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1 ype I), IFN-gamma (type II), and IFN-lambda (type III).
2 avage is required to allow signaling of NRG1 type III.
3  I, 17 (26.2%) as type II, and 21 (32.4%) as type III.
4 st common phenotype was type I (50.3%), with type III (29.6%), type II (14.5%) and type IV (5.7%).
5                        Type I: 6, Type 2: 6, Type III: 6, Type IV: 11, Type V: 4.
6 rRNA maturation and establish a link between Type III-A CRISPR-Cas immunity and central nucleic acid
7  targeting by the Staphylococcus epidermidis type III-A CRISPR-Cas system does not require PAM or see
8        Staphylococcus epidermidis harbours a Type III-A CRISPR-Cas system that encodes the Cas10-Csm
9                                              Type III-A CRISPR-Cas systems defend prokaryotes against
10 dition, mutations in the active sites of the type III-A RNases Csm3 and Csm6 lead to the accumulation
11  should be considered as primary therapy for type III achalasia; 4) if the expertise is available, PO
12  secretion by suppressing fluid transport in type III acini.
13 ding structures opening towards the lumen in type-III acini.
14 egulation (p < 0.01) with increased Collagen type III and increased expression of several apoptosis r
15            When mutations in the fibronectin type III and kinase domains of EPHB1 were compared with
16 saliva formation, mediated by Na/K-ATPase in type III and type II acini, is followed by a dopamine-in
17             Here we test the ability of 200 type III and type IV effector proteins from six Gram-neg
18 rentially expressed during infection and the type III and VI secretion systems were highly expressed
19  hydrocarbon-dominated organic matter types (types III and IV; mainly land plant, metamorphosed or de
20 , acquired angioedema, hereditary angioedema type III, and angiotensin converting enzyme inhibitor-in
21                  The effector complex of the Type III-B Cmr system cleaves invader RNAs recognized by
22                    The Sulfolobus islandicus type III-B Cmr-alpha system targets invading nucleic aci
23 erranean seagrass meadows, we found that the type III-B machinery co-opts type I-F CRISPR-RNAs.
24                                       In the Type III-B system, the Cmr effector complex has been fou
25  type I-F spacers by a horizontally-acquired type III-B system.
26                             A second system (type III-B) is broadly capable of acquiring spacers in e
27 otic activity, and osteotomy site healing in type III bone and high endogenous Wnt signaling.
28 ) bone versus more trabeculated, cancellous (type III) bone.
29 yses to identify and characterize type I and type III bones in murine jaws.
30 IL-18 are cell-specific and were observed in Type III but not in Type I/II neurons.
31 ylated viral promoters that are expressed in type III (but not type I) latency.
32 -dentin area showed significant increases in type III, but not in types I or II cases.
33                            This evolved into type III by aggravating both mechanical substrates.
34 sinaemia type I into the benign tyrosinaemia type III by deleting Hpd (hydroxyphenylpyruvate dioxigen
35 ic responses could explain why a minority of type III cells (34%) had AI salt responses but lacked an
36                                       All AI type III cells had osmotic responses to cellobiose, whic
37 he transduction machinery for salty taste in type III cells is sensitive to anion size.
38 se responses were significantly larger in AI type III cells that did not exhibit the anion effect.
39                      The sour sensing cells, Type III cells, release serotonin (5-HT) in response to
40 ed to neuronal function were up-regulated in type III cells.
41 type II cells and physiologically identified type III cells.
42 ctyostelium and mutant cells lacking ChdC, a Type III CHD protein ortholog.
43                                              Type III CHDs are required for multicellular development
44 opment, establish an in vivo function of CHD Type III chromatin remodeling proteins in this process,
45 ypes of ependymal cilia, type-I, type-II and type-III classified based upon their beating frequency,
46                         In many prokaryotes, type III clustered regularly interspaced short palindrom
47  effect by increasing the amount of refolded type III collagen in vitro and FKBP19 seems to interact
48 agen, the unhydroxylated quarter fragment of type III collagen, and synthetic peptides as substrates.
