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Introduction: Cardiac hypertrophy is an important contributor of heart failure, and the mechanisms remain unclear. Leucine zipper protein 1 (LUZP1) is essential for the development and function of cardiovascular system; however, its role in cardiac hypertrophy is elusive. Objectives: This study aims to investigate the molecular basis of LUZP1 in cardiac hypertrophy and to provide a rational therapeutic approach. Methods: Cardiac-specific Luzp1 knockout (cKO) and transgenic mice were established, and transverse aortic constriction (TAC) was used to induce pressure overload-induced cardiac hypertrophy. The possible molecular basis of LUZP1 in regulating cardiac hypertrophy was determined by transcriptome analysis. Neonatal rat cardiomyocytes were cultured to elucidate the role and mechanism of LUZP1 in vitro. Results: LUZP1 expression was progressively increased in hypertrophic hearts after TAC surgery. Gain- and loss-of-function methods revealed that cardiac-specific LUZP1 deficiency aggravated, while cardiac-specific LUZP1 overexpression attenuated pressure overload-elicited hypertrophic growth and cardiac dysfunction in vivo and in vitro. Mechanistically, the transcriptome data identified Stat3 pathway as a key downstream target of LUZP1 in regulating pathological cardiac hypertrophy. Cardiac-specific Stat3 deletion abolished the pro-hypertrophic role in LUZP1 cKO mice after TAC surgery. Further findings suggested that LUZP1 elevated the expression of Src homology region 2 domain-containing phosphatase 1 (SHP1) to inactivate Stat3 pathway, and SHP1 silence blocked the anti-hypertrophic effects of LUZP1 in vivo and in vitro. Conclusion: We demonstrate that LUZP1 attenuates pressure overload-induced cardiac hypertrophy through inhibiting Stat3 signaling, and targeting LUZP1 may develop novel approaches to treat pathological cardiac hypertrophy.

Abstract Background Neuroblastoma (NB) is a common extracranial malignancy with high mortality in children. Recently, super-enhancers (SEs) have been reported to play a critical role in the tumorigenesis and development of NB via regulating a wide range of oncogenes Thus, the synthesis and identification of chemical inhibitors specifically targeting SEs are of great urgency for the clinical therapy of NB. This study aimed to characterize the activity of the SEs inhibitor GNE987, which targets BRD4, in NB. Results In this study, we found that nanomolar concentrations of GNE987 markedly diminished NB cell proliferation and survival via degrading BRD4. Meanwhile, GNE987 significantly induced NB cell apoptosis and cell cycle arrest. Consistent with in vitro results, GNE987 administration (0.25 mg/kg) markedly decreased the tumor size in the xenograft model, with less toxicity, and induced similar BRD4 protein degradation to that observed in vitro. Mechanically, GNE987 led to significant downregulation of hallmark genes associated with MYC and the global disruption of the SEs landscape in NB cells. Moreover, a novel candidate oncogenic transcript, FAM163A, was identified through analysis of the RNA-seq and ChIP-seq data. FAM163A is abnormally transcribed by SEs, playing an important role in NB occurrence and development. Conclusion GNE987 destroyed the abnormal transcriptional regulation of oncogenes in NB by downregulating BRD4, which could be a potential therapeutic candidate for NB.

Abstract Recent studies uncovered the emerging roles of SAPCD2 (suppressor anaphase-promoting complex domain containing 2) in several types of human cancer. However, the functions and underlying mechanisms of SAPCD2 in the progression of neuroblastoma (NB) remain elusive. Herein, through integrative analysis of public datasets and regulatory network of GSK-J4, a small-molecule drug with anti-NB activity, we identified SAPCD2 as an appealing target with a high connection to poor prognosis in NB. SAPCD2 promoted NB progression in vitro and in vivo. Mechanistically, SAPCD2 could directly bind to cytoplasmic E2F7 but not E2F1, alter the subcellular distribution of E2F7 and regulate E2F activity. Among the E2F family members, the roles of E2F7 in NB are poorly understood. We found that an increasing level of nuclear E2F7 was induced by SAPCD2 knockdown, thereby affecting the expression of genes involved in the cell cycle and chromosome instability. In addition, Selinexor (KTP-330), a clinically available inhibitor of exportin 1 (XPO1), could induce nuclear accumulation of E2F7 and suppress the growth of NB. Overall, our studies suggested a previously unrecognized role of SAPCD2 in the E2F signaling pathway and a potential therapeutic approach for NB, as well as clues for understanding the differences in subcellular distribution of E2F1 and E2F7 during their nucleocytoplasmic shuttling.

