Biomedical subjects

Jie Liu

Publications and source records attributed to Jie Liu.

At least 253 records · Page 14Linked to original sources

PubMed2004

Changes in the gene expression associated with carbon tetrachloride-induced liver fibrosis persist after cessation of dosing in mice.

Recent studies have shown that gene expression profiles change in the livers of animals treated acutely with toxic chemicals such as carbon tetrachloride (CCl(4)). This study was undertaken to evaluate the changes in gene expression in mouse liver immediately after a long-term treatment with CCl(4) and possible effects of treatment cessation on these changes. Adult 129/Sv(pc)J mice were treated twice a week with CCl(4) at 1 ml/kg in olive oil for 4 weeks. Hepatic pathological changes observed in the CCl(4)-treated mice included necrosis, inflammation, and fibrosis, along with increased serum alanine aminotransferase activities. Consistent with these changes, expression of genes involved in cell death, cell proliferation, metabolism, DNA damage, and fibrogenesis were upregulated as detected by microarray analysis and confirmed by real-time RT-PCR. Four weeks after CCl(4) treatment cessation, the pathological changes were recovered, with the exception of fibrosis, which was not completely reversed. Most of the gene expression profiles also returned to the control level; however, the fibrogenetic genes remained at a high level of expression. These results demonstrate that changes in gene expression profile correlate with pathological alterations in the liver in response to CCl(4) intoxication. Most of these changes are recoverable upon withdrawal of the toxic insult. However, liver fibrosis is a prolonged change both in gene expression and histopathological alterations.

Alanine Transaminase↗

PubMed2004

Estrogen signaling in livers of male mice with hepatocellular carcinoma induced by exposure to arsenic in utero.

BACKGROUND: Exposure of pregnant mice to inorganic arsenic induces a spectrum of tumors, including hepatocellular carcinoma (HCC), in their adult offspring similar to that induced by exposing adult mice to estrogenic compounds. To investigate whether arsenic exposure in utero causes altered estrogen signaling, we examined expression of estrogen receptor-alpha (ER-alpha), cyclin D1 (an estrogen-responsive hepatic oncogene), and several cytochrome P450 genes (with sexually dimorphic liver expression patterns) in livers from adult male mice with in utero arsenic-induced HCC. METHODS: Quantitative real-time reverse transcription-polymerase chain reaction was used to evaluate gene expression in livers of adult male mice that had (i.e., exposed mice; n = 8) or had not (i.e., control mice; n = 5) been exposed to arsenic in utero. DNA methylation status of portions of the ER-alpha and cyclin D1 gene promoters in liver tissue was measured using methylation-specific polymerase chain reaction. Statistical tests were two-sided. RESULTS: ER-alpha mRNA levels were 3.1-fold (95% confidence interval [CI] = 2.0-fold to 4.3-fold) higher in livers of exposed mice than in those of control mice, and cyclin D1 levels were 3.0-fold (95% CI = 1.7-fold to 4.3-fold) higher. Exposed mice showed a feminized expression pattern of several cytochrome P450 genes, expressing the female-dominant CYP2A4 (P =.017 versus control) and CYP2B9 (P<.001) genes at 8.7 and 10.5 times, respectively, the level in control mice and expressing the male-dominant CYP7B1 at approximately one-fourth the level in control mice(P =.0012). Exposed mice exhibited reduced (by approximately 90%) methylation of the ER-alpha gene promoter in liver DNA as compared with control mice; the cyclin D1 gene promoter was not methylated in either exposed or control mice. CONCLUSION: Altered estrogen signaling may play a role in induction of HCC by arsenic exposure in utero. Specifically, overexpression of ER-alpha, potentially through promoter region hypomethylation, in livers of such mice may be linked to the hepatocarcinogenicity of arsenic.

Animals↗

PubMed2004

The nitric oxide donor, O2-vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), protects against cadmium-induced hepatotoxicity in mice.

