The effect of behavioural and morphological plasticity on foraging efficiency in the threespine stickleback (Gasterosteus sp.)

We conducted an experiment to assess the change in foraging efficiency resulting from diet-induced morphological and behavioural plasticity in a species of freshwater, threespine stickleback (Gasterosteus sp.). Different degrees of morphological and behavioural change were induced using two prey items commonly found in the diet of this species, allowing us to estimate the relative importance of each type of plasticity. The purpose of the experiment was twofold. First, earlier work had suggested that diet variability might be an important factor in the evolution of trophic morphological plasticity in sticklebacks. The present results extend this work by revealing the adaptive significance of morphological plasticity. The current experiment also qualitatively assessed the compatibility of the time scale of morphological change with that of the natural resource variability experienced by this species. The results indicate that diet-induced plasticity improves foraging efficiency continuously for up to 72 days of prey exposure. This is probably due in part to plasticity of the external trophic morphology but our results also suggest a complex interplay between morphology and behaviour. The time scale appears to be matched to that of natural diet variability although it is possible that some traits exhibit non-labile plasticity. Our discussion highlights the important distinction between conditions favouring the evolution of labile versus non-labile plasticity. The second objective of the experiment was to determine the relative importance of morphological and behavioural plasticity. Few studies have attempted to quantify the adaptive significance of morphological plasticity and no study to our knowledge has separated the effects of morphological and behavioural plasticity. Our experiment reveals that both behavioural and morphological plasticity are important and it also suggests a dichotomy between the two: behavioural plasticity predominately affects searching efficiency whereas morphological plasticity predominately affects handling efficiency.     

One hospital's experience with a "Do not resuscitate" policy.

A "No not resuscitate" policy was instituted at McMaster University Medical Centre, Hamilton, in January 1979. Its objectives were to ensure that physicians decide on the appropriateness of resuscitation attempts before they might be needed; to have each physician consult his or her patients, or the families of incompetent patients, to determine their wishes concerning further treatment; and to provide legal protection of or physicians and the hospital in regard to the policy. To determine the effectiveness of the "Do not resuscitate" policy a questionnaire was sent to a sample of the professional staff of the hospital; the overall response rate was 87%. The respondents felt that a better way of informing hospital staff of the policy and its objectives was needed. However, the results of the questionnaire suggested that, on the whole, the policy was perceived as beneficial to both patients and physicians at the hospital.     

Phosphatidic acid and diacylglycerol directly activate NADPH oxidase by interacting with enzyme components

The enzyme NADPH oxidase is regulated by phospholipase D in intact neutrophils and is activated by phosphatidic acid (PA) plus diacylglycerol (DG) in cell-free systems. We showed previously that cell-free NADPH oxidase activation by these lipids involves both protein kinase-dependent and -independent pathways. Here we demonstrate that only the protein kinase-independent pathway is operative in a cell-free system of purified and recombinant NADPH oxidase components. Activation by PA + DG was ATP-independent and unaffected by the protein kinase inhibitor staurosporine, indicating the lack of protein kinase involvement. Both PA and DG were required for optimal activation to occur. The drug reduced activation of NADPH oxidase by either arachidonic acid or PA + DG, with IC(50) values of 46 and 25 microm, respectively. The optimal concentration of arachidonic acid or PA + DG for oxidase activation was shifted to the right with, indicating interference of the drug with the interaction of lipid activators and enzyme components. inhibited the lipid-induced aggregation/sedimentation of oxidase components p47(phox) and p67(phox), suggesting a disruption of the lipid-mediated assembly process. The direct effects of on NADPH oxidase activation complicate its use as a "specific" inhibitor of DG kinase. We conclude that the protein kinase-independent pathway of NADPH oxidase activation by PA and DG involves direct interaction with NADPH oxidase components. Thus, NADPH oxidase proteins are functional targets for these lipid messengers in the neutrophil.     

The autonomic nervous control of heart rate in ducks during voluntary diving

Autonomic nervous control of heart rate was studied in voluntarily diving ducks (Aythya affinis). Ducks were injected with the muscarinic blocker atropine, the beta-adrenergic blocker nadolol, the beta-adrenergic agonist isoproterenol, and a combination of both atropine and nadolol. Saline injection was used as a control treatment. The reduction in heart rate (from the predive level) normally seen during a dive was abolished by atropine. Nadolol reduced heart rate during all phases of diving activity-predive, dive, and postdive-indicating that sympathetic output to the heart was not withdrawn during diving. Isoproterenol increased heart rate before, during, and after the dive, although the proportional increase in heart rate was not as high during the dive as compared with the increase in routine heart rate or heart rate during the predive or postdive phase. The parasympathetic system predominates in the control of heart rate during diving despite the maintenance of efferent sympathetic influences to the heart, perhaps due to accentuated antagonism between the two branches of the autonomic nervous system.     

