Inputs to the hormonal control of egg development in Rhodnius prolixus

This paper re-examines existing data on the environmental inputs governing egg production in Rhodnius prolixus. Feeding has a direct effect on egg production such that the product of the unfed weight of the female times the weight of the blood meal is a good predictor of the number of eggs produced. Mating modifies this input, so that mated females produce more eggs. Egg production is governed by the corpus allatum, and indirect evidence suggests that the number of eggs producted by a female is a function of the length of time that juvenile hormone is secreted by the corpus allatum. The input which determines the times at which the corpus allatum is switched off originates in the stretch induced by the amount of the meal remaining in the crop, modified by the matedness status of the female. The precise nature of the sensors detecting stretch is not yet clear, but the integrity of the dorsal aorta is essential to the transmission of the information. These data are related to the survival strategy for Rhodnius.

Morphological evidence by scanning electron microscopy of excretion of metacyclic forms of Trypanosoma cruzi in vector's urine

Comparision by scanning electron microscopy (SEM) of Trypanosoma cruzi flagellates attached to the cuticle of the rectal gland of infected Dipetalogaster maxima nymphs, showed marked differences before amd after feeding. Before feeding numerous metacyclic trypomastigotes were observed among the abundant epimastigotes that formed the carpet of flagellates. On the other hand, in insects that were allowed to urinate for 24 hours after a meal, the metacyclics were scarce,indicating that they had been detached by the urine flow. An asymetric type of cell division, probably originating both an epi-and a trypomastigote, was occasionally observed. The occurrence of swellings at different levels of the flagella of epimastigotes suggests that secondary sites of attachment may be common.

A functional equation related to the product in a quadratic number field

"Vegeu el resum a l'inici del document del fitxer adjunt."

The interaction between Poultry and Triatoma infestans Klug, 1834 (Hemiptera: Reduviidae) in an experimental model

This paper compares the predation pressure that ducks and chickens exert on triatomines. For the tests, these birds were placed in individual boxes together with a known number of Triatoma infestans and left to interact from 6 p.m. till the next morning, involving a long lasting period of complete darkness limited by two short-term periods of semi-darkness. There was a shelter which could prevent the bugs from being predated. The number of live and dead triatomines was recorded, considering missing bugs as predated by the birds. Ducks exhibited a greater predatory activity than chickens, that could be due to a long term active period at night while chickens sleep motionless from sunset to dawn. Surviving triatomines that had fed on chickens outnumbered those fed on ducks suggesting that these were less accessible to the triatomine biting. If ducks are better than chickens to detect and eat bugs and to interfere with their feeding in the field, an increase in duck number might help to diminish triatomine density. Further research is needed to determine the feasibility of application of these experimental results.

Specific Identification of Biomphalaria tenagophila and Biomphalaria occidentalis Populations by the Low Stringency Polymerase Chain Reaction

Although Biomphalaria occidentalis and B. tenagophila are indistinguishable on the basis of shell morphology and the majority of their genital organs, only the latter is susceptible to infection with Schistosoma mansoni. Thus, the identification of these species is fundamental to epidemiological studies of schistosomiasis. Here we describe a simple and rapid method for differentiating B. tenagophila from B. occidentalis based on low stringency polymerase chain reaction and using a pair of primers specific for the amplification of the 18S rRNA gene. Analysis of the low stringency product profiles of populations of these snails from different geographical regions confirmed this approach as being applicable to the identification of B. tenagophila and B. occidentalis in cases where classical morphology is inconclusive

Whole body protein metabolism and resting energy expenditure in pregnant Gambian women.

Whole body protein metabolism and resting energy expenditure (REE) were measured at 11, 23, and 33 wk of pregnancy in nine pregnant (not malnourished) Gambian women and in eight matched nonpregnant nonlactating (NPNL) matched controls. Rates of whole body nitrogen flux, protein synthesis, and protein breakdown were determined in the fed state from the level of isotope enrichment of urinary urea and ammonia during a period of 9 h after a single oral dose of [15N]glycine. At regular intervals, REE was measured by indirect calorimetry (hood system). Based on the arithmetic end-product average of values obtained with urea and ammonia, a significant increase in whole body protein synthesis was observed during the second trimester (5.8 +/- 0.4 g.kg-1.day-1) relative to values obtained both for the NPNL controls (4.5 +/- 0.3 g.kg-1.day-1) and those during the first trimester (4.7 +/- 0.3 g.kg-1.day-1). There was a significant rise in REE during the third trimester both in the preprandial and postprandial states. No correlation was found between REE after meal ingestion and the rate of whole body protein synthesis.

