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1 sis and epithelial injury induced by dextran sodium sulfate.
2 itis in mice after administration of dextran sodium sulfate.
3 its stability at different concentrations of sodium sulfate.
4 ration with diatomaceous earth and anhydrous sodium sulfate.
5 r administration of azoxymethane and dextran sodium sulfate.
6 e after exposure to azoxymethane and dextran sodium sulfate.
7 susceptibility to colitis induced by dextran sodium sulfate.
8 y 3 cycles of oral administration of dextran sodium sulfate.
9 xymethane followed by treatment with dextran sodium sulfate.
10 aused by chemical irritants, such as dextran sodium sulfate.
11 hesis was measured by incorporation of [35S]-sodium sulfate.
12 e to wounding of the epithelium with dextran sodium sulfate.
13 ments are repeated in the presence of 400 mM sodium sulfate.
14  absence and presence of a stabilizing salt, sodium sulfate.
15 uced by exposure to azoxymethane and dextran sodium sulfate.
16 given oral Salmonella Typhimurium or dextran sodium sulfate.
17 as induced by oral administration of dextran sodium sulfate.
18  signaling during colitis induced by dextran sodium sulfate.
19 ed by the high sodium content of the dextran sodium sulfate.
20 loys treatment with azoxymethane and dextran sodium sulfate.
21 inflammation induced by azoxymethane/dextran sodium sulfate.
22  a mouse model of colitis induced by dextran sodium sulfate.
23 stration of azoxymethane followed by dextran sodium sulfate.
24 l injury following administration of dextran sodium sulfate.
25 colitis induced by a single cycle of dextran sodium sulfate administration.
26 presence of the stabilizing additives 0.23 M sodium sulfate and 1 M sodium chloride.
27 ults were found when 0.5g mussel shell, 0.5g sodium sulfate and 5mL ethanol were used.
28 entium infection and exacerbation of dextran sodium sulfate and anti-IL10R-triggered colitis.
29 al tumorigenesis in the azoxymethane-dextran sodium sulfate and Apc(Min/+) mouse models and in human
30 c epithelium after administration of dextran sodium sulfate and azoxymethane than control mice.
31 cer was induced by administration of dextran sodium sulfate and azoxymethane.
32              Here we report that the dextran sodium sulfate and CD4+CD45RBhigh T-cell transfer models
33            We found that in both the dextran sodium sulfate and Citrobacter rodentium models of colit
34  was not observed after ingestion of dextran sodium sulfate and correlated with exacerbation of the m
35 ator (Cftr) knockout mice exposed to dextran sodium sulfate and in vitro in primary cholangiocytes is
36 tis was induced by administration of dextran sodium sulfate, and colitis-associated cancer was induce
37 hobiont challenge, administration of dextran sodium sulfate, and high-fat diets.
38 in C57/Bl6 mice by administration of dextran sodium sulfate, and mice were given 10(8) bacteria for 1
39 litis was induced in mice using 2.5% dextran sodium sulfate, and severity was assessed with histology
40 ry (ATOFMS) revealed the presence of halite, sodium sulfates, and sodium carbonates that were strongl
41    Similarly, Spns2 deletion reduced dextran sodium sulfate- and oxazolone-induced colitis.
42 nogenesis protocol [azoxymethane and dextran sodium sulfate (AOM-DSS) administration] exhibited a two
43 on tumorigenesis in the azoxymethane-dextran sodium sulfate (AOM-DSS) model of colitis-associated car
44 c-deficient mice in the azoxymethane/dextran sodium sulfate (AOM/DSS) model of colorectal cancer.
45 arcinogenesis using the azoxymethane/dextran sodium sulfate (AOM/DSS) model.
46           Using the azoxymethane and dextran sodium sulfate (AOM/DSS) murine model of colitis-associa
47 nfected ApcP (Min/+) or azoxymethane/dextran sodium sulfate (AOM/DSS)-treated mice had high LRP5/6 or
48 ecreased in both the presence and absence of sodium sulfate, as previously reported for a variety of
49 n of a 3.41 mol/kg water aqueous solution of sodium sulfate at 1.54 GPa in a diamond-anvil cell resul
50 (PAA) and Amplon (blend of sulfuric acid and sodium sulfate) at a poultry processing pilot plant scal
51  formation following an azoxymethane/dextran sodium sulfate challenge.
