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1 mice exhibited hemophagocytosis, anemia, and splenomegaly.
2 consequent extramedullary hematopoiesis and splenomegaly.
3 terized by thrombocytosis, neutrophilia, and splenomegaly.
4 icantly higher hemoglobin levels and reduced splenomegaly.
5 s (group B) progressed, of whom 15 developed splenomegaly.
6 echogenicity on ultrasonography, and 65% had splenomegaly.
7 less than or equal to 174,000 per mm(3) and splenomegaly.
8 ditionally presented anemia, leukopenia, and splenomegaly.
9 f the Hopx(-/-) mice developed cytopenia and splenomegaly.
10 ultrasound imaging showed the development of splenomegaly.
11 n leukemia cell counts, lymphadenopathy, and splenomegaly.
12 xtramedullary hematopoiesis in the liver and splenomegaly.
13 ] > 100 x 10(9)/L), as well as resolution of splenomegaly.
14 ation of RA characterized by neutropenia and splenomegaly.
15 e models showed dermatitis, blepharitis, and splenomegaly.
16 eticulocytosis, erythropoietin abundance and splenomegaly.
17 with a bleeding tendency, myelofibrosis, and splenomegaly.
18 sponse rates were 30% for anemia and 42% for splenomegaly.
19 matic increase in splenic megakaryocytes and splenomegaly.
20 ative disease (LPD) that results in dramatic splenomegaly.
21 ating their infection and resulting in acute splenomegaly.
22 6 release, extramedullary hematopoiesis, and splenomegaly.
23 ultimately results in cytopenias and massive splenomegaly.
24 17 population in the spleen, and ameliorated splenomegaly.
25 hite blood cells, associated with increasing splenomegaly.
26 llary hematopoiesis (myeloid metaplasia) and splenomegaly.
27 varices or ascites or low platelet count and splenomegaly.
28 such as hypoalbuminemia, bilirubinemia, and 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%).
35 urrently, Cdc42 deficiency caused anemia and splenomegaly accompanied with decreased bone marrow eryt
37 mice exhibited reduced bacterial burden and splenomegaly, along with distinct effector T-cell and mo
38 at C. burnetii infection induced more-severe splenomegaly and a higher bacterial burden in the spleen
41 demonstrate that anti-CD47 (MIAP410) causes splenomegaly and activation of DCs and T cells, without
42 t the mutated kinase indicate a reduction in splenomegaly and alleviation of night sweats, fatigue, a
43 expatriate patient who presented with acute splenomegaly and anemia 3 years after visiting Ecuador.
46 17F(+) MPN, oral INCB018424 markedly reduced splenomegaly and circulating levels of inflammatory cyto
47 oreductive drugs such as hydroxyurea for the splenomegaly and constitutional symptoms, and splenectom
49 ciated with marked and durable reductions in splenomegaly and disease-related symptoms, improvements
50 llenged BCG-immune mice developed a striking splenomegaly and elevated CD4 and CD8 T-cell responses b
51 hus, 4- to 6-week-old IRP1(-/-) mice exhibit splenomegaly and extramedullary hematopoiesis, which is
54 d of malaria is increased by the presence of splenomegaly and hepatomegaly but individual findings ar
55 showed a delayed onset of leukemia, reduced splenomegaly and hepatomegaly, and a longer survival tha
57 meaningful benefits, particularly decreased splenomegaly and improvement in constitutional symptoms,
58 ost-ET MF achieved significant reductions in splenomegaly and improvements in symptoms with ruxolitin
59 alleviating the symptomatic burden, reducing splenomegaly and improving quality of life in patients w
60 phase 3 studies to be effective in reducing splenomegaly and improving symptoms in myelofibrosis pat
61 o3 causes a myeloproliferative syndrome with splenomegaly and increased hematopoietic progenitors (HP
63 eletion using MxCre or Scl-CreER(T) leads to splenomegaly and leukemia formation, which occurs after
66 ead, C9orf72 null mice developed progressive splenomegaly and lymphadenopathy with accumulation of en
67 nt lyn(-/-)IL-10(-/-) mice manifested severe splenomegaly and lymphadenopathy, dramatically increased
68 efore disease initiation resulted in reduced splenomegaly and lymphadenopathy, impaired expansion and
70 Map3k7(DeltaM/DeltaM)) led to development of splenomegaly and lymphomegaly associated with neutrophil
