ライフサイエンスコーパス: splenomegaly

1 echogenicity on ultrasonography, and 65% had splenomegaly.

2 less than or equal to 174,000 per mm(3) and splenomegaly.

3 ditionally presented anemia, leukopenia, and splenomegaly.

4 ultrasound imaging showed the development of splenomegaly.

5 n leukemia cell counts, lymphadenopathy, and splenomegaly.

6 xtramedullary hematopoiesis in the liver and splenomegaly.

7 ] > 100 x 10(9)/L), as well as resolution of splenomegaly.

8 ation of RA characterized by neutropenia and splenomegaly.

9 eticulocytosis, erythropoietin abundance and splenomegaly.

10 with a bleeding tendency, myelofibrosis, and splenomegaly.

11 sponse rates were 30% for anemia and 42% for splenomegaly.

12 matic increase in splenic megakaryocytes and splenomegaly.

13 ative disease (LPD) that results in dramatic splenomegaly.

14 ating their infection and resulting in acute splenomegaly.

15 al vein was common (80%) and associated with splenomegaly.

16 atients with moderate to severe cytopenia or splenomegaly.

17 a decrease in peripheral-blood blasts and in splenomegaly.

18 imals displayed systemic lymphadenopathy and splenomegaly.

19 ttributed to hemolysis and is accompanied by splenomegaly.

20 ultimately results in cytopenias and massive splenomegaly.

21 17 population in the spleen, and ameliorated splenomegaly.

22 hite blood cells, associated with increasing splenomegaly.

23 llary hematopoiesis (myeloid metaplasia) and splenomegaly.

24 varices or ascites or low platelet count and splenomegaly.

25 such as hypoalbuminemia, bilirubinemia, and splenomegaly.

26 consequent extramedullary hematopoiesis and splenomegaly.

27 terized by thrombocytosis, neutrophilia, and splenomegaly.

28 s (group B) progressed, of whom 15 developed splenomegaly.

29 ty to trigger massive lymphoid expansion and splenomegaly; 2) the proportion of Th1 cells among infil

30 ing two of the following: (1) hepatomegaly+/-splenomegaly; (2)>6 months elevation of ALT (>1.5x upper

31 ake value [SUVmax], 6.0; range, 2.0-8.0) and splenomegaly (3.4; 1.2-11.0), with increased metabolism

32 vated interleukin 6 (57/63), hepatomegaly or splenomegaly (52/67), fever (33/64), oedema, ascites, an

33 s (100%), peripheral lymphadenopathy (100%), splenomegaly (72%), hepatomegaly (50%), and edema (28%).

34 Splenomegaly, a characteristic feature of E. muris infec

35 on, reduced plasma Na+, hyperal-dosteronism, splenomegaly, abnormal dentition, intestinal obstruction

36 urrently, Cdc42 deficiency caused anemia and splenomegaly accompanied with decreased bone marrow eryt

37 We describe a patient who had fever and splenomegaly after traveling to Peru and also had bacter

38 at C. burnetii infection induced more-severe splenomegaly and a higher bacterial burden in the spleen

39 developed a myelofibrosis associated with a splenomegaly and a marked osteosclerosis.

40 ls develop a myeloproliferative disease with splenomegaly and aberrant myelopoiesis.

41 t the mutated kinase indicate a reduction in splenomegaly and alleviation of night sweats, fatigue, a

42 expatriate patient who presented with acute splenomegaly and anemia 3 years after visiting Ecuador.

43 17F(+) MPN, oral INCB018424 markedly reduced splenomegaly and circulating levels of inflammatory cyto

44 oreductive drugs such as hydroxyurea for the splenomegaly and constitutional symptoms, and splenectom

45 is the current best available therapy for MF splenomegaly and constitutional symptoms.

46 ciated with marked and durable reductions in splenomegaly and disease-related symptoms, improvements

47 llenged BCG-immune mice developed a striking splenomegaly and elevated CD4 and CD8 T-cell responses b

48 hus, 4- to 6-week-old IRP1(-/-) mice exhibit splenomegaly and extramedullary hematopoiesis, which is

49 A 14-year-old boy presented with splenomegaly and hemolysis.

50 d of malaria is increased by the presence of splenomegaly and hepatomegaly but individual findings ar

51 showed a delayed onset of leukemia, reduced splenomegaly and hepatomegaly, and a longer survival tha

52 splay a lupus-like autoimmune phenotype with splenomegaly and high autoantibodies titers.