52 enomas formed following azoxymethane/dextran sodium sulfate challenge.
53          We identified and characterized the sodium/sulfate co-transporter (NaS-1; Slc13a1) as an Fxr
54  signaling protected mice from acute dextran sodium sulfate colitis because DR3(-/-) mice showed more
55 (DeltaIEC)) mice develop more severe dextran sodium sulfate colitis due to delayed ulcer healing and
56 issue from Ier3(-/-) mice subject of dextran sodium sulfate colitis exhibit greater Nrf2 activity tha
57 /2(-/-) BM chimera mice with chronic dextran sodium sulfate colitis exhibited delayed ulcer healing,
58                           Studies of dextran sodium sulfate colitis in intestinal epithelial-specific
59                                      Dextran sodium sulfate colitis led to increased levels of inflam
60 e were similarly more susceptible to dextran sodium sulfate colitis, although without mortality and w
61           Using the azoxymethane and dextran sodium sulfate colitis-associated colorectal cancer mode
62 esults in enhanced susceptibility to dextran sodium sulfate colitis-induced systemic inflammation and
63 lity and increased susceptibility to dextran sodium sulfate colitis.
64 ins in macrophages protect mice from dextran sodium sulfate-colitis by enhancing 15-PGDH-dependent ox
65                       In response to dextran sodium sulfate, colonic infiltration of neutrophils and
66 himurium and after administration of dextran sodium sulfate compared with wild-type mice.
67 nt gas, the extract was dried with anhydrous sodium sulfate, concentrated through evaporation, and th
68 of one-dimensional bonded chains observed in sodium sulfate decahydrate (mirabilite).
69 stinal inflammation upon exposure to dextran sodium sulfate, demonstrating a previously unrecognized
70 e mice treated with azoxymethane and dextran sodium sulfate developed approximately 7-10 tumors per m
71 burdens following azoxymethane (AOM)/dextran sodium sulfate (DSS) administration compared with wild-t
72  We administered 2 exogenous agents, dextran sodium sulfate (DSS) and acetic acid, to assess the susc
73                               In the dextran sodium sulfate (DSS) and adoptive T-cell transfer models
74 tis and colitis-associated CRC using dextran sodium sulfate (DSS) and azoxymethane (AOM)-DSS experime
75                                      Dextran sodium sulfate (DSS) and Citrobacter rodentium colitis (
76 mely sensitive to colitis induced by dextran sodium sulfate (DSS) and developed spontaneous ileitis a
77  using two models, administration of dextran sodium sulfate (DSS) and Salmonella enterica subsp. sero
78 nitrobenzene sulfonic acid (TNBS) or dextran sodium sulfate (DSS) and the inflammatory responses were
79                                  The dextran sodium sulfate (DSS) and trinitrobenzene sulfonic acid (
80 ucosal injury and colitis induced by dextran sodium sulfate (DSS) are ameliorated in epimorphin-/- mi
81 nted diets was assayed after a 7-day dextran sodium sulfate (DSS) challenge by quantitative real-time
82 sessment of mucosal damage in murine dextran sodium sulfate (DSS) colitis and human IBD.
83 DeltaIEC) mice) were subjected to 2% dextran sodium sulfate (DSS) colitis for 7 days.
84 eficient mice and chemically induced dextran sodium sulfate (DSS) colitis have led to inconsistent re
85 he development of azoxymethane (AOM)/dextran sodium sulfate (DSS) colitis-associated cancer (CAC).
86 eoplasia, we compared differences in dextran sodium sulfate (DSS) colitis-associated neoplasia betwee
87 nistering the specific inhibitors in dextran sodium sulfate (DSS) colitis.
88 e (10 mg/kg) and two treatments with dextran sodium sulfate (DSS) during a 20-week assay period.