71 or that has demonstrated rapid reductions in splenomegaly and marked improvement in disease-related s
72 asing the burden of symptoms associated with splenomegaly and MF-related constitutional symptoms, it
73 d for at least 5 weeks, displaying increased splenomegaly and more severe splenitis than infected mic
77 or activity to gossypol in terms of reducing splenomegaly and reducing B-cell counts in spleens of Bc
81 d significantly reduces Nras(G12D/+)-induced splenomegaly and spontaneous colony formation and prolon
83 e I (NMI), SCID mice developed pneumonia and splenomegaly and succumbed to infection, whereas wild-ty
86 xolitinib produced significant reductions in splenomegaly and symptomatic burden and improved surviva
87 cular those with myelofibrosis and extensive splenomegaly and symptomatic burden, after the introduct
88 apy at controlling haematocrit and improving splenomegaly and symptoms in patients with polycythaemia
89 fter the operation portal hypertension, with splenomegaly and symptoms of the liver cirrhosis occurre
91 K2 inhibitor therapy improves MPN-associated splenomegaly and systemic symptoms but does not signific
92 ough clinically tested JAK inhibitors reduce splenomegaly and systemic symptoms, molecular responses
93 otective immunity that significantly reduces splenomegaly and the bacterial burden in spleen and lung
95 MHV68 lytic replication, including increased splenomegaly and the presence of infectious virus in the
98 range, reduced reticulocytosis, reversal of splenomegaly and up to 7% beta-globin gene correction in
99 , mice infected with FMLV-IL-1beta exhibited splenomegaly and viral loads 300-fold higher than those
100 h male and female IL-3 KO mice had increased splenomegaly and were more anemic than corresponding WT
101 USP21-deficient mice spontaneously developed splenomegaly and were more resistant to VSV infection wi
102 hematopoietic cells developed virus-induced splenomegaly and were more resistant to VSV infection.
103 t for foxp3a displayed excess T lymphocytes, splenomegaly, and a profound inflammatory phenotype that
104 lary hematopoiesis, circulating CD34+ cells, splenomegaly, and a propensity to evolve to acute myeloi
105 ation of ineffective erythropoiesis (IE) and splenomegaly, and an increase in total hemoglobin levels
106 , reversal of ineffective erythropoiesis and splenomegaly, and an increase in total hemoglobin levels
107 racterized by myeloid-dominant leukocytosis, splenomegaly, and an increase of hematopoietic stem/prog
109 ome of chronic nonmalignant lymphadenopathy, splenomegaly, and autoimmunity associated with a mutatio
111 omplications of IE, including iron overload, splenomegaly, and bone pathology, while reducing erythro
115 blast cells in the peripheral blood, reduced splenomegaly, and corrected a pathologically low myeloid
116 Decreased body temperature, weight loss, splenomegaly, and deformation of the tails were observed
117 deficiency (hypogammaglobulinemia [low IgA], splenomegaly, and diminished immunization responses).
118 megakaryocyte emperipolesis of neutrophils, splenomegaly, and elevated serum vitamin B12 levels.
120 sia in the bone marrow and spleen, displayed splenomegaly, and had reduced levels of plasma erythropo
121 ever, otitis media, pneumonia, hepatomegaly, splenomegaly, and hospitalization in HIV-infected infant
122 years) with polycythaemia vera, no palpable splenomegaly, and hydroxyurea resistance or intolerance
125 st completely abrogates cellular expansions, splenomegaly, and liver inflammation associated with ant
127 ized by cytopenias, constitutional symptoms, splenomegaly, and marrow histopathological abnormalities
129 rder characterized by macrothrombocytopenia, splenomegaly, and paucity of alpha-granules in megakaryo
131 IL-33trap inhibits eosinophil infiltration, splenomegaly, and production of signature cytokines in s
133 hil CD18 silencing resulted in neutrophilia, splenomegaly, and significant defects in neutrophil traf
134 0 decreases leukemic allelic burden, reduces splenomegaly, and significantly increases survival of Ja
135 frequency of thromboembolic events, palpable splenomegaly, and splenectomy; chemotherapy exposure; le
137 hal phenotype characterized by pancytopenia, splenomegaly, and the accumulation of monocytoid cells.
