Oat cover cropping and soil insecticides in an integrated sugarbeet root maggot (Diptera: Otitidae) management program

Sugarbeet, Beta vulgaris L., producers occasionally establish cereal cover crops to minimize early-season soil erosion, wind abrasion, and mechanical injury of seedlings. We evaluated the use of living oat, Avena sativa L., cover cropping as a cultural tactic to minimize feeding injury from sugarbeet root maggot, Tetanops myopaeformis (R?der), larvae at five field sites during 1996, 1998, and 1999. Sweep-net sampling yielded 4.8-, 11.2-, and 7.2-fold more flies from oat cover-cropped chlorpyrifos, terbufos, and untreated control plots, respectively, than in noncover counterparts. However, larval feeding injury in terbufos-treated plots was reduced when cover-cropped (383 seeds/m2) at St. Thomas in all years. A reduced oat seeding rate (224 seeds/m2) also enhanced root protection in terbufos-treated plots at St. Thomas in 1999. Less root injury was sustained in cover-cropped chlorpyrifos plots than in noncover counterparts at St. Thomas in 2 study yr. Oat cover cropping also frequently resulted in reduced T. myopaeformis feeding injury in the absence of a soil insecticide. Although trends toward increased yields were often evident, significant yield benefits were limited to a 6.8% root yield increase in oat cover plots when compared with noncover treatments overall at St. Thomas in 1996 and an 18.4% sucrose yield increase in terbufos-treated plots at St. Thomas in 1999. These findings suggest that beneficial interactions between planting-time soil insecticides and cereal cover crops are achievable in areas infested by T. myopaeformis. Demonstrated reductions in root feeding injury, combined with additional agronomic benefits, may warrant use of this production practice as part of an integrated management program for this key insect pest of sugarbeet.     

Effects of nicotine on target biting and resident-intruder attack

The effects of acute administration of nicotine on target biting (defensive) and resident-intruder (offensive) attack of male mice were assessed. In the target biting procedure confined mice received tail shock on a fixed time, 2-min schedule. Under baseline conditions, biting attack directed toward an inanimate target occurred at three distinct rates. A high target biting rate (13.5 +/- 3.8 bites/15 sec) followed shock delivery, an intermediate biting rate (9.6 +/- 4.1 bites/15 sec) occurred during the inter-shock interval, and a low biting rate (1.0 +/- 0.5 bites/15 sec) occurred during a tone stimulus which signalled the impending shock. Nicotine (administered IP, 15 min presession) reduced post-shock and inter-shock interval target biting in a dose-dependent manner (ED50 values estimated at 0.13 and 0.14 mg/kg, respectively) but exerted more variable effects on target biting during the tone. In the resident-intruder paradigm the same mice were exposed to an intruder introduced into its home cage for a 10-min test session. Under baseline conditions, residents directed 20 +/- 3.2 biting attacks toward the intruder during the session with an average latency of 89 +/- 40 sec to the first attack. Nicotine caused a dose-dependent decrease in this attack behavior (ED50 values estimated to be 0.48 and 0.49 mg/kg, respectively). These observations are interpreted to indicate that nicotine has an increased potency at reducing "defensive" aggression.     

Altered gene expression in mouse livers after dichloroacetic acid exposure

Dichloroacetic acid (DCA) is a major by-product of water disinfection by chlorination. Several studies have demonstrated that DCA exhibits hepatocarcinogenic effects in rodents when administered in drinking water. This chemical does not appear to be highly mutagenic, and the mechanism(s) involved in DCA induction of cancer are not clear. The present work was aimed at identifying changes in gene expression which may indicate critical alterations/pathways involved in this chemical's carcinogenic activities. We used cDNA microarray methods for analyses of gene expression in livers of mice treated with the tumorigenic dose of 2 g/l DCA in drinking water for 4 weeks. Total RNA samples obtained from livers of the control and DCA-treated mice were evaluated for gene expression patterns with Clontech Atlas Mouse 1.2 cDNA and Atlas mouse stress/toxicology arrays, and the data analyzed with AtlasImage 2.01 and one-way ANOVA in JMP4 software. From replicate experiments, we identified 24 genes with altered expression, of which 15 were confirmed by Northern blot analysis. Of the 15 genes, 14 revealed expression suppressed two- to five-fold; they included the following: MHR 23A, cytochrome P450 (CYP) 2C29, CYP 3A11, serum paraoxonase/arylesterase 1 (PON 1), liver carboxylesterase, alpha-1 antitrypsin, ER p72, glutathione S-transferase (GST) Pi 1, angiogenin, vitronectin precursor, cathepsin D (CTSD), plasminogen precursor (contains angiostatin), prothrombin precursor and integrin alpha 3 precursor (ITGA 3). An additional gene, CYP 2A4/5, had a two-fold elevation in expression. Further, in ancillary Northern analyses of total RNA isolated from DCA-induced hepatocellular carcinomas (from earlier reported studies of mice treated with 3.5 g/l DCA for 93 weeks), many of the same genes (11 of 15) noted above showed a similar alteration in expression. In summary, we have identified specific genes involved in the functional categories of cell growth, tissue remodeling, apoptosis, cancer progression and xenobiotic metabolism that have altered levels of expression following exposures to DCA. These findings serve to highlight new pathways in which to further probe DCA effects that may be critical to its tumorigenic activity.     