89                                      Dextran sodium sulfate (DSS) exposure induced STAT-6 and NF-kapp
90                           Mice given dextran sodium sulfate (DSS) followed by NP-KPV were protected a
91 type littermates by administering 3% dextran sodium sulfate (DSS) for 7 days followed by 2-week recov
92    Mice (C57BL/6) were exposed to 3% dextran sodium sulfate (DSS) for 7 days or 4% DSS for 5 days fol
93 tis was induced by administration of dextran sodium sulfate (DSS) in distilled water.
94  and wild-type mice by administering dextran sodium sulfate (DSS) in drinking water.
95 litis based on the administration of dextran sodium sulfate (DSS) in the drinking water, we sought to
96  extracellular osmolarity induced by dextran sodium sulfate (DSS) in vivo Collectively, these finding
97  gammadelta IEL was evaluated in the dextran sodium sulfate (DSS) induced mouse colitis model system.
98 duces the severity of colitis in the dextran sodium sulfate (DSS) model of murine colonic injury.
99 evels in colon contents, we used the dextran sodium sulfate (DSS) model to test the enzyme's ability
100 itrobenzene sulfonic acid (TNBS) and dextran sodium sulfate (DSS) models of colitis.
101                    Administration of dextran sodium sulfate (DSS) significantly increased intestinal
102 thane followed by multiple rounds of dextran sodium sulfate (DSS) to induce colitis and tumorigenesis
103                                Using dextran sodium sulfate (DSS) to induce colitis in mice, we ident
104 ymethane followed by three cycles of dextran sodium sulfate (DSS) to induce colitis-associated cancer
105                 Some mice were given dextran sodium sulfate (DSS) to induce colitis.
106                     Mice were fed 3% dextran sodium sulfate (DSS) to induce colonic inflammation, wit
107 beta(-/-) mice, and, when exposed to dextran sodium sulfate (DSS) to induce inflammatory bowel diseas
108 tis was induced by administration of dextran sodium sulfate (DSS) to mice or transfer of T cells to l
109 X-2(-/-), and heterozygous mice with dextran sodium sulfate (DSS) to provoke acute colonic inflammati
110                         We show that dextran sodium sulfate (DSS) treatment promotes the recruitment
111                              Chronic Dextran sodium sulfate (DSS) treatment, an inflammatory inducer
112 microbiota was achieved via low-dose dextran sodium sulfate (DSS) treatment.
113                                      Dextran sodium sulfate (DSS) was used to induce colitis in C57BL
114 lowed by three 1-week cycles of 2.5% dextran sodium sulfate (DSS) water, each cycle separated by 2 we
115                                      Dextran sodium sulfate (DSS), 2,4,6-trinitrobenzene sulfonic aci
116  intestinal inflammation elicited by dextran sodium sulfate (DSS), a model of experimental colitis.
117  exposure to the oral innate trigger dextran sodium sulfate (DSS), a nonredundant proinflammatory rol
118 induced in mice by administration of dextran sodium sulfate (DSS), and carcinogenesis was induced by
119                                      Dextran sodium sulfate (DSS), at doses that resulted in little e
120 ice, or given azoxymethane (AOM) and dextran sodium sulfate (DSS), or 1,2-dimethylhydrazine and DSS,
121 nvironmental epithelial injury using dextran sodium sulfate (DSS), Tfeb (DeltaIEC) mice exhibited exa
122          In acute colitis induced by dextran sodium sulfate (DSS), Vim KO mice develop significantly
123 epithelium with low-molecular-weight dextran sodium sulfate (DSS), which is a well-studied model of m
124 is were induced by administration of dextran sodium sulfate (DSS), with or without azoxymethane (AOM)
125 pecifically in mice with infectious, dextran sodium sulfate (DSS)-, and T-cell-induced colitis.
126  of Gal2 in colitis, we employed the dextran sodium sulfate (DSS)-induced acute colitis model in mice
127 taIEC) mice were less susceptible to dextran sodium sulfate (DSS)-induced acute colitis.
128                              We used dextran sodium sulfate (DSS)-induced chronic colitis to investig
129        In this article, we show that dextran sodium sulfate (DSS)-induced clinical disease and histol
130    Mucosal repair was assessed after dextran sodium sulfate (DSS)-induced colitis in mice receiving i
131 antioxidants on gut permeability and dextran sodium sulfate (DSS)-induced colitis in mice was tested.
