ライフサイエンスコーパス: be severely impaired

1 e impairment, respectively (with 62% and 36% being severely impaired).

2 nges in the microenvironment, blood flow may be severely impaired.

3 ion of tumor-infiltrating lymphocytes (TILs) is severely impaired.

4 ize, and activate the downstream AKT pathway is severely impaired.

5 genes are poorly activated, and virus growth is severely impaired.

6 E (CENP-E), a kinesin-related motor protein, is severely impaired.

7 ckin mice expressing the human ApoE4 isoform is severely impaired.

8 that in vivo protease secretion by the T2SS is severely impaired.

9 cification of migratory myogenic progenitors is severely impaired.

10 lineages; however, neuronal differentiation is severely impaired.

11 plication capacity of HIV-1 containing I132M is severely impaired.

12 toreactive activation, but calcium signaling is severely impaired.

13 oteins RAD51 and DMC1 to meiotic chromosomes is severely impaired.

14 hat myelination by Schwann cells lacking FAK is severely impaired.

15 y reduced, and the activation of p38 and Akt is severely impaired.

16 Cognitive development is severely impaired.

17 gRP projections to hypothalamic target sites is severely impaired.

18 As a result, granule cell production is severely impaired.

19 ption of some H chain constant regions genes is severely impaired.

20 iated at the synapse, mitochondrial dynamics are severely impaired.

21 )-DJ(H) and V(kappa)-J(kappa) rearrangements are severely impaired.

22 CD4+ T cell responses, CD8+ T cell responses are severely impaired.

23 on of replication and possibly fork movement are severely impaired.

24 dent responses (including activation of PKB) are severely impaired.

25 self-administer a threshold dose of cocaine, was severely impaired.

26 uced activation of transcription factor AP-1 was severely impaired.

27 entiation to neural progenitors cells (NPCs) was severely impaired.

28 s K562 showed that the uptake of transferrin was severely impaired.

29 ighly sensitive to ACh levels and locomotion was severely impaired.

30 of the flagellar motor, monolayer formation was severely impaired.

31 eplication of a genome with four stop codons was severely impaired.

32 e assays, epithelial branching morphogenesis was severely impaired.

33 , synthesis of viral late mRNAs and proteins was severely impaired.

34 modulation of layer 5 (L5) pyramidal neurons was severely impaired.

35 ugh the endothelium-dependent vasodilatation was severely impaired.

36 and propagation of the TCR signaling cascade was severely impaired.

37 odendrocyte progenitor cell (OPC) generation was severely impaired.

38 Health status was severely impaired.

39 tion and NF-kappaB p65 nuclear translocation were severely impaired.

40 ut those initially trained with a 750-ms ISI were severely impaired.

41 Both rod and cone system functions were severely impaired.

42 and the induction of neutralizing antibodies were severely impaired.

43 and Ab responses to T cell-dependent antigen were severely impaired.

44 onal damage to neocortex, and these patients were severely impaired.

45 emical signals and to promote cell migration were severely impaired.

46 th the acquisition of longevity and dormancy were severely impaired.

47 In contrast, CT-transected rats were severely impaired (59% accuracy).

48 l receptor and Toll-like receptor triggering were severely impaired after ERT and improved significan

49 voked by action potentials and hypertonicity were severely impaired after the same treatments.

50 tolic and diastolic function of VM/RC hearts was severely impaired already before the onset of cardia

51 In this study, we show that mTEC development is severely impaired and autoimmune manifestations occur

52 In fbl17 mutant plants, DNA replication is severely impaired and endoreplication is fully suppre

53 Hb degradation is severely impaired and large amounts of undigested Hb

54 nstrate that Igkappa germ line transcription is severely impaired and recombination is blocked in the

55 In its absence, chondrocyte hypertrophy is severely impaired and there is no vascularization of

56 Thrombin generation at low triggers was severely impaired and mixing experiments suggested t

57 poisomerase II (Top2) activity, processivity was severely impaired and polymerases were unable to tra

58 ripts for the viral F17R and A10L genes also was severely impaired and was shown to be a direct inhib

59 utants lacking both YidC2 and SRP components were severely impaired and barely able to grow, even in

60 In the place task, DTN-lesioned rats were severely impaired and displayed little evidence of

61 DTN-lesioned rats, however, were severely impaired and showed reduced heading accura

62 Type I IFN-mediated JAK-STAT signaling is severely impaired, and activation of MAPKs and PI3K s

63 f compatible osmolytes, the formation of SGs is severely impaired, and cells increase their chances o