Abstract Background Acute myeloid leukemia (AML) is a myeloid neoplasm accounts for 7.6% of hematopoietic malignancies. AML is a complex disease, and understanding its pathophysiology is contributing to the improvement in the treatment and prognosis of AML. In this study, we assessed the expression profile and molecular functions of CCAAT enhancer binding protein gamma (CEBPG), a gene implicated in myeloid differentiation and AML progression. Methods shRNA mediated gene interference was used to down-regulate the expression of CEBPG in AML cell lines, and knockdown efficiency was detected by RT-qPCR and western blotting. The effect of knockdown on the growth of AML cell lines was evaluated by CCK-8. Western blotting was used to detect PARP cleavage, and flow cytometry were used to determine the effect of knockdown on apoptosis of AML cells. Genes and pathways affected by knockdown of CEBPG were identified by gene expression analysis using RNA-seq. One of the genes affected by knockdown of CEBPG was Eukaryotic translation initiation factor 4E binding protein 1 (EIF4EBP1), a known repressor of translation. Knockdown of EIF4EBP1 was used to assess its potential role in AML progression downstream of CEBPG. Results We explored the ChIP-Seq data of AML cell lines and non-AML hematopoietic cells, and found CEBPG was activated through its distal enhancer in AML cell lines. Using the public transcriptomic dataset, the Cancer Cell Line Encyclopedia (CCLE) and western blotting, we also found CEBPG was overexpressed in AML. Moreover, we observed that CEBPG promotes AML cell proliferation by activating EIF4EBP1, thus contributing to the progression of AML. These findings indicate that CEBPG could act as a potential therapeutic target for AML patients. Conclusion In summary, we systematically explored the molecular characteristics of CEBPG in AML and identified CEBPG as a potential therapeutic target for AML patients. Our findings provide novel insights into the pathophysiology of AML and indicate a key role for CEBPG in promoting AML progression.

Abstract It’s a challenge for detecting the therapeutic targets of a polypharmacological drug from variations in the responsed networks in the differentiated populations with complex diseases, as stable coronary heart disease. Here, in an adaptive, 31-center, randomized, double-blind trial involving 920 patients with moderate symptomatic stable angina treated by 14-day Danhong injection(DHI), a kind of polypharmacological drug with high quality control, or placebo (0.9% saline), with 76-day following-up, we firstly confirmed that DHI could increase the proportion of patients with clinically significant changes on angina-frequency assessed by Seattle Angina Questionnaire (ΔSAQ-AF ≥ 20) (12.78% at Day 30, 95% confidence interval [CI] 5.86–19.71%, P = 0.0003, 13.82% at Day 60, 95% CI 6.82–20.82%, P = 0.0001 and 8.95% at Day 90, 95% CI 2.06–15.85%, P = 0.01). We also found that there were no significant differences in new-onset major vascular events (P = 0.8502) and serious adverse events (P = 0.9105) between DHI and placebo. After performing the RNA sequencing in 62 selected patients, we developed a systemic modular approach to identify differentially expressed modules (DEMs) of DHI with the Zsummary value less than 0 compared with the control group, calculated by weighted gene co-expression network analysis (WGCNA), and sketched out the basic framework on a modular map with 25 functional modules targeted by DHI. Furthermore, the effective therapeutic module (ETM), defined as the highest correlation value with the phenotype alteration (ΔSAQ-AF, the change in SAQ-AF at Day 30 from baseline) calculated by WGCNA, was identified in the population with the best effect (ΔSAQ-AF ≥ 40), which is related to anticoagulation and regulation of cholesterol metabolism. We assessed the modular flexibility of this ETM using the global topological D value based on Euclidean distance, which is correlated with phenotype alteration (r 2: 0.8204, P = 0.019) by linear regression. Our study identified the anti-angina therapeutic module in the effective population treated by the multi-target drug. Modular methods facilitate the discovery of network pharmacological mechanisms and the advancement of precision medicine. (ClinicalTrials.gov identifier: NCT01681316).