132 ions that increase susceptibility to dextran sodium sulfate (DSS)-induced colitis in mice, we identif
133 l thrombosis that is associated with dextran sodium sulfate (DSS)-induced colitis in mice.
134 ve component of the host response to dextran sodium sulfate (DSS)-induced colitis in the mouse is med
135                             Although dextran sodium sulfate (DSS)-induced colitis is a commonly used
136 i in male mice, in formalin test and dextran sodium sulfate (DSS)-induced colitis model, respectively
137 estinal tract, significantly reduced dextran sodium sulfate (DSS)-induced colitis severity, whereas d
138 alactosylceramide (alpha-GalCer), on dextran sodium sulfate (DSS)-induced colitis were examined.
139 IL-6-deficient (IL-6(-/-)) mice with dextran sodium sulfate (DSS)-induced colitis.
140 caspase-1 were highly susceptible to dextran sodium sulfate (DSS)-induced colitis.
141 f Pirb-/- and wild-type (WT) mice to dextran sodium sulfate (DSS)-induced colitis.
142 at causes enhanced susceptibility to dextran sodium sulfate (DSS)-induced colitis.
143  inflammation or crypt damage during dextran sodium sulfate (DSS)-induced colitis.
144 protect intestinal epithelium during dextran sodium sulfate (DSS)-induced colitis.
145  or 50 mg/kg), in an animal model of dextran sodium sulfate (DSS)-induced colitis.
146  in vivo, and enhances recovery from dextran sodium sulfate (DSS)-induced colonic damage.
147   Here we address this issue using a dextran sodium sulfate (DSS)-induced colonic regeneration model.
148 han WT mice using Azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colorectal cancer model.
149  to induce IL-36gamma in response to dextran sodium sulfate (DSS)-induced damage, suggesting that gut
150 pared with wild-type (WT) mice after dextran sodium sulfate (DSS)-induced injury.
151                            Using the dextran sodium sulfate (DSS)-induced intestinal epithelial injur
152       Colon was examined after acute dextran sodium sulfate (DSS)-induced mucosal injury or after azo
153 oethylene-o,o') tellurate (AS101) on dextran sodium sulfate (DSS)-induced murine colitis.
154 ell repopulation of steady-state and dextran sodium sulfate (DSS)-inflamed small intestine/colon and
155 )Apc(Min/+) mice, azoxymethane (AOM)/dextran sodium sulfate (DSS)-treated mice and de-identified huma
156 ring TNFalpha-siRNA-loaded NPs to 3% dextran sodium sulfate (DSS)-treated mice and investigated the t
157   In comparison with wild-type mice, Dextran Sodium Sulfate (DSS)-treated TRPM8 knockout mice showed
158  Colitis was chemically induced with dextran sodium sulfate (DSS).
159 ion and tissue repair in response to dextran sodium sulfate (DSS).
160 equently exposed to colonic irritant dextran sodium sulfate (DSS).
161 d IL-8Tg mice given azoxymethane and dextran sodium sulfate (DSS).
162 mical colitis induced by exposure to dextran sodium sulfate (DSS).
163 then subjected to repeated cycles of dextran sodium sulfate (DSS).
164 ollowed by induction of colitis with dextran sodium sulfate (DSS).
165 d the severity of colitis induced by dextran sodium sulfate (DSS).
166     We induced colitis in mice using Dextran Sodium Sulfate (DSS).
167 he mouse model of colitis induced by dextran sodium sulfate (DSS).
168 mipenem before or after receiving 5% dextran sodium sulfate (DSS).
169 by continuous oral administration of dextran sodium sulfate (DSS).
170  treatment in severe IBD induced via dextran sodium sulfate (DSS).
171 alities after oral administration of dextran sodium sulfate (DSS).
172 he mouse, which are augmented during dextran sodium sulfate (DSS)/azoxymethane (AOM)-induced CAC.