64 IET in G473W is severely impaired, and no IET is observed for G473D/R

65 o fibronectin and ICAM1, 2 integrin ligands, was severely impaired, and CYTH1-deficient cells showed

66 Growth of the double mutant nhx1 nhx2 was severely impaired, and plants were extremely sensiti

67 yonic fibroblasts, adipocyte differentiation was severely impaired, and reexpression of SRC-3 was abl

68 on), 31 (18%) were mildly impaired, 25 (14%) were severely impaired, and 3 (1%) were in a vegetative

69 Mitochondrial biogenesis is severely impaired as evidenced by reduced mtDNA repli

70 se animals to develop the allergic phenotype was severely impaired as evidenced by attenuated eosinop

71 erall release efficiency of affected neurons was severely impaired, as demonstrated by a smaller read

72 A vaccinia virus G5 deletion mutant was severely impaired, as the yield of infectious virus

73 Neutrophil infiltration in Mac-1 KO mice was severely impaired at 24 hours.

74 e, the photoreceptor outer segment structure was severely impaired at 4 weeks of age, although a full

75 mal levels, but that memory for conjunctions was severely impaired at 8 s delays.

76 Swimming was severely impaired at approximately 5 h after peptide

77 olished; clathrin-mediated endocytosis (CME) was severely impaired at the step of membrane fission, w

78 Following PFC-IT disconnection monkeys were severely impaired at reacquiring the rule (to avoid

79 lues in object-reward associations, but they were severely impaired at updating choices after reversa

80 nant G473D sulfite oxidase indicated that it is severely impaired both in the ability to bind sulfite

81 th previous reports, hippocampectomized rats were severely impaired both in acquiring and recalling t

82 wild type, whereas others (S138T and A156V) were severely impaired both in RNA replication and infec

83 Episodic and emotional memories are severely impaired, but both are rescued with the tyr

84 Bone formation in homozygotes was severely impaired, but no obvious phenotypic change

85 vities of three different FGF10 LADD mutants are severely impaired by different mechanisms.

86 ty of the truncated GLI1 factor was found to be severely impaired by cell culture and in vivo assays,

87 Fertility in adult life can be severely impaired by gonadotoxic therapies and with r

88 O2-consumption and aerobic growth proved to be severely impaired by sulfide when respiration was sus

89 The role of RAB7A is severely impaired by a mutation, K157N, that causes C

90 OR to the COI1-JAZ complex requires COI1 and is severely impaired by a point mutation in the putative

91 many memory tests varies across the day and is severely impaired by disruptions in circadian timing.

92 achieved in 2D spectra whose interpretation is severely impaired by scintillation noise.

93 Mitochondrial biogenesis and function is severely impaired by TNF as evidenced by downregulati

94 mma, such as interferon regulatory factor-1, was severely impaired by both STAT1 silencing and by con

95 n was not affected by VTA microinfusions but was severely impaired by bupivacaine microinfusions into

96 e two procofactors by membrane-bound rMZ-IIa was severely impaired by D5Q1,2.

97 Accordingly, DNA-binding by Cmr was severely impaired by nitrosation.

98 The efficiency of reverse transcription was severely impaired by nonconservative substitution of

99 at the ability of S. mutans to form biofilms was severely impaired by oxygen exposure, transcription

100 mation of an RNP complex with poliovirus RNA was severely impaired by substitution of a lysine, highl

101 Proliferating HepaRG bioenergetic parameters were severely impaired by day 8, with 1 and 12 muM ddC,

102 synaptotagmin-10-dependent IGF-1 exocytosis were severely impaired by knockdown of complexins, demon

103 imicking a non-acetylated NP lysine residue, is severely impaired compared to wildtype or the mutant

104 urface expression of mutant murine GABA(A)Rs is severely impaired compared with WT, due to retention

105 by lipopolysaccharide-stimulated leukocytes was severely impaired compared with control subjects, wi

106 neration in CXCL16-deficient (CXCL16KO) mice was severely impaired compared with regeneration in wild

107 he bone marrow and peripheral reconstitution was severely impaired compared with wild-type (WT) mice.

