Image classification and auxiliary diagnosis system for hyperpigmented skin diseases based on deep learning.

Background and aim: Melasma (ML), naevus fusco-caeruleus zygomaticus (NZ), freckles (FC), cafe-au-lait spots (CS), nevus of ota (NO), and lentigo simplex (LS), are common skin diseases causing hyperpigmentation. Deep learning algorithms learn the inherent laws and representation levels of sample data and can analyze the internal details of the image and classify it objectively to be used for image diagnosis. However, deep learning algorithms that can assist clinicians in diagnosing skin hyperpigmentation conditions are lacking. Methods: The optimal deep-learning image recognition algorithm was explored for the auxiliary diagnosis of hyperpigmented skin disease. Pretrained models, such as VGG-19, GoogLeNet, InceptionV3, ResNet50V2, ResNet101V2, ResNet152V2, InceptionResNetV2, DesseNet201, MobileNet, and NASNetMobile were used to classify images of six common hyperpigmented skin diseases. The best deep learning algorithm for developing an online clinical diagnosis system was selected by using accuracy and area under curve (AUC) as evaluation indicators. Results: In this research, the parameters of the above-mentioned ten deep learning algorithms were 18333510, 5979702, 21815078, 23577094, 42638854, 58343942, 54345958, 18333510, 3235014, and 4276058, respectively, and their training time was 380, 162, 199, 188, 315, 511, 471, 697, 101, and 144 min respectively. The respective accuracies of the training set were 85.94%, 99.72%, 99.61%, 99.52%, 99.52%, 98.84%, 99.61%, 99.13%, 99.52%, and 99.61%. The accuracy rates of the test set data were 73.28%, 57.40%, 70.04%, 71.48%, 68.23%, 71.11%, 71.84%, 73.28%, 70.39%, and 43.68%, respectively. Finally, the areas of AUC curves were 0.93, 0.86, 0.93, 0.91, 0.91, 0.92, 0.93, 0.92, 0.93, and 0.82, respectively. Conclusions: The experimental parameters, training time, accuracy, and AUC of the above models suggest that MobileNet provides a good clinical application prospect in the auxiliary diagnosis of hyperpigmented skin.

A novel cationic covalent organic framework as adsorbent for simultaneous removal of methyl orange and hexavalent chromium.

The simultaneous removal of toxic, carcinogenic organic dyes and metal ions from water by one material offers significant advantages when fast, facile, and robust water purification is required. Ionic covalent organic frameworks (ICOFs) have the combined properties of COFs and ion exchange resins and are expected to achieve simultaneous capture of heavy metal ions and organic dyes from water. Herein, a novel guanidinium-based ICOF was synthesized using a solvothermal method. Benefitting from the cationic character, porosity and nanoscale pore size of ICOFs, the adsorbent exhibited high simultaneous adsorption capacities of 290 mg g-1 and 158 mg g-1 for methyl orange (MO) and Cr(vi), respectively, and retained more than 90% adsorption capacity after six adsorption-desorption cycles. In addition, based on dual control of size-exclusion and charge-selection, precisely selective adsorption is achieved towards diverse mixed anionic and cationic pollutants. This strategy offers a practical solution for COFs to confront environmental pollution issues.

Myocardial work and energy loss of left ventricle obtained by pressure-strain loop and vector flow mapping: a new perspective on idiopathic left bundle branch block.