The development and manufacture of room-temperature NH3 respiratory gas sensors are particularly important in the medical field. However, current NH3 sensors either lack sensitivity or have slow response and recovery. Herein, in situ growth of TiO2 nanosheet on the layered amorphous C derived from oxidation of Ti3C2Tx by a hydrothermal method is proposed. The resultant gas sensing performance showed that the TiO2-C-2 (hydrothermal reactor for 12 h) specimen exhibited a high gas response value (10.3) and short response and recovery times (69 and 82 s, respectively) to 100 ppm of NH3 at room temperature. In the UV light environment, gas sensitivity is further improved (from 10.3 to 14.2 for 100 ppm of NH3 response value) and response and recovery times are reduced from 69 and 82 s to 50 and 60 s, respectively. Finally, selective adsorption of NH3 was characterized by density functional theory (DFT). This study confirms that the in situ growth of a TiO2 nanosheet on the layered amorphous C for gas-sensitive detection is expected to be a strategy. [ABSTRACT FROM AUTHOR]

Abstract Background Propionic acidemia (PA)(OMIM#606054) is an inborn error of branched-chain amino acid metabolism, caused by defects in the propionyl-CoA carboxylase (PCC) enzyme which encoded by the PCCA and PCCB genes. Case presentation Here we report a Chinese neonate diagnosed with suspected PA based on the clinical symptoms, gas chromatography-mass spectrometry (GC/MS), and brain imaging tests. Targeted next-generation sequencing (NGS) was performed on the proband. We detected only one heterozygous recurrent nonsense variant (c.937C > T, p.Arg313Ter) in the PCCA gene. When we manually checked the binary alignment map (BAM) diagram of PCCA gene, we found a heterozygous deletion chr13:100915039-100915132delinsAA (c.773_819 + 47delinsAA) (GRCh37.p13) inside the exon 10 in the PCCA gene. The results were validated by Sanger sequencing and qPCR method in the family: the variant (c.937C > T, p.Arg313Ter) was in the maternal allele, and the delins was in the paternal allele. When the mother was pregnant again, prenatal diagnosis was carried out through amniocentesis at 18 weeks gestation, the fetus carried neither of the two mutations. After birth, newborn screening was undertaken, the result was negative. Conclusions We identified a recurrent c.937C > T and a novel c.773_819 + 47delinsAA mutations in the PCCA gene, which may be the genetic cause of the phenotype of this patient. Our findings expanded the spectrum of causative genotype-phenotype of the PCCA gene. For the cases, the NGS results revealed only a heterozygous mutation in autosomal recessive disease when the gene is associated with phenotypes, it is necessary to manually check the BAM diagram to improve the detection rate. Targeted NGS is an effective technique to detect the various genetic lesions responsible for the PA in one step. Genetic testing is essential for genetic counselling and prenatal diagnosis in the family to avoid birth defects.

Background: The clinical characteristics of patients with tuberculosis (TB) and schizophrenia remain largely unknown. Furthermore, TB retreatment is associated with a poor outcome. Hence, we aimed to address the risk factors of TB retreatment in schizophrenia patients in this retrospective cohort.Methods: Between March 2005 and August 2020, patients diagnosed with schizophrenia and TB were included in the study. Patient characteristics, such as demographics, medical history, underlying diseases, symptoms, outcome, and lab examinations, were collected from medical records using a structured questionnaire. TB retreatment was defined as treatment failures and relapses. Subsequently, multivariate logistic regression was performed using variables selected based on prior findings as well as factors found to be associated with a retreatment episode in univariate analyses (p < 0.1).Results: A total of 113 TB patients with schizophrenia were included. Of them, 94 (83.2%) patients were classified as initial treatment group, and 19 (16.8%) were classified as retreatment group. The mean age was 53.0 ± 23.2 years, and males accounted for 61.9% of all cases. Multivariate analysis revealed that continuous antipsychotics treatment (OR = 0.226, 95% CI: 0.074, 0.693; p = 0.009) and extra-pulmonary TB (OR = 0.249, 95% CI: 0.080, 0.783; p = 0.017) were associated with the retreatment in TB patients with schizophrenia.Conclusion: Retreatment is a significant concern for TB patients with schizophrenia. To improve the current dilemma, continuous antipsychotics treatment is required, and increasing awareness of schizophrenia would reduce the disease burden.

