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1 hy, Oral-Facial-Digital syndrome Type I (OFD Type I).
2 ppaB signaling, and increases AngII receptor type I a expression, thus potentiating AngII signaling i
3 g and increases expression of AngII receptor type I a.
4                     Derivation of these cell types is a critical step toward understanding the basis
5                The comparative study of cell types is a powerful approach toward deciphering animal e
6  basal concentration of cAMP in several cell types is about 1 muM.
7 his plasticity was dependent on the Rutabaga type I adenylyl cyclase, linking cAMP-dependent plastici
8 gnaling pathway that preferentially uses two type I (ALK2 and ALK3) and two type II (ActRIIA and BMPR
9               The herpes simplex virus (HSV) type I alkaline nuclease, UL12, has 5'-to-3' exonuclease
10 en-specific IgE antibodies are a hallmark of type I allergy.
11 odes on a low-cost disposable chip; one cell type is allowed to pass through the chip whereas the oth
12 h" and then assigned levels of causality for type I and II autoimmunity in patients with CSU from lev
13                              Using siRNAs to type I and II BMP receptors and the signaling intermedia
14                                          For type I and II CRISPR-Cas systems, single-nucleotide muta
15 us and tibialis anterior muscles (with mixed type I and II fiber content), while a significant increa
16 found that supporting cells phagocytose both type I and II hair cells.
17 lates with SAMHD1 protein up-regulation upon type I and II interferon stimulation in primary human mo
18 r ruxolitinib reduced hyperresponsiveness to type I and II interferons, normalized TH1 and follicular
19 rentiation and exaggerated responsiveness to type I and II interferons.
20           Our work shows that, as opposed to type I and II systems, the relaxed specificity of type I
21 ces PGC1alpha expression and a switch toward type I and IIa fibers in rat muscle and myotubes in vitr
22     Isolated collagens were characterized as type I and maintained their triple-helical structure, co
23 wed that BAnOCC performs well as measured by type I and type II error rates.
24           How can neural tissue exhibit both type I and type II excitability?
25                       KEY POINTS: Vestibular type I and type II hair cells and their afferent fibres
26 at anti-Ebola virus activity was overlooked, type I and type II IFNs (alpha-2a, alpha-2b, -beta, -gam
27  blocked binding of their cognate ligands to type I and type II TGF-beta receptors, indicating that C
28 iscale analyses to identify and characterize type I and type III bones in murine jaws.
29 y decreased protein expression of intestinal types I and II IFNRs.
30 at produced ECM proteins, including collagen types I and III and fibronectin.
31                               Genes encoding types I and IV pili, quorum sensing components, and prot
32 ulated by cGMP/cGMP-dependent protein kinase type I, and recent ex vivo studies implicated that incre
33 s than RBM when no information regarding DTI types is available.
34 SMA is subdivided into four main types, with type I being the most severe.
35           Type I EBV infection, particularly type I BL, stimulates strong responses of innate immune
36 erentiation by their activation of different type I BMP receptors and distinct modulations of the cel
37 e proportion of densely compact, homogenous (type I) bone versus more trabeculated, cancellous (type
38 which a fall in oxygen levels might initiate Type I cell activation.
39 asmalemmal-mitochondrial microenvironment in Type I cells and how theories of acute oxygen sensing ar
40  factor (TF) binding sites in different cell types is challenging.
41 dicate that dominant forest tree mycorrhizal type is closely linked with understory invasions.
42 o be a selective biomarker of type II versus type I cochlear afferents (Vyas et al., ).
43 pe I procollagen (PINP) and C-telopeptide of type I collagen (CTX-I) are markers of bone formation an
44 chondral bone were determined by MicroCT and type I collagen alpha1/alpha2 ratio was determined by SD
45 lant with recombinant resistin increased the Type I collagen alpha1/alpha2 ratio.
46                      Excessive deposition of type I collagen causes fibrotic diseases.
47 th altered subchondral bone architecture and type I collagen composition.
48                        Outcome measures were type I collagen crosslinked beta C-telopeptide (betaCTX)
49  their translation and is necessary for high type I collagen expression.
