ライフサイエンスコーパス: KS

1 KS and NHL diagnoses during 1996 to 2011 were identified

2 KS and PEL are aggressive KSHV-associated malignancies w

3 KS can develop following organ transplantation through r

4 KS incidence rates per 100000 person-years were 52 in th

5 KS incidence was lower at 12-23 (IRR = 0.47; 95% CI, .23

6 KS is a highly disseminated and vascularized tumor.

7 KS risk was 5 times higher in South African women (aHR,

8 KS risk was lower in girls than in boys (adjusted HR [aH

9 KS spindle cells, the main tumor cells, all contain KSHV

10 KS tumors support both latent and lytic KSHV replication

11 KS was identified by >/= 1 inpatient or >/= 2 outpatient

12 Over a period of 1066572 person-years, 2046 KS cases were diagnosed.

13 There were 341 KS cases among 25 529 HIV-infected male veterans (incide

14 ation in RAP1B in a second individual with a KS-like phenotype.

15 mpound 2 for all anions investigated, with a KS/KR ratio of up to 2.

16 , the reduction in insulin sensitivity after KS-oil supplementation was more marked [27% lower than w

17 R gene frequencies in 250 classic (non-AIDS) KS cases, 280 KSHV-seropositive controls, and 576 KSHV-s

18 be an attractive therapeutic target for AIDS-KS.

19 ially effective therapeutic approach in AIDS-KS patients.

20 rtial regression of AIDS-associated KS (AIDS-KS) in five of 10 patients.

21 athogenesis underlying AIDS-related KS (AIDS-KS) remains unknown.

22 The high incidence of AIDS-KS has been ascribed to the interaction of KSHV and HIV-

23 hogenesis and extensive angiogenesis of AIDS-KS remains unclear.

24 way is important in the pathogenesis of AIDS-KS, which could be an attractive therapeutic target for

25 gressive AIDS-related Kaposi's sarcoma (AIDS-KS) characterized by abnormal angiogenesis.

26 ions of KS, the pathogenesis underlying AIDS-KS remains largely unknown.

27 ernative therapy for some patients with AIDS-KS.

28 In Europe, Latin, and North America KS risk was 6 times higher in men who have sex with men

29 Activity of the CPS and KS found in this phytopathogen was verified - that is, X

30 ical characterization of the encoded CPS and KS, and the impact of insertional mutagenesis on virulen

31 phosphate and ent-kaurene synthases (CPS and KS, respectively), which are found within a well-conserv

32 ratio and hydrogen bonding between Reb D and KS.

33 Both KSHV and KS are endemic in sub-Saharan Africa where approximately

34 eir potential role in HHV-8 pathogenesis and KS.IMPORTANCE Here we show that HHV-8, a DNA tumor virus

35 vIL-6 also plays a role in PEL and KS.

36 d the relationship between cART regimens and KS using multivariable Poisson regression, stratified or

37 urene synthase1 (SrKS1) homologs, SrCPS2 and KS-like (SrKSL), which were specifically expressed in tr

38 nical characteristics, overall survival, and KS progression-free survival were analyzed according to

39 her CD4 counts and lower HIV RNA values, and KS occurred more frequently after ART initiation.

40 not pathological aggregates, but rather are KS-WNK1-dependent microdomains of the DCT cytosol that m

41 nduced partial regression of AIDS-associated KS (AIDS-KS) in five of 10 patients.

42 r with aberrant neovascularization caused by KS-associated herpesvirus (KSHV).

43 ciated malignancy is etiologically caused by KS-associated herpesvirus (KSHV).

44 Kgamma were backcrossed into db/+ mice C57BL/KS (>10 generations) to obtain db/db-PI3Kgamma(-/-) mice

45 ation of a protein previously shown to cause KS-like lesions in mice (Rac1), an increase in KS-associ

46 ide Innovations and Technology, Kansas City, KS) designed to protect the head from radiation exposure

47 mmunodeficiency virus (HIV)-negative classic KS cases to plasma from 29 matched controls, using a mul

48 have reported a higher prevalence of classic KS in diabetic patients.

49 istic support for the association of classic KS with diabetes.