53 meaningful benefits, particularly decreased splenomegaly and improvement in constitutional symptoms,

54 ost-ET MF achieved significant reductions in splenomegaly and improvements in symptoms with ruxolitin

55 alleviating the symptomatic burden, reducing splenomegaly and improving quality of life in patients w

56 phase 3 studies to be effective in reducing splenomegaly and improving symptoms in myelofibrosis pat

57 o3 causes a myeloproliferative syndrome with splenomegaly and increased hematopoietic progenitors (HP

58 ar of age, Lpla2-/- mice demonstrated marked splenomegaly and increased lung surfactant phospholipid

59 eletion using MxCre or Scl-CreER(T) leads to splenomegaly and leukemia formation, which occurs after

60 proliferation, extramedullary hematopoiesis, splenomegaly and leukemic progression.

61 od and, at 6 months of age, exhibited marked splenomegaly and leukophilia.

62 ead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of en

63 s, produced autoantibodies, exhibited marked splenomegaly and lymphadenopathy, and elevated serum IL-

64 nt lyn(-/-)IL-10(-/-) mice manifested severe splenomegaly and lymphadenopathy, dramatically increased

65 efore disease initiation resulted in reduced splenomegaly and lymphadenopathy, impaired expansion and

66 increased T-independent antibody responses, splenomegaly and lymphadenopathy.

67 Map3k7(DeltaM/DeltaM)) led to development of splenomegaly and lymphomegaly associated with neutrophil

68 or that has demonstrated rapid reductions in splenomegaly and marked improvement in disease-related s

69 Diseased rats showed splenomegaly and massive enlargement of the mesenteric l

70 asing the burden of symptoms associated with splenomegaly and MF-related constitutional symptoms, it

71 while surviving mice had even more prominent splenomegaly and normal-appearing lungs.

72 ration of minihepcidin significantly reduces splenomegaly and normalizes hematocrit levels.

73 Female Prkca(-/-) mice develop splenomegaly and reduced marrow GBA1 expression reminisc

74 or activity to gossypol in terms of reducing splenomegaly and reducing B-cell counts in spleens of Bc

75 247), which, contrastingly, produced greater splenomegaly and reticulocytosis.

76 Splenomegaly and spleen toxicity in Nrf2(-/-) mice raise

77 d significantly reduces Nras(G12D/+)-induced splenomegaly and spontaneous colony formation and prolon

78 We observed severe splenomegaly and structural destruction in the spleen wi

79 e I (NMI), SCID mice developed pneumonia and splenomegaly and succumbed to infection, whereas wild-ty

80 Fedratinib therapy significantly reduced splenomegaly and symptom burden in patients with MF.

81 The splenomegaly and symptom reductions achieved with ruxoli

82 xolitinib produced significant reductions in splenomegaly and symptomatic burden and improved surviva

83 cular those with myelofibrosis and extensive splenomegaly and symptomatic burden, after the introduct

84 apy at controlling haematocrit and improving splenomegaly and symptoms in patients with polycythaemia

85 We found that responses in splenomegaly and symptoms, as well as the risk of develo

86 K2 inhibitor therapy improves MPN-associated splenomegaly and systemic symptoms but does not signific

87 ough clinically tested JAK inhibitors reduce splenomegaly and systemic symptoms, molecular responses

88 Splenomegaly and the increased neoplastic stem cell pool

89 MHV68 lytic replication, including increased splenomegaly and the presence of infectious virus in the

90 All patients had baseline splenomegaly and thrombocytopenia (mostly moderate or se

91 orrected immunological abnormalities such as splenomegaly and thymic atrophy in Apc(Min/+) mice.

