ライフサイエンスコーパス: leprosy

1 nerve demyelination characteristic of human leprosy.

2 e drug discovery target for tuberculosis and leprosy.

3 ing to the control of host susceptibility to leprosy.

4 lopment of nerve injuries and deformities in leprosy.

5 mportance, such as plague, tuberculosis, and leprosy.

6 raphy in examination of peripheral nerves in leprosy.

7 t increases the risk for Crohn's disease and leprosy.

8 rkinson's disease (PD), Crohn's disease, and leprosy.

9 in biopsy specimens from 85 individuals with leprosy.

10 ns from patients with a disseminated form of leprosy.

11 identified gene conferring susceptibility to leprosy.

12 t a considerable proportion of patients with leprosy.

13 rae, the intracellular bacterium that causes leprosy.

14 detect latent tuberculosis in patients with leprosy.

15 xico, was diagnosed with diffuse lepromatous leprosy.

16 n the clinical diagnosis and surveillance of leprosy.

17 8 gene were associated with T1R but not with leprosy.

18 CIITA-SOCS1 as new susceptibility genes for leprosy.

19 ost exclusively in patients with lepromatous leprosy.

20 testing was performed on 39 US patients with leprosy.

21 be used as an additional control measure for leprosy.

22 terium leprae challenge in a murine model of leprosy.

23 t with no evidence of active tuberculosis or leprosy.

24 y lead to tools applicable to elimination of leprosy.

25 ing that 248S is a susceptibility factor for leprosy.

26 ypersensitivity syndrome among patients with leprosy.

27 ion in patients with the progressive form of leprosy.

28 n the genetic control of Crohn's disease and leprosy.

29 rkinson's disease (PD), Crohn's disease, and leprosy.

30 difies susceptibility to Crohn's disease and leprosy.

31 ohn disease, psoriasis, alopecia areata, and leprosy.

32 that cause diseases such as tuberculosis and leprosy.

33 atients and 101 control participants without leprosy.

34 teraction in the peripheral nerve lesions of leprosy.

35 contributes to nerve injury in patients with leprosy.

36 leprae, contributing to the pathogenesis of leprosy.

37 e expression profiles in the skin lesions of leprosy.

38 rium leprae is the noncultivable pathogen of leprosy.

39 identification of chains of transmission of leprosy.

40 he major cause of irreversible neuropathy in leprosy.

41 xpression levels as potential biomarkers for leprosy.

42 des and main contributors to nerve damage in leprosy.

43 rs in clinical diagnosis and surveillance of leprosy.

44 prived individuals have the greatest risk of leprosy.

45 iptomic biomarkers as correlates of risk for leprosy.

46 lation are associated with increased risk of leprosy.

47 the mycobacteria that cause tuberculosis or leprosy.

48 (Th1) inflammatory episode in patients with leprosy.

49 . leprae PGL-1 in initiating nerve damage in leprosy.

50 (5,577 to 2,871), trachoma (506 to 159), and leprosy (36 to 26).

51 ved dapsone as part of multidrug therapy for leprosy (39 participants with the dapsone hypersensitivi

52 p of 5-7 years, out of 104 HHCs, 7 developed leprosy (6.7%).

53 fic antibodies: the visual immunogold OnSite Leprosy Ab Rapid test [Gold-LFA] and the quantitative, l

54 However, due to the spectral character of leprosy, additional, cellular biomarkers are required to

55 on WHO multidrug therapy for paucibacillary leprosy along with antiinflammatory drugs.

56 and Texas, there are autochthonous cases of leprosy among native-born Americans with no history of f

57 ssion in mycobacterial infection by studying leprosy, an intracellular infection caused by Mycobacter

58 galectin-3 with unfavorable host response in leprosy and a potential mechanism for impaired host defe

59 pathogen associated with diffuse lepromatous leprosy and a reactional state known as Lucio's phenomen

60 besides diagnosing enlargement of nerves in leprosy and acute neuritis due to lepra reactions, guide

61 sed analysis revealed an association between leprosy and allele G of marker rs295340 (P = .042) and b

62 orderline evidence of an association between leprosy and alleles C and A of markers rs4880 (P = .077)

63 assist in the diagnosis and monitoring of MB leprosy and can detect a significant number of earlier-s

64 luding Parkinson's disease, Crohn's disease, leprosy and cancer.

