ライフサイエンスコーパス: aplastic

1 a daughter dome, presence of hypoplastic or aplastic A1 arteries and hypoplastic or fetal PCoA, perp

2 oplastic lungs, hypoplastic/ectopic kidneys, aplastic adrenal glands and spleen, as well as atretic t

3 c stem cell transplantation (HSCT) in severe aplastic anaemia (SAA) have improved steadily over the p

4 the placebo-controlled period: one event of aplastic anaemia and five serious adverse events related

5 ns have severe disease, with most developing aplastic anaemia by the age of 10 years.

6 Acquired aplastic anaemia can be effectively treated by allogenei

7 Similarly to other autoimmune diseases, aplastic anaemia has a varied clinical course; some pati

8 Aplastic anaemia in adults is usually acquired, but rare

9 Aplastic anaemia is a bone-marrow-failure syndrome chara

10 Aplastic anaemia is a rare haemopoietic stem-cell disord

11 Aplastic anaemia is caused by an intrinsic defect of hae

12 The pathophysiology of acquired aplastic anaemia is immune mediated in most cases; autor

13 The use of alternative donor sources for aplastic anaemia patients remains limited and problemati

14 The main cause of aplastic anaemia remains elusive.

15 rrow transplantation in patients with severe aplastic anaemia remains to be established.

16 To test the hypothesis that aplastic anaemia results from antigen-specific lymphocyt

17 The CDR3 sequence repertoire in aplastic anaemia showed much redundancy compared with he

18 Blood samples from 54 patients with aplastic anaemia were subjected to flow cytometry to def

19 ponse (no longer meeting criteria for severe aplastic anaemia).

20 udy, patients (aged </=65 years) with severe aplastic anaemia, adequate organ function, and an unrela

21 ia, three of 27 patients with constitutional aplastic anaemia, but in none of 214 normal controls (p<

22 order associated with chromosomal fragility, aplastic anaemia, congenital abnormalities and a high ri

23 rited disorder associated with a progressive aplastic anaemia, diverse congenital abnormalities and c

24 tic syndrome commonly arise in patients with aplastic anaemia, showing a pathophysiological link betw

25 indicate that, in a subset of patients with aplastic anaemia, the disorder might be associated with

26 ations in two of 17 patients with idiopathic aplastic anaemia, three of 27 patients with constitution

27 onse can be identified in many patients with aplastic anaemia, which is evidence for an underlying an

28 unosuppressive agent for treatment of severe aplastic anaemia, with a response rate similar to that w

29 not develop leukaemia spontaneously develop aplastic anaemia, with the concomitant accumulation of d

30 c" immune response in the pathophysiology of aplastic anaemia.

31 ormal adults, and can masquerade as acquired aplastic anaemia.

32 nita--an inherited syndrome characterised by aplastic anaemia.

33 r unrelated donor transplantation for severe aplastic anaemia.

34 r unrelated donor transplantation for severe aplastic anaemia.

35 ematopoietic stem cell pool confers profound aplastic anaemia.

36 ndromes including dyskeratosis congenita and aplastic anaemia.

37 tumors (3), leukemia (3), lymphoma (1), and aplastic anemia (1).

38 The distinction between acquired aplastic anemia (AA) and hypocellular myelodysplastic sy

39 Some (~ 3%) sporadic aplastic anemia (AA) and idiopathic pulmonary fibrosis c

40 Aplastic anemia (AA) and myelodysplasia (MDS) are forms

41 nisms are involved in the pathophysiology of aplastic anemia (AA) and myelodysplastic syndrome (MDS).

42 cytopenias and can cooccur in the context of aplastic anemia (AA) and myelodysplastic syndromes (MDS)

43 Acquired aplastic anemia (AA) and paroxysmal nocturnal hemoglobin

44 patients with previously untreated nonsevere aplastic anemia (AA) as defined by a neutrophil count of

45 ain (VB) T-cell receptor (TCR) repertoire in aplastic anemia (AA) at initial presentation and after i

46 in 4 of 91 patients with apparently acquired aplastic anemia (AA) but not in 276 ethnically matched c