92 range, reduced reticulocytosis, reversal of splenomegaly and up to 7% beta-globin gene correction in

93 , mice infected with FMLV-IL-1beta exhibited splenomegaly and viral loads 300-fold higher than those

94 h male and female IL-3 KO mice had increased splenomegaly and were more anemic than corresponding WT

95 USP21-deficient mice spontaneously developed splenomegaly and were more resistant to VSV infection wi

96 hematopoietic cells developed virus-induced splenomegaly and were more resistant to VSV infection.

97 response rates were 22% for anemia, 33% for splenomegaly, and 50% for thrombocytopenia.

98 t for foxp3a displayed excess T lymphocytes, splenomegaly, and a profound inflammatory phenotype that

99 lary hematopoiesis, circulating CD34+ cells, splenomegaly, and a propensity to evolve to acute myeloi

100 ation of ineffective erythropoiesis (IE) and splenomegaly, and an increase in total hemoglobin levels

101 , reversal of ineffective erythropoiesis and splenomegaly, and an increase in total hemoglobin levels

102 racterized by myeloid-dominant leukocytosis, splenomegaly, and an increase of hematopoietic stem/prog

103 evidenced by the lack of glomerulonephritis, splenomegaly, and antinuclear autoantibody production se

104 gnificant decrease in DNTs, lymphadenopathy, splenomegaly, and autoantibodies after only 4 weeks when

105 ical manifestations include lymphadenopathy, splenomegaly, and autoimmune cytopenias.

106 ome of chronic nonmalignant lymphadenopathy, splenomegaly, and autoimmunity associated with a mutatio

107 omplications of IE, including iron overload, splenomegaly, and bone pathology, while reducing erythro

108 cued chronic activation of conventional DCs, splenomegaly, and colitis.

109 manifestations, including pancreatic cysts, splenomegaly, and common bile duct dilation.

110 a myeloid malignancy associated with anemia, splenomegaly, and constitutional symptoms.

111 blast cells in the peripheral blood, reduced splenomegaly, and corrected a pathologically low myeloid

112 ffected birds were inclusion body hepatitis, splenomegaly, and enteritis.

113 autoantibodies, reduced lymphadenopathy and splenomegaly, and extended survival.

114 sia in the bone marrow and spleen, displayed splenomegaly, and had reduced levels of plasma erythropo

115 ever, otitis media, pneumonia, hepatomegaly, splenomegaly, and hospitalization in HIV-infected infant

116 years) with polycythaemia vera, no palpable splenomegaly, and hydroxyurea resistance or intolerance

117 including leukocytosis, reduced hematocrit, splenomegaly, and increased bone marrow reticulin.

118 emia and reduces ineffective erythropoiesis, splenomegaly, and iron loading.

119 for disease complications, including anemia, splenomegaly, and leukemic transformation.

120 st completely abrogates cellular expansions, splenomegaly, and liver inflammation associated with ant

121 acterized by dermatitis, liver inflammation, splenomegaly, and loss of Peyer's patches.

122 ized by cytopenias, constitutional symptoms, splenomegaly, and marrow histopathological abnormalities

123 bited reduced thrombocythemia, neutrophilia, splenomegaly, and neoplastic stem cell pool.

124 rder characterized by macrothrombocytopenia, splenomegaly, and paucity of alpha-granules in megakaryo

125 ll formation, surfactant lipid accumulation, splenomegaly, and phospholipidosis in mice.

126 on in mice leads to multiorgan inflammation, splenomegaly, and premature death.

127 characterized by leukocytosis, monocytosis, splenomegaly, and progressive anemia.

128 strating markedly elevated leukocyte counts, splenomegaly, and reticulin fibrosis compared with C57Bl

129 a, extramedullary hematopoiesis resulting in splenomegaly, and reticulin fibrosis in the bone marrow.

130 hil CD18 silencing resulted in neutrophilia, splenomegaly, and significant defects in neutrophil traf

131 0 decreases leukemic allelic burden, reduces splenomegaly, and significantly increases survival of Ja

132 frequency of thromboembolic events, palpable splenomegaly, and splenectomy; chemotherapy exposure; le

133 hal phenotype characterized by pancytopenia, splenomegaly, and the accumulation of monocytoid cells.

134 in T and B cell activation, lymphadenopathy, splenomegaly, and the production of IgG antichromatin an

135 kopenia, higher blast count, symptoms, large splenomegaly, and unfavorable karyotype.

