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Resistance and the control of sheep ectoparasites.

For about 100 years Australian woolgrowers have used a variety of chemicals to control blowflies, lice and other ectoparasites of sheep. While the chemicals have changed considerably the application technology has not changed very much at all. Chemicals registered for use on sheep have paralleled the evolution of synthetic insecticides with the unfortunate consequence of the development of resistance in the Australian sheep blowfly, Lucilia cuprina, following closely behind. Organochlorine (dieldrin) resistance peaked at about 70% in 1958 when unacceptable residues in meat and wool forced their withdrawal. Organophosphate (OP) resistance appeared in 1965. With no alternative insecticide classes until 1979, OP resistance reached near fixation levels by the early 1970s and has remained unchanged. OP resistance has reduced the protection period from over 16 weeks to about 6 weeks. Moreover, resistance has decreased the effectiveness of many flystrike dressings to unacceptably low levels. OPs are still very effective against sheep body lice, Bovicola ovis but control is hampered by inadequate application via plunge or shower dipping. Synthetic pyrethroid (SP) pour-on products were released in 1981 but resistance developed by 1985 and many woolgrowers were unable to eradicate lice with pour-on products. Highest Resistance Factors at this time were only about 26 x but this was sufficient to prevent pour-ons working efficiently. By 1991 a population from Hartley in NSW was found to be 642 x resistant to cypermethrin with side-resistance conferred to the other SPs. SP resistance was partially suppresible by piperonyl butoxide but field trials suggested that the resulting improvement in efficacy was not sufficient to be commercially attractive. OPs remain very effective if applied correctly and the release of ivermectin and 2 benzoylphenyl urea products significantly improves the prospects for resistance management. However the increasing environmental concern about the persistence of chemical residues in wool has stimulated interest in biological control of sheep lice by Bacillus thuringiensis.

Animals↗

Isotype, distribution and target analysis of lymphocyte reactive antibodies in patients with human immunodeficiency virus infection.

Anti-lymphocyte (ALA) antibodies were investigated by using both microcytotoxicity and immunofluorescence analyses in 87 subjects with different clinical features of human immunodeficiency virus (HIV) infection. A similar mean percentage of killing in microcytotoxicity assays using heterologous lymphocytes as cellular target was recorded in four groups of patients, including 36 HIV-seropositive asymptomatic subjects, 34 patients with HIV-induced lymphadenopathy syndrome (LAS), 13 with acquired immunodeficiency syndrome (AIDS)-related complex (ARC), and 4 patients with the full-blown AIDS. Conversely, an increasing percentage of ALA-positive subjects paralleled the evolution of the HIV infection. The majority of ALA were IgM isotype with a significant reactivity against T cells. This specificity was indifferently directed to CD3+, CD4+, and CD8+ lymphocytes. In additional experiments employing enzymatic digestion of lymphocyte membrane antigens, we demonstrated that CD4 and CD8 receptors were digested by the pronase, whereas CD3 molecules were highly resistant. Subsequent flow cytometry analyses using these pronase-digested T cells showed that reactivity of ALA for their target was unchanged. Our data suggest that antigenic specificities of ALA in HIV infection are resistant to pronase treatment and are not related to CD4 and CD8 molecules.

Antigens, Differentiation, T-Lymphocyte↗

Adaptational response in transcription factors during development of myocardial hypertrophy.

Cardiac hypertrophy is characterized, among others, by the molecular events which selectively activate the expression of genes for contractile proteins within individual myocardial cells. As such, myosin light chain 2 (MLC-2), which is upregulated in the hypertrophic state in both rat and human, serves as a marker for hypertrophy. In an attempt to investigate the gene regulatory mechanisms of this phenomenon, we tested the hypothesis that certain transcription factors are directly involved in the development of cardiac hypertrophy by demonstrating the presence of cardiac tissue-specific regulatory elements in the 5'-flanking region of the MLC-2 promoter and testing them in the gel mobility shift assay for their binding activity to nuclear proteins from hypertrophied and normal cardiac tissue. In nuclear extracts from the ventricular tissues of the spontaneously hypertensive rat (SHR), distinctive changes in two families of activator proteins, the A/T-rich DNA-binding transcription factors, myocyte enhancer factor (MEF-2) and CArG-binding factor, manifested in a developmentally dictated manner paralleling the evolution of cardiac hypertrophy in these animals. Extracts isolated from brains and skeletal muscle tissues from the same animals did not exhibit the changes in binding activity. Also, the changes were not apparent when a distal negative regulatory element (CSS), which confers cardiac-specific expression, was tested in gel mobility shift assays. The ubiquitous TATA-binding proteins remained unchanged in comparing SHR with the control strain WKY in the same assay. These data support the notion that the expression of specific transcription factors is modulated in response to hypertrophy related signals which execute changes at the gene level effecting the enrichment of certain contractile proteins in an effort discrete and estranged from the basal transcription machinery.

