Biomedical subjects

H Li

Publications and source records attributed to H Li.

At least 37 records · Page 2Linked to original sources

PubMed2006

Usefulness of traditionally defined herbal properties for distinguishing prescriptions of traditional Chinese medicine from non-prescription recipes.

Traditional Chinese medicine (TCM) has been widely practiced and is considered as an attractive to conventional medicine. Multi-herb recipes have been routinely used in TCM. These have been formulated by using TCM-defined herbal properties (TCM-HPs), the scientific basis of which is unclear. The usefulness of TCM-HPs was evaluated by analyzing the distribution pattern of TCM-HPs of the constituent herbs in 1161 classical TCM prescriptions, which shows patterns of multi-herb correlation. Two artificial intelligence (AI) methods were used to examine whether TCM-HPs are capable of distinguishing TCM prescriptions from non-TCM recipes. Two AI systems were trained and tested by using 1161 TCM prescriptions, 11,202 non-TCM recipes, and two separate evaluation methods. These systems correctly classified 83.1-97.3% of the TCM prescriptions, 90.8-92.3% of the non-TCM recipes. These results suggest that TCM-HPs are capable of separating TCM prescriptions from non-TCM recipes, which are useful for formulating TCM prescriptions and consistent with the expected correlation between TCM-HPs and the physicochemical properties of herbal ingredients responsible for producing the collective pharmacological and other effects of specific TCM prescriptions.

Algorithms↗

PubMed2006

Detachment-induced upregulation of XIAP and cIAP2 delays anoikis of intestinal epithelial cells.

Detachment of normal epithelial cells from the extracellular matrix triggers apoptosis, a phenomenon called anoikis. Conversely, carcinoma cells tend to be relatively more anoikis-resistant than their normal counterparts, and this increased resistance represents a critical feature of the malignant phenotype. Mechanisms that control susceptibility and resistance to anoikis are not fully understood. It is now known that detachment of non-malignant epithelial cells triggers both pro- and antiapoptotic signals, and it is the balance between these signals and the duration of detachment that determine further fate of the cells. Detachment-induced antiapoptotic events delay anoikis and if cells reattach relatively soon after detachment they survive. Direct regulators of apoptosis responsible for this delay of anoikis are unknown. We found that detachment of non-malignant intestinal epithelial cells triggers upregulation of inhibitors of apoptosis protein (IAP) family, such as X-chromosome-linked inhibitor of apoptosis protein and cellular inhibitor of apoptosis-2 (cIAP2). We demonstrated that this upregulation requires detachment-dependent activation of the transcription factor nuclear factor-kappaB. We further observed that various IAP antagonists accelerate anoikis, indicating that upregulation of the IAPs delays detachment-triggered apoptosis. We conclude that the IAPs are important regulators of the balance between detachment-triggered life and death signals. Perhaps, not by coincidence, these proteins are often upregulated in carcinomas, tumors composed of cells that tend to be anoikis-resistant.

Anoikis↗

PubMed2006

Endogenous overproduction of beta-amyloid induces tau hyperphosphorylation and decreases the solubility of tau in N2a cells.

Although neurofibrillary tangles and senile plaques have been identified as the hallmark pathological changes in the brain of Alzheimer's disease (AD), the relationship between them is still not fully understood. In the present study, we have studied the effect of endogenously overproduced amyloid beta (A beta) on tau by using wild type amyloid precursor protein (APP) transfected (N2a/APP695), or Swedish mutant APP plus Delta 9 deleted presenilin-1 co-transfected (N2a/APPswe.Delta 9) and APP vector transfected (N2a/vector) cell lines. We measured the secreted and intracellular A beta, including A beta(1-40) and A beta(1-42), by Sandwich ELISA assay. It was shown that the levels of A beta were increased time-dependently in N2a/APP695 and N2a/APPswe.Delta 9 but not in N2a/vector upon butyric acid (BA) treatment. Compared with N2a/vector cells, tau in N2a/APP695 and N2a/APPswe.Delta 9 cells was not extracted by RIPA buffer, and the SDS-extracted tau protein was hyperphosphorylated at Tau-1 and PHF-1 epitopes upon BA treatment. Obvious accumulation of the hyperphosphorylated tau in N2a/APP695 and N2a/APPswe.Delta 9 cells was observed at 48 h after BA treatment. The total level of the extracted tau was reduced in N2a/APP695 and N2a/APPswe.Delta 9 lines compared with N2a/vector cells by Western blot, and this reduction of total tau was also detected by immunofluorescence staining. No obvious alteration of tau mRNA was observed in both N2a/APP695 and N2a/APPswe.Delta 9 cells compared with N2a/vector. This study provides direct evidence demonstrating that endogenously overproduced A beta not only induces tau hyperphosphorylation but also decreases the level and solubility of tau in N2a cell lines.