47 We studied the role of Th17 cells in aplastic anemia (AA) by isolating Th17 cells from patien

48 Idiopathic aplastic anemia (AA) has 2 key characteristics: an autoi

49 Immune mediation of aplastic anemia (AA) has been inferred from clinical res

50 An immune pathophysiology for acquired aplastic anemia (AA) has been inferred from the responsi

51 Improved survival in aplastic anemia (AA) has shown a high incidence of late

52 Severe aplastic anemia (AA) is a bone marrow (BM) failure (BMF)

53 Aplastic anemia (AA) is a disease characterized by T-cel

54 accumulating evidence strongly suggests that aplastic anemia (AA) is a T cell-mediated autoimmune dis

55 Idiopathic aplastic anemia (AA) is an immune-mediated and serious f

56 Aplastic anemia (AA) is characterized by hypocellular ma

57 Refractory aplastic anemia (AA) is defined as a lack of response to

58 A serious complication of aplastic anemia (AA) is its evolution to clonal hematolo

59 ole of CD4(+) T cells in the pathogenesis of aplastic anemia (AA) is not well characterized.

60 We have hypothesized that in aplastic anemia (AA) the presence of antigen-specific T

61 teristics and outcome of posttransplantation aplastic anemia (AA) were determined in 12 of 1,736 pati

62 Aplastic anemia (AA), a potentially fatal disease, may b

63 in 55, 34, 43, and 5 patients with acquired aplastic anemia (AA), autoimmune uveitis, systemic lupus

64 In aplastic anemia (AA), contraction of the stem cell pool

65 in bone marrow failure syndromes, including aplastic anemia (AA), paroxysmal nocturnal hemoglobinuri

66 samples from a large number of patients with aplastic anemia (AA), paroxysmal nocturnal hemoglobinuri

67 patients with dyskeratosis congenita (DC) or aplastic anemia (AA).

68 ematologic improvement in most patients with aplastic anemia (AA).

69 its serologic split HLA-DR15 in both MDS and aplastic anemia (AA).

70 ch a relationship also has been reported for aplastic anemia (AA).

71 th suppressed hematopoiesis, including frank aplastic anemia (AA).

72 of patients with congenital neutropenia and aplastic anemia (AA).

73 Hepatitis-associated aplastic anemia (HAA) is a syndrome of bone marrow failu

74 inant hepatitis (FH) or hepatitis-associated aplastic anemia (HAA).

75 lose relationship between PNH and idiopathic aplastic anemia (IAA), it has been suggested that the 2

76 We treated 17 patients with moderate aplastic anemia (mAA) with 1 mg/kg every 2 weeks for 3 m

77 ation for the treatment of refractory severe aplastic anemia (rSAA) based on treatment of 43 patients

78 Severe aplastic anemia (SAA) appears to be an immunologically m

79 bone marrow (BM) transplantation for severe aplastic anemia (SAA) has improved, with survival rates

80 Survival in severe aplastic anemia (SAA) has markedly improved in the past

81 Severe aplastic anemia (SAA) is a life-threatening bone marrow

82 Severe aplastic anemia (SAA) is a life-threatening bone marrow

83 Severe aplastic anemia (SAA) is a rare disorder characterized b

84 Acquired severe aplastic anemia (SAA) is a rare hematologic disease asso

85 First-line therapy of severe aplastic anemia (SAA) with high-dose cyclophosphamide ca

86 In contrast to severe aplastic anemia (sAA), the appropriate management of pat

87 bone marrow transplantation (BMT) for severe aplastic anemia (SAA).

88 been promoted as curative therapy for severe aplastic anemia (SAA).

89 fective in restoring hematopoiesis in severe aplastic anemia (SAA).

90 itioning regimen in HSCT for acquired severe aplastic anemia (SAA).

91 About one-third of patients with acquired aplastic anemia also have short telomeres, which in some

92 s from 124 patients with apparently acquired aplastic anemia and 282 control subjects for sequence va

93 durable treatment-free remissions in severe aplastic anemia and a variety of other autoimmune disord

94 ightened cellular sensitivity to DNA damage, aplastic anemia and cancer susceptibility.

95 activation in the bone marrow occurs such as aplastic anemia and certain infectious conditions.

