Chemical Ecology of the host searching behavior in an Egg Parasitoid: are Common Chemical Cues exploited to locate hosts in Taxonomically Distant Plant Species?

Parasitoids are known to exploit volatile cues emitted by plants after herbivore attack to locate their hosts. Feeding and oviposition of a polyphagous herbivore can induce the emission of odor blends that differ among distant plant species, and parasitoids have evolved an incredible ability to discriminate them and locate their hosts relying on olfactive cues. We evaluated the host searching behavior of the egg parasitoid Cosmocomoidea annulicornis (Ogloblin) (Hymenoptera: Mymaridae) in response to odors emitted by two taxonomically distant host plants, citrus and Johnson grass, after infestation by the sharpshooter Tapajosa rubromarginata (Signoret) (Hemiptera: Cicadellidae), vector of Citrus Variegated Chlorosis. Olfactory response of female parasitoids toward plants with no herbivore damage and plants with feeding damage, oviposition damage, and parasitized eggs was tested in a Y-tube olfactometer. In addition, volatiles released by the two host plant species constitutively and under herbivore attack were characterized. Females of C. annulicornis were able to detect and significantly preferred plants with host eggs, irrespectively of plant species. However, wasps were unable to discriminate between plants with healthy eggs and those with eggs previously parasitized by conspecifics. Analysis of plant volatiles induced after sharpshooter attack showed only two common volatiles between the two plant species, indole and ß-caryophyllene. Our results suggest that this parasitoid wasp uses common chemical cues released by many different plants after herbivory at long range and, once on the plant, other more specific chemical cues could trigger the final decision to oviposit.

Previous herbivory alerts conspecific gravid sawflies to avoid unsuitable host plants.

The willow sawfly, Nematus oligospilus (Förster), is a pest in Salix commercial forests and has been reported worldwide. Female adults must recognize a suitable host plant to oviposit, since her offspring lack the ability to move to another host. We evaluated the effect of conspecific herbivory on the oviposition choices of N. oligospilus females by providing damaged (DP) and undamaged (UP) plants of Salix humboldtiana, a native willow from South America, as oviposition substrates. Local and systemic effects were studied. For the local treatment, a twig from the DP with damaged leaves was contrasted to a twig from a UP in dual choice experiments. For systemic treatment, a twig from the DP with intact leaves was contrasted to a twig from a UP. We estimated the use of olfactory and contact cues by comparing volatile emission of DP and UP, and by analysing the behaviour of the females during host recognition after landing on the leaf surface. In the context of the preference-performance hypothesis (PPH), we also tested if oviposition site selection maximizes offspring fitness by evaluating neonate hatching, larval performance and survival of larvae that were born and bred on either DP or UP. Our results demonstrate that previous conspecific herbivory on S. humboldtiana has a dramatic impact on female oviposition choices and offspring performance of the sawfly N. oligospilus. Females showed a marked preference for laying eggs on UP of S. humboldtiana. This preference was found for both local and systemic treatments. Volatile emission was quantitatively changed after conspecific damage suggesting that it could be related to N. oligospilus avoidance. In the dual choice preference experiments, the analysis of the behaviour of the females once landing on the leaf surface suggested the use of contact cues triggering egg laying on leaves from UP and avoidance of leaves from DP. Furthermore, 48 h of previous conspecific feeding was sufficient to dramatically impair neonate hatching, as well as larval development and survival, suggesting a rapid and effective reaction of the induced resistance mechanisms of the tree. In agreement with the PPH, these results support the idea that decisions made by colonizing females may result in optimal outcomes for their offspring in a barely studied insect model, and also opens the opportunity for studying tree-induced defences in the unexplored South American willow S. humboldtiana.

Volatiles mediate host-selection in the corn hoppers Dalbulus maidis (Hemiptera: Cicadellidae) and Peregrinus maidis (Hemiptera: Delphacidae).