Amyloid beta-Peptides↗

PubMed2006

Prevention of murine experimental autoimmune encephalomyelitis by in vivo expression of a novel recombinant immunotoxin DT390-RANTES.

Experimental autoimmune encephalomyelitis (EAE) is a T-cell-mediated autoimmune disease. Chemokine receptor CCR5 has been shown to be essential for the T-cell recruitment to the inflammatory site in EAE. In this study, we assumed that an immunotoxin directed at CCR5+ cells would be able to reduce the disease activity of EAE. A recombinant immunotoxin, DT390-RANTES-SRalpha, was constructed in an eukaryotic cell expression plasmid consisting of regulated on activation normal T cells expressed and secreted (RANTES) as the targeting moiety and DT390 as the toxic moiety. DT390-RANTES was expressed in vitro and was highly toxic to activated mouse T cells with the inhibitory concentration 50 at 0.18 ng/ml. To evaluate whether DT390-RANTES was effective in preventing EAE, C57BL/6 mice were immunized with myelin basic protein, emulsified with complete Freund's adjuvant and were treated by injecting cationic liposome-embedded plasmid DNA into the muscle of hind limbs. Mice treated with DT390-RANTES-SRalpha developed a much milder EAE compared to mice treated with phosphate-buffered saline or the empty plasmid DNA. Much less CCR5+-infiltrating cells were found in the central nervous system in DT390-RANTES-SRalpha-treated mice than in the control mice. This study indicates that recombinant immunotoxin can be expressed in vivo, and targeting CCR5 can attenuate the disease activity of EAE in mice.

3T3 Cells↗

PubMed2006

AP-2alpha and AP-2gamma are transcriptional targets of p53 in human breast carcinoma cells.

Activating enhancer-binding protein 2alpha (AP-2alpha) and activating enhancer-binding protein 2gamma (AP-2gamma) are transcription factors that bind GC-rich consensus sequences and regulate the expression of many downstream genes. AP-2alpha and AP-2gamma interact with p53 both physically and functionally. Expression microarray results in human breast carcinoma cells with forced p53 expression revealed AP-2gamma as a putative transcriptional target of p53. To confirm and extend these findings we measured the effects of forced p53 expression in human breast carcinoma cells by real-time reverse transcription-PCR, Western blotting, electrophoretic gel mobility shift assays, promoter reporter, chromatin immunoprecipitation and chromatin accessibility assays. Wild-type p53 expression rapidly induced not only AP-2gamma but also AP-2alpha mRNA. The subsequent increase in these proteins led to increased AP-2 DNA-binding and transactivating activity. Candidate p53-binding sites were identified in the AP-2alpha and AP-2gamma promoters. p53 binding to these cis-elements in vivo was also observed, together with a relaxation of chromatin structure in these regions. Finally, expression of either AP-2alpha or gamma inhibited growth of human breast carcinoma cells in vitro. Taken together, our findings indicate that these AP-2 genes are targets for transcriptional activation by p53 and suggest that AP-2 proteins may mediate some of the downstream effects of p53 expression such as inhibition of proliferation.

Adenocarcinoma↗

PubMed2006

TA-p63-gamma regulates expression of DeltaN-p63 in a manner that is sensitive to p53.