Background: To date, no research has been conducted on the electrical activity and mechanical dyssynchrony of idiopathic left bundle branch block (iLBBB) with normal left ventricular ejection fraction (LVEF). This study sought to assess the left ventricular summation of energy loss (EL-SUM) and average energy loss (EL-AVE) using vector flow mapping as well as myocardial work using pressure-strain loop (PSL) in patients with iLBBB and normal LVEF. Methods: We prospectively recruited 35 patients with iLBBB and 35 control participants with normal LVEF. Echocardiography was performed. Conventional echocardiographic parameters, myocardial work, and energy loss (i.e., the EL-SUM and EL-AVE) were calculated. Results: In relation to global myocardial work, compared to the control participants, the iLBBB patients showed decreased global longitudinal strain (GLS; -15.32%±2.58% vs. -18.27%±2.12%; P=0.001), a decreased global work index (GWI; 1,428.24±338.18 vs. 1,964.87±264.16 mmHg%; P<0.001), decreased global work efficiency (GWE) (84.48±5.19 vs. 91.73±5.31 mmHg%; P<0.001), and significantly increased global waste work (GWW; 341.60±132.62 vs. 161.80±106.81 mmHg%; P<0.001). In relation to the regional index, the iLBBB patients had a significantly reduced basal anteroseptal segment (879.15±370.50 vs. 1,746.38±154.44 mmHg%; P<0.001), basal inferoseptal segment (1,111.42±389.04 vs. 1,677.25±223.10 mmHg%; P<0.001), mid-anteroseptal segment (1,097.54±394.83 vs. 1,815.06±291.22 mmHg%; P<0.001), mid-inferoseptal segment (1,012.54±353.33 vs. 1,880.88±254.39 mmHg%; P<0.001), apical anterior segment (1,592.42±366.64 vs. 1,910.00±170.27 mmHg%; P=0.001), apical lateral segment (1,481.62±342.95 vs. 1,817.19±227.55 mmHg%; P=0.001), apical septal segment (1,437.65±428.22 vs. 1,852.25±275.19 mmHg%; P=0.001), and apex (1,542.62±342.89 vs. 1,907.06±197.94 mmHg%; P<0.001). The iLBBB patients had increased EL-AVE and EL-SUM during the late-diastole, isovolumic-systole, and rapid-ejection periods [EL-AVE in T2: 28.3 (8.7, 49.0) vs. 6.8 (5.4, 9.4) J/(s·m3); P=0.029]; [EL-AVE in T3: 24.7 (13.0, 46.8) vs. 7.2 (5.4, 10.8) J/(s·m3), P<0.001]; [EL-AVE in T4: 18.3 (12.0, 27.6) vs. 7.7 (4.1, 11.6) J/(s·m3), P=0.002]; [EL-SUM in T2: 8.3 (2.2, 14.5) vs. 2.1 (1.6, 3.2) J/(s·m), P=0.049]; [EL-SUM in T3: 7.6 (4.0, 14.5) vs. 2.2 (1.7, 3.3) J/(s·m), P<0.001]; [EL-SUM in T4: 5.3 (3.6, 9.7) vs. 2.2 (1.4, 3.0) J/(s·m), P=0.004]. Conclusions: The GWI and GWE were reduced in patients with iLBBB, especially in the septum and apex. The EL-SUM and EL-AVE were higher in patients with iLBBB during the late-diastole, isovolumic-systole, and rapid-ejection periods. EL and PSL reflect the LV hemodynamics of patients with iLBBB.

Randomized Trial of Left Bundle Branch vs Biventricular Pacing for Cardiac Resynchronization Therapy.

BACKGROUND: Left bundle branch pacing (LBBP) is the most rapidly growing conduction system pacing technique that is capable of correcting intrinsic left bundle branch block (LBBB). As such, it is potentially an optimal alternative to cardiac resynchronization therapy (CRT) with biventricular pacing (BiVP). OBJECTIVES: The authors sought to compare the efficacy of LBBP-CRT with BiVP-CRT in patients with heart failure and reduced left ventricular ejection fraction (LVEF). METHODS: This is a prospective, randomized trial of patients with nonischemic cardiomyopathy and LBBB with 6-month preplanned follow-up. Crossovers were allowed if LBBP or BiVP were unsuccessful. The primary endpoint was the difference in LVEF improvement between 2 groups. The secondary endpoints included changes in echocardiographic measurements, N-terminal pro-B-type natriuretic peptide (NT-proBNP), New York Heart Association functional class, 6-minute walk distance, QRS duration, and CRT response. RESULTS: The study included 40 consecutive patients (20 males, mean age 63.7 years, LVEF 29.7% ± 5.6%). Crossovers occurred in 10% of LBBP-CRT and 20% of BiVP-CRT. All patients completed follow-up. Intention-to-treat analysis showed significantly higher LVEF improvement at 6 months after LBBP-CRT than BiVP-CRT (mean difference: 5.6%; 95% CI: 0.3-10.9; P = 0.039). LBBP-CRT also appeared to have greater reductions in left ventricular end-systolic volume (-24.97 mL; 95% CI: -49.58 to -0.36 mL) and NT-proBNP (-1,071.80 pg/mL; 95% CI: -2,099.40 to -44.20 pg/mL), and comparable changes in New York Heart Association functional class, 6-minute walk distance, QRS duration, and rates of CRT response compared with BiVP-CRT. CONCLUSIONS: LBBP-CRT demonstrated greater LVEF improvement than BiVP-CRT in heart failure patients with nonischemic cardiomyopathy and LBBB. (Left Bundle Branch Pacing Versus Biventricular Pacing for Cardiac Resynchronization Therapy [LBBP-RESYNC]; NCT04110431).

