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1 virus and innate receptors that may underlie disease pathogenesis.
2 ata, enable new, systems-level insights into disease pathogenesis.
3 g that tRNA charging plays a central role in disease pathogenesis.
4 alaria, the retina can be used to understand disease pathogenesis.
5 th an established regulatory role in Crohn's disease pathogenesis.
6 , whereas inhibition of SR-A ameliorates the disease pathogenesis.
7 larized immune response did not affect prion disease pathogenesis.
8 n self-antigens as important contributors to disease pathogenesis.
9 ization of the genome in gene regulation and disease pathogenesis.
10 between the gut and the brain may influence disease pathogenesis.
11 tly advanced our understanding of infectious disease pathogenesis.
12 e cells is considered to be important in the disease pathogenesis.
13 viral load may be an important parameter in disease pathogenesis.
14 ls are thought to contribute specifically to disease pathogenesis.
15 matory cytokines associated with periodontal disease pathogenesis.
16 inth co-infection would influence oral prion disease pathogenesis.
17 omponent of high-grade endometrial carcinoma disease pathogenesis.
18 standing tissue-specific immune responses in disease pathogenesis.
19 accumulate in human brains and contribute to disease pathogenesis.
20 , including migration during homeostasis and disease pathogenesis.
21 the link between alpha-syn accumulation and disease pathogenesis.
22 d burden and is thought to drive Alzheimer's disease pathogenesis.
23 such individuals may uncover insights about disease pathogenesis.
24 produce antibodies that are associated with disease pathogenesis.
25 r have been shown to play essential roles in disease pathogenesis.
26 L-17A(+) cells that could play a role in the disease pathogenesis.
27 laxis, we aimed to assess the role of C5a in disease pathogenesis.
28 that metabolic alterations are important to disease pathogenesis.
29 sions, suggesting a role for this protein in disease pathogenesis.
30 matory microenvironment play a vital role in disease pathogenesis.
31 d mitochondrial/oxidative stress pathways in disease pathogenesis.
32 y the mechanisms of endothelial function and disease pathogenesis.
33 or antigen stimulation in early iBA and BASM disease pathogenesis.
34 ytosis (SVE) as a significant contributor to disease pathogenesis.
35 nd the nature of the immune cells that drive disease pathogenesis.
36 s that unknown genetic factors contribute to disease pathogenesis.
37 rovide insight into the role of structure in disease pathogenesis.
38 ion and methylation, which may contribute to disease pathogenesis.
39 response, which worsened inflammatory bowel disease pathogenesis.
40 gamma-secretase is implicated in Alzheimer's disease pathogenesis.
41 s (GWAS) has provided critical insights into disease pathogenesis.
42 merular epithelial cell, as major factors in disease pathogenesis.
43 l as dendritic spine dysgenesis may underlie disease pathogenesis.
44 y diseases, multiple cytokines contribute to disease pathogenesis.
45 that environmental exposures play a role in disease pathogenesis.
46 bility and the role of TDP-43 aggregation in disease pathogenesis.
47 important factors that influence oral prion disease pathogenesis.
48 ental models suggest that CD8+ T cells drive disease pathogenesis.
49 IgE-mediated anaphylaxis and stress-related disease pathogenesis.
50 at neuronal ER impairment contributes to HSP disease pathogenesis.
51 ly limited by our molecular understanding of disease pathogenesis.
52 estinal microbiome, the immune response, and disease pathogenesis.
53 ns in Peyer's patches can directly influence disease pathogenesis.
54 ls, is upregulated during GvHD, and mediates disease pathogenesis.
55 on profiles in asthmatic patients can inform disease pathogenesis.
56 inflammation may identify new mechanisms of disease pathogenesis.
57 Genetic risk loci provide new insights into disease pathogenesis.
58 critical factor contributing to Alzheimer's disease pathogenesis.
59 igen presentation, as pivotal mechanisms for disease pathogenesis.
60 derstood about the role of CD4(+) T cells in disease pathogenesis.
