkers of Renal Dysfunction in Cisplatin-Treated Rats
This study analyzes the fluorimetric determination of alanyl- (Ala), glutamyl- (Glu), leucyl-cystinyl- (Cys) and aspartyl-aminopeptidase (AspAp) urinary enzymatic activities as early and predictive biomarkers of renal dysfunction in cisplatin-treated rats. Male Wistar rats (n = 8 each group) received a single subcutaneous injection of either saline or cisplatin 3.5 or 7 mg/kg, and urine samples were taken at 0, 1, 2, 3 and 14 days after treatment. In urine samples we determined Ala, Glu, Cys and AspAp activities, proteinuria, N-acetyl-β-D-glucosaminidase (NAG), albumin, and neutrophil gelatinase-associated lipocalin (NGAL). Plasma creatinine, creatinine clearance and renal morphological variables were measured at the end of the experiment. CysAp, NAG and albumin were increased 48 hours after treatment in the cisplatin 3.5 mg/kg treated group. At 24 hours, all urinary aminopeptidase activities and albuminuria were significantly increased in the cisplatin 7 mg/kg treated group. Aminopeptidase urinary activities correlated (p0.259) with plasma creatinine, creatinine clearance and/or kidney weight/body weight ratio at the end of the experiment and they could be considered as predictive biomarkers of renal injury severity. ROC-AUC analysis was made to study their sensitivity and specificity to distinguish between treated and untreated rats at day 1. All aminopeptidase activities showed an AUC>0.633. We conclude that Ala, Cys, Glu and AspAp enzymatic activities are early and predictive urinary biomarkers of the renal dysfunction induced by cisplatin. These determinations can be very useful in the prognostic and diagnostic of renal dysfunction in preclinical research and clinical practice.This study was supported by a grant (R1/12/2010/66) from the University of Jaén with the participation of Caja Rural of Jaén, and from the Carlos III Health Institute of the Spanish Ministry of Health and Consumer Affairs (Red de Investigación Renal, REDinREN RD06/0016/0017 and RD07/0016/2008), “FEDER una manera de hacer Europa.
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)
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
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
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