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1. This study evaluated the effectiveness of different types of acidifiers on reproductive performance, body weight loss and plasma biochemical indices of breeding pigeons as well as on growth performance, carcass characteristics, meat quality and plasma biochemical indices of squabs.2. In a 45 d trial, 144 pairs of European white Mimas pigeons were selected and randomly divided into three experimental groups. Three groups of pigeons were fed plain pigeon grit (NC), pigeon grit supplemented with 5% single acidifier (SAG) and pigeon grit supplemented with 5% combined acidifiers (CAG).3. Supplementing with SAG and CAG significantly increased the weight gain in male pigeons from 1-12 d of incubation. However, SAG and CAG had no significant effect on the feed intake of breeding pigeons during incubation, but significantly increased total feed intake of breeding pigeons during the lactation period. Breeder pigeons fed SAG and CAG had significantly higher egg-laying rate at 40 d. In addition, feeding SAG and CAG significantly increased growth rate and slaughter weight of squabs, but SAG reduced the diameter of pectoral muscle fibres. Biochemical indices showed that feeding SAG and CAG improved metabolism and increased the liver function of breeder pigeons and squabs.4. In conclusion, supplementing pigeon grit with acidifiers increased feed intake of breeding pigeons during lactation, protected liver function, enhanced reproductive performance and promoted the growth and development of squabs.

Aim: To develop and validate a nomogram model that combines computed tomography (CT)-based radiological factors extracted from deep-learning and clinical factors for the early predictions of immune checkpoint inhibitor-related pneumonitis (ICI-P)., Materials and Methods: Forty ICI-P patients and 101 patients without ICI-P were divided randomly into the training (n=113) and test (n=28) sets. The convolution neural network (CNN) algorithm was used to extract the CT-based radiological features of predictable ICI-P and calculated the CT score of each patient. A nomogram model to predict the risk of ICI-P was developed by logistic regression., Results: CT score was calculated from five radiological features extracted by the residual neural network-50-V2 with feature pyramid networks. Four predictors of ICI-P in the nomogram model included a clinical feature (pre-existing lung diseases), two serum markers (absolute lymphocyte count and lactate dehydrogenase), and a CT score. The area under curve of the nomogram model in the training (0.910 versus 0.871 versus 0.778) and test (0.900 versus 0.856 versus 0.869) sets was better than the radiological and clinical models. The nomogram model showed good consistency and better clinical practicability., Conclusion: The nomogram model that combined CT-based radiological factors and clinical factors can be used as a new non-invasive tool for the early prediction of ICI-P in lung cancer patients after immunotherapy with low cost and low manual input., (Copyright © 2023. Published by Elsevier Ltd.)

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline, amyloid-β (Aβ) plaques and the formation of neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau. Increasing evidence has demonstrated that the damage of cell plays an important role in AD. Cell death is a critical phenomenon for physiological functions, which promotes AD pathogenesis. Programmed cell death, including necroptosis, pyroptosis, autophagy, and ferroptosis, have been discovered that have unique biological functions and pathophysiological characteristics. Here, we review the available evidence detailing the mechanisms of programmed microglial death, including pyroptosis, autophagy, and ferroptosis. We also highlight the role of programmed death of microglia during the process of AD and focus on the connection between the disease and cell death., Competing Interests: All authors claim that there are no conflicts of interest.

Telomere length (TL) in blood cells is commonly used as a proxy for TL in other tissue types. The source of DNA of adequate quality and quantity is important for TL analysis. Compared to blood cells, buccal cells easy for genomic DNA preparation would facilitate the rapid and reliable TL analysis. However, the feasibility of buccal cells for TL analysis remains yet unestablished. We characterized TL of buccal cells and blood cells collected from 52 individuals using buccal cell swabs and fingertip sticks. Relative TL (RTL) determined by quantitative PCR showed that there is a strong correlation between buccal RTL and blood RTL (r=0.877, p<0.001), suggesting that buccal cells are adequate sources of DNA for TL analysis. The validity of sampling using buccal cell swabs provides simple operation and good reproducibility for TL analysis, that overcomes the discomfort and risk of infection caused by blood sampling., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature.)

BACKGROUND: Gabapentin and baclofen are recommended for the treatment of chronic refractory cough (CRC). We investigated the efficacy of flupentixol/melitracen in patients unresponsive to these neuromodulators. METHODS: A total of 101 patients with CRC who failed to respond to gabapentin and baclofen were recruited, and treated with flupentixol/melitracen. The prevalence of cough resolution and changes in the Cough Symptom Score (CSS), cough thresholds to capsaicin, Hull Airway Reflux Questionnaire (HARQ), Leicester Cough Questionnaire (LCQ), Generalized Anxiety Disorder-7, Hamilton Anxiety Rating Scale, Patient Health Questionnaire-9, and Hamilton Depression Rating Scale-24 were evaluated after treatment. RESULTS: Ninety-eight patients (97.0%) completed the study. The overall successful cough resolution rate was 62.4% (63/101). Cough resolution was accompanied by an obvious decrease in the CSS and HARQ score and a remarkable increase in cough thresholds to capsaicin challenge and LCQ score, whereas anxiety and depression scores did not change significantly. The prevalence of adverse effects (e.g., insomnia and dizziness) was 21.8%. The prevalence of cough recurrence within 2 weeks after treatment cessation was 17.8%. CONCLUSION: Flupentixol/melitracen may be an efficacious option for CRC unresponsive to other neuromodulators.

Non-small cell lung cancer (NSCLC) is a major source of cancer mortality. Long non-coding RNA DSCAM-AS1 has been certified to be involved in the pathogenesis of NSCLC. This study aimed to further investigate the potential mechanism of DSCAM-AS1 in NSCLC progression. The expressions of DSCAM-AS1, miR-577, and high mobility group box 1 (HMGB1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot assay. Cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. Flow cytometry assay was conducted to monitor cell apoptosis. Cell migration and invasion were measured by transwell assay. Wnt/β-catenin pathway-related factors were detected by western blot assay. The relationship between DSCAM-AS1, miR-577, and HMGB1 was validated by bioinformatics analysis and dual-luciferase reporter assay. The xenograft mouse model was established to analyze tumor growth in vivo. DSCAM-AS1 and HMGB1 were upregulated, while miR-577 was downregulated in NSCLC tissues and cells. DSCAM-AS1 promoted cell proliferation, migration and invasion, and restrained cell apoptosis in NSCLC cells. Overexpression of HMGB1 reversed the effects of DSCAM-AS1 depletion on the progression of NSCLC. DSCAM-AS1 modulated HMGB1 expression by sponging miR-577. DSCAM-AS1 regulated the Wnt/β-catenin pathway by regulating miR-577 and HMGB1. DSCAM-AS1 knockdown blocked the tumor growth in vivo. In conclusion, DSCAM-AS1 facilitated NSCLC progression by regulating the HMGB1-mediated Wnt/β-catenin pathway, providing a promising therapeutic target for NSCLC.