Volatile organic compounds (VOCs) released by plants are generally involved in host recognition and host selection for many phytophagous insects. However, for leafhoppers and planthoppers, host recognition is mainly thought to involve a phototactic response, but it is not clear if a host plant could be selected based on the volatile cues it emits. In this study we evaluated olfactory responses in dual choice tests of two Hemiptera species, Dalbulus maidis (De Long) (Cicadellidae) and Peregrinus maidis (Ashmead) (Delphacidae), vectors of maize-stunting diseases, to three maize (Zea mays L.) germplasms, a temperate and a tropical hybrid and a landrace. VOCs emitted by the germplasms were collected and identified using gas chromatography-mass spectrometry. The temperate hybrid released significantly more VOCs than the tropical hybrid and the landrace, and its volatile profile was dominated by (±)-linalool. D. maidis preferred odours emitted from the temperate hybrid, whereas P. maidis preferred odours from the tropical hybrid and the landrace over the temperate one. In order to test if linalool plays a role in the behavioural responses, we assayed this compound in combination with the tropical hybrid, to provide other contextual olfactory cues. D. maidis was attracted to the tropical hybrid plus a 0.0001% linalool solution, indicating that this compound could be part of a blend of attractants. Whereas addition of linalool resulted in a slight, though not significant, reduction in host VOC attractiveness for P. maidis. Both hopper species responded to olfactory cues in the absence of supplementary visual cues.

Perspectives on skeletal muscle stem cells.

Skeletal muscle has remarkable regeneration capabilities, mainly due to its resident muscle stem cells (MuSCs). In this review, we introduce recently developed technologies and the mechanistic insights they provide to the understanding of MuSC biology, including the re-definition of quiescence and Galert states. Additionally, we present recent studies that link MuSC function with cellular heterogeneity, highlighting the complex regulation of self-renewal in regeneration, muscle disorders and aging. Finally, we discuss MuSC metabolism and its role, as well as the multifaceted regulation of MuSCs by their niche. The presented conceptual advances in the MuSC field impact on our general understanding of stem cells and their therapeutic use in regenerative medicine.

Study of the renal tubular interactions of thyrocalcitonin, cyclic adenosine 3',5'-monophosphate, 25-hydroxycholecalciferol, and calcium ion.

Acute clearance studies were performed in thyroparathyroidectomized animals to determine the actions and interactions of thyrocalcitonin (TCT), cyclic adenosine 3'5'-monophosphate (cAMP), 25-hydroxycholecalciferol (25HCC), and calcium ion on the reabsorption of phosphate, calcium, sodium, and potassium by the kidney. The infusion of 25HCC in a dosage of 60 U/h to moderately saline-expanded animals (2.5% body weight) induced a fall in the excretion of all of the ions under study after 90-120 min similar to that observed in previous experiments from this laboratory. Mean decrements in fractional excretion were: phosphate, 42.0% (P < 0.005); calcium, 25.0% (P < 0.005); sodium, 23.4% (P < 0.001); and potassium, 14.7% (P < 0.005). The superimposition of either porcine or salmon TCT (1-100 MRC U/h for 2 h) resulted in no further alterations in electrolyte excretion. However, the infusion of TCT during steady-state saline expansion, before the administration of 25HCC, obviated the renal transport effects of the vitamin D metabolite. Both in the latter studies, as well as those in which similar doses of TCT were given to hydropenic animals, the hormone itself failed to induce any consistent alteration in electrolyte excretion. Cyclic AMP (50 mg/h) caused an increase in the excretion of phosphate, sodium, and potassium and no change in calcium excretion. Like TCT, the nucleotide blocked the action of 25HCC on the kidney. Raising the mean level of serum ultrafilterable calcium to 3.02+/-0.25 mEq/liter from 1.62+/-0.17 mEq/liter likewise prevented enhanced ionic reabsorption due to 25HCC.

Male sexual enhancement after methoprene treatment in Anastrepha fraterculus (Diptera: Tephritidae): A sustained response that does not fade away after sexual maturation.