Dihydroaeruginoic acid synthetase and pyochelin synthetase, products of the pchEF genes, are induced by extracellular pyochelin in Pseudomonas aeruginosa.

The siderophore pyochelin of Pseudomonas aeruginosa is derived from one molecule of salicylate and two molecules of cysteine. Two cotranscribed genes, pchEF, encoding peptide synthetases have been identified and characterized. pchE was required for the conversion of salicylate to dihydroaeruginoate (Dha), the condensation product of salicylate and one cysteine residue and pchF was essential for the synthesis of pyochelin from Dha. The deduced PchE (156 kDa) and PchF (197 kDa) proteins had adenylation, thiolation and condensation/cyclization motifs arranged as modules which are typical of those peptide synthetases forming thiazoline rings. The pchEF genes were coregulated with the pchDCBA operon, which provides enzymes for the synthesis (PchBA) and activation (PchD) of salicylate as well as a putative thioesterase (PchC). Expression of a translational pchE'-'lacZ fusion was strictly dependent on the PchR regulator and was induced by extracellular pyochelin, the end product of the pathway. Iron replete conditions led to Fur (ferric uptake regulator)-dependent repression of the pchE'-'lacZ fusion. A translational pchD'-'lacZ fusion was also positively regulated by PchR and pyochelin and repressed by Fur and iron. Thus, autoinduction by pyochelin (or ferric pyochelin) and repression by iron ensure a sensitive control of the pyochelin pathway in P. aeruginosa.

Product differentiation, competitive pressure and the effects of innovation on the success and survivability of firms in oligopoly markets

In a recent paper Tishler and Milstein (2009) fi…nd that increased competition may increase aggregate R&D spending while market output decreases. Therefore, they obtain the surprising result that R&D spending is excessive when competition becomes intense. Their result is based on the standard linear demand function for differentiated products introduced by Bowley (1924) where decreased product differentiation is interpreted as more competitive pressure. In this paper I show that at an aggregate level this interpretation is problematic because equilibrium effects are dominated by a demand reduction effect. A slight modifi…cation of the standard demand function eliminates this effect. For the Tishler and Milstein (2009) setting it is shown that then increased competition increases both R&D spending and aggregate market output. Therefore, at least for consumers, more intense competition increases welfare. Journal of Economic Literature Classi…fication Numbers: D43, L1, O3. Keywords: Oligopoly markets, Product differentiation, Competitive pressure.

Activation of the heat shock response in plants by chlorophenols: transgenic Physcomitrella patens as a sensitive biosensor for organic pollutants.

The ability to detect early molecular responses to various chemicals is central to the understanding of biological impact of pollutants in a context of varying environmental cues. To monitor stress responses in a model plant, we used transgenic moss Physcomitrella patens expressing the beta-glucuronidase reporter (GUS) under the control of the stress-inducible promoter hsp17.3B. Following exposure to pollutants from the dye and paper industry, GUS activity was measured by monitoring a fluorescent product. Chlorophenols, heavy metals and sulphonated anthraquinones were found to specifically activate the hsp17.3B promoter (within hours) in correlation with long-term toxicity effects (within days). At mildly elevated physiological temperatures, the chemical activation of this promoter was strongly amplified, which considerably increased the sensitivity of the bioassay. Together with the activation of hsp17.3B promoter, chlorophenols induced endogenous chaperones that transiently protected a recombinant thermolabile luciferase (LUC) from severe heat denaturation. This sensitive bioassay provides an early warning molecular sensor to industrial pollutants under varying environments, in anticipation to long-term toxic effects in plants. Because of the strong cross-talk between abiotic and chemical stresses that we find, this P. patens line is more likely to serve as a direct toxicity bioassay for pollutants combined with environmental cues, than as an indicator of absolute toxicity thresholds for various pollutants. It is also a powerful tool to study the role of heat shock proteins (HSPs) in plants exposed to combined chemical and environmental stresses.

Characterization of human fibroleukin, a fibrinogen-like protein secreted by T lymphocytes.