136 rombocytopenia; HGF, MIG, IL-1RA, and marked splenomegaly; and IL-1RA, IL-2R, IP-10, MIP-1beta, and J

137 is involved in inhibiting the development of splenomegaly, anemia, and erythropoiesis.

138 es), strong progenitor and LKS mobilization, splenomegaly, anemia, and loss of lymphoid lineages.

139 ivary glands pathology, lymphadenopathy, and splenomegaly are dramatically suppressed in CSF-1-defici

140 pleural effusion, ascites, hepatomegaly, and splenomegaly are highly suggestive of dengue fever in cl

141 Reductions in lymphadenopathy and splenomegaly are seen within weeks and are frequently ac

142 Interestingly, EPCR(R84A/R84A) mice develop splenomegaly as a result of bone marrow (BM) failure.

143 c twofold decrease in mSin3A protein develop splenomegaly as well as kidney disease indicative of a d

144 ldhood with nonmalignant lymphadenopathy and splenomegaly associated with a characteristic expansion

145 is results in chronic lymphadenopathy and/or splenomegaly associated with autoimmune phenomena.

146 The Irf5(-/-) mice develop an age-related splenomegaly, associated with a dramatic accumulation of

147 These symptoms were preceded by splenomegaly at an early age, which was associated with

148 who presented with chronic lymphadenopathy, splenomegaly, autoantibodies, elevated immunoglobulins a

149 normalities characteristic of SLE, including splenomegaly, autoantibody production, frequencies of ma

150 inactive mutants of IRAK1 or IRAK4 prevented splenomegaly, autoimmunity, and liver and kidney inflamm

151 Penumbra(-/-) mice develop massive splenomegaly, basophilic macrocytic red blood cells, and

152 umococcal infection can, under conditions of splenomegaly, be readily compensated for by activated re

153 nonleukemic hCG-PR x PU.1+/- mice developed splenomegaly because of the abnormal expansion of myeloi

154 , at least 2 prior pregnancies, male gender, splenomegaly, bleeding, fever, infection, disseminated i

155 ontributing to extramedullary hematopoiesis, splenomegaly, BM failure, and decreased levels of circul

156 hibitors improve constitutional symptoms and splenomegaly but do not significantly reduce mutant alle

157 lutary effect on constitutional symptoms and splenomegaly but have yet to produce histopathologic or

158 mice exhibited marked reductions in AEAs and splenomegaly but not in anti-nuclear Abs.

159 one or with fusion vaccine induced transient splenomegaly but without apparent toxicity.

160 nias, occurrence of autoimmune diseases, and splenomegaly, but was undetectable in control cases with

161 Splenectomy for massive splenomegaly can be performed safely and offers durable

162 te pathology induced by FV, which was severe splenomegaly caused by erythroproliferation, the immunos

163 e marrow dysfunction that was accompanied by splenomegaly caused by extramedullary hematopoiesis.

164 d a more complete spectrum of HLH, including splenomegaly, coagulopathy, and decreased NK cell cytoto

165 6-treated animals had complete resolution of splenomegaly, compared with none of the imatinib mesylat

166 It is notably characterized by splenomegaly, complex skeletal involvement, ischemic eve

167 myeloproliferative neoplasm characterised by splenomegaly, cytopenias, bone marrow fibrosis, and debi

168 litating disease manifestations (eg, massive splenomegaly, cytopenias, constitutional symptoms, and t

169 liferative neoplasm characterized by anemia, splenomegaly, debilitating constitutional symptoms, and

170 ematocrit, white blood cells, platelets, and splenomegaly, deletion of Stat5 in the Jak2V617F knockin

171 The study found that thrombocytopenia, splenomegaly, didanosine use, elevated aminotransferases

172 rast to residual lymphadenopathy, persisting splenomegaly does not impact outcome in patients with MR

173 These changes were accompanied by splenomegaly due to lymphoid hyperplasia and increased h

174 ound that systemic infection induced anemia, splenomegaly, elevated erythropoietin (EPO) levels, and

175 typical clinical features of HLH, including splenomegaly, elevated serum IFNgamma, and anemia.

