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 Sunday, 2011 Mar 13Search 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. | Analyst. 2011 Mar 11. [Epub ahead of print]Aptasensor based on the selective electrodeposition of protein-linked gold nanoparticles on screen-printed electrodes.Moreno M, González VM, Rincón E, Domingo A, Domínguez E.Departamento Bioquímica y Biología Molecular, Facultad de Medicina, Universidad de Alcalá, 28871, Alcalá de Henares, Madrid, Spain. morenomm@cab.inta-csic.es. AbstractThe electrodeposition of DNA-gold nanoparticles previously developed in our group has been used as starting point for the electrodeposition of proteins attached to gold nanoparticles. We have performed a proof of principle by developing a methodology based on the electrodeposition of proteins bound to gold nanoparticles on screen-printed gold microelectrodes using, in a first approach, horseradish peroxide-conjugated gold nanoparticles (gold-HRP). The electrodeposition was achieved at a current positive potential of 800 mV vs. Ag/AgCl and the functionality of the electrodeposited HRP-particles was tested by electrochemical reduction of H(2)O(2). Furthermore, we used this proof of concept in an aptasensor application to detect Leishmania infantum KMP-11. Hence, we have demonstrated not only the functionality of the electrodeposition of proteins bound to gold nanoparticles, but also the utility of the method with the aim of developing a real biosensor containing multiple enzymes or proteins in a multimodular device. |
PMID: 21394378 [PubMed - as supplied by publisher] | |
Related citations | |
![]() |
2. | PLoS One. 2011 Mar 4;6(3):e14751.Visceral leishmaniasis in muzaffarpur district, bihar, India from 1990 to 2008.Malaviya P, Picado A, Singh SP, Hasker E, Singh RP, Boelaert M, Sundar S.Institute of Medical Sciences, Banaras Hindu University, Varanasi, India. AbstractBACKGROUND: Visceral Leishmaniasis (VL) is a vector-borne disease transmitted by Phlebotomus argentipes. To understand the VL seasonality, annual and monthly variations of VL incidence and its relationship to meteorological variables, the numbers of VL cases reported in Muzaffarpur district, Bihar, India from 1990 to 2008 were studied. METHODS: Annual VL incidence per 10,000 and the total number of annual VL cases reported at block Community Health Centres (CHC), Public Hospitals or Non-Governmental Organisations (NGO) and the number of VL cases per month from 2000 to 2008 as well as the monthly average of cases for 2000-08, 2000-04 and 2005-08 periods along with the monthly averages of temperature, rainfall and relative humidity were plotted. VL Standardised Incidence Ratios per block were computed for the periods of 1990-1993, 1994-1998, 1999-2004 and 2005-2008 and month wise from 2002 to 2008. A negative binomial regression model was used to evaluate the association between meteorological variables and the number of VL cases per month from 2000 to 2008. RESULTS: A total of 68,358 VL cases were reported in Muzaffarpur district from 1990 to 2008, ranging from 1,2481 in 1992 to 1,161 in 2001. The blocks with the highest number of cases shifted from East (1990-98) to West (1999-2008). Monthly averages of cases ranged from 149 to 309, highest peak in March-April and another one in July. Monthly VL incidence was associated positively to rainfall and negatively to relative humidity and the numbers of VL cases in the previous month. INTERPRETATION: The number of cases reported to the public health sector allowed the describing of the spatial distribution and temporal variations in the Muzaffarpur from 1990 to 2008. However, to assess the actual VL burden, as well as the efficacy of the control measures applied in the district, reporting from private practices and NGOs should be encouraged. |
PMID: 21394195 [PubMed - in process] | |
Related citations | |
![]() |