Genetic analysis indicates that TP63 is required for establishment and preservation of self-renewing progenitors within the basal layer of several epithelial structures, however, the specific contributions of transactivating (TA-p63) and dominant-negative (DeltaN-p63) isoforms remain largely undefined. Recent studies have suggested a model in which TA-p63 plays an important role in the establishment of progenitor populations in which expression of DeltaN-p63 contributes to the preservation of self-renewing capacity. Our previous studies indicate that DeltaN-p63 is a transcriptional target of p53, however, the absence of overt epithelial deficiencies in p53-/- mice and reports of increased expression of DeltaN-p63 in p53-/- mice suggest p53-independent mechanisms also contribute to expression of DeltaN-p63. Here, we present data indicating that, prolonged loss of p53 leads to the activation of a p53-independent mechanism for transcriptional regulation of DeltaN-p63. This p53-independent mechanism is sensitive to ectopic p53 but not to a p53 mutant that lacks the transactivation domain. We further show that in cells in which p53 is expressed TA-p63-gamma protein is destabilized in a manner that is p53 dependent and sensitive to pharmacologic inhibition of the 26S proteosome. Consistent with this observation, we demonstrate that loss of p53 leads to the stabilization of TA-p63-gamma that is reversible by ectopic p53. Finally, we present evidence that disruption of TA-p63-gamma expression leads to decreased expression of DeltaN-p63 and that overexpression of TA-p63-gamma was sufficient to enhance the activity of the DeltaN-p63 promoter. Taken together, our studies indicate that TA-p63-gamma is capable of activating expression of DeltaN-p63 and that this mechanism may account for p53-independent expression of DeltaN-p63.

Breast↗

PubMed2006

Safety enhanced photodynamic therapy with half dose verteporfin for chronic central serous chorioretinopathy: a short term pilot study.

AIM: To evaluate short term safety of an enhanced photodynamic therapy (PDT) protocol with half dose verteporfin for treating chronic central serous chorioretinopathy (CSC). METHODS: 20 eyes of 18 patients with symptomatic chronic CSC underwent PDT using 3 mg/m2 verteporfin. Verteporfin was infused over 8 minutes followed by indocyanine green angiography guided laser application 2 minutes later. Serial optical coherence tomography (OCT) and multifocal electroretinography (mfERG) recordings were performed before PDT, at 4 days, 2 weeks, and 1 month after PDT. The best corrected visual acuity (BCVA), OCT central retinal thickness, and mean mfERG response amplitudes and peak latencies were compared longitudinally. Subgroup analysis was further performed for eyes with or without pigment epithelial detachment (PED). RESULTS: At 1 month after PDT, the median BCVA improved from 20/40 to 20/30 (p = 0.001). The mean central retinal thickness also reduced from 276 microm to 158 microm (p < 0.001) and 17 (85%) eyes had complete resolution of serous retinal detachment and/or PED. MfERG showed no significant changes in the mean N1 and P1 response amplitude and latency for all eyes. Subgroup analysis demonstrated that eyes without PED had a significant increase in the mean central mfERG P1 response amplitude with reduction in P1 peak latency at 1 month post-PDT. For eyes with PED, transient reduction in the mean central P1 response amplitude was observed at 4 days post-PDT. CONCLUSIONS: The modified safety enhanced PDT protocol with half dose verteporfin appeared to be a beneficial treatment option for patients with chronic CSC, especially in eyes without serous PED. Further controlled study is warranted to demonstrate the long term safety and efficacy of this treatment option.

Adult↗

PubMed2006

Functional and clinical characterization of a mutation in KCNJ2 associated with Andersen-Tawil syndrome.

BACKGROUND: Andersen-Tawil syndrome (ATS) is a rare inherited disorder, characterised by periodic paralysis, cardiac dysarrhythmias, and dysmorphic features, and is caused by mutations in the gene KCNJ2, which encodes the inward rectifier potassium channel, Kir2.1. This study sought to analyse KCNJ2 in patients with familial ATS and to determine the functional characteristics of the mutated gene. METHODS AND RESULTS: We screened a family with inherited ATS for the mutation in KCNJ2, using direct DNA sequencing. A missense mutation (T75R) of Kir2.1, located in the highly conserved cytoplasmic N-terminal domain, was identified in three affected members of this family. Using the Xenopus oocyte expression system and whole cell voltage clamp analyses, we found that the T75R mutant was non-functional and possessed a strong dominant negative effect when co-expressed with the same amount of wild type Kir2.1. Transgenic (Tg) mice expressing the mutated form of Kir2.1 in the heart had prolonged QTc intervals compared with mice expressing the wild type protein. Ventricular tachyarrhythmias were observed in 5 of 14 T75R-Tg mice compared with 1 of 7 Wt-Tg and none of 6 non-transgenic littermates. In three of five T75R-Tg mice with ventricular tachycardia, their ECG disclosed bidirectional tachycardia as in our proband. CONCLUSIONS: The in vitro studies revealed that the T75R mutant of Kir2.1 had a strong dominant negative effect in the Xenopus oocyte expression system. It still preserved the ability to co-assemble and traffic to the cell membrane in mammalian cells. For in vivo studies, the T75R-Tg mice had bidirectional ventricular tachycardia after induction and longer QT intervals.

