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#34525443   2021/04/27 To Up

Phosphorus equivalency of phytase with various evaluation indicators of meat duck.

The objective of the present experiment was to determine the efficacy and the phosphorus (P) equivalency of phytase in the corn-soybean meal-rapeseed meal diets of Cherry Valley ducks from 1 to 35 d of age. 320 ducks were randomly divided into 8 blocks of 5 cages with 8 ducks per cage. This experiment included eight treatments diets. The available P levels of I to IV treatments were respectively 0.25%, 0.32%, 0.39%, 0.46% (d 1-14) and 0.20%, 0.27%, 0.34%, 0.41% (d 15-35). And 4 levels of phytase added to low-P basal diet (treatment I) with 300, 600, 900, and 1,200 U/kg (treatment V to VIII). Among them, treatment IV was a P-adequate positive control, treatment I was a low-P negative control. The ratio of calcium (Ca) to P was 1.3:1 for all diets. The other nutritional indexes in all diets were basically the same. Ducks were provided ad libitum access to water and experimental diets. The negative control diet reduced (P < 0.05) body weight, carcase weight, eviscerated weigh, breast muscle weight, leg muscle weight, bone ash, tibia Ca and tibia P, and increasing levels of available P and supplementary phytase significantly (P < 0.05) improved the growth performance and slaughtering performance of meat ducks. Phytase supplementation at a dose of 900 U/kg in the low-P basal diet increased the growth performance of ducks to a level comparable to that of a P-adequate diet. The available P level of 0.39% (1-14 d) and 0.34% (15-35 d) could meet the nutritional needs of meat ducks for P, and the apparent P utilization rate was high, and the effective utilization effect of P was the best. In addition, with the evaluation indexes of feed intake, body weight gain, tibia ash, tibia Ca, tibia P, content of blood Ca and P, the addition of 500 U/kg phytase could release available P of 0.02%, 0.02%, 0.02%, 0.02%, 0.01%, 0.04%, and 0.03%, respectively. In the same way, the addition of 1,000 U/kg phytase could release available phosphorus of 0.14%, 0.04%, 0.04%, 0.05%, 0.02%, 0.12%, and 0.01%, respectively.
Yan Wu, Shujing Xu, Xinhui Wang, Hongyang Xu, Peiyao Liu, Xiaoguang Xing, Zhili Qi

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#34525415   2021/09/12 To Up

Exposure to hydroxyapatite nanoparticles enhances Toll-like Receptor 4 signal transduction and overcomes endotoxin tolerance in vitro and in vivo.

Emerging studies indicate hydroxyapatite nanoparticles (HANPs) exhibit modest immunogenicity to elicit innate immune response which might involve Toll-like receptor 4 (TLR4) activation. This study was proposed to elucidate how HANPs direct over TLR4 signal activity in macrophage in response to TLR4 ligand, lipopolysaccharide (LPS). The present study for the first time reveals that HANPs themselves can induce TLR4 endocytosis and activate pathways both of nuclear factor-kappa B (NF-κB) and interferon regulatory factor 3 (IRF3), which potentially trigger the production of inflammatory cytokine by macrophage. Further, HANPs dose-dependently reprogram over LPS driven TLR4 signaling transduction in macrophage, leading to synergistically augmented innate immune response. In particular, HANPs synergize with LPS to promote macrophage polarization toward M1 phenotype. Moreover, HANPs abrogate the endotoxin tolerance in macrophages by restoring the production of inflammatory cytokines from macrophage in response to secondary LPS stimulation, and enhance the responsiveness of the body to LPS re-challenge in the endotoxin tolerance mice model. Therefore, this study sheds a new light on the mechanism by which HANPs drive the innate immune response, and offers a powerful strategy to potentiate LPS mediated TLR4 signaling activation in macrophage. STATEMENT OF SIGNIFICANCE: In recent years, increasing attention has been given to hydroxyapatite nanoparticles (HANPs) on how they interact with immune cells for achieving appropriate biological effect such as bone tissue repair, soft tissue filler, tumor treatment, vaccine delivery, et al. This study indicated HANPs can induce TLR4 signaling activation. In the further, HANPs dose-dependently synergize with LPS to program over LPS induced TLR4 signaling transduction in macrophage, to favor macrophage polarizing toward M1 phenotype, as well as to abrogate immune tolerance in macrophage in response to repeated LPS stimulation. This work opens a window for the intrinsic mechanism of HANPs to drive immune response and facilitate to direct the rational use or design of HANPs for their better biomedical application.
Yuchen Hua, Jinjie Wu, Hongfeng Wu, Cheng Su, Xiangfeng Li, Qiang Ao, Qin Zeng, Xiangdong Zhu, Xingdong Zhang

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#34525248   2021/09/15 To Up

Disruption of the circadian rhythms and its relationship with pediatric obesity.