50 t inactivation of Fam20C in cells expressing type I collagen led to skeletal defects and hypophosphat
51  imperfecta (OI) is a bone disease caused by type I collagen mutations and characterized by bone frag
52 as to investigate the use of self-assembling type I collagen oligomers as an injectable therapeutic d
53  regulates cell survival, proliferation, and type I collagen synthesis.
54           On a larger scale, deformations in Type I collagen vary with a periodicity consistent with
55 f intron 36 of the Col1a1 gene, encoding the type I collagen, alpha1 chain, was responsible for the p
56 n, metabolism, and pharmacokinetics of a new type I collagen-targeted magnetic resonance (MR) probe,
57 h Fam20C was inactivated in cells expressing Type I collagen.
58 FKBP19 seems to interact with triple helical type I collagen.
59  and was further increased after adhesion to type I collagen.
60 p.G736D) substitution in the alpha1 chain of type I collagen.
61 cal profiling was conducted to confirm a CDG type I defect.
62 has been identified and it is shown that its type is dependent on the nanoribbon length.
63 ecause LBH gene variants are associated with type I diabetes mellitus, systemic lupus erythematosus,
64  remains the gold standard for treatment for type I diabetes providing an insulin-independent, normog
65 .c. islet delivery as a treatment option for type I diabetes, the more immediate benefit may be for t
66 onton Protocol, is a promising treatment for type I diabetics.
67  class of reactions four pathways (Type I Z, Type I E, Type II Z, Type II E) are possible, leading to
68                                           In type I-E and II-A CRISPR-Cas systems, this adaptation pr
69  genomic regions and of different transcript types (i.e., protein coding, noncoding, and pseudogenes)
70 kine response to IL-1beta in the tested cell types, i.e., neutrophils, macrophages, and fibroblasts,
71                                              Type I EBV infection, particularly type I BL, stimulates
72 ymer-GNR intraribbon heterostructures have a type-I energy level alignment and strongly localized int
73 any other genetic study, including stringent type I error control.
74 s showed that the new method can control the type I error rate and is a bit conservative when compare
75                       To control the overall type I error rate at 0.05, a hierarchical testing strate
76 s with modified standard errors have correct type I error under the null.
77 methods in terms of both empirical power and Type I error.
78                                     However, Type-I error rates are controlled after applying the dat
79  dispersed, the NB regression shows inflated Type-I error rates but the Classical logistic and Bayes
80  power while retaining similar, and reliable type I errors.
81 sting methods, while maintaining the correct type I errors.
82 ation, a model with random effects for event types is estimated.
83  that cortical tissue normally operates as a type I excitable medium but it is locally transformed in
84                                          The type I-F CRISPR adaptive immune system in Pseudomonas ae
85 at many Tn7-like transposons contain minimal type I-F CRISPR-Cas systems that consist of fused cas8f
86 pe I-F system can be overcome through use of type I-F spacers by a horizontally-acquired type III-B s
87 n 'arms race' in which phage escape from the type I-F system can be overcome through use of type I-F
88 ive immune system in Pseudomonas aeruginosa (type I-F) relies on a 350 kDa CRISPR RNA (crRNA)-guided
89                                  One system (type I-F) targets DNA.
90 observed in the soleus muscle (predominantly type I fibers).
91 tween the myofibers adjacent to the collagen type I fibers.
92 ps, lipid infusion increased IMTG content in type I fibres (trained: +62%, sedentary: +79%; P < 0.05)
93 IN3 (+73%) and PLIN5 (+40%; all P < 0.05) in type I fibres.
94 n about the allergen molecules causative for type I food allergy in animals, which, like in human pat
95    KEY POINTS: In the synaptic cleft between type I hair cells and calyceal afferents, K(+) ions accu
96                                              Type I hair cells are not restored by Plp1-CreER(T2)-exp
97  vitro, the afferent nerve calyx surrounding type I hair cells causes unstable intercellular K(+) con
98 nd that in the absence of the calyx, IK,L in type I hair cells exhibited unique biophysical activatio
99                The characteristic feature of type I hair cells is the expression of a low-voltage-act
100 el was established; within a dilute collagen-type I hydrogel, a novel clonal strain of rat cancer-ass
101  inhibitors (PPIs) have been known to induce type I hypersensitivity reactions.
102 est Nile virus (WNV) infection by regulating type I IFN (IFN-I) response.