The juvenile hormone (JH) of insects triggers physiological changes related to reproduction in adults of both sexes. Methoprene is a sesquiterpene with some effects that are analogous to those of JH. Treatments with methoprene accelerate sexual maturation in males of the South American fruit fly Anastrepha fraterculus, giving young males a mating advantage over non-treated males of the same age. Here, we evaluated the effects of methoprene treatment on A. fraterculus males after the sexual maturation phase and tested whether this compound provides a long-term mating advantage. Moreover, we took the first step to unravel the mechanisms that underlie male sexual enhancement. We treated males 1day or 8days after adult emergence and compared mate choice between recently matured (young) females and females that had been mature for ca. 10days (aged females). We also addressed methoprene treatment effects on male sexual signalling. We found that methoprene treatment enhanced male sexual competitiveness even after the sexual maturation phase, and the effect did not decrease until males were older than 20days. However, when methoprene treatment was carried out close to sexual maturity, the mating enhancement was no longer observed, suggesting a non-immediate effect and excluding the possibility that methoprene acts as a pheromonal compound. Young and aged females tended to mate more frequently with treated-males. This might indicate that in a context of sexual selection, the potential benefits associated with reproductive success would be similar for females of both ages. Treated males released larger amounts of pheromonal compounds than non-treated males, but their courtship behaviour was not altered to the same extent, suggesting that methoprene treatment may accelerate differently the components of male courtship. We discuss potential benefits of using methoprene to increase the efficiency of the sterile insect technique, which is an environmentally safe method to control this important South American fruit pest.

N-acetylcysteine blocks apoptosis induced by N-alpha-tosyl-L-phenylalanine chloromethyl ketone in transformed T-cells.

The serine protease inhibitor N-alpha-tosyl-L-phenylalanine chloromethyl ketone (TPCK) can interfere with cell-cycle progression and has also been shown either to protect cells from apoptosis or to induce apoptosis. We tested the effect of TPCK on two transformed T-cell lines. Both Jurkat T-cells and Theileria parva-transformed T-cells were shown to be highly sensitive to TPCK-induced growth arrest and apoptosis. Surprisingly, we found that the thiol antioxidant, N-acetylcysteine (NAC), as well as L- or D-cysteine blocked TPCK-induced growth arrest and apoptosis. TPCK inhibited constitutive NF-kappaB activation in T. parva-transformed T-cells, with phosphorylation of IkappaBalpha and IkappaBbeta being inhibited with different kinetics. TPCK-mediated inhibition of IkappaB phosphorylation, NF-kappaB DNA binding and transcriptional activity were also prevented by NAC or cysteine. Our observations indicate that apoptosis and NF-kappaB inhibition induced by TPCK result from modifications of sulphydryl groups on proteins involved in regulating cell survival and the NF-kappaB activation pathway(s).

Ticrynafen and probenecid in hyperuricemic, hypertensive men.

In a double-blind crossover study of ticrynafen (TCN) and probenecid (PBC), 9 hypertensive, hyperuricemic men completed 12-wk courses of each drug. With a TCN dose of 125 mg daily, the fall in serum uric acid was prompt, dramatic, and lasting; it was equal to that after PBC, 500 or 1,000 mg daily. There was a small but significant early weight loss (diuresis) after TCN but no antihypertensive effect. Twelve days after resuming TCN for a proposed additional extension study 1 patient suffered acute, reversible bilateral ureteral obstruction, probably caused by sudden urinary uric acid precipitation.

Characterisation of NF-kappa B complexes in Theileria parva-transformedT cells.

Transformation of T cells by the intracellular parasite Theileria parva is accompanied by constitutive I-kappa B degradation and NF-kappa B activation, a process which is essential to prevent the spontaneous apoptosis of these parasite-transformed cells. NF-kappa B-mediated responses are regulated by selective combinations of NF-kappa B proteins as homo- or heterodimers and by distinct kappa B motifs. We characterised the NF-kappa B complexes induced by T. parva infection in TpM(803) T cells. By western blot, we demonstrated that all members of the NF-kappa B/Rel family of proteins translocate to the nucleus of infected cells. Using two different kappa B oligonucleotides (kappa B-1 and kappa B-2), both containing the decameric consensus kappa B motif (GGGACTTTCC), clearly distinct patterns of DNA binding activities could be demonstrated in electrophoretic mobility shift assays. Supershift analysis and UV cross-linking assays showed that complexes binding to kappa B-1 consisted of p50, p65 and RelB homo and/or heterodimers. We could also detect an association of ATF-2 and c-Fos with one of the complexes. The HIV-derived kappa B-2 oligo only bound p50 and p65. Additionally, several agents known to inhibit a wide range of NF-kappa B activation pathways had no inhibitory effect on the activation of NF-kappa B DNA binding in TpM(803) T cells.