A Comparison of Elevation, Perforation Rate, and Time Spent for the Crestal Sinus Elevation Intervened by Piezosurgery, CAS-Kit, and Osteotome in a Novel Goat Model.

Purpose: This study aimed to compare the differences among Piezosurgery, CAS-kit, and Osteotome regarding safe elevation, perforation rate, and time spent and to observe and analyze different sinus lifting efficacy of the three methods. Materials and Methods: Twenty-one fresh goat heads (42 sinuses) were investigated. CBCT images confirmed the feasibility of the goat model. The maxillary sinus was successively lifted to 5, 7, and 9 mm by Piezosurgery, CAS-kit, and Osteotome until the sinus membrane was perforated or lifted to 9 mm. In the end, final elevation, sinus perforation, and time spent were recorded. Results: Piezosurgery and CAS-kit lifted sinuses to relatively higher heights than did Osteotome (P = 0.000). Perforation rates (14.29, 21.43%) of the Piezosurgery and CAS-kit were far lower than that of the Osteotome (85.71%). In the Osteotome group, the time of lifting to 9 mm was significantly shorter than that of Piezosurgery and CAS-kit (P = 0.000). There was no statistical difference in time spent between the latter two (P = 0.115). Conclusions: The lifting height of the Osteotome was limited, but it took the shortest time for sinus lifting. Piezosurgery and CAS-kit had higher lifting heights and lower perforation rates compared with Osteotome.

The combined induction of liver progenitor cells and the suppression of stellate cells by small molecules reverts chronic hepatic dysfunction.

Rationale: We developed a cocktail of soluble molecules mimicking the in vivo milieu supporting liver regeneration that could convert mature hepatocytes to expandable liver progenitor-like cells in vitro. This study aimed to induce endogenous liver progenitor cells by the administration of the soluble molecules to provide an alternative approach for the resolution of liver fibrosis. Methods:In vitro cultured hepatocyte-derived liver progenitor-like cells (HepLPCs) were transplanted into CCL4-treated mice to investigate the therapeutic effect against liver fibrosis. Next, we used HGF in combination with a cocktail of small molecules (Y-27632, A-83-01, and CHIR99021 (HACY)) to induce endogenous CD24+ liver progenitor cells and to inhibit the activation of hepatic stellate cells (HSCs) during CCL4-induced hepatic injury. RNA sequencing was performed to further clarify the features of HACY-induced CD24+ cells compared with CCL4-induced CD24+ cells and in vitro derived HepLPCs. Finally, we evaluated the expansion of HACY-induced CD24+ cells in human hepatocyte-spheroids from fibrotic liver tissues. Results: HepLPCs exhibited the capacity to alleviate liver fibrosis after transplantation into CCL4-treated mice. The in vivo administration of HACY not only induced the conversion of mature hepatocytes (MHs) to CD24+ progenitor cells but prevented the activation of HSCs, thus leading to enhanced improvement of liver fibrosis in CCL4-treated mice. Compared to CD24+ cells induced by CCL4 alone, HACY-induced CD24+ cells retained an enhanced level of hepatic function and could promote the restoration of liver function that exhibited comparable gene expression profiles with HepLPCs. CD24+ cells were also observed in human liver fibrotic tissues and were expanded in three-dimensional (3D) hepatic spheroids in the presence of HACY in vitro. Conclusions: Hepatocyte-derived liver progenitor-like cells are crucial for liver regeneration during chronic hepatic injuries. The administration of HACY, which allowed the induction of endogenous CD24+ progenitor cells and the inactivation of HSCs, exerts beneficial effects in the treatment of liver fibrosis by re-establishing a balance favoring liver regeneration while preventing fibrotic responses.

Enrichment and identification of differentially expressed genes in hepatocellular carcinoma stem-like cells.