Model reference adaptive control takes the output of a reference model as the target and ensures that the actual output is consistent with the target. In this scenario, the reference model determines the performance of the control system. Constructing a reference model with specific performance is challenging, and most researchers construct the reference model by experience. As alternative frameworks, we propose two novel reference model construction methods, namely, zero-pole method and frequency response method. The zero-pole method establishes a nonlinear optimization model to ensure that the added zeros and poles are as far away from the imaginary axis as possible. In the case where this cannot be done, the frequency response method matches the system frequency response of the reference model and the given model to the extent possible using a nonlinear optimization model. Experimental results are presented to confirm that both methods can construct a reference model based on a given transfer function. Deviations in response between the reference models constructed using the two methods and the given model are compared, and the reasons for higher accuracy of the frequency response method are discussed.

Two pilot contamination reduction methods in very large MIMO cellular network were proposed by dividing all cells into two types of one-dimensional very large MIMO network.The same pilot sequences were used in cells in the same category while orthogonal pilot sequences were used between these two categorie.Then the pilot power control method can be used to achieve the purpose of alleviating pilot contamination.By coordinating among base stations,the nearly optimal length of pilot sequences and assignment of pilot transmission could be found through minimizing the sum of channel estimation mean square error of all base stations.Thus,much better performance of channel estimation could be obtained,greatly enhancing the sum rate in downlink in all cells.

The performance of the zero-forcing (ZF) coordinated transmit strategy in multiple-input multiple-output (MIMO) interference channels was investigated.With the goal to derive analytical expression of its performance metric such as the sum rate and the outage probability,the asymptotic behavior of the performance metric was examined with the MIMO dimension tending to infinity.Using the random ma ix theory,an asymptotic estimate of all the eigenvalues of the effective channel matrix in the ZF coordinated transmit strategy was first proposed.Based on that,two closed-form expressions of the sum rate were derived,from which the scaling law of the sum rate with the MIMO dimension was obtained.Furthermore,using the multivariate statistics about the probability density distribution of the minimum eigenvalue of a Wishart matrix,the analytical expression of the outage probability for the coordinated transmit scheme was achieved under two special cases.Simulation results show that the proposed tical expression of the performance metric is valid not only in the large-dimension regime,but also in the normal-dimension regime.

A joint network coding (NC) and superposition coding scheme was proposed to realize a cooperative transmission.The use of NC was able to improve spectral efficiency over classical decode and forward relaying strategy by relaxing the orthogonality constraint between different data streams and mitigating the resultant interference through precoding.In contrast to using the CSI based beamforming scheme which could achieve near optimal performance but involves huge computational complexity,designing the beamforming vector using the form of superposition coding was proposed,such that CSI at the transmitters were not required and the involved computation was greatly reduced.The theoretical analysis and simulation results reveal that the proposed scheme shows performances close to the near-optimal CSIT based scheme.

Endovascular mechanical thrombectomy is emerging as a promising therapeutic approach for acute ischemic stroke and show some advantages. However, the data of predicting clinical outcome after thrombectomy with Solitaire retriever were limited. We attempt to identify prognostic factors of clinical outcome in patients with acute ischemic stroke undergoing thrombectomy with Solitaire retriever.We conducted a retrospective analysis of consecutive acute ischemic strokes cases treated between December 2010 and December2013 where the Solitaire stent retriever was used for acute ischemic stroke. We assessed the effect of selected demographic characteristics, clinical factors on poor outcome at 3 months (modified Rankin score 3-6), mortality at 3 months, and hemorrhage within 24 h (symptomatic and asymptomatic). Clinical, imaging and logistic variables were analyzed. A multivariate logistic regression analysis was used to identify variables influencing clinical outcome, based on discharge NIHSS score change and mRS at 3 months.Eighty nine consecutive patients with acute ischemic stroke underwent mechanical thrombectomy. Multivariate analysis revealed that admission NIHSS score, Serum glucose and endovascular procedure duration were independently associated with clinical outcome. Sex, NIHSS score at admission, diabetes and time of operation were associated with sICH in 1 day. NIHSS score ≥20 (OR 9.38; 95% CI 2.41-36.50), onset to reperfusion >5 hours (OR 5.23; 95% CI1.34,20.41) and symptomatic intracranial hemorrhage (OR 10.19; 95% CI1.80,57.83) were potential predictive factors of mortality at 3 months.Multiple pre- and intra-procedural factors can be used to predict clinical outcome, symptomatic intracranial hemorrhage and mortality in acute ischemic stroke patients undergoing endovascular therapy. This knowledge is helpful for patients selection for endovascular mechanical thrombectomy.