Key Message: A novel QTL (qSCN-PL10) for SCN resistance and related candidate genes were identified in the soybean variety Pingliang xiaoheidou, and plant basal immunity seems to contribute to the SCN resistance. Soybean cyst nematode (SCN, Heterodera glycines Ichinohe) is one of the most devastating soybean pests worldwide. The development of host plant resistance represents an effective strategy to control SCN. However, owing to the lack of diversity of resistance genes in soybean varieties, further investigation is necessary to identify new SCN resistance genes. By analyzing the resistance phenotypes of soybean variety Pingliang xiaoheidou (Pingliang, ZDD 11047), we found that it exhibited the different resistance phenotypes from PI 88788 and Peking varieties. Because Pingliang variety contains the Rhg1-a (low copy) haplotype and lacks the resistant Rhg4 haplotype, novel quantitative trait locus might account for their SCN resistance. After sequencing parental lines (Magellan and Pingliang) and 200 F 2:3 progenies, a high-density genetic map was constructed using the specific length amplified fragment sequencing method and qSCN-PL10 was identified as a novel locus for SCN resistance. Candidate genes were predicted by RNA sequencing (RNA-seq) in the qSCN-PL10 locus region. The RNA-seq analysis performed also indicated that plant basal immunity plays an important role in the resistance of Pingliang to SCN. These results lay a foundation for the use of marker-assisted breeding to enhance the resistance to SCN.

Objective: This study aimed to investigate the effects of prostaglandin E2 receptor subtypes 1 (EP1) and 2 (EP2) on endoplasmic reticulum (ER) stress induced by TGF-β1 in mouse mesangial cells (MCs) and to explore its potential mechanisms., Materials and Methods: Mouse mesangial cells were isolated and cultured. EP-siRNAs were transfected into mesangial cells for silencing EP1 and EP2. Mesangial cell proliferation was assessed by the CCK-8 method. Expression of PGE2 was measured by enzyme-linked immunosorbent assay (ELISA). GRP78, TRPC1, ERK1/2, and phospho-ERK1/2 levels were examined by Western blot., Results: TGF-β1 induced mesangial cell proliferation and increased PGE2 secretion. Besides, TGF-β1 significantly upregulated GRP78 and TRPC1 expression at the protein level. Phospho-ERK1/2 protein amounts were also increased (p<0.05). Compared with the TGF-β1 group, cell proliferation in the EP1-siRNA+TGF-β1 group was reduced, while GRP78, TRPC1, and ERK1/2 protein amounts were downregulated (p<0.05). EP1 agonist significantly enhanced above changes and their activities (p<0.05). EP1 antagonist significantly attenuated the above changes (p<0.05). Compared with TGF-β1 group, cell proliferation in EP2-siRNA+TGF-β1 group was increased, while GRP78, TRPC1, and ERK1/2 protein amounts were increased (p<0.05). EP2 agonist significantly attenuated the above changes (p<0.05)., Conclusions: EP1 receptor may increase TGF-β1-induced cell damage by increasing the activities of GRP78, TRPC1, and ERK1/2 via ER stress. Meanwhile, the EP2 receptor may reduce TGF-β1-induced cell damage by suppressing GRP78, TRPC1, and ERK1/2 activities, also via ER stress. EP1 inhibition and EP2 stimulation may be a therapeutic option for delaying renal fibrosis.

The soft tick Argas japonicus mainly infests birds and can cause human dermatitis; however, no pathogen has been identified from this tick species in China. In the present study, the microbiota in A. japonicus collected from an epidemic community was explored, and some putative Rickettsia pathogens were further characterized. The results obtained indicated that bacteria in A. japonicus were mainly ascribed to the phyla Proteobacteria, Firmicutes and Actinobacteria. At the genus level, the male A. japonicus harboured more diverse bacteria than the females and nymphs. The bacteria Alcaligenes, Pseudomonas, Rickettsia and Staphylococcus were common in nymphs and adults. The abundance of bacteria belonging to the Rickettsia genus in females and males was 7.27% and 10.42%, respectively. Furthermore, the 16S rRNA gene of Rickettsia was amplified and sequenced, and phylogenetic analysis revealed that 13 sequences were clustered with the spotted fever group rickettsiae (Rickettsia heilongjiangensis and Rickettsia japonica) and three were clustered with Rickettsia limoniae, which suggested that the characterized Rickettsia in A. japonicus were novel putative pathogens and also that the residents were at considerable risk for infection by tick-borne pathogens., (© 2019 The Royal Entomological Society.)

Objective: To investigate the influences of urinary kallidinogenase on neuronal apoptosis in rats with cerebral infarction through the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) oxidative stress pathway., Materials and Methods: A total of 30 male rats were divided into group A (model control group), group B (rat model of cerebral infarction) and group C (rat model of cerebral infarction + medical treatment with urinary kallidinogenase). The percentage of cerebral infarct volume and the apoptosis of brain cells in the three groups of rats were detected via 2,3,5-Triphenyltetrazolium chloride (TTC) staining, the pathological morphology of brain tissues in the three groups of rats was observed via hematoxylin and eosin (HE) staining, and the protein levels of Nrf2 and superoxide dismutase 1 (SOD1) in the brain tissues in the three groups of rats were measured using the Western blotting assay., Results: The degree of neurological deficit in group B was remarkably higher than that in group A (p<0.05), and it was markedly decreased in group C compared to that in group B, displaying statistically significant differences (p<0.05). Compared to that in group A, the cell apoptosis was significantly aggravated in group B, while a remarkably alleviated cell apoptosis was observed in group C compared to that of group B, and the differences were statistically significant (p<0.05). The cerebral infarct volume accounted for 34.87% of the whole brain volume in group B, and a mild cerebral infarction was detected in group C, with a percentage of cerebral infarct volume of 21.14%. Group B showed a more evident increase in the cerebral infarct volume than in group C (p<0.05). Compared to those of group A, pyknotic nuclei and neuron staining of brain tissue cells were evidently increased, and the neuronal cell injury was aggravated in group B. Moreover, prominently decreased pyknotic nuclei and neuron staining (p<0.05) as well as mild neuronal cell injury (p<0.05) were detected in group C compared to those in group B. The levels of Nrf2 and SOD1 protein in the brain tissues in group B were remarkably lower than those of group C (p<0.05)., Conclusions: Urinary kallidinogenase can inhibit the neuronal apoptosis in rats and protect the rats from cerebral infarction, whose mechanism is associated with the activation of the Nrf2/ARE oxidative stress pathway.