61 e to the antiviral immune response and liver disease pathogenesis.
62 re thought to facilitate specific aspects of disease pathogenesis.
63 enable effective prioritization of iSNVs for disease pathogenesis.
64 ect disease risk can yield relevant clues to disease pathogenesis.
65 ng pulmonary fibrosis that are important for disease pathogenesis.
66 t attempts to explain the role of HLA-B27 in disease pathogenesis.
67 ic markers that may provide new knowledge on disease pathogenesis.
68 ests that this pathway may play a role in AD disease pathogenesis.
69 ions, mounting an inflammatory response, and disease pathogenesis.
70 el may be beneficial to our understanding of disease pathogenesis.
71 bonuclease (RMRP) in cellular physiology and disease pathogenesis.
72 ha-SYN) is a central molecule in Parkinson's disease pathogenesis.
73 istics and investigate their contribution in disease pathogenesis.
74 2A in axon guidance also suggested a role in disease pathogenesis.
75 tion to altered environmental conditions and disease pathogenesis.
76 unction is thought to play a crucial role in disease pathogenesis.
77 tribute to dissect the complex mechanisms of disease pathogenesis.
78 n ciliary compartmentalization might play in disease pathogenesis.
79 and to provide novel molecular insights into disease pathogenesis.
80 RNAs (miRNAs) can have a detrimental role in disease pathogenesis.
81 lso potentially contribute to cardiovascular disease pathogenesis.
82 of ALS, highlighting its relevance to study disease pathogenesis.
83 role for oligodendrocyte dysfunction in SCA3 disease pathogenesis.
84 understanding of normal cell physiology and disease pathogenesis.
85 rculosis or sarcoidosis, and is decisive for disease pathogenesis.
86 al pathways and processes that contribute to disease pathogenesis.
87 ll dysfunction might be a key contributor to disease pathogenesis.
88 of identifying putative cellular pathways of disease pathogenesis.
89 range of normal physiological processes and disease pathogenesis.
90 egulation plays an important role in cardiac disease pathogenesis.
91 modium parasite defines the start of malaria disease pathogenesis.
92 o DNA vaccines, gene therapy, and autoimmune disease pathogenesis.
93 sting a primary role for glia in the complex disease pathogenesis.
94 d which reveals novel features of underlying disease pathogenesis.
95 , can provide a window into cell biology and disease pathogenesis.
96 icture of the complex pathway leading to SSc disease pathogenesis.
97 h may contribute to accelerate or exacerbate disease pathogenesis.
98 oactive lipids implicated in alcoholic liver disease pathogenesis.
99 ) to influence inflammation, cell death, and disease pathogenesis.
100 immune system, metabolic rate, and at times, disease pathogenesis.
101 that this model is suitable for studying the disease pathogenesis.
102 tance of lysosomal mechanisms in Parkinson's disease pathogenesis.
103 gests that this biomarker may play a role in disease pathogenesis.
104 d gain-of-function mechanisms play a role in disease pathogenesis.
105 s indicates their central pathogenic role in disease pathogenesis.
106 elopmental processes but also contributes to disease pathogenesis.
107 complement and how these affect immunity and disease pathogenesis.
108 expressed genes is necessary for unraveling disease pathogenesis.
109 OC and ACS episodes to better understand ACS disease pathogenesis.
110 exert both adaptive and maladaptive roles in disease pathogenesis.
111 st 10 days of illness while the virus drives disease pathogenesis.
112 and proposed potential non-HLA mechanisms in disease pathogenesis.
113 with MS points to a role for CD8+ T cells in disease pathogenesis.
114 in which Th17 cells play a major role in the disease pathogenesis.
115 pro-fibrotic response in the multifactorial disease pathogenesis.
116 hanges along this axis are a core feature of disease pathogenesis.
117 l infection would similarly affect CNS prion disease pathogenesis.
118 nd their interplay with the immune system in disease pathogenesis.
119 metabolism and heterogeneity play a role in disease pathogenesis.