49  preferences of these PPIases in vitro using type III collagen, the unhydroxylated quarter fragment o
50 icated cracks, a combination of a Type I and Type III cracks, which may or may not be confluent with
51                     Although most type I and type III CRISPR systems require four or more distinct pr
52                                   In several type III CRISPR systems, Cas1 is naturally fused to a re
53 I and II systems, the relaxed specificity of type III CRISPR-Cas targeting provides robust immune res
54 22 in strain 26695, encodes a N(6)-adenosine type III DNA methyltransferase.
55  activating mutation in the fibronectin-like type III domain of the extracellular region of CSF3R (W3
56 -binding proteins based upon the fibronectin type III domain, and we find that variations in sequence
57 F splice variants 1, 2, 4, 6 and fibronectin type III domain-containing protein 5 (FNDC5) mRNA levels
58 en the membrane-proximal (third) Fibronectin type III domains (Fn3) of Tie2.
59 ose cryptic FN-FN binding sites buried in FN Type III domains.
60  II (e.g. the Tas1r genes, Plcb2, Trpm5) and type III (e.g. Pkd2l1, Ncam, Snap25) taste cells.
61 EBV infection and suggest that TET2 promotes type III EBV latency in B cells with an ABC or naive phe
62 ed Xam strains in which individual predicted type III effector (T3E) genes were mutated and applied m
63 interaction between the Pseudomonas syringae type III effector AvrPtoB and NPR1.
64 ttom-up approach, showing that the bacterial type III effector AvrRxo1 of plant pathogens is an authe
65                    Finally, we show that the type III effector IpgB1 from Shigella flexneri may bind
66        We isolated Response to the bacterial type III effector protein HopBA1 (RBA1), a gene that enc
67                                  HopAF1 is a type III effector protein of unknown function encoded in
68                                 A screen for type III effector proteins from Pst for their ability to
69 plex contact host cell membranes and deliver type III effector proteins.
70 from an extensive phylogenetic analysis, and type III effector translocation and host cell invasion a
71 viously unstudied Pseudomonas syringae (Psy) type III effector, HopBB1, interacts with TCP14 and targ
72 y to delete the coding sequences for a known type III effector.
73  DC3000 (Pst DC3000), demonstrating that the type-III effector HopG1 is required for pathogen-induced
74 oduce a computational method that identifies type III effectors by combining homology-based inference
75 h is required for efficient translocation of type III effectors into host cells.
76       Most plant bacterial pathogens rely on type III effectors to cause diseases.
77 erstanding of the basis of host specificity, type III effectors, microbe-associated molecular pattern
78  The spike resonance of these phasic-firing (type III excitable) MSO neurons and of the model is of p
79 A marked shift in collagen predominance from type III (fetal/early wound) to type I (adult/mature) wa
80   PavA and PavB target at least 13 out of 15 type III fibronectin domains as demonstrated in ligand o
81 t antigen to be MrkA, a major protein in the type III fimbriae complex, and showed that these serotyp
82 a highly conserved region of the fibronectin type III (FN3) domain of the receptor tyrosine kinase Ep
83  C2 type (IgC2) domains and four fibronectin type III (FnIII) domains that are shared with many other
84 is mediated by membrane-proximal fibronectin type III (FNIII) domains that were omitted in previous s
85 ructural switch within its first fibronectin type III (FnIII-1) domain to control RbmA structural dyn
86 d-optimal temperatures, predators may have a type III functional response, and prey carrying capacity
87             Reducing the excitatory input on Type III GABAergic neurons, IL-18 can increase the firin
88 it feeding by inhibiting the activity of BST Type III GABAergic neurons.
89 sentative of the protective response against type III GBS polysaccharide.
90 ram-positive group B Streptococcus, capsular type III (GBS-III) bacteria resulted in augmented serum
91 ncing similar to what is seen in EBV latency type III genomes.
92 ally (occluso-gingival) oriented cracks; and Type III - hybrid or complicated cracks, a combination o
93  skin, but the mechanisms that regulate this type III hypersensitivity process remain poorly understo
94                 Small immune complexes cause type III hypersensitivity reactions that frequently resu
95 ms made with IBPs (both from winter rye, and type III IBP) had aggregates of ice crystals that entrap
96 ound that adding recombinantly produced fish type III IBPs at a concentration 3mg.L(-1) made ice crea
97 pha/beta) controls systemic replication, and type III IFN (IFN-lambda) controls MNV persistence in th
98              Type I IFN (IFN-alpha/beta) and type III IFN (IFN-lambda) function at the epithelial lev
99 se to infection both in vitro and in vivo is type III IFN and acid labile.
