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Abstract Initial research indicates a possible connection between exposure to phthalates and the development of anemia. To fill the gap in epidemiological data, our study utilized data from across the United States, representative on a national scale, to evaluate the association between the concentration of phthalate metabolites in urine and both anemia and iron levels. We gathered data on 11,406 individuals from the National Health and Nutrition Examination Survey (NHANES) database, spanning 2003–2018. We conducted logistic and linear regression analyses, adjusted for potential confounding factors, to evaluate the correlations between different phthalate metabolites and anemia, as well as serum iron levels, including gender-stratified analysis. Most urinary phthalate metabolites were positively correlated with an increased risk of anemia, and the majority were negatively correlated with serum iron levels. The study revealed that for every unit increase in ln-transformed metabolite concentrations, the odds ratios (ORs) for anemia increased to varying degrees, depending on the phthalate: Monobutyl phthalate (MBP) at 1.08 (95% CI 1.01–1.17, P = 0.0314), mono(3-carboxypropyl) phthalate (MCPP) at 1.17 (95% CI 1.10–1.24, P

ABSTRACT: The continuous expansion of intestinal stem cells (ISCs) is crucial for maintaining the renewal of the intestinal epithelium, particularly in inflammatory conditions. It remains largely unknown how the internal microbiota repair damage to the internal mucosal barrier. Hence, investigating potential anti-inflammatory probiotics from the intestinal symbolic microbes of broilers and analyzing their mechanism of action to support the intestinal mucosal barrier function can offer novel regulatory tools to alleviate broiler enteritis. In this research, we utilized in vivo broilers plus ex vivo organoids model to thoroughly examine the effectiveness of Lactobacillus reuteri (LR) in protecting the integrity of the intestinal mucosa during lipopolysaccharide-induced (LPS-induced) enteritis in broilers. The findings indicated that LR feeding maintained intestinal morphological and structural integrity, enhanced proliferation of intestinal epithelial cells, and inhibited cell apoptosis and inflammatory response against the deleterious effects triggered by LPS. Simultaneously, LR enhanced ISCs activity and stimulated intestinal epithelial regeneration to protect the intestinal barrier during LPS-induced injury conditions. The coculture system of LR and ileum organoids revealed that LR increased the growth of organoids and attenuated LPS-stimulated damage to organoids. Furthermore, the LPS-induced decrease in ISC activity was rescued by reactivation of Wnt/β-catenin signaling by LR ex vivo and in vivo. This research revealed that LR promoted the expansion of ISCs and intestinal epithelial cell renewal by regulating the Wnt/β-catenin signaling pathway, thereby maintaining the integrity of the intestinal mucosal barrier. This finding provided theoretical support for lactobacillus as a probiotic additive in livestock feed to improve intestinal inflammation and treat intestinal diseases.

PurposeWhile strengthening exercises are recommended for knee osteoarthritis (KOA) treatment, the optimal type of muscle contraction remains unclear, with current research showing conflicting results. This network meta-analysis (NMA) aims to evaluate the efficacy of lower limb strengthening exercises based on different muscle contraction characteristics for KOA patients and provide clinical references.MethodsWe conducted the NMA following the PRISMA-NMA. A comprehensive search of five databases (PubMed, Web of Science, CENTRAL, Embase, and SPORTDiscus) up to August 2024 identified randomized controlled trials (RCTs) investigating lower limb strengthening exercises in KOA patients. Control groups included receiving usual care, only providing health education, or no intervention at all. Outcomes analyzed included pain, physical function, quality of life, and muscle strength.ResultsForty-one studies (2,251 participants) were included. Twenty-eight studies used rigorous randomization; eighteen reported allocation concealment. All had high performance bias risk due to exercise interventions. Regarding efficacy, isokinetic exercise ranked highest in pain relief (SMD = 0.70, 95% CI: 0.50–0.91, SUCRA = 82.6%), function improvement (SMD = 0.75, 95% CI: 0.57–0.92, SUCRA = 96.1%), and enhancement in muscle strength (SMD = 0.56, 95% CI: 0.34–0.78, SUCRA = 90.1%). Isometric exercise ranked highest in improving quality of life (SMD = 0.80, 95% CI: 0.28–1.31, SUCRA = 90.5%). Mixed strengthening exercise ranked lowest across all outcomes. High-frequency interventions (≥5 times/week) showed superior pain relief compared with low-frequency (≤3 times/week) for isotonic, isometric, and isokinetic exercise.ConclusionThis NMA suggests isokinetic exercise may be most effective for pain, function, and muscle strength in KOA patients, while isometric exercise benefits quality of life most. Mixed strengthening exercise ranked lowest across all outcomes. High-frequency interventions appear more effective than low-frequency ones. These findings support personalized KOA treatment, considering efficacy, accessibility, and patient-specific factors. Study biases, heterogeneity, and other limitations may affect result reliability. Future research should focus on high-quality studies with standardized protocols and analyze dose–response relationships to refine KOA treatment strategies.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024582525, identifier: CRD42024582525.