Objective: This study was conducted to analyze the effect of miR-7 on the inflammatory response of microglia in vitro and in vivo by constructing an intracerebral hemorrhage model., Patients and Methods: In this study, we first established a model of cerebral hemorrhage in rat for in vivo experiments, and used lipoprotein (LPS) to induce an inflammatory response development in microglial cells, and constructed microglial inflammation models for in vitro experiments. Quantitative Real-time-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-7 in the rat model of cerebral hemorrhage and microglia with inflammation. The effect of miR-7 on the inflammation caused by intracerebral hemorrhage was evaluated through measuring the expression of IL-1β, IL-8 and TNF-α by enzyme-linked immunosorbent assay (ELISA). Dual luciferase reporter assay was used to detect the binding site of miR-7 to TLR4. Western blot was used to evaluate the level of TLR4 after overexpression and knockdown of miR-7 and to evaluate whether miR-7 alleviated the secondary inflammatory response of microglia after cerebral hemorrhage by inhibiting the expression of TLR4., Results: The expression of miR-7 in the rat cerebral hemorrhage model and microglial inflammation model tissue was significantly lower than that in the normal control group. Expression of inflammatory cytokines including IL-1β, IL-8 and TNF-α was significantly increased in rats with intracerebral hemorrhage and microglial inflammation in rats, and the expression of these inflammatory cytokines was partially reversed after overexpression of miR-7. Double luciferase reporter gene and ELISA results showed that miR-7 could inhibit the expression of TLR4 and relieve the secondary inflammatory response of microglia after cerebral hemorrhage., Conclusions: We demonstrated that, in in vivo and in vitro experiments, miR-7 could reduce the LPS-induced inflammatory response produced by microglial cells, and alleviate the inflammation in the brain of rats with cerebral hemorrhage.

The murine monoclonal anti-idiotypic antibody, NP30, is a potential vaccine candidate against Schistosoma japonicum. Previous studies have revealed that NP30 has an immunoregulatory effect, but the underlying mechanism for this effect remains unknown. This study shows that NP30 induces dendritic cell (DC) maturation and increases the production of pro-inflammatory cytokines. The expression of CD86 and MHC II was upregulated in DCs following stimulation with NP30 in vitro. Moreover, NP30 induced Th17 polarization by increasing the production of IL-6 and TGF-β. In vivo, Th17 differentiation was induced by the production of key pro-inflammatory cytokines, including IL-6and TGF-β, from DCs of NP30-immunized mice. These results indicate that NP30 promotes Th17 polarization through DC activation, preventing serious schistosomiasis., (© 2018 The Authors. Parasite Immunology Published by John Wiley & Sons Ltd.)

Purpose: The objective of the study was to investigate the role of NFBD1 in the proliferation and apoptosis of laryngeal squamous cell carcinoma (LSCC) cells., Methods: Immunohistochemistry (IHC) and qRT-PCR was employed to determine the expressions of NFBD1 protein and mRNA in LSCC tissues and adjacent noncancerous tissues. After the downregulation of NFBD1 expression, the colony formation assay, MTS assay and apoptosis assay were used to investigate the changes in the proliferation and apoptosis of Hep2 cells. The mechanisms by which silencing NFBD1 promote apoptosis of Hep2 cells were examined by western blotting. Furthermore, xenograft models were used to evaluate the proliferation of Hep2 cells in vivo., Results: NFBD1 protein was upregulated in 55.6% of LSCC cancer tissues compared with adjacent normal tissues (26.7%). NFBD1 knockdown in Hep2 cells significantly impacted proliferation and apoptosis, and silencing NFBD1 might promote apoptosis of Hep2 cells by activating the mitochondrial apoptotic pathway. Xenograft models showed that silencing NFBD1 also significantly inhibited tumor growth., Conclusions: Our data highlight that NFBD1 participates in the regulation of proliferation and apoptosis in LSCC, and suggest that NFBD1 could be a promising therapy target.

Neutral alpha-1,4-glucosidase (NAG) is a crucial biomarker for the function of epididymis and is reported to be associated with semen quality. However, the correlation between NAG and Chinese semen quality has never been reported. This study aimed to investigate the level of NAG in the seminal plasma of Chinese men. A total of 394 cases of seminal plasma samples from normal, subfertile and infertile men were enrolled in this study. Male subfertility was caused by teratozoospermia, asthenospermia, severe oligozoospermia, asthenoteratozoospermia, oligoasthenospermia and oligoasthenoteratozoospermia. Male infertility was resulted from azoospermatism. The level of NAG was detected by spectrophotometry. Results showed that the level of NAG in normal men was significantly higher than that in subfertile and infertile men (p = .000). Meanwhile, the level of NAG in subfertile men was significantly greater than that in infertile men (p = .000). In addition, a significant difference was observed in normozoospermia, teratozoospermia, asthenospermia, severe oligozoospermia, asthenoteratozoospermia, oligoasthenospermia, oligoasthenoteratozoospermia and azoospermatism (p < .05). In conclusion, these data indicate that NAG is a crucial marker for assessing seminal plasma quality in Chinese men, which might be helpful for the assistant diagnosis of male infertility., (© 2017 Blackwell Verlag GmbH.)

We demonstrate theoretically that a toroidal Alfvén eigenmode (TAE) can parametrically decay into a geodesic acoustic mode and kinetic TAE in a toroidal plasma. The corresponding threshold condition for the TAE amplitude is estimated to be |δB&#95;{⊥}/B&#95;{0}|∼O(10^{-4}). Here, δB&#95;{⊥} and B&#95;{0} are, respectively, the perturbed magnetic field of the pump TAE and the equilibrium magnetic field. This novel decay process, in addition to contributing to the nonlinear saturation of energetic-particle or α-particle driven TAE instability, could also contribute to the heating as well as regulating the transports of thermal plasmas.