Cancer stem cells are considered to be tumor-initiating cells. To explain the initiation or progression of hepatocellular carcinoma (HCC), we previously established a culture system that may enrich hepatic cancer stem-like cells (HCSCs). However, the regulatory mechanisms by which HCSCs acquire stem cell properties remain unclear. In the present study, three pairs of HCSCs and case-matched human HCC cells were analyzed by high-throughput screening, and novel biomarkers and pathways for the regulation of HCSCs were identified. The results led to the identification and stratification of 406 differentially expressed genes (DEGs), among which 73 GO terms were found to be significantly associated with DEGs in HCSCs, and only complement and coagulation cascade pathways were identified during the development of HCSCs. By combining the results of the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses, it was revealed that 7 genes were downregulated in the complement and coagulation cascade pathways, and 7 miRNAs were predicted to target several downregulated genes involved in these pathways. The results may contribute toward hepatic cancer stem cell studies and novel drug research for HCC treatment.

CsZn2 BO3 X2 (X2 =F2 , Cl2 , and FCl): A Series of Beryllium-Free Deep-Ultraviolet Nonlinear-Optical Crystals with Excellent Properties.

Designing deep-ultraviolet (DUV) nonlinear-optical (NLO) crystals is one of the major current research interests, but it faces a great challenge. In order to overcome the problem of crystal growth and the toxicity of BeO raw materials in KBe2 BO3 F2 (KBBF), the only applicable DUV NLO crystal so far, we substitute Be2+ cations with Zn2+ in the KBBF structure and modify the halogen anions, by which three new Zn-containing KBBF-like compounds, CsZn2 BO3 X2 (X2 =F2 , Cl2 , and FCl), have been successfully synthesized. They all exhibit excellent NLO properties, including improved SHG responses (2.8-3.5×KDP) and short UV cut-off edges (<190 nm). In comparison with KBBF, CsZn2 BO3 X2 (X2 =F2 , Cl2 , and FCl) are all chemically benign and have better growth habits, so they are all promising as DUV NLO crystals. Further study on structure-property relationships indicates that the mixing of halogen anions is a feasible strategy to enhance the SHG responses of the KBBF family.

Extracellular vesicles-derived OncomiRs mediate communication between cancer cells and cancer-associated hepatic stellate cells in hepatocellular carcinoma microenvironment.

Tumor microenvironment (TME) is a critical determinant for hepatocellular carcinoma (HCC). Hepatic stellate cells (HSCs) are main interstitial cells in TME and play a vital role in early intrahepatic invasion and metastasis of HCC. The potential mechanism on the interactions between HSCs and HCC cells remains unclear. In this study, the effects of extracellular vesicles (EVs)-derived OncomiRs that mediate communication between HCC cells and cancer-associated hepatic stellate cells (caHSCs) and remold TME were investigated. The results found that the HCC cells-released EVs contained more various OncomiRs, which could activate HSCs (LX2 cells) and transform them to caHSCs, the caHSCs in turn exerted promotion effects on HCC cells through HSCs-released EVs. To further simulate the effects of OncomiRs in EVs on construction of pro-metastatic TME, a group of OncomiRs, miR-21, miR-221 and miR-151 was transfected into HCC cells and LX2 cells. These microRNAs in the EVs from OncomiRs-enhanced cells were demonstrated to have oncogenic effects on HCC cells by upregulating the activities of protein kinase B (AKT)/extracellular signal-regulated kinase (ERK) signal pathways. Equivalent results were also found in HCC xenografted tumor models. The findings suggested that the OncomiR secretion and transference by cancer cells-released EVs can mediate the communication between HCC cells and HSCs. HCC cells and caHSCs, as well as their secreted EVs, jointly construct a pro-metastatic TME suitable for invasion and metastasis of cancer cells, all these TME components form a positive feedback loop to promote HCC progression and metastasis.

FoxOs could play an important role during influenza A viruses infection via microarray analysis based on GEO database.

Influenza is a highly contagious respiratory illness caused by influenza A viruses (IAVs). The response and reaction from the host vary due to different subtypes. In this study, we identified the global transcriptomics of HUVEC (human umbilical vein endothelial cells) and macrophage cells after infection of H5N1 and H1N1 strains using microarray data from Gene Expression Omnibus (GEO), respectively. Our data showed that influenza A viruses (IAVs) could induce more global profound transcriptomics in HUVEC than macrophage cells. H5N1 infection led to much more rigorous apoptosis than H1N1 did in macrophage cells. Our data is consistent with the idea that by maintaining normal levels of FoxO1 could be maintained, the pro-apoptotic effects of IAV virus infection could be reduced. Anti-inflammatory and anti-apoptosis responses could be manipulated via FoxOs in response to IAVs infection, indicating that FoxOs could function as candidate target for the treatment of IAVs infection. Our result thus provides new insight for the future strategy of anti-IAVs therapy.

iTRAQ-based proteomic and bioinformatic characterization of human mast cells upon infection by the influenza A virus strains H1N1 and H5N1.