The nitric oxide (NO) donor, O2-vinyl 1-(pyrrolidin-1-yl)diazen-1-ium-1,2-diolate (V-PYRRO/NO), is metabolized by P450 enzymes to release NO within the liver and is effective in protecting against hepatotoxicity of endotoxin and acetaminophen. This study examined the effects of V-PYRRO/NO on cadmium (Cd) hepatotoxicity in mice. Mice were given multiple injections of V-PYRRO/NO (10 mg/kg, s.c. at 2-h intervals) before and after a hepatotoxic dose of Cd (3.7 mg/kg Cd as CdCl2, i.p.). V-PYRRO/NO administration reduced Cd-induced hepatotoxicity as evidenced by reduced serum alanine aminotransferase activity, improved pathology, and reduced hepatic lipid peroxidation. The protection by V-PYRRO/NO was not mediated by altered Cd distribution to the liver or within hepatic subcellular fractions. Similar inductions of metallothionein, a metal-binding protein, were observed in mice receiving Cd alone or Cd plus V-PYRRO/NO. Real-time reverse transcription-polymerase chain reaction analysis revealed that V-PYRRO/NO administration suppressed the expression of inflammation-related genes such as macrophage inflammatory protein-2, CXC chemokine, thrombospondin-1, intracellular adhesion molecular-1, and interleukin-6. V-PYRRO/NO also suppressed the expression of acute phase protein genes and genes related to cell-death pathways, such as c-jun/AP-1, nuclear factor-kappaB, early response growth factor-1, heme oxygenase-1, caspase-3, growth arrest, and DNA-damaging protein-153. In summary, the liver-selective NO donor, V-PYRRO/NO, protects against Cd hepatotoxicity in mice. This protection is not mediated through altered distribution of Cd but may be related to reduced hepatic inflammation, reduced acute phase responses, and the suppression of cell-death-related components.

Animals↗

PubMed2004

Structure and protein design of a human platelet function inhibitor.

Hematophagous arthropods secrete a salivary apyrase that inhibits platelet activation by catabolizing ADP released from damaged tissues and blood cells. We report the X-ray crystal structures of a human enzyme of the soluble apyrase family in its apo state and bound to a substrate analog. The structures reveal a nucleotide binding domain comprising a five-blade beta propeller, binding determinants of the substrate and the active site, and an unusual calcium binding site with a potential regulatory function. Using a comparative structural biology approach, we were able to redesign the human apyrase so as to enhance its ADPase activity by more than 100-fold. The engineered enzyme is a potent inhibitor of platelet aggregation and may serve as the basis for the development of a new class of antithrombotic agents.

Amino Acid Sequence↗

PubMed2004

Minocycline treatment reduces delayed oligodendrocyte death, attenuates axonal dieback, and improves functional outcome after spinal cord injury.

Minocycline has been demonstrated to be neuroprotective after spinal cord injury (SCI). However, the cellular consequences of minocycline treatment on the secondary injury response are poorly understood. We examined the ability of minocycline to reduce oligodendrocyte apoptosis, microglial/macrophage activation, corticospinal tract (CST) dieback, and lesion size and to improve functional outcome after SCI. Adult rats were subjected to a C7-C8 dorsal column transection, and the presence of apoptotic oligodendrocytes was assessed within the ascending sensory tract (AST) and descending CST in segments (3-7 mm) both proximal and distal to the injury site. Surprisingly, the numbers of dying oligodendrocytes in the proximal and distal segments were comparable, suggesting more than the lack of axon-cell body contiguity played a role in their demise. Minocycline or vehicle control was injected into the intraperitoneal cavity 30 min and 8 hr after SCI and thereafter twice daily for 2 d. We report a reduction of apoptotic oligodendrocytes and microglia within both proximal and distal segments of the AST after minocycline treatment, using immunostaining for active caspase-3 and Hoechst 33258 staining in combination with cell-specific markers. Activated microglial/macrophage density was reduced remote to the lesion as well as at the lesion site. Both CST dieback and lesion size were diminished after minocycline treatment. Footprint analysis revealed improved functional outcome after minocycline treatment. Thus, minocycline ameliorates multiple secondary events after SCI, rendering this clinically used drug an attractive candidate for SCI treatment trials.

Animals↗

PubMed2004

Tissue-specific imprinting of the G protein Gsalpha is associated with tissue-specific differences in histone methylation.

