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1 tivity against the axenic form of Leishmania donovani .
2 elenocysteinyl-tRNA synthase from Leishmania donovani.
3 ceral leishmaniasis(VL) caused by Leishmania donovani.
4 caused by the protozoan parasite Leishmania donovani.
5 aniasis in children infected with Leishmania donovani.
6 cted against Trypanosoma cruzi or Leishmania donovani.
7 d 3) lower miltefosine-induced killing of L. donovani.
8 intracellular amastigotes form of Leishmania donovani.
9 on of the intracellular protozoan Leishmania donovani.
10 visceral leishmaniasis caused by Leishmania donovani.
11 and increased the early dissemination of L. donovani.
12 and kinetic analysis of ASNA from Leishmania donovani.
13 ctivity against T. brucei rhodesiense and L. donovani.
14 atalyses beta-oxidation of fatty acids in L. donovani.
15 1) and its conjugation pathway in Leishmania donovani.
16 nucleobases and nucleosides as wild type L. donovani.
17 nt importance of AAH to purine salvage by L. donovani.
18 tion by macrophages infected with Leishmania donovani.
19 ne protease activity expressed by Leishmania donovani.
20 eral leishmaniasis (VL) caused by Leishmania donovani.
21 e replacement within a virulent strain of L. donovani.
22 g this large (> 358 kDa) motor protein in L. donovani.
23 nst T. b. rhodesiense, P. falciparum, and L. donovani.
24 restrict the replication of intracellular L. donovani.
25 ch are associated with protection against L. donovani.
26 s involved in mediating susceptibility to L. donovani.
27 0) against the protozoan parasite Leishmania donovani.
28 mg/kg) for the treatment of VL caused by L. donovani.
29 onocytes, which mediate susceptibility to L. donovani.
30 throponotic transmission cycle of Leishmania donovani.
31 eral leishmaniasis (VL) caused by Leishmania donovani.
32 g of L. tropica and to a lesser extent of L. donovani.
33 caused by the protozoan parasite Leishmania donovani, a causative agent of visceral leishmaniasis (V
37 tor of ODC, inhibited growth of wild-type L. donovani amastigotes and effectively cured macrophages o
39 highly active with IC(50) values against L. donovani amastigotes of 0.5 +/- 0.2 and 2.3 +/- 0.8 micr
40 dies, these data support a model in which L. donovani amastigotes readily salvage ornithine and have
41 lquinoline derivatives, targeting Leishmania donovani, among which CQFC1 showed the highest efficacy
42 erize chemokine action in the response to L. donovani and also reemphasize that (i) recruited mononuc
43 rine salvage by both life cycle stages of L. donovani and authenticate ASL as a potential drug target
44 iense, Plasmodium falciparum, and Leishmania donovani and cytotoxicities for mammalian cells were inf
45 iense, Plasmodium falciparum, and Leishmania donovani and cytotoxicity against mammalian cells were i
46 STAT1(-/-) mice were highly resistant to L. donovani and developed less immunopathology, whereas T-b
47 es, we generated Deltaarg null mutants in L. donovani and evaluated their ability to proliferate in v
48 determined the structures of the Leishmania donovani and human ribosomes at 2.9 A and 3.6 A, respect
49 caused by infection of C57BL/6 mice with L. donovani and identified an early suppressive role for IL
50 en synthesized and tested against Leishmania donovani and L. amazonensis intracellular amastigotes.
51 ites of the Leishmania donovani complex - L. donovani and L. infantum - cause the fatal disease visce
54 caused by the protozoan parasites Leishmania donovani and Leishmania infantum, is one of the major pa
56 fective for the treatment of VL caused by L. donovani and mediates its antileishmanial activity by pr
57 rypanosoma brucei rhodesiense and Leishmania donovani and nanomolar potency against Plasmodium falcip
58 e cytochrome c oxidase complex in Leishmania donovani and that upon deletion of its gene the parasite
59 iense, Plasmodium falciparum, and Leishmania donovani and their cytotoxicity for mammalian cells.
61 plastid species, putative stem-loops from L. donovani and Trypanosoma brucei nucleobase transporter m
64 odesiense, Trypanosoma cruzi, and Leishmania donovani), and two compounds (14 and 21) showed good act
65 Expression of ISP2 was not detected in L. donovani, and a transgenic line constitutively expressin
66 iense, Plasmodium falciparum, and Leishmania donovani, and for cytotoxicity against mammalian cells.