176 provoke disease, while its absence produced splenomegaly, enlarged lymph nodes, and mild social inte

177 ozygous FOG-1(R3K5A) mice were found to have splenomegaly, extramedullary erythropoiesis, granulocyto

178 pendent autoimmune manifestations, including splenomegaly, extramedullary hematopoiesis, and autoanti

179 These mice develop severe neutrophilia, splenomegaly, extramedullary hematopoiesis, decreased bo

180 patients presented with lymphadenopathy and splenomegaly; fever, hepatitis, and pancytopenia were co

181 The phenotype included splenomegaly, fibrotic and hypercellular bone marrow, ex

182 Enteropathy, autoimmunity, granulomas, and splenomegaly formed a set of interrelated features, wher

183 characterized with a female predominance, a splenomegaly, gain of chromosome 3, and CD27 expression.

184 Other main inclusion criteria were palpable splenomegaly (>/=5 cm below the left costal margin), Eas

185 Splenectomy for massive splenomegaly (>1500 g) provides palliation but is associ

186 isease was observed until platelet count and splenomegaly had improved.

187 MRD-negative PR who presented with residual splenomegaly had only a similar PFS (63 months) compared

188 Patients with >/= 50% reduction in splenomegaly had significantly prolonged survival versus

189 BB agonists given to unimmunized mice induce splenomegaly, hepatitis, and other immune system anomali

190 The Id3(-/-) mice with lymphoma showed splenomegaly, hepatomegaly, and lymphadenopathy with inv

191 mia: leukocytosis with maturing neutrophils, splenomegaly, hepatomegaly, and myeloid infiltration int

192 On gross examination these mice present with splenomegaly, hepatomegaly, and severe lymphadenopathy.

193 a associated pathological changes, including splenomegaly, hepatomegaly, or granulomatous disease.

194 cells began to hyperproliferate and induced splenomegaly; however, isotype switching and autoantibod

195 lls, which culminates in lymphadenopathy and splenomegaly, hypergammaglobulinemia, and autoantibodies

196 cted B6.PD-1(-/-) mice developed more severe splenomegaly, hypergammaglobulinemia, and immunodeficien

197 LE)-like disease that included leukocytosis, splenomegaly, hypergammaglobulinemia, antinuclear autoan

198 the murine retroviral isolate LP-BM5 induces splenomegaly, hypergammaglobulinemia, profound B- and T-

199 haracterized by early-onset lymphadenopathy, splenomegaly, immune cytopenias, and an increased risk f

200 Hepatomegaly was found in 34% and splenomegaly in 56% of patients.

201 ele (CRTC2/3m mice) develop neutrophilia and splenomegaly in adulthood due to the up-regulation of gr

202 y, these results reveal that the age-related splenomegaly in Irf5(-/-) mice is associated with an acc

203 peripheral blood counts and markedly reduced splenomegaly in Jak2V617F knock-in mice compared with pl

204 ortant role in the management of symptomatic splenomegaly in MF patients.

205 The safety was revealed by the absence of splenomegaly in mice that were inoculated with the mutan

206 monella infection commonly induces prolonged splenomegaly in murine or human hosts.

207 for treatment of constitutional symptoms and splenomegaly in myelofibrosis, but the effect of these a

208 igher in VAD pigs in spleen (coincident with splenomegaly in other VAD animals) prechallenge and inte

209 exception of a higher prevalence of palpable splenomegaly in patients with fibrosis (P < .01).

210 electively improves liver pathology, but not splenomegaly in the mice.

211 therapeutic algorithm of RA, neutropenia and splenomegaly in the spectrum of LGL leukemia and Felty's

212 vo) significantly decreased tumor weight and splenomegaly in tumor-bearing mice with reduced accumula

213 ed to increased WBC counts, monocytosis, and splenomegaly in WT recipient mice.