139 rombocytopenia; HGF, MIG, IL-1RA, and marked splenomegaly; and IL-1RA, IL-2R, IP-10, MIP-1beta, and J
141 es), strong progenitor and LKS mobilization, splenomegaly, anemia, and loss of lymphoid lineages.
142 pleural effusion, ascites, hepatomegaly, and splenomegaly are highly suggestive of dengue fever in cl
144 Interestingly, EPCR(R84A/R84A) mice develop splenomegaly as a result of bone marrow (BM) failure.
145 nternational Normal Ratio levels were lower, splenomegaly, ascites, and cirrhosis were more common (a
146 ldhood with nonmalignant lymphadenopathy and splenomegaly associated with a characteristic expansion
148 The Irf5(-/-) mice develop an age-related splenomegaly, associated with a dramatic accumulation of
150 who presented with chronic lymphadenopathy, splenomegaly, autoantibodies, elevated immunoglobulins a
151 normalities characteristic of SLE, including splenomegaly, autoantibody production, frequencies of ma
152 inactive mutants of IRAK1 or IRAK4 prevented splenomegaly, autoimmunity, and liver and kidney inflamm
153 umococcal infection can, under conditions of splenomegaly, be readily compensated for by activated re
154 ontributing to extramedullary hematopoiesis, splenomegaly, BM failure, and decreased levels of circul
155 hibitors improve constitutional symptoms and splenomegaly but do not significantly reduce mutant alle
156 lutary effect on constitutional symptoms and splenomegaly but have yet to produce histopathologic or
159 nias, occurrence of autoimmune diseases, and splenomegaly, but was undetectable in control cases with
162 d a more complete spectrum of HLH, including splenomegaly, coagulopathy, and decreased NK cell cytoto
164 myeloproliferative neoplasm characterised by splenomegaly, cytopenias, bone marrow fibrosis, and debi
165 litating disease manifestations (eg, massive splenomegaly, cytopenias, constitutional symptoms, and t
166 liferative neoplasm characterized by anemia, splenomegaly, debilitating constitutional symptoms, and
167 ematocrit, white blood cells, platelets, and splenomegaly, deletion of Stat5 in the Jak2V617F knockin
169 rast to residual lymphadenopathy, persisting splenomegaly does not impact outcome in patients with MR
171 ound that systemic infection induced anemia, splenomegaly, elevated erythropoietin (EPO) levels, and
173 provoke disease, while its absence produced splenomegaly, enlarged lymph nodes, and mild social inte
174 ozygous FOG-1(R3K5A) mice were found to have splenomegaly, extramedullary erythropoiesis, granulocyto
175 pendent autoimmune manifestations, including splenomegaly, extramedullary hematopoiesis, and autoanti
176 These mice develop severe neutrophilia, splenomegaly, extramedullary hematopoiesis, decreased bo
177 patients presented with lymphadenopathy and splenomegaly; fever, hepatitis, and pancytopenia were co
179 Enteropathy, autoimmunity, granulomas, and splenomegaly formed a set of interrelated features, wher
180 characterized with a female predominance, a splenomegaly, gain of chromosome 3, and CD27 expression.
181 lytic anemia, or neutropenia, in addition to splenomegaly, generalized or worrisome lymphadenopathy,
182 Other main inclusion criteria were palpable splenomegaly (>/=5 cm below the left costal margin), Eas
185 MRD-negative PR who presented with residual splenomegaly had only a similar PFS (63 months) compared
187 BB agonists given to unimmunized mice induce splenomegaly, hepatitis, and other immune system anomali
189 mia: leukocytosis with maturing neutrophils, splenomegaly, hepatomegaly, and myeloid infiltration int
190 a associated pathological changes, including splenomegaly, hepatomegaly, or granulomatous disease.