65 atment of multiple myeloma, complications of leprosy and cancers.

66 for systemic juvenile idiopathic arthritis, leprosy and Crohn's disease.

67 sk variant function in rheumatoid arthritis, leprosy and Crohn's disease.

68 bility genes shared with Crohn's disease and leprosy and implicate mucosal factors and the innate imm

69 ), which occurs in patients with lepromatous leprosy and is characterized by neutrophil infiltration

70 Mycobacterium leprae causes leprosy and is unique among mycobacterial diseases in pr

71 teria, are associated with susceptibility to leprosy and its clinical outcomes.

72 ed by the World Health Organization to treat leprosy and multi-drug-resistant tuberculosis.

73 y decrease an individual's susceptibility to leprosy and offer a novel therapeutic target for IL-1-de

74 tic intervention in modulating the course of leprosy and other chronic infectious diseases.

75 as a facile, genetically tractable model for leprosy and reveal the interplay between innate and adap

76 riants are associated with susceptibility to leprosy and the development of leprosy reactive states.

77 cting findings about the association between leprosy and TLR1 variants N248S and I602S have been repo

78 ts to develop tools and approaches to detect leprosy and to stop the transmission of Mycobacterium le

79 Leprosy and tuberculosis were widespread in the past and

80 protects against the mycobacterial diseases leprosy and tuberculosis.

81 ulosis (tuberculosis), Mycobacterium leprae (leprosy) and Treponema pallidum pallidum (syphilis).

82 ics that are effective against tuberculosis, leprosy, and AIDS-related mycobacterial infections.

83 at possess activity against tuberculosis and leprosy, and an inhibitor of para-aminobenzoate biosynth

84 mples from patients with multibacillary (MB) leprosy, and the rate of positive results declined with

85 h leprosy; screening the traced contacts for leprosy; and administering SDR to eligible contacts.

86 atients with the different clinical types of leprosy as well as between the patients and 101 control

87 n = 0.82, 95% CI: 0.68, 0.98) and cases with leprosy-associated disabilities (IRRPoisson = 0.79, 95%

88 ts related to operational classification and leprosy-associated disabilities at diagnosis.

89 including the inflammatory bowel disease and leprosy-associated tumor necrosis factor ligand superfam

90 s, despite their ancient separation, the two leprosy bacilli are remarkably conserved and still cause

91 suggest that the viability and purity of the leprosy bacilli used for in vitro studies determines the

92 when macrophages had a heavy burden of live leprosy bacilli.

93 Fortunately, the leprosy bacillus is sensitive to several antibiotics.

94 Here, we show that the leprosy bacterium hijacks this property to reprogram adu

95 The first serum diagnosis of leprosy based on the detection of antibodies of patients

96 associated with inflammatory bowel disease, leprosy, Behcet disease, and systemic juvenile idiopathi

97 A phylogeographic survey of 227 leprosy biopsies by differential PCR revealed that 221 c

98 ce of LTalpha on the control of experimental leprosy, both low- and high-dose Mycobacterium leprae fo

99 rial diseases explored include tuberculosis, leprosy, bubonic plague, typhoid, syphilis, endemic and

100 cells participate in the immune response in leprosy by their ability to activate T cells that recogn

101 ns to estimate incidence rate ratios for new leprosy case detection and secondary endpoints related t

102 P) conditional cash transfer program and new leprosy case detection using linked records from 12,949,

103 In an analysis of a leprosy case-control study, iBVS selected 94 SNPs as pre

104 rium leprae was obtained from biopsies of 37 leprosy cases (18 relapses and 19 new cases): 16 (43.24%

105 on to validate the findings of WES using 151 leprosy cases and 226 healthy controls by Sanger sequenc

106 Confirmed leprosy cases were investigated for bacterial resistance

107 pite the dramatic reduction in the number of leprosy cases worldwide in the 1990s, transmission of th

108 Leprosy, caused by infection with Mycobacterium leprae o

109 e against intracellular bacteria, we studied leprosy, caused by the obligate intracellular pathogen M

110 bacterium lepromatosis is a newly discovered leprosy-causing organism.

