Novel ΔJ=1 Sequence in

A sequence of low-energy levels in _{32}^{78}Ge_{46} has been identified with spins and parity of 2^{+}, 3^{+}, 4^{+}, 5^{+}, and 6^{+}. Decays within this band proceed strictly through ΔJ=1 transitions, unlike similar sequences in neighboring Ge and Se nuclei. Above the 2^{+} level, members of this sequence do not decay into the ground-state band. Moreover, the energy staggering of this sequence has the phase that would be expected for a γ-rigid structure. The energies and branching ratios of many of the levels are described well by shell-model calculations. However, the calculated reduced transition probabilities for the ΔJ=2 in-band transitions imply that they should have been observed, in contradiction with the experiment. Within the calculations of Davydov, Filippov, and Rostovsky for rigid-triaxial rotors with γ=30°, there are sequences of higher-spin levels connected by strong ΔJ=1 transitions which decay in the same manner as those observed experimentally, yet are calculated at too high an excitation energy.

Probing the Single-Particle Character of Rotational States in

A beam containing a substantial component of both the J^{π}=5^{+}, T_{1/2}=162 ns isomeric state of ^{18}F and its 1^{+}, 109.77-min ground state is utilized to study members of the ground-state rotational band in ^{19}F through the neutron transfer reaction (d,p) in inverse kinematics. The resulting spectroscopic strengths confirm the single-particle nature of the 13/2^{+} band-terminating state. The agreement between shell-model calculations using an interaction constructed within the sd shell, and our experimental results reinforces the idea of a single-particle-collective duality in the descriptions of the structure of atomic nuclei.

Masses and ß-Decay Spectroscopy of Neutron-Rich Odd-Odd

The structure of deformed neutron-rich nuclei in the rare-earth region is of significant interest for both the astrophysics and nuclear structure fields. At present, a complete explanation for the observed peak in the elemental abundances at A∼160 eludes astrophysicists, and models depend on accurate quantities, such as masses, lifetimes, and branching ratios of deformed neutron-rich nuclei in this region. Unusual nuclear structure effects are also observed, such as the unexpectedly low energies of the first 2^{+} levels in some even-even nuclei at N=98. In order to address these issues, mass and ß-decay spectroscopy measurements of the ^{160}Eu_{97} and ^{162}Eu_{99} nuclei were performed at the Californium Rare Isotope Breeder Upgrade radioactive beam facility at Argonne National Laboratory. Evidence for a gap in the single-particle neutron energies at N=98 and for large deformation (ß_{2}∼0.3) is discussed in relation to the unusual phenomena observed at this neutron number.

Superallowed α Decay to Doubly Magic

We report the first observation of the ^{108}Xe→^{104}Te→^{100}Sn α-decay chain. The α emitters, ^{108}Xe [E_{α}=4.4(2) MeV, T_{1/2}=58_{-23}^{+106} µs] and ^{104}Te [E_{α}=4.9(2) MeV, T_{1/2}<18 ns], decaying into doubly magic ^{100}Sn were produced using a fusion-evaporation reaction ^{54}Fe(^{58}Ni,4n)^{108}Xe, and identified with a recoil mass separator and an implantation-decay correlation technique. This is the first time α radioactivity has been observed to a heavy self-conjugate nucleus. A previous benchmark for study of this fundamental decay mode has been the decay of ^{212}Po into doubly magic ^{208}Pb. Enhanced proton-neutron interactions in the N=Z parent nuclei may result in superallowed α decays with reduced α-decay widths significantly greater than that for ^{212}Po. From the decay chain, we deduce that the α-reduced width for ^{108}Xe or ^{104}Te is more than a factor of 5 larger than that for ^{212}Po.