50 mumax), nitrite half saturation coefficient (KS), oxygen half saturation coefficient (KO), and biomas

51 n both the discovery and validation cohorts, KS was associated with HLA-A*11:01 (adjusted OR for the

52 nce (Kleaf) and stem hydraulic conductivity (KS).

53 -out coefficients (or Setschenow constants) (KS [M(-1)]) for 38 diverse neutral compounds in ammonium

54 nowledge about Setschenow salting constants, KS, the exponential dependence of Henry's Law coefficien

55 potentially be used in treatment to control KS/PEL.

56 Moreover, knocking out CPS, KS or CYP112 led to mutant Xoc that exhibited reduced vi

57 During R-Dox therapy, cutaneous KS developed in 1 patient, whereas 5 of 6 patients with

58 r regimens was not associated with decreased KS incidence.

59 iofacial, intellectual, and cardiac defects, KS is also characterized by humoral immune deficiency an

60 We describe a case of probable donor-derived KS in the recipient of a liver-kidney transplant.

61 uthern Africa, Europe and Asia; 26 developed KS after starting cART.

62 idence rates and risk factors for developing KS in different periods after starting cART in patients

63 idence rates and risk factors for developing KS up to 90 and 180 days and 1, 2, 5, and 8 years after

64 ther regions, have a high risk of developing KS after cART initiation.

65 not associated with the hazard of developing KS in the first year after cART initiation, but was over

66 cell counts increased the risk of developing KS throughout all observation periods after cART initiat

67 than those from GGAs or even from the exact KS potential.

68 stable disease, and seven (23.3%) exhibited KS progression.

69 erm generally overpredicted the experimental KS, predicted and experimental values were correlated.

70 We screened STAT4 in additional 18 familial KS cases and the variant site from 56 sporadic KS cases

71 L occurred at higher CD4 counts (P < .05 for KS and NHL) and with undetectable HIV RNA (P < .05 for K

72 ) and with undetectable HIV RNA (P < .05 for KS and NHL).

73 rug has potential as a therapeutic agent for KS.

74 ys provides novel therapeutic approaches for KS tumors.

75 ion, providing novel therapeutic avenues for KS tumors.IMPORTANCE KSHV is the etiologic agent of Kapo

76 ng cART, both incidence and risk factors for KS change with time since starting cART.

77 ests a potential of using YAP inhibitors for KS intervention.

78 The prediction error is generally larger for KS(NaCl) than for KS((NH4)2SO4).

79 Since current treatment methods for KS and PEL are fraught with unwanted side effects and lo

80 othelial cells (LTC) as a cellular model for KS, we demonstrated that KSHV infection induces Nrf2 con

81 al of lipoxin using in vitro cell models for KS and PEL.

82 ld provide potential therapeutic targets for KS.

83 or is generally larger for KS(NaCl) than for KS((NH4)2SO4).

84 Here we show that keratinocytes derived from KS patients are unable to undergo electrotaxis, and this

85 mine whether consuming Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and B. longum MM-2

86 sitive responses to Stona IB Gel(R), gelatin KS and gelatin RP600, of which the latter two were inclu

87 In this study, we use ketosynthase gene (KS) PCR amplicon sequences (sequence tags) to explore th

88 a simple proof of a theorem: In generalized KS theory (GKS), the band gap of an extended system equa

89 ) theory is shown to be valid in generalized KS theory.

90 ran Africa where approximately 84% of global KS cases occur.

91 V LSSE and the sudden increases in H K and H KS at 175 K are associated with the spin reorientation

92 e perpendicular magnetic anisotropy field (H KS) in the same Pt/YIG system.

93 V LSSE peak at 75 K is attributed to the H KS and M S (saturation magnetization) whose peaks also o

94 es mL (median 72, range <50-74 375); all had KS and 2 also had PEL.

95 act as control valves for species with high KS , or a low safety margin.

96 tro, KS-like mouse tumors and clinical human KS specimens.

97 clear serine-40-phosphorylated Nrf2 in human KS lesions compared to that in healthy tissues.

98 Pomalidomide is well tolerated and active in KS regardless of HIV status.

99 evelopment of organs and tissues affected in KS patients.