Association of neuregulin 1 with schizophrenia confirmed in a Scottish population

Recently, we identified neuregulin 1 (NRG1) as a susceptibility gene for schizophrenia in the Icelandic population, by a combined linkage and association approach. Here, we report the first study evaluating the relevance of NRG1 to schizophrenia in a population outside Iceland. Markers representing a core at-risk haplotype found in Icelanders at the 5' end of the NRG1 gene were genotyped in 609 unrelated Scottish patients and 618 unrelated Scottish control individuals. This haplotype consisted of five SNP markers and two microsatellites, which all appear to be in strong linkage disequilibrium. For the Scottish patients and control subjects, haplotype frequencies were estimated by maximum likelihood, using the expectation-maximization algorithm. The frequency of the seven-marker haplotype among the Scottish patients was significantly greater than that among the control subjects (10.2% vs. 5.9%, P=.00031). The estimated risk ratio was 1.8, which is in keeping with our report of unrelated Icelandic patients (2.1). Three of the seven markers in the haplotype gave single-point P values ranging from .000064 to .0021 for the allele contributing to the at-risk haplotype. This direct replication of haplotype association in a second population further implicates NRG1 as a factor that contributes to the etiology of schizophrenia.     

Mussel disturbance dynamics: signatures of oceanographic forcing from local interactions

Local interactions, biotic and abiotic, can have a strong influence on the large-scale properties of ecosystems. However, ecological models often explore the influence of local biotic interactions where physical disturbance is included as a large-scale and imposed source of variability but is not allowed to interact with biotic processes at the local scale. In marine intertidal communities dominated by mussels, wave disturbances create gaps in the mussel bed that recover through a successional sequence. We present a lattice model of mussel disturbance dynamics that allows local interactions between wave disturbance and mussel recolonization, in which each cell of the lattice can be empty, occupied by a mussel bed element, or disturbed (which corresponds to a newly disturbed cell that has unstable edges). As in natural ecosystems, wave disturbance can also spread from disturbed to adjacent occupied cells, and recolonization can also spread from occupied to adjacent empty cells. We first validate the local rules from artificial gap experiments and from natural gap monitoring along the Oregon coast. We analyze the properties of the model system as a function of different oceanographic forcings of productivity and disturbance. We show that the mussel bed can go through phase transitions characterized by a large sensitivity of mussel cover and patterns to oceanographic forcings but also that criticality (scale invariance) is observed over wide ranges of parameters, which suggests self-organization. We also show that spatial patterns in the intertidal can provide a robust signature of local processes and can inform about oceanographic regimes. We do so by comparing the large-scale patterns of the simulation (scaling exponents) with field data, which suggest that some experimental sites are close to criticality. Our results suggest that regional patterns in disturbed populations can be explained by local biotic and abiotic processes submitted to oceanographic forcing.     

A quantitative diffraction-based sandwich immunoassay

It is shown that diffraction-based sensing can be enhanced for diagnostic purposes through the use of a secondary label. The limit of detection for anti-rabbit IgG was reduced more than 40-fold by using a gold-conjugated secondary antibody. The response to secondary antibody binding was linear for concentrations from 25 to 500 ng/ml of anti-rabbit IgG, suggesting that quantitative determinations can be readily done. Moreover, the binding of the secondary antibody was observed as soon as 1 min after its introduction to the surface-bound primary complex.     