Study of the

The existence of ^{26}Al (t_{1/2}=7.17×10^{5} yr) in the interstellar medium provides a direct confirmation of ongoing nucleosynthesis in the Galaxy. The presence of a low-lying 0^{+} isomer (^{26}Al^{m}), however, severely complicates the astrophysical calculations. We present for the first time a study of the ^{26}Al^{m}(d,p)^{27}Al reaction using an isomeric ^{26}Al beam. The selectivity of this reaction allowed the study of ℓ=0 transfers to T=1/2, and T=3/2 states in ^{27}Al. Mirror symmetry arguments were then used to constrain the ^{26}Al^{m}(p,γ)^{27}Si reaction rate and provide an experimentally determined upper limit of the rate for the destruction of isomeric ^{26}Al via radiative proton capture reactions, which is expected to dominate the destruction path of ^{26}Al^{m} in asymptotic giant branch stars, classical novae, and core collapse supernovae.

Transverse wobbling in

A pair of transverse wobbling bands is observed in the nucleus ^{135}Pr. The wobbling is characterized by ΔI=1, E2 transitions between the bands, and a decrease in the wobbling energy confirms its transverse nature. Additionally, a transition from transverse wobbling to a three-quasiparticle band comprised of strong magnetic dipole transitions is observed. These observations conform well to results from calculations with the tilted axis cranking model and the quasiparticle rotor model.

Identification and analysis of organic explosives from post-blast debris by nuclear magnetic resonance.

The growing threat of terrorism has triggered an urgent need to find effective ways to improve the analysis of explosives. This will aid forensic scientists in analysing the post-blast debris, which in turn helps the law enforcement agencies to frame suitable regulations. Analysis of post-blast debris is challenging as it hosts a massive amount of complexity. There are various techniques reported till date such as mass spectrometry, gas chromatography, high-performance liquid chromatography, Fourier transform infrared spectroscopy, and Raman spectroscopy for the analysis of post-blast residues. However, none of them has been able to identify the structural composition of the explosives. The current research study focuses on identifying the structural composition of the explosives from the post-blast debris using the nuclear magnetic resonance (NMR) technology. The post-blast analytes were extracted from soil samples, cleaned by the solid phase extraction (SPE) method and were rapidly analysed by the nuclear magnetic resonance spectrometer. This paper reports the identification of nitro organic explosives such as pentaerythritol tetranitrate (PETN), trinitrotoluene (TNT) and 2,4,6-trinitrophenylmethylnitramine (tetryl) in post-blast debris by 400 MHz nuclear magnetic resonance spectrometer.

Secreted frizzled-related protein 1 regulates adipose tissue expansion and is dysregulated in severe obesity.

AIM: The Wnt/ß-catenin signaling network offers potential targets to diagnose and uncouple obesity from its metabolic complications. In this study, we investigate the role of the Wnt antagonist, secreted frizzled-related protein 1 (SFRP1), in promoting adipogenesis in vitro and adipose tissue expansion in vivo. METHODS: We use a combination of human and murine, in vivo and in vitro models of adipogenesis, adipose tissue expansion and obesity-related metabolic syndrome to profile the involvement of SFRP1. RESULTS: SFRP1 is expressed in both murine and human mature adipocytes. The expression of SFRP1 is induced during in vitro adipogenesis, and SFRP1 is preferentially expressed in mature adipocytes in human adipose tissue. Constitutive ectopic expression of SFRP1 is proadipogenic and inhibits the Wnt/ß-catenin signaling pathway. In vivo endogenous levels of adipose SFRP1 are regulated in line with proadipogenic states. However, in longitudinal studies of high-fat-diet-fed mice, we observed a dynamic temporal but biphasic regulation of endogenous SFRP1. In agreement with this profile, we observed that SFRP1 expression in human tissues peaks in patients with mild obesity and gradually falls in morbidly obese subjects. CONCLUSIONS: Our results suggest that SFRP1 is an endogenous modulator of Wnt/ß-catenin signaling and participates in the paracrine regulation of human adipogenesis. The reduced adipose expression of SFRP1 in morbid obesity and its knock-on effect to prevent further adipose tissue expansion may contribute to the development of metabolic complications in these individuals.

