Triton calculations with π\pi and ρ\rho exchange three-nucleon forces

The Faddeev equations are solved in momentum space for the trinucleon bound state with the new Tucson-Melbourne $\pi$ and $\rho$ exchange three-nucleon potentials. The three-nucleon potentials are combined with a variety of realistic two-nucleon potentials. The dependence of the triton binding energy on the $\pi NN$ cut-off parameter in the three-nucleon potentials is studied and found to be reduced compared to the case with pure $\pi$ exchange. The $\rho$ exchange parts of the three-nucleon potential yield an overall repulsive effect. When the recommended parameters are employed, the calculated triton binding energy turns out to be very close to its experimental value. Expectation values of various components of the three-nucleon potential are given to illustrate their significance for binding.Comment: 17 pages Revtex 3.0, 4 figures. Accepted for publication in Phys. Rev.

Hepatic autophagy contributes to the metabolic response to dietary protein restriction

© 2016 Elsevier Inc. All rights reserved. Autophagy is an essential cellular response which acts to release stored cellular substrates during nutrient restriction, and particularly plays a key role in the cellular response to amino acid restriction. However, there has been limited work testing whether the induction of autophagy is required for adaptive metabolic responses to dietary protein restriction in the whole animal. Here, we found that moderate dietary protein restriction led to a series of metabolic changes in rats, including increases in food intake and energy expenditure, the downregulation of hepatic fatty acid synthesis gene expression and reduced markers of hepatic mitochondrial number. Importantly, these effects were also associated with an induction of hepatic autophagy. To determine if the induction of autophagy contributes to these metabolic effects, we tested the metabolic response to dietary protein restriction in BCL2-AAA mice, which bear a genetic mutation that impairs autophagy induction. Interestingly, BCL2-AAA mice exhibit exaggerated responses in terms of both food intake and energy expenditure, whereas the effects of protein restriction on hepatic metabolism were significantly blunted. These data demonstrate that restriction of dietary protein is sufficient to trigger hepatic autophagy, and that disruption of autophagy significantly alters both hepatic and whole animal metabolic response to dietary protein restriction

Gauging the three-nucleon spectator equation

We derive relativistic three-dimensional integral equations describing the interaction of the three-nucleon system with an external electromagnetic field. Our equations are unitary, gauge invariant, and they conserve charge. This has been achieved by applying the recently introduced gauging of equations method to the three-nucleon spectator equations where spectator nucleons are always on mass shell. As a result, the external photon is attached to all possible places in the strong interaction model, so that current and charge conservation are implemented in the theoretically correct fashion. Explicit expressions are given for the three-nucleon bound state electromagnetic current, as well as the transition currents for the scattering processes \gamma He3 -> NNN, Nd -> \gamma Nd, and \gamma He3 -> Nd. As a result, a unified covariant three-dimensional description of the NNN-\gamma NNN system is achieved.Comment: 23 pages, REVTeX, epsf, 4 Postscript figure

Double heterozygous pathogenic variants in TP53 and CHEK2 in boy with undifferentiated embryonal sarcoma of the liver

Undifferentiated embryonal sarcoma of the liver is a rare mesenchymal malignancy that predominantly occurs in children. The relationship between this tumor entity and germline pathogenic variants (PVs) remains undefined. Here, we present the clinical case of a male patient diagnosed with undifferentiated embryonal sarcoma of the liver. Both germline and tumor samples were analyzed using next-generation sequencing. In the tumor tissue, PVs in TP53 (NM_000546.5):c.532del p.(His178Thrfs*69) and CHEK2 (NM_007194.4):c.85C>T p.(Gln29*) were identified, with both confirmed to be of germline origin. Copy number analyses indicated a loss of the wildtype TP53 allele in the tumor, consistent with a second hit, while it was the variant CHEK2 allele that was lost in the tumor. Our data indicate that the germline TP53 PV acts as a driver of tumorigenesis in the reported case and support a complex interaction between the germline TP53 and CHEK2 PVs. This case highlights the dynamic interplays of genetic alterations in tumorigenesis and emphasizes the need for continued investigation into the complex interactions between TP53 and CHEK2 PVs and into the association of undifferentiated embryonal sarcoma of the liver and Li–Fraumeni syndrome

Analysis of De Novo HOXA 13 Polyalanine Expansions Supports Replication Slippage Without Repair in Their Generation

Polyalanine repeat expansion diseases are hypothesized to result from unequal chromosomal recombination, yet mechanistic studies are lacking. We identified two de novo cases of hand‐foot‐genital syndrome (HFGS) associated with polyalanine expansions in HOXA13 that afforded rare opportunities to investigate the mechanism. The first patient with HFGS was heterozygous for a de novo nine codon polyalanine expansion. Haplotype investigation showed that the expansion arose on the maternally inherited chromosome but not through unequal crossing over between homologs, leaving unequal sister chromatid exchange during mitosis or meiosis or slipped mispairing as possible explanations. The asymptomatic father of the second patient with HFGS was mosaic for a six codon polyalanine expansion. Multiple tissue PCR and clonal analysis of paternal fibroblasts showed only expansion/WT and WT/WT clones, and haplotype data showed that two unaffected offspring inherited the same paternal allele without the expansion, supporting a postzygotic origin. Absence of the contracted allele in the mosaic father does not support sister chromatid exchange in the origin of the expansion. Mosaicism for HOXA13 polyalanine expansions may be associated with a normal phenotype, making examination of parental DNA essential in apparently de novo HFGS cases to predict accurate recurrence risks. We could not find an example in the literature where unequal sister chromatid exchange has been proven for any polyalanine expansion, suggesting that the principal mechanism for polyalanine expansions (and contractions) is slipped mispairing without repair or that the true frequency of unequal sister chromatid exchange involving these repeats is low. © 2013 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97454/1/ajmga35843.pd