3. | Indian J Dermatol Venereol Leprol. 2011 Mar-Apr;77(2):251.Unresponsive cutaneous leishmaniasis and HIV co-infection: Report of three cases.Soni P, Prasad N, Khandelwal K, Ghiya BC, Mehta RD, Bumb RA, Salotra P.Department of Dermatology, SP Medical College and PBM Group of Hospitals, Bikaner, Rajasthan, India. AbstractCutaneous leishmaniasis (CL) is a vector borne disease caused by various species of Leishmania parasite. CL is endemic in the Thar desert of Rajasthan state and Himachal Pradesh in India. Immune suppression caused by human immunodeficiency virus (HIV) infection is associated with atypical clinical presentation of CL which responds poorly to the standard treatment and causes frequent relapses. We are reporting three cases of localized and disseminated CL due to Leishmania tropica which failed to respond to conventional intralesional/intramuscular sodium stibogluconate (SSG) injections. Initially, we did not think of HIV infection because CL is endemic in this region. When patients did not respond to SSG injections, we performed enzyme-linked immunosorbent assay (ELISA) tests for HIV and they turned out to be HIV positive. Our report showed that CL is emerging as an opportunistic infection associated with HIV/AIDS and may be the first manifestation in HIV positive patients in an endemic area. |
PMID: 21393971 [PubMed - in process] | |
Related citations | |
4. | Indian J Dermatol Venereol Leprol. 2011 Mar-Apr;77(2):214-7.Exacerbation reaction (Hypersensitivity) in Post-kala-azar dermal leishmaniasis with Miltefosine.Bansal S, Ghate SS, Jerajani H.Department of Dermatology, Lokmanya Tilak Municipal Medical College and General Hospital, Mumbai, India. |
PMID: 21393963 [PubMed - in process] | |
Related citations | |
5. | Int Immunol. 2011 Mar;23(3):195-202.Aberrant IL-4 production by SOCS3-over-expressing T cells during infection with Leishmania major exacerbates disease manifestations.Nakaya M, Hamano S, Kawasumi M, Yoshida H, Yoshimura A, Kobayashi T.Division of Molecular and Cellular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan. AbstractSuppressor of cytokine signaling (SOCS) 3 is a major negative feedback regulator of signal transducer and activator of transcription 3-activating cytokines. Studies using T-cell-specific SOCS3-deficient mice indicate that the absence of SOCS3 in T cells results in exacerbation of disease progression after infection by Leishmania major due to skewing of the T(h)3 cell phenotype accompanied by hyper-production of IL-10 and transforming growth factor β (TGF-β). Here we show that transgenic mice over-expressing the SOCS3 gene in T cells (Lck-SOCS3 Tg mice) are also susceptible to infection by L. major. Forced expression of SOCS3 in T cells did not affect the production of the anti-inflammatory cytokines IL-10 and TGF-β or that of the protective T(h)1 type cytokine IFN-γ, which is required for parasite clearance. CD4(+) T cells isolated from infected-Lck-SOCS3 Tg mice produced much higher levels of IL-4 when they were re-stimulated with L. major antigen in vitro. Exacerbation of disease progression in Lck-SOCS3 Tg mice was completely reversed by administration of a neutralizing antibody against IL-4. These data suggest that tight regulation of SOCS3 expression in T(h) cells is crucial for disease control during infection by L. major. |
PMID: 21393635 [PubMed - in process] | |
Related citations | |
![]() |
6. | J Antimicrob Chemother. 2011 Mar;66(3):677-9. Epub 2011 Jan 11.Drug susceptibilit y of Leishmania infantum (syn. Leishmania chagasi) isolates from Brazilian HIV-positive and HIV-negative patients.Inocêncio da Luz R, Romero GA, Dorval ME, Cruz I, Cañavate C, Dujardin JC, Van Assche T, Cos P, Maes L.Laboratory for Microbiology, Parasitology and Hygiene (LMPH), Faculty of Pharmaceutical, Biomedical and Veterinary Sciences, University of Antwerp, Groenenborgerlaan 171, B-2020 Antwerp, Belgium. |
PMID: 21393233 [PubMed - in process] | |
Related citations | |
![]() |