Abstract Lumpy skin disease virus (LSDV) infection is a major socio-economic issue that seriously threatens the global cattle-farming industry. Here, a recombinant virus LSDV-ΔTK/EGFP, expressing enhanced green fluorescent protein (EGFP), was constructed with a homologous recombination system and applied to the high-throughput screening of antiviral drugs. LSDV-ΔTK/EGFP replicates in various kidney cell lines, consistent with wild-type LSDV. The cytopathic effect, viral particle morphology, and growth performance of LSDV-ΔTK/EGFP are consistent with those of wild-type LSDV. High-throughput screening allowed to identify several molecules that inhibit LSDV-ΔTK/EGFP replication. The strong inhibitory effect of theaflavin on LSDV was identified when 100 antiviral drugs were screened in vitro. An infection time analysis showed that theaflavin plays a role in the entry of LSDV into cells and in subsequent viral replication stages. The development of this recombinant virus will contribute to the development of LSDV-directed antiviral drugs and the study of viral replication and mechanisms of action.

Background and aimsAnemia is a widespread global health concern, and recent research has unveiled a link between anemia and inflammation. The Dietary Inflammation Index (DII) is a novel tool used to assess the overall inflammatory potential of an individual’s diet. However, until now, there have been no studies demonstrating a connection between DII and anemia. This study aimed to explore the relationship between DII and the risk of anemia among Americans, as well as to examine the influence of other risk factors on this association.MethodsData from 32,244 patients were collected from the National Health and Nutrition Examination Survey (NHANES) database spanning from 1999 to 2018. Using multivariable logistic regression, we examined the correlation between DII and anemia. Subgroup analyses and smoothed curve analyses were conducted to further investigate the association between DII and anemia.ResultsThe analysis revealed a significant positive association between higher DII scores and increased anemia risk in the American population (Odds Ratio [OR] = 1.06, 95% Confidence Interval [CI] = 1.03 to 1.09, p

SIRT1 is a highly conserved nicotinamide adenine dinucleotide (NAD+)-dependent histone deacetylase. It is involved in the regulation of various pathophysiological processes, including cell proliferation, survival, differentiation, autophagy, and oxidative stress. Therapeutic activation of SIRT1 protects the heart and cardiomyocytes from pathology-related stress, particularly myocardial ischemia/reperfusion (I/R). Autophagy is an important metabolic pathway for cell survival during energy or nutrient deficiency, hypoxia, or oxidative stress. Autophagy is a double-edged sword in myocardial I/R injury. The activation of autophagy during the ischemic phase removes excess metabolic waste and helps ensure cardiomyocyte survival, whereas excessive autophagy during reperfusion depletes the cellular components and leads to autophagic cell death. Increasing research on I/R injury has indicated that SIRT1 is involved in the process of autophagy and regulates myocardial I/R. SIRT1 regulates autophagy through various pathways, such as the deacetylation of FOXOs, ATGs, and LC3. Recent studies have confirmed that SIRT1-mediated autophagy plays different roles at different stages of myocardial I/R injury. By targeting the mechanism of SIRT1-mediated autophagy at different stages of I/R injury, new small-molecule drugs, miRNA activators, or blockers can be developed. For example, resveratrol, sevoflurane, quercetin, and melatonin in the ischemic stage, coptisine, curcumin, berberine, and some miRNAs during reperfusion, were involved in regulating the SIRT1-autophagy axis, exerting a cardioprotective effect. Here, we summarize the possible mechanisms of autophagy regulation by SIRT1 in myocardial I/R injury and the related molecular drug applications to identify strategies for treating myocardial I/R injury.