The circadian clock system is an evolutionarily conserved system by which organisms adapt their metabolic activities to environmental inputs, including nutrient availability. The disruption of this system has been pathogenically linked to the disintegration of metabolic homeostasis, leading to the development of metabolic complications, including obesity. Lifestyle factors that disrupt this system have recently been emerging and associated with the development of obesity, which is most evidenced by the finding that shift workers are at an increased risk of developing various disorders, such as obesity and obesity-related complications. Lifestyle factors that contribute to a misalignment between the internal clock system and environmental rhythms have also been identified in the pediatric field. A short sleep duration and breakfast skipping are prevalent in children and there is mounting evidence that these lifestyle factors are associated with an increased risk of pediatric obesity; however, the underlying mechanisms have not yet been elucidated in detail. Our current understanding of the impact of lifestyle factors that cause a misalignment between the internal clock system and environmental rhythms on the development of pediatric obesity is summarized herein with a discussion of potential mechanistic insights.
Masanobu Kawai

2041 related Products with: Disruption of the circadian rhythms and its relationship with pediatric obesity.

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#34525226   2021/09/15 To Up

Naringin promotes osteogenesis and ameliorates osteoporosis development by targeting JAK2/STAT3 signaling.

Osteoporosis is a systemic bone metabolism disorder, which increases the risk of fractures, and in severe cases it may cause disability or even death. An important factor contributing to osteoporosis is the imbalance between bone formation and resorption. Naringin was reported to promote osteoblast differentiation, thus enhancing bone formation and alleviating osteoporosis development. However, the signaling pathways related to the regulatory mechanism of naringin in osteoporosis development are not clear. Proliferation of bone mesenchymal stem cells (BMSCs) treated with naringin in vitro was detected by CCK-8. An osteogenesis differentiation medium supplemented with naringin was applied to explore the effects of naringin on BMSC osteogenic differentiation, as detected by Alizarin red staining. Ovariectomy (OVX)-induced postmenopausal osteoporosis (PMOP) rats were orally administered with naringin. Dual-energy X-ray absorptiometry (DEXA) and micro-CT were applied to measure bone mineral density (BMD), bone volume/total volume (BV/TV), trabecula thickness (Tb.Th), trabecula number (Tb.N), trabecular separation (Tb.Sp) and bone surface/bone volume (BS/BV). H&E staining was performed to show pathological changes of the femur in PMOP rats after naringin treatment. Bone metabolism indicators were assessed by ELISA. We found that naringin suppressed the activation of the JAK2/STAT3 pathway. Naringin promoted BMSC proliferation and osteogenic differentiation. Furthermore, naringin alleviates bone loss and improves abnormal bone metabolism of PMOP rats. Collectively, naringin promotes BMSC osteogenic differentiation to ameliorate osteoporosis development by targeting JAK2/STAT3 signaling.
Wang Wang, Jie Mao, Yan Chen, Lin Chen, Jing Zuo, Yajing Li, Yingqian Gao, Qibin Lu

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#34525208   2021/09/15 To Up

Observation of Unique Circulating miRNA Signatures in Non-Human Primates Exposed to Total-Body vs. Whole Thorax Lung Irradiation.