7. | J Antimicrob Chemother. 2011 Mar;66(3):618-25. Epub 2011 Jan 14.Fucoidan cures infec tion with both antimony-susceptible and -resistant strains of Leishmania donovani through Th1 response and macrophage-derived oxidants.Kar S, Sharma G, Das PK.Molecular Cell Biology Laboratory, Infectious Diseases and Immunology Division, Indian Institute of Chemical Biology, Kolkata, India. AbstractObjectives The aim of this study was to evaluate and characterize the antileishmanial efficacy of fucoidan, a polyanionic sulphated polysaccharide from brown algae, in experimental infections of BALB/c mice with antimony-susceptible (AG83) and -resistant (GE18ER) Leishmania donovani. Methods The effect of fucoidan was assessed against intracellular parasites in cultured macrophages and in suppressing splenic and liver parasite burdens in a BALB/c mouse model of visceral leishmaniasis by microscopic evaluation of surviving intracellular amastigotes stained with Giemsa. To evaluate the type of immunological responses, real-time PCR and ELISA were performed for various Th1 and Th2 cytokines in both in vitro and in vivo infected conditions. To determine the effector mechanism, reactive oxygen species (ROS) and NO were measured in fucoidan-treated animals by H(2)DCFDA-based fluorometric analysis and Griess reaction, respectively. Results In addition to having appreciable inhibitory effect on amastigote multiplication within macrophages (>93% inhibition at 50 μg/mL), complete elimination of liver and spleen parasite burden was achieved by fucoidan at a dose of 200 mg/kg/day given orally, 3 times weekly, in a 6-week mouse model of both antimony-susceptible and -resistant strains. This curative effect is associated with switching of T cell differentiation from Th2 to Th1 mode. Further, splenocytes of fucoidan-treated infected (AG83 and GE18FR) mice generated significantly enhanced levels of superoxide and NO. Not only was this treatment curative when administered orally 15 days post-infection, but it also imparted resistance to reinfection. Conclusions These results suggest the effectiveness of fucoidan as potent immunomodulator for controlling both antimony-susceptible and -resistant visceral leishmaniasis. |
PMID: 21393231 [PubMed - in process] | |
Related citations | |
![]() |
8. | J Antimicrob Chemother. 2011 Feb 3. [Epub ahead of print]Targeted killing of Leishman ia donovani in vivo and in vitro with amphotericin B attached to functionalized carbon nanotubes.Prajapati VK, Awasthi K, Gautam S, Yadav TP, Rai M, Srivastava ON, Sundar S.Infectious Disease Research Laboratory, Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221 005, India. AbstractObjectives This study describes the antileishmanial efficacy of the novel drug formulation of amphotericin B (AmB) attached to functionalized carbon nanotubes (f-CNTs) and compares it with AmB. Methods f-CNTs were prepared in a two-step chemical carboxylation and amidation process. The AmB was then attached to make f-CNT-AmB and its construction was confirmed by Fourier transform infrared (FTIR) spectroscopy and transmission electron microscopy (TEM). The cytotoxicity of the constructed compound, f-CNT-AmB, was assessed in vitro using the J774A.1 macrophage cell line and in vivo using healthy BALB/c mice. Antileishmanial activity of AmB and f-CNT-AmB was assessed in vitro using a macrophage (J774A.1 cell line) model of Leishmania donovani infection. Antileishmanial activity was assessed in vivo by comparing the parasite load of hamsters treated with a 5 day course of AmB, f-CNTs or f-CNT-AmB initiated at 30 days after infection with L. donovani parasites. Results The FTIR spectroscopy and TEM data demonstrate the successful attachment of AmB to f-CNTs. The in vitro cytotoxicity of AmB, f-CNTs and f-CNT-AmB was measured by the cytotoxic concentration required to kill 50% of the cells: 0.48 ± 0.06 μg/mL; 7.31 ± 1.16 μg/mL; 0.66 ± 0.17 μg/mL, respectively, in the J774A.1 cell line. The in vivo toxicity assessment of the compounds in BALB/c mice revealed no hepatic or renal toxicity. Against intracellular amastigotes the in vitro antileishmanial efficacy of f-CNT-AmB was significantly higher than that of AmB (IC(50) 0.00234 ± 0.00075 μg/mL versus 0.03263 ± 0.00123 μg/mL; P ≤ 0.0001). The percentage inhibition of amastigote replication in hamsters treated with f-CNT-AmB was significantly more than that with AmB (89.85% ± 2.93% versus 68.97% ± 1.84%; P = 0.0004). Conclusions The results of these experiments clearly demonstrate that f-CNT-AmB has significantly greater antileishmanial efficacy than AmB and had no significant cytotoxic effects. |
PMID: 21393222 [PubMed - as supplied by publisher] | |
Related citations | |
![]() |