This study aimed to investigate the effects of different levels of xylanase supplementation in a wheat-based diet on growth performance, short-chain fatty acids, intestinal health, microbial composition, and serum metabolism. A total of 1200 male chicks were randomly assigned to four wheat-based diet treatments: Group C (adding 0 mg/kg of xylanase), Group L (adding 50 mg/kg of xylanase), Group M (adding 100 mg/kg of xylanase), and Group H (adding 150 mg/kg of xylanase). The experiment lasted for 56 days. The results indicated that Group H broilers experienced a decreased feed-to-gain ratio throughout the study period. Additionally, dietary supplementation with xylanase led to an increase in the physical barrier, as indicated by increased VH and VH/CD in the gut (p < 0.05). Furthermore, levels of D-lactic acid and endotoxin were reduced. Xylanase supplementation also increased the abundance of Muc-2, ZO-1, and Occludin (p < 0.05). Moreover, xylanase supplementation enhanced the activity of sucrase and maltase in the duodenum (p < 0.05), which may be attributable to the upregulation of the abundance of SI and MGA (p < 0.05). Furthermore, xylanase addition promoted propionic acid produced by specific bacteria, such as Phascolarctobacterium, and influenced the microbial composition to some extent, promoting intestinal health. Additionally, 150 mg/kg of xylanase supplementation increased the amino acid, peptide, and carbohydrate content and upregulated the metabolism of amino acids related to histidine, cysteine, methionine, and other pathways (p < 0.05). These findings suggest adequate xylanase supplementation can enhance nutritional digestibility and absorption, improve growth performance, stimulate endogenous enzyme activity, optimize intestinal morphology and barrier function, and positively influence acid-producing bacteria and amino acid metabolic pathways.

Oxidative stress refers to the imbalance between the production of reactive oxygen species (ROS) and the endogenous antioxidant defense system. Its involvement in cell senescence, apoptosis, and series diseases has been demonstrated. Advances in carcinogenic research have revealed oxidative stress as a pivotal pathophysiological pathway in tumorigenesis and to be involved in lung cancer, glioma, hepatocellular carcinoma, leukemia, and so on. This review combs the effects of oxidative stress on tumorigenesis on each phase and cell fate determination, and three features are discussed. Oxidative stress takes part in the processes ranging from tumorigenesis to tumor death via series pathways and processes like mitochondrial stress, endoplasmic reticulum stress, and ferroptosis. It can affect cell fate by engaging in the complex relationships between senescence, death, and cancer. The influence of oxidative stress on tumorigenesis and progression is a multi-stage interlaced process that includes two aspects of promotion and inhibition, with mitochondria as the core of regulation. A deeper and more comprehensive understanding of the effects of oxidative stress on tumorigenesis is conducive to exploring more tumor therapies.

Earlier studies have shown that selenomethionine (SM) supplements in broiler breeders had higher deposition in eggs, further reduced the mortality of chicken embryos, and exerted a stronger antioxidant ability in offspring than sodium selenite (SS). Since previous studies also confirmed that Se deposition in eggs was positively correlated with maternal supplementation, this study aimed to directly investigate the antioxidant activities and underlying mechanisms of SS and SM on the chicken hepatocellular carcinoma cell line (LMH). The cytotoxicity results showed that the safe concentration of SM was up to 1000 ng/mL, while SS was 100 ng/mL. In Se treatments, both SS and SM significantly elevated mRNA stability and the protein synthesis rate of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), two Se-containing antioxidant enzymes. Furthermore, SM exerted protective effects in the H2O2-induced oxidant stress model by reducing free radicals (including ROS, MDA, and NO) and elevating the activities of antioxidative enzymes, which performed better than SS. Furthermore, the results showed that cotreatment with SM significantly induced apoptosis induced by H2O2 on elevating the content of Bcl-2 and decreasing caspase-3. Moreover, investigations of the mechanism revealed that SM might exert antioxidant effects on H2O2-induced LMHs by activating the Nrf2 pathway and enhancing the activities of major antioxidant selenoenzymes downstream. These findings provide evidence for the effectiveness of SM on ameliorating H2O2-induced oxidative impairment and suggest SM has the potential to be used in the prevention or adjuvant treatment of oxidative-related impairment in poultry feeds.