LEM-PCR: a method for determining relative transcript isoform proportions using real-time PCR without a standard curve.

Many genes express multiple transcript isoforms generated by alternative splicing of mRNA. Using real-time PCR, it is straightforward to determine the relative expression level of each isoform independently. However, it is less trivial to determine the relative proportions of different isoforms in a cDNA sample. The relative proportions of different isoforms can be important, as a small change in a highly abundant transcript may be more relevant than a large change in a minimally expressed transcript. Currently, determining the relative proportions of isoforms requires the construction of a standard curve using recombinant plasmid DNA or genomic DNA. As recombinant or genomic DNA standards often amplify with different efficiencies to cDNA samples, they may give under- or overestimations of isoform abundances. The method described in this article uses a titration curve generated from the same cDNA samples measured in the experiment. By using samples with different levels of separate isoforms, it is possible to derive linear equations which, when solved, allow the determination of the proportion of each isoform within the samples under study.

Antioxidant effect of Triticum aestivium (wheat grass) in high-fat diet-induced oxidative stress in rabbits.

Wheat grass is used as a general health tonic and is reported to be effective against several medical disorders, although detailed literature is not available. Besides drug therapy, a number of medicinal plants are effective in treating hyperlipidemia. This study examined the effects of wheat grass on high-fat diet-induced hyperlipidemia in rabbits. Thirty rabbits were divided into 3 groups of 10 rabbits each, group I receiving a control diet, group II a high-fat diet and group III a high-fat diet together with wheat grass over a period of 10 weeks. Fasting serum samples from the animals were analyzed for total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), malondialdehyde (MDA), reduced glutathione (GSH) and vitamin C, and the results were compared. The high-fat diet resulted in hyperlipidemia and an increase in oxidative stress, indicated by a significant rise in MDA levels, whereas antioxidant levels of GSH and vitamin C were significantly reduced. Wheat grass supplementation with a high-fat diet resulted in improved lipid levels (decreased total cholesterol and increased HDL-C) together with significantly reduced MDA levels and increased GSH and vitamin C levels. These results indicate the beneficial role of wheat grass in ameliorating hyperlipidemia and the associated oxidative stress.

Multiple flow rates measurement of exhaled nitric oxide in patients with sarcoidosis: a pilot feasibility study.

Fraction of end tidal exhaled nitric oxide (FeNO) has been introduced as a non-invasive marker of airway inflammation in patients with asthma and may have value in monitoring disease activity in patients with sarcoidosis. This pilot study explored: 1) feasibility of the multiple flow rates maneuver to estimate alveolar (C(AlV)NO) and airway wall (J(AW)NO) NO in patients with sarcoidosis; and 2) utility of exhaled NO (FeNO, C(Alv)NO and J(AW)NO) measurements to detect and monitor treatment response in patients with active pulmonary sarcoidosis. Patients with sarcoidosis (n = 42) and healthy non-smokers (n = 20) underwent FeNO measurement at 7 flow-rates (50 to 400 ml/s). Using the Tsoukias and George (1998) model, C(Alv)NO and J(AW)NO were estimated. Both patients and healthy non-smokers were able to perform the multiple flow rates maneuver without discomfort, with first measurement success rate of 57% and 65%, respectively. No significant difference was found between patients with sarcoidosis and healthy non-smokers in exhaled NO. None were correlated with pulmonary function tests, except a significant negative correlation between C(Alv)NO and FVC% (p = 0.001) and DLCO% (p = 0.012). In 8 patients with active sarcoidosis, FeNO, C(Alv)NO or J(AW)NO were not different from those of patients with inactive sarcoidosis. Treatment of active sarcoidosis using oral prednisone and methotrexate did not show any consistent pattern of changes in C(Alv)NO or J(AW)NO. Due to a large inter-subject variability and difficulty controlling use of the inhaled corticosteroids, exhaled NO measurement did not appear to be a clinically useful method of monitoring disease progression in sarcoidosis.