IMDA/aldol strategy for transforming carbohydrates into functionalized trans-decalins

L-Rhamnal is readily converted into an allyl 2, 3-unsaturated-C-glycopyranoside. The (S) configuration of the alphaL-anomer defines the stereochemical outcome of the future IMDA reaction, leading to the absolute stereochemistry for the trans-decalin moiety in naturally occurring terpenoids. Selective cleavage of the terminal double bond of the allyl group provides an aldehydo function which serves for an aldol/Claisen addition with ethyl sorbate. Of the four possible diastereomers, one is obtained in pure form and processed to give the IMDA precursor. Cyclocondensation is achieved by heating in xylene to give a tricyclic trans-decalin whose structure is established by NMR and X-ray analysis.     

Inhibition of human neutrophil chemotaxis by the protein kinase inhibitor, 1-(5-isoquinolinesulfonyl) piperazine

The protein kinase inhibitor, 1-(5-isoquinolinesulfonyl) piperazine (C-I), inhibits superoxide release from human neutrophils (PMN) stimulated with phorbol myristate acetate or synthetic diacylglycerol, without inhibiting superoxide release from PMN stimulated with the chemoattractants C5a or N-formyl-methionyl-leucyl-phenylalanine (f-Met-Leu-Phe). In this study, we investigated the effect of C-I on human PMN chemotaxis to C5a, f-Met-Leu-Phe, leukotriene B4 (LTB4), and fluoresceinated N-formyl-methionyl-leucyl-phenylalanine-lysine (f-Met-Leu-Phe-Lys-FITC). PMN, preincubated for 5 min at 37 degrees C with 0 to 200 microM C-I, were tested for their migratory responses to the chemoattractants. C-I (greater than or equal to 1 microM) significantly inhibited PMN chemotaxis to f-Met-Leu-Phe, f-Met-Leu-Phe-Lys-FITC, and C5a without affecting random migration. Maximal inhibition of chemotaxis to these attractants occurred with greater than or equal to 50 microM C-I, at which chemotaxis was inhibited by 80 to 95%. The C-I inhibition was reversible. In contrast, 200 microM C-I did not inhibit the number of PMN migrating to LTB4, although, the leading front of PMN migration to LTB4 was inhibited by C-I. C-I inhibited PMN orientation to C5a and f-Met-Leu-Phe without affecting orientation to LTB4. C-I did not inhibit the binding of radiolabeled f-Met-Leu-Phe or f-Met-Leu-Phe-Lys-FITC to PMN. These findings suggest that the chemotactic responses of PMN to f-Met-Leu-Phe and C5a involve a protein kinase-dependent reaction which is inhibited by C-I.     

Activated p53 in the anti-apoptotic milieu of tuberous sclerosis gene mutation induced diseases leads to cell death if thioredoxin reductase is inhibited

Apoptosis - Tuberous sclerosis, angiomyolipoma and lymphangioleiomyomatosis are a group of diseases characterized by mutation in tuberous sclerosis genes (TSC 1-2). TSC mutation leads to continuous...     

Reduced IgG anti-small nuclear ribonucleoprotein autoantibody production in systemic lupus erythematosus patients with positive IgM anti-cytomegalovirus antibodies

Introduction

In rheumatoid arthritis (RA), synovial fluid (SF) contains a large number of neutrophils that contribute to the inflammation and destruction of the joints. The SF also contains granulocyte-macrophage colony-stimulating factor (GM-CSF), which sustains viability of neutrophils and activates their functions. Using proteomic surveillance, we here tried to elucidate the effects of GM-CSF on neutrophils.

Methods

Neutrophils stimulated by GM-CSF were divided into four subcellular fractions: cytosol, membrane/organelle, nuclei, and cytoskeleton. Then, proteins were extracted from each fraction and digested by trypsin. The produced peptides were detected using matrix-assisted laser desorption ionisation-time-of-flight mass spectrometry (MALDI-TOF MS).

