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1.
Euro Surveill ; 16(13)2011 Mar 31.
Article in English | MEDLINE | ID: mdl-21489375

ABSTRACT

We present a summary of the main findings of the latest report of the European Food Safety Authority and European Centre for Disease Prevention and Control on zoonoses, zoonotic agents and food-borne outbreaks in the European Union (EU), based on data from 2009. Zoonoses are prevalent and widely distributed across several countries in the EU. The most important highlight of this report was the continuous decrease of human salmonellosis since 2005, probably due to effective control programmes in livestock.


Subject(s)
Foodborne Diseases/epidemiology , Zoonoses/epidemiology , Animals , Bacterial Infections/epidemiology , European Union , Humans , Parasitic Diseases/epidemiology , Rabies/epidemiology
2.
Med. cután. ibero-lat.-am ; 39(1): 13-18, ene.-feb. 2011. ilus
Article in Spanish | IBECS | ID: ibc-92753

ABSTRACT

La leishmaniasis es un grupo de enfermedades producida por protozoos del genero leishmania, que se transmite al hombre por la picadura de un mosquito.Dependiendo de la especie y del estado inmunológico del huésped, presenta diferentes formas clínicas: cutánea, mucocutánea y visceral.Afecta a 12 millones de personas y el aumento de su incidencia la coloca a la cabeza de las enfermedades emergentes. Contribuyen a su expansiónfactores ambientales, de emigración, e inmigración, y globalización del trabajo y del ocio. También contribuye, la inmunodepresión de las personasinfectadas debida al consumo de medicamentos que alteran la inmunidad o coinfecciones víricas como el HIV. Presentamos los 5 casos de leishmaniasisatendidos en nuestro hospital de Huesca (España), en 2007, que reflejan su incidencia y variabilidad clínica (AU)


Infection whith protozoan parasites of the genus Leishmania causes a variety of clinical diseases called leishmaniases, which is transmited to humanhost by the bite of a sandfly. The clinical manifestation depends on the interaction among series of parasite and host inmunity: cutaneous, mucocutaneousor visceral. Worldwide, an estimated 12 million people are infected with leishmaniases. The number of cases of leishmaniases is increasing,globally at an alarming rate, and the leishmaniases are among in the top the emergent diseases. The ecological chaos, differents phenomena such asmigration, immunosupression caused by drughs and viral infections, globalization of work and leisure contribute to the spread and increase of the disease.We report five cases with leishmaniasis who had been atended in 2007 at our hospital in Huesca (Spain), reflecting its clinical diversity (AU)


Subject(s)
Humans , Leishmaniasis/epidemiology , /epidemiology , Leishmania/pathogenicity , Immunocompromised Host , Risk Factors , Human Migration/trends
4.
Eur J Pharmacol ; 403(1-2): 9-15, 2000 Sep 01.
Article in English | MEDLINE | ID: mdl-10969138

ABSTRACT

Recent studies have demonstrated that serotonin (5-hydroxytryptamine, 5-HT) may interact with either specific receptors or with a specific transporter that takes up 5-HT in the gastrointestinal tract. The purpose of the present work was to study the 5-HT interactions with brush border membrane from rabbit jejunum enterocytes. The results obtained showed that 5-HT did not seem to be transported by any specific system of transport in brush border membrane vesicles. Nevertheless, [3H]5-HT seemed to bind specifically to this membrane. The kinetic analysis indicated a saturable and dissociable specific binding with a dissociation constant K(D)=14x10(-9) M. The saturation studies with [3H]5-HT indicated the presence of one specific site in the brush border membrane. The results of displacement of [3H]5-HT specific binding from the brush border membrane showed that both unlabelled 5-HT and unlabelled GR113080 ([1-[(2-methyl sulphonyl) amino] ethyl-4-piperidinyl] methyl-1-methyl-1H-indole-3-carboxylate), a specific competitive antagonist of 5-HT(4) receptors, inhibited the specific binding of [3H]5-HT to this membrane.


Subject(s)
Enterocytes/metabolism , Jejunum/metabolism , Microvilli/metabolism , Serotonin/metabolism , Animals , Binding, Competitive/drug effects , Biological Transport , Cell Membrane/metabolism , Dose-Response Relationship, Drug , Enterocytes/cytology , Ergolines/pharmacology , Indoles/pharmacology , Jejunum/cytology , Kinetics , Male , Ondansetron/pharmacology , Rabbits , Serotonin/pharmacokinetics , Serotonin Antagonists/pharmacology , Sulfonamides/pharmacology , Tritium
5.
J Neurochem ; 62(2): 686-96, 1994 Feb.
Article in English | MEDLINE | ID: mdl-8294931

ABSTRACT

Defective protein kinase C (PKC) has been implicated in impaired Na+,K(+)-ATPase activity in the sciatic nerve of streptozotocin-induced diabetic rats. In the present study, alpha, beta I, beta II, gamma, delta, and epsilon isoform-specific antibodies were used in parallel to the measurement of compound PKC activity for the characterization of PKC distribution and isoform expression in sciatic nerves of normal and diabetic rats. To distinguish isoform expression between the axonal and glial compartments, PKC isoforms were evaluated in nerves subjected to Wallerian degeneration and in a pure primary Schwann cell culture. alpha, beta I, beta II, delta, and epsilon but no gamma isoforms were detected in sciatic nerve. Similar immunoreactivity was observed in degenerated nerves 3-4 days after transection except for diminished beta I and epsilon species; in Schwann cell cultures, only alpha, beta II, delta, and epsilon were detected. In normal nerves, two-thirds of PKC compound activity was found in the cytosol and 50% of total enzyme activity translocated to the Na+,K(+)-ATPase-enriched membrane fraction with phorbol myristate acetate. Similar redistribution patterns were observed for the immunoreactivity of all isoforms with the exception of delta, which did not translocate to the membrane with phorbol myristate acetate. No abnormality in compound PKC activity, in the immunoreactive intensity, or in the distribution of PKC isoforms could be detected in rat sciatic nerve after 6-12 weeks of diabetes. Thus, defective activation rather than decreased intrinsic PKC activity may occur in diabetic neuropathy.


Subject(s)
Diabetes Mellitus, Experimental/enzymology , Isoenzymes/metabolism , Protein Kinase C/metabolism , Sciatic Nerve/enzymology , Animals , Blotting, Western , Calcium/metabolism , Cell Membrane/enzymology , Cytosol/enzymology , In Vitro Techniques , Intracellular Membranes/metabolism , Male , Rats , Rats, Wistar , Reference Values , Tissue Distribution
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