100                      IFN-lambda4 is a unique type III IFN because it is produced only in individuals
101              Since these miRNAs can suppress type III IFN family members, these data collectively def
102                 The mechanisms that regulate type III IFN gene expression tracked with those that pro
103             However, the roles of type I and type III IFN in restricting human enteric viruses are po
104  has a positive role in enhancing type I and type III IFN production.
105     Early after HRV infection, low levels of type III IFN protein activate IFN-stimulated genes.
106 se replication-competent HRV antagonizes the type III IFN response at pre- and posttranscriptional le
107 overned by genetic polymorphisms that affect type III IFN signaling and virus-specific cellular immun
108 tion, with type I IFN being more potent than type III IFN, suggesting that extraepithelial sources of
109   In addition, we found that fetuses lacking type III IFN-lambda signaling had increased ZIKV replica
110 tional pathway induced by HRV infection is a type III IFN-regulated response.
111 alpha/beta) and the more recently identified type III IFNs (IFN-lambda) function as the first line of
112                                              Type III IFNs (IFN-lambdas) are secreted factors that ar
113 hoblasts through the constitutive release of type III IFNs (IFNlambda1 and IFNlambda2) and become res
114      IRF1 is necessary for the expression of type III IFNs (IFNLs 1 and 2/3).
115 ter of pregnancy also constitutively release type III IFNs and use these IFNs in autocrine and paracr
116                                              Type III IFNs are important mediators of antiviral immun
117 ly expressed from TLRs present on endosomes, type III IFNs could be induced by TLRs that reside at th
118          IFN-lambda4 acted faster than other type III IFNs in inducing antiviral genes, as well as ne
119 on and new human models to study the role of type III IFNs in the vertical transmission of ZIKV and o
120  hepatocytes (PHHs) treated with recombinant type III IFNs or infected with Sendai virus to model acu
121 ctions in cell-intrinsic antiviral immunity, type III IFNs protect epithelial barrier integrity, an a
122           Lambda interferons (IFNlambdas) or type III IFNs share homology, expression patterns, signa
123                                              Type III IFNs were originally identified as a novel liga
124 ormed in 47.2% (type II) and apical closure (type III) in 38.9% cases.
125                                        Gigot type III individuals scored numerically higher than type
126  through a second messenger generated by the type III interference complex.
127 zontal uptake and maintenance of promiscuous type III interference modules that supplement existing h
128 ay, suppress IFNL2 and IFNL3, members of the type III interferon (IFN) gene family, to support viral
129         PHT cells constitutively release the type III interferon (IFN) IFNlambda1, which functions in
130                                              Type III interferon (IFNlambda) and type I IFN (IFNalpha
131 L-10R family and highlight the plasticity of type III interferon signaling and its therapeutic potent
132                                              Type III interferons (IFN-lambda) control enteric viral
133                                              Type III interferons (IFN-lambdas) signal through a hete
134 ctors, including the constitutive release of type III interferons (IFNs).
135 se, including strong induction of type I and type III interferons (IFNs).
136        This in turn stimulates production of type III interferons and hence enhances tumour antigen p
137                   We focus here on desmin, a type III intermediate filament, which is specifically ex
138 ncept of sphincter of Oddi dysfunction (SOD) type III is discarded.
139 pe 2-oriented membrane-retained stub of NRG1 type III is further processed by signal peptide peptidas
140                                   Thus, NRG1 type III is the first protein substrate that is not only
141                  Neuregulin 1 type III (NRG1 type III) is a major physiological substrate of beta-sec
142 lar resistance, proteolysis, quorum sensing, Type III/IV secretion systems, phages and toxins in the
143                  Type I (alpha and beta) and type III (lambda) IFNs are induced upon viral infection
144  H3 at lysine 4) and H3 acetylation at Cp in type III latency and Qp in type I latency, as well as an
145 e transcripts are regulated similarly to EBV type III latency genes and that TET2 protein is a cofact
146 cofactor of EBNA2 and coregulator of the EBV type III latency program and DNA methylation state.IMPOR
147 n correlate with the highly demethylated EBV type III latency program permissive for expression of EB
148 a germinal center (GC) B cell phenotype, and type III latency with an activated B cell (ABC) phenotyp
149 e whether EBV enters the highly transforming type III latency, versus the more restricted type I late
150 to convert EBV-infected cells from type I to type III latency.