120 cular and cellular mechanisms that drive MKD disease pathogenesis.
121 involvement and cortical lesion formation in disease pathogenesis.
122 r vTRs and discuss the role of vTRs in human disease pathogenesis.
123 GluSph or GalSph play a significant role in disease pathogenesis.
124 in mechanosensation and mechanically induced disease pathogenesis.
125 gly being recognized as crucial mediators of disease pathogenesis.
126 lammatory damage plays a significant role in disease pathogenesis.
127 achoma due to an incomplete understanding of disease pathogenesis.
128 disease variants in STAT genes contribute to disease pathogenesis.
129 ed contribution of adipocyte inflammation in disease pathogenesis.
130 presymptomatic, developmental components to disease pathogenesis.
131 likely mediate the genotype effect on kidney disease pathogenesis.
132 s cooperate to regulate pathways relevant to disease pathogenesis.
133 hildren and adults that mediate differential disease pathogenesis.
134 ween these 2 mucosal sites in the context of disease pathogenesis.
135 ses suggest a role for impaired autophagy in disease pathogenesis.
136 intestinal microbes in human physiology and disease pathogenesis.
137 ation as an important mechanism of leiomyoma disease pathogenesis.
138 to question a prevailing view of Alzheimer's disease pathogenesis.
139 sfunction is likely a crucial contributor to disease pathogenesis.
140 at ARSA is a genetic modifier of Parkinson's disease pathogenesis, acting as a molecular chaperone fo
141 data reveal that JNK is a key pathway in the disease pathogenesis and add new therapeutic entry point
142 analyses could increase our understanding of disease pathogenesis and allow us to better predict pati
143 useful as an end point for investigation of disease pathogenesis and as an outcome measure for thera
146 ite notable advances in the understanding of disease pathogenesis and considerable investment in anti
147 erved in patients, they can be used to study disease pathogenesis and determine whether ocular findin
148 of LAM that can advance our understanding of disease pathogenesis and develop therapeutic strategies
149 eratoconus could be useful for understanding disease pathogenesis and discovering biomarkers for earl
151 possible role of diverse T-cells subsets in disease pathogenesis and emphasize the systemic nature o
152 ellular and molecular mechanisms involved in disease pathogenesis and enable the discovery of therape
153 quently to inform a greater understanding of disease pathogenesis and endotypes and prediction of the
154 hnologies could provide unique insights into disease pathogenesis and expedite bench-to-bedside trans
155 ential for understanding the fundamentals of disease pathogenesis and for developing safe and effecti
156 f these transcription factors contributes to disease pathogenesis and found that LEC-specific deletio
157 ibrosis will provide an opportunity to study disease pathogenesis and has potential to be used in pre
160 private spliceosomal mutations contribute to disease pathogenesis and illustrate the utility of molec
161 t implications in the understanding of human disease pathogenesis and immunotherapeutic strategies fo
163 sponse of the host is crucial in determining disease pathogenesis and is the basis for the developmen
164 ing miRNAs are both candidate biomarkers for disease pathogenesis and mediators of cell-to-cell commu
166 ether, our results provide new insights into disease pathogenesis and offer new prospective targets f
167 disease-associated SNPs in lncRNAs influence disease pathogenesis and open the door to the developmen
170 cal manifestations and immune dysregulation, disease pathogenesis and phenotype vary greatly among RA
171 ectrodes are now providing new insights into disease pathogenesis and physiology, while cardiomyocyte
172 r necrosis factor alpha and interleukin 6 in disease pathogenesis and possibly also for granulocyte-m
173 y which dysfunction of TDP-43 contributes to disease pathogenesis and progression remain unclear.
176 erstanding of the mechanisms contributing to disease pathogenesis and provide critical information fo
177 s with a facile and reliable method to study disease pathogenesis and support the development of ther
178 SARS-CoV-2 MA model demonstrates age-related disease pathogenesis and supports the clinical use of pe
179 myelitis (EAE), is widely used to understand disease pathogenesis and test novel therapeutic agents.