214 assigned phlebotomy-dependent patients with splenomegaly, in a 1:1 ratio, to receive ruxolitinib (11

215 ciated with increasing portal vein diameter, splenomegaly, increased serum immunoglobulin G level, an

216 d survival and reduced serum autoantibodies, splenomegaly, intrarenal leukocyte trafficking, and end

217 lacrimal glands, lungs, lymphadenopathy, and splenomegaly) is equivalent in ICOS-/- MRL-Faslpr and WT

218 reduced white blood cell count, blast cells, splenomegaly, lactate dehydrogenase levels, and bone pai

219 apid objective response (>/=50% reduction of splenomegaly) lasting for 12 months or more, and this th

220 els, including extra-corporeal loss of iron, splenomegaly leading to red blood cell sequestration, au

221 myeloproliferative disease, characterized by splenomegaly, leukocytosis, and myeloid hypercellularity

222 The APL disease was characterized by splenomegaly, leukocytosis, extramedullary hematopoiesis

223 kly administration of the naked mAbs reduced splenomegaly, liver tumor spots, and tumor burden in BLC

224 ed infants with P/EP CMV, symptoms including splenomegaly, lymphadenopathy, and hepatomegaly were ass

225 including loss of marginal zone macrophages, splenomegaly, lymphadenopathy, autoantibodies (including

226 its measures of B-cell hyperactivity such as splenomegaly, lymphadenopathy, elevated serum IL-6, elev

227 These included splenomegaly, lymphadenopathy, hepatomegaly, multifocal

228 BM5 retrovirus-infected C57BL/6 mice develop splenomegaly, lymphadenopathy, hypergammaglobulinemia, a

229 eport here that Rabgef1-/- mice also develop splenomegaly, lymphadenopathy, myeloid hyperplasia, and

230 phages, and dendritic cells and did not have splenomegaly, lymphadenopathy, or inflammation in multip

231 layed a dramatic phenotype, characterized by splenomegaly, lymphadenopathy, thymic atrophy, and multi

232 with CEP-33779 extended survival and reduced splenomegaly/lymphomegaly.

233 As in GPS, Nbeal2(-/-) mice exhibit splenomegaly, macrothrombocytopenia, and a deficiency of

234 Future care of MF patients, including splenomegaly management, will continue to require the he

235 duction was dependent on three subloci, with splenomegaly mapping to two of the subloci and expansion

236 The phenotype was characterized by splenomegaly, megakaryocytic hyperplasia, and marked thr

237 ological syndrome akin to typhoid fever with splenomegaly, microcytic anemia, extramedullary erythrop

238 oked a clonal myelomonocytic cell expansion, splenomegaly, multi-organ infiltration, genomic instabil

239 res of human plasma cell-type MCD, including splenomegaly, multifocal lymphadenopathy, hypergammaglob

240 and childhood onset chronic lymphadenopathy, splenomegaly, multilineage cytopenias, and an increased

241 Autopsy of sick mice demonstrated splenomegaly, myeloid bone marrow hyperplasia, and extra

242 deletion of Pten in mice lacking G-CSF, the splenomegaly, myeloproliferative disease, and splenic HS

243 and laboratory manifestations include fever, splenomegaly, neurologic dysfunction, coagulopathy, live

244 optive transfer of CRTC2/3m BM conferred the splenomegaly/neutrophilia phenotype in WT recipients.

245 The reduced splenomegaly observed following infection with SL1344 tr

246 roved erythroid differentiation, and reduced splenomegaly of iron-deficient Hri(-/-) and eAA mice.

247 therapeutic dose of anti-GITR did not induce splenomegaly or increase serum alanine transaminase.

248 botomy) with complete resolution of palpable splenomegaly or symptoms in the absence of a thrombotic

249 achieved before the patients develop massive splenomegaly or undergo splenectomy.

250 o significant difference in lymphadenopathy, splenomegaly, or anti-chromatin autoantibody titer betwe

251 or axillary adenopathy, palatine petechiae, splenomegaly, or atypical lymphocytosis is associated wi

252 erial or venous thrombosis, marrow fibrosis, splenomegaly, or transformation to acute leukemia, albei

253 abnormal liver echogenicity (P < 0.001); and splenomegaly (P = 0.001) at ultrasound.

254 ore portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platele

255 09 to July 2012 among eligible patients with splenomegaly plus thrombocytopenia and/or anemia.