Results

We detected 33 peptide peaks whose expression was upregulated by more than 2.5-fold in GM-CSF stimulated neutrophils and identified 11 proteins out of the 33 peptides using MALDI-TOF/TOF MS analysis and protein database searches. One of the identified proteins was neutrophil gelatinase-associated lipocalin (NGAL). We confirmed that the level of NGAL in SF was significantly higher in patients with RA than in those with osteoarthritis. We next addressed possible roles of the increased NGAL in RA. We analysed proteome alteration of synoviocytes from patients with RA by treatment with NGAL in vitro. We found that, out of the detected protein spots (approximately 3,600 protein spots), the intensity of 21 protein spots increased by more than 1.5-fold and the intensity of 10 protein spots decreased by less than 1 to 1.5-fold as a result of the NGAL treatment. Among the 21 increased protein spots, we identified 9 proteins including transitional endoplasmic reticulum ATPase (TERA), cathepsin D, and transglutaminase 2 (TG2), which increased to 4.8-fold, 1.5-fold and 1.6-fold, respectively. Two-dimensional electrophoresis followed by western blot analysis confirmed the upregulation of TERA by the NGAL treatment and, moreover, the western blot analysis showed that the NGAL treatment changed the protein spots caused by post-translational modification of TERA. Furthermore, NGAL cancelled out the proliferative effects of fibroblast growth factor (FGF)-2 and epidermal growth factor (EGF) on chondrocytes from a patient with RA and proliferative effect of FGF-2 on chondrosarcoma cells.

Conclusions

Our results indicate that GM-CSF contributes to the pathogenesis of RA through upregulation of NGAL in neutrophils, followed by induction of TERA, cathepsin D and TG2 in synoviocytes. NGAL and the upregulated enzymes may therefore play an important role in RA.     

Molecular characterization of PoGT8D and PoGT43B, two secondary wall-associated glycosyltransferases in poplar

Dicot wood is mainly composed of cellulose, lignin and glucuronoxylan (GX). Although the biosynthetic genes for cellulose and lignin have been studied intensively, little is known about the genes involved in the biosynthesis of GX during wood formation. Here, we report the molecular characterization of two genes, PoGT8D and PoGT43B, which encode putative glycosyltransferases, in the hybrid poplar Populus alba x tremula. The predicted amino acid sequences of PoGT8D and PoGT43B exhibit 89 and 75% similarity to the Arabidopsis thaliana IRREGULAR XYLEM8 (IRX8) and IRX9, respectively, both of which have been shown to be required for GX biosynthesis. The PoGT8D and PoGT43B genes were found to be expressed in cells undergoing secondary wall thickening, including the primary xylem, secondary xylem and phloem fibers in stems, and the secondary xylem in roots. Both PoGT8D and PoGT43B are predicted to be type II membrane proteins and shown to be targeted to Golgi. Overexpression of PoGT43B in the irx9 mutant was able to rescue the defects in plant size and secondary wall thickness and partially restore the xylose content. Taken together, our results demonstrate that PoGT8D and PoGT43B are Golgi-localized, secondary wall-associated proteins, and PoGT43B is a functional ortholog of IRX9 involved in GX biosynthesis during wood formation.     

Linking bioprospecting with sustainable development and conservation: the Panama case

The limited international resources for economic aid and conservation can only mitigate poverty and losses of biodiversity. Hence, developing nations must establish the capacity to resolve their problems. Additionally, policy-makers and donors need to obtain scientific input on issues such as global change and ecosystem services. We propose that for nations rich in biodiversity, ecosystem services derived from bioprospecting, or drug discovery, could contribute to economic development. In the case where unstudied samples are shipped abroad for research, the chances of obtaining royalties are infinitesimally small. Therefore developing nations will only realize benefits from bioprospecting through in-country research on their own biodiversity. Policy-makers and donors have failed to appreciate the value of this approach. In order to provide an example of the inherent links between conservation and sustainable economic development, we initiated a drug discovery effort in Panama that emphasizes local benefit. As much of the drug discovery process as possible is conducted in Panamanian laboratories, providing jobs dependent on intact biodiversity and enhancing local research and training. In short, research, plus the spin-offs from research, provide immediate and long-lasting benefits to Panama. The connection between conservation and development has been highlighted in publicity about the project in Panama’s urban media. This provides a constructive alternative to the perception the among the urban populace that economic development inevitably competes with conservation. In summary, our program uses biodiversity to promote human health as well as to support research capacity, economic development and conservation within Panama. The program provides an example of the widely recognized but little developed concept of bioprospecting research as an ecosystem service.