Hypokalemia and the pathology of ion transport molecules.

Serum potassium is normally maintained within a narrow range through an exquisite balance between cellular K+ efflux and influx, and between the intake and output of potassium from the body. Ultimately such balances are determined by cell membrane molecules which effect K+ transfer from one milieu to another. Over the last decade, electrophysiological and molecular techniques of study, briefly reviewed in this article, have helped to define the biochemical and functional characteristics of many of the molecules responsible for potassium homeostasis. When combined with molecular genetics, the same technology allows for the ultimate definition of hereditary or familial disease states characterized by hypokalemia. Familial hypokalemic periodic paralysis is associated with mutations of the dihydropyridine receptor gene encoding the L-type Ca+2 channel, but how such mutations result in episodic hypokalemia and paralysis remains a mystery. Mutations in several genes involved in renal ion transport also result in hypokalemia. Among them, Liddle's syndrome, or pseudohyperaldosteronism, has been linked to increased surface expression of the epithelial sodium channel (ENaC) responsible for Na+ transport in the cortical collecting duct. On the other hand, Bartter's syndrome, characterized by defective salt reabsorption by the ascending limb of Henle's loop, is associated with mutations in either the NKCC2 gene encoding the loop's 1Na+-1K+-2Cl- cotransporter, or in the ROMK gene, which allows K+ recycling in the loop to occur from cell to lumen, making Na+ reabsorption via the cotransporter possible. In Gitelman's syndrome, which clinically appears as a milder form of Bartter's, the abnormal gene encodes the thiazide sensitive Na+-Cl- cotransporter operating in the distal convoluted tubule.

Principles of diuretic therapy.

This section discusses the reasons different diuretic agents inhibit salt reabsorption at specific sites within the renal tubule. It also includes a brief review of how diuretics reach their target site of action along the nephron, together with a discussion of how disease states may affect the delivery of diuretics to those sites. When diuretics are administered to edematous patients, the natriuretic response is often blunted. In addition, increased renal tubular salt avidity is observed after administration of loop diuretics. The elements required to successfully achieve adequate natriuresis under such conditions are analyzed. Because achieving diuresis may result in significant hypokalemia, hyponatremia, metabolic alkalosis, and worsening prerenal azotemia, the prevention and management of these complications of diuretic therapy are also reviewed. A description of successful use of diuretics in specific edematous states, such as congestive heart failure, chronic renal failure, nephrotic syndrome, and liver disease, is followed by a brief discussion of the management of resistant edema and the use of diuretics in nonedematous states, including essential hypertension and other conditions.

[Inhibition of growth hormone in insulin-dependent diabetics after oral administration of pirenzepine. Fluorophotometric study of the vitreous body]. / Inhibition de l'hormone de croissance chez les sujets diabétiques insulino-dépendants après administration par voie orale de pirenzépine. Etude par fluorophotométrie du vitré.

The purpose of our study was to quantify the blood-retinal barrier permeability in five patients with insulin-dependent diabetic (mean age 14.96 +/- 2.45 years) without retinopathy, after six month with oral pirenzepine, a growth hormone inhibitor. Blood-retinal barrier permeability was determined by vitreous fluorophotometry before and after treatment with a nocturnal oral dose of pirenzepine (0.6 mg/kg the first month and 1 mg/kg the following five months). We found a significant diminution (p < 0.05) in growth hormone levels (10.48 +/- 4.94 ng/ml before treatment and 4.35 +/- 2.53 ng/ml after treatment), nevertheless, no changes in the blood-retinal barrier permeability values were observed (4.84 +/- 2.08 x 10(-6) min-1 before treatment and 4.53 +/- 2.54 x 10(-6) min-1 after treatment). We found no modifications in the levels of somatomedin C or HbA1c either. It can be concluded that oral pirenzepine used at this dose for six months, in spite of a significant decrease in growth hormone secretion, does not decrease the permeability of the blood-retinal barrier.

Ceramide synergizes with phorbol ester or okadaic acid to induce IkappaB degradation.