ObjectiveIn the treatment of cervical spondylotic radiculopathy (CSR), spinal endoscopy has been developed vigorously in the past 30 years. However, its effectiveness and subsequent problem of cervical spine stability have always been the controversial hotspots. This study aims to conduct a retrospective study using posterior cervical full-endoscopic technique for the treatment of CSR with foraminal bony stenosis, and evaluate its clinical effect and application value.MethodsAll 22 patients treated for CSR with foraminal bony stenosis using posterior cervical full-endoscopic technique were analyzed since Dec 1, 2016, to Apr 30, 2020. The data collection included operation time, length of stay, wound healing, surgical complications, visual analog scale (VAS), Japanese Orthopaedic Association (JOA) scores, intervertebral foramen diameter, intervertebral foramen area and cervical instability. The relevant indicators were observed on admission, at postoperative 1 week and 3 months, and at the last follow-up.ResultsThe operation time was 141.6 ± 13.7 min. The length of stay was 6.0 ± 2.5 days. VAS and JOA at different time points after operation were decreased compared with before operation (p 0.05). The height, anteroposterior diameter and area of intervertebral foramen after operation were significantly increased compared with before operation (p

Hypoxic training improves the microcirculation function of human skeletal muscle, but its mechanism is still unclear. Silent information regulator 2 homolog 3 (Sirt3) can improve mitochondrial function and oxidative status. We aimed to examine the role of Sirt3 in the process of hypoxic training, which affects skeletal muscle microcirculation. C57BL/6 mice were assigned to control (C), hypoxic training (HT), Sirt3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP), and 3-TYP + hypoxic training (3-TYP + HT) groups (n = 6/group). Sirt3 inhibition was induced by intraperitoneal injection of Sirt3 inhibitor 3-TYP. After 6 weeks of intervention, microcirculatory capillary formation and vasomotor capacity were evaluated using immunofluorescence, Western blot, biochemical tests, and transmission electron microscopy (TEM). Laser Doppler flowmetry was used to evaluate skeletal muscle microcirculation blood flow characteristics. Six weeks of hypoxic training enhanced skeletal muscle microcirculation function and increased microcirculatory vasodilation capacity and capillary formation. After the pharmacological inhibition of Sirt3, the reserve capacity of skeletal muscle microcirculation was reduced to varying degrees. After the inhibition of Sirt3, mice completed the same hypoxic training, and we failed to observe the microcirculation function adaptation like that observed in hypoxic training alone. The microcirculation vasodilation and the capillaries number did not improve. Hypoxic training improved skeletal muscle microcirculation vasodilation capacity and increased skeletal muscle microcirculation capillary density. Sirt3 is involved in the adaptation of skeletal muscle microcirculation induced by hypoxic training.

Objective: Traditional Mongolian Medicine Qiqirigan-8 (MMQ-8) is a Chinese botanical drug with effective pharmacological properties in obesity. However, the pharmacological mechanism of MMQ-8 remains unclear. This study aimed to determine the active metabolites of MMQ-8 and its therapeutic effects on lipid metabolism and inflammation.Methods: The active metabolites of MMQ-8 were identified by ultrahigh-performance liquid chromatograph Q extractive mass spectrometry (UHPLC-QE-MS) assay and network analysis. An obesity rat model induced by high-fat diet was used in the study. Serum levels of lipids and inflammatory factors were detected using biochemical analysis and enzyme-linked immunosorbent assay (ELISA). Pathological analysis of liver tissues and arteries was conducted with hematoxylin and eosin (H&E) staining and immunohistochemistry. Protein expression of the tumor necrosis factor (TNF) signaling pathway was investigated by Western-blot. Simultaneously, bone marrow cells were used for RNA sequencing and relevant results were validated by cell culture and quantitative real-time polymerase chain reaction (RT-qPCR).Results: We identified 69 active metabolites and 551 target genes of MMQ-8. Of these, there are 65 active metabolites and 225 target genes closely related to obesity and inflammation. In vivo, we observed that MMQ-8 had general decreasing effects on body weight, white adipose tissue weight, and serum lipids. MMQ-8 treatment notably decreased the liver function markers and hepatic steatosis, and significantly decreased inflammation. In serum, it notably decreased TNF-α, interleukin (IL)-6, and inducible nitric oxide synthase (INOS), while elevating IL-10 levels. MMQ-8 treatment also significantly inhibited proteins phosphorylation of nuclear factor-kappa B inhibitor alpha (IκBα), mitogen-activated protein kinase (p38), extracellular regulated kinase 1/2(ERK1/2), and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and decreased vascular endothelium damage and macrophage infiltration and polarization to M1. These findings coincide with the RNA-sequencing data of bone marrow cells and results of in vitro experiments.Conclusion: We determined the pharmacological actions and relevant metabolites of MMQ-8 in obesity for the first time. Our study revealed MMQ-8 can optimize lipid metabolism and reduce chronic inflammation in obesity. However, more in-depth research is needed, for example, to understand the principle of compound compatibility and the inhibition effects on hepatic steatosis, T cell differentiation, and inflammatory signal transduction.