The G protein Gsalpha is imprinted in a tissue-specific manner, being primarily expressed from the maternal allele in some tissues, such as renal proximal tubules. The Gsalpha promoter is unmethylated, but is downstream of a differentially methylated region [the exon 1A differentially methylated region (DMR)] that is methylated on the maternal allele. Maternal Gsalpha null mutations or loss of maternal-specific exon 1A methylation leads to pseudohypoparathyroidism types 1A or 1B, respectively. We now have examined the chromatin state of each parental allele within the exon 1A-Gsalpha promoter region by chromatin immunoprecipitation of samples derived from mice with heterozygous deletions within the region using antibodies to covalently modified histones. The exon 1A DMR had allele-specific differences in histone acetylation and methylation, with histone acetylation and H3 lysine 4 (H3K4) methylation of the paternal allele, and H3 lysine 9 (H3K9) methylation of the maternal allele. Both parental alleles had similar levels of histone acetylation and H3K4 methylation within the Gsalpha promoter and first exon, with no H3K9 methylation. In liver, where Gsalpha is biallelically expressed, both parental alleles had similar levels of tri- and dimethylated H3K4 within the Gsalpha first exon. In contrast, in renal proximal tubules there was a greater ratio of tri- to dimethylated H3K4 of Gsalpha exon 1 in the more transcriptionally active maternal as compared with the paternal allele. These results show that allele-specific differences in Gsalpha expression correlate in a tissue-specific manner with allele-specific differences in the extent of H3K4 methylation, and are the first demonstration that chronic transcriptional activation in mammals is correlated with trimethylation of H3K4.

Animals↗

PubMed2004

Solution-phase synthesis of single-crystalline iron phosphide nanorods/nanowires.

A solution-phase route for the preparation of single-crystalline iron phosphide nanorods and nanowires is reported. We have shown that the mixture of trioctylphosphine oxide (TOPO) and trioctylphosphine (TOP), which are commonly used as the solvents for semiconductor nanocrystal synthesis, is not entirely inert. In the current process, TOP, serving as phosphor source, reacts with Fe precursors to form FeP nanostructures with large aspect ratios. In addition, the experimental results show that both TOP and TOPO are necessary for the formation of FeP nanowires and their ratio appears to control the morphology of the produced FeP structures. A possible growth mechanism is discussed.

Journal Article↗

PubMed2004

Transition to instability in a kicked bose-einstein condensate.

A periodically kicked ring of a Bose-Einstein condensate is considered as a nonlinear generalization of the quantum kicked rotor. For weak interactions between atoms, periodic motion (antiresonance) becomes quasiperiodic (quantum beating) but remains stable. There exists a critical strength of interactions beyond which quasiperiodic motion becomes chaotic, resulting in an instability of the condensate manifested by exponential growth in the number of noncondensed atoms. Similar behavior is observed for dynamically localized states (essentially quasiperiodic motions), where stability remains for weak interactions but is destroyed by strong interactions.

Journal Article↗

PubMed2004

GSSI, a general model for solute-solvent interactions. 1. Description of the model.

A novel, semiempirical approach for the general treatment of solute-solvent interactions (GSSI) was developed to enable the prediction of solution-phase properties (e.g., free energies of desolvation, partition coefficients, and membrane permeabilities). The GSSI approach is based on the principle that all solution-phase processes can be modeled in terms of one or more gas-to-solution transfer processes. The free energy of each gas-to-solution transfer process is calculated as the sum of the free energy of cavity formation and the free energy of solute-solvent interaction. The solute's contributions to these free energies are modeled on the basis of various quantities computed from the solute's three-dimensional (3D) structure, whereas the solvent's contributions are modeled by empirically determined regression coefficients. More specifically, the free energy of cavity formation is modeled on the basis of the total solvent-accessible surface area of the solute. The enthalpy of solute-solvent interaction is modeled on the basis of intermolecular interaction potentials calculated at many uniformly distributed points on the solvent-accessible surface of the solute. The entropy of solute-solvent interaction is modeled on the basis of an effective number of rotatable bonds in the solute and by the regression coefficients characteristic of the solvent. The potential utility of the GSSI approach was demonstrated by modeling the free energy of gas-to-solution transfer for 111 solutes in water, 250 solutes in hexadecane, and 84 solutes in octanol.

Kinetics↗

PubMed2004

Reduced oncotic necrosis in Fas receptor-deficient C57BL/6J-lpr mice after bile duct ligation.