Ceramide is a lipid second messenger which is generated in response to stimulation of a number of surface receptors, treatment with chemotherapeutic agents, or ionising radiation. Depending on the target cell, ceramide induces diverse biological responses including apoptosis, cell-cycle arrest, differentiation, and also proliferation. We studied the effect of ceramide on the degradation of IkappaB, the cytoplasmic inhibitor of the transcription factor NF-kappaB. We show that ceramide treatment results in reduced levels of phosphorylated IkappaBalpha and degradation of both IkappaBalpha and IkappaBbeta. Ceramide synergised with okadaic acid (OA), a compound which interferes with the protein phosphatase 2A-controlled component of the NF-kappaB activation pathway, enhancing OA-induced IkappaB degradation. Ceramide also synergised with phorbol 12-myristate 13-acetate, which mimics protein kinase C activation. Finally, we show that the synergistic effect of ceramide with OA or phorbol ester can be observed in primary lymph node T-cells as well as in transformed T-cells.

Relationship between serum phosphate concentration and proximal tubular bicarbonate transport.

Micropuncture studies were performed in intact and thyroparathyroidectomized (TPTX) dogs to evaluate the relationship between the absolute level of serum ultrafilterable phosphate concentration (SUFP) and proximal bicarbonate reabsorption. In both groups of animals, a reverse linear relationship was noted between the serum phosphate level and the tubular fluid bicarbonate concentration (TFHCO3). For the intact dogs, TFHCO3=32.27 SUFP+/-2.17, r=0.715, p=0.02, and for the TPTX dogs, TFHCO3=35.68-2.39 SUFP+/-2.26; r=0.619, p less than 0.02. Furthermore, when late-proximal tubular values for absolute bicarbonate reabsorptive rate (THCO3)/100 nl single nephron filtrate were plotted against SUFP, a direct relationship was found for both groups; intact dogs: THCO3=205 SUFP-169+/-136, r=0.707, p less than 0.05; TPTX dogs: THCO3=224 SUFP-882+/-221, r=0.625, p less than 0.01. Variations in plasma bicarbonate concentration or PCO2 did not contribute to the relationship between SUFP and bicarbonate reabsorption. The data suggest that extracellular fluid phosphate concentration is an important modulator of proximal bicarbonate transport, independent of the action of parathyroid hormone.

Theileria parva: taking control of host cell proliferation and survival mechanisms.

The intracellular parasite Theileria parva infects and transforms bovine T-cells, inducing their uncontrolled proliferation and spread in non-lymphoid as well as lymphoid tissues. This parasite-induced transformation is the predominant factor contributing to the pathogenesis of a lymphoproliferative disease, called East Coast fever. T. parva-transformed cells become independent of antigenic stimulation or exogenous growth factors. A dissection of the signalling pathways that are activated in T. parva-infected cells shows that the parasite bypasses signalling pathways that normally emanate from the T-cell antigen receptor to induce continuous proliferation. This review concentrates on the influence of the parasite on the state of activation of the mitogen-activated protein kinase (MAPK), NF-kappaB and phosphoinositide-3-kinase (PI3-K) pathways in the host cell. Of the MAPKs, JNK, but not ERK or p38, is active, inducing constitutive activation of the transcription factors AP-1 and ATF-2. A crucial step in the transformation process is the persistent activation of the transcription factor NF-kappaB, which protects T. parva-transformed cells from spontaneous apoptosis accompanying the transformation process. Inhibitor studies also suggest an important role for the lipid kinase, PI-3K, in the continuous proliferation of T. parva-transformed lymphocytes.

Clinical and metabolic factors associated with the blood retinal barrier permeability in insulin dependent diabetes mellitus without retinopathy.