Mast cells can support the replication of influenza A virus, although how this occurs is poorly understood. In the present study, using quantitative MS, we analyzed the proteome of human mast cells infected with different influenza A virus strains at 12 h post-infection. Forty-one differentially expressed proteins were identified in human mast cells upon infection by the virulent H5N1 (A/Chicken/Henan/1/04) virus compared to the seasonal H1N1 (A/WSN/33) virus. Bioinformatic analyses confirmed that H1N1 significantly regulates the RNA degradation pathway via up-regulation of CCR4-NOT transcription complex subunit 4, whereas apoptosis could be suppressed by H5N1 via down-regulation of the tumor protein p53 signaling pathway with P ≤ 0.05 at 12 h post-infection. The hypoxia-inducible factor-1 signaling pathway of human mast cells is more susceptible to infection by H5N1 than by H1N1 virus.

Bioinformatics analysis of evolutionary characteristics and biochemical structure of FGF5 Gene in sheep.

Fibroblast growth factor (FGF) 5 regulates the development and periodicity of hair follicles, which can affect hair traits. Loss-of-function mutations associated with long-hair phenotypes have been described in several mammalian species. Sheep is an important economic animal, however, the evolution characterizations and biological mechanism of oFGF5 (Ovis aries FGF5) gene are still poorly understood. In this study, oFGF5 gene was obtained by resequencing the whole genome of three Dorper sheep and RACE of two Kazakh sheep FGF5. We proposed FGF5 was phylogenetically related to FGF4 family and oFGF5 clearly orthologed to goat FGF5. Six loci were found from the positive selection results of FGF5 and half of them located on signal peptide. The basically similar rates of function-altering substitutions in sheep and goat lineage and the rest of the mammalian lineage of 365 SNPs indicated that the FGF5 gene was quite conservative during evolution. Homology modeling of the oFGF5 suggested that it has a highly conserved FGF superfamily domain containing 10 ß-strands. Furthermore, the protein-protein docking analysis revealed that oFGF5 have the potential to form heterodimers with oFGFR1, the predicted interaction interface of FGF5-FGFR1 heterodimer was formed mainly by residues from FGF superfamily domain. Our observations suggested the evolutionary and structural biology features of oFGF5 might be relevant to its function about hair follicle development and modulating hair growth, and we confirmed our speculation by using the FGF5 gene editing sheep produced by CRISPR/Cas9 technology.

Expansion and differentiation of human hepatocyte-derived liver progenitor-like cells and their use for the study of hepatotropic pathogens.

The study of pathophysiological mechanisms in human liver disease has been constrained by the inability to expand primary hepatocytes in vitro while maintaining proliferative capacity and metabolic function. We and others have previously shown that mouse mature hepatocytes can be converted to liver progenitor-like cells in vitro with defined chemical factors. Here we describe a protocol achieving efficient conversion of human primary hepatocytes into liver progenitor-like cells (HepLPCs) through delivery of developmentally relevant cues, including NAD + -dependent deacetylase SIRT1 signaling. These HepLPCs could be expanded significantly during in vitro passage. The expanded cells can readily be converted back into metabolically functional hepatocytes in vitro and upon transplantation in vivo. Under three-dimensional culture conditions, differentiated cells generated from HepLPCs regained the ability to support infection or reactivation of hepatitis B virus (HBV). Our work demonstrates the utility of the conversion between hepatocyte and liver progenitor-like cells for studying HBV biology and antiviral therapies. These findings will facilitate the study of liver diseases and regenerative medicine.

Draft genome Sequence of Phosphate-Accumulating Bacterium Acinetobacter tandoii SC36 from a Mangrove Wetland Ecosystem Provides Insights into Elements of Phosphorus Removal.