Neutrophils aggravate cholestatic liver injury after bile duct ligation (BDL). Recently, it was suggested that hepatocellular apoptosis might be critical for liver injury in this model. To test the hypothesis that apoptosis could be a signal for neutrophil extravasation and injury, we assessed parameters of apoptosis and inflammation after BDL using 2 different approaches: (1) wild-type and Fas receptor-deficient lpr mice of the C57BL/6J or C3H/HeJ strains, and (2) treatment with the pancaspase inhibitor z-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk)in C3HeB/FeJ mice. After BDL for 3 days, total cell death was estimated to be between 10% and 50% of all cells evaluated. However, less than 0.1% of hepatocytes showed apoptotic morphology in all 3 strains. Processing of procaspase-3, caspase-3 enzyme activities, and immunohistochemical staining for cytokeratin 18 cleavage products indicated no activation of caspases. Real-time reverse-transcriptase polymerase chain reaction analysis revealed increased expression of many inflammatory mediators but no effect on proapoptotic genes. More than 50% of all accumulated neutrophils were extravasated and colocalized with foci of oncotic hepatocytes and chlorotyrosine adducts. z-VAD-fmk treatment had no effect on apoptosis or liver injury after BDL but eliminated apoptosis after galactosamine/endotoxin in C3HeB/FeJ mice. In Fas receptor-deficient lpr mice (C57BL/6J), expression of inflammatory mediators, neutrophil accumulation and extravasation, chlorotyrosine adduct formation, and liver injury were reduced. This protection was not observed in lpr mice of the endotoxin-resistant C3H/HeJ strain. In conclusion, liver injury (oncotic necrosis) after BDL correlated with the severity of the inflammatory response. The minimal amount of apoptosis had no effect on inflammation or on the overall injury.

Amino Acid Chloromethyl Ketones↗

PubMed2004

Hepatitis C virus replication in stably transfected HepG2 cells promotes hepatocellular growth and tumorigenesis.

HepG2 cells stably transfected with a full-length, infectious hepatitis C virus (HCV) cDNA demonstrated consistent replication of HCV for more than 3 years. Intracellular minus strand HCV RNA was present. Minus strand synthesis was NS5B dependent, and was sensitive to interferon alpha (IFN alpha) treatment. NS5B and HCV core protein were detectable. HCV stimulated HepG2 cell growth and survival in culture, in soft agar, and accelerated tumor growth in SCID mice. These mice became HCV RNA positive in blood, where the virus was also sensitive to IFN alpha. The RNA banded at the density of HCV, and was resistant to RNase prior to extraction. Hence, HCV stably replicates in HepG2 cells, stimulates hepatocellular growth and tumorigenesis, and is susceptible to IFN alpha both in vitro and in vivo.

Animals↗

PubMed2004

Human S15a expression is upregulated by hepatitis B virus X protein.

The hepatitis B virus (HBV)-encoded X antigen (HBxAg) may contribute to the development of hepatocellular carcinoma (HCC) through the upregulated expression of selected cellular genes. To identify these genes, RNAs isolated from HBxAg-positive and -negative HepG2 cells were compared by PCR select cDNA subtraction. One gene overexpressed in HBxAg-positive cells by Northern and Western blotting is the ribosomal protein S15a. The S15a mRNA is 535 base pairs, encoding a protein 130 amino acids long with a molecular weight of 14.3 kDa. S15a expression was upregulated in HBV-infected livers, where it costained with HBxAg. Overexpression of S15a stimulated cell growth, colony formation in soft agar, and tumor formation in SCID mice. Hence, HBxAg upregulated the expression of S15a, the latter of which participates in the development of HCC, perhaps by altering the integrity of translation.

Amino Acid Sequence↗

PubMed2004

Function of a low molecular peptide generated by cellulolytic fungi for the degradation of native cellulose.

Peptides (MW < 5 kDa) produced by 57 cellulolytic fungi can form free radicals. Scanning tunneling microscopy (STM) and IR spectroscopy showed that the peptide produced by Trichoderma pseudokoningii can break the hydrogen bond network of cellulose. The synergic action of these peptides and cellulases increased production of reducing sugars during degradation of native cellulose.

Biodegradation, Environmental↗

PubMed2004

Synthesis, characterization and antiviral activity against influenza virus of a series of novel manganese-substituted rare earth borotungstates heteropolyoxometalates.