108 Aryl hydrocarbon receptor signaling is severely impaired despite the ligand (Trp dimer) bein

109 l production of these peptides in plants can be severely impaired due to the toxicity exerted on the

110 liver hematopoietic stem cell (HSC) function is severely impaired due to Cited2 deficiency.

111 ion was not affected; however, its outgrowth was severely impaired due to reduced epithelial and mese

112 Synaptic vesicle endocytosis was severely impaired during strong exogenous stimulatio

113 icity after brief monocular deprivation (MD) was severely impaired during the critical period (CP) in

114 antibodies to TNP-keyhole limpet hemocyanin were severely impaired, even after adoptive transfer of

115 several key aspects of presynaptic function are severely impaired following even brief interruptions

116 itro and in vivo, and strains lacking site 2 are severely impaired for growth following nutritional s

117 shifted to mild heat shock temperatures, but are severely impaired for survival at 48 degrees C.

118 protein, including mutant Est3 proteins that are severely impaired for telomere replication in vivo,

119 p53(25,26) is severely impaired for the transactivation of numerous

120 itrate, MnO2, and Mn(III) pyrophosphate] yet was severely impaired for growth on electron acceptors w

121 nal mutation into the osuD gene (Omega osuD) was severely impaired for growth on starch media.

122 In contrast, beta(148-152) was severely impaired for Pol II and Pol IV replication

123 ut4 elicited robust interferon responses and was severely impaired for replication in PK1 cells.

124 Finally, beta(+)/beta(C) was severely impaired for unloading from DNA using eithe

125 Venus-ICP27, was constructed, and this virus was severely impaired for virus replication.

126 eatments that caused double-chain breaks and were severely impaired for growth; recB growth suppresso

127 t mutants lacking the Dot/Icm substrate SdhA were severely impaired for intracellular growth within m

128 ropofol inhibition and enhancement of GluCls were severely impaired (IC50 and EC50 values could not b

129 This activation is severely impaired if the CD4-binding site on the agon

130 onstrated that fibrinolysis and angiogenesis are severely impaired in A2-deficient mice.

131 w that both recombinant AAC1 mutant proteins are severely impaired in ADP/ATP transport, affecting mo

132 ce deficient either in IL-7 or in IL-7Ralpha are severely impaired in anti-PPS responses and do not s

133 n, including three disease-associated forms, are severely impaired in ATPase activity.

134 Thus mutant seedlings are severely impaired in beta-oxidation, even though mic

135 s of the border zone of infarcted myocardium are severely impaired in db/db mice compared with wild-t

136 sst3 knock-out mice are severely impaired in discriminating novel objects, w

137 Knockdown rice plants, however, are severely impaired in growth and development.

138 CKS1 deletion mutants are severely impaired in hyphal growth, sexual reproduct

139 Nevertheless, Itk-deficient NKT cells are severely impaired in IL-4 protein production.

140 es its lysosomal degradation, functions that are severely impaired in LRP6(R611C).

141 nfection with mouse-adapted DENV strains but are severely impaired in mounting functional immune resp

142 long condition in which affected individuals are severely impaired in navigating around their environ

143 ls with reduced levels of SMC that lack ParB are severely impaired in origin resolution.

144 CCL22/CCL17 and effector T cell recruitment are severely impaired in Pla2g5-null mice.

145 nsgenic, RAG-, and CD4-deficient mice, which are severely impaired in positive selection, and asked w

146 and secondary responses of all Ig subclasses are severely impaired in response to specific antigens.

147 fically pheromone response-defective mutants are severely impaired in shmoo formation and fail to loc

148 TLR4-mediated NF-kappaB and AP-1 activation are severely impaired in Tak1(m/m) cells, but they are n

149 y impaired in the absence of XLF or ATM, but are severely impaired in the absence of both.

150 rabidopsis mutants deficient in BR signaling are severely impaired in the production of bioactive GA,

151 that cells expressing a mutated form of Bves are severely impaired in the recycling of these molecule

152 We found that S. aureus lacking lukAB are severely impaired in their ability to kill phagocyte

153 Ia.2(-) tethered peptide-class II molecules are severely impaired in their ability to present both t

154 Similar to porA-1, speechless seedlings are severely impaired in their development.

155 f in vivo reconstitution of the RNR cofactor are severely impaired in two conditional tah18 mutants.