151 vation from lymphoblastoid cells (LCLs) with type III latency.
152 ients in Europe are also consistent with the type III lineage.
153         The basic defect in long-QT syndrome type III (LQT3) is an excessive inflow of sodium current
154 lvability, while non-neutral correlations of type iii) may instead facilitate evolutionary exploratio
155 hase-variable methylation by both Type I and Type III methyltransferases is associated with altered g
156 ed MegaSTAR to identify pairs of fibronectin type III monobodies for three human proteins.
157                                Expression of type III neuregulin-1 (TIIINRG1) in induced pluripotent
158                Interestingly, IL-18-sensitve Type III neurons were recorded in the juxtacapsular BST,
159                                            n-Type III-nitride nanowires decorated with Ru sub-nanoclu
160                              Both type I and type III NRG1 improves deficits in the Morris water-maze
161  II) were conditionally ablated, leaving the type III Nrg1 intact.
162  that soluble ectodomains of both type I and type III NRG1 significantly increased expression of Abet
163 test this possibility, full-length type I or type III NRG1 was overexpressed via lentiviral vectors i
164                                 Neuregulin 1 type III (NRG1 type III) is a major physiological substr
165                                 Neuregulin 1 type III (Nrg1III) and laminin alpha2beta1gamma1 (Lm211)
166  B cells support a highly transforming form (type III) of viral latency; however, long-term EBV infec
167  Hereditary sensory and autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian
168 opsis showed that exposure to LS upregulated type III peroxidase genes, of which some are involved in
169 led by NADPH oxidases as well as by secreted type III peroxidases has a great impact on cell wall pro
170                                              Type III phosphatidylinositol 4-kinase (PI4KIIIbeta) is
171 istical association between strains from the type III phylogenetic lineage and PMH lesions (P = 0.001
172                   Chalcone synthase (CHS), a type III plant polyketide synthase, is critical for flav
173 oding proteins of several families including type-III polyketide synthases, hydrolases, and cytochrom
174 ecies (type II), Staphylococcus epidermidis (type III), Porphyromonas and Peptoniphilus species (type
175 ganization of the collagen network, collagen type III predominance, and lack of collagen fiber insert
176 various substrates, thus classifying it as a type III PRMT.
177                RNA polymerase III (RNAP III) type III promoters (U6 or H1) are typically used to driv
178            Using a high-throughput assay for type III protein secretion in Salmonella enterica serova
179                                              Type III protein secretion machines have evolved to deli
180                                              Type III protein secretion systems have specifically evo
181  The Chromodomain-Helicase-DNA binding (CHD) Type III proteins are a subfamily of SWI2/SNF2 proteins
182              Transforming growth factor beta type III receptor (TbetaRIII/betaglycan) is a transmembr
183 ly secreted from cardiomyocytes, as were the type III repeat (T3R) and TSP-C domains, while the LamG
184 tural comparisons revealed that the targeted type III repeat epitopes cluster on the inner strands of
185 ing matricryptic RWRPK sequence in the first type III repeat of fibrillar fibronectin.
186 icryptic heparin-binding region of the first type III repeat of fibrillar FN (FNIII1H) mediates vasod
187 FnBPs recognize similar peptides in targeted type III repeats.
188 i) metal coordination to the organic ligand (type III), respectively.
189                                 In contrast, type III responses convey stability at intermediate temp
190  a combination of random fragmentation and a type III restriction enzyme to derive a densely covering
191 tion system as a molecular syringe to inject type III secreted effector (T3SE) proteins in plants.
192  the reactive oxygen species burst using two type III secreted effector proteins, ExoS and ExoT.
193 e roles of toxins, type II secreted enzymes, type III secreted effectors and motility as well as thei
194 wn about the prerequisites for deployment of type III secreted proteins during infection.
195 cytosolic interface of the membrane spanning type III secretion 'injectisome'.
196                                          The type III secretion (T3S) injectisome is a specialized pr
197                                              Type III secretion (T3S), a protein export pathway commo
198  amylovoran, and had increased expression of type III secretion (T3SS) genes in vitro.