191 cells began to hyperproliferate and induced splenomegaly; however, isotype switching and autoantibod
192 cted B6.PD-1(-/-) mice developed more severe splenomegaly, hypergammaglobulinemia, and immunodeficien
193 LE)-like disease that included leukocytosis, splenomegaly, hypergammaglobulinemia, antinuclear autoan
194 the murine retroviral isolate LP-BM5 induces splenomegaly, hypergammaglobulinemia, profound B- and T-
195 haracterized by early-onset lymphadenopathy, splenomegaly, immune cytopenias, and an increased risk f
197 ele (CRTC2/3m mice) develop neutrophilia and splenomegaly in adulthood due to the up-regulation of gr
199 y, these results reveal that the age-related splenomegaly in Irf5(-/-) mice is associated with an acc
200 peripheral blood counts and markedly reduced splenomegaly in Jak2V617F knock-in mice compared with pl
202 The safety was revealed by the absence of splenomegaly in mice that were inoculated with the mutan
204 for treatment of constitutional symptoms and splenomegaly in myelofibrosis, but the effect of these a
205 igher in VAD pigs in spleen (coincident with splenomegaly in other VAD animals) prechallenge and inte
208 therapeutic algorithm of RA, neutropenia and splenomegaly in the spectrum of LGL leukemia and Felty's
209 vo) significantly decreased tumor weight and splenomegaly in tumor-bearing mice with reduced accumula
211 assigned phlebotomy-dependent patients with splenomegaly, in a 1:1 ratio, to receive ruxolitinib (11
212 ciated with increasing portal vein diameter, splenomegaly, increased serum immunoglobulin G level, an
214 d survival and reduced serum autoantibodies, splenomegaly, intrarenal leukocyte trafficking, and end
215 reduced white blood cell count, blast cells, splenomegaly, lactate dehydrogenase levels, and bone pai
216 apid objective response (>/=50% reduction of splenomegaly) lasting for 12 months or more, and this th
217 myeloproliferative disease, characterized by splenomegaly, leukocytosis, and myeloid hypercellularity
218 kly administration of the naked mAbs reduced splenomegaly, liver tumor spots, and tumor burden in BLC
219 ed infants with P/EP CMV, symptoms including splenomegaly, lymphadenopathy, and hepatomegaly were ass
220 including loss of marginal zone macrophages, splenomegaly, lymphadenopathy, autoantibodies (including
221 its measures of B-cell hyperactivity such as splenomegaly, lymphadenopathy, elevated serum IL-6, elev
223 eport here that Rabgef1-/- mice also develop splenomegaly, lymphadenopathy, myeloid hyperplasia, and
224 layed a dramatic phenotype, characterized by splenomegaly, lymphadenopathy, thymic atrophy, and multi
228 duction was dependent on three subloci, with splenomegaly mapping to two of the subloci and expansion
229 ological syndrome akin to typhoid fever with splenomegaly, microcytic anemia, extramedullary erythrop
230 e changes were accompanied by a reduction in splenomegaly, more organized T and B cell zones, and an
231 oked a clonal myelomonocytic cell expansion, splenomegaly, multi-organ infiltration, genomic instabil
232 res of human plasma cell-type MCD, including splenomegaly, multifocal lymphadenopathy, hypergammaglob
233 and childhood onset chronic lymphadenopathy, splenomegaly, multilineage cytopenias, and an increased
234 deletion of Pten in mice lacking G-CSF, the splenomegaly, myeloproliferative disease, and splenic HS
235 and laboratory manifestations include fever, splenomegaly, neurologic dysfunction, coagulopathy, live
236 ind spontaneous MPD that is characterized by splenomegaly, neutrophilia, and extramedullary hematopoi
237 optive transfer of CRTC2/3m BM conferred the splenomegaly/neutrophilia phenotype in WT recipients.