Adolescent↗

PubMed2006

Highly purified CD44+ prostate cancer cells from xenograft human tumors are enriched in tumorigenic and metastatic progenitor cells.

CD44 is a multifunctional protein involved in cell adhesion and signaling. The role of CD44 in prostate cancer (PCa) development and progression is controversial with studies showing both tumor-promoting and tumor-inhibiting effects. Most of these studies have used bulk-cultured PCa cells or PCa tissues to carry out correlative or overexpression experiments. The key experiment using prospectively purified cells has not been carried out. Here we use FACS to obtain homogeneous CD44(+) and CD44(-) tumor cell populations from multiple PCa cell cultures as well as four xenograft tumors to compare their in vitro and in vivo tumor-associated properties. Our results reveal that the CD44(+) PCa cells are more proliferative, clonogenic, tumorigenic, and metastatic than the isogenic CD44(-) PCa cells. Subsequent molecular studies demonstrate that the CD44(+) PCa cells possess certain intrinsic properties of progenitor cells. First, BrdU pulse-chase experiments reveal that CD44(+) cells colocalize with a population of intermediate label-retaining cells. Second, CD44(+) PCa cells express higher mRNA levels of several 'stemness' genes including Oct-3/4, Bmi, beta-catenin, and SMO. Third, CD44(+) PCa cells can generate CD44(-) cells in vitro and in vivo. Fourth, CD44(+) PCa cells, which are AR(-), can differentiate into AR(+) tumor cells. Finally, a very small percentage of CD44(+) PCa cells appear to undergo asymmetric cell division in clonal analyses. Altogether, our results suggest that the CD44(+) PCa cell population is enriched in tumorigenic and metastatic progenitor cells.

Animals↗

PubMed2006

Degradation of benzo[a]pyrene in an experimentally contaminated paddy soil by vetiver grass (Vetiveria zizanioides).

A pot experiment was conducted to study the effect of growing vetiver grass on the biodegradation of benzo[a]pyrene (B[a]P) under glasshouse conditions. Plant biomass, microbial biomass C and degradation of B[a]P were determined. B[a]P disappeared faster in the plant treatments than in unplanted controls. Disappearance of B[a]P was accompanied by an increase in soil microbial biomass C. Vetiver grass may promote the biodegradation of B[a]P under flooded conditions by plant roots by stimulating the microbial biomass. Microbial biomass was the main factor affecting dissipation of B[a]P under flooded conditions.

Benzopyrenes↗

PubMed2006

Prediction of estrogen receptor agonists and characterization of associated molecular descriptors by statistical learning methods.

Specific estrogen receptor (ER) agonists have been used for hormone replacement therapy, contraception, osteoporosis prevention, and prostate cancer treatment. Some ER agonists and partial-agonists induce cancer and endocrine function disruption. Methods for predicting ER agonists are useful for facilitating drug discovery and chemical safety evaluation. Structure-activity relationships and rule-based decision forest models have been derived for predicting ER binders at impressive accuracies of 87.1-97.6% for ER binders and 80.2-96.0% for ER non-binders. However, these are not designed for identifying ER agonists and they were developed from a subset of known ER binders. This work explored several statistical learning methods (support vector machines, k-nearest neighbor, probabilistic neural network and C4.5 decision tree) for predicting ER agonists from comprehensive set of known ER agonists and other compounds. The corresponding prediction systems were developed and tested by using 243 ER agonists and 463 ER non-agonists, respectively, which are significantly larger in number and structural diversity than those in previous studies. A feature selection method was used for selecting molecular descriptors responsible for distinguishing ER agonists from non-agonists, some of which are consistent with those used in other studies and the findings from X-ray crystallography data. The prediction accuracies of these methods are comparable to those of earlier studies despite the use of significantly more diverse range of compounds. SVM gives the best accuracy of 88.9% for ER agonists and 98.1% for non-agonists. Our study suggests that statistical learning methods such as SVM are potentially useful for facilitating the prediction of ER agonists and for characterizing the molecular descriptors associated with ER agonists.