100 Despite important ART-related declines in KS incidence, men and women in South Africa and men who

101 and rescued the wound-healing deficiency in KS-TG mice.

102 dlin-1 also failed to rescue electrotaxis in KS cells, indicating that both integrin and lipid bindin

103 the dermal endothelium and hair follicles in KS-TG mice.

104 ceptor/formyl peptidyl receptor (ALX/FPR) in KS patient tissue sections and in vitro KS and PEL cell

105 -like lesions in mice (Rac1), an increase in KS-associated phenotypes (tube formation in endothelial

106 n of antioxidant genes and genes involved in KS pathogenesis such as the NAD(P)H quinone oxidase 1 (N

107 s and mechanisms of action of KSHV miRNAs in KS development.

108 and reduction of SHP1 were also observed in KS patient tissue.

109 d find that glyoxal consistently "salts-in" (KS of -0.16, -0.06, -0.065, -0.1 molality(-1), respectiv

110 clinical cohorts in Europe with 916 incident KS cases.

111 en who have sex with men remain at increased KS risk, likely due to high human herpesvirus 8 coinfect

112 cally active agents, possess a ketosynthase (KS) domain within each module to catalyze chain elongati

113 cyl carrier protein (ACP), and ketosynthase (KS) domains.

114 from a newly developed coupled ketosynthase (KS)-ketoreductase (KR) assay that established that the d

115 denylation (AD) and polyketide ketosynthase (KS) domain fragments amplified from these microbiomes pr

116 lly, we determined that dysfunction of known KS genes and the genes identified in this study results

117 Lower KS incidence was observed with longer BPI use, after acc

118 Months on BPIs was associated with lower KS incidence (P = .02).

119 The main KS tumor cell is the spindle cell, a cell of endothelial

120 We have measured KS of glyoxal and methylglyoxal for the atmospherically

121 AIOMFAC tends to underpredict the measured KS((NH4)2SO4) but always overpredicts KS(NaCl).

122 derlying pathogenic mechanism for this novel KS-associated variant.

123 A close correspondence between the observed KS selectivity and that predicted by phylogenetic analys

124 s evidence that KSHV, the etiologic agent of KS, induces aberrant angiogenesis.

125 Supplementation with a blend of KS oil is associated with decreased insulin sensitivity.

126 therwise healthy, received 5 1-g capsules of KS oil or a control (canola oil) for 8 wk and crossed ov

127 Most cases of KS show a marked reduction or complete absence of the ki

128 of polymicrogyria are not characteristic of KS, and we found only a few previous reports of this ass

129 Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV) infection.

130 To date, the precise contribution of KS selectivity in controlling product fidelity has been

131 AIOMFAC also predicted a dependence of KS on the salt concentrations, which is not observed in

132 betic patients contributes to development of KS by promoting KSHV lytic replication and infection.

133 ncogenic activity of KSHV and development of KS, and also suggests a potential of using YAP inhibitor

134 have an important role in the development of KS.

135 showed a mutation in COL18A1, diagnostic of KS.

136 roles of KMT2D and KDM6A in the etiology of KS by using a vertebrate model organism to provide direc

137 harbored within a unique N-terminal exon of KS-WNK1.

138 d testes growth, a characteristic feature of KS.

139 t of structures represents a larger group of KS domains from both canonical and AT-less type I PKSs t

140 s the fundamental gap, a major limitation of KS density-functional theory.

141 KMT2D have been identified in a majority of KS patients, a few patients have mutations in KDM6A.

142 n promoting the aggressive manifestations of KS in AIDS patients; however, the pathogenesis underlyin

143 n promoting the aggressive manifestations of KS, the pathogenesis underlying AIDS-KS remains largely

144 dings provide insights into the mechanism of KS selectivity in this important group of PKSs, can serv

145 cycle) is necessary for the pathogenesis of KS.

146 The clinical phenotype of KS includes moderate to severe intellectual disability w

147 itical for the initiation and progression of KS.

148 ergic antagonist, decreased proliferation of KS-associated herpesvirus (KSHV)-infected cells.