239 roved erythroid differentiation, and reduced splenomegaly of iron-deficient Hri(-/-) and eAA mice.
240 therapeutic dose of anti-GITR did not induce splenomegaly or increase serum alanine transaminase.
241 s, or any combination of these together with splenomegaly or myelofibrosis, and it can take years for
242 botomy) with complete resolution of palpable splenomegaly or symptoms in the absence of a thrombotic
244 o significant difference in lymphadenopathy, splenomegaly, or anti-chromatin autoantibody titer betwe
245 or axillary adenopathy, palatine petechiae, splenomegaly, or atypical lymphocytosis is associated wi
246 erial or venous thrombosis, marrow fibrosis, splenomegaly, or transformation to acute leukemia, albei
247 e developed gastric hyperplasia (P < .0001), splenomegaly (P < .0001), and increased serum antibody t
248 tations (P = .015), deletion 13q (P = .006), splenomegaly (P = .02), and thrombocytopenia (P = .004),
250 ore portosystemic collaterals (P = 0.01) and splenomegaly (P = 0.01) on ultrasound, and lower platele
252 erative neoplasm associated with cytopenias, splenomegaly, poor quality of life, and shortened surviv
254 red with that of a normal control), ascites, splenomegaly, portal hypertension (portal vein velocity,
255 d blood cells, leukocytosis, thrombocytosis, splenomegaly, reduced serum erythropoietin (Epo) levels
256 In particular, management of symptomatic splenomegaly remains one of the most perplexing aspects
259 taIEC) mice had low-grade inflammation (mild splenomegaly, shortened colons, and increased fecal leve
260 .95; positive LR, 5.3 [95% CI, 2.1-13]), and splenomegaly (specificity range, 0.71-0.99; positive LR
262 r disease symptoms such as IC generation and splenomegaly, suggesting that GN and other inflammatory
263 f limited diagnostic utility but presence of splenomegaly (summary likelihood ratio [LR], 3.3; 95% co
264 resence of fever (LR, 5.1; 95% CI, 4.9-5.3), splenomegaly (summary LR, 6.5; 95% CI, 3.9-11.0), hyperb
266 arginal zone macrophages associated with the splenomegaly that follows a variety of viral and protozo
267 y, including anti-nuclear autoantibodies and splenomegaly, that are not found in Unc93b1(3d/3d) DKO m
268 a-subunit of the type 1 IFNR did not prevent splenomegaly, the appearance of high serum levels of aut
269 th receptor function causes lymphadenomegaly/splenomegaly, the expansion of T-cell receptor alphabeta
270 e rheumatoid arthritis (RA), neutropenia and splenomegaly, thereby resembling the manifestations obse
272 in mice revealed Hippo kinase loss to induce splenomegaly, thrombocytopenia, megakaryocytic dysplasia
274 ice exhibited marked facial edema and marked splenomegaly upon gross examination, while the intraderm
275 WT mice, RdRP mice had significantly reduced splenomegaly, viral loads, and infection of multiple tar
276 diet animal model, a significant increase in splenomegaly was observed, but no significant change in
278 t from New Caledonia presenting with febrile splenomegaly,weight loss, life-threatening autoimmune ha
280 ative MRI relaxation times as well as severe splenomegaly were observed in the heart, liver and splee
282 ion, spontaneous intestinal inflammation and splenomegaly, which can be rescued by antibiotic treatme
283 riction (by targeting Tmprss6) would improve splenomegaly while preserving the beneficial effects on
285 oms in patients with polycythaemia vera with splenomegaly who were inadequately controlled with hydro
287 major reduction of bone marrow IgD(+) cells, splenomegaly with a loss of white pulp and grossly expan
289 ted growth retardation, premature death, and splenomegaly with altered architecture and extramedullar
290 ficient CAR T cells reexpanded, resulting in splenomegaly with disruption of normal splenic architect
293 blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis and eryt
296 ction in SCD/NRF2(-/-) mice produced greater splenomegaly with red pulp expansion and obscured archit
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