156 in-proteasome system (UPS) has been shown to be severely impaired in vitro in cells overexpressing mu

157 Despite being severely impaired in visual shape recognition, M.C

158 Arbuscule formation is severely impaired in a Medicago truncatula Mtdella1/M

159 r experiments revealed that Notch2 signaling is severely impaired in ADAM10-null B cells.

160 ry for specific object-location associations is severely impaired in aged Tg2576 mice.

161 arin complexes, and that antibody production is severely impaired in B-cell-specific Notch2-deficient

162 response of neurons to transcallosal stimuli is severely impaired in cortex containing substantial pl

163 e show that T-cell development in the thymus is severely impaired in Cxxc1-deficient mice.

164 ent-derived progenitor cell (PC) dysfunction is severely impaired in diabetes, but the molecular trig

165 However, in vivo development is severely impaired in embryos covered by a ZP4-devoide

166 ls of theta burst afferent stimulation (TBS) is severely impaired in hippocampal field CA1 of young a

167 cycle, undergoes little phosphorylation, and is severely impaired in its ability to function as a tra

168 An hfq mutant is severely impaired in its ability to invade plant cell

169 Additionally, DeltaSPD0247 is severely impaired in its attachment to an abiotic sur

170 r regulator of granulocytic differentiation, is severely impaired in leukemic promyelocytes with the

171 We found that the hpf null strain is severely impaired in long-term viability concomitant

172 echanism controlling chromosome segregation, is severely impaired in metaphase oocytes following Sirt

173 r responses depend on type 1 immunity, which is severely impaired in mice deficient for the T-box exp

174 Host defense against the spirochete is severely impaired in mice deficient in the adaptor mo

175 Here, we found that NK cell development is severely impaired in mice deficient in the histone H2

176 Microcirculation is severely impaired in patients with refractory cardiog

177 (Asp(L210) --> Asn + Asp(M17) --> Asn) that is severely impaired in proton transfer capability over

178 Here we show that angiogenesis is severely impaired in PSMA-null animals and that this

179 osis where (129)Xe replenishment of the RBCs is severely impaired in regions of lung injury.

180 rmal neutrophil numbers, neutrophil function is severely impaired in Srf knockout (KO) neutrophils.

181 roduction in response to T cell-dependent Ag is severely impaired in the Abl mutant mice.

182 enance of intestinal stem cells after damage is severely impaired in the absence of ILC3s or the ILC3

183 revealed that auxin-induced gene expression is severely impaired in the arf7 single and arf7 arf19 d

184 We report here that UPS proteolytic function is severely impaired in the heart of a mouse model of in

185 The development of chloroplasts is severely impaired in the IspH-deficient albino tissue

186 However, this functional recovery is severely impaired in the presence of CD13 antagonists

187 idative phosphorylation dependent, mitophagy is severely impaired in the PRKN mutant patient neurons.

188 mbles Crohn's disease, and that DC migration is severely impaired in these mice compared with AKR mic

189 dings demonstrate that synaptic transmission is severely impaired in these mutants.

190 of these defects since pituitary development is severely impaired in these mutants.

191 lex class I negative tumors, a response that is severely impaired in Txb21(-/-) mice.

192 I-2) Ags, such as bacterial polysaccharides, is severely impaired in X-linked immunodeficient (XID) m

193 Although B cell development was severely impaired in 2F5 V(H) x V(L) KI animals, we

194 the first postoperative week, hand function was severely impaired in all monkeys.

195 t maturation of excitatory cortical circuits was severely impaired in Angelman syndrome model mice de

196 Endocytosis was severely impaired in apolar fimA disruption cells.

197 reserved LV ejection fraction (55+/-12%), LS was severely impaired in CA.

198 Furthermore, LMP1 packaging was severely impaired in CD63 knockout cells, concomitan

199 nversely, induction of ZAP by virus or dsRNA was severely impaired in cells expressing a dominant-neg

200 Infectivity for all Envs was severely impaired in cells expressing low levels of

201 comparable with Wt progenitors, this process was severely impaired in E2a heterozygote mutant mice.

202 Further, 17dmiR-H1/H6 was severely impaired in epinephrine-induced reactivatio

203 -derived macrophages from BALB/c.D2 mice and was severely impaired in extraintestinal growth but not

204 secondary infection with H. polygyrus bakeri was severely impaired in IL-25(-/-) mice, including dela

205 This process was severely impaired in ILC2-deficient mice.

206 of the LCMV NP(396)-specific CD8(+) T cells was severely impaired in IRF7 KO mice.