67 iense, Plasmodium falciparum, and Leishmania donovani, and for cytotoxicity against mammalian cells.
68 oma brucei rhodesiense, T. cruzi, Leishmania donovani, and Plasmodium falciparum, the causative agent
70 nneled to hypoxanthine and/or xanthine by L. donovani, and that the purine sources within the macroph
71 l components of purine salvage in Leishmania donovani, and therefore Deltaadss and Deltaasl null muta
73 iense, Plasmodium falciparum, and Leishmania donovani, as well as cytotoxicity against mammalian cell
74 sion in Escherichia coli implied that the L. donovani ASL could also recognize 5-aminoimidazole-(N-su
75 unds 14, 15, and 25 selectively inhibited L. donovani at nanomolar concentrations and showed much low
77 /day) was further studied against Leishmania donovani/BALB/c mice via the intraperitoneal route for 5
81 that miR155 contributes to the control of L. donovani but is not essential for infection resolution.
82 erimental visceral leishmaniasis (Leishmania donovani) but more severe disease in a model of malaria
84 in mice and humans infected with Leishmania donovani, but their contribution to host resistance agai
85 sand flies favor the transmissibility of L. donovani by infected hosts, owing to a systemic effect t
86 f IL-17A rendering susceptibility against L. donovani by regulating the IFN-gamma response and promot
87 hibit sterol biosynthesis in T. cruzi and L. donovani by the inhibition of the enzyme sterol 24-methy
88 ana infection, suggesting that attenuated L. donovani can provide protection against heterologous L.
89 mation such as chronic infection (Leishmania donovani), cancer (melanoma and colorectal carcinoma), a
92 lipid, in successful survival of Leishmania donovani, causative agent of the fatal visceral leishman
93 he pathogenic protozoan parasite, Leishmania donovani, causative agent of the tropical infectious dis
96 w that in muMT mice infected with Leishmania donovani, CD8 T cells displayed a greater cytotoxic pote
97 e C57BL/6 (B6) mice infected with Leishmania donovani, CD8(+) T cell mechanisms are required for gran
99 ave implications for human S. mansoni and L. donovani co-infections and also demonstrate that granulo
100 nst T. b. rhodesiense, P. falciparum, and L. donovani combined with high antitrypanosomal efficacy in
104 us in aggregate; the Leishmania (Leishmania) donovani complex in aggregate; the species L (L) tropica
105 leishmaniasis (VL), caused by the Leishmania donovani complex, is a fatal, neglected tropical disease
110 were compared on small amounts of Leishmania donovani DNA, testing their ability to preserve specific
111 agent of visceral leishmaniasis, Leishmania donovani, does not prime human DC for IL-12 production.
113 Our results reveal the complexity of L. donovani evolution in the ISC in response to drug treatm
114 Collectively our results showed that L. donovani exploited the macrophage anti-apoptotic protein
115 llectively, our findings demonstrate that L. donovani exploits specific histone lysine methyltransfer
116 mmunoprecipitation analysis revealed that L. donovani facilitated H3K36 dimethylation at TNF-alpha pr
117 mice intravenously infected with Leishmania donovani form heterogeneous skin parasite patches that g
121 egg granuloma, consistent with a lack of L. donovani granuloma assembly in this tissue microenvironm
124 Hs-SAHH > Tc-SAHH > Ld-SAHH (from Leishmania donovani) > Pf-SAHH (from Plasmodium falciparum), which
130 and Kenya, where the disease is caused by L. donovani Here, we report the discovery and characterizat
132 or the growth of the promastigote form of L. donovani in culture, that all uracil and pyrimidine nucl
133 d to kill approximately 90-95% of Leishmania donovani in livers of mice deficient in mechanisms of ac
134 We report poor intracellular growth of L. donovani in macrophages from knockout mice for NE (ela(-
136 show that HSCs are infected with Leishmania donovani in vivo and in vitro and that this infection le
137 visceral leishmaniasis, caused by Leishmania donovani, in contrast to infection in mice, mimics the p
138 udies with nucleoside transport-deficient L. donovani indicate that this phenomenon is mediated by th
139 asis in both life cycle stages of Leishmania donovani, individual mutant lines deficient in either ca
140 s by which resistant clinical isolates of L. donovani induce intracellular events relevant to drug re
142 Our data revealed that L. major, but not L. donovani, induces expression of IRF2, IRF7, and IFIT5, i