96 ies had shown that LCMV infection results in aplastic anemia and death in most of these mice and that

97 In FA-C, there was a later age of onset of aplastic anemia and fewer somatic abnormalities in patie

98 the diagnosis and treatment of patients with aplastic anemia and highlight a role for the THPO-MPL pa

99 cytopenia of undetermined significance, and aplastic anemia and how genetic approaches may help to b

100 For example, aplastic anemia and hypoplastic MDS can be difficult to

101 omerase, cause short telomeres in congenital aplastic anemia and in some cases of apparently acquired

102 , remains controversial for the treatment of aplastic anemia and inherited bone marrow failure syndro

103 Hematologic disorders such as aplastic anemia and leukemia induced by chloramphenicol

104 mphomas, Hodgkins disease, immunodeficiency, aplastic anemia and lymphohistiocytic disorders that cha

105 omere attrition in bone marrow cells rescues aplastic anemia and mouse survival compared with mice tr

106 lso are significantly lower in patients with aplastic anemia and NFAT1 protein levels are decreased o

107 f novel therapeutic agents for patients with aplastic anemia and other autoimmune diseases.

108 rescue, has been used successfully to treat aplastic anemia and other autoimmune disorders.

109 tion leads to durable complete remissions in aplastic anemia and other autoimmune disorders.

110 kinase may prove useful in the treatment of aplastic anemia and other cytokine-mediated bone marrow

111 enita have shed light on the pathobiology of aplastic anemia and other forms of bone marrow dysfuncti

112 the skin in an 11-year-old child with severe aplastic anemia and prolonged neutropenia is reported.

113 he second featured a 31-year-old female with aplastic anemia and prolonged neutropenia who developed

114 d with telomere dysfunction, including AIDS, aplastic anemia and pulmonary fibrosis, has bolstered in

115 isorder associated with premature death from aplastic anemia and pulmonary fibrosis.

116 ave been described in patients with acquired aplastic anemia and the autosomal dominant form of dyske

117 r patients with hematologic malignancies and aplastic anemia are almost certain to follow up patients

118 emoglobinuria (PNH) is intimately related to aplastic anemia because many patients with bone marrow f

119 ssays in 18 consecutive patients with severe aplastic anemia before and after treatment with high-dos

120 nts of HLA-identical sibling transplants for aplastic anemia between 1976 and 1992, reported to the I

121 , progressive loss of bone marrow, and fatal aplastic anemia between 3 and 4 months of age.

122 hemopoietic progenitor colony formation from aplastic anemia bone marrows in vitro.

123 telomere length have been reported in severe aplastic anemia but their clinical significance is unkno

124 Aplastic anemia can be a presenting manifestation of T-L

125 Aplastic anemia can be effectively treated by stem cell

126 Aplastic anemia can be effectively treated by stem-cell

127 ce polymorphisms found in some patients with aplastic anemia can inhibit telomerase activity by disru

128 st universally fatal just a few decades ago, aplastic anemia can now be cured or ameliorated by stem-

129 sted telomere length of patients with severe aplastic anemia consecutively enrolled in immunosuppress

130 The hepatitis of the hepatitis-associated aplastic anemia does not appear to be caused by any of t

131 e Tert gene in 2 independent mouse models of aplastic anemia due to short telomeres (Trf1- and Tert-d

132 ns associated with dyskeratosis congenita or aplastic anemia either impair the specific activity of t

133 ion, marrow transplantation in patients with aplastic anemia established long-term normal hematopoies

134 mia is a variant of aplastic anemia in which aplastic anemia follows an acute attack of hepatitis.

135 cal to exploring therapies to counteract the aplastic anemia for the treatment of FA patients.

136 cal sibling bone marrow transplantations for aplastic anemia has improved since 1976.

137 rtant role in the pathogenesis of idiopathic aplastic anemia in humans.

138 His brother had aplastic anemia in the course of his EBV infection and d

139 C partial loss-of-function allele results in aplastic anemia in the homozygous state and mild thrombo

140 tinct cell surface receptor and cause severe aplastic anemia in vivo and erythroblast destruction in

141 s-associated aplastic anemia is a variant of aplastic anemia in which aplastic anemia follows an acut

142 Aplastic anemia is a fatal bone marrow disorder characte

143 Severe aplastic anemia is a life-threatening bone marrow failur

144 Hepatitis-associated aplastic anemia is a variant of aplastic anemia in which

145 Aplastic anemia is caused by several diverse factors, in

146 Aplastic anemia is known to respond to immunosuppressive

147 The pathophysiology of aplastic anemia is now believed to be immune-mediated, w

148 d tumor may become even higher as death from aplastic anemia is reduced and as patients survive longe