111 A key drug for the treatment of leprosy, clofazimine has recently been associated with h

112 We believe an all-out campaign by a global leprosy coalition is needed to bring that figure down to

113 a Village, an isolated, hyperendemic, former leprosy colony located in the Brazilian Amazon.

114 48S is associated with an increased risk for leprosy, consistent with its hypoimmune regulatory funct

115 Lesions in lepromatous leprosy contained macrophages with a regulatory phenotyp

116 Leprosy continues to be the belligerent public health ha

117 of single-dose rifampicin (SDR) into routine leprosy control activities.

118 social policies might contribute to ongoing leprosy control efforts in high-burden communities.

119 Leprosy control has seen little innovation and only limi

120 tre feasibility study implemented within the leprosy control programmes of Brazil, India, Indonesia,

121 DR is safe; can be integrated into different leprosy control programmes with minimal additional effor

122 The programme has also invigorated local leprosy control through the availability of a prophylact

123 Innovative approaches are required for leprosy control to reduce cases and curb transmission of

124 equired to block transmission and to improve leprosy control.

125 ons of patients with progressive lepromatous leprosy, correlating and colocalizing with IFN-beta and

126 Decubitus ulcer, psoriasis, and leprosy demonstrated review/protocol overrepresentation

127 e association study in Chinese patients with leprosy detected association signals in 16 single-nucleo

128 Since efficient leprosy diagnosis requires field-friendly test condition

129 With a prompt leprosy diagnosis, an early and effective treatment coul

130 th ESI-HRMS is a promising fast and sensible leprosy diagnostic method.

131 ed transcriptomic biomarkers associated with leprosy disease, different leprosy phenotypes as well as

132 form of leprosy known as diffuse lepromatous leprosy (DLL).

133 form of leprosy known as diffuse lepromatous leprosy (DLL).

134 Mycobacterium leprae, the causative agent of leprosy, due to difficulties with culturing of the organ

135 will be a critical component of an effective leprosy elimination campaign.

136 Leprosy elimination has been a goal of the WHO for the p

137 ew strategies are required in the pursuit of leprosy elimination.

138 This multi-site study, situated in four leprosy endemic areas, demonstrates the potential of hos

139 did not distinguish patients from EC in one leprosy-endemic area based on IFN-gamma.

140 Simple tests to facilitate referral to leprosy experts are not widely available, and the correc

141 and four healthy control relatives from two leprosy families.

142 , and CHGB48 and CHGB23 were susceptibile to leprosy for the male population, respectively).

143 e likely represents the first report of this leprosy form and its agent in the southeastern tip of Me

144 ere built from a cohort of 409 patients with leprosy from central Brazil, monitored for T1R and T2R.

145 de Informacao de Agravos de Notificacao) for leprosy from Jan 1, 2007, to Dec 31, 2014.

146 e and adaptive immune determinants mediating leprosy granuloma formation and function.

147 Understanding the pathogenesis of leprosy granulomas has been hindered by a paucity of tra

148 Mycobacterium leprae, which causes leprosy, grows optimally at approximately 30 degrees C,

149 ectious disease, biopsies from patients with leprosy (Hanseniasis) were analyzed.

150 Leprosy has been treated with multidrug therapy, which h

151 Leprosy has long been thought to have a strong genetic c

152 stigation into the innate immune response in leprosy has provided insight into immunoregulation in hu

153 Since 2000, about 250 000 new cases of leprosy have been detected every year.

154 , the etiological agents of tuberculosis and leprosy, have coevolved with mammals for millions of yea

155 nd adaptive immunity, in the pathogenesis of leprosy, highlighting the merits of protein-coding varia

156 distinguishing between positive and negative leprosy human sera samples diluted from 1:640 up to 1:10

157 In the third cohort of schoolchildren from a leprosy hyperendemic region in Brazil, both tests detect

158 h T1R or T2R and controls with nonreactional leprosy identified the gene for interleukin 6 (IL-6) as

159 nal candidate gene SOD2 for association with leprosy in 2 independent population samples.