Adaptation, Physiological↗

Glial reaction to volkensin-induced selective degeneration of central neurons.

Volkensin, a highly toxic protein retrogradely transported through axons, was used to target primary neuronal death in brainstem precerebellar relays after injection in the cerebellar cortex of rats. The reaction of astrocytes and microglia was studied with immunohistochemistry in the inferior olivary and pontine nuclei from 6 h to 14 days. Neurodegenerative features were evident since the first hours, especially in the pontine nuclei, and neuronal loss reached a plateau at 7 days in the inferior olive and at 10 days in the pons. Astrocytic activation, revealed by glial fibrillary acidic protein immunoreactivity, was concomitant with early signs of neuronal death and gradually increased. Microglia activation, revealed by OX-42 immunoreactivity, was evident at 2 days and became rapidly intense in precerebellar relays. At 1 week, marked ED-1 immunoreactivity also revealed phagocytic features of microglia, which persisted during the second week. In addition, major histocompatibility complex antigens (MHC) class I and II were induced in cells exhibiting microglial features. In the inferior olive, MHC I immunoreactivity was evident since 4 days and persisted at 14 days, whereas MHC II induction was intense at 7 days and subsided at 2 weeks. In the pontine nuclei high expression of both MHC antigens persisted instead at 14 days, probably reflecting the progression of neuronal death. Thus, targeted lethal injury of central neurons elicited prompt activation of both astrocytes and microglia; the marked microglia activation resulted in phagocytic features and immunophenotypic changes, with a temporal regulation that paralleled the evolution of neurodegenerative phenomena.

Animals↗

Effects of disulfiram on the amphetamine-induced behavioral syndrome in the cat as a model of psychosis.

We have previously reported that, from a phenomenological standpoint, the behavioral manifestations of cats chronically intoxicated with amphetamine parallel the evolution of the paranoid psychosis induced by the drug in humans. However, certain manifestations in the cat, such as frozen postures, disjunctive behaviors and postures, cataleptic-like phenomena, obstinate progression, loss of righting reflex and pupillary changes, did not appear to be consistent with the phenomenology of the paranoid psychosis. Since treatment of schizophrenic patients with disulfiram, an inhibitor of norepinephrine synthesis that acts at the level of the enzyme dopamine beta-hydroxylase, thereby leading to increased dopamine concentrations, had been found to profoundly exaggerate psychotic symptomatology, amphetamine behavioral syndrome in the cat as it is modified by pretreatment with disulfiram. Following such pretreatment, a faster development of certain end-stage components of the amphetamine syndrome was obtained. Thus, on the first day, development of a Reactive attitude and of more prominent behavioral disjunction occurred with the combined drug administration as compared with amphetamine alone. In contrast with the facilitation of these behaviors was the absence of dyskinesias and hyperreflexia on that day. Stereotyped behavior, loss of motor initiative and hyperkinetic activity were markedly enhanced and appeared with a shorter latency period on subsequent days of the intoxication cycle. Loss of righting reflex was an early manifestation in these animals. During the later days, the particularly high level of compulsive activity was evident from the occurrence of an obstinate progression syndrome and the performance of stereotyped movements of the head in the presence of a crucifixion posture. In general, modification of the amphetamine effects on behavior was in a direction consistent with comparable features in experimental catatonia and the catatonic form of schizophrenia. The need to integrate such phenomena in any amphetamine model of psychosis is stressed and analogies are drawn with similar features reported in animals treated with bulbocapnine or other psychotogenic compounds and with symptoms of human amphetamine psychosis and schizophrenia.

Animals↗

The olfactory receptor gene repertoire in primates and mouse: evidence for reduction of the functional fraction in primates.