Forecasting↗

PubMed2006

Functional epigenetics identifies a protocadherin PCDH10 as a candidate tumor suppressor for nasopharyngeal, esophageal and multiple other carcinomas with frequent methylation.

Protocadherins constitute the largest subgroup in the cadherin superfamily of cell adhesion molecules. Their major functions are poorly understood, although some are implicated in nervous system development. As tumor-specific promoter methylation is a marker for tumor suppressor genes (TSG), we searched for epigenetically inactivated TSGs using methylation-subtraction combined with pharmacologic demethylation, and identified the PCDH10 CpG island as a methylated sequence in nasopharyngeal carcinoma (NPC). PCDH10 is broadly expressed in all normal adult and fetal tissues including the epithelia, though at different levels. It resides at 4q28.3--a region with hemizygous deletion detected by array-CGH in NPC cell lines; however, PCDH10 itself is not located within the deletion. In contrast, its transcriptional silencing and promoter methylation were frequently detected in multiple carcinoma cell lines in a biallelic way, including 12/12 nasopharyngeal, 13/16 esophageal, 3/4 breast, 5/5 colorectal, 3/4 cervical, 2/5 lung and 2/8 hepatocellular carcinoma cell lines, but not in any immortalized normal epithelial cell line. Aberrant methylation was further frequently detected in multiple primary carcinomas (82% in NPC, 42-51% for other carcinomas), but not normal tissues. The transcriptional silencing of PCDH10 could be reversed by pharmacologic demethylation with 5-aza-2'-deoxycytidine or genetic demethylation with double knockout of DNMT1 and DNMT3B, indicating a direct epigenetic mechanism. Ectopic expression of PCDH10 strongly suppressed tumor cell growth, migration, invasion and colony formation. Although the epigenetic and genetic disruptions of several classical cadherins as TSGs have been well documented in tumors, this is the first report that a widely expressed protocadherin can also function as a TSG that is frequently inactivated epigenetically in multiple carcinomas.

Azacitidine↗

PubMed2006

Hint1 is a haplo-insufficient tumor suppressor in mice.

The HINT1 protein, a member of the histidine triad (HIT) family, is highly conserved in diverse species and ubiquitously expressed in mammalian tissues. However, its precise function in mammalian cells is not known. As a result of its structural similarity to the tumor-suppressor protein FHIT, we used homozygous-deleted Hint1 mice to study its role in tumorigenesis. We discovered that after 2 to 3 years of age the spontaneous tumor incidence in Hint1 -/- mice was significantly greater than that in wild-type Hint1 +/+ mice (P < 0.05). Using a well-established mouse model of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary carcinogenesis we found a marked and significant (P < 0.05) increase in the incidence of mammary and ovarian tumors in both, Hint1 -/- and +/- mice versus +/+ mice. The Hint1 -/- and +/- mice had similar tumor incidence and similar tumor histologies. Therefore, deletion of Hint1 in mice enhances both spontaneous tumor development and susceptibility to tumor induction by DMBA. In addition, since the Hint1 +/- tumors retained expression of the unmutated wild-type allele, Hint1 is haplo-insufficient with respect to tumor suppression in this model system.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2006

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis.

To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.

Adenocarcinoma↗

PubMed2006

Ion-pair reversed-phase HPLC: assay validation of sodium tanshinone IIA sulfonate in mouse plasma.

Sodium tanshinone IIA sulfonate (STS), a hydrophilic ionic substance, is used as a cardiovascular drug. An ion-pair reversed-phase high-performance liquid chromatography (IP-RP-HPLC) method for the determination of STS in mouse plasma was initially developed. The assay involved a rapid and simple extraction process and subsequent detection at 271 nm. The retention time for STS was 7.5 min. Based on extracted STS standard mouse plasma at 1.5,10 and 50 microg/ml, the assay precision were 2.7, 2.1 and 1.7% with a mean accuracy of 96.7, 98.5 and 99.4%, respectively. At plasma concentration of 1.5, 50 and 75 microg/ml, the mean recovery of STS were 93.1, 96.3 and 97.5%. The limit of detection (LOD) and limit of quantification (LOQ) for STS was 0.1 microg/ml and 0.5 microg/ml, respectively. Linear responses were observed over a wide concentration range (0.5-100 microg/ml) for STS in mouse plasma. STS can be detected after intravenous administration. This method was performed for the first time in pharmacokinetic studies of STS in the mouse.