160 on were associated with an increased risk of leprosy in Brazil.

161 To address the persisting problem of leprosy in Cebu, Philippines, we compiled a database of

162 dapsone (DDS) resistance has led to fear of leprosy in more unfortunate people of certain developing

163 ssary to investigate ongoing transmission of leprosy in regions of endemicity.

164 Red squirrels are thus a reservoir for leprosy in the British Isles.

165 dicated an association between TLR1 248S and leprosy in the case-control study (SS genotype odds rati

166 We performed a 3-stage GWAS of leprosy in the Chinese population using 8,313 cases and

167 socioeconomic factors with risk of incident leprosy in the full cohort and in children (aged 0-15 ye

168 Wild armadillos and many patients with leprosy in the southern United States are infected with

169 e clinically progressive lepromatous form of leprosy; in contrast, galectin-3 was almost undetectable

170 sociated with an up to two-times increase in leprosy incidence (incidence rate ratio 1.46, 95% CI 1.3

171 north, and northeast regions) had a risk of leprosy incidence five-to-eight times greater than did o

172 g, BFP participation was not associated with leprosy incidence overall (incidence rate ratio (IRR)Poi

173 Overall, cumulative leprosy incidence was 17.4/100,000 person-years at risk

174 I: 0.90, 1.04) but was associated with lower leprosy incidence when restricted to families living in

175 ng policies might be associated with reduced leprosy incidence, we evaluated the association between

176 2 individuals including 18 518 patients with leprosy, increased levels of deprivation were associated

177 the frequency of CD1b(+) DCs at the site of leprosy infection correlated with the clinical presentat

178 prae, the intracellular etiological agent of leprosy, infects Schwann promoting irreversible physical

179 exist in fields such as oncology, diabetes, leprosy, inflammatory bowel disease, among others, howev

180 nd with the potential for quality control in leprosy investigations.

181 Leprosy is a chronic but treatable infectious disease ca

182 Leprosy is a chronic disease characterized by skin and p

183 Leprosy is a chronic infectious disease caused by Mycoba

184 Leprosy is a neglected tropical disease predominately af

185 ts well-defined immunological complications, leprosy is a useful disease for studying genetic regulat

186 Leprosy is an infectious disease caused by Mycobacterium

187 on from both tuberculosis and multibacillary leprosy is associated with heterozygosity for LTA4H poly

188 ently, the gold standard diagnostic test for leprosy is based on skin lesion biopsy, which is invasiv

189 Early diagnosis of leprosy is challenging, particularly its inflammatory re

190 prae DNA is present in soil of regions where leprosy is endemic or areas with possible animal reservo

191 on of M. leprae in different countries where leprosy is endemic.

192 Early detection of leprosy is key to reduce the ongoing transmission.

193 razil, Ethiopia) and from South Korea, where leprosy is not endemic anymore.

194 Leprosy is not eradicable with currently available diagn

195 dely available, and the correct diagnosis of leprosy is often delayed.

196 Leprosy is present in more than 100 countries, where it

197 Although leprosy is recognised as a disease of poverty, there is

198 ence a diagnostic tool for bacterium causing leprosy is successfully fabricated in a facile manner wh

199 Leprosy is the most common form of treatable peripheral

200 or the prevention of immune pathology during leprosy, it will not control bacterial burden and is the

201 epromatosis was identified in a rare form of leprosy known as diffuse lepromatous leprosy (DLL).

202 epromatosis was identified in a rare form of leprosy known as diffuse lepromatous leprosy (DLL).

203 vation correlated with mo-DC infiltration in leprosy lesions.

204 L-12, relative to macrophages in tuberculoid leprosy lesions.

205 lgaris) have increasingly been observed with leprosy-like lesions on the head and limbs.

206 r, UK, showing skeletal signs of lepromatous leprosy (LL) have been studied using a multidisciplinary

207 istological sections (n = 10), 1 lepromatous leprosy (LL), 1 DLL, and 3 Lucio reactions contained M.

