The effects of crossbreed and of RN phenotype on pork and its eating quality were evaluated in four different pig crossbreeds [involving Swedish Landrace (L) × Yorkshire (Y) sows and Hampshire (H), Duroc (D), Yorkshire (Y) or Hampshire × Yorkshire (HY) as the terminal sire]. Pigs from the LYH crossbreed were also classified as either carriers or non-carriers of the RN(-) allele. In the crossbreeds investigated, M. longissimus dorsi (LD) and M. semimembranosus (SM) from LYH were found to have the lowest pH as measured 24h post-mortem (pH(24h)). The low pH in the LYH crossbreed was due to the large proportion of RN(-) carriers it had (approximately 70%). The non-carriers of the RN(-) allele in the LYH crossbreed had a pH(24h) close to that of LYD, LYY and LYHY. In a selected group of pigs (N=50), the ultimate pH in the ham muscles M. biceps femoris (BF), M. quadriceps femoris (QF), M. gluteus medius (GM) and M. semitendinosus (ST) was also found to be lower in RN(-) carriers of LYH than in the other crossbreeds. As determined visually, LYD had the highest frequency (2%) of pale, soft and exudative meat (PSE), in LD. Ham from RN(-) carriers of LYH had the highest frequency (23%) of PSE meat around the femur, indicating that when the pH is low, the deep musculature, in which the chilling rate can be slow, is particularly sensitive to the development of PSE. According to assessments by members of a trained sensory panel, tenderness was significantly greater in LD from carriers of the RN(-) allele in LYH than in LD from LYD, LYHY and non-carriers of LYH. The tenderness of LD from LYY was rated as intermediate. The intramuscular fat content was found to be highest in LD from LYD, no relationship between intramuscular fat content and tenderness being found. The RN(-) carriers of LYH received the highest ratings in terms of juiciness. In conclusion, the sensory ratings demonstrated the great eating quality of LD from carriers of the RN(-) allele, indicating that abandoning the Hampshire crossbreed or eliminating the RN(-) allele from it, would result in the meat being less tender.
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http://dx.doi.org/10.1016/S0309-1740(02)00268-1 | DOI Listing |
Cancer Med
December 2024
Niguarda Hospital, Department of Hematology and Oncology, Milano, Italy.
Background: Despite recurrent and activating mutations, including MYD88, CXCR4, ARID1A, KMT2D, and CD79B were identified, the genetic basis for Waldenström's Macroglobulinemia (WM) and the risk of progression of IgM MGUS to WM remain to be fully elucidated.
Methods: We investigated the mutation status of WM (n = 8), sWM (n = 7), and IgM MGUS (n = 5) patients, by performing high-throughput targeted AmpliSeq NGS on 117 target genes. Specifically, we analyzed the CD19+ cells from 15 WM/sWM patients and five IgM MGUS patients.
Sci Rep
November 2024
Center of Oncology Research, Federal University of Pará (UFPA), Belém, 66073- 005, PA, Brazil.
Despite all the efforts acquired in four years of the COVID-19 pandemic, the path to a full understanding of the biological mechanisms involved in this disease remains complex. This is partly due to a combination of factors, including the inherent characteristics of the infection, socio-environmental elements, and the variations observed within both the viral and the human genomes. Thus, this study aimed to investigate the correlation between genetic host factors and the severity of COVID-19.
View Article and Find Full Text PDFClin Epigenetics
October 2024
Genomic Medicine Laboratory UILDM, IRCCS Santa Lucia Foundation, Via Ardeatina 306-354, 00179, Rome, Italy.
medRxiv
October 2024
Department of Medicine, Division of Nephrology, Columbia University, College of Physicians & Surgeons, New York, NY, USA.
Proc Natl Acad Sci U S A
October 2024
Division of Molecular and Cellular Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215.
Loss-of-function germline () tumor suppressor mutations cause VHL disease, which predisposes individuals to kidney cancer, hemangioblastomas, and paragangliomas. The risk that a given VHL disease family will manifest some or all these tumor types is profoundly influenced by the allele it carries. For example, almost all VHL disease families that develop paraganglioma have missense mutations.
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