256 erative neoplasm associated with cytopenias, splenomegaly, poor quality of life, and shortened surviv

257 Eligible patients had clinical splenomegaly poorly controlled with standard therapies o

258 younger adults with normal cytogenetics AML, splenomegaly predicts a lower CR rate, and the postremis

259 d blood cells, leukocytosis, thrombocytosis, splenomegaly, reduced serum erythropoietin (Epo) levels

260 In particular, management of symptomatic splenomegaly remains one of the most perplexing aspects

261 expansion of leukocytes, the actual cause of splenomegaly remains unclear.

262 or activity included > or = 50% reduction in splenomegaly (seven of 17 patients; 41%), complete disap

263 tive mononuclear cells causing hepatomegaly, splenomegaly, severe anemia, and death.

264 taIEC) mice had low-grade inflammation (mild splenomegaly, shortened colons, and increased fecal leve

265 .95; positive LR, 5.3 [95% CI, 2.1-13]), and splenomegaly (specificity range, 0.71-0.99; positive LR

266 om humans with sickle cell disease in having splenomegaly, splenic hematopoiesis, more severe hepatic

267 Splenomegaly started early in life; 60% of children youn

268 f limited diagnostic utility but presence of splenomegaly (summary likelihood ratio [LR], 3.3; 95% co

269 resence of fever (LR, 5.1; 95% CI, 4.9-5.3), splenomegaly (summary LR, 6.5; 95% CI, 3.9-11.0), hyperb

270 n shortening, colon histological damage, and splenomegaly than did wild-type (WT) mice.

271 arginal zone macrophages associated with the splenomegaly that follows a variety of viral and protozo

272 y, including anti-nuclear autoantibodies and splenomegaly, that are not found in Unc93b1(3d/3d) DKO m

273 a-subunit of the type 1 IFNR did not prevent splenomegaly, the appearance of high serum levels of aut

274 th receptor function causes lymphadenomegaly/splenomegaly, the expansion of T-cell receptor alphabeta

275 munized mice had many gross lung lesions and splenomegaly; the counts were 5.97 +/- 0.14 and 3.54 +/-

276 e rheumatoid arthritis (RA), neutropenia and splenomegaly, thereby resembling the manifestations obse

277 e to A. phagocytophilum infection and showed splenomegaly, thrombocytopenia, and monocytopenia.

278 linked to survival, glomerulonephritis, and splenomegaly, to investigate its role in AIHA.

279 ice exhibited marked facial edema and marked splenomegaly upon gross examination, while the intraderm

280 diet animal model, a significant increase in splenomegaly was observed, but no significant change in

281 Splenectomy for massive splenomegaly was performed most commonly for non-Hodgkin

282 Splenomegaly was present in all groups, but only mono-in

283 Ascites and splenomegaly were independent predictors for the presenc

284 ative MRI relaxation times as well as severe splenomegaly were observed in the heart, liver and splee

285 Lymphadenopathy and splenomegaly, which are characteristic traits of the MRL

286 in patients with polycythaemia vera without splenomegaly who need second-line therapy.

287 oms in patients with polycythaemia vera with splenomegaly who were inadequately controlled with hydro

288 Tumor progression induced splenomegaly with a dramatic increase (22.1%) in CD11b(+

289 At this stage mice exhibited severe splenomegaly with abnormal B-cell-derived white pulp exp

290 ted growth retardation, premature death, and splenomegaly with altered architecture and extramedullar

291 erized by elevated erythropoietin levels and splenomegaly with excess erythropoiesis.

292 We report that W(sh) animals exhibit splenomegaly with expanded myeloid and megakaryocyte pop

293 blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis and eryt

294 Ultrasound demonstrated hepato-splenomegaly with multiple granulomas as well as ascites

295 utropenia, bone marrow hypercellularity, and splenomegaly with myeloid infiltration.

296 ction in SCD/NRF2(-/-) mice produced greater splenomegaly with red pulp expansion and obscured archit

297 Nix null mice exhibited massive splenomegaly, with splenic and bone marrow erythroblasto

298 in autoimmune disease, lymphadenopathy, and splenomegaly within 1 to 3 months of starting sirolimus.

299 ations is the simplest approach for reducing splenomegaly, yet achieving symptomatic response without

300 esults in a rapid reduction of the degree of splenomegaly, yet the mechanism underlying this effect r