We have recently cloned the human homologue of the murine pT49 cDNA (hpT49h), a transcript encoding a protein homologous to the beta- and gamma-chains of fibrinogen. Here, we report the identification of the hpT49h gene product using mAbs generated against a peptide corresponding to the carboxyl-terminal end of the deduced protein and a recombinant protein fragment expressed in Escherichia coli. mAbs 23A6, 7B12, and 3F4 specifically recognized a protein of 70 kDa in reducing SDS-PAGE in the culture supernatant of 293T cells transiently transfected with the full length hpT49h cDNA and freshly isolated PBMC. Under nonreducing conditions, the material migrated with a molecular mass of 250 to 300 kDa, indicating that the 70-kDa protein forms a disulfide bonded complex. Because of its homology with fibrinogen, we have termed this protein fibroleukin. Fibroleukin is spontaneously secreted in vitro by freshly isolated CD4+ and CD8+ T lymphocytes. RT-PCR analysis revealed preferential expression of fibroleukin mRNA in memory T lymphocytes (CD3+/CD45R0+) compared with naive T lymphocytes (CD3+/CD45RA+). Fibroleukin production by PBMC was rapidly lost in culture. Production could be partially maintained in the presence of IFN-gamma, while T lymphocyte activation had no effect. To demonstrate fibroleukin production in vivo, we analyzed colon mucosa by immunohistology. Fibroleukin staining was detected in the extracellular matrix of the T lymphocyte-rich upper portion of the lamina propria mucosa. While the exact function of fibroleukin remains to be defined, these data suggest that fibroleukin may play a role in physiologic lymphocyte functions at mucosal sites.

Profitability, uncertainty and multi-product firm product proliferation: The Spanish car industry

This article studies how product introduction decisions relate to profitability and uncertainty in the context of multi-product firms and product differentiation. These two features, common to many modern industries, have not received much attention in the literature as compared to the classical problem of firm entry, even if the determinants of firm and product entry are quite different. The theoretical predictions about the sign of the impact of uncertainty on product entry are not conclusive. Therefore, an econometric model relating firms’ product introduction decisions with profitability and profit uncertainty is proposed. Firm’s estimated profits are obtained from a structural model of product demand and supply, and uncertainty is proxied by profits’ variance. The empirical analysis is carried out using data on the Spanish car industry for the period 1990-2000. The results show a positive relationship between product introduction and profitability, and a negative one with respect to profit variability. Interestingly, the degree of uncertainty appears to be a driving force of entry stronger than profitability, suggesting that the product proliferation process in the Spanish car market may have been mainly a consequence of lower uncertainty rather than the result of having a more profitable market. Keywords: Product introduction, entry, uncertainty, multiproduct firms, automobile JEL codes: L11, L13

Regulation of gastric and pancreatic lipase secretion by CCK and cholinergic mechanisms in humans.

Gastric lipase (HGL) contributes significantly to fat digestion. However, little is known about its neurohormonal regulation in humans. We studied the role of CCK and cholinergic mechanisms in the postprandial regulation of HGL and pancreatic lipase (HPL) secretion in six healthy subjects. Gastric emptying of a mixed meal and outputs of HGL, pepsin, acid, and HPL were determined with a double-indicator technique. Three experiments were performed in random order: intravenous infusion of 1) placebo, 2) low-dose atropine (5 micrograms.kg-.h-1), and 3) the CCK-A receptor antagonist loxiglumide (22 mumol.kg-.h-1). Atropine decreased postprandial outputs of HGL, pepsin, gastric acid, and HPL (P < 0.03) while slowing gastric emptying (P < 0.05). Loxiglumide markedly increased the secretion of HGL, pepsin, and acid while distinctly reducing HPL outputs and accelerating gastric emptying (P < 0.03). Plasma CCK and gastrin levels increased during loxiglumide infusion (P < 0.03). Atropine enhanced gastrin but not CCK release. Postprandial HGL, pepsin, and acid secretion are under positive cholinergic but negative CCK control, whereas HPL is stimulated by cholinergic and CCK mechanisms. We conclude that CCK and cholinergic mechanisms have an important role in the coordination of HGL and HPL secretion to optimize digestion of dietary lipids in humans.

Dynamic product diversity

The goal of this paper is to study the frequency of new product introductions in monopoly markets where demand is subject to transitory saturation. We focus on those types of goods for which consumers purchase at most one unit of each variety, but repeat purchases in the same product category. The model considers infinitely-lived, forward-looking consumers and firms. We show that the share of potential surplus that a monopolist is able to appropriate increases with the frequency of introduction of new products and the intensity of transitory saturation. If the latter is sufficiently strong then the rate of introduction of new products is higher than socially desirable (excessive dynamic product diversity.)