A series of novel manganese-substituted mixed-valence rare earth borotungsto-heteropoly blues, Ln2H3[BW9(VI)W2(V)Mn(H2O)O39] x 12H2O (Ln(2), Ln = La, Ce, Pr, Nd, Sm, Eu and Gd), as well as their corresponding heteropoly acids (Ln(0)), have been prepared and characterized by cyclic voltammetry (CV), infrared (IR), ultraviolet (UV), thermal gravimetric (TG) and differential thermal (DTA) analysis, X-ray photoelectron spectroscopy (XPS) and electrochemistry. It's shown that the heteropoly blues anion in Ln(2) still retains the alpha-Keggin structure but with a slight distortion as heteropoly acids do, and Mn and W atoms distribute statistically in the whole molecular. At the same time, the cell toxicity and antiviral activity of these rare earth borotungstateheteropoly blues against influenza virus type A and type B in MDCK cells have been investigated using plaque reduction assay. The results elucidated that these complexes exhibit a significantly inhibitory activity and almost no cytotoxicity comparable with those obtained from virazole, and the anti-virus activity depend on the structure of these complexes.

Animals↗

PubMed2004

St John's wort induces both cytochrome P450 3A4-catalyzed sulfoxidation and 2C19-dependent hydroxylation of omeprazole.

OBJECTIVE: St John's wort, an extract of the medicinal plant Hypericum perforatum, is widely used as an herbal antidepressant. Although the ability of St John's wort to induce cytochrome P450 (CYP) 3A4-mediated reaction has been well established, the effect on CYP2C19 is still not determined. Thus the objective of this study was to determine the impact of St John's wort on the pharmacokinetic profiles of omeprazole and its metabolites. METHODS: Twelve healthy adult men (6 CYP2C19*1/CYP2C19*1, 4 CYP2C19*2/CYP2C19*2 and 2 CYP2C19*2/CYP2C19*3) were enrolled in a 2-phase randomized crossover design. In each phase the volunteers received placebo or a 300-mg St John's wort tablet 3 times daily for 14 days. Then all subjects took a 20-mg omeprazole capsule orally. Blood samples were collected up to 12 hours after omeprazole administration. Omeprazole and its metabolites were quantified by use of HPLC with ultraviolet detection. RESULTS: Omeprazole and its metabolites all exhibit CYP2C19 genotype-dependent pharmacokinetic profiles. After a 14-day treatment with St John's wort, substantial decreases in plasma concentrations of omeprazole were observed. The peak plasma concentration (C(max)) significantly decreased by 37.5% +/- 13.3% (P =.001) in CYP2C19*2/CYP2C19*2 or *3 and by 49.6% +/- 20.7% (P =.017) in CYP2C19*1/CYP2C19*1; the area under the concentration-time curve extrapolated to infinity [AUC(0- infinity )] decreased by 37.9% +/- 21.3% (P =.014) and 43.9% +/- 23.7% (P =.011) in CYP2C19 mutant and wild genotypes, respectively. Moreover, the C(max) and AUC(0- infinity ) of omeprazole sulfone increased by 160.3% +/- 45.5% (P =.001) and by 136.6% +/- 84.6% (P =.014), 155.5% +/- 58.8% (P =.001), and 158.7% +/- 101.4% (P =.017) in mutant and wild genotypes, respectively. St John's wort increased the C(max) of 5-hydroxyomeprazole by 38.1% +/- 30.5% (P =.028) and the AUC(0- infinity ) by 37.2% +/- 26% (P =.005) in CYP2C19 wild-type subjects, whereas it did not produce any significant alterations to the corresponding pharmacokinetic parameters in subjects with variant genotypes. CONCLUSION: St John's wort induces both CYP3A4-catalyzed sulfoxidation and CYP2C19-dependent hydroxylation of omeprazole and enormously decreases the plasma concentrations of omeprazole. Clinically relevant interactions with other drugs may occur and must be taken into account when St John's wort is being taken.

Adolescent↗

PubMed2004

Optimizing mechanical properties of laser-welded gold alloy through heat treatment.