173 as induced by oral administration of dextran sodium sulfate (DSS, 5 g/dL) to knockout mice, their gen
174 of IFN-gamma to G2A(-/-) mice during dextran sodium sulfate exposure abolished the excess colitic inf
175 methane alone or in combination with dextran sodium sulfate; formation of aberrant crypt foci and col
176 s of sodium sulfate is the highly metastable sodium sulfate heptahydrate (Na(2)SO(4).7H(2)O).
177 ted in the formation of a previously unknown sodium sulfate hydrate, which we have determined by sing
178 is of proteoglycans via incorporation of 35S-sodium sulfate in the culture medium.
179   Acute colitis was induced using 4% dextran sodium sulfate in wild-type mice maintained on Se-defici
180 e models (Salmonella typhimurium and dextran sodium sulfate) in PHB transgenic mice and wild-type lit
181 naturation were observed; for example, 0.4 M sodium sulfate increased the free energy of wild-type SN
182 in altering the onset and relapse of dextran sodium sulfate induced murine colitis.
183 ccordingly, knockdown of ORMDL3 in a dextran sodium sulfate -induced colitis mouse model showed reduc
184 is under normal conditions; however, dextran sodium sulfate-induced (DSS-induced) colitis promoted th
185                               In the dextran sodium sulfate-induced acute colitis model, systemic tre
186                                 In a dextran sodium sulfate-induced acute colitis model, WT mice lost
187  wound healing was corroborated in a dextran sodium sulfate-induced acute colitis mouse model.
188 tes, and increases susceptibility to dextran sodium sulfate-induced bowel injury.
189  in mice inhibited azoxymethane- and dextran sodium sulfate-induced CAC, IL-6 expression, STAT3 phosp
190 CDDO-Me suppressed azoxymethane plus dextran sodium sulfate-induced carcinogenesis in wild-type anima
191 d neutrophil infiltration in a mouse dextran sodium sulfate-induced chronic inflammatory bowel diseas
192  in epithelial cells during both the dextran sodium sulfate-induced colitic and the recovery phase.
193   Further, administration of EGCG to dextran sodium sulfate-induced colitic mice significantly reduce
194                      Mouse models of dextran sodium sulfate-induced colitis and a T cell transfer mod
195 ts were observed in a mouse model of dextran sodium sulfate-induced colitis and in Caco2-BBE cells tr
196 th trinitrobenzene sulfonic acid- or dextran sodium sulfate-induced colitis and in Il10(-/-) mice.
197                                      Dextran sodium sulfate-induced colitis and Salmonella typhimuriu
198 that the presence of GIV ameliorates dextran sodium sulfate-induced colitis and sepsis-induced death.
199 bsence of villin predisposes mice to dextran sodium sulfate-induced colitis by promoting apoptosis.
200 od2 results in higher sensitivity to dextran sodium sulfate-induced colitis compared with a single de
201 ve effects of engineered EcN against dextran sodium sulfate-induced colitis in mice, associated with
202 ignificantly reduced the severity of dextran sodium sulfate-induced colitis in mice.
203             Increased sensitivity to dextran sodium sulfate-induced colitis in Pglyrp3(-/-)Nod2(-/-)
204 ministration of MDP does not prevent dextran sodium sulfate-induced colitis in SAMP mice and that the
205 ed lymphoid follicles and attenuates dextran sodium sulfate-induced colitis independent of endothelia
206 d ameliorating disease phenotypes in dextran sodium sulfate-induced colitis mice.
207  repair during recovery in the acute dextran sodium sulfate-induced colitis model in GH-overexpressin
208    Treatment of mice with HDACi in a dextran sodium sulfate-induced colitis model resulted in a stron
209                                      Dextran sodium sulfate-induced colitis model was established in
210 etermined in vitro as well as in the dextran sodium sulfate-induced colitis mouse model.
211 nt model of allergic airway disease, dextran sodium sulfate-induced colitis was significantly reduced
212 1(-/-) mice and CRHR2(-/-) mice with dextran sodium sulfate-induced colitis were analyzed in comparis
213 R (NCM460-NK-1R cells) and mice with dextran sodium sulfate-induced colitis were used.
214 rom TNF exposure, and exhibit severe dextran sodium sulfate-induced colitis, ameliorated by TNF inhib
215  led to impaired resolution of acute dextran sodium sulfate-induced colitis, which was characterized
216  elevated in the colons of mice with dextran sodium sulfate-induced colitis, which was reduced by tre
217 re transferred to CD1 nude mice with dextran sodium sulfate-induced colitis, with or without oral adm
218 epithelial cell-derived IL-33 during dextran sodium sulfate-induced colitis.