Olfactory receptors (ORs) located in the cell membrane of olfactory sensory neurons of the nasal epithelium are responsible for odor detection by binding specific odorant ligands. Primates are thought to have a reduced sense of smell (microsmatic) with respect to other mammals such as dogs or rodents. We have previously demonstrated that over 70% of the human OR genes have become nonfunctional pseudogenes, leading us to hypothesize that the reduced sense of smell could correlate with the loss of functional genes. To extend these results, we sampled the OR gene repertoire of 10 primate species, from prosimian lemur to human, in addition to mouse. About 221 previously unidentified primate sequences and 33 mouse sequences were analyzed. These sequences encode ORs distributed in seven families and 56 subfamilies. Analysis showed a high fraction ( approximately 50% on average) of pseudogenes in hominoids. In contrast, only approximately 27% of OR genes are pseudogenes in Old World monkeys, and New World monkeys are almost free of pseudogenes. The prosimian branch seems to have evolved differently from the other primates and has approximately 37% pseudogene content. No pseudogenes were found in mouse. With the exception of New World monkeys, we demonstrate that primates have a high fraction of OR pseudogenes compared with mouse. We hypothesize that under relaxed selective constraints, primates would have progressively accumulated pseudogenes with the highest level seen in hominoids. The fraction of pseudogenes in the OR gene repertoire could parallel the evolution of the olfactory sensory function.

Animals↗

Epidemiology of infections due to Pseudomonas aeruginosa.

Pseudomonas aeruginosa is responsible for an increasing proportion of infections acquired in the modern hospital setting. It accounts for 8.5% of all nosocomial infections and has an attack rate of 36 infections per 10,000 hospital discharges. P. aeruginosa represents the single most frequently isolated pathogen in patients with nosocomial pneumonia and burn-wound infections. The organism's bioepidemiology is linked to its ability to thrive in marginal econiches, and its ascendency as a nosocomial pathogen parallels the evolution of high-technology intensive care units, the large numbers of immunocompromised patients, and the liberal use of antibiotics. The reservoirs and modes of transmission for this organism are reviewed along with recent studies aimed at the prevention of both colonization and infection by this organism.

Cross Infection↗

Pattern of morphological diversification in the Leptocarabus ground beetles (Coleoptera: Carabidae) as deduced from mitochondrial ND5 gene and nuclear 28S rDNA sequences.

Most of the mitochondrial NADH dehydrogenase subunit 5 (ND5) gene and a part of nuclear 28S ribosomal RNA gene were sequenced for 14 species of ground beetles belonging to the genus Leptocarabus. In both the ND5 and the 28S rDNA phylogenetic trees of Leptocarabus, three major lineages were recognized: (1) L. marcilhaci/L. yokoael/Leptocarabus sp. from China, (2) L. koreanus/L. truncaticollis/L. seishinensis/L. semiopacus/L. canaliculatus/L. kurilensis from the northern Eurasian continent including Korea and Hokkaido, Japan, and (3) all of the Japanese species except L. kurilensis. Clustering of the species in the trees is largely linked to their geographic distribution and does not correlate with morphological characters. The species belonging to different species groups are clustered in the same lineages, and those in the same species group are scattered among the different lineages. One of the possible interpretations of the present results would be that morphological transformations independently took place in the different lineages, sometimes with accompanying parallel morphological evolution, resulting in the occurrence of the morphological species belonging to the same species group (= type) in the different lineages.

Animals↗

Complete congruence between morphological and rbcL-based molecular phylogenies in birches and related species (Betulaceae).

Estimations of phylogenies from morphological and molecular data often show contrasting results. We compared morphological and molecular phylogenies in an ancient family of woody dicots, the Betulaceae (birch family). The phylogeny of the family was estimated from parsimony analysis of morphological characters in the genera Alnus, Betula, Carpinus, Corylus, Ostrya, and Ostryopsis and from parsimony and distance-matrix analyses of DNA sequences of the chloroplast gene encoding the large subunit of ribulose-1,5-biphosphate carboxylase (rbcL) in the genera Alnus, Betula, Carpinus, Corylus, and Ostrya and in two outgroups, Quercus and Liquidambar. The topologies obtained by the different methods were completely congruent, and bootstrapping strongly supported the division of the family Betulaceae into two major clades, Betuleae (Alnus and Betula) and Coryleae (other members). Only slightly more homoplasy was present in the rbcL sequence data set than in the morphological set. Relative-rate tests indicated that the Coryleae clade had a faster rate of rbcL evolution than did the Betuleae clade. Heterogeneity of rates of morphological evolution also paralleled those for rbcL.