149 etect serum antibodies in 104 asymptomaticL. donovani-infected individuals (qualified as positive for
154 sphatases, thioredoxin, SOCS, and Egr1 in L. donovani-infected macrophages was found to be unaffected
157 how that the enhanced early resistance in L. donovani-infected mice is entirely due to the activity o
161 l role for ceramide in the perspective of L. donovani infection and help formulate an antileishmanial
162 IFN-gamma) controls intracellular Leishmania donovani infection and the efficacy of antimony (Sb) che
163 ecruited into the spleen and liver during L. donovani infection and they are preferential targets for
165 uring C57BL/6 mice, intracellular Leishmania donovani infection enhanced Toll-like receptor 4 (TLR4)
166 l zone macrophages resulting from Leishmania donovani infection have increased resistance to Streptoc
167 in VL, we monitored the course of Leishmania donovani infection in miR155 knockout (miR155KO) and wil
169 maniasis (VL) by monitoring the course of L. donovani infection in TCCR-deficient C57BL/6 (TCCR-/-) m
170 uired resistance in intracellular Leishmania donovani infection in the liver, inducing gamma interfer
172 -6, responses to an intracellular Leishmania donovani infection in the livers of IL-6(-/-) and wild-t
173 ed resistance of p110delta(D910A) mice to L. donovani infection is due in part to impaired expansion
176 hi) iMOs into the liver and spleen during L. donovani infection using a CCR2 antagonist reduces the f
178 tment of Ly6C(hi) iMOs into organs during L. donovani infection, and adaptive transfer of wild type L
179 an efficient Th1 response during Leishmania donovani infection, but they play distinct roles in dete
180 ng, revamping Wnt5a signaling can inhibit L. donovani infection, irrespective of drug sensitivity or
181 afficking and hepatic inflammation during L. donovani infection, it is not essential for immunity aga
182 sults showed that compared with wild-type L. donovani infection, LdCen(-/-) parasites induce signific
183 luation in a mouse model of acute Leishmania donovani infection, one phenylpyridine derivative (37) s
191 ound with modest activity against Leishmania donovani intracellular amastigotes and excellent selecti
192 une evasion strategies adopted by Leishmania donovani involve the exploitation of suppressor of cytok
195 The pathogenic protozoan parasite Leishmania donovani is capable of both de novo pyrimidine biosynthe
196 or absent expression of parasite ISP2 in L. donovani is necessary to preserve the activation of the
199 he lymph node barrier to dissemination of L. donovani is related to insufficient numbers of lymph nod
200 l leishmaniasis (PKDL), caused by Leishmania donovani is the dermal sequel of Visceral Leishmaniasis
201 mice with the protozoan parasite Leishmania donovani, is characterized by focal accumulation of infl
203 regulation in which the parasite Leishmania donovani (Ld) causes mitochondrial depolarization, reduc
204 characterization of two new biomarkers of L. donovani (Ld-mao1 and Ld-ppi1) present in the urine of V
206 e attenuated centrin gene-deleted Leishmania donovani (LdCen(-/-) ) parasites through induction of Th
207 er a live attenuated centrin gene-deleted L. donovani (LdCen1(-/-)) parasite can persist and be both
209 solution significantly suppressed Leishmania donovani liver parasite burdens (p<0.05) but could not i
210 aken together, these results suggest that L. donovani may exploit SOCS for subverting macrophage apop
213 In this study, we showed that Leishmania donovani modulates the TLR2-mediated pathway in macropha
219 resulting in novel, highly potent Leishmania donovani NMT inhibitors with good selectivity over the h
220 ated a computational model of the Leishmania donovani nucleoside transporter 1.1 (LdNT1.1) that captu
221 cted transmembrane domains of the Leishmania donovani nucleoside transporter 1.1, LdNT1.1, which tran
223 tly, we have demonstrated that a Deltaodc L. donovani null mutant lacking ornithine decarboxylase (OD
225 using a transgenic luciferase-expressing L. donovani parasite and longitudinally quantified the infe
226 etically modified live-attenuated Leishmania donovani parasite cell lines (LdCen(-/-) and Ldp27(-/-))
227 our PfCENs in a centrin knock-out Leishmania donovani parasite line that exhibited a severe growth de
229 vaccines such as centrin deleted Leishmania donovani parasites (LdCen (-/-)) showed protective immun
231 onstrate the potential of live-attenuated L. donovani parasites as pan-Leishmania species vaccines.