OBJECTIVE: The goal of this work was to improve the mechanical strength of laser-welded gold alloy with age-hardenability at intraoral temperature. METHODS: The gold alloy was cast conventionally in plate patterns (0.5 mm x 3.0 mm x 20 mm). After bench-cooling the mold to room temperature (as-cast state), transverse sections of the plate were made at mid-span. They were butted against one another and welded using Nd:YAG laser (current: 320 A; time: 10 ms; spot diameter: 1 mm). Three laser pulses were applied from both sides to cover the joint width (3.0 mm) of the specimens before or after solution heat treatment at 700 degrees C/5 min. Uncut control specimens (non-welded) were also prepared. After solution treatment, two different heat treatments were given the laser-welded specimens: high-temperature aging at 250 degrees C/15 min, or intraoral aging at 37 degrees C/3 days. Control specimens underwent all of the heat treatments after solution treatment. Tensile testing was conducted at a crosshead speed of 2 mm/min and a gauge length of 10 mm. RESULTS: Solution treatment of the gold alloy before laser-welding did not improve the mechanical strength of laser-welded gold alloy after high-temperature aging or intraoral aging. The joint strengths of laser-welded gold alloy were improved only by solution heat treatments after laser-welding and subsequent aging treatment at high or intraoral temperatures. SIGNIFICANCE: The results of this study indicated that laser-welded cast gold alloy prostheses aged at high or intraoral temperatures produce high strength when they are solution-treated after laser-welding.

Dental Soldering↗

PubMed2004

Rubrospinal neurons fail to respond to brain-derived neurotrophic factor applied to the spinal cord injury site 2 months after cervical axotomy.

Numerous experimental therapies to promote axonal regeneration have shown promise in animal models of acute spinal cord injury, but their effectiveness is often found to diminish with a delay in administration. We evaluated whether brain-derived neurotrophic factor (BDNF) application to the spinal cord injury site 2 months after cervical axotomy could promote a regenerative response in chronically axotomized rubrospinal neurons. BDNF was applied to the spinal cord in three different concentrations 2 months after cervical axotomy of the rubrospinal tract. The red nucleus was examined for reversal of neuronal atrophy, GAP43 and Talpha1 tubulin mRNA expression, and trkB receptor immunoreactivity. A peripheral nerve transplant paradigm was used to measure axonal regeneration into peripheral nerve transplants. Rubrospinal axons were anterogradely traced and trkB receptor immunohistochemistry performed on the injured spinal cord. We found that BDNF treatment did not reverse rubrospinal neuronal atrophy, nor promote GAP-43 and Talpha1 tubulin mRNA expression, nor promote axonal regeneration into peripheral nerve transplants. TrkB receptor immunohistochemistry demonstrated immunoreactivity on the neuronal cell bodies, but not on anterogradely labeled rubrospinal axons at the injury site. These findings suggest that the poor response of rubrospinal neurons to BDNF applied to the spinal cord injury site 2 months after cervical axotomy is not related to the dose of BDNF administered, but rather to the loss of trkB receptors on the injured axons over time. Such obstacles to axonal regeneration will be important to identify in the development of therapeutic strategies for chronically injured individuals.

Animals↗

PubMed2004

Genomic organization of an avermectin receptor subunit from Haemonchus contortus and expression of its putative promoter region in Caenorhabditis elegans.

Avermectins and milbemycins are believed to exert their anthelmintic effects by binding to glutamate-gated chloride channels (GluCls). Two GluCl subunits have been localized in the pharynx in Caenorhabditis elegans, and the pharynx has been implicated as a major target for avermectins in C. elegans. However, in parasitic nematodes, the pharyngeal localization of the GluCl subunits needs to be determined. The HcGluCla gene encoding an alpha-type GluCl subunit has been cloned from Haemonchus contortus previously. To investigate the expression site of the HcGluCla gene we have isolated a 1439bp 5'-flanking region and determined the genomic organization of this gene. The HcGluCla gene is composed of 12 exons separated by 11 introns and spans approximately 7.3kb of genomic DNA. Analysis of the 1439bp 5'-flanking region of the HcGluCla gene revealed that it contained TATA, CCAAT boxes, and several other consensus transcriptional factor recognition sequences. The 1439bp 5'-flanking region and the first exon and intron and part of the second exon of the HcGluCla gene were fused to green fluorescence protein (GFP) reporter gene and microinjected into the gonads of C. elegans. After microinjection of the construct into C. elegans, four stable transformed lines were established and assayed for GFP expression. The transformed animals exhibited fluorescence in the two pairs of MC and M2 pharyngeal neurons, but no expression was detected in the muscle cells. Expression of HcGluCla in pharyngeal neurons suggests a mechanism for the effects of avermectins and milbemycins on pharyngeal function in parasitic nematodes.

3' Untranslated Regions↗