9. | J Antimicrob Chemother. 2011 Feb 3. [Epub ahead of print]In vitro interactions between si tamaquine and amphotericin B, sodium stibogluconate, miltefosine, paromomycin and pentamidine against Leishmania donovani.Seifert K, Munday J, Syeda T, Croft SL.London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. AbstractObjectives To evaluate in vitro interactions between sitamaquine and the current antileishmanial drugs amphotericin B, sodium stibogluconate, miltefosine, paromomycin and pentamidine against intracellular Leishmania donovani amastigotes in peritoneal mouse macrophages. A second objective was to evaluate the susceptibility of antimony-resistant L. donovani isolates to sitamaquine. Methods Mouse peritoneal macrophages were infected with L. donovani amastigotes. Drug susceptibility was assessed in a standard 5 day assay and drug interactions with a modified fixed ratio isobologram method. Fractional inhibitory concentrations (FICs), sum FICs (∑FICs) and an overall mean ∑FIC were calculated for each combination. The nature of interaction was classified on the basis of the mean ∑FIC as follows: synergy as mean ∑FIC ≤0.5, indifference as mean ∑FIC between >0.5 and ≤4 and antagonism as mean ∑FIC >4. Results Interactions between sitamaquine and amphotericin B, sodium stibogluconate, paromomycin and miltefosine were classified as indifferent at the 50% and 90% effective concentration (EC(50) and EC(90), respectively) levels. The sitamaquine/pentamidine combination was synergistic, with overall mean ∑FICs from 0.5 to 0.6 at the EC(50) level and from 0.3 to 0.7 at the EC(90) level. Sitamaquine displayed in vitro activity against L. donovani isolates resistant to sodium stibogluconate. Conclusions This study expands the preclinical data on drug combinations and provides the basis for further studies as antileishmanial chemotherapy is moving towards multidrug treatment regimens. |
PMID: 21393188 [PubMed - as supplied by publisher] | |
Related citations | |
![]() |
10. | J Antimicrob Chemother. 2011 Jan 28. [Epub ahead of print]Biological activity of three n ovel complexes with the ligand 5-methyl-1,2,4-triazolo[1,5-a]pyrimidin-7(4H)-one against Leishmania spp.Ramírez-Macías I, Marín C, Salas JM, Caballero A, Rosales MJ, Villegas N, Rodríguez-Dieguez A, Barea E, Sánchez-Moreno M.Department of Parasitology, University of Granada, Severo Ochoa s/n, E-18071 Granada, Spain. AbstractObjectives We report on new 1,2,4-triazolo[1,5-a]pyrimidine complexes that have been developed and examined for both antiproliferative in vitro activity against Leishmania infantum and Leishmania braziliensis, and report their possible mechanism of action on L. infantum and L. braziliensis. Results Antileishmanial effects are described for newly synthesized Cu(II) and Co(II) complexes containing 5-methyl-1,2,4-triazolo[1,5-a]pyrimidin-7(4H)-one (HmtpO) as a ligand. These complexes display a wide structural diversity: (i) mononuclear unit, [Cu(HmtpO)(2)(H(2)O)(3)](ClO(4))(2)·H(2)O (1); (ii) two-dimensional framework, {[Cu(HmtpO)(2)(H(2)O)(2)](ClO(4))(2)·2HmtpO}(n) (2); and (iii) chains, {[Co(HmtpO)(H(2)O)(3)](ClO(4))(2)·2H(2)O}(n) (3). Compounds 1 and 2 appeared to be the most active against L. infantum (IC(50) 20.0 and 24.4 μM, respectively), and compounds 1 and 3 the most active against L. braziliensis (IC(50) 22.1 and 23.5 μM, respectively), with IC(50)s similar to those of the reference drug, glucantime (18.0 μM for L. infantum and 25.6 μM for L. braziliensis). These compounds were not toxic towards J774.2 macrophages. IC(25) decreased infection capacity and severely reduced the multiplication of intracellular amastigotes, following the trend 1 > 3 > 2 for L. infantum and 3 > 1 > 2 for L. braziliensis. These complexes had an effect on the energy metabolism of the parasites at the level of the NAD(+)/NADH balance and the organelle membranes, causing their degradation and cell death. Conclusions Cellular proliferation, metabolic and ultrastructural studies showed that the compounds 2 > 1 > 3 were highly active against L. infantum and L. braziliensis. |
PMID: 21393181 [PubMed - as supplied by publisher] | |
Related citations | |
![]() |
No comments:
Post a Comment