A radiological/nuclear (RAD-NUC) incident, especially in an urban setting, results in diverse radiation-induced injuries due to heterogeneities in dose, the extent of partial-body shielding, human biodiversity and pre-existing health conditions. For example, acute radiation syndrome (ARS) can result in death within days to weeks of exposure to 0.7-10 Gy doses and is associated with destruction of the bone marrow, known as hematopoietic ARS (H-ARS). However, partial-body shielding that spares a portion of the bone marrow from exposure can significantly reduce the occurrence of H-ARS, but delayed effects of acute radiation exposure (DEARE) can still occur within months or years after exposure depending on the individual. In a mass casualty event, ideal triage must be able to pre-symptomatically identify individuals likely to develop radiation-induced injuries and provide an appropriate treatment plan. Today, while there are FDA approved treatments for hematopoietic ARS, there are no approved diagnosis for radiation injury and no approved treatments for the broad spectra of injuries associated with radiation. This has resulted in a major capability gap in the nations preparedness to a potentially catastrophic RAD-NUC event. Circulating microRNA (miRNA) are a promising class of biomarkers for this application because the molecules are accessible via a routine blood draw and are excreted by various tissues throughout the body. To test if miRNA can be used to predict distinct tissue-specific radiation-induced injuries, we compared the changes to the circulating miRNA profiles after total-body irradiation (TBI) and whole thorax lung irradiation (WTLI) in non-human primates at doses designed to induce ARS (day 2 postirradiation; 2-6.5 Gy) and DEARE (day 15 postirradiation; 9.8 or 10.7 Gy), respectively. In both models, miRNA sequences were identified that correlated with the onset of severe neutropenia (counts <500 μL-1; TBI) or survival (WTLI). This method identified panels of eleven miRNA for both model and assigned functional roles for the panel members using gene ontology enrichment analysis. A common signature of radiation-induced injury was observed in both models: apoptosis, DNA damage repair, p53 signaling, pro-inflammatory response, and growth factor/cytokine signaling pathways were predicted to be disrupted. In addition, injury-specific pathways were identified. In TBI, pathways associated with ubiquitination, specifically of histone H2A, were enriched, suggesting more impact to DNA damage repair mechanisms and apoptosis. In WTLI, pro-fibrotic pathways including transforming growth factor (TGF-β) and bone morphogenetic protein (BMP) signaling pathways were enriched, consistent with the onset of late lung injury. These results suggest that miRNA may indeed be able to predict the onset of distinct types of radiation-induced injuries.
Claude J Rogers, Espoir M Kyubwa, Agnes I Lukaszewicz, Mark A Starbird, Michelle Nguyen, Ben T Copeland, Jason Yamada-Hanff, Naresh Menon

1948 related Products with: Observation of Unique Circulating miRNA Signatures in Non-Human Primates Exposed to Total-Body vs. Whole Thorax Lung Irradiation.

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#34525198   2021/09/15 To Up

IL-1 Mediates Microbiome-Induced Inflamm-Ageing of Hematopoietic Stem Cells in Mice.

Ageing is associated with impaired hematopoietic and immune function. This is caused in part by decreased hematopoietic stem cell (HSC) population fitness and an increased myeloid differentiation bias. The reasons for this aging-associated HSC impairment are incompletely understood. We here demonstrate that aged specific pathogen free (SPF) wild-type mice in contrast to young SPF mice produce more IL-1a/b in steady-state bone marrow (BM), with most of IL-1a/b being derived from myeloid BM cells. Further, blood of steady-state aged SPF wild-type mice contains higher levels of microbe associated molecular patterns (MAMPs), specifically TLR4 and TLR8 ligands. Also, BM myeloid cells from aged mice produce more IL-1b in vitro, and aged mice show higher and more durable IL-1a/b responses upon LPS stimulation in vivo. To test if HSC ageing is driven via IL-1a/b, we evaluated HSCs from IL-1 receptor 1 (IL-1R1) knock-out mice. Indeed, aged HSCs from IL-1R1 knock-out mice show significantly mitigated ageing-associated inflammatory signatures. Moreover, HSCs from aged IL-1R1KO and also from germ-free mice maintain unbiased lympho-myeloid hematopoietic differentiation upon transplantation, thus resembling this functionality of young HSCs. Importantly, in vivo antibiotic suppression of microbiota or pharmacologic blockade of IL-1 signaling in aged wild-type mice was similarly sufficient to reverse myeloid biased output of their HSC populations. Collectively, our data defines the microbiome-IL-1/IL-1R1 axis as a key, self-sustaining, but also therapeutically partially reversible driver of HSC inflamm-ageing.
Larisa Vladimirovna Kovtonyuk, Francisco Caiado, Santiago Garcia-Martin, Eva-Maria Manz, Patrick Michael Helbling, Hitoshi Takizawa, Steffen Boettcher, Fatima Al-Shahrour, Cesar Nombela-Arrieta, Emma Slack, Markus G Manz

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#34525188   2021/09/15 To Up

Long-term outcomes in severe aplastic anemia patients treated with immunosuppression and eltrombopag: a phase 2 study.