103  disease-exacerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and s
104                                              Type I IFN activation is induced by pattern-recognition
105 ated Th1 cells to prevent abberant autocrine type I IFN and downstream signaling.
106  although the inflammation is independent of type I IFN and the nucleic acid sensing TLRs, blocking t
107       In this study, we examined the role of type I IFN and TLR trafficking and signaling in xenobiot
108 FN treatment restricts HRV replication, with type I IFN being more potent than type III IFN, suggesti
109 L-6 production by control keratinocytes, and type I IFN blockade decreased IL-6 secretion by lupus ke
110 , CHOP and spliced XBP1 gene expression, and type I IFN by measuring IFNB1 (IFN-beta) and CXCL10 expr
111                        Our results show that type I IFN can suppress CD8(+) T cell responses to cross
112                   In this work, we show that type I IFN expression is derived from the recognition of
113  of IFN-responsive genes, and the release of type I IFN from transfected cells.
114 3 and increased rhinovirus-induced HSPA5 and type I IFN gene expression.
115  interval, and confirmed the contribution of type I IFN genes to Lyme arthritis.
116 ate that PRDM16 diminishes responsiveness to type I IFN in adipose cells to promote thermogenic and m
117  ORMDL3 and rhinovirus-induced ER stress and type I IFN in human leucocytes.
118                                     Although type I IFN induces an antiviral state in many cell types
119       Therefore, we investigated the role of type I IFN induction in the antiviral effects of the miR
120  of chicken IFN-kappa (chIFN-kappa) near the type I IFN locus on the sex-determining Z chromosome.
121 , suggesting that extraepithelial sources of type I IFN may be the critical IFN for limiting enteric
122 alpha in immunosuppression and predicts that type I IFN modulation will be pivotal to cure human chro
123 peared to be independent of the induction of type I IFN or the effects of type II and III IFNs but we
124 se findings suggest that the STING-dependent type I IFN pathway is critical for the GBP-mediated rele
125                           In conclusion, the type I IFN pathway is dysfunctional at the epigenetic le
126                 As bat IFN-gamma induced the type I IFN pathway, its antiviral effect is likely to be
127  fatal response to MI by activating IRF3 and type I IFN production.
128 l host factors involved in DNA detection and type I IFN production.
129 the treatment did not reduce the spontaneous type I IFN response and did not ameliorate lethal inflam
130 triggers a cyclic GMP-AMP synthase-dependent type I IFN response and systemic autoimmunity.
131          These results identify IRF3 and the type I IFN response as a potential therapeutic target fo
132                     This SAM vaccine-induced type I IFN response has the potential to provide an adju
133                            However, when the type I IFN response of mice was suppressed, then the ada
134           To determine the role of the early type I IFN response, SAM vaccines were evaluated in IFN
135 es have indicated that ZIKV evades the human type I IFN response, suggesting a role for the adaptive
136  community highlighting key paradigms of the type I IFN response.
137                   These mice have suppressed type I IFN responses and lack adaptive immune responses,
138 ter, without which inflammatory cytokine and type I IFN responses to the double-stranded RNA analogue
139 1 play important roles in the ISG15-mediated type I IFN sensitivity of HEV.
140 7A NP-induced protection is mediated through type I IFN signaling and requires monocytes in PBMCs.
141 munomodulatory role by negatively regulating type I IFN signaling and, thus, HEV sensitivity to type
142  that DCIR deficiency impairs STAT1-mediated type I IFN signaling in DCs, leading to increased produc
143 on and pathogen's control through sustaining type I IFN signaling in DCs.
144      This study highlights the importance of type I IFN signaling in inflammatory monocytes and the i
145 horiomeningitis virus infection, blockade of type I IFN signaling partially restores antiviral respon
146                            For example, when type I IFN signaling was blocked by Abs in Rag1(-/-) mic
147                            Mice deficient in type I IFN signaling, Ifnar(-/-) and Irf9(-/-) mice, had
148  in the cytoplasm of host cells can initiate type I IFN signaling.
149 herpes simplex virus 1 (HSV-1) that modulate type I IFN signaling.
150 he host by priming the amplification loop of type I IFN signaling.
151 ls was partially regulated by both IL-27 and type I IFN signaling.
152 irus chronic infections display a persistent type I IFN signature.