The authors assessed a study pointing out the relationship between the permeability of Blood Retinal Barrier (BRB), using vitreous fluorophotometry, and several risk clinical and laboratory data in Insulin Dependent Diabetes Mellitus (IDDM). Eighty eyes of 40 IDDM patients were evaluated. Their mean age was 14.8 +/- 3.2 years. Twenty healthy volunteers served as control group (mean age 15.3 +/- 3.2 years). Preexisting diabetic retinopathy was dismissed after funduscopy and fluorescein angiography. The studied risk factors were: age, duration of diabetes, HLA antigens, blood pressure, cholesterol and triglycerides levels, glycosylated hemoglobin, insulin dose/kg body weight and fructosamine. Vitreous and lens fluorophotometry was performed in both groups (VPRt). The mean VPRt in IDDM patients was 3.56 +/- 1.47 x 10(-6) min-1. In healthy subjects it was 2.53 +/- 0.55 x 10(-6) min-1, establishing a significant difference (p < 0.01). We found a statistically significant correlation between VPRt and duration of diabetes, insulin dose/kg body weight and HbAlc. No correlation was found between VPRt and the rest of parameters. We conclude that vitreous fluorophotometry is a valid method to measure BRB; and the three factors mentioned above are related to the BRB permeability.

Charcot arthropathy secondary to amyloid neuropathy.

Neuropathic (Charcot) ankle joints developed in a 50-year-old patient with end-stage renal disease from primary, nonfamilial amyloidosis. Sensory neuropathy in the legs had been noted three years before the onset of uremia and had porgressed. Sural nerve, but not synovial biopsy specimen, showed amyloid in and around arteriolar walls by light and electron microscopy. Since Charcot joints are only rarely associated with amyloid neuropathy, it is possible that uremic neuritis, or prolonged survival by dialysis, contributed to progression of the neuropathy, allowing subsequent joint degeneration.

The inhibition of NF-kappaB activation pathways and the induction of apoptosis by dithiocarbamates in T cells are blocked by the glutathione precursor N-acetyl-L-cysteine.

Nuclear factor-kappaB regulates genes that control immune and inflammatory responses and are involved in the pathogenesis of several diseases, including AIDS and cancer. It has been proposed that reactive oxygen intermediates participate in NF-kappaB activation pathways, and compounds with putative antioxidant activity such as N-acetyl-L-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) have been used interchangeably to demonstrate this point. We examined their effects, separately and combined, on different stages of the NF-kappaB activation pathway, in primary and in transformed T cells. We show that NAC, contrary to its reported role as an NF-kappaB inhibitor, can actually enhance rather than inhibit IkappaB degradation and, most importantly, show that in all cases NAC exerts a dominant antagonistic effect on PDTC-mediated NF-kappaB inhibition. This was observed at the level of IkappaB degradation, NF-kappaB DNA binding, and HIV-LTR-driven reporter gene expression. NAC also counteracted growth arrest and apoptosis induced by dithiocarbamates. Antagonistic effects were further observed at the level of jun-NH2-terminal kinase, p38 and ATF-2 activation. Our findings argue against the widely accepted assumption that NAC inhibits all NF-kappaB activation pathways and shows that two compounds, previously thought to function through a common inhibitory mechanism, can also have antagonistic effects.

The intracellular parasite Theileria parva protects infected T cells from apoptosis.

Parasites have evolved a plethora of strategies to ensure their survival. The intracellular parasite Theileria parva secures its propagation and spreads through the infected animal by infecting and transforming T cells, inducing their continuous proliferation and rendering them metastatic. In previous work, we have shown that the parasite induces constitutive activation of the transcription factor NF-kappaB, by inducing the constitutive degradation of its cytoplasmic inhibitors. The biological significance of NF-kappaB activation in T. parva-infected cells, however, has not yet been defined. Cells that have been transformed by viruses or oncogenes can persist only if they manage to avoid destruction by the apoptotic mechanisms that are activated on transformation and that contribute to maintain cellular homeostasis. We now demonstrate that parasite-induced NF-kappaB activation plays a crucial role in the survival of T. parva-transformed T cells by conveying protection against an apoptotic signal that accompanies parasite-mediated transformation. Consequently, inhibition of NF-kappaB nuclear translocation and the expression of dominant negative mutant forms of components of the NF-kappaB activation pathway, such as IkappaBalpha or p65, prompt rapid apoptosis of T. parva-transformed T cells. Our findings offer important insights into parasite survival strategies and demonstrate that parasite-induced constitutive NF-kappaB activation is an essential step in maintaining the transformed phenotype of the infected cells.