199 , a direct physiologic role for the Shigella type III secretion apparatus (T3SA) in mediating phagoso
200 recisely with the activation of the Shigella type III secretion apparatus, thus evidencing injectisom
201  free cytosolic complexes, which include the type III secretion ATPase, constitute a highly dynamic a
202 g a microcompartment shell protein (PduA), a type III secretion effector protein (SteA), and a metabo
203           Here we report that the Salmonella type III secretion effector, SipA, is responsible for P-
204                                     The ExoU type III secretion enzyme is a potent phospholipase A2 s
205  will be instrumental for the development of type III secretion inhibitors.
206 ation and characterization of the Salmonella type III secretion machine in live bacteria by 2D and 3D
207 situ structure of the Salmonella Typhimurium type III secretion machine obtained by high-throughput c
208 reviously unknown effectors, suggesting that type III secretion may have evolved prior to the archaea
209 epends in part on its pathogenicity island 2 type III secretion system (SPI-2 T3SS), which is require
210  inflammasome upon sensing components of the type III secretion system (T3SS) and flagellar apparatus
211 ne and expression dose of the antiphagocytic type III secretion system (T3SS) and induces functions c
212 opathogenic Escherichia coli (EPEC) uses the type III secretion system (T3SS) effector EspL to degrad
213 . Typhimurium pathogenicity island-1 (SPI-1) type III secretion system (T3SS) effectors and transloca
214                    P. aeruginosa expresses a type III secretion system (T3SS) needle complex that ind
215                                    The SPI-2 type III secretion system (T3SS) of intracellular Salmon
216 e receptors sense host-cell targeting by the type III secretion system (T3SS) of pathogenic Yersinia.
217 ny pathogenic Gram-negative bacteria use the type III secretion system (T3SS) to deliver effector pro
218 tive pathogens infect eukaryotes and use the type III secretion system (T3SS) to deliver effector pro
219                 Citrobacter rodentium uses a type III secretion system (T3SS) to induce colonic crypt
220                          Many bacteria use a type III secretion system (T3SS) to inject effector prot
221 gative pathogens, Shigella rely on a complex type III secretion system (T3SS) to inject effector prot
222                               EHEC employs a type III secretion system (T3SS) to translocate 50 effec
223 dosomal membrane damage by components of the type III secretion system (T3SS) translocon.
224 rV is an essential part of the P. aeruginosa type III secretion system (T3SS), and its oligomeric nat
225 and regulatory components of the P. syringae type III secretion system (T3SS), essential for coloniza
226 m-negative bacteria secrete proteins using a type III secretion system (T3SS), which functions as a n
227 e characterize a regulatory node involving a type III secretion system (T3SS)-exported protein, BtrA,
228 ence effectors into the cell cytoplasm via a type III secretion system (T3SS).
229 d P. aeruginosa virulence determinant is the type III secretion system (T3SS); the production of T3SS
230 is organism requires a horizontally acquired type III secretion system (T3SS2) to infect the small in
231 B, are required for activating the virulence type III secretion system 2 in response to bile salts.
232 he epithem and is actively suppressed by the type III secretion system and its effector proteins.
233 syringae and Xanthomonas campestris, use the type III secretion system as a molecular syringe to inje
234 's immune response, Y. enterocolitica uses a type III secretion system consisting of an injectisome a
235                   The Pseudomonas aeruginosa type III secretion system delivers effector proteins dir
236 fication of two homologous Shigella flexneri type III secretion system effector E3 ligases IpaH1.4 an
237                      Exoenzyme Y (ExoY) is a type III secretion system effector found in 90% of the P
238 tium strains bearing deletions in individual type III secretion system effector genes to determine wh
239                                          The type III secretion system effector protein NleE from ent
240                                    Y. pestis type III secretion system effectors YopJ and YopM can in
241 mbrella term given to E. coli that possess a type III secretion system encoded in the locus of entero
242 leum, a virulence process carried out by the type III secretion system encoded within Salmonella path
243 depends on effector proteins secreted by its type III secretion system for the pathogenesis of plants
244                                              Type III secretion system is a key bacterial symbiosis a
245 er Gram-negative bacterial pathogens, uses a type III secretion system to deliver multiple proteins,
246 domonas syringae secretes effectors from its type III secretion system to infect plants.