180 ed for autoreactive CD4 T cell-mediated skin disease pathogenesis and that the NLRP3-dependent inflam
181 rscore its crucial importance to elucidating disease pathogenesis and the design of next-generation A
182 d new opportunities for better understanding disease pathogenesis and the development of new diagnost
183 nificant implications for both mechanisms of disease pathogenesis and the development of therapeutics
184 are suggested to be important players in the disease pathogenesis and the experimental autoimmune enc
185 ver, the importance of these alpha-chains in disease pathogenesis and the paired TCRbeta-chain remain
186 zation may bring to light insights regarding disease pathogenesis and the reprogramming of macrophage
187 me coronavirus 2 is crucial to understanding disease pathogenesis and the usefulness of bridge therap
188 lement activation that could be important in disease pathogenesis and therapeutic interventions.
190 n a clinical setting, both the mechanisms of disease pathogenesis and therapeutic targets to modify e
191 intermediates can play an important role in disease pathogenesis and thus provide potential targets
192 biological pathways that underly Alzheimer's disease pathogenesis and to identify novel drug targets.
193 developing a more profound understanding of disease pathogenesis and ultimately targeted therapies.
194 rofiles, suggesting potential differences in disease pathogenesis and/or disease characteristics.
195 iron dysregulation that are associated with disease pathogenesis and/or progression are becoming inc
197 he progressive, site-specific nature of CLN1 disease pathogenesis, and highlight the importance of th
198 at have generated new insights into allergic disease pathogenesis, and how these could potentially be
199 discovery in APS1 can illuminate fundamental disease pathogenesis, and many of the antigens found in
200 xis will shed new light on the mechanisms of disease pathogenesis, and may help to guide the developm
201 studying human kidney development, modeling disease pathogenesis, and performing patient-specific dr
202 evolution, in vivo systems for dissection of disease pathogenesis, and the relationship between genet
203 s for diagnostic criteria, poorly understood disease pathogenesis, and very few studies of therapeuti
208 r's disease (AD) pathology are implicated in disease pathogenesis, as they may promote elevated redox
209 ture of PAH, which includes RNAs relevant to disease pathogenesis, associates with disease severity a
210 Although there are important differences in disease pathogenesis between diabetes and glaucoma, they
211 L will not only improve our understanding of disease pathogenesis but also provide further insight in
212 virus 2 (SARS-CoV-2) is key to understanding disease pathogenesis, but few studies have evaluated T c
213 ) likely plays a primary role in Alzheimer's disease pathogenesis, but longitudinal Abeta, tau, and n
214 e polarization is important for inflammatory disease pathogenesis, but the mechanisms regulating pola
215 gesting that Chmp7 may play a causal role in disease pathogenesis by disrupting the endosome-lysosome
216 a This microbial imbalance can contribute to disease pathogenesis by either a depletion in or the pro
217 ld aid in better understanding of cerebellar disease pathogenesis caused due to deregulation of Wnt s
218 vel approaches based on new knowledge of the disease pathogenesis, cell and gene therapies are curren
220 ion of the basic mechanisms underlying human disease pathogenesis depends on the findings afforded to
221 ese findings have important implications for disease pathogenesis: development of Graves TSHR Abs is
224 vations suggest a mechanism of Legionnaires' disease pathogenesis due to the presence of type IVA sec
225 their limitations, advances in understanding disease pathogenesis, emerging targeted treatments, and
226 brate model for evaluating gene function and disease pathogenesis, especially because large numbers o
227 These observations may provide insight into disease pathogenesis for FIRES and other inflammatory se
228 Neutrophilic inflammation is central to disease pathogenesis, for example, in chronic obstructiv
229 opment as a major contributor to psychiatric disease pathogenesis, from common variants acting as exp
232 unctions as signaling molecules and roles in disease pathogenesis have been emerging to be BA species
235 CT) has been implicated in neurodegenerative disease pathogenesis; however, the mechanisms by which d
236 dvances that underlie expanding knowledge of disease pathogenesis, improvements in disease management
237 a powerful tool for the exploration of human disease pathogenesis in biomedical research, as well as
238 tion pathology may contribute to Alzheimer's disease pathogenesis in both synergistic and additive ma
239 TS-1 may play a role in advanced periodontal disease pathogenesis in correlation with tissue hypoxia
241 tes dysregulated ILC responses as drivers of disease pathogenesis in multiple inflammatory disorders.
