Investigating the features of PDO green hams during salting: Insights for new markers and genomic regions in commercial hybrid pigs

Protected Designation of Origin (PDO) dry-cured hams production is greatly dependent on raw meat quality. This study was performed to identify genetic markers associated with the quality of dry-cured ham. Carcass traits of 229 heavy pigs belonging to three commercial genetic lines were registered (weight, EUROP classification). Phenotypic traits (Semimembranosus muscle ultimate pH, ham weight and lean meat content, adsorbed salt) of the corresponding thighs, undergone PDO ham process in three different plants, were measured, using a fast and non-invasive technology. Green ham weight and lean meat percentage influenced the estimated salt content and the weight loss during salting, even if the processing plant greatly affected the variability of the measured ham traits. The genomic data were obtained with the GeneSeek Genomic Profiler (GGP) 70k HD Porcine Array, using the slaughter day and the sex of the animals in the statistical analyses. The phenotypic traits were associated with the genotypes through GenAbel software. The results showed that 18 SNPs located on nine porcine chromosomes were found to be associated with nine phenotypic traits, mainly related to ham weight loss during salting. New associations were found between markers in the genes Neural Precursor Cell Expressed Developmentally Down-Regulated 9 (NEDD9, SSC7), T-Cell Lymphoma Invasion and Metastasis 2 (TIAM2, SSC1), and the ham quality traits. After validation, these SNPs may be useful to improve the quality of thighs for the production of PDO dry-cured hams

The Stellar Ages and Masses of Short GRB Host Galaxies: Investigating the Progenitor Delay Time Distribution and the Role of Mass and Star Formation in the Short GRB Rate

[Abridged] We present optical and NIR observations of 19 short GRB host galaxies, aimed at measuring their stellar masses and population ages. The goals of this study are to evaluate whether short GRBs track the stellar mass distribution of galaxies, to investigate the progenitor delay time distribution, and to explore any connection between long and short GRB progenitors. Using single stellar population models we infer masses of log(M/M_sun)=8.8-11.6 and population ages of tau=0.03-4.4 Gyr. We further infer maximal masses of log(M/M_sun)=9.7-11.9 by assuming stellar population ages equal to the age of the universe at each host's redshift. Comparing the distribution of stellar masses to the general galaxy mass function we find that short GRBs track the cosmic stellar mass distribution only if the late-type hosts generally have maximal masses. However, there is an apparent dearth of early-type hosts compared to the equal contribution of early- and late-type galaxies to the cosmic stellar mass budget. These results suggest that stellar mass may not be the sole parameter controlling the short GRB rate, and raise the possibility of a two-component model with both mass and star formation playing a role. If short GRBs in late-type galaxies indeed track the star formation activity, the resulting typical delay time is ~0.2 Gyr, while those in early-type hosts have a typical delay of ~3 Gyr. Using the same stellar population models we fit the data for 22 long GRB hosts and find that they have lower masses and younger population ages, with =9.1 and =0.06 Gyr, respectively; their maximal masses are similarly lower, =9.6. Most importantly, the two host populations remain distinct even if we consider only the star-forming hosts of short GRBs, supporting our previous findings that the progenitors of long GRBs and short GRBs in late-type galaxies are distinct.Comment: Submitted to ApJ; 20 pages, 3 tables, 8 figure

Protect the natives to combat the aliens: Could octopus vulgaris cuvier, 1797 be a natural agent for the control of the lionfish invasion in the mediterranean sea?

[No abstract available

The association between maternal reproductive age and progression of refractive error in urban students in Beijing

To investigate the association between maternal reproductive age and their children' refractive error progression in Chinese urban students.The Beijing Myopia Progression Study was a three-year cohort investigation. Cycloplegic refraction of these students at both baseline and follow-up vision examinations, as well as non-cycloplegic refraction of their parents at baseline, were performed. Student's refractive change was defined as the cycloplegic spherical equivalent (SE) of the right eye at the final follow-up minus the cycloplegic SE of the right eye at baseline.At the final follow-up, 241 students (62.4%) were reexamined. 226 students (58.5%) with completed refractive data, as well as completed parental reproductive age data, were enrolled. The average paternal and maternal age increased from 29.4 years and 27.5 years in 1993-1994 to 32.6 years and 29.2 years in 2003-2004, respectively. In the multivariate analysis, students who were younger (β = 0.08 diopter/year/year, P<0.001), with more myopic refraction at baseline (β = 0.02 diopter/year/diopter, P = 0.01), and with older maternal reproductive age (β = -0.18 diopter/year/decade, P = 0.01), had more myopic refractive change. After stratifying the parental reproductive age into quartile groups, children with older maternal reproductive age (trend test: P = 0.04) had more myopic refractive change, after adjusting for the children's age, baseline refraction, maternal refraction, and near work time. However, no significant association between myopic refractive change and paternal reproductive age was found.In this cohort, children with older maternal reproductive age had more myopic refractive change. This new risk factor for myopia progression may partially explain the faster myopic progression found in the Chinese population in recent decades

Modeling the high-energy emission in GRB 110721A and implications on the early multiwavelength and polarimetric observations