Tumour necrosis factor-alpha inhibits adipogenesis via a beta-catenin/TCF4(TCF7L2)-dependent pathway.

Tumour necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, is a potent negative regulator of adipocyte differentiation. However, the mechanism of TNF-alpha-mediated antiadipogenesis remains incompletely understood. In this study, we first confirm that TNF-alpha inhibits adipogenesis of 3T3-L1 preadipocytes by preventing the early induction of the adipogenic transcription factors peroxisome proliferator-activated receptor-gamma (PPARgamma) and CCAAT/enhancer binding protein-alpha (C/EBPalpha). This suppression coincides with enhanced expression of several reported mediators of antiadipogenesis that are also targets of the Wnt/beta-catenin/T-cell factor 4 (TCF4) pathway. Indeed, we found that TNF-alpha enhanced TCF4-dependent transcriptional activity during early antiadipogenesis, and promoted the stabilisation of beta-catenin throughout antiadipogenesis. We analysed the effect of TNF-alpha on adipogenesis in 3T3-L1 cells in which beta-catenin/TCF signalling was impaired, either via stable knockdown of beta-catenin, or by overexpression of dominant-negative TCF4 (dnTCF4). The knockdown of beta-catenin enhanced the adipogenic potential of 3T3-L1 preadipocytes and attenuated TNF-alpha-induced antiadipogenesis. However, beta-catenin knockdown also promoted TNF-alpha-induced apoptosis in these cells. In contrast, overexpression of dnTCF4 prevented TNF-alpha-induced antiadipogenesis but showed no apparent effect on cell survival. Finally, we show that TNF-alpha-induced antiadipogenesis and stabilisation of beta-catenin requires a functional death domain of TNF-alpha receptor 1 (TNFR1). Taken together these data suggest that TNFR1-mediated death domain signals can inhibit adipogenesis via a beta-catenin/TCF4-dependent pathway.

Complement-fixing antigen of human sarcomas.

Further investigation of the humoral immune responses of patients with sarcoma to their tumors revealed a sarcoma-associated antigen that was readily detected by complement fixation. Circulating levels of antibody to this antigen, tentatively labeled S3, rose markedly after surgical removal of the tumor. Antibody to S3, as to S1 and S2, was highly prevalent in patients with various malignant tumors other than sarcoma.

7-Deaza cyclic adenosine 5'-diphosphate ribose: first example of a Ca(2+)-mobilizing partial agonist related to cyclic adenosine 5'-diphosphate ribose.

BACKGROUND: Cyclic adenosine 5'-diphosphate ribose (cADPR), a naturally occurring metabolite of nicotinamide adenine dinucleotide (NAD+), mobilizes Ca2+ from non-mitochondrial stores in a variety of mammalian and invertebrate tissues. It has been shown that cADPR activates ryanodine-sensitive Ca(2+)-release channels, working independently of inositol 1,4,5-trisphosphate (IP3) to mobilize intracellular Ca2+ stores. In some systems, cADPR has been shown to be more potent than IP3. The chemo-enzymatic synthesis of structurally modified analogues of cADPR can provide pharmacological tools for probing this new Ca(2+)-signaling pathway. In this work, we describe the synthesis and evaluation of a structural mimic of cADPR with different Ca(2+)-releasing properties. RESULTS: 7-Deaza cyclic adenosine 5'-diphosphate ribose (7-deaza cADPR), a novel cADPR analogue modified in the purine ring, was synthesized and its ability to release Ca2+ from non-mitochondrial pools in homogenates made from sea urchin eggs was investigated. 7-Deaza cADPR was more effective in releasing Ca2+ than cADPR, but it only released approximately 66% of the Ca2+ released by a maximal concentration of cADPR. It was also more resistant to hydrolysis than cADPR. If we administered increasing concentrations of 7-deaza cADPR at the same time as a maximal concentration of cADPR, the induction of Ca2+ release by cADPR was antagonized. CONCLUSIONS: 7-Deaza cADPR has a Ca(2+)-release profile consistent with that of a partial agonist, and it is the first reported example of such a compound to act at the cADPR receptor. The imidazole ring of cADPR is clearly important in stimulating the Ca(2+)-release machinery, and the present results demonstrate that structural modification of a site other than position 8 of the purine ring can affect the efficacy of Ca2+ release. 7-Deaza cADPR represents a significant step forwards in designing modulators of the cADPR signaling pathway.

beta-Adrenergic regulation of IL-6 release from adipose tissue: in vivo and in vitro studies.