243 w the virology of EBV, mechanisms underlying disease pathogenesis in PIDs, and developments in immune
245 oll-like receptor 9 (TLR9) is a regulator of disease pathogenesis in systemic lupus erythematosus (SL
246 contribution of defects in CD4(+) T cells to disease pathogenesis in these patients has not been thor
247 ation is a druggable epigenetic mechanism of disease pathogenesis in this heritable HF syndrome.
248 that support a current model of Alzheimer's disease pathogenesis in which Abeta appears early, follo
250 ollectively implicated four main pathways in disease pathogenesis, including RNA metabolism and trans
251 has evoked environmental factors involved in disease pathogenesis, including the gut microbiota, diet
254 he contribution of IFNs to skin and systemic disease pathogenesis is key to development of new therap
259 ating the interactions between autophagy and disease pathogenesis is thus a critical area for further
260 nsglutaminase is critical to activate celiac disease pathogenesis making the addition of mTG to wheat
261 of IFI16 and AIM2 contribute to periodontal disease pathogenesis may lead to treatment options that
262 tic system, which are important in Alzheimer disease pathogenesis, may also be involved in CKD-associ
263 olved mechanisms of health are distinct from disease pathogenesis mechanisms and suggest that we deve
264 ic approaches, increase our understanding of disease pathogenesis, monitor disease progression, and d
265 understanding of the molecular basis of SMA, disease pathogenesis, natural history, and recognition o
267 ure to hyperoxia is thought to contribute to disease pathogenesis.Objectives: To determine the effect
268 ssue-specific modulations, pharmacology, and disease pathogenesis of K(V)7.1, and likely applies to n
269 robes and their products contribute to liver disease pathogenesis, putative microbial biomarkers of d
270 infection, we achieved uniform lethality and disease pathogenesis reflective of that observed in huma
271 pathogenesis with the underlying theme that disease pathogenesis relates to a failure of damage resp
273 ular characteristics of LAM cells underlying disease pathogenesis remain elusive.Objectives: Identifi
279 of ALS/FTD pathology; however, their role in disease pathogenesis remains incompletely understood.
282 oned by tumour lineage-with implications for disease pathogenesis, screening, design of clinical tria
284 oxin is postulated to have a central role in disease pathogenesis, the establishment of chronic infec
285 onary artery disease-and its contribution to disease pathogenesis, there is increased interest in und
287 nonstructural protein 1 (NS1) contributes to disease pathogenesis through the inhibition of host inna
288 otential involvement of TREM-1 in the severe disease pathogenesis, thus providing new insights for fu
289 sing on the elucidation of the mechanisms of disease pathogenesis to enhance health, treat disease, a
290 elin-specific CD8+ T cells may contribute to disease pathogenesis via a FasL-dependent mechanism that
292 ress whether this phenomenon plays a role in disease pathogenesis, we generated a knock-in mouse mode
293 c and immunological insights into autoimmune disease pathogenesis were initially uncovered in the con
294 tokine axes and other mechanisms involved in disease pathogenesis, which are currently being tested f
295 lecular markers and limited understanding of disease pathogenesis, which has made diagnosis challengi
296 l, in turn, provide additional insights into disease pathogenesis, which will inform the development
297 derlying the prodromic stages of Alzheimer's disease pathogenesis will aid the development of new, ta
299 and elucidation of the mechanistic basis of disease pathogenesis will depend on an increased basic u
300 and adaptive immune pathways contributes to disease pathogenesis, with prominent interferon (IFN) si