Animals↗

PubMed2006

In vitro bioactivity and osteoblast response of porous NiTi synthesized by SHS using nanocrystalline Ni-Ti reaction agent.

Porous NiTi with an average porosity of 55 vol % and a general pore size of 100-600 microm was synthesized by self-propagating high temperature synthesis (SHS) with the addition of mechanically alloyed nanocrystalline Ni-Ti as the reaction agent. The SHS of porous NiTi using elemental powders was also performed for comparison. To enhance the bioactivity of the metal surface, porous NiTi synthesized by nanocrystalline Ni-Ti was subjected to chemical treatment to form a layer of TiO(2) coating. The porous NiTi with TiO(2) coating was subsequently immersed in a simulated body fluid (SBF) to investigate its apatite forming ability. The effects of the addition of nanocrystalline Ni-Ti as reaction agent and the application of apatite coating on osteoblastic behavior were studied in primary cultures of human osteoblast cells. Results showed that the main phases in porous NiTi synthesized by elemental powders were NiTi, Ti(2)Ni, and unreacted free Ni. By using nanocrystalline Ni-Ti as reaction agent, the secondary intermetallic phase of Ti(2)Ni was significantly reduced and the free Ni was eliminated. TiO(2) coating with anatase phase was formed on the surface of porous NiTi after the chemical treatment. A layer consisting of nanocrystalline carbonate-containing apatite was formed on the surface of TiO(2) coating after soaking in SBF. The preliminary cell culture studies showed that the porous NiTi synthesized with the addition of nanocrystalline Ni-Ti attracted marked attachment and proliferation of the osteoblast cells. This gives the evidence of the potential biomedical applications of the porous NiTi.

Biocompatible Materials↗

PubMed2006

The antibacterial effects of zinc ion migration from zinc-based glass polyalkenoate cements.

Zinc-based glass polyalkenoate cements have been synthesised and their potential use in orthopaedic applications investigated. Zinc ions were released from the materials in a rapid burst over the first 24 h after synthesis, with the release rate falling below detectable levels after 7 days. Cement-implanted bone samples were prepared and the released zinc was shown, using energy dispersive X-ray analysis, to penetrate from the cement into the adjacent bone by up to 40 microm. Finally, the cements exhibited antibacterial activity against Streptococcus mutans and Actinomyces viscosus that reflected the pattern of zinc release, with the inhibition of growth greatest shortly after cement synthesis and little or no inhibition measureable after 30 days.

Actinomyces viscosus↗

PubMed2006

The recombinant nonstructural polyprotein NS1 of porcine parvovirus (PPV) as diagnostic antigen in ELISA to differentiate infected from vaccinated pigs.

To differentiate pigs infected with porcine parvovirus (PPV) from those vaccinated with inactivated whole-virus vaccine, an enzyme-linked immunosorbent assay (ELISA) based on detection of a nonstructural polyprotein 1 (NS1) was developed. A threshold of 0.23 optical density units was established and the assay had high specificity (100), sensitivity (88), accuracy (90) and positive predictive value (100) using haemagglutination inhibition as the standard method. A reproducibility test revealed that the coefficients of variation of sera within-plates and between-run were less than 10%. The assay showed no cross-reactivity with antibodies to porcine reproductive respiratory syndrome virus, pseudorabies virus, foot and mouth disease virus, Actinobacillus pleuropneumoniae, Toxoplasma or Chlamydia. Sera obtained from pigs infected with PPV reacted with recombinant NS1 protein in the ELISA. Sera from pigs vaccinated with inactivated whole virus did not recognize this protein in the ELISA. In contrast, antibodies against PPV whole virus were present in both PPV-infected and vaccinated animals. Serum conversion against NS1 was first detected 10 days after infection and NS1-specific antibodies were detectable up to half a year post infection. In conclusion, the PPV-NS1 ELISA can differentiate PPV-infected versus inactivated PPV-vaccinated pigs and could be applied in disease diagnosis and surveillance.

Animals↗