149 An increasing proportion of KS and NHL occurred at higher CD4 counts (P < .05 for KS

150 9%; 54 patients have died, 15 as a result of KS.

151 new insight into the potential treatment of KS and PEL using nature's own anti-inflammatory molecule

152 s and long-term benefits of PI-based cART on KS in other cohorts and prospective studies.

153 -control design preclude firm conclusions on KS risk or pathogenesis.

154 owever, effects of cART type and duration on KS remain difficult to interpret secondary to KS-associa

155 KIR influences the risk of KSHV infection or KS.

156 e oral microenvironment plays a role in oral KS tumor development.

157 spectively) while methylglyoxal "salts-out" (KS of +0.16, +0.075, +0.02, +0.06 molality(-1)).

158 asured KS((NH4)2SO4) but always overpredicts KS(NaCl).

159 ed technique (Analyze Direct, Overland Park, KS).

160 ed controlled viremia with either persistent KS despite 3 months of antiretroviral therapy (ART) or p

161 ystal structures of seven AT-less type I PKS KS domains that represent various sequence clusters, rev

162 the structural consequences of a type I PKS KS evolving into an AT-less type I PKS KS.

163 ural diversity within the AT-less type I PKS KS family, and most important, provide a unique opportun

164 Structures of canonical type I PKS KS-AT didomains reveal structured linkers that connect t

165 I PKS KS evolving into an AT-less type I PKS KS.

166 eir substrates, whereas canonical type I PKS KSs are monophyletic.

167 AT-less type I PKS KSs have remnants of these linkers, which have been hypo

168 AT-less type I PKS KSs possess substrate specificity and fall into phylogen

169 the current version of COSMOtherm to predict KS.

170 advanced (T1) disease, and 19 (86%) previous KS therapy excluding ART.

171 antiretroviral therapy (ART) or progressive KS despite 2 months of ART.

172 the infected host gene regulation to promote KS pathogenesis.

173 RT initiation in these children might reduce KS risk.

174 nhibitors (BPIs) was associated with reduced KS incidence in the third year of cART (incidence rate r

175 ell counts are essential to further reducing KS incidence worldwide, but additional measures might be

176 er, the pathogenesis underlying AIDS-related KS (AIDS-KS) remains unknown.

177 opsy specimens compared with non-HIV-related KS and NST.

178 lated KS cases compared with non-HIV-related KS and NST.

179 32gamma isoforms was observed in HIV-related KS biopsy specimens compared with non-HIV-related KS and

180 oform, followed by IL-32beta, in HIV-related KS cases compared with non-HIV-related KS and NST.

181 unctional interaction between the respective KS-associated genes and their products in zebrafish mode

182 o dietary potassium loading and restriction, KS-WNK1 knockout mice were deficient in these structures

183 ementation with a blend of krill and salmon (KS) oil [which is rich in eicosapentaenoic acid (EPA) an

184 8) is the causative agent of Kaposi sarcoma (KS) and multicentric Castleman disease (MCD), a life-thr

185 The burden of Kaposi sarcoma (KS) in human immunodeficiency virus (HIV)-infected child

186 Kaposi sarcoma (KS) incidence has decreased since combination antiretrov

187 Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV

188 Kaposi sarcoma (KS) remains a frequent cancer in human immunodeficiency

189 We compared Kaposi sarcoma (KS) risk in adults who started antiretroviral therapy (A

190 Kaposi sarcoma (KS) risk is affected by perturbed immunity.

191 rit behind the human disease Kaposi sarcoma (KS), an AIDS-defining malignancy.

192 V-related, 7 non-HIV-related Kaposi sarcoma (KS), and 7 normal skin tissues (NSTs) of Dutch origin we

193 V) is the causative agent of Kaposi sarcoma (KS), one of the leading cancers in human immunodeficienc

194 virus (KSHV) is the cause of Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a form of Cast

195 ) is the causative agent for Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and a subset of mu

196 rstanding of the burden of Kaposi's sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretro

197 Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL) are two well-kno

198 ed malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

199 an malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

200 ed malignancies, including Kaposi's sarcoma (KS) and primary effusion lymphoma (PEL).