153 flammatory syndromes in diseases with active type I IFN signature.
154              Increased virus replication and type I IFN specifically inhibited the response to two im
155                    HMBA also increased early type I IFN transcription in human monocytic and epitheli
156 nce of T-bet, IFN-gamma aberrantly induced a type I IFN transcriptomic program.
157 LgyLRV1(-) ) strain of parasites followed by type I IFN treatment increased lesion size and parasite
158                            This induction of type I IFN was independent of IFI16.
159 enic analyses indicate that chIFN-kappa is a type I IFN with conserved genetic features and promoter
160  we tested whether chronic administration of type I IFN, at doses mimicking chronic viral infection,
161  by pretreatment of AMPK-deficient MEFs with type I IFN, illustrating that de novo production of IFN-
162                                         In a type I IFN-accelerated lupus model, treatment with an an
163   Moreover, significant associations between type I IFN-alpha/beta protein levels with the DNA methyl
164  induced early during HIV infection and that type I IFN-associated gene signatures persist, even duri
165 ing that hypomethylation and upregulation of type I IFN-associated genes might be critical in systemi
166 n stage, we confirmed these changes for five type I IFN-associated genes.
167 immune responses through the initiation of a type I IFN-dependent DDR.
168      These findings identify HgIA as a novel type I IFN-independent model of systemic autoimmunity an
169 r studies define a TRIF-dependent, TLR4- and type I IFN-independent pathway of sterile liver injury i
170                           By obstructing the type I IFN-induced antiviral response, miR-BART16 provid
171 sting that HIV-1 exploits CD169 to attenuate type I IFN-induced restrictions.
172                                              Type I IFN-mediated neutrophil activation and NET format
173 cy also leads to persistently high levels of type I IFN-stimulated gene expression and to increased r
174  critical initial step in the elaboration of type I IFN.
175  IFN signaling and, thus, HEV sensitivity to type I IFN.
176 e and regulates HEV sensitivity to exogenous type I IFN.IMPORTANCE Hepatitis E virus (HEV) infection
177 ways between Nb and DBP-FITC, but revealed a type-I IFN (IFN-I) signature unique to DCs from Nb-prime
178 ition receptors (TLR9 and TLR3) leading to a type-I IFN mediated innate immune response that is modul
179                                              Type-I IFN treatment triggers the interaction of STAT1 w
180              Here, we have demonstrated that type I IFNAR signaling in astrocytes regulates BBB perme
181 /-) mice or wild-type mice treated with anti-type I IFNR alone.
182 ited an alpha-helical fold characteristic of type I IFNs and bound to IFNalpha/beta receptor 1 (IFNAR
183 se studies were limited to a small number of type I IFNs and, during the most recent outbreak of Ebol
184                                              Type I IFNs are key mediators of immune defense against
185 also been shown to regulate transcription of type I IFNs during HSV infection.
186                               More recently, type I IFNs were shown to be important during bacterial
187 cerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and signaling in
188 ive, and antibacterial activities typical of type I IFNs, albeit with 100-1000-fold reduced potency c
189  exhibit pro-inflammatory activation only to type I IFNs.
190 illion years ago, predating the evolution of type I IFNs.
191 etal (M) replacement in the framework nodes (type I), (ii) metal node extension (type II), and (iii)
192           Here, we find that RV degrades the types I, II, and III IFN receptors (IFNRs) in vitro In a
193 pregnant C57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice against let
194               Single-pass NRGs, such as NRG1 Types I/II and NRG2, accumulate as unprocessed proforms
195 mily that signals through the IL-20 receptor type I (IL-20Ralpha:IL-20Rbeta), is a cytokine whose fun
196 s are differentiated into >220 different emm types, is immunogenic and elicits protective antibodies.
197 a humanized mouse model and demonstrate that type I interferon (IFN) is induced early during HIV infe
198         Both genes play significant roles in type I interferon (IFN) production and signalling.
199 d that the brain parenchyma has a functional type I interferon (IFN) response that can limit VSV spre
200                                              Type I interferon (IFN) signaling engenders an antiviral
201 ost karyopherin alpha (KPNA) proteins blocks type I interferon (IFN) signaling, which is a central co
202 r T-bet acts as a selective repressor of the type I interferon (IFN) transcriptional program in respo
203 icles via cytoplasmic RNA sensors to produce type I interferon (IFN).