207 ic activity with NAEs, but the latter enzyme was severely impaired in its ability to catabolize NATs.

208 establish latency, the G50DblKo virus mutant was severely impaired in its ability to reactivate from

209 The completely "regenerated" Pdr5 protein was severely impaired in its function of ATP hydrolysis

210 The data showed that fV(Q3) was severely impaired in its interaction with fXa before

211 regulation of T lymphocytes and erythrocytes was severely impaired in Kcnn4 null mice but was normal

212 plication of ovalbumin to tape-stripped skin was severely impaired in Ltb4r1(-/-) mice and required e

213 Moreover, autoreactive T cell activation was severely impaired in MALT1-deficient T cells, sugges

214 inding, the capacity for muscle regeneration was severely impaired in mice deficient for skeletal-mus

215 ell expansion following Plasmodium infection was severely impaired in mice genetically deficient for

216 Strikingly, GC formation was severely impaired in mice in which Irf4 was conditio

217 Growth of S40 was severely impaired in minimal medium.

218 FIXa(Y225P), a Na+ site mutant, was severely impaired in Na+ potentiation of its catalyt

219 ation of DC-SIGN(+) MoDCs in response to LPS was severely impaired in Nr4a3 (-/-) mice, which resulte

220 that the functional bone resorbing capacity was severely impaired in OCLs depleted of Orai1, potenti

221 s inhibited, and spreading viral replication was severely impaired in PSIP1-/- Jurkat cells infected

222 sed hydrolysis of triacylglycerols 7 (cht7), was severely impaired in regrowth following removal of d

223 Notably, this rkpM mutant was severely impaired in symbiosis with its host, Macrop

224 hly differentiated, and leukemia progression was severely impaired in the absence of AMD1 in vivo.

225 at early Bcl6(+)CXCR5(+) Tfh differentiation was severely impaired in the absence of IL-6; however, S

226 (TCM) and effector memory (TEM) CD8+ T cells was severely impaired in the absence of MCP-1.

227 epatobiliary clearance of (99m)Tc-mebrofenin was severely impaired in the bile duct-ligated animal, a

228 We found stimulated mucus release was severely impaired in the cystic fibrosis F508 reprod

229 n the hindlimb field and that Shh expression was severely impaired in the hindlimb bud.

230 Nuclear targeting of LHP1 was severely impaired in the impalpha triple mutant, res

231 The initial outgrowth of the palate was severely impaired in the mutant embryos, due to decr

232 The repair of UV-induced (6-4)photoproducts was severely impaired in these cells, and they were hype

233 HIV-1 replication was severely impaired in these PSIP1 knockout cells.

234 VA), a potential model of atopic dermatitis, was severely impaired in TSLPR(-/-) mice, as evidenced b

235 al of HNF1A(-/-) common lymphoid progenitors was severely impaired in vitro, and the expression of th

236 Furthermore, megakaryopoiesis was severely impaired in vitro.

237 enic mice showed normal 1-day memories, they were severely impaired in 10-day contextual fear memory.

238 AC5KO mice were severely impaired in acquisition of a response stra

239 S. marcescens oxyR mutants were severely impaired in biofilm formation, in contrast

240 tigens and antibody responses to vaccination were severely impaired in both patients.

241 memory responses to the pathogen reinfection were severely impaired in CCR10-KO mice.

242 ng individual pair discriminations, but they were severely impaired in contextual retrieval.

243 ere decreased and hepatic responses to FGF19 were severely impaired in dietary obese mice that have e

244 ment-dependent gene transcription activities were severely impaired in EPCs obtained from ER alpha-kn

245 - and glutamine-stimulated insulin secretion were severely impaired in H454Y mice.

246 Cells reacted with a thiol-blocking reagent were severely impaired in Hg(0) oxidation activity.

247 Furthermore, AC8 KO mice were severely impaired in hippocampus-dependent episodic

248 g and the hyperglycemic response to glucagon were severely impaired in HKO mice.

249 hymus and spleen, but only NF90(-/-) T cells were severely impaired in IL-2 gene expression.