We aimed to investigate the effects of dietary supplementation with gallus epidermal growth factor (gEGF) from chicken embryos on growth performance, immunity, and intestinal morphology in broilers. 480 1-day-old AA broilers were randomly divided into 5 groups with 6 replicates of 16 chicks each. The control group was fed basal diet and other treatment diets were supplemented with 4, 6, 8, 12 ng/kg gEGF, respectively. The whole experiment lasted for 42 d. Broilers were harvested at the end of the experiment, and spleen, thymus, bursa, serum samples and small intestine were collected. Results showed that average daily growth (ADG) of 1–21d at the 4, 6 and 12 ng/kg groups were significantly increased (p

The aim of this study was to evaluate the impacts of dietary phytosterol (PS) addition at different levels on serum parameters, nutrient digestibility and digestive enzyme activities of white feather broilers. A total of 600, 1-day-old male broilers were randomly divided into five groups with six replicates and were fed a basal diet supplemented with 0 (control group), 10, 20, 40, or 80 mg PS/kg for 42 days. The results showed that dietary supplementation with PS at 20 and 40 mg/kg decreased malondialdehyde accumulation and increased glutathione peroxidase concentrations compared with the control group (p

The current study investigated the effects of the maternal Zn source in conjunction with their offspring’s dietary Zn supplementation on the growth performance, antioxidant status, Zn concentration, and immune function of the offspring. It also explored whether there is an interaction between maternal Zn and their offspring’s dietary Zn. One-day-old Lingnan Yellow-feathered broilers (n = 800) were completely randomized (n = 4) between two maternal dietary supplemental Zn sources [maternal Zn–Gly (oZn) vs. maternal ZnSO4 (iZn)] × two offspring dietary supplemental Zn doses [Zn-unsupplemented control diet (CON), the control diet + 80 mg of Zn/kg of diet as ZnSO4]. oZn increased progeny ADG and decreased offspring mortality across all periods, especially during the late periods (p < 0.05). The offspring diet supplemented with Zn significantly improved ADG and decreased offspring mortality over the whole period compared with the CON group (p < 0.05). There were significant interactions between the maternal Zn source and offspring dietary Zn with regards to progeny mortality during the late phase and across all phases as a whole (p < 0.05). Compared with the iZn group, the oZn treatment significantly increased progeny liver and serum Zn concentrations; antioxidant capacity in the liver, muscle, and serum; and the IgM concentration in serum; while also decreasing progeny serum IL-1 and TNF-α cytokine secretions (p < 0.05). Similar results were observed when the offspring diet was supplemented with Zn compared with the CON group; moreover, adding Zn to the offspring diet alleviated progeny stress by decreasing corticosterone levels in the serum when compared to the CON group (p < 0.05). In conclusion, maternal Zn–Gly supplementation increased progeny performance and decreased progeny mortality and stress by increasing progeny Zn concentration, antioxidant capacity, and immune function compared with the same Zn levels from ZnSO4. Simultaneously, Zn supplementation in the progeny’s diet is necessary for the growth of broilers.