We identified a novel large fragment deletion from intron 9 to 3'UTR in PLS3 (E10-E16del) in one Chinese boy with X-linked early-onset osteoporosis and vertebral fractures, which expanded the pathogenic spectrum of X-linked early-onset osteoporosis. Treatment with zoledronic acid was beneficial for increasing BMD and reshaping the vertebral bodies of this patient., Introduction: X-linked early-onset osteoporosis is a rare disease, which is characterized by low bone mineral density (BMD), vertebral compression fractures (VCFs), and/or long bone fractures. We aimed to detect the phenotype and the underlying pathogenic mutation of X-linked early-onset osteoporosis in a boy from a nonconsanguineous Chinese family., Methods: We investigated the pathogenic mutation of the patient with X-linked early-onset osteoporosis by targeted next-generation sequencing and confirmed it by Sanger sequencing. We also observed the effects of zoledronic acid on fracture frequency and BMD of the patient., Results: Low BMD and multiple VCFs were the main phenotypes of X-linked early-onset osteoporosis. We identified a total of 12,229 bp deletion in PLS3, involving intron 9 to the 3'UTR (E10-E16 del). This large fragment deletion might be mediated by Alu repeats and microhomology of 26 bp at each breakpoint junction. Zoledronic acid treatment could significantly increase the Z-score of BMD and reshape the compressed vertebral bodies., Conclusion: We identified a large fragment deletion mutation in PLS3 for the first time and elucidated the possible mechanism of the deletion, which led to X-linked early-onset osteoporosis and multiple vertebral fractures. Our findings would enrich the etiology spectrum of this rare disease.

Mucosal antigen-specific CD4 T-cell responses to intestinal pathogens remain incompletely understood. Here we examined the CD4 T-cell response after oral infection with an internalin A 'murinized' Listeria monocytogenes (Lm). Oral Lm infection induced a robust endogenous listeriolysin O (LLO)-specific CD4 T-cell response with distinct phenotypic and functional characteristics in the intestine. Circulating LLO-specific CD4 T cells transiently expressed the 'gut-homing' integrin α 4 β 7 and accumulated in the intestinal lamina propria and epithelium where they were maintained independent of interleukin (IL)-15. The majority of intestinal LLO-specific CD4 T cells were CD27 - Ly6C - and CD69 + CD103 - while the lymphoid LLO-specific CD4 T cells were heterogeneous based on CD27 and Ly6C expression and predominately CD69 - . LLO-specific effector CD4 T cells transitioned into a long-lived memory population that phenotypically resembled their parent effectors and displayed hallmarks of residency. In addition, intestinal effector and memory CD4 T cells showed a predominant polyfunctional Th1 profile producing IFNγ, TNFα, and IL-2 at high levels with minimal but detectable levels of IL-17A. Depletion of CD4 T cells in immunized mice led to elevated bacterial burden after challenge infection highlighting a critical role for memory CD4 T cells in controlling intestinal intracellular pathogens.

Nodule development directly affects nitrogen fixation efficiency during soybean growth. Although abundant genome-based information related to nodule development has been released and some studies have reported the molecular mechanisms that regulate nodule development, information on the way nodule genes operate in nodule development at different developmental stages of soybean is limited. In this report, notably different nodulation phenotypes in soybean roots inoculated with Bradyrhizobium japonicum strain 113-2 at five developmental stages (branching stage, flowering stage, fruiting stage, pod stage and harvest stage) were shown, and the expression of nodule genes at these five stages was assessed quantitatively using RNA-Seq. Ten comparisons were made between these developmental periods, and their differentially expressed genes were analysed. Some important genes were identified, primarily encoding symbiotic nitrogen fixation-related proteins, cysteine proteases, cystatins and cysteine-rich proteins, as well as proteins involving plant-pathogen interactions. There were no significant shifts in the distribution of most GO functional annotation terms and KEGG pathway enrichment terms between these five development stages. A cystatin Glyma18g12240 was firstly identified from our RNA-seq, and was likely to promote nodulation and delay nodule senescence. This study provides molecular material for further investigations into the mechanisms of nitrogen fixation at different soybean developmental stages., Competing Interests: The authors declare no competing financial interests.

Recent data suggest that common genetic risks for metabolic disorders such as obesity may be human-specific and exert effects via the central nervous system. To overcome the limitation of human tissue access for study, we have generated induced human pluripotent stem cell (hiPSC)-derived neuronal cultures that recapture many features of hypothalamic neurones within the arcuate nucleus. In the present study, we have comprehensively characterised this model across development, benchmarked these neurones to in vivo events, and demonstrate a link between obesity risk variants and hypothalamic development. The dynamic transcriptome across neuronal maturation was examined using microarray and RNA sequencing methods at nine time points. K-means clustering of the longitudinal data was conducted to identify co-regulation and microRNA control of biological processes. The transcriptomes were compared with those of 103 samples from 13 brain regions reported in the Genotype-Tissue Expression database (GTEx) using principal components analysis. Genes with proximity to body mass index (BMI)-associated genetic variants were mapped to the developmentally expressed genesets, and enrichment significance was assessed with Fisher's exact test. The human neuronal cultures have a transcriptional and physiological profile of neuropeptide Y/agouti-related peptide arcuate nucleus neurones. The neuronal transcriptomes were highly correlated with adult hypothalamus compared to any other brain region from the GTEx. Also, approximately 25% of the transcripts showed substantial changes in expression across neuronal development and potential co-regulation of biological processes that mirror neuronal development in vivo. These developmentally expressed genes were significantly enriched for genes in proximity to BMI-associated variants. We confirmed the utility of this in vitro human model for studying the development of key hypothalamic neurones involved in energy balance and show that genes at loci associated with body weight regulation may share a pattern of developmental regulation. These data support the need to investigate early development to elucidate the human-specific central nervous system pathophysiology underlying obesity susceptibility., (© 2017 British Society for Neuroendocrinology.)