Address by Michea¡l Martin to the Conference - Legislating for Tobacco Free Society

Thank you Chairman I would like to extend a warm welcome to our keynote speakers, David Byrne of the European Commission, Derek Yach from the World Health Organisation, and Paul Quinn representing Congressman Marty Meehan who sends his apologies. When we include the speakers who will address later sessions, this is, undoubtedly, one of the strongest teams that have been assembled on tobacco control in Europe. The very strength of the team underlines what I see as a shift – a very necessary shift – in the way we perceive the tobacco issue. For the last twenty years, we have lived out a paradox. It isn´t a social side issue. I make no apology for the bluntness of what I´m saying, and will come back, a little later, to the radicalism I believe we need to bring – nationally – to this issue. For starters, though, I want to lay it on the line that what we´re talking about is an epidemic as deadly as any suffered by human kind throughout the centuries. Slower than some of those epidemics in its lethal action, perhaps. But an epidemic, nonetheless. According to the World Health Organisation tobacco accounted for just over 3 million annual deaths in 1990, rising to 4.023 million annual deaths in 1998. The numbers of deaths due to tobacco will rise to 8.4 million in 2020 and reach roughly 10 million annually by 2030. This is quite simply ghastly. Tobacco kills. It kills in many different ways. It kills increasing numbers of women. It does its damage directly and indirectly. For children, much of the damage comes from smoking by adults where children live, study, play and work. The very least we should be able to offer every child is breathable air. Air that doesn´t do them damage. We´re now seeing a global public health response to the tobacco epidemic. The Tobacco Free Initiative launched by the World Health Organisation was matched by significant tobacco control initiatives throughout the world. During this conference we will hear about the experiences our speakers had in driving these initiatives. This Tobacco Free Initiative poses unique challenges to our legal frameworks at both national and international levels; in particular it raises challenges about the legal context in which tobacco products are traded and asks questions about the impact of commercial speech especially on children, and the extent of the limitations that should be imposed on it. Politicians, supported by economists and lawyers as well as the medical profession, must continue to explore and develop this context to find innovative ways to wrap public health considerations around the trade in tobacco products – very tightly. We also have the right to demand a totally new paradigm from the tobacco industry. Bluntly, the tobacco industry plays the PR game at its cynical worst. The industry sells its products without regard to the harm these products cause. At the same time, to gain social acceptance, it gives donations, endowments and patronage to high profile events and people. Not good enough. This model of behaviour is no longer acceptable in a modern society. We need one where the industry integrates social responsibility and accountability into its day-to-day activities. We have waited for this change in behaviour from the tobacco industry for many decades. Unfortunately the documents disclosed during litigation in the USA and from other sources make very depressing reading; it is clear from them that any trust society placed in the tobacco industry in the past to address the health problems associated with its products was misplaced. This industry appears to lack the necessary leadership to guide it towards just and responsible action. Instead, it chooses evasion, deception and at times illegal activity to protect its profits at any price and to avoid its responsibilities to society and its customers. It has engaged in elaborate ´spin´ to generate political tolerance, scientific uncertainty and public acceptance of its products. Legislators must act now. I see no reason why the global community should continue to wait. Effective legal controls must be laid on this errant industry. We should also keep these controls under review at regular intervals and if they are failing to achieve the desired outcomes we should be prepared to amend them. In Ireland, as Minister for Health and Children, I launched a comprehensive tobacco control policy entitled “Towards a Tobacco Free Society“. OTT?Excessive?Unrealistic? On the contrary – I believe it to be imperative and inevitable. I honestly hold that, given the range of fatal diseases caused by tobacco use we have little alternative but to pursue the clear objective of creating a tobacco free society. Aiming at a tobacco free society means ensuring public and political opinion are properly informed. It requires help to be given to smokers to break the addiction. It demands that people are protected against environmental tobacco smoke and children are protected from any inducement to experiment with this product. Over the past year we have implemented a number of measures which will support these objectives; we have established an independent Office of Tobacco Control, we have introduced free nicotine replacement therapy for low-income earners, we have extended our existing prohibitions on tobacco advertising to the print media with some minor derogations for international publications. We have raised the legal age at which a person can be sold tobacco products to eighteen years. We have invested substantially more funds in health promotion activities and we have mounted sustained information campaigns. We have engaged in sponsorship arrangements, which are new and innovative for public bodies. I have provided health boards with additional resources to let them mount a sustained inspection and enforcement service. Health boards will engage new Directors of Tobacco Control responsible for coordinating each health board´s response and for liasing with the Tobacco Control