247                                 It deploys a type III secretion system to inject effector proteins in
248 hogens use a syringe-like apparatus called a type III secretion system to inject virulence factors in
249 effectors into host cells via a prototypical type III secretion system to promote pathogenesis.
250          In many Gram-negative bacteria, the type III secretion system transports effector proteins i
251 at the introduction of a functional Shigella type III secretion system, but none of its effectors, in
252 -silenced plants are more susceptible to the type III secretion system-deficient bacterial strain Pse
253 ets identified the mRNA for the regulator of type III secretion system.
254 s across its vacuolar membrane via the SPI-2 type III secretion system.
255 ctors delivered into plant cells through the type III secretion system.
256                                              Type III Secretion Systems (T3SS) are complex bacterial
257                                    Flagellar type III secretion systems (T3SS) contain an essential c
258                                              Type III secretion systems (T3SSs) are essential devices
259                                              Type III Secretion Systems (T3SSs) are structurally cons
260                                              Type III secretion systems (T3SSs) inject bacterial effe
261                   Salmonella species utilize type III secretion systems (T3SSs) to translocate effect
262 inject effector proteins into host cells via type III secretion systems (T3SSs).
263 e inner rod and needle proteins of bacterial type III secretion systems (T3SSs).
264 he injectisome (iT3SS) and flagellar (fT3SS) type III secretion systems are 2 virulence factors assoc
265                                              Type III secretion systems are complex nanomachines used
266 sponse, attaching and effacing pathogens use type III secretion systems to introduce effectors target
267 e homology to ring-forming proteins found in type III secretion systems, assembles into an oligomeric
268 quired the presence of functional Salmonella type III secretion systems.
269 e intermembrane space, as has been found for type III secretion systems.
270  of proteins involved in central metabolism, type III secretion, and protein synthesis were associate
271 w that Pst inhibits proteasome activity in a type III secretion-dependent manner.
272 tial mechanism involved in the regulation of type III secretion.
273 dant to IcsA; its activity is independent of type III secretion.
274        This mode of protein export is termed type-III secretion (T3S).
275 d action of the cargo-conducting part of the type-III secretion apparatus.
276 isomes of gram-negative pathogens, is termed type-III secretion.
277 functional analyses, may help to explain why type III strains are associated with PMH.
278 gions that are specific for, or absent from, type III strains compared to other phylogroups.
279 the natural history of mucopolysaccharidosis type III syndromes, neurocognitive progression was impro
280 lfataricus has two divergent subtypes of the type III system (Sso-IIID and a Cmr7-containing variant
281                                              Type III systems (Cmr, Csm) have been shown to cleave RN
282               As has been observed for other Type III systems, Cmr eliminates plasmid invaders in Pyr
283 lex and provide a unifying mechanism for all Type III systems.
284  mild post-systolic shortening (n = 35); and type III: systolic stretching with large post-systolic s
285 e information involves communication between Type III taste cells and 5-HT3 -expressing afferent nerv
286 um imaging, we identified AI salt-responsive type III taste cells and demonstrated that they compose
287 o separate populations of AI salt-responsive type III taste cells distinguished by their sensitivity
288 bsence of TPs, many (66%) AI salt-responsive type III taste cells still exhibited the anion effect, d
289 chanisms could underlie AI salt responses in type III taste cells, one of which may contribute to the
290 ly contact and receive synaptic contact from Type III taste cells.
291 e mechanism contributes to salt responses in type III taste cells.
292 ular PAR levels were up to 2-fold greater in type III than type I latently infected EBV B cells.
293 study, we show that a representative of fold type III, the Escherichia coli alanine racemase (ALR), i
294 ling and maturation with a shift in collagen type III to I.
295                             We show that the type III transforming growth factor beta (TGF-beta) rece
296        Because of the hairpin nature of NRG1 type III, two membrane-bound stubs with a type 1 and a t
297                               Usher syndrome type III (USH3) characterized by progressive loss of vis
298 re identified from water buffalo and a third type (III) was isolated from goat.
299  of structural staged mutation carriers were type III, whereas a large proportion of both electrical
300 ine (Type II) or manifest as a chronic form (Type III) with a wide spectrum of neurological signs.

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