Cefquinome is a fourth-generation cephalosporin with broad-spectrum antibacterial activity, including activity against enteric gram-negative bacilli such as Riemerella anatipestifer. The pericarditis model was used to examine the pharmacodynamic characteristics of cefquinome against R. anatipestifer. Serum levels of cefquinome following the administration of different doses were determined by LC-MS/MS. Ducks with ca. 10(6) CFU/mL at the initiation of therapy were treated with cefquinome at doses that ranged from 0.0156 to 2 mg/kg of body weight/day (in 3, 6, 12, or 24 divided doses) for 24 h. The percentage of a 24-h dosing interval that the unbound serum cefquinome concentrations exceeded the MIC (fT > MIC) were the pharmacokinetic (PK)-pharmacodynamic (PD) parameter that best correlated with efficacy (R(2) 86.3% for R. anatipestifer, compared with 58.9% for the area under the concentration-time curve/MIC and 10.6% for peak/MIC). A sigmoid Emax model was used to estimate the magnitudes of the %fT > MIC associated with net bacterial stasis, a 1-log10 CFU reduction from baseline, and a 2-log10 CFU reduction from baseline; the corresponding values were (22.5 ± 1.3) %, (35.2 ± 4.5) %, and (42.4 ± 2.7) %. These data showed that treatment with cefquinome results in marked antibacterial effects in vivo against R. anatipestifer and that the host's immunity may also play a key role in the anti-infective therapy process., (© 2015 John Wiley & Sons Ltd.)

In this report we investigate the self-discharge in a positively charged polypyrrole-cellulose composite material in water solution. Rate constants for the self-discharge reaction are determined by potential step methods and their dependence on pH, temperature and applied potential are reported. Based on the results, we propose that two fundamentally different self-discharge mechanisms operate in parallel; one of faradaic origin with a rate constant increasing exponentially with applied potential and one mechanism comprising an initial reaction of the charged polymer with hydroxide ions. The second mechanism dominates at high pH as the rate constant for this reaction increases exponentially with pH whilst the faradaic reaction dominates at low pH. With this report we hope to shed light on the complex and elusive nature of self-discharge in conducting polymers to serve as guidance for the construction of electrical energy storage devices with conducting polymer components.

Background: Experimental and clinical studies have suggested that the presence of fragmented QRS complex (fQRS) is associated with various cardiovascular diseases. fQRS may predict major adverse cardiovascular events (MACE). The current meta-analysis was performed using clinical outcome studies to evaluate the role of fQRS in coronary artery disease (CAD)., Methods: A systematic search of electronic databases (Cochrane, Medline, Embase and Pubmed) from their inception to April 2014 was performed. Data were extracted from applicable articles to evaluate the prognostic value of fQRS in CAD., Results: A total of 16 observational studies about fQRS and CAD (n = 3,997 patients) were identified. Compared with the non-fQRS group, MACE and mortality were significantly higher in the fQRS group -odds ratios (OR) 3.19, 95 % confidence interval (95 % CI) [2.3, 4.42], p < 0.00001; OR 2.24, 95 % CI [1.71, 2.94], p < 0.0001. Patients developed Q waves, anterior-wall myocardial infarction (MI), and low left ventricular ejection fraction (LVEF) more frequently in the fQRS group than in the non-fQRS group-OR 2.59, 95 % CI [1.76, 3.81], p < 0.00001; OR 2.43, 95 % CI [1.07, 5.52], p = 0.03; OR - 6.43, 95 % CI [- 9.11, - 3.74], p < 0.00001., Conclusion: Based on current evidence, fQRS was associated with increased MACE, mortality, Q waves, anterior-wall MI, and decreased LVEF in CAD. These findings show that fQRS is a reliable marker in CAD.

Surface plasmons, free-electron collective oscillations in metallic nanostructures, provide abundant routes to manipulate light-electron interactions that can localize light energy and alter electromagnetic field distributions at subwavelength scales. The research field of plasmonics thus integrates nano-photonics with electronics. In contrast, electronics is also entering a new era of spintronics, where spin currents play a central role in driving devices. However, plasmonics and spin-current physics have so far been developed independently. Here we report the generation of spin currents by surface plasmon resonance. Using Au nanoparticles embedded in Pt/BiY(2)Fe(5)O(12) bilayer films, we show that, when the Au nanoparticles fulfill the surface-plasmon-resonance conditions, spin currents are generated across the Pt/BiY(2)Fe(5)O(12) interface. This spin-current generation cannot be explained by conventional heating effects, requiring us to introduce nonequilibrium magnons excited by surface-plasmon-induced evanescent electromagnetic fields in BiY(2)Fe(5)O(12). This plasmonic spin pumping integrates surface plasmons with spin-current physics, opening the door to plasmonic spintronics.

Epigenetic regulation of long interspersed nucleotide element-1 (LINE-1) retrotransposition events plays crucial roles during early development. Previously we showed that LINE-1 hypomethylation in neuronal tissues is associated with pathogenesis of neural tube defect (NTD). Herein, we further evaluated LINE-1 Homo sapiens (L1Hs) methylation in tissues derived from three germ layers of stillborn NTD fetuses, to define patterns of tissue specific methylation and site-specific hypomethylation at CpG sites within an L1Hs promoter region. Stable, tissue-specific L1Hs methylation patterns throughout three germ layer lineages of the fetus, placenta, and maternal peripheral blood were observed. Samples from maternal peripheral blood exhibited the highest level of L1Hs methylation (64.95%) and that from placenta showed the lowest (26.82%). Between samples from NTDs and controls, decrease in L1Hs methylation was only significant in NTD-affected brain tissue at 7.35%, especially in females (8.98%). L1Hs hypomethylation in NTDs was also associated with a significant increase in expression level of an L1Hs-encoded transcript in females (r = -0.846, p = 0.004). This could be due to genomic DNA instability and alternation in chromatins accessibility resulted from abnormal L1Hs hypomethylation, as showed in this study with HCT-15 cells treated with methylation inhibitor 5-Aza.

Lipusu is the first paclitaxel liposome preparation approved in the world and has been widely used in China for the treatment of ovary, breast and non-small cell lung cancer. In present study we evaluated the pharmacokinetic and tissue distribution characteristics of paclitaxel liposome in Sprague-Dawley rats and Beagle dogs. A rapid and simple liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay was developed for the determination of paclitaxel in plasma and tissues. The plasma concentrations of paclitaxel in both rats and dogs initially declined steeply, followed by slow elimination after intravenous administration of Lipusu at 5 mg/kg and 1 mg/kg, respectively. The pharmacokinetic parameters calculated by a non-compartmental method in rats and dogs were as follows: AUC0-24: 3 566.5±1 366.1 and 443.2±165.7 μg · h/L, CL: 1.5±0.5 and 2.1±0.6 L/h/kg, Vd: 20.0±7.8 and 38.4±12.5 L/kg, t1/2: 9.3±2.9 and 14.1±6.9 h, respectively. Biodistribution results in rats showed that except for brain and testis, liposomal paclitaxel was extensively distributed into various tissues, especially highly in liver and spleen., (© Georg Thieme Verlag KG Stuttgart · New York.)