208 istological sections (n=10), one lepromatous leprosy (LL), one DLL, and three Lucio reactions contain

209 a large natural reservoir for M. leprae, and leprosy may be a zoonosis in the region.

210 The chronic course of lepromatous leprosy may be interrupted by acute inflammatory episode

211 nal support from MAP International, American Leprosy Missions, Fondation Raoul Follereau France, Buru

212 Leprosy morbidity is increased by 2 pathologic immune re

213 ls and mitochondrial swelling in pure neural leprosy nerves.

214 The impact of this regulation in leprosy neuropathy is discussed.

215 ypersensitivity syndrome among patients with leprosy (odds ratio, 6.18; P=3.84x10(-13)).

216 We found three new susceptible loci of leprosy, one in GAL3ST4 and two in CHGB.

217 h (trachoma and onchocerciasis), ulcer care (leprosy), or renal support (schistosomiasis).

218 tic challenge, particularly in tuberculosis, leprosy, P. aeruginosa and S. aureus infections, where i

219 ae infection causes demyelination to mediate leprosy pathogenesis has been a long-standing question.

220 s identified in 16.0% of soil from houses of leprosy patients (Bangladesh), in 10.7% from armadillos'

221 kin tests from the same individual, from 113 leprosy patients and 104 household contacts of patients

222 variants in Han Chinese, of whom were 7,048 leprosy patients and 14,398 were healthy control subject

223 low improved diagnosis and classification of leprosy patients and detection of infection.

224 es induced by M. leprae proteins in blood of leprosy patients and endemic controls (EC) from high lep

225 In this study, we used WES approach on four leprosy patients and four healthy control relatives from

226 sponses from both TB and paucibacillary (PB) leprosy patients and from healthy household contacts of

227 ollection of M. leprae isolates derived from leprosy patients and propagated in armadillo hosts.

228 n, intra-individual longitudinal analyses of leprosy patients before, during and after treatment of r

229 f this work was to identify lipid markers in leprosy patients directly from skin imprints, using a ma

230 sting was performed on skin biopsies from 24 leprosy patients from Guinea-Conakry for the first time.

231 We selected 474 Vietnamese leprosy patients of which 237 were T1R-affected and 237

232 Forty multibacillary leprosy patients were negative.

233 Five of 10 paucibacillary leprosy patients were Quantiferon Gold (Q-G) positive wi

234 Pentraxin-3 (PTX3) analyses of sera from 87 leprosy patients with or without reactions were conducte

235 y and apoptotic molecules were identified as leprosy patients' markers.

236 on incubation with blood from paucibacillary leprosy patients, a group who limit M. leprae growth and

237 Prospective cohorts of newly diagnosed leprosy patients, including reactions, and healthy contr

238 a major cause of peripheral nerve damage in leprosy patients, the immunopathogenesis of ENL remains

239 event permanent neuropathy and disability in leprosy patients.

240 esults of a genome-wide association study of leprosy per se, we investigated the TNFSF15 chromosomal

241 Leprosy persists as a public health problem.

242 s associated with leprosy disease, different leprosy phenotypes as well as high exposure to Mycobacte

243 In addition to new findings on leprosy physiopathology, the discovery of relevant piRNA

244 h antileprosy drug resistance occurs in this leprosy population, resistance does not appear to be a m

245 The leprosy post-exposure prophylaxis (LPEP) programme was a

246 ffered between EC from areas with dissimilar leprosy prevalence.

247 patients and endemic controls (EC) from high leprosy-prevalence areas (Bangladesh, Brazil, Ethiopia)

248 erence Laboratory (NTRL) and National TB and Leprosy Program redesigned the tuberculosis specimen tra

249 screening of contacts of known patients with leprosy promises to strengthen early diagnosis, while pr

250 Leprosy provides a model to investigate mechanisms of im

251 Identifying genetic predictive factors for leprosy reactions may have a major impact on preventive

252 eptibility to leprosy and the development of leprosy reactive states.