GRB 110721A was detected by the Gamma-ray Burst Monitor and the Large Area Telescope (LAT) onboard the Fermi satellite and the Gamma-ray Burst Polarimeter onboard the IKAROS solar mission. Previous analysis done of this burst showed: i) a linear polarization signal with position angle stable ($\phi_p= 160^\circ\pm11$) and high degree of $\Pi=84^{+16}_{-28}$, ii) an extreme peak energy of a record-breaking at 15$\pm$2 MeV, and iii) a subdominant prompt thermal component observed right after the onset of this burst. In this paper, the LAT data around the reported position of GRB 110721A are analysed with the most recent software and then, the LAT light curve above 100 MeV was obtained. The LAT light curve is modelled in terms of adiabatic early-afterglow external shocks when the outflow propagates into a stellar wind. Additionally, we discuss the possible origins and also study the implications of the early-afterglow external shocks on the extreme peak energy observed at 15$\pm$2 MeV, the polarization observations and the subdominant prompt thermal component.Comment: 9 pages and one figure. Accepted for publication in Ap

A giant ectopic hidradenoma papilliferum in a Niger delta region of Nigeria

Hidradenoma papilliferum is a known example of adnexal skin tumours with apocrine differentiation. It is a rare benign tumour which tends to arise from areas with rich concentration of aporine glands such as anogenital region, vulval, perineal, axillae, and periumbilical areas. In this report, the tumour was found in the upper outer quadrant of left breast, being one of the ectopic sites for this tumour. Contrary to most reports where male preponderance was popular for ectopic hidradenoma papilliferum, the patient in this report is a 71-year-old female. Considering the location of this tumour in this report, the likely histopathological differential diagnoses such as tubular apocrine adenoma, clear cell (apocrine) adenoma, lipoma, intraductal papilloma and papillary carcinoma of the breast should be considered for exclusion. This is the first reported case of a giant ectopic hidradenoma papilliferum of the breast in a Niger Delta region of Nigeria which also highlights the role of fine needle aspiration and cytology in the diagnosis of breast lesions

Histone Acetylation Defects in Brain Precursor Cells: A Potential Pathogenic Mechanism Causing Proliferation and Differentiation Dysfunctions in Mitochondrial Aspartate-Glutamate Carrier Isoform 1 Deficiency

Mitochondrial aspartate-glutamate carrier isoform 1 (AGC1) deficiency is an ultra-rare genetic disease characterized by global hypomyelination and brain atrophy, caused by mutations in the SLC25A12 gene leading to a reduction in AGC1 activity. In both neuronal precursor cells and oligodendrocytes precursor cells (NPCs and OPCs), the AGC1 determines reduced proliferation with an accelerated differentiation of OPCs, both associated with gene expression dysregulation. Epigenetic regulation of gene expression through histone acetylation plays a crucial role in the proliferation/differentiation of both NPCs and OPCs and is modulated by mitochondrial metabolism. In AGC1 deficiency models, both OPCs and NPCs show an altered expression of transcription factors involved in the proliferation/differentiation of brain precursor cells (BPCs) as well as a reduction in histone acetylation with a parallel alteration in the expression and activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs). In this study, histone acetylation dysfunctions have been dissected in in vitro models of AGC1 deficiency OPCs (Oli-Neu cells) and NPCs (neurospheres), in physiological conditions and following pharmacological treatments. The inhibition of HATs by curcumin arrests the proliferation of OPCs leading to their differentiation, while the inhibition of HDACs by suberanilohydroxamic acid (SAHA) has only a limited effect on proliferation, but it significantly stimulates the differentiation of OPCs. In NPCs, both treatments determine an alteration in the commitment toward glial cells. These data contribute to clarifying the molecular and epigenetic mechanisms regulating the proliferation/differentiation of OPCs and NPCs. This will help to identify potential targets for new therapeutic approaches that are able to increase the OPCs pool and to sustain their differentiation toward oligodendrocytes and to myelination/remyelination processes in AGC1 deficiency, as well as in other white matter neuropathologies

Deficiency of mitochondrial aspartate-glutamate carrier 1 leads to oligodendrocyte precursor cell proliferation defects both in vitro and in vivo

Aspartate-Glutamate Carrier 1 (AGC1) deficiency is a rare neurological disease caused by mutations in the solute carrier family 25, member 12 (SLC25A12) gene, encoding for the mitochondrial aspartate-glutamate carrier isoform 1 (AGC1), a component of the malate-aspartate NADH shuttle (MAS), expressed in excitable tissues only. AGC1 deficiency patients are children showing severe hypotonia, arrested psychomotor development, seizures and global hypomyelination. While the effect of AGC1 deficiency in neurons and neuronal function has been deeply studied, little is known about oligodendrocytes and their precursors, the brain cells involved in myelination. Here we studied the effect of AGC1 down-regulation on oligodendrocyte precursor cells (OPCs), using both in vitro and in vivo mouse disease models. In the cell model, we showed that a reduced expression of AGC1 induces a deficit of OPC proliferation leading to their spontaneous and precocious differentiation into oligodendrocytes. Interestingly, this effect seems to be related to a dysregulation in the expression of trophic factors and receptors involved in OPC proliferation/differentiation, such as Platelet-Derived Growth Factor α (PDGFα) and Transforming Growth Factor βs (TGFβs). We also confirmed the OPC reduction in vivo in AGC1-deficent mice, as well as a proliferation deficit in neurospheres from the Subventricular Zone (SVZ) of these animals, thus indicating that AGC1 reduction could affect the proliferation of different brain precursor cells. These data clearly show that AGC1 impairment alters myelination not only by acting on N-acetyl-aspartate production in neurons but also on OPC proliferation and suggest new potential therapeutic targets for the treatment of AGC1 deficiency