201 Kaposi's sarcoma (KS) as the most common AIDS-associated malignancy is eti

202 Kaposi's sarcoma (KS) is a disease of multifocal vascular proliferation th

203 Purpose Kaposi's sarcoma (KS) is a multicentric tumor caused by Kaposi's sarcoma-a

204 Kaposi's sarcoma (KS) is an AIDS-defining cancer with aberrant neovascular

205 Kaposi's sarcoma (KS) is common in Africa, but economic constraints hinder

206 High prevalence of Kaposi's sarcoma (KS) is seen in diabetic patients.

207 is the etiologic agent of Kaposi's sarcoma (KS), a vascular tumor frequently found in immunodeficien

208 ologically associated with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric C

209 rus (KSHV) is the cause of Kaposi's sarcoma (KS), which is the most common AIDS-associated malignancy

210 Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) infection is linked to

211 Kaposi's sarcoma (KS)-associated herpesvirus (KSHV) is a human gammaherpes

212 the etiological agent for Kaposi's sarcoma (KS).

213 rs for development of oral Kaposi's sarcoma (KS).

214 genic virus that can cause Kaposi's sarcoma (KS).

215 is the etiologic agent of Kaposi's sarcoma (KS).

216 sed individuals, including Kaposi's sarcoma (KS).

217 ffusion lymphoma (PEL) and Kaposi's sarcoma (KS).

218 man herpesvirus 8 (HHV-8) (Kaposi's sarcoma [KS]-associated herpesvirus) and have an important role i

219 was proposed to use the kinetic-segregation (KS) mechanism.

220 cture of the exact multiplicative Kohn-Sham (KS) potential substantially underestimates the fundament

221 pression for the work function in Kohn-Sham (KS) theory is shown to be valid in generalized KS theory

222 Six KS domains from trans-acyltransferase (trans-AT) PKSs we

223 gistic regression and by Kolmogorov-Smirnov (KS) statistics.

224 between countries using Kolmogorov-Smirnov (KS) tests, Degree Distribution Quantification and Compar

225 Potassium sorbate (KS) was chosen as the carrier and two different concentr

226 cases and the variant site from 56 sporadic KS cases but detected no pathogenic mutations.

227 s within the Upper Neosho River subdrainage, KS, from June-August 2013 yielded three generalizable ec

228 rmatan sulfate (CS/DS), and keratan sulfate (KS)-mainly novel glycosylation strategies, elongation se

229 dulatory agent, in patients with symptomatic KS.

230 Kabuki syndrome (KS) is a complex multisystem developmental disorder asso

231 Kabuki syndrome (KS) is a rare multiple congenital anomaly syndrome chara

232 The genetic disorder Kabuki syndrome (KS) is characterized by developmental delay and congenit

233 EMA3E) in 2 brothers with Kallmann syndrome (KS), which causes inherited GnRH deficiency.

234 Kindler syndrome (KS) is an autosomal recessive blistering skin disease re

235 Kleefstra syndrome (KS) (Mendelian Inheritance in Man (MIM) no.

236 -chromosome (45X), and Klinefelter syndrome (KS), where males have an additional X-chromosome (47XXY)

237 Knobloch Syndrome (KS) is a rare congenital syndrome characterized by occip

238 Overall 5-year survival was 92% for T0 KS and 83% to T1 KS (P = .0024).

239 Patients with T0 KS had higher CD4 cell counts (P < .001); 90% of patient

240 l counts (P < .001); 90% of patients with T0 KS who were not receiving cART and 84% of those with T1

241 Patients with early-stage (T0) KS are treated with cART alone; patients with advanced-s

242 ear survival was 92% for T0 KS and 83% to T1 KS (P = .0024).

243 not receiving cART and 84% of those with T1 KS were treated in accordance with the stage-stratified

244 ART alone; patients with advanced-stage (T1) KS receive cART plus liposomal anthracycline chemotherap

245 We show that KS values for different salts are additive and present a

246 The KS incidence rates were 0/100 000 PYs in children of non

247 The KS model postulates that, when small receptors engage th

248 The KS test is sensitive to variation in network scale, and

249 The KS was successfully treated by switching immunosuppressi

250 0% lower (adjusted OR, 0.6; P = .01) but the KS risk 80% higher with HLA-C group 1 homozygosity (adju

251 the combined cohorts, 0.6; P = .01), but the KS risk was 2-fold higher (adjusted OR, 2.1; P = .002).