234 tes (compared to that with wild-type [WT] L. donovani parasites) induced significantly higher product
235 e shown that genetically modified Leishmania donovani parasites, here described as live attenuated pa
237 M s) and CD4(+) T cells, we observed that L. donovani preferentially upregulates SOCS1 and SOCS3 expr
238 sary for the viability and growth of both L. donovani promastigotes and amastigotes and intimate that
239 fectively inhibited the growth of Leishmania donovani promastigotes and amastigotes, and iron did not
245 eral leishmaniasis (VL) caused by Leishmania donovani requires interferon-gamma production by CD4+ T
246 ive protozoan pathogen of humans, Leishmania donovani, resides and multiplies in highly restricted mi
247 tant of L. donovani that establishes that L. donovani salvages purines primarily through hypoxanthine
248 Infection with antimony-resistant Leishmania donovani (Sb(R)LD) induces aggressive pathology in the m
249 r mechanism of antimony-resistant Leishmania donovani (Sb(R)LD)-driven up-regulation of IL-10 and mul
252 val of the intracellular parasite Leishmania donovani Screening of macrophage antioxidant enzymes dur
253 rts extensive skin infection with Leishmania donovani, spatial analyses at macro-(quantitative PCR) a
255 ted individuals (qualified as positive forL. donovani-specific antibodies by direct agglutination tes
257 istance in two clinically derived Leishmania donovani strains with different inherent resistance to a
259 pite the development of a functional anti-L. donovani Th1 response that can mediate granuloma formati
261 acellular replication of residual Leishmania donovani that escape chemotherapy evolves to a host mech
262 nal lethal Deltahgprt/Deltaxprt mutant of L. donovani that establishes that L. donovani salvages puri
263 sis is a deadly illness caused by Leishmania donovani that provokes liver and spleen inflammation and
264 parasites Leishmania infantum and Leishmania donovani The gold standard diagnostic test for VL is the
265 polyamine biosynthetic pathway of Leishmania donovani, the causal agent of visceral leishmaniasis, ar
266 In this study the interactions of Leishmania donovani, the causative agent of visceral Leishmaniasis,
267 ens against the tropical parasite Leishmania donovani, the causative agent of visceral leishmaniasis.
270 t, IL-12p40 expression is not elicited by L. donovani, the etiological agent of deadly visceral leish
271 polyamine biosynthetic pathway of Leishmania donovani, the etiological agent of visceral leishmaniasi
272 d a proof-of-concept of SL-seq in Leishmania donovani, the main causative agent of visceral leishmani
273 stigated the interactions between Leishmania donovani, the main etiological agent of visceral leishma
276 by the intra-macrophage parasite Leishmania donovani to protect their "home" from actinomycin D-indu
277 ans were quantified and the sensitivity of L donovani to sodium stibogluconate assessed at each passa
278 y in Leishmania, has not been analyzed in L. donovani To test ARG function in intact parasites, we ge
279 A crystal structure of an active truncated L.donovani TOP1L/TOP1S heterodimer bound to nicked double-
280 t relevant to human disease, i.e. Leishmania donovani, Trypanosoma cruzi and Trypanosoma brucei.
281 involving Schistosoma mansoni and Leishmania donovani, two important human pathogens affecting the li
290 ease (SUB; Clan SB, family S8) of Leishmania donovani was cloned and found to possess a unique cataly
294 n mice infected with the parasite Leishmania donovani, we identified a transcriptomic network operati
295 th antimony drug-sensitive and -resistant L. donovani, we noted disruption in the steady-state level
296 is expressed in both life cycle stages of L. donovani, whereas subcellular fractionation and immunofl
298 exhibited potent activity against Leishmania donovani with IC(50) values ranging from 3.75 to 10.37 m
299 rypanosoma brucei rhodesiense and Leishmania donovani with IC50 values of 1.55 and 0.22 muM, respecti
300 3.75 muM, respectively) forms of Leishmania donovani with negligible cytotoxicity toward the host (J