Agency I set up earlier this year. Most recently, I have published a comprehensive Bill – The Public Health (Tobacco) Bill, 2001. This Bill will, among other things, end all forms of product display and in-store advertising and will require all retailers to register with the new Tobacco Control Agency. Ten packs of cigarettes will be banned and transparent and independent testing procedures of tobacco products will be introduced. Enforcement officers will be given all the necessary powers to ensure there is full compliance with the law. On smoking in public places we will extend the existing areas covered and it is proposed that I, as Minister for Health and Children, will have the powers to introduce further prohibitions in public places such as pubs and the work place. I will also provide for the establishment of a Tobacco Free Council to advise and assist on an ongoing basis. I believe the measures already introduced and those additional ones proposed in the Bill have widespread community support. In fact, you´re going to hear a detailed presentation from the MRBI which will amply illustrate the extent of this support. The great thing is that the support comes from smokers and non-smokers alike. Bottom line, Ladies and Gentlemen, is that we are at a watershed. As a society (if you´ll allow me to play with a popular phrase) we´ve realised it´s time to ´wake up and smell the cigarettes.´ Smell them. See them for what they are. And get real about destroying their hold on our people. The MRBI survey makes it clear that the single strongest weapon we have when it comes to preventing the habit among young people is price. Simple as that. Price. Up to now, the fear of inflation has been a real impediment to increasing taxes on tobacco. It sounds a serious, logical argument. Until you take it out and look at it a little more closely. Weigh it, as it were, in two hands. I believe – and I believe this with a great passion – that we must take cigarettes out of the equation we use when awarding wage increases. I am calling on IBEC and ICTU, on employers and trade unions alike, to move away from any kind of tolerance of a trade that is killing our citizens. At one point in industrial history, cigarettes were a staple of the workingman´s life. So it was legitimate to include them in the ´basket´ of goods that goes to make up the Consumer Price Index. It isn´t legitimate to include them any more. Today, I´m saying that society collectively must take the step to remove cigarettes from the basket of normality, from the list of elements which constitute necessary consumer spending. I´m saying: “We can no longer delude ourselves. We must exclude cigarettes from the considerations we address in central wage bargaining. We must price cigarettes out of the reach of the children those cigarettes will kill.” Right now, in the monthly Central Statistics Office reports on consumer spending, the figures include cigarettes. But – right down at the bottom of the page – there´s another figure. Calculated without including cigarettes. I believe that if we continue to use the first figure as our constant measure, it will be an indictment of us as legislators, as advocates for working people, as public health professionals. If, on the other hand, we move to the use of the second figure, we will be sending out a message of startling clarity to the nation. We will be saying “We don´t count an addictive, killer drug as part of normal consumer spending.” Taking cigarettes out of the basket used to determine the Consumer Price Index will take away the inflation argument. It will not be easy, in its implications for the social partners. But it is morally inescapable. We must do it. Because it will help us stop the killer that is tobacco. If we can do it, we will give so much extra strength to health educators and the new Tobacco Control Association. This new organisation of young people who already have branches in over fifteen counties, is represented here today. The young adults who make up its membership are well placed to advise children of the dangers of tobacco addiction in a way that older generations cannot. It would strengthen their hand if cigarettes move – in price terms – out of the easy reach of our children Finally, I would like to commend so many public health advocates who have shown professional and indeed personal courage in their commitment to this critical public health issue down through the years. We need you to continue to challenge and confront this grave public health problem and to repudiate the questionable science of the tobacco industry. The Research Institute for a Tobacco Free Society represents a new and dynamic form of partnership between government and civil society. It will provide an effective platform to engage and mobilise the many different professional and academic skills necessary to guide and challenge us. I wish the conference every success.

A review of coccidiostat residues in poultry

safefood, the Food Safety Promotion Board, is responsible for increasing food safety awareness and for supporting north/south scientific co-operation. safefood is currently funding a project entitled "Poultry Meat: improving food safety by improving chemical residue surveillance". This joint project between the Veterinary Sciences Division, Queen's University, Belfast and the National Food Centre, Teagasc, Dublin, is addressing the problem of anti-coccidial drug residues in poultry meat and eggs through an all-island research and residue testing initiative. The project started in 2001 and will continue until 2004. Poultry have a high susceptibility to the parasitic disease, coccidiosis. Because of this susceptibility, veterinary drugs, commonly known as coccidiostats are routinely used in intensively-reared poultry. The coccidiostats are potent drugs and, where residues occur in food, they may exacerbate certain coronary disease conditions. It is important, therefore, for poultry and egg producers to prevent the occurrence of residues of coccidiostats in food products.