Patients with severe aplastic anemia (SAA) are either treated with bone marrow transplant (BMT) or immunosuppression (IST) depending on their age, comorbidities, and available donors. In 2017, our phase 2 trial reported improved hematologic responses with the addition of eltrombopag (EPAG) to standard IST for SAA when compared to a historical cohort treated with IST alone. However, the rates and characteristics of long-term complications, relapse, and clonal evolution, previously described in patients treated with IST alone are not yet known with this new regimen, IST and EPAG. Patients were accrued from 2012 to 2020 with a total of 178 subjects included in this secondary endpoint analysis. With double the sample size and a much longer median follow-up (4 years) since the original report in 2017, we report a cumulative relapse rate of 39% in responding patients who received CSA maintenance, and clonal evolution of 15% in all treated patients at 4 years. Relapse occurred at distinct timepoints: after cyclosporine dose reduction and EPAG discontinuation at six months, and after two years when cyclosporine was discontinued. Most relapsed patients were retreated with therapeutic doses of cyclosporine +/- EPAG, and two-thirds responded. Clonal evolution to a myeloid malignancy or chromosome 7 abnormality (high-risk) was noted in 5.7% of patients and conferred a poorer overall survival. Neither relapse nor high-risk evolution occurred at a higher rate than was observed in a historical comparator cohort but the median time to both events were earlier in IST and EPAG treated patients. Trial registered in (NCT01623167).
Bhavisha A Patel, Emma M Groarke, Jennifer Lotter, Ruba N Shalhoub, Fernanda Gutierrez-Rodrigues, Olga Julia Rios, Diego Quinones Raffo, Colin O Wu, Neal S Young

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#34525183   2021/09/15 To Up

Characterization of HLH-Like Manifestations as a CRS Variant in Patients Receiving CD22 CAR T-Cells.

CAR T-cell toxicities resembling hemophagocytic lymphohistiocytosis (HLH) occur in a subset of patients with cytokine release syndrome (CRS). As a variant of conventional CRS, a comprehensive characterization of CAR T-cell associated HLH (carHLH) and investigations into associated risk factors are lacking. In the context of 59 patients infused with CD22 CAR T-cells where a substantial proportion developed carHLH, we comprehensively describe the manifestations and timing of carHLH as a CRS variant and explore factors associated with this clinical profile. Amongst 52 subjects with CRS, 21 (40.4%) developed carHLH. Clinical features of carHLH included hyperferritinemia, hypertriglyceridemia, hypofibrinogenemia, coagulopathy, hepatic transaminitis, hyperbilirubinemia, severe neutropenia, elevated lactate dehydrogenase and occasionally hemophagocytosis. Development of carHLH was associated with pre-infusion NK-cell lymphopenia and higher bone marrow T/NK-cell ratio, which was further amplified with CAR T-cell expansion. Following CRS, more robust CAR T-cell and CD8 T-cell expansion in concert with pronounced NK-cell lymphopenia amplified pre-infusion differences in those with carHLH without evidence for defects in NK-cell mediated cytotoxicity. CarHLH was further characterized by persistent elevation of HLH-associated inflammatory cytokines, which contrasted with declining levels in those without carHLH. In the setting of CAR T-cell mediated expansion, clinical manifestations and immunophenotypic profiling in those with carHLH overlap with features of secondary HLH, prompting consideration of an alternative framework for identification and management of this toxicity profile to optimize outcomes following CAR T-cell infusion.
Daniel A Lichtenstein, Fiorella Schischlik, Lipei Shao, Seth M Steinberg, Bonnie Yates, Hao-Wei Wang, Yanyu Wang, Jon Inglefield, Alina Dulau Florea, Francesco Ceppi, Leandro C Hermida, Kate Stringaris, Kim Dunham, Philip John Homan, Parthav Jailwala, Justin Mateen Mirazee, Welles Robinson, Karen Chisholm, Constance M Yuan, Maryalice Stetler-Stevenson, Amanda K Ombrello, Jianjian Jin, Terry J Fry, Naomi Taylor, Steven L Highfill, Ping Jin, Rebecca A Gardner, Haneen Shalabi, Eytan Ruppin, David F Stroncek, Nirali N Shah

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