UNLABELLED: Circulating IL-6 levels are elevated in obesity. Although IL-6 is expressed in adipose tissue, neither its regulation nor cell of origin is well characterized. Here we investigated the beta-adrenergic regulation of IL-6 release in a combination of studies on humans and animals in vivo and cultured adipocytes in vitro. Human in vivo study: Human volunteers were infused with isoproterenol, norepinephrine, or saline [4 M:4F; mean (SD) age 35.5 (5.8) yr; body mass index 24.6 (4.2) kg/m(-2)]. Plasma IL-6 levels increased during a 3-h infusion of isoproterenol (P = 0.01) and fell 2 h post infusion (P = 0.05). IL-6 levels did not change significantly with either norepinephrine or saline. Murine in vivo study: C57BL6/J male mice were injected ip with dobutamine (beta(1) agonist), clenbuterol (beta(2)), CL316243 (beta(3)), or saline placebo. Plasma IL-6 levels at 3 h were increased by clenbuterol (P = 0.02) and CL316243 (P = 0.02) but not dobutamine (P = 0.51), compared with placebo. IN VITRO STUDIES: In human peripheral blood cells, lipopolysaccharide treatment enhanced secretion of IL-6 (vs. controls; P < 0.001), whereas isoproterenol inhibited IL-6 secretion (P = 0.012) and norepinephrine had no significant effect. In contrast, isolated human adipocytes and differentiated 3T3F442A adipocytes all rapidly secreted IL-6 in response to adrenergic agonists (P < 0.01, compared with untreated cells). We conclude that beta 2/beta 3 adrenoceptor stimulation on adipocytes, rather than macrophages, may be responsible for the increases in plasma IL-6 concentrations observed during sympathetic activation and in obesity.

Characterisation of receptor-specific TNFalpha functions in adipocyte cell lines lacking type 1 and 2 TNF receptors.

Tumour necrosis factor-alpha (TNFalpha) is a multifunctional cytokine that exerts a myriad of biological actions in numerous different tissues including adipocytes through its two distinct cell surface receptors. To address the role of each TNF receptor in the biological actions of TNFalpha in adipocytes, we have developed four new preadipocyte cell lines. These were established from wild type controls (TNFR1(+/+)R2(+/+)) and from mice lacking TNFR1 (TNFR1(-/-)), TNFR2 (TNFR2(-/-)) or both (TNFR1(-/-)R2(-/-)). All four new cell lines can fully differentiate to form mature adipocytes, under appropriate culture conditions, as judged by cell morphology, expression of multiple adipogenic markers and the ability to mediate agonist-stimulated lipolysis and insulin-stimulated glucose transport. In wild type (TNFR1(+/+)R2(+/+)) and TNFR2(-/-) adipocytes, TNFalpha stimulated lipolysis and inhibited insulin-stimulated glucose transport as well as insulin receptor autophosphorylation. In contrast, these activities were completely lost in the TNFR1(-/-)R2(-/-) and TNFR1(-/-) cells. Taken together, these studies demonstrate that TNFalpha-induced lipolysis, as well as inhibition of insulin-stimulated glucose transport are predominantly mediated by TNFR1 and that the presence of TNFR2 is not necessary for these functions. This new experimental system promises to be useful in dissecting the molecular pathways activated by each TNF receptor in mediating the biological functions of TNFalpha in differentiated adipocytes.