Base Sequence↗

Chronic ethanol consumption induces the production of tumor necrosis factor-alpha and related cytokines in liver and adipose tissue.

Increases in monocyte/macrophage production of the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha), parallel the evolution of liver injury in rats and humans with alcoholic liver disease. However, the possibility that TNF-alpha expression may be induced in other cell populations before serious liver disease develops has not been evaluated. To clarify this issue, mRNAs and/or protein levels of TNF-alpha and cytokines [interleukin (IL)-6, IL-10, transforming growth factor-beta (TGF)-beta, IL-12, and interferon-gamma] that regulate its biological activity were measured in sera, liver, and adipose tissues of rats that had developed hepatic steatosis after consuming ethanol-containing diets for 6 weeks. Cytokine expression in the ethanol-fed groups was compared with that of pair-fed controls rats that had received isocaloric amounts of a similar, ethanol-free diet for the same time period. Animals were studied both before and after a surgical stress (partial hepatectomy) that is known to provoke cytokine production. Chronic ethanol consumption led to increased serum concentrations of TNF and related cytokines, at least in part, by inducing the overproduction of these factors in the liver and peripheral adipose tissues. Despite the pair-feeding protocol that ensured similar calorie consumption in both groups, adipose tissues in ethanol-fed rats also expressed more leptin, a TNF-alpha-inducible mRNA that encodes an appetite-suppressing hormone. Thus, white adipose tissue can be an important source of cytokines in nonobese animals and may be a target for ethanol's actions. These data implicate TNF-alpha as a potential mediator of the nutritional-metabolic aberrations that often accompany chronic alcohol intake, even in the absence of advanced liver disease.

Adipose Tissue↗

Professionalizing domesticity: a synthesis of selected nursing historiography.

The 19th century consolidation of the ideology of domesticity and the ideology of professionalism paralleled the evolution of nursing as a formal occupation for women. Efforts to combine these ideologies, which are based on markedly different foundational assumptions, have been central to the history of American nursing. A meaningful understanding of nursing's history necessitates a synthesis of the interpretations generated by individual historians who have studied similar events in nursing's past. Three feminist historians have studied the professionalizing process in nursing. Generated from diverse perspectives and source materials, the work of these historians illuminates the tensions resulting from nursing's efforts to blend the ideologies of domesticity and professionalism and provides insight into the lessons that can be learned from history.

Female↗

Parallel genetic adaptation amid a background of changing effective population sizes in divergent yellow perch (Perca flavescens) populations.

Aquatic ecosystems are highly dynamic environments vulnerable to natural and anthropogenic disturbances. High-economic-value fisheries are one of many ecosystem services affected by these disturbances, and it is critical to accurately characterize the genetic diversity and effective population sizes of valuable fish stocks through time. We used genome-wide data to reconstruct the demographic histories of economically important yellow perch (Perca flavescens) populations. In two isolated and genetically divergent populations, we provide independent evidence for simultaneous increases in effective population sizes over both historic and contemporary time scales including negative genome-wide estimates of Tajima's D, 3.1 times more single nucleotide polymorphisms than adjacent populations, and contemporary effective population sizes that have increased 10- and 47-fold from their minimum, respectively. The excess of segregating sites and negative Tajima's D values probably arose from mutations accompanying historic population expansions with insufficient time for purifying selection, whereas linkage disequilibrium-based estimates of Ne also suggest contemporary increases that may have been driven by reduced fishing pressure or environmental remediation. We also identified parallel, genetic adaptation to reduced visual clarity in the same two habitats. These results suggest that the synchrony of key ecological and evolutionary processes can drive parallel demographic and evolutionary trajectories across independent populations.

Animals↗

Ultrametricity in three-dimensional edwards-anderson spin glasses

We perform an accurate test of ultrametricity in the aging dynamics of the three-dimensional Edwards-Anderson spin glass. Our method consists in considering the evolution in parallel of two identical systems constrained to have fixed overlap. This turns out to be a particularly efficient way to study the geometrical relations between configurations at distant large times. Our findings strongly hint towards dynamical ultrametricity in spin glasses, while this is absent in simpler aging systems with domain growth dynamics. A recently developed theory of linear response in glassy systems allows us to infer that dynamical ultrametricity implies the same property at the level of equilibrium states.