Acinetobacter tandoii SC36 was isolated from a mangrove wetland ecosystem in the Dongzhaigang Nature Reserve in Haikou, China. This bacterium was found to have a capacity for polyphosphate accumulation. To provide insight into its phosphorus metabolism and facilitate its application in phosphorus removal, we developed a draft genome of this strain. KEGG (Kyoto Encyclopedia of Genes and Genomes) annotation revealed three ppk genes and several phosphate metabolic related pathways in the genome of SC36. These genome data of Acinetobacter tandoii SC36 will facilitate elucidation of the mechanism of polyphosphate accumulation.

Synergistic antitumoral efficacy of a novel replicative adenovirus SG611-PDCD5 and daunorubicin in human leukemic cells.

BACKGROUND: Daunorubicin is a traditional chemotherapeutic agent that plays a pivotal role in leukemia therapy. However, the dose-related toxicity remains a considerable challenge. The apoptosis-regulating gene, PDCD5, is downregulated in various tumors, including leukemias, and may provide a potential target for the diagnosis and treatment of leukemia. The purpose of this study was to construct a triple-regulated oncolytic adenovirus carrying a PDCD5 gene expression cassette (SG611-PDCD5) and explore the combined antitumor efficacy of SG611-PDCD5 in combination with low dose daunorubicin on leukemic cells. MATERIALS AND METHODS: A variety of leukemic cell lines, including K562, MEG-01, KG-1a, HL-60, SUP-B15, and BV-173, were cultured according to the providers' instructions. The insertion and orientation of all recombined plasmids were confirmed by restriction enzyme digestion and PCR. The tumor-selective replication of the constructed conditionally replicating SG611-PDCD5 and its antitumor efficacy in combination with daunorubicin were characterized in leukemic cell lines in vitro and in a nude mouse xenograft model. Cell viability was detected using cell-counting kit-8. Apoptosis was detected in whole living cells using flow cytometry and in paraffin-embedded tumor tissues using a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. RESULTS: The triple-regulated CRAd carrying SG611-PDCD5 and nude mouse xenograft models of K562 cells were successfully constructed. In vitro treatment with SG611-PDCD5 in combination with low-dose daunorubicin elicited more potent anti-proliferative and proapoptotic effects in leukemic cells in a dose-dependent manner. The Chou-Talalay analysis revealed synergistic anti-proliferative effects in all of the above cell lines. In the nude mice xenograft model, the tumor size in the control, daunorubicin, SG611-PDCD5, and combined treatment groups on day 10 were 170.1±47.8, 111.9±81.1, 60.7±12.3, and 33.2±17.5 mm3, respectively (all P<0.05). The results of the TUNEL assay showed significantly more apoptotic cells in the SG611-PDCD5 plus daunorubicin group than in the SG611-PDCD5 or daunorubicin groups alone (25±0.82, 12.5±2.27, and 7.8±2.67 apoptotic cells/field, respectively) (P<0.05). CONCLUSION: The findings suggest that combined treatment with SG611-PDCD5 and daunorubicin may be a promising strategy for enhancing chemosensitivity and thus lowering the dose-related toxicity of daunorubicin in leukemia therapy.

Dwarf chickens with low monocytes/macrophages phagocytic activity show low antibody titers but greater performance.

Monocytes/macrophages phagocytosis has key roles in inflammatory responses. However, systematic research on the effects of monocytes/macrophages phagocytosis on production and reproductive performance in dwarf chickens is lacking. In this study, we developed the HCT-8-MTT method to detect monocytes/macrophages phagocytosis product (PP) which was accuracy, flexible, and saving time. Based on PP in 990 dwarf chickens (890 hens and 100 cocks), chickens were divided into high phagocytosis product group (HPPG) and low phagocytosis product group (LPPG). In production performance, chickens in LPPG have higher laying rate at 24 wk and 71 wk and higher average egg weight at 23 wk and 24 wk than in HPPG (P < 0.05). The levels of follicle-stimulating hormone and luteinizing hormone were higher in LPPG than in HPPG at 58 wk (P < 0.01). In the reproductive performance, the fertilization rate in LPPG was higher than that in HPPG at 45 wk, 49 wk, and 53 wk (P < 0.05). Chickens in LPPG have higher hatchability than HPPG at 45 wk and 49 wk (P < 0.05). In LPPG, the mRNA expression levels of follicle-stimulating hormone receptor and CD9 in the follicle were higher than HPPG (P < 0.05). In the immune response, chickens with higher PP levels showed higher antibody titers for the avian influenza virus H9 inactivated vaccine (P < 0.01). Therefore, monocytes/macrophages PP was positively associated with antibody titers and negatively related to production and reproductive performance, and these findings have practical applications for the optimization of production in the poultry industry.