253 associated with increased susceptibility to leprosy (recessive, P = 1.4 x 10(-3)) and with increased

254 search for M. leprae resistance in suspected leprosy relapse cases and contacts was performed in Prat

255 Leprosy remains a major global health problem and typica

256 Leprosy remains an important health problem in a number

257 infection should therefore be emphasized in leprosy research.

258 Study of IFN responses in human leprosy revealed an inverse correlation between IFN-beta

259 wild armadillo and three U.S. patients with leprosy revealed that the infective strains were essenti

260 on, we investigated socioeconomic markers of leprosy risk in Brazil.

261 contacts of individuals newly diagnosed with leprosy; screening the traced contacts for leprosy; and

262 report, we evaluate the performance of a new leprosy serological test (NDO-LID).

263 ecommended that all registered patients with leprosy should receive combination therapy with three an

264 osy susceptibility factors in 474 Vietnamese leprosy simplex families.

265 Analysis of leprosy skin lesions by gene expression profiling and im

266 ies of gene expression profiles derived from leprosy skin lesions suggested a link between IL-27 and

267 of the piRNAs examined are downregulated in leprosy skin lesions.

268 Development of a leprosy-specific vaccine that boosts long-lasting T-cell

269 dge potential for diagnosis across the whole leprosy spectrum.

270 cohort and in children (aged 0-15 years), by leprosy subtype and region of residence.

271 Here, we studied these 16 SNPs as potential leprosy susceptibility factors in 474 Vietnamese leprosy

272 HLA-DR-DQ, RIPK2, CCDC122-LACC1, and NOD2 as leprosy susceptibility factors in Vietnam.

273 pic effects demonstrated a high tendency for leprosy susceptibility loci to show association with aut

274 contribution of common noncoding variants to leprosy susceptibility, protein-coding variants have not

275 an the alternative, the Standard Diagnostics leprosy test (87.0% versus 81.7% and 32.3% versus 6.5%,

276 er proportions of MB and paucibacillary (PB) leprosy than the alternative, the Standard Diagnostics l

277 control nerve damage, a prominent feature of leprosy that has no currently available pharmaceutical t

278 Mycobacterium leprae, a well-known cause of leprosy, that justifies the status of M. lepromatosis as

279 ns to tuberculosis and reversal reactions in leprosy, the exact mechanisms, and therefore potential d

280 Leprosy, the leading infectious cause of disability worl

281 ment could be feasible and thus the chain of leprosy transmission could be abbreviated.

282 or targeted approaches to search and confirm leprosy transmission in various scenarios.

283 The first antibiotic to be widely used for leprosy treatment was dapsone in the 1950s, which had to

284 In leprosy, type 1 reaction (T1R) and type 2 reaction (T2R)

285 We report a case of leprosy unmasking and downgrading reaction after stem ce

286 ought to be the exclusive causative agent of leprosy until Mycobacterium lepromatosis was identified

287 was thought the exclusive causative agent of leprosy until Mycobacterium lepromatosis was identified

288 Research on tuberculosis and leprosy was revolutionized by the development of a plasm

289 In the human mycobacterial infection leprosy, we found that activation of monocytes via nucle

290 hisms were associated with susceptibility to leprosy when comparing allele frequencies, and 8 were as

291 Mycobacterium leprae causes endemic disease leprosy which becomes chronic if not treated timely.

292 Leprosy, which is caused by the human pathogen Mycobacte

293 used to study the genetic susceptibility to leprosy,while whole exome sequencing (WES) approach has

294 discovery of several susceptibility loci for leprosy with robust evidence, providing biological insig

295 estations seen in patients, from tuberculoid leprosy with robust production of Th1-type cytokines to

296 ted by comparing results in HHCs who develop leprosy with those not affected.

297 y was consistent with borderline tuberculoid leprosy with type 1 lepra reaction.

298 cally expressed in the polar immune forms of leprosy, with type I IFNs inducing IL-10 that interferes

299 lary disease is similar to human lepromatous leprosy, with variable/high levels of antibody and a dys

300 been implicated in the pathogenesis of human leprosy, yet it is not clear whether Mycobacterium lepra