Summary: Intermittent treatment with high-dose parathyroid hormone (PTH) enhances the quantity and quality of the fusion callus and reduces healing time of posterolateral spinal fusion with autologous iliac bone grafts in ovariectomized osteoporotic female Sprague-Dawley rats. Intermittent PTH (1-34) could be an appropriate adjunctive therapy for osteoporotic patients undergoing posterolateral intertransverse process fusion., Introduction: The study was designed to test the hypothesis that intermittent administration of PTH improves spinal fusion rates in a randomized controlled, ovariectomized osteoporotic rat spinal fusion model., Methods: Thirty-six 10-week-old Sprague-Dawley rats were ovariectomized and underwent bilateral posterolateral L4-L5 spinal fusion with autologous iliac bone graft 6 weeks later. The experimental (PTH) group (18 rats) received daily subcutaneously administered injections of PTH (1-34) at 30 μg/kg/day starting on the day of operation. The control group (18 rats) received a subcutaneously administered injection of normal saline of the same volume. Nine rats from each group were sacrificed at 4 and 6 weeks. After sacrifice, the L4-L5 vertebral segments were removed and analyzed by plain radiographs, μ-CT, histomorphometry, and serum bone metabolism marker., Results: The PTH group had a significantly higher fusion rate and X-ray fusion score than the control group at 4 and 6 weeks (p < 0.05). μ-CT and histological analysis showed that the fusion bone volume and cortical thickness for the PTH group were significantly higher than those for the control group at 4 and 6 weeks (p < 0.05). Metabolic marker analysis also showed significant difference between the two groups. The serum osteocalcin was significantly higher in the PTH group at 4 and 6 weeks, and levels of N-terminal peptide of type I collagen were significantly higher at 4 weeks (p < 0.05)., Conclusion: Intermittent treatment with high-dose PTH enhances the quantity of the fusion callus and reduces the healing time of posterolateral spinal fusion with autologous iliac bone grafts in ovariectomized osteoporotic female Sprague-Dawley rats.

Introduction: The relative expression of T cell receptor (TCR) beta variable (TRBV) and TCR diversity was compared between recipients receiving human leukocyte antigen (HLA)-mismatched transplants and those receiving HLA-matched transplants, using granulocyte colony-stimulating factor (G-CSF)-mobilized peripheral blood stem cells and bone marrow as grafts., Methods: The kinetics of the relative expression of TRBV family members were analyzed using real-time quantitative PCR. Additionally, the association of TRBV clonotype with acute graft-versus-host disease (aGVHD) was determined by cloning and sequence analysis of the CDR3 region., Results: The TCR diversity in recipients receiving HLA-mismatched transplants was significantly lower than in those receiving HLA-matched transplants at 1 month and 2 months after hematopoietic stem cell transplantation (HSCT) (both P < 0.05). However, these differences disappeared 3 months after transplantation. The relative expression of TRBV27 (n = 7 recipients) at the onset of aGVHD was higher than in corresponding donors (P = 0.025), but no significant differences were observed between recipients lacking aGVHD and their donors at serial time points after HSCT., Conclusion: Our results suggest that HLA disparity may affect the relative expression of TRBV in the early phase after transplantation, and TRBV27 may be associated with the onset of aGVHD., (© 2012 Blackwell Publishing Ltd.)

Background: Neonatal Bacillus Calmette-Guérin (BCG) vaccination induces vigorous T-helper type 1 (Th1) responses and inhibits allergy-related airway dysfunction, but the exact mechanisms remain unclear. The objective of this study was to address where the Th1 cells induced by neonatal BCG vaccination are generated and stored, and how they are recruited into the inflamed airway for the prevention of allergen-induced airway inflammation., Methods: We vaccinated neonatal C57BL/6 mice with BCG in a mouse model of asthma and analyzed the expression and function of Th1 cells in vivo and in vitro., Results: BCG vaccination-induced Th1 cells in the local inguinal lymph nodes (ILN) migrated into the lungs upon inhaled ovalbumin (OVA) challenge in OVA-sensitized mice. These CD4(+) T cells in the ILN exhibited potentials of activation, proliferation and cytokine secretion and expressed high levels of CXCR3. Adoptive transfer of CD4(+) T cells from BCG-treated ILN significantly decreased allergic airway responses. In addition, the protective effect of BCG vaccination against allergic airway inflammation was lost upon the excision of the ILN., Conclusions: These data demonstrate that ILN serves as a 'weapon' pool of Th1 cells following BCG vaccination, and these cells are ready for the migration into the inflamed lungs upon the allergen challenge, thereby inhibiting allergen-induced airway disorder., (© 2013 John Wiley & Sons A/S. Published by Blackwell Publishing Ltd.)

This Letter provides evidence for intrinsic longitudinal spin Seebeck effects (LSSEs) that are free from the anomalous Nernst effect (ANE) caused by an extrinsic proximity effect. We report the observation of LSSEs in Au/Y(3)Fe(5)O(12) (YIG) and Pt/Cu/YIG systems, showing that the LSSE appears even when the mechanism of the proximity ANE is clearly removed. In the conventional Pt/YIG structure, furthermore, we separate the LSSE from the ANE by comparing the voltages in different magnetization and temperature-gradient configurations; the ANE contamination was found to be negligibly small even in the Pt/YIG structure.