149 Most acquired aplastic anemia is the result of immune-mediated destruc

150 Our understanding of the pathophysiology of aplastic anemia is undergoing significant revision, with

151 netically identical twins into patients with aplastic anemia may help define how frequently these fac

152 uced in patients' peripheral blood and in an aplastic anemia murine model, infusion of regulatory T c

153 e more common in developing countries, where aplastic anemia occurs more frequently than it does in t

154 rformed on a limited number of patients with aplastic anemia or acute leukemia, but only transient en

155 tent stem cells (iPSCs) from 4 patients with aplastic anemia or hypocellular bone marrow carrying het

156 rvival after bone marrow transplantation for aplastic anemia or leukemia was poor in both cohorts.

157 cted by high-sensitivity flow cytometry have aplastic anemia or low-risk myelodysplastic syndrome.

158 a may be warranted in selected patients with aplastic anemia or myelodysplastic syndrome, as this may

159 bset of patients presumed to have idiopathic aplastic anemia or myelodysplastic syndrome.

160 rating an immune-mediated process underlying aplastic anemia pathogenesis.

161 t the increased IFN-gamma levels observed in aplastic anemia patients are the result of active transc

162 Bone marrow (BM) and lymphocyte samples from aplastic anemia patients show up-regulated Fas and Fas-l

163 esents a novel therapeutic strategy to treat aplastic anemia provoked or associated with short telome

164 In a cohort of patients with severe aplastic anemia receiving immunosuppressive therapy, tel

165 Most patients with aplastic anemia recover bone marrow function after recei

166 is efficacious in a subset of patients with aplastic anemia refractory to immunosuppressive therapy,

167 patibility in 16 alloimmunized patients with aplastic anemia refractory to random donor platelet tran

168 About a quarter of patients with severe aplastic anemia remain pancytopenic despite immunosuppre

169 Acquired aplastic anemia results from immune-mediated destruction

170 In most patients, aplastic anemia results from T-cell-mediated immune dest

171 d in patients with dyskeratosis congenita or aplastic anemia show loss of function without any indica

172 were noted in analyses stratified on severe aplastic anemia subtype, recipient age, HLA matching, ca

173 ron-gamma promoter region, is upregulated in aplastic anemia T cells.

174 atologic response among patients with severe aplastic anemia than in a historical cohort.

175 al infection, myelodysplasia, lymphedema, or aplastic anemia that progress to myeloid leukemia.

176 In patients with aplastic anemia that was refractory to immunosuppression

177 cted a phase 2 study involving patients with aplastic anemia that was refractory to immunosuppression

178 mance score, graft type, HLA matching, prior aplastic anemia therapy, race/ethnicity, and calendar ye

179 he records and reevaluated 212 patients with aplastic anemia transplanted at the Fred Hutchinson Canc

180 Approximately half of patients with severe aplastic anemia treated with antithymocyte globulin and

181 ween 1970 and 1996, 333 patients with severe aplastic anemia underwent HLA-matched related marrow tra

182 Complete remission of aplastic anemia was achieved in four of these five patie

183 Bone marrow transplants for severe aplastic anemia were first performed in the 1970s.

184 even patients with hematologic malignancy or aplastic anemia were prepared to receive a transplant wi

185 Ten patients with hepatitis-associated aplastic anemia were referred to the NIH between 1990 an

186 viduals is highlighted by an individual with aplastic anemia who appears to lack six contiguous IGHD

187 ested that survivors of childhood cancer and aplastic anemia who are infected with the hepatitis C vi

188 serves further study in patients with severe aplastic anemia who are not suitable candidates for allo

189 In 87 patients with aplastic anemia who failed to respond to immunosuppressi

190 me of unrelated transplants in patients with aplastic anemia who had received multiple transfusions.

191 preferred for younger patients with acquired aplastic anemia who have matched, related donors.

192 itution analysis of 183 patients with severe aplastic anemia who were treated in sequential prospecti

193 s of patients with dyskeratosis congenita or aplastic anemia with mutations in telomerase genes can i

194 The patient had aplastic anemia with prolonged neutropenia and was treat

195 mphoma, 1 Chronic Myeloid Leukemia, 2 Severe Aplastic Anemia) undergoing allo-HSCT.