Rate of biodistribution of STEALTH liposomes to tumor and skin: influence of liposome diameter and implications for toxicity and therapeutic activity

The influence of diameter on the pharmacokinetic and biodistribution of STEALTH liposomes into the tumor (4T1 murine mammary carcinoma) and cutaneous tissues (skin and paws) of mice was studied to ascertain the time course of liposome accumulation and to determine if a preferential accumulation of liposomes into tumor over skin or paws could be achieved by altering liposome size. These tissues were chosen as the dose-limiting toxicity for Caelyx/Doxil in humans is palmar-plantar erythrodysesthesia, a cutaneous toxicity. We examined liposomes of four diameters: 82, 101, 154, or 241 nm. Liposomes with the three smallest diameters showed similar accumulation profiles that were significantly higher than the largest liposomes in all three tissues of interest. We were unable to achieve a preferential accumulation of liposomes into tumor over skin or paws based on size alone, as evidenced by the tumor to skin and tumor to paw ratios. However, there were differences in the time courses of liposome accumulation in these three tissues. Liposome levels plateaued in tumors and paws within 24 h, whereas skin levels plateaued between 24 and 48 h. The therapeutic activity of liposomal doxorubicin of three diameters (100, 157, and 255 nm) was tested in the same model. All formulations delayed tumor growth, with liposomes of 100 or 157 nm being equally efficacious and superior to liposomes of 255 nm.     

Characterisation of a potential biomarker of phospholipidosis from amiodarone-treated rats

A novel and relatively simple analytical method for the separation, characterisation and semi-quantitation of phospholipids (PLs) from extracts of complex biological samples has been developed. This methodology allows PL extracts from cells and tissues to be analysed by liquid chromatography (LC) coupled to electrospray ionisation mass spectrometry (ESI-MS). Complex mixtures of PLs were separated on a high-performance liquid chromatography (HPLC) system using 0.5% ammonium hydroxide in methanol/water/hexane/formate mixture with UV detection at 205 nm. Identification and structural characterisation of molecular species were carried out utilising ESI-MS and MS/MS in the negative ion mode.The abnormal accumulation of PLs (phospholipidosis) was induced in male Sprague-Dawley rats by administration of the cationic amphiphilic drug (CAD), amiodarone. Analysis of the PL profile of liver and lung tissues, lymphocytes and serum from treated rats was carried out using this analytical procedure (LC-ESI/MS/MS). Differences in PL profiles between treated and untreated animals were highlighted by principal component analysis (PCA). This led to the selection of a potential metabolic marker of phospholipidosis (PLD) identified as a lyso-bis-phosphatidic acid (LBPA) derivative, also known as bis(monoglycero)phosphate (BMP). This PL was absent in control animals but was present in quantifiable amounts in all samples from amiodarone-treated rats.     

A single point mutation resulting in an adversely reduced expression of DPM2 in the Lec15.1 cells

Mammalian dolichol-phosphate-mannose (DPM) synthase consists of three subunits, DPM1, DPM2, and DPM3. Lec15.1 Chinese hamster ovary cells are deficient in DPM synthase activity. The present paper reports that DPM1 cDNA from wild type and Lec15.1 CHO cells were found to be identical, and transfection with CHO DPM1 cDNA did not reverse the Lec15.1 phenotype. Neither did a chimeric cDNA containing the complete hamster DPM1 open reading frame fused to the Saccharomyces cerevisiae DPM1 C-terminal transmembrane domain. In contrast, Lec15.1 cells were found to have a single point mutation G29A within the coding region of the DPM2 gene, resulting in a glycine to glutamic acid change in amino acid residue 10 of the peptide. Moreover, mutant DPM2 cDNA expressed a drastically reduced amount of DPM2 protein and poorly corrects the Lec15.1 cell phenotype when compared with wild type CHO DPM2 cDNA (G(29) form).     

The divergent 5' ends of DPM2 mRNAs originate from the alternative splicing of two adjacent introns: characterization of the hamster DPM2 gene

Mammalian dolichol-phosphate-mannose (DPM) synthase has three subunits, DPM1, DPM2, and DPM3. In this report, an analysis of the gene and cDNAs of hamster DPM2 is presented. The CHO DPM2 gene has two special features. First, the initiation codon ATG is separated from the remainder of the coding region by intron sequences. Second, within these intron sequences the DPM2 gene contains an adjacent 3' splice site (acceptor) and a 5' splice site (donor), suggestive of a deleted exon between the first and second codons. In fact, these sites overlap by four nucleotides (nt) of AGGT. Splicing intermediates using both of these alternative splice sites were observed. This latter feature appears unique and is particularly unusual considering the relatively small size of the gene (2.7 kb) and of introns a (123 bp) and b (152 bp).