Whole exome sequencing identifies novel candidate mutations in a Chinese family with left ventricular noncompaction.

Left ventricular noncompaction (LVNC) is an inherited cardiomyopathy involving numerous genes. To identify novel candidate causal mutations, a whole exome sequencing study was performed on a Chinese LVNC family. Exons of the most prevalent pathogenic genes of LVNC (myosin heavy chain 7 and actin, α­cardiac muscle 1) were sequenced, although no mutations were identified. Following this, Burrows­Wheeler Aligner, PICARD and Genome Analysis Toolkit (v.2.8) were used to analyze the exome sequencing data. Non­silent single nucleotide variants (SNVs) that were identified in patients with LVNC, although not in the healthy individual, were investigated further using SNV prioritization via the integration of genomic data (SPRING) based on P­values. Co­expressed gene enrichment analysis was performed using Genotype Tissue Expression (GTEx) data in order to investigate the potential roles of the genes containing SNVs in the myocardium. In the Chinese LVNC family, seven novel SNVs were identified that were only present in patients with LVNC and annotated by SPRING with P<0.05. Among these SNVs, hemicentin 1 [c. thymine (T) 9776 cytosine (C)], tolloid like 2 [c. cytosine (C) 2615 thymine (T)], fms related tyrosine kinase 3 [c. guanine (G) 976 adenine (A)] and nucleotide binding protein like [c. guanine (G) 91 thymine (T)] were located in conserved regions and annotated as deleterious by PolyPhen2, LRT and MutationTaster database analyses. Based on GTEx data, it was revealed that NUBPL was co­expressed with almost all previously established LVNC pathogenic genes. Furthermore, the results of the present study demonstrated that genes co­expressed with NUBPL were additionally enriched in the Notch signaling pathway. In addition, the results revealed numerous novel mutations that may be causal SNVs for the development of LVNC in the family involved in the present study.

Application of the dimensional reduction formalism to Pb9-xBax[Li2(P2O7)2(P4O13)2] (x = 0, 2, 6, 7): a series of phosphates with two types of isolated polyphosphate groups.

A series of phosphates, Pb9-xBax[Li2(P2O7)2(P4O13)2] (x = 0, 2, 6, 7), have been synthesized by a high temperature solution method and the crystal structures were determined by single crystal X-ray diffraction. They are isostructural and crystallize in the triclinic space group P1[combining macron]. It is interesting that there are two kinds of isolated polyphosphate anionic groups coexisting in the crystal structure, which is rare among phosphates. Their structures exhibit zero-dimensional [Li2(P2O7)2(P4O13)2]18- anionic clusters constructed by the LiO4, P2O7 and P4O13 groups, which are separated by the Pb2+ or Ba2+ cations. The structure of Pb9[Li2(P2O7)2(P4O13)2] could be obtained using Li2O as a dimensional reduction agent to dismantle Pb3P4O13. In addition, the infrared spectra and the UV-Vis-NIR diffuse reflectance spectra, as well as thermal analyses are reported. The first-principles theoretical studies are also carried out to understand the relationship between their electronic structures and linear optical properties.

Inhibition of SIRPα in dendritic cells potentiates potent antitumor immunity.

Despite their central function in tumor immunity, dendritic cells (DCs) can respond to inhibitory signals and become tolerogenic, curtailing T cell responses in vivo. Here, we provide the evidence for an inhibitory function of signal regulatory protein (SIRP) α in DC survival and activation. In tumors from human liver cancer patients, infiltrative DCs expressed elevated levels of SIRPα, which is correlated with the induction of immune tolerance within the tumors. Silencing of SIRPα resulted in a significant increase in the longevity of antigen-pulsed DCs in the draining lymph nodes. In addition, SIRPα controls the activation and output of DCs. Silencing of DC-expressed SIRPα induced spontaneous and enhanced production of IL12 and costimulatory molecules, resulting in more potent cytotoxic T lymphocyte responses, including the eradication of previously established solid tumors. SIRPα exerted such effects, at least in part, via the association and sequestration of p85 subunit of PI3K. Thus, SIRPα is a critical regulator of DC lifespan and activity, and its inhibition might improve the clinical efficacy of DC-based tumor vaccines.