Reuterin is well-known for its broad-spectrum antimicrobial ability, while the other potential bioactivity is not yet clear. The present study aims to investigate the immunomodulatory activity of reuterin on chicken macrophage HD11 cells for the first time and evaluate whether reuterin is able to regulate the lipopolysaccharide-stimulated inflammatory response. The results showed that the safe medication range of reuterin was less than 250 μM. Reuterin treatment for 6 h decreased the transcriptional of CD86, IL-1β and iNOS and increased the expression of CD206 in a dose-dependent way, but reuterin treatment for 12 h contrary increased the expression of IL-1β, IL-6 and IL-10. However, it was noticed that reuterin treatment for 12 h significantly decreased the production of reactive oxygen species (ROS) and suppressed the phagocytosis activity of HD11 macrophages against bacteria. Further, the results showed that preincubation or coincubation with reuterin significantly attenuated the promotive effects of lipopolysaccharide (LPS) on transcription of proinflammatory cytokines (including IL-1β, IL-6 and TNF-α) and obviously inhibited nitric oxide (NO) production as well as the protein expression of inducible nitric oxide synthase (iNOS). Meanwhile, Mechanism studies implied that reuterin might exert an anti-inflammatory effect on LPS-stimulated cells by downregulating the expression of TLR4/MyD88/TRAF6 and blocking the activation of NF-κB as well as MAPKs signaling pathways. Additionally, it was found that both pretreatment and cotreatment with reuterin remarkably inhibited the oxidative stress induced by LPS stimulation by activating the Nrf2/HO-1 signaling pathway and enhancing the activities of antioxidative enzymes. These findings suggested the immunoregulatory function of reuterin and indicated this bacterial metabolite was able to inhibit the inflammation and oxidative stress of HD11 macrophages once exposed to LPS stimulation.

Environmental factors such as high temperature can cause oxidative stress and negatively affect the physiological status and meat quality of broiler chickens. The study was conducted to evaluate the effects of dietary maternal Zn-Gly or ZnSO4 supplementation on embryo mortality, hepatocellular mitochondrial morphology, liver antioxidant capacity and the expression of related genes involved in liver oxidative mechanisms in heat-stressed broilers. A total of 300 36-week-old Lingnan Yellow broiler breeders were randomly divided into three treatments: (1) control (basal diet, 24 mg zinc/kg); (2) inorganic ZnSO4 group (basal diet +80 mg ZnSO4/kg); (3) organic Zn-Gly group (basal diet +80 mg Zn-Gly/kg). The results show that maternal zinc alleviated heat stress-induced chicken embryo hepatocytes’ oxidative stress by decreasing the content of ROS, MDA, PC, 8-OHdG, and levels of HSP70, while enhancing T-SOD, T-AOC, CuZn-SOD, GSH-Px, CTA activities and the content of MT. Maternal zinc alleviated oxidative stress-induced mitochondrial damage in chick embryo hepatocytes by increasing mitochondrial membrane potential and UCP gene expression; and Caspase-3-mediated apoptosis was alleviated by increasing CuZn-SOD and MT gene expression and decreasing Bax gene expression and reducing the activity of caspase 3. Furthermore, maternal zinc treatment significantly increased Nrf2 gene expression. The results above suggest that maternal zinc can activate the Nrf2 signaling pathway in developing chick embryos, enhance its antioxidant function and reduce the apoptosis-effecting enzyme caspase-3 activities, thereby slowing oxidative stress injury and tissue cell apoptosis.

Background: Tamoxifen is one of the medicines for adjuvant endocrine therapy of hormone-dependent breast cancer. However, development of resistance to tamoxifen occurs inevitably during treatment. This study aimed to determine whether sensitivity of tamoxifen-resistant breast cancer cells (TAM-R) could be reinstated by tetrandrine (Tet). Methods: All experiments were conducted in TAM-R cells derived from the MCF-7 breast cancer cell line by long-term tamoxifen exposure. Cell growth, apoptosis, and autophagy were end-points that evaluated the effect of Tet (0.9 μg/ml, 1.8 μg/ml, and 3.75 μg/ml) alone or in combination with TAM (1 μM). Cell apoptosis was determined by an ELISA assay and autophagy was determined by fluorescent staining using the Enzo autophagy detection kit. Immunoblotting was used to evaluate markers for apoptosis, autophagy, and related signal pathway molecules. Results: Growth of TAM-R cells was significantly inhibited by Tet. Combination of Tet with tamoxifen induced a greater inhibition on cell growth than tamoxifen alone, which was predominantly due to enhancement of pro-apoptotic effect of TAM by Tet. Autophagy was significantly inhibited in TAM-R cells treated with Tet plus TAM as shown by increased autophagosomes and the levels of LC3-II and p62. At 0.9 μg/ml, Tet increased the levels of both apoptosis and autophagy markers. Among them increase in p53 levels was more dramatic. Conclusions: Tet as a monotherapy inhibits TAM-R cells. Tet potentiates the pro-apoptotic effect of TAM via inhibition of autophagy.