252 distributions differed significantly by the KS test.

253 In contrast, recombinant SEMA3E carrying the KS-associated mutation did not protect GnRH neurons from

254 Because IL-1 is abundant in the KS microenvironment and inhibits KSHV replication, this

255 hose whose counts were <50 cells/microL, the KS risk was halved in South Africa (aHR, 0.53; 95% CI, .

256 Acylation of the KS active site Cys residue is followed by transfer to ma

257 o detailed molecular characterization of the KS-associated immune phenotype has been reported.

258 2 production by T cells and suggest that the KS mechanism contributes to CD28 signaling.

259 Taken together, our studies suggest that the KS pathophysiology overlaps with the RASopathies and pro

260 er the Matsuda index) was 14% lower with the KS oil than with the control oil (P = 0.049).

261 Over time, KS and NHL occurred at higher CD4 counts and lower HIV R

262 itivity to electric fields and contribute to KS disease pathology.

263 NAs suppress host proteins and contribute to KS-associated pathogenesis.

264 logical condition of diabetes contributes to KS development.

265 gene expression, ultimately contributing to KS development.

266 d disrupted histone mark binding can lead to KS.

267 nhance KSHV dissemination and progression to KS if infection occurs.

268 o missense mutations in EHMT1 giving rise to KS have been described.

269 S remain difficult to interpret secondary to KS-associated immune reconstitution inflammatory syndrom

270 e and with that the risk for post-transplant KS.

271 on is one of the strategies adopted to treat KS and PEL, a primary motivation for exploring and evalu

272 dels offers a novel possibility for treating KS and PEL with lipoxins.

273 ) in KS patient tissue sections and in vitro KS and PEL cell models offers a novel possibility for tr

274 tors involved in this process using in vitro KS and PEL cells as models.

275 e activated in KSHV-infected cells in vitro, KS-like mouse tumors and clinical human KS specimens.

276 sub-Saharan Africa, a geographic area where KS is highly endemic.

277 using isolates from Western countries-where KS is not endemic.

278 n of the KSHV lytic cycle is associated with KS pathogenesis.

279 e strongly and significantly associated with KS, after adjustment for age and smoking status.

280 KSHV, the etiological agent associated with KS.

281 th complex medical histories consistent with KS in whom next generation sequencing identified the sam

282 shoots, Kleaf was negatively correlated with KS , supporting the HSH.

283 zed 40 individuals clinically diagnosed with KS for mutations in KMT2D and KDM6A.

284 Although several families with KS have been described previously, our case is noteworth

285 issues that are affected in individuals with KS, including craniofacial structures, heart and brain.

286 r proliferation that requires infection with KS herpes virus (KSHV/HHV-8).

287 assess the association of these markers with KS.

288 niparental isodisomy (UPD) in a patient with KS and a de novo, dominant mutation in RAP1B in a second

289 nd we find evidence of only one patient with KS who had an RD identified at an earlier age.

290 nction in a cohort (n = 13) of patients with KS (age, 4 months to 27 years).

291 V-8 MCD and compared them with patients with KS (n = 24) and healthy donors (n = 29).

292 We identified 466 patients with KS and 258 with NHL.

293 All patients with KS should undergo serial clinical immune evaluations.

294 umoral immune defects found in patients with KS with lysine methyltransferase 2D (KMT2D) mutations.

295 In patients with KS, autosomal dominant KMT2D mutations are associated wi

296 Chemical probes capable of reacting with KS (ketosynthase)-bound biosynthetic intermediates were

297 RESENTATIONS: We report on two siblings with KS.

298 Here, we show that kidney-specific WNK1 (KS-WNK1), a truncated kinase-defective WNK1 isoform that

299 In recent years, KS was more frequently diagnosed after ART initiation (5

300 we generated and analyzed 16 unique Zambian, KS-derived, KSHV genomes.