MiR-155 is known to participate in various cellular processes by targeting gene expression. We previously revealed a link between miR-155 and perturbation of trophoblast invasion and differentiation. This study aimed to investigate the target molecule(s) of miR-155 on the influence on the proliferation and migration of trophoblast cells. Bioinformatics analysis showed that, at the 3' untranslated region (UTR) of cyclin D1, six bases are complementary to the seed region of miR-155. Luciferase assays and cyclin D1 3'UTR transfection assays validated that cyclin D1 3'UTR was the target of miR-155 in HTR-8/SVneo cells. Overexpression of miR-155 in HTR-8/SVneo cells reduced the level of cyclin D1 protein, decreased cell proliferation and invasion, and increased cell number at the G1 stage. Furthermore, the increased expression of miR-155 also regulated the protein levels of kinase inhibitory protein p27 and phosphorylated cytoskeletal protein filamin A. In conclusion, we found that cyclin D1 may be a target of miR-155 in HTR-8/SVneo cells, and demonstrated a negative regulatory role of miR-155 involved in cyclin D1/p27 pathway in proliferation and migration of the cells., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Mucopolysaccharidosis I (MPS I) is a lysosomal storage disease that results from the deficiency of α-l-iduronidase and is transmitted in an autosomally recessive manner. This report describes the first systematic screening for mutations in Chinese MPS I patients from mainland China, wherein we have summarized the phenotype/genotype correlation of the individuals in Chinese MPS I patients. Mutational analyses were performed in 57 unrelated Chinese MPS I patients. Overall, 105 mutant alleles were identified from a set of 41 different mutations. Notably, of these 41 mutations, 27 were novel mutations that consisted of 8 splicing mutations (c.1-2C>G, c.296+4G>A, c.300-1G>C, c.792+1G>C, c.973-4G>A, c.1189+5G>T, c.1402+1G>T and c.1402+2T>G), 1 nonsense mutation (p.W41X), 1 insertion (c.668-670ins GCG), 5 duplications (c.531dupT, c.657dupG, c.883dupC, c.1147dupG and c.1225dupG), 3 deletions (c.349delT, c.1593delG and c.1244-1271del27),1 nucleotide substitution c.2T>C and 8 missense mutations (p.H33P,p.F52L, p.G168V,p.T179R,p. E182D, p.L237R, p.L238R and p.L421P). The missense mutations p.A79V and p.L346R, which accounted for 16.7% (19/114) and 12.3% (14/114) respectively, were the common mutations in Chinese patients but were rare in the mutational profiles reported for other populations. These results indicate that Chinese MPS I patients may have a different mutational spectrum compared to those of other populations. Moreover, for the first time in China, molecular genetic methods were used for prenatal diagnosis of six cases in five families., (© 2011 John Wiley & Sons A/S.)

Signal transducers and activators of transcription 3 (STAT3) is a central cytoplasmic transcription factor and regulates a number of pathways important in tumorigenesis including cell cycle progression, apoptosis, tumor angiogenesis, invasion and metastasis.This study aims to investigate the expression of pSTAT3, VEGF and VEGF-C in pancreatic adenocarcinoma and their relations to the clinicopathological features, tumor angiogenesis and prognosis. In the present study, the expression of pSTAT3, VEGF and VEGF-C and microvascular density (MVD) were examined via immunohistochemistry. The clinicopathological information was collected and patients were regularly followed up. The relationship between the parameters and the clinicopathological features were analyzed, and the univariate and multivariate prognostic factors were also analyzed. The expression of pSTAT3 in tumor tissues was significantly higher in contrast to that in normal tissues, and pSTAT3 was related to VEGF and VEGF-C expression, MVD, tumor size, lymphogenous status and TNM staging (P<0.05). Survival analysis suggested that tumor size, TNM staging, pSTAT3 and VEGF expression were risk factors of prognosis, but no independent factors were found. We concluded that pSTAT3, which was a risk factor of prognosis, was abnormally expressed in pancreatic adenocarcinoma and related to tumor size, TNM staging and lymphatic metastasis. pSTAT3 may promote tumor angiogenesis via up-regulating VEGF on protein and even gene levels, and enhance the early lymphatic metastasis through VEGF-C. Better understanding of STAT3 signaling pathways in angiogenesis may contribute to the development of novel therapeutic strategies in angiogenesis and metastasis of pancreatic cancer.

A 184 kb gap in an ovine MHC physical map was successfully closed by identification of two overlapping clones (304C7 and 222G18) from a Chinese fine wool merino sheep BAC library. The location and tiling path of the two clones were confirmed by BAC-end sequencing and PCR amplification of loci in overlapping regions. Full-length sequencing of the clones identified 13 novel ovine genes in the gap between loci Notch4 and Btnl2, and eight of them belonging to the Butyrophilin-like (Btn-like or Btnl) gene family. The scattered distribution of the Btnl gene cluster at the gap provided a clue to explain the difficulties previously experienced in closing the gap. Completed BAC contigs of the ovine MHC will facilitate sequencing of the entire ovine leukocyte antigen (OLA) region, providing detailed information for comparative studies of MHC evolution., (© 2010 The Authors, Animal Genetics © 2010 Stichting International Foundation for Animal Genetics.)

Aberrant Signal transducers and activators of transcription-3 (STAT3) signaling pathway is a major cause of tumor invasion and metastasis; the underlying mechanisms, however, are not well understood. Epithelial-mesenchymal transition (EMT) is an early event that occurs during invasion of cancers of an epithelial origin. It remains elusive whether STAT3signaling pathway is involved in EMT. The objective of this study was to evaluate the effect of blockage of STAT3 signaling pathway on IL-6 inducing EMT in human pancreatic cancer cells. We used SW1990 cells and induced them to undergo EMT by exposing these cells to soluble factor interleukin-6 (IL-6). The expression of Snail, E-cadherin, and Twist was detected by reverse transcription-PCR, real-time PCR, and Western blotting. Cell morphology was observed under invert phase-contrast microscope.The invasion ability was determined by cell invasion assay in vitro. Our results demonstrated that STAT3 signaling pathway was involved in pancreatic cancer cell invasion and EMT, and that EMT induced by IL-6 was associated with the activation of STAT3 signaling pathway. Inhibition of STAT3 signaling pathway by silencing of the STAT3 gene with RNAi blocked STAT3 signaling pathway activation and suppressed EMT in pancreatic cancer cells. Collectively, the STAT3 signaling pathway plays an important role in the process of EMT of pancreatic cancer by regulating Snail gene expression. Better understanding of STAT3 signaling pathways in EMT may contribute to development of novel therapeutic strategies in invasion and metastasis of pancreatic cancer.

Active immunotherapy of cancer has yet to yield effective therapies in the clinic. To evaluate the translatability of DNA-based vaccines we analyzed the profile of T-cell immunity by plasmid vaccination in a murine model, using transcriptome microarray analysis and flow cytometry. DNA vaccination resulted in specific T cells expressing low levels of co-inhibitory molecules (most notably PD-1), strikingly different from the expression profile elicited by peptide immunization. In addition, the T-cell response primed through this dual-antigen-expressing plasmid (MART-1/Melan-A and tyrosinase) translated into a substantial proliferation capacity and functional conversion to antitumor effector cells after tyrosinase and MART-1/Melan-A peptide analog boost. Furthermore, peptide boost rescued the immune response against the subdominant tyrosinase epitope. This immunization approach could be adapted to elicit potent immunity against multiple tumor antigens, resulting in a broader immune response that was more effective in targeting human tumor cells. Finally, this study sheds light on a novel mechanism of immune homeostasis through synchronous regulation of co-inhibitory molecules on T cells, highly relevant to heterologous prime boost approaches involving DNA vaccines as priming agents.