204 tive CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct
205 rica serovar Typhimurium exploits the host's type I interferon (IFN-I) response to induce receptor-in
206        Furthermore, VA1 was sensitive to the type I interferon (IFN-I) response, as VA1 RNA levels we
207 antiretroviral therapy (cART), low levels of type I interferon (IFN-I) signaling persist in some indi
208 sly and induces the subsequent expression of type I interferon and other proinflammatory cytokines.
209 he authors show that the chronic presence of type I interferon in aged mouse brain impedes cognitive
210 eronopathies) characterized by expression of type I interferon in the brain.
211                                    The STING/type I interferon pathway enhances suppressive inflammat
212 cal roles in coordinating both virus-induced type I interferon production and apoptosis; however, the
213 e, a synthetic analogue of histamine reduces type I interferon production in a mouse model of influen
214 e the neuropathogenesis of ZIKV infection in type I interferon receptor IFNAR knockout (Ifnar1 (-/-)
215 NAR(fl/fl) C57BL/6 (H-2(b)) mice lacking the type I interferon receptor in a subset of myeloid cells.
216 ing the viral gene B19R, an inhibitor of the type I interferon response (NYVAC-C-KC-DeltaB19R).
217 onstrated impaired viral clearance, a slower type I interferon response and delayed production of vir
218              Additionally, we found that the type I interferon response and sex hormones can alter bo
219                        One such pathway, the type I interferon response, recognizes viral or mitochon
220 cinia virus B19 protein, an inhibitor of the type I interferon response.
221  through induction of a microbiota-dependent type I interferon response.
222 n of host responses, including inhibition of type I interferon responses, suppression of dendritic ce
223 stimulation with anti-CD3/CD28 antibodies or type I interferon resulted in upregulation of distinct s
224 h functional importance in the regulation of type I interferon signaling.
225 toantibodies (including anti-DNA IgG), and a type I interferon signature.
226 rategically target crucial components of the type I interferon system.
227 ol, preventing accumulation and a subsequent type I interferon-associated inflammatory response.
228  in conjunction with a global suppression of type I interferon-signalling pathway and an aberrant exp
229                                 We validated type-I interferon expression in neurofibroma by protein
230 ce with polyethylene glycolyated (PEGylated) type-I interferon-alpha2b reduces the expression of many
231                          These data define a type I interferonopathy due to DNase II deficiency in hu
232                                              Type I interferons (IFN-1) are cytokines that affect the
233                            Pretreatment with type I interferons (IFN-alpha and IFN-kappa) increased I
234 ion of toll-like receptor 7 (TLR7)-dependent type I interferons (IFN-alpha/beta) from plasmacytoid de
235                                              Type I interferons (IFN-I) are critical in antimicrobial
236 be a driving force in immune exhaustion, and type I interferons (IFN-I) are emerging as critical comp
237                                              Type I interferons (IFN-Is) can now be considered as the
238                                              Type I interferons (IFNalpha/beta) are critical mediator
239 ctivates the adaptor protein STING to induce type I interferons (IFNs) and other immune modulatory mo
240                                              Type I interferons (IFNs) are essential mediators of ant
241                 While induction of antiviral type I interferons (IFNs) is the major outcome of STING
242                                              Type I interferons (IFNs) play a central role in the imm
243 ta support a model wherein the production of type I interferons driven by an autoimmune risk variant
244 387 of U-STAT2 might enhance the efficacy of type I interferons in many different clinical settings.
245 d that the proinflammatory cytokines TNF and type I interferons induced transcriptional cascades that
246               The full-length cDNA encodes a type-I IPPI containing a plastid transit peptide (PTP) a
247                                              Type I IRES elements require auxiliary host proteins to
248  To evaluate the safety of concurrent Boston type I keratoprosthesis (KPro) and glaucoma drainage dev
249                       Interleukin-1 receptor type I knockout mice, which display braked immune respon
250 type III latency, versus the more restricted type I latency, have not been well characterized.
251 ters that are expressed in type III (but not type I) latency.
