This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.
Sender's message:
Sent on Wednesday, 2010 Jul 21Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
Click here to view complete results in PubMed. (Results may change over time.)
To unsubscribe from these e-mail updates click here.
| PubMed Results |
| 1. | PLoS Negl Trop Dis. 2010 Jul 13;4(7):e743.Kinetic analysis of ex vivo human blood infection by leishmania.Moreno I, Domínguez M, Cabañes D, Aizpurua C, Toraño A.Servicio de Inmunología, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain. AbstractThe leishmanioses, vector-borne diseases caused by the trypanosomatid protozoan Leishmania, are transmitted to susceptible mammals by infected phlebotomine sand flies that inoculate promastigotes into hemorrhagic pools created in host skin. We assumed that promastigotes are delivered to a blood pool, and analyzed early promastigote interactions (0-5 min) with host components, which lead to parasite endocytosis by blood leukocytes, and to host infection. Promastigotes were incubated with NHS or with heparinized blood in near-physiological conditions, and we used cell radioimmunoassay and flow cytometry to measure the on-rate constants (k(+1)) of promastigote interactions with natural opsonins and erythrocytes. We obtained quantitative data for parasitized cells to determine the time-course of promastigote binding and internalization by blood leukocytes. In these reactions, promastigotes bind natural opsonins, immune adhere to erythrocytes and activate complement cytolysis, which kills approximately 95% of promastigotes by 2 min post-infection. C3-promastigote binding is a key step in opsonization; nascent C3-promastigotes are the substrate for two simultaneous reactions, C3-promastigote immune adherence (IA) to erythrocytes and complement-mediated promastigote killing. The k(+1) for IA was 75-fold greater than that for promastigote killing, showing that IA facilitates promastigote endocytosis and circumvents lysis. At 5 min post-infection, when reaction velocity is still linear and promastigote concentration is not limiting, 17.4% of granulocytes and 10.7% of monocytes had bound promastigotes, of which approximately 50% and approximately 25%, respectively, carried surface-bound (live) or internalized (live and dead) leishmanias. Of other leukocyte types, 8.5% of B cells bound but did not internalize promastigotes, and T cells, NK cells and CD209(+) dendritic cells did not bind parasites. These data show that, once in contact with blood, promastigote invasion of human leukocytes is an extremely rapid and efficient reaction, and suggest that the IA reaction constitutes a central strategy for this parasite in subverting host innate immune defenses. |
| PMID: 20644618 [PubMed - in process] | |
| Related citations | |
| 2. | J Coll Physicians Surg Pak. 2010 Jul;20(7):496.Glucantime Fever with Parenteral Meglumine Antimonate in Patients of Cutaneous Leishmaniasis.Rashid BN Dr, Tabassum S Dr, Ullah Rao MS Dr, Masood S Dr, Abbas MM Dr, Mumtaz MJ Dr.Head of Dermatology Department, Combined Military Hospital, Lahore Cant. |
| PMID: 20642959 [PubMed - as supplied by publisher] | |
| Related citations | |
| 3. | Curr Pharm Des. 2010 Jul 20. [Epub ahead of print]QSAR, Docking, and CoMFA Studies of GSK3 Inhibitors.García I, Fall Y, Gómez G.Department of Organic Chemistry, University of Vigo, Spain. iselapintos@yahoo.es. AbstractGSK-3 inhibitors are interesting candidates to develop Anti-Alzheimer compounds. GSK-3beta are also interesting as Anti-parasitic compounds active against Plasmodium falciparum, Trypanosoma brucei, and Leishmania donovani; the causative agents for Malaria, African Trypanosomiasis and Leishmaniosis. The high number of possible candidates creates the necessity of Quantitative Structure-Activity Relationship models in order to guide the GSK3 (glycogen synthase kinase 3 inhibitor) synthesis. In this work, we revised different computational studies for a very large and heterogeneous series of GSK-3Is. First, we revised QSAR studies with conceptual parameters such as flexibility of rotation, probability of availability, etc. we then used the method of regression analysis and QSAR studies in order to understand the essential structural requirement for binding with receptor. Next, we reviewed 3D-QSAR, CoMFA and CoMSIA with different compounds to find out the structural requirements for GSK-3 inhibitory activity. |
| PMID: 20642432 [PubMed - as supplied by publisher] | |
| Related citations | |
| 4. | J Infect Dis. 2010 Aug 15;202(3):416-26.Gene expression changes associated with myocarditis and fibrosis in hearts of mice with chronic chagasic cardiomyopathy.Soares MB, de Lima RS, Rocha LL, Vasconcelos JF, Rogatto SR, dos Santos RR, Iacobas S, Goldenberg RC, Iacobas DA, Tanowitz HB, de Carvalho AC, Spray DC.Centro de Pesquisas Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil. milena@bahia.fiocruz.br AbstractChronic chagasic cardiomyopathy is a leading cause of heart failure in Latin American countries. About 30% of Trypanosoma cruzi-infected individuals develop this severe symptomatic form of the disease, characterized by intense inflammatory response accompanied by fibrosis in the heart. We performed an extensive microarray analysis of hearts from a mouse model of this disease and identified significant alterations in expression of approximately 12% of the sampled genes. Extensive up-regulations were associated with immune-inflammatory responses (chemokines, adhesion molecules, cathepsins, and major histocompatibility complex molecules) and fibrosis (extracellular matrix components, lysyl oxidase, and tissue inhibitor of metalloproteinase 1). Our results indicate potentially relevant factors involved in the pathogenesis of the disease that may provide new therapeutic targets in chronic Chagas disease. |
| PMID: 20565256 [PubMed - indexed for MEDLINE] | |
| Related citations | |
| 5. | J Nat Prod. 2009 May 22;72(5):906-11.Biologically active cannabinoids from high-potency Cannabis sativa.Radwan MM, Elsohly MA, Slade D, Ahmed SA, Khan IA, Ross SA.Department of Pharmaceutics, National Center for Natural Products Research, School of Pharmacy, The University of Mississippi, Mississippi 38677, USA. AbstractNine new cannabinoids (1-9) were isolated from a high-potency variety of Cannabis sativa. Their structures were identified as (+/-)-4-acetoxycannabichromene (1), (+/-)-3''-hydroxy-Delta((4'',5''))-cannabichromene (2), (-)-7-hydroxycannabichromane (3), (-)-7R-cannabicoumarononic acid A (4), 5-acetyl-4-hydroxycannabigerol (5), 4-acetoxy-2-geranyl-5-hydroxy-3-n-pentylphenol (6), 8-hydroxycannabinol (7), 8-hydroxycannabinolic acid A (8), and 2-geranyl-5-hydroxy-3-n-pentyl-1,4-benzoquinone (9) through 1D and 2D NMR spectroscopy, GC-MS, and HRESIMS. The known sterol beta-sitosterol-3-O-beta-d-glucopyranosyl-6'-acetate was isolated for the first time from cannabis. Compounds 6 and 7 displayed significant antibacterial and antifungal activities, respectively, while 5 displayed strong antileishmanial activity. |
| PMID: 19344127 [PubMed - indexed for MEDLINE] | |
| Related citations | |
No comments:
Post a Comment