This study assessed cardiac diastolic dysfunction (DD) in HIV-infected subjects without cardiovascular symptoms in China. Eighty-four HIV-infected patients without cardiovascular symptoms were recruited and compared with 30 HIV-negative control subjects. Cardiac DD was evaluated using echocardiography including tissue Doppler imaging. DD was detected in 47.6% of AIDS patients and 42.8% of HIV-positive patients, which was significantly higher than in HIV-negative controls. After logistic regression analysis, HIV infection was independently correlated with cardiac DD (P < 0.05). Among HIV-positive subjects, logistic regression analysis showed that zidovudine exposure was associated with higher prevalence of DD (P < 0.05). Asymptomatic cardiac DD was observed frequently in HIV-infected subjects. HIV infection itself and zidovudine exposure were correlated with a higher prevalence of cardiac DD.

The purpose of this study was to investigate the effects of combination therapy with methylprednisolone (MP) and Nogo-66 antagonistic peptide (NEP1-40) on morphological and functional recovery in adult rats subjected to thoracic compression spinal cord injury (SCI). Animals were randomized into four groups: a trauma control group, an MP group, an NEP1-40 group, and a combined treatment group. The inflammatory reaction, neuronal and oligodendrocyte survival, and ultrastructure were assessed at the injury site. Functional analysis was also performed using Basso, Beattie and Bresnahan (BBB) scoring. Rat behaviour was evaluated regularly up to week 4. NEP1-40 did not alter the beneficial effect of MP on haematogenous inflammatory cell infiltration, while combined treatment resulted in greater neuronal and oligodendrocyte survival compared with monotherapy or control. Combination therapy resulted in better locomotor scores. These results in a clinically-relevant SCI model showed that significant neuroprotection can be obtained by combining an initial acute IV injection of MP with continuously infused NEP1-40.

This study investigated the effects of the ionic dissolution products of NovaBone on osteoblastic proliferation and cell cycle regulation. MG63 osteoblast-like cells were cultured in NovaBone-conditioned Dulbecco's Modified Eagle's Medium (DMEM) or control DMEM for 10 days. The concentration of silicon ions was significantly higher in NovaBone-conditioned DMEM than control DMEM. MG63 cells cultured in NovaBone -conditioned DMEM exhibited greater proliferation on days 1 and 4 than control cells. There were increased proportions of Novabone-conditioned DMEM-cultured cells in the S and G(2)/M phases, and decreased proportions in the G(0)/G(1) phase on days 1 and 4 versus control cells, while no differences were observed on days 7 and 10 between the two groups. Bone morphogenic protein 2 production increased in both groups, but was significantly higher for the NovaBone-conditioned DMEM-cultured cells on day 10 compared with the controls. In conclusion, the NovaBone ionic dissolution products, particularly the silicon ions, promoted proliferation of MG63 osteoblast-like cells in vitro via influences on the cell cycle.

Objectives: Type 1 diabetes mellitus, characterized by loss of pancreatic beta-cells, can be ameliorated by islet transplantation, but this treatment is restricted by the scarcity of islet tissue and by allograft rejection., Materials and Methods: We isolated and characterized skin-derived precursors (SKPs)--an abundant source of autologous cells--and developed an experimental strategy to convert them into insulin-producing cells (IPCs) in vitro within a short period of time, through extracellular factor modification and analyses of IPCs by reverse transcription-polymerase chain reaction, immunocytochemistry and enzyme-linked immunosorbent assay., Results: SKPs could self-assemble to form three-dimensional islet cell-like clusters (dithizone-positive) and co-express insulin and C-peptide. In addition, they expressed multiple genes related to pancreatic beta-cell development and function (e.g. insulin 1, insulin 2, islet-1, Pdx-1, NeuroD/beta2, glut-2 and Nkx6.1), but not other pancreas-specific hormones and enzymes (e.g. glucagon, somatostatin and amylase). Moreover, when stimulated with glucose, these cells synthesized and secreted insulin in a glucose-regulated manner., Conclusions: The findings of this study indicate that SKPs can differentiate into functional IPCs and can provide an abundant source of autologous cells for transplantation. This study also provides strategies to derive autologous islet-replacement tissues from human skin stem cells.

Aims: To enhance the recovery of f(2) bacteriophage and poliovirus by an established method based on the adsorption to and elution from positively-charged Al(OH)(3)-treated silica gel., Methods and Results: Polyaluminum Chloride (PAC) was added to water samples to neutralize the negatively charged materials, which can reduce virus recovery by providing a competing adsorption mode on the media surface. Using this improved process (PAC 30 mg l(-1), pH 6.5, temperature 20 approximately 30 degrees C), the recoveries of Poliovirus I and f(2) from small-volume sewage (100 ml) were 110.76 +/- 36.0% and 92.06 +/- 8.65%, respectively (P < 0.05 vs. traditional methods). Recovery from a 20-L volume of sewage averaged 85.65 +/- 4.43% for f(2) and 88.73 +/- 9.76% for poliovirus, significantly higher than the recoveries in the traditional methods (P < 0.05)., Conclusions: PAC could enhance concentration efficiency of poliovirus and f(2) phage from sewage water., Significance and Impact of the Study: This method should significantly improve the recovery of viruses from sewage.

Background: During endotoxaemia, neutrophils activated by inflammatory cytokines release reactive oxygen species and neutrophil elastase, resulting in hepatic necrosis and dysfunction. This study investigated the possible mechanism underlying the protective effect of sivelestat, a neutrophil elastase inhibitor, on endotoxin-induced liver injury following partial hepatectomy., Methods: Lipopolysaccharide (LPS) was administered intravenously to male Sprague-Dawley rats 48 h after 70 per cent hepatectomy. Sivelestat or normal saline was given intravenously before LPS administration,, Results: Treatment with sivelestat significantly improved the survival rate. Sivelestat prevented increases in the concentration of serum enzymes and total bilirubin related to liver injury. Levels of inflammatory cytokines in serum and liver tissue were significantly lower in the sivelestat-treated group than in the control group. The degree of neutrophil infiltration, necrosis and apoptosis in the remnant liver was significantly decreased in sivelestat-treated rats. Sivelestat pretreatment inhibited the activation of nuclear factor (NF) kappaB, caspase 3 and 8 activities, and cytochrome c release., Conclusion: Sivelestat prevents LPS-induced liver injury by inhibition of NF-kappaB activation and apoptosis.