250 umoral immune responses against C. rodentium were severely impaired in infected miR-155-deficient mic

251 performance during whisking and licking, but were severely impaired in learning this task compared wi

252 rp2 alleles with mutations at the barbed end were severely impaired in nucleation, providing the firs

253 vel locations, both DG and CA3 lesion groups were severely impaired in reexploring the displaced obje

254 nd LEF-1 exhibited an effector phenotype and were severely impaired in secondary expansion upon recha

255 m Ca2+ cycling and beta-adrenergic signaling were severely impaired in SKO-MI myocardium but preserve

256 liferation of GCPs and their response to SHH were severely impaired in the cerebellum of subjects wit

257 st or memory B-cell response, although these were severely impaired in the group with a CD4+ T-cell c

258 R211A and K214A mutants were severely impaired in the oxidation of S-HPC or redu

259 on transport and carbon dioxide assimilation were severely impaired in the silenced plant lines.

260 lines engineered to express the mutant CD13 were severely impaired in their ability to migrate into

261 MyD88-deficient mice were severely impaired in their ability to mount an acut

262 (Etx-Y29E, Etx-Y30E, Etx-Y36E and Etx-Y196E) were severely impaired in their ability to not only kill

263 ingly, neutrophils from EP-infected chambers were severely impaired in their ability to phagocytose a

264 nor Tregs lacking CCR8 (CCR8(-/-)), however, were severely impaired in their ability to prevent letha

265 After MCMV infection, these NK cells were severely impaired in their ability to proliferate.

266 In contrast, MyD88-deficient AECs were severely impaired in their ability to respond to Pn

267 /) (-) HSPCs were able to home to the BM but were severely impaired in their capacity to reconstitute

268 tential of HSC and early lymphoid progenitor is severely impaired, in tandem with reduced early lymph

269 RV EF was severely impaired (</=35%) in 63 patients (30%), and

270 episodic memory that require intact PFC, but were severely impaired on a spatial working memory task.

271 ogressive aphasia with non-semantic subtypes were severely impaired on an odour naming task, in compa

272 NMS task at either the 5- or 30-s delays but were severely impaired on the Obj-SO task.

273 rd chromatin and other lupus nuclear targets is severely impaired or absent.

274 but the nucleotide selectivity of the enzyme is severely impaired, providing a mechanistic explanatio

275 ir follicle morphogenesis of Ift27-null mice was severely impaired, reminiscent of phenotypes observe

276 ouse post-implantation placental development is severely impaired, resulting in early embryonic death

277 the assembly of viral replication factories is severely impaired, revealing a second critical role f

278 ndroitin sulfate chain alone; however, there is severely impaired secretion of core protein devoid of

279 nt in the optic nerves of Eomes(-/-) embryos is severely impaired, suggesting that Eomes regulates th

280 r, the reconstitution capacity of these HSCs is severely impaired, suggesting that SHIP expression mi

281 pseudohyphal formation in the OLE1 KO cells was severely impaired, suggesting that Ole1 regulates mo

282 ce development in the Shh(N/-) telencephalon were severely impaired, suggesting that telencephalic pa

283 ore clones with residue rtS202 substitutions were severely impaired than those at rtT184 or rtM250.

284 iary clearance in the respiratory epithelium is severely impaired, the disorder is referred to as pri

285 Whereas rad53-TA in vitro kinase activity is severely impaired, the rad53-TA strains are not compl

286 well maintained, whereas peripheral strength was severely impaired throughout hospitalization.

287 VCC localization and virus release of HIV-1 are severely impaired upon 5ptaseIV overexpression, sugg

288 tic potential of PTPN12-deficient TNBC cells is severely impaired upon restoration of PTPN12 function

289 However, fluorescence is severely impaired when concentrations climb above 5 m

290 so affect HvG tolerance, since its induction is severely impaired when donor hematopoietic cells have

291 Our results revealed that pollen hydration is severely impaired when multiple PCP-Bs are lost from

292 ation, postresuscitation myocardial function was severely impaired when compared with the normothermi

293 In contrast, organelle segregation was severely impaired when complementing with a TgADF mu

294 Parasite development was severely impaired when treated with 18, thus reinfor

295 However, the monkeys were severely impaired when the cue was switched frequen

296 B-cell proliferation in response to mitogens was severely impaired, whereas that of T cells appeared

297 Q knock-in mouse embryos, the BER efficiency was severely impaired, which subsequently resulted in do

298 es (cleistothecia) in self-fertilization and was severely impaired with cleistothecial development in

299 Mutant endosperms are severely impaired, with highly irregular differentia

300 Skeletal development was severely impaired, with chondrocytes showing swellin