219 lfonic acid (DNBS)-, oxazolone-, and dextran-sodium sulfate-induced colitis.
220 en associated with susceptibility to dextran sodium sulfate-induced colitis.
221 ver, the IGF2BP1 deletion aggravated dextran sodium sulfate-induced colitis.
222  while promoting Treg development in dextran sodium sulfate-induced colitis.
223 , it exerted protective functions in dextran sodium sulfate-induced colitis.
224 cking colonic RelA were sensitive to dextran sodium sulfate-induced colitis.
225 oth autoimmune encephalomyelitis and dextran sodium sulfate-induced colitis.
226 enhance or attenuate the severity of dextran sodium sulfate-induced colitis.
227 rfering (si)RNA to C57BL/6 mice with dextran sodium sulfate-induced colitis.
228 , TNF-alpha, and IL-17) in mice with dextran sodium sulfate-induced colitis.
229 comparing healthy mice and mice with dextran sodium sulfate-induced colitis.
230 ing are transmissible and exacerbate dextran sodium sulfate-induced colitis.
231  and exaggerated inflammation during dextran sodium sulfate-induced colitis.
232 reater incidence of azoxymethane and dextran sodium sulfate-induced colon carcinoma.
233 rotected the colonic epithelium from dextran sodium sulfate-induced damage.
234    We show that this antibody blocks dextran sodium sulfate-induced HK cleavage and bradykinin produc
235 e highly susceptible to azoxymethane/dextran sodium sulfate-induced inflammation and suffered from dr
236 than Rag(-/-) mice to development of dextran sodium sulfate-induced intestinal inflammation, indicati
237 tenance of intestinal homeostasis in dextran sodium sulfate-induced intestinal injury.
238                              Using a dextran sodium sulfate-induced mouse model of acute colitis, we
239 n in Cftr-knockout mice exposed to a dextran sodium sulfate-induced portal endotoxemia.
240 revention and recovery rat models of dextran-sodium-sulfate-induced colitis.
241 portantly, PPARdelta is required for dextran sodium sulfate induction of proinflammatory mediators, i
242 in TNBS-inflamed guinea pigs, and in dextran sodium sulfate-inflamed mice, treated with a free radica
243 yl dipeptide (to stimulate NOD2), or dextran sodium sulfate; intestinal lamina propria cells were col
244 sis was measured as the incorporation of 35S-sodium sulfate into macromolecules separated from uninco
245  the crystallization of aqueous solutions of sodium sulfate is the highly metastable sodium sulfate h
246 ption of the epithelial barrier with dextran sodium sulfate leads to increased IL-19 expression.
247 served for sulfate in some samples with high sodium/sulfate mass ratios.
248 colon into the lymphatic system in a dextran sodium sulfate mediated model of inflammatory bowel dise
249 letion failed to modify azoxymethane/dextran sodium sulfate-mediated tumorigenesis.
250  models of colonic inflammation: the dextran sodium sulfate model and multidrug resistance gene 1a-de
251   Here, studies utilizing the murine dextran sodium sulfate model of colitis revealed the crucial rol
252 ENT FINDINGS: Using the azoxymethane-dextran sodium sulfate model, wound healing pathways seem to be
253 ion and colitis-associated cancer in dextran sodium sulfate model.
254 he trinitrobenzene sulfonic acid and dextran sodium sulfate models of colitis, we show the importance
255     Separate sets of mice were given dextran sodium sulfate or 2,4,6-trinitrobenzenesulfonic acid to
256 d ulcers following administration of dextran sodium sulfate or 2,4,6-trinitrobenzenesulfonic acid.