In order to realize mechanical properties test of the emergency towing arrangements, anchor chain and other large marine components, a large-tonnage and multi-function horizontal tension test platform is put forward in this paper. The paper analyzes the disadvantages of the frame structure of the existing experimental platform and designs the composite structure of the concrete and steel. The steel has good elasticity and toughness, the concrete has good performance of high rigidity and compression resistance, so the composite structure takes the advantages of both. The sharp of the frame is like “L”, which can be used to testing different projects. The paper gives the detailed size and analysis procedure of the frame. And it finds a more reasonable structure by means of finite element to analyze and optimize. The frame structure has the advantages of low weight and cost. The platform has been installed in Zhoushan, China successfully.

In the title compound, [Co(C12H8NO2)2(H2O)4], the Co atom lies on a twofold rotation axis and has an N2O4 octahedral coordination environment formed by four O atoms of water molecules in the equatorial plane and two apical N atoms of pyridine groups. An intricate three-dimensional supramolecular network is formed by multiple O—H...O hydrogen bonds between the coordinated water molecules and the uncoordinated carboxylate groups.

In the title compound, [Fe(C9H6N3O3S)2(H2O)4] or [Fe(POA)2(H2O)4], the FeII atom is located on an inversion center and is ligated by four O atoms of coordinated water molecules in the equatorial plane while two POA ligands acting as monodentate ligands occupy the axial positions through their pyridyl N atoms, completing a slightly distorted octahedral coordination geometry. A three-dimensional supramolecular network is formed by multiple O—H...O hydrogen-bonding interactions between the coordinated water donors and the uncoordinated carboxyl acceptors.

Isoquercetin has exhibited a wide range of therapeutic properties, including antioxidant, anti-inflammatory and anti-allergic activities. The aim of the present study was to investigate the effect of isoquercetin on rats with 2 h middle cerebral artery occlusion (MCAO) and evaluate the neuroprotective effect of isoquercetin on a primary culture of rat hippocampal neuronal cells subjected to oxygen-glucose deprivation followed by reoxygenation (OGD/R). In vivo, the rats treated with isoquercetin exhibited a lower degree of neurological dysfunction and smaller infarct volume than the vehicle-treated rats. In vitro, it was found that isoquercetin prevented the OGD/R-induced increase in apoptosis, lactate dehydrogenase release and reduction in cell viability. Additionally, isoquercetin induced the upregulation of nuclear factor erythroid 2-related factor 2 gene and protein expression, and increased extracellular signal-regulated kinase 1 and 2 (ERK1/2) phosphorylation. This indicates that the ERK1/2 pathway may contribute to the neuroprotective effect of isoquercetin against OGD/R-induced oxidative damage in rat hippocampal neurons. These findings suggest the potential importance of isoquercetin in the treatment of ischemia/reperfusion-related brain injury and associated diseases. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the effects of high mobility group protein B1 (HMGB1), which is expressed in the serum of patients with sepsis, on vascular endothelial permeability. Sera from patients with sepsis were used to treat endothelial cells (ECs), and the effect on endothelial permeability was evaluated using immunofluorescence. The morphologies of endothelial cytoskeletal actin and vascular endothelial (VE)-cadherin were assessed using laser scanning confocal microscopy. The protein expression levels of HMGB1, B-cell lymphoma 2 (BCL-2) and BCL-2-associated X protein (BAX) were detected using western blotting. EC apoptosis was measured using flow cytometry. The results demonstrated that HMGB1 was significantly expressed in the serum 24 h following the onset of sepsis, and the expression levels peaked at 48 h, which were sustained until 96 h post-onset. Compared with the control group, treatment of the ECs with 20% septic serum in vitro significantly increased endothelial monolayer permeability (P<0.01), markedly induced transcellular filamentous (F)-actin rearrangement with stress fiber formation, and resulted in the localization of VE-cadherin fragmentations at the cell borders with increased gaps between ECs. Furthermore, flow cytometry showed that the apoptotic rate of ECs was significantly increased following treatment with septic serum. In addition, the expression levels of BAX were significantly increased, whereas the expression levels of BCL-2 were significantly decreased. Pretreatment with an HMGBI inhibitor (ethyl pyruvate; 5 µM) 24 h prior to treatment with the septic serum attenuated the effects of septic serum treatment. Together, these findings suggested that treatment of ECs with sera from patients with sepsis may induce the loss of vascular endothelial monolayer integrity, elicit the formation of endothelial F-actin stress fibers and initiate VE-cadherin redistribution, which may be attributed to high levels of HMGB1 in the serum. This mechanism also appears to involve changes in the activation of BAX and BCL-2, resulting in EC apoptosis. [ABSTRACT FROM AUTHOR]