252 hangiogenesis (in melanomas and other tumour types) is limited by the paucity of mouse models for liv
253 s around 125 K, leading to the presence of a type-I multiferroic phase with huge electric polarizatio
254  Fitzpatrick skin phototype (for type IV vs. type I, multivariable-adjusted RR = 0.99, 95% CI: 0.92,
255 munotherapy, whereas the chromosome-instable type is negatively associated with it.
256  antiviral pathways mediated by multiple IFN types is not well understood.
257 lex ciliopathy, Oral-Facial-Digital syndrome Type I (OFD Type I).
258 (FTase) or protein geranylgeranyltransferase type I or II (GGTase-I and GGTase-II).
259 f ZIKV in pregnant C57BL/6 mice and protects type I or type I/II interferon receptor-deficient mice a
260 tially fatal condition caused by deficiency (type I) or dysfunction (type II) of the C1 inhibitor pro
261   We recently reported 1a (skepinone-L) as a type I p38alpha MAP kinase inhibitor with high potency a
262 I crystal lattice in contrast to the typical type I packing seen from membrane protein structures cry
263 ed levels of plasminogen activator inhibitor type I (PAI-1) have been shown to promote fibrosis in mu
264                              This metabolism-type is particularly elaborated in Catharanthus roseus t
265 duced aquaporin-2 phosphorylation within the type I PDZ-ligand motif disrupted the interaction, in as
266       The method involves sequential Norrish Type I photocleavage of a ketone (7b) and beta-fragmenta
267                                      We used type I plaids formed by the additive superposition of mo
268             Detailed analysis of the modular Type I polyketide synthase (PKS) involved in the biosynt
269             However, manipulation of modular type I polyketide synthases (PKSs) to make unnatural met
270 eveals two distinct tumor types: the mutator type is positively associated with potential response to
271                     N-terminal propeptide of type I procollagen (PINP) and C-telopeptide of type I co
272 mergency department visits as separate event types is proposed.
273              A lower diversity of land cover types is purported to decrease arthropod diversity in ag
274 approximately 60% of all PV-IR synapses, and Type I PV-IR synapses from putative thalamocortical term
275 Se2(1-x) alloys from n-type to bipolar and p-type is realized.
276        New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle atrophy a
277 ral motif essential for binding the TGF-beta type I receptor (TbetaRI) but dispensable for binding th
278 binding to the N-terminal globular domain or type I repeats of hTSP-1.
279 ungus Blastocladiella emersonii, combining a type I rhodopsin domain with a guanylyl cyclase domain.
280 netobacter species produce both a functional type I secretion system (T1SS) and a contact-dependent i
281 confirmed that the labeled SGNs were neither type I SGNs nor olivocochlear efferents.
282 end not only on TLR9, but also on interferon type I signaling, and both mechanisms can be inhibited b
283 d stream by the scavenger receptor, class B, type I (SR-BI), the so-called HDL receptor.
284           This is the case for the zorO-orzO type I system where the OrzO antitoxin base pairs to the
285                            We found that the Type I TARP gamma-2 (stargazin) is present in lamina II
286  a partial agonist at AMPARs associated with Type I TARPs, evoked whole-cell currents in lamina II ne
287                  TWSs can be classified into type-I that respect Lorentz symmetry and type-II that do
288                          Common to most cell types is the asymmetric establishment and regulation of
289 hat used by the previous study, wherein case Types I to IV defined increasing severity of periodontal
290 mbining the historical nomenclature for penA types I to XXXVIII with novel nucleotide sequence design
291 ive infantile paralysis and premature death (type I) to limited motor neuron loss and normal life exp
292                               Many bacterial type I toxin mRNAs possess a long 5 untranslated region
293         Here, we reveal that, in contrast to Type I, Type II animal cryptochromes lack the structural
294 ort three distinct types of ependymal cilia, type-I, type-II and type-III classified based upon their
295                      We argue that each song type is unique to a population and these changes represe
296 pe usage (i.e., how many times each syllable type is used) or syllable sequences.
297 caSR is similar to the adenovirus-associated type I (VAI) RNA in terms of both nucleotide sequence an
298  To test the hypothesis that muscles rich in type I vs. type II muscle fibers would exhibit similar c
299 emia is categorized into two main subgroups: type I, which is seen exclusively in clonal hematologic
300   For this class of reactions four pathways (Type I Z, Type I E, Type II Z, Type II E) are possible,

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