The objective of the existing investigation was to determine the effect of dietary inclusion of threonine amino acid at different levels during feed restriction on growth indices, liver and kidney function parameters, and some hormonal profiles along with economic indicators in broiler chickens. A total of 1,600 from 2 different breeds (800 Ross 308 and 800 Indian River) at 21-day-old age were incorporated. Chicks were randomly assigned into 2 main groups, control and feed-restricted (8 h/d), during the fourth week of age. Each main group was subdivided into 4 groups. The first group was fed a basal diet without adding extra threonine (100%), the second, third, and fourth groups were fed a basal diet with extra threonine levels of 110, 120, and 130%, respectively. Each subgroup consisted of 10 replicates of 10 birds. We noticed that the dietary inclusion of threonine at extra levels in the basal diets significantly enhanced final body weight, body weight gain, and better feed conversion ratio. This was mainly due to the enhanced levels of growth hormone (GH), insulin-like growth factor (IGF1), triiodothyronine (T3), and thyroxine (T4). Moreover, the lowest feed cost per kilogram body weight gain and improved return parameters were reported in control and feed-restricted birds fed higher levels of threonine than other groups. Also, a significant increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and urea levels was observed in feed-restricted birds supplemented with 120 and 130% levels of threonine. Hence, we recommend supplementing threonine at levels of 120 and 130% in the diet of broilers to promote growth and profitability.
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http://dx.doi.org/10.1016/j.psj.2023.102796 | DOI Listing |
We describe a new release of the PeptideAtlas proteomics spectral resource (build 2024-03), providing a sequence coverage of 79.5% at the canonical protein level, matched mass spectrometry spectra, and experimental evidence identifying 3382 and 536 phosphorylated serine and threonine sites with false localization rates of 1% and 5.3%, respectively.
View Article and Find Full Text PDFOrphanet J Rare Dis
January 2025
Division of Pediatric Epileptology, Department of Pediatrics I, Medical Faculty of Heidelberg, Heidelberg University, Heidelberg, Germany.
Background: Tuberous sclerosis complex (TSC) is an autosomal dominant genetic disorder affecting multiple organ systems, with a prevalence of 1:6,760-1:13,520 live births in Germany. On the molecular level, TSC is caused by heterozygous loss-of-function variants in either of the genes TSC1 or TSC2, encoding the Tuberin-Hamartin complex, which acts as a critical upstream suppressor of the mammalian target of rapamycin (mTOR), a key signaling pathway controlling cellular growth and metabolism. Despite the therapeutic success of mTOR inhibition in treating TSC-associated manifestations, studies with mTOR inhibitors in children with TSC above two years of age have failed to demonstrate beneficial effects on disease-related neuropsychological deficits.
View Article and Find Full Text PDFAlzheimers Res Ther
January 2025
Center for Cognitive and Computational Neuroscience, Complutense University of Madrid, Pozuelo de Alarcón, 28223, Spain.
Background: Changes in amyloid beta (Aβ) and phosphorylated tau brain levels are known to affect brain network organization but very little is known about how plasma markers can relate to these measures. We aimed to address the relationship between centrality network changes and two plasma pathology markers: phosphorylated tau at threonine 231 (p-tau231), a proxy for early Aβ change, and neurofilament light chain (Nfl), a marker of axonal degeneration.
Methods: One hundred and four cognitively unimpaired individuals were divided into a high pathology load (33 individuals; HP) group and a low pathology (71 individuals; LP) one.
Cardiovasc Diabetol
January 2025
Department of Clinical Pharmacy, School of Preclinical Medicine and Clinical Pharmacy, China Pharmaceutical University, 24 Tong jia Lane, Nanjing, 210009, People's Republic of China.
Background: Inflammatory diseases impair the reparative properties of endothelial progenitor cells (EPC); however, the involvement of diabetes in EPC dysfunction associated with myocardial infarction (MI) remains unknown.
Methods: A model was established combining high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mice with myocardial infarction. The therapeutic effects of transplanted wild-type EPC, Nlrp3 knockout EPC, and Nlrp3 overexpression EPC were evaluated.
Cell Commun Signal
January 2025
School of Medicine, Southeast University, Nanjing, Jiangsu, China.
Tribbles homolog 2 (TRIB2), a pseudoserine/threonine kinase, is a member of the TRIB family. TRIB2 primarily regulates cell proliferation through its scaffold or adaptor effect on promoting the degradation of target proteins by E3 ligase-dependent ubiquitination and regulating mitogen-activated protein kinase (MAPK) and protein kinase B (AKT) signaling pathways. TRIB2 is not only involved in the physiological proliferation of cells (granulosa cells, myoblasts, naive T cells, and thymocytes) during normal development but also in the pathological proliferation of vascular smooth muscle cells and a variety of cancer cells (lung cancer cells, liver cancer cells, leukemia cells, pancreatic cancer cells, gastric cancer cells, prostate cancer cells, thyroid cancer cells, cervical cancer cells, melanoma cells, colorectal cancer cells, ovarian cancer cells and osteosarcoma cells) under disease conditions.
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