196 than leukemia (odds ratio=6.5 compared with aplastic anemia), and grade 4 graft-versus-host disease

197 a rate similar to that seen in patients with aplastic anemia).

198 115 patients with aplastic anemia, 39 patients with myelodysplasia, 28 pat

199 failure syndromes dyskeratosis congenita and aplastic anemia, acute myeloid leukemia, liver cirrhosis

200 hemoglobinuria is frequently associated with aplastic anemia, although the basis of this relation is

201 Aplastic anemia, an unusual hematologic disease, is the

202 5%) of 26 patients with hepatitis-associated aplastic anemia, and 0 of 17 patients with cryptogenic a

203 progressive immunoglobulin deficiency, FIM, aplastic anemia, and B-cell lymphoma.

204 plain the association between B19 infection, aplastic anemia, and chronic neutropenia of childhood.

205 MECOM patients presented early-onset severe aplastic anemia, and ERCC6L2 patients, mild pancytopenia

206 ggesting mutations in patients with acquired aplastic anemia, and for selection of suitable hematopoi

207 ions associated with dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis disru

208 ow failure syndromes dyskeratosis congenita, aplastic anemia, and idiopathic pulmonary fibrosis.

209 ed for children and young adults with severe aplastic anemia, and immunosuppressive therapy is employ

210 dyskeratosis congenita, pulmonary fibrosis, aplastic anemia, and liver fibrosis.

211 sis, thalassemia major, sickle cell disease, aplastic anemia, and myelodysplasia, among others.

212 ompared with other hematologic malignancies, aplastic anemia, and myelodysplastic syndrome.

213 BAF53a resulted in multilineage BM failure, aplastic anemia, and rapid lethality.

214 In patients with post-hepatitis aplastic anemia, antibodies to the known hepatitis virus

215 to horse ATG as a first treatment for severe aplastic anemia, as indicated by hematologic response an

216 factors for immunocompromise included AIDS, aplastic anemia, asplenia, hematological cancer, chemoth

217 ailure, dyskeratosis congenita, and acquired aplastic anemia, both diseases that predispose to acute

218 n associated with dyskeratosis congenita and aplastic anemia, both typified by impaired haemopoietic

219 ty syndrome characterized by childhood-onset aplastic anemia, cancer or leukemia susceptibility, and

220 utosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sen

221 utosomal recessive disorder characterized by aplastic anemia, cancer susceptibility, and cellular sen

222 tability disorder characterized by childhood aplastic anemia, developmental abnormalities and cancer

223 ant dyskeratosis congenita (DKC), as well as aplastic anemia, has been linked to mutations in the RNA

224 Androgens, used in the treatment of aplastic anemia, have been reported to block proliferati

225 those obtained in a series of patients with aplastic anemia, healthy donors, and patients with a his

226 In aplastic anemia, hematopoiesis fails: Blood cell counts

227 In severe acquired aplastic anemia, hematopoietic failure is the result of

228 in chronic inflammatory conditions, such as aplastic anemia, HIV, and graft-versus-host disease, is

229 The aplastic anemia, however, is often fatal if untreated.

230 In aplastic anemia, immune destruction of hematopoietic cel

231 keratosis congenita, pulmonary fibrosis, and aplastic anemia, is characterized by severely short telo

232 der individual or after recovery from immune aplastic anemia, is uncertain.

233 ening is also described in cases of acquired aplastic anemia, most likely secondary to increased turn

234 Patients with aplastic anemia, myelodysplasia, or renal allografts rec

235 rast, bone marrow from karyotypically normal aplastic anemia, myelodysplastic syndrome, or healthy in

236 dels of marrow failure, and to patients with aplastic anemia, myeloid, and lymphoid cell malignancies

237 In aplastic anemia, oligoclonally expanded cytotoxic T cell

238 utations and the effects of THPO agonists in aplastic anemia, our results have clinical implications

239 Patients with acquired aplastic anemia, primary immune deficiencies, and congen

240 h diseases including dyskeratosis congenita, aplastic anemia, pulmonary fibrosis and cancer.