Effect of single intralesional treatment of surgically induced equine superficial digital flexor tendon core lesions with adipose-derived mesenchymal stromal cells: a controlled experimental trial

Background: Adipose tissue is a promising source of mesenchymal stromal cells (MSCs) for the treatment of tendon disease. The goal of this study was to assess the effect of a single intralesional implantation of adipose tissue-derived mesenchymal stromal cells (AT-MSCs) on artificial lesions in equine superficial digital flexor tendons (SDFTs). Methods: During this randomized, controlled, blinded experimental study, either autologous cultured AT-MSCs suspended in autologous inactivated serum (AT-MSC-serum) or autologous inactivated serum (serum) were injected intralesionally 2 weeks after surgical creation of centrally located SDFT lesions in both forelimbs of nine horses. Healing was assessed clinically and with ultrasound (standard B-mode and ultrasound tissue characterization) at regular intervals over 24 weeks. After euthanasia of the horses the SDFTs were examined histologically, biochemically and by means of biomechanical testing. Results: AT-MSC implantation did not substantially influence clinical and ultrasonographic parameters. Histology, biochemical and biomechanical characteristics of the repair tissue did not differ significantly between treatment modalities after 24 weeks. Compared with macroscopically normal tendon tissue, the content of the mature collagen crosslink hydroxylysylpyridinoline did not differ after AT-MSC-serum treatment (p = 0.074) while it was significantly lower (p = 0.027) in lesions treated with serum alone. Stress at failure (p = 0.048) and the modulus of elasticity (p = 0.001) were significantly lower after AT-MSC-serum treatment than in normal tendon tissue. Conclusions: The effect of a single intralesional injection of cultured AT-MSCs suspended in autologous inactivated serum was not superior to treatment of surgically created SDFT lesions with autologous inactivated serum alone in a surgical model of tendinopathy over an observation period of 22 weeks. AT-MSC treatment might have a positive influence on collagen crosslinking of remodelling scar tissue. Controlled long-term studies including naturally occurring tendinopathies are necessary to verify the effects of AT-MSCs on tendon disease

The pion-three-nucleon problem with two-cluster connected-kernel equations

It is found that the coupled piNNN-NNN system breaks into fragments in a nontrivial way. Assuming the particles as distinguishable, there are indeed four modes of fragmentation into two clusters, while in the standard three-body problem there are three possible two-cluster partitions and conversely the four-body problem has seven different possibilities. It is shown how to formulate the pion-three-nucleon collision problem through the integral-equation approach by taking into account the proper fragmentation of the system. The final result does not depend on the assumption of separability of the two-body t-matrices. Then, the quasiparticle method a' la Grassberger-Sandhas is applied and effective two-cluster connected-kernel equations are obtained. The corresponding bound-state problem is also formulated, and the resulting homogeneous equation provides a new approach which generalizes the commonly used techniques to describe the three-nucleon bound-state problem, where the meson degrees of freedom are usually suppressed.Comment: 20 pages, REVTeX, with 3 COLOR figures (PostScript

Reply to: Soils need to be considered when assessing the impacts of land-use change on carbon sequestration

Industrial Ecolog

An Equine Model for Vaccination against a Hepacivirus: Insights into Host Responses to E2 Recombinant Protein Vaccination and Subsequent Equine Hepacivirus Inoculation

Equine hepacivirus (EqHV) is the closest known genetic homologue of hepatitis C virus. An effective prophylactic vaccine is currently not available for either of these hepaciviruses. The equine as potential surrogate model for hepacivirus vaccine studies was investigated, while equine host responses following vaccination with EqHV E2 recombinant protein and subsequent EqHV inoculation were elucidated. Four ponies received prime and booster vaccinations (recombinant protein, adjuvant) four weeks apart (day −55 and −27). Two control ponies received adjuvant only. Ponies were inoculated with EqHV RNA-positive plasma on day 0. Blood samples and liver biopsies were collected over 26 weeks (day −70 to +112). Serum analyses included detection of EqHV RNA, isotypes of E2-specific immunoglobulin G (IgG), nonstructural protein 3-specific IgG, haematology, serum biochemistry, and metabolomics. Liver tissue analyses included EqHV RNA detection, RNA sequencing, histopathology, immunohistochemistry, and fluorescent in situ hybridization. Al-though vaccination did not result in complete protective immunity against experimental EqHV inoculation, the majority of vaccinated ponies cleared the serum EqHV RNA earlier than the control ponies. The majority of vaccinated ponies appeared to recover from the EqHV-associated liver insult earlier than the control ponies. The equine model shows promise as a surrogate model for future hepacivirus vaccine research