257 litis was induced in mice by oral 5% dextran sodium sulfate or rectal 5% acetic acid, followed by ene
258 OD, and B6.AKR) by administration of dextran sodium sulfate or rectal application of trinitrobenzene
259             MMP-9-/- mice exposed to dextran sodium sulfate or salmonella had a significantly reduced
260 vere colitis after administration of dextran sodium sulfate or trinitrobenzene sulfonate than mice wi
261            Colitis was induced using dextran sodium sulfate or trinitrobenzene sulfonic acid (TNBS).
262 olitis, induced by administration of dextran sodium sulfate or trinitrobenzene sulfonic acid.
263 e signal response was found to be linear for sodium sulfate over the concentration ranges of 0.2-100
264 05% of the total protein population in 20 mM sodium sulfate, respectively.
265  response, induction of colitis with dextran sodium sulfate resulted in a MyD88-dependent serum Ab re
266 s following initiation of refolding in 0.4 M sodium sulfate revealed weak protection in the first bet
267                                  Addition of sodium sulfate shifts the rate profile to higher denatur
268  in the rectum following injury with dextran sodium sulfate, similarly treated Myd88(-/-) (TLR signal
269  studied the influence of a number of salts (sodium sulfate, sodium fluoride, sodium acetate, and sod
270 mmonium sulfate (AS), ammonium nitrate (AN), sodium sulfate (SS), or sodium nitrate (SN) solutions wi
271 ic (Step 5A) and, when combined with dextran sodium sulfate (Step 5B), inflammation-associated tumor
272 ablated all but the first exon of SLC13A1, a sodium/sulfate symporter responsible for regulating seru
273 and four saline water treatments dominant in sodium-sulfate (T2), sodium-chloride (T3), sodium-chlori
274  all HPP starches and was generally lower in sodium sulfate than in water.
275 vere colitis after administration of dextran sodium sulfate than mice infected with LF82-DeltachiA or
276 oncentrations, especially in the presence of sodium sulfate), the kinetics of folding shows evidence
277                     This resembles anhydrous sodium sulfate (thenardite) but contrasts with the hepta
278 o Rag(-/-) mice or administration of dextran sodium sulfate to C57BL/6 mice.
279 ced in some mice by addition of 2.5% dextran sodium sulfate to drinking water for 5-9 consecutive day
280 ice were exposed to azoxymethane and dextran sodium sulfate to induce colitis and tumorigenesis.
281 n was measured; some mice were given dextran sodium sulfate to induce colitis and/or gavage with an a
282 ice (controls); some mice were given dextran sodium sulfate to induce colitis, with or without a FFAR
283 l polyinosinic:polycytidylic acid or dextran sodium sulfate to induce colitis.
284 t-free (control) diet and then given dextran sodium sulfate to induce colitis; we also studied Il10(-
285 n of sodium chloride, potassium chloride, or sodium sulfate to leptospiral medium to physiological os
286 tis was induced by administration of dextran sodium sulfate to wild-type and Cav-1(-/-) mice, as well
287 e, or given azoxymethane followed by dextran sodium sulfate, to assess intestinal tumor formation.
288                                      Dextran sodium sulfate-treated SLC15A4-deficient mice exhibit de
289 g azoxymethane injection followed by dextran sodium sulfate treatment in TLR4-deficient or wild-type
290 nuated colon inflammation induced by dextran sodium sulfate treatment or Citrobacter rodentium infect
291 rcinogenesis induced by azoxymethane/dextran sodium sulfate treatment.
292 e gut in response to indomethacin or dextran sodium sulfate treatment.
293 uced tumor burden after azoxymethane/dextran sodium sulfate treatment.
294 ation compared with WT animals after dextran sodium sulfate treatment.
295 ion-driven tumor model (azoxymethane/dextran sodium sulfate), VS28 mice developed a significantly hig
296 njury induced by the toxic substance dextran sodium sulfate was fundamentally altered to include path
297 mon colitis model, administration of dextran sodium sulfate, was hopelessly confounded by the high so
298  alpha-d-glucose and citric acid, along with sodium sulfate, were produced using established and newl
299 human FN promoter, given water or 3% dextran sodium sulfate, were used as animal models of colitis.
300                               For example, a sodium sulfate with single, oligomeric vinyl acetate (VA

 
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