241 mbilical cord blood transplantation and with aplastic anemia, results from insufficient numbers of ea

242 play a critical role in the pathogenesis of aplastic anemia, suggesting that selective pharmacologic

243 Aplastic anemia, the paradigm of immune-mediated bone ma

244 Severe aplastic anemia, which is characterized by immune-mediat

245 uch as sickle cell disease, thalassemia, and aplastic anemia--necessitate chronic transfusion before

246 coexpression of wild-type TERT and TERT with aplastic anemia-associated mutations in a telomerase-def

247 telomere length (LTL) and increased risk for aplastic anemia.

248 transfusion, such as sickle cell disease and aplastic anemia.

249 amide is highly effective therapy for severe aplastic anemia.

250 and choice of graft source for patients with aplastic anemia.

251 expression and diminished Treg frequency in aplastic anemia.

252 ng the immunodominant Ag H60, produced fatal aplastic anemia.

253 ns in the perforin gene occurred in acquired aplastic anemia.

254 ) is increased in T cells from patients with aplastic anemia.

255 (total of 99 immunosuppressive courses) with aplastic anemia.

256 osomy 7 in severe congenital neutropenia and aplastic anemia.

257 other components of telomerase also occur in aplastic anemia.

258 in previously untreated patients with severe aplastic anemia.

259 e is an additional feature shared by PNH and aplastic anemia.

260 l-depleted inoculum and transplantations for aplastic anemia.

261 nfused with aplasia and can also evolve from aplastic anemia.

262 s durable treatment-free remission in severe aplastic anemia.

263 myelodysplasia and one of four patients with aplastic anemia.

264 h hematopoietic malignancy or progression to aplastic anemia.

265 atients, T-LDGL is reported as presenting as aplastic anemia.

266 cal characteristics were similar to acquired aplastic anemia.

267 ed in the differential diagnosis of acquired aplastic anemia.

268 n cases of leukopenia, thrombocytopenia, and aplastic anemia.

269 H was found in 25 of 115 (22%) patients with aplastic anemia.

270 , providing a unique insight into a cause of aplastic anemia.

271 degree of neutropenia or a prior history of aplastic anemia.

272 le, complete remission in most patients with aplastic anemia.

273 ay be relevant to the pathogenesis of MDS in aplastic anemia.

274 on are accepted treatments for patients with aplastic anemia.

275 red immunodeficiency syndrome, and 1 case of aplastic anemia.

276 en with MDS secondary to therapy or acquired aplastic anemia.

277 atients with therapy-related MDS or acquired aplastic anemia.

278 e associated with dyskeratosis congenita and aplastic anemia.

279 thality due to acute bone marrow failure and aplastic anemia.

280 diseases, such as dyskeratosis congenita and aplastic anemia.

281 ival in patients who received HCT for severe aplastic anemia.

282 ytic leukemic, myelodysplastic syndrome, and aplastic anemia.

283 flicted with idiopathic, autosomal recessive aplastic anemia.

284 nomucor elegans in a patient with refractory aplastic anemia.

285 nses in some patients with refractory severe aplastic anemia.

286 an, phase 2 pilot study, in 35 patients with aplastic anemia.

287 une thrombocytopenia, Evans syndrome, severe aplastic anemia/refractory cytopenia, and others.

288 at presentation in almost all patients with aplastic anemia; FOXP3 protein and mRNA levels also are

289 great majority of young patients with severe aplastic anemia; the major challenges are extending the

290 Acquired and congenital aplastic anemias recently have been linked molecularly a

291 linically-relevant vascular features such as aplastic arteries, stenosis, aneurysms, and vessel calip

292 ypes of Tbx1 heterozygotes as hypoplastic or aplastic at the conclusion of pharyngeal artery formatio

293 eomalacia and, more recently, by adynamic or aplastic bone disease.

294 infection is the primary cause of transient aplastic crisis.

295 arthritis, myocarditis, hydrops fetalis, and aplastic crisis.

296 ds in mice aged 80 d bore claudin-4-positive aplastic lesions and accumulated (111)In-cCPE.GST (3.17

297 We examined the presence of hypoplastic, aplastic or fetal PCoAs, vertebral dominance, and diamet

298 al syndrome characterized by microphthalmia, aplastic skin and agenesis of the corpus callosum, and i

299 required to switch the mature neuron from an aplastic state to a state capable of growth.

300 arian strip may play a role in governing the aplastic transport of these elements.