Objective:As4S4 is an effective drug for the treatment of acute promyelocytic leukemia but its mechanism of action remains largely unknown. In a previous study, we identified PNAS-2, a human apoptosis-related protein gene, using gene expression profiling. In this study, we tried to clarify the role of PNAS-2 in apoptosis and leukemogenesis. Methods: NB4 and U937 leukemia cell lines and serial clinical samples were studied. RNA interference (RNAi) and RNA overexpression were used to address the potential role of PNAS-2 in apoptosis. PNAS-2 expression was examined using Northern blot in multiple tissues, and real-time PCR was applied to analyze PNAS-2 expression in various patient samples. Results: Functional analyses of PNAS-2 by RNAi and RNA overexpression indicate PNAS-2 is an anti-apoptosis gene. PNAS-2 expression is significantly increased in de novo or relapsed acute leukemia, but in patients in complete remission PNAS-2 levels decrease to levels comparable to those found in normal controls. In carcinomas, PNAS-2 expression was not upregulated, indicating that PNAS-2 overexpression was specific for leukemia. Conclusion: Based on the preliminary data, we suggest that the PNAS-2 gene functions as an anti-apoptotic gene and probably participates in leukemogenesis. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC), one of the most common and malignant tumors worldwide, is unresponsive to any of the available therapies. Using intact HCC cells as therapeutic targets, we isolated a novel peptide, denoted HCC79 (KSLSRHDHIHHH), from a phage display peptide library. HCC79 can bind to hepatoma cell membranes with high affinity and specificity. Remarkably, competitive binding assays demonstrated that HCC79 competed with HAb25, a specific antibody for HCC, in binding to hepatoma cells. The corresponding synthetic peptide did not inhibit tumor proliferation directly, but repressed tumor invasion significantly in a cell migration assay. Moreover, we explored the potential of the selected peptide to deliver a superantigen (SAg) to cancer cells, to attain a significant cell-targeting effect. When the peptide is fused to the TSST-1 SAg, the resulting fusion protein could bind to hepatoma cells with high affinity in vitro and improved the tumor inhibition effect by activating T lymphocyte cells in vitro and in vivo, compared with TSST-1 alone. Taken together, our results indicate that this peptide and its future derivatives may have the potential to be developed into highly specific therapeutic agents against cancer. [ABSTRACT FROM AUTHOR]

At present, cancer is one of the most lethal diseases in the world, and researchers are committed to developing effective anticancer drugs. Isoginkgetin (IGG) is a kind of biflavone with the potential to treat cancer due to the features of altering the cell cycle and inhibiting tumor cell infiltration. However, its solubility, absorbability and bioavailability are poor, so in this study, IGG was prepared into mixed nanomicelles and evaluated in vitro and in vivo. After condition optimization, IGG-loaded TPGS/soluplus mixed nanomicelles with particle size of 62.34 ± 1.10 nm, entrapment efficiency of 96.92 ± 0.66% and drug loading of 2.42 ± 0.02% were successfully prepared. The physicochemical properties of the nanomicelles were stable within 60 days, and the cytotoxicity of the nanomicelles was significantly higher than that of IGG. The metabolism results showed that 32 kinds of metabolites of IGG and 21 kinds of IGG-loaded nanomicelles were detected. The metabolites of IGG can only be detected in feces of rats, while the metabolites of IGG-loaded nanomicelles can be detected in plasma, bile, urine and feces. All these indicated that after prepared into nanomicelles, the stability, solubility, cytotoxicity and bioavailability of IGG were increased significantly, which provided a new choice for the development of new drugs. [ABSTRACT FROM AUTHOR]