Journal Article↗

Transition from the incommensurately modulated structure to the lock-in phase in Co-åkermanite.

The adaptation of the incommensurate structure modulation in Ca(2)CoSi(2)O(7) (dicalcium cobalt disilicate) single crystals to decreasing temperature has been examined using in situ high-resolution transmission electron microscopy and electron diffraction. The transition from the incommensurate to the commensurate lock-in phase of Co-åkermanite exhibits a pronounced hysteresis of a highly strained metastable state with a characteristic microdomain morphology. A network of domain walls surrounding single orientation domains develops out of the room-temperature tartan pattern, the domains increase in size and their alignment changes from crystallographic to random. At 100 K the phase transition becomes almost complete. In parallel, the evolution of the modulation structure can be described by a change from a loose arrangement of octagonal tilings into a close-packed configuration of overlapping octagons in the commensurate low-temperature lock-in phase. Thereby, the octagon represents the ordered distribution of low-coordinated Ca clusters within a nanodomain extending over 4 x 4 subunits, on average [Riester et al. (2000). Z. Kristallogr. 215, 102--109]. The modulation wavevector was found to change from q(1,2) = 0.295 (a* +/- b*) at 300 K to q(1,2) = 0.320 (a* +/- b*) at 100 K.

Journal Article↗

Aspirin prevention of cholesterol gallstone formation in prairie dogs.

When prairie dogs (Cynomys ludovicianus) are fed a diet containing cholesterol, a marked increase in gallbladder mucin secretion parallels the evolution of cholesterol supersaturated bile. Gelation of mucin precedes the precipitation of cholesterol liquid and solid crystals and the development of gallstones. Aspirin given to prairie dogs inhibited mucin hypersecretion and gel accumulation and prevented gallstone formation without influencing the cholesterol content of supersaturated bile. This suggests that gallbladder mucin is a nucleation matrix for cholesterol gallstones.

Animals↗

Systemic response to local urate crystal induced inflammation in man: a possible model to study the acute phase response.

The production of a systemic inflammatory response to intradermal monosodium urate crystal injection is described. A transient, self-limiting local response is associated with a systemic response detectable by a rise in the white cell count and serum amyloid A protein. The white cell change parallels the evolution of the local response, whereas the serum amyloid A response lags behind the local lesion, peaking after the local lesion is resolving. Intradermal monosodium urate injection is proposed as a possible inflammatory stimulus to explore the acute phase protein response in different disease states.

Acute Disease↗

Correlation of interleukin-2 and soluble interleukin-2 receptor with clinical activity of multiple sclerosis.

Concentrations of interleukin-2 (IL-2) and soluble IL-2 receptor (sIL-2R) in serum and CSF samples were measured in 63 patients with multiple sclerosis (MS) to evaluate their usefulness as markers of disease activity. CSF concentrations of IL-2 and sIL-2R were significantly higher in MS relapse compared with MS patients in remission or with control subjects. These concentrations correlated with the clinical score by which disease severity was assessed, with the number of relapses per year, and with the total disease duration. Furthermore, there was evidence of intrathecal release of IL-2 and sIL-2R in clinically active MS. The results extend the notion that an activated cellular immune state parallels the evolution of the pathological process in MS and suggest that measurement of IL-2 and sIL-2R concentrations may provide an objective marker of disease activity in patients with MS.

Adult↗

Antibody-induced degradation of acetylcholine receptor in myasthenia gravis: clinical correlates and pathogenetic significance.

Sera of myasthenic patients containing anti-AChR antibodies increase the rate of degradation of mammalian AChR. This phenomenon, antigenic modulation (AMd), was tested on AChR of rat myotubes in serum from 48 myasthenic patients. Sixty-six percent of the sera increased AChR degradation. AMd activity was higher in more severely affected patients, paralleled clinical evolution in individual patients, and was related to AChR-antibody titer. Steroid treatment and thymectomy did not affect AMd activity. Patients who had a thymoma always had greater AMd activity.

Adolescent↗