The present study evaluated the impact of dietary multienzyme complex (MEC) supplementation on growth performance, digestive enzyme activity, histomorphology, serum metabolism and hepatopancreas glycometabolism in snakeheads (Channa argus). A total of 600 fish (initial weight, 69.70 ± 0.30 g) were randomly divided into four groups. Four diets were formulated: (1) control (basic diet); (2) E1 (400 U kg−1 amylase, 150 U kg−1 acid protease, 1900 U kg−1 neutral protease and basic diet); (3) E2 (800 U kg−1 amylase, 300 U kg−1 acid protease, 3800 U kg−1 neutral protease and basic diet); and (4) E3 (1200 U kg−1 amylase, 450 U kg−1 acid protease, 5700 U kg−1 neutral protease and basic diet). The results show that the E2 group increased the specific growth rate, weight gain rate and the final body weight, as well as decreasing the blood urea nitrogen, alanine aminotransferase and triglyceride. The mRNA levels and activities of digestive enzymes and key glucose metabolism enzymes in the hepatopancreas were enhanced in snakeheads fed the MEC. Meanwhile, moderate MEC diet (E2 groups) supplementation improved digestive tract morphology, increased the glycogen in the hepatopancreas and the lipids in the dorsal muscle. Moreover, plasma metabolomics revealed differential metabolites mainly involved in amino acid metabolism. These findings suggest that dietary supplementation with the MEC improved growth performance, digestive tract morphology, gene expression and the activity of digestive enzymes, enhanced the glycolysis-gluconeogenesis and amino acid metabolism of snakeheads, and the optimal composition of the MEC was group E2.

This study investigated the dietary supplementation of tea residue fermented by Bacillus subtilis, Aspergillus niger, and Saccharomyces cerevisiae, to explore its effects on growth performance, digestion performance, meat quality, serum antioxidant capacity, and intestinal morphology in pigs bred for rapid growth, also known as fatteners. One hundred and ninety-two healthy “Duroc × Landrace × Yorkshire” ternary hybrid pigs (body weight 70 ± 1.0 kg) were randomly divided into four groups according to the feeding test requirements, with four replicates in each group, and 12 fatteners per replicate. The control group (CG) was fed the basal diet. Treatments 1 (T1), 2 (T2), and 3 (T3), comprising ratios of 10%, 15%, and 20% of tea residue were added to the basal diet. The test period was 60 days. The results showed that supplementation of FTR in fatteners’ diets increased final body weight (FBW), average daily gain (ADG), and feed conversion ratio (FCR) in the T1 and T2 groups (p < 0.05). Compared with the other groups, the lightness (L*) and pH were significantly affected in the T2 group (p < 0.05). Compared with the CG, dietary supplementation of FTR significantly increased the nutrient digestibility of crude protein (CP), ether extract (EE), calcium (Ca), and phosphorus (P), improved the lipase and trypsin activities, and reduced drip loss and the shear force of fatteners (p < 0.05). Glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) were significantly increased in the T2 and T3 groups compared with the other groups (p < 0.05). Supplementation of FTR in the jejunum significantly increased the villi height of the T2 group and the ratio of villi height to crypt depth of the FTR groups. Compared with the other two groups, the T2 and T3 groups significantly reduced the ratio of the villous height to crypt depth in the duodenum (p < 0.05). In conclusion, the tea residue after fermentation was shown to have beneficial effects on the fattening performance, digestion performance, meat quality, serum antioxidant capacity, and intestinal morphology of fatteners.

Degradable, flame retardant, and flexible nanocomposite films with low dielectric constant were prepared with poly (lactic acid) (PLA), nano ZIF-8@GO, and degradable flame-retardant resorcinol di(phenyl phosphate) (RDP). The SEM results of the fractured surfaces indicated that ZIF-8@GO and RDP were dispersed uniformly in the PLA matrix. The prepared films had good mechanical properties and the tensile strength of the film with 1.5 wt% of ZIF-8@GO was increased to 48.2 MPa, compared with 38.5 MPa of pure PLA. Meanwhile, the nanocomposite films were flexible due to the toughing effect of RDP. Moreover, above 27.0% of limited oxygen index (LOI) and a VTM-0 rating were achieved for the nanocomposite films. The effects of nano ZIF-8@GO hybrids and RDP on the dielectric properties were investigated, and the results showed that ZIF-8@GO and RDP were beneficial in reducing the dielectric constant and dielectric loss of the nanocomposites.