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1 % of the activation of the positive control (rosiglitazone).
2 played iWAT browning, even in the absence of rosiglitazone.
3 tures were treated with the PPARgamma ligand rosiglitazone.
4 sly reported amorfrutins, similar to that of rosiglitazone.
5 e loss side effect of the PPAR-gamma agonist rosiglitazone.
6  types may be different for pioglitazone and rosiglitazone.
7 ytes was increased by the anti-diabetic drug rosiglitazone.
8  edema side effects of the PPARgamma agonist rosiglitazone.
9 erent from metformin alone or metformin plus rosiglitazone.
10 ly, down-regulated by the anti-diabetic drug rosiglitazone.
11 sis by AFC was also attenuated compared with rosiglitazone.
12 e-proliferator-activated receptor-gamma with rosiglitazone.
13 roliferator-activated receptor-gamma agonist Rosiglitazone.
14 activated receptor-gamma (PPARgamma) ligand, rosiglitazone.
15  different from responses induced by the TZD rosiglitazone.
16 c acid (13-HODE) and thiazolidinedione (TZD)-rosiglitazone.
17 creased mainly in women randomly assigned to rosiglitazone.
18 ta was also up-regulated by pioglitazone and rosiglitazone.
19  effect profile compared to the full agonist rosiglitazone.
20 d) in the presence of the PPARgamma agonist, rosiglitazone.
21 an the median expected percentage prescribed rosiglitazone.
22 ical response to antidiabetic treatment with rosiglitazone.
23 gonists such as TZD diabetes drugs including rosiglitazone.
24 t but also impairs the anti-tumor effects of rosiglitazone.
25 ates the anti-tumor effects of PPARgamma and rosiglitazone.
26 ) or without (n = 8) the anti-diabetes drug, rosiglitazone.
27  weight and with effectiveness comparable to rosiglitazone.
28 , is reversed by the upregulation of NRF2 by rosiglitazone.
29 alter the activity of the anti-diabetic drug rosiglitazone.
30 reatment of mice with the insulin sensitizer rosiglitazone.
31 ator-activated receptor gamma sensitivity to rosiglitazone.
32                  Supplementing the diet with rosiglitazone (1.5 mg/g body weight) for an additional 4
33 ted for 7 days with metformin (10 mM) and/or rosiglitazone (10 muM).
34 endently up-regulated IGF-1R protein levels (rosiglitazone, 10 mumol/liter, 67% increase, n = 4, p <
35 ollows: 1) metformin (100 mg/kg per day), 2) rosiglitazone (2 mg/kg per day), and 3) no drug.
36 sistance were randomized to rhGH 3 mg daily, rosiglitazone 4 mg twice daily, combination rhGH + rosig
37 etformin alone or to metformin combined with rosiglitazone (4 mg twice a day) or a lifestyle-interven
38 signed to receive either 4 mg twice-daily of rosiglitazone, 4 mg of rosiglitazone and 500 mg of metfo
39  to the known insulin-sensitizing effects of rosiglitazone (6 mg kg(-1) day(-1) ).
40 ently evaluated the therapeutic potential of rosiglitazone (6 mg/kg at 5 min, 6 h and 24 h; i.p.) fol
41 7 days with metformin (250 mg/kg/day) and/or rosiglitazone (8 mg/kg/day).
42 and anemia characteristics of treatment with rosiglitazone (a TZD).
43                                              Rosiglitazone, a blood-brain barrier-impermeant PPARgamm
44        In our type 2 diabetes/obesity model, rosiglitazone, a peroxisome proliferator-activated recep
45 tment of selenium-deficient macrophages with rosiglitazone, a peroxisome proliferator-activated recep
46                                              Rosiglitazone, a peroxisome proliferator-activated recep
47                            Here we show that rosiglitazone, a PPAR-gamma agonist, rescued the dendrit
48 egulation by TNFalpha, which was reversed by rosiglitazone, a result consistent with altered high man
49 tion or when mice were treated for 1 wk with rosiglitazone, a specific agonist of peroxisome prolifer
50                                              Rosiglitazone, a specific peroxisome proliferator-activa
51               Recent studies have associated rosiglitazone, a thiazolidinedione drug, with adverse ca
52                                              Rosiglitazone, a well known insulin sensitizer, stimulat
53 roliferator-activated receptor-gamma agonist rosiglitazone abrogated diet-induced mammary growth.
54                              The addition of rosiglitazone abrogated the adverse effects of rhGH on i
55 that ped/pea-15 repression may contribute to rosiglitazone action on glucose disposal.
56  down-regulation, whereas metformin reversed rosiglitazone activity at the translational level.
57 10-fold) treatment, or the antidiabetic drug rosiglitazone, all known PPAR activators.
58 glitazone and -22.7% in rhGH) but not in the rosiglitazone alone (-2.5%) or control arms (-1.9%).
59 and losartan confers no greater benefit than rosiglitazone alone with respect to histopathology.
60 rsus rosiglitazone and losartan, compared to rosiglitazone alone, after 48 weeks of therapy.
61                 The insulin-sensitizing drug rosiglitazone also increases the expression of CTRP13 in
62 adverse effect, and long-term treatment with rosiglitazone altered liver enzymes and caused hepatic f
63 5 expression and caused nonresponsiveness to rosiglitazone, although c-jun overexpression enhanced th
64 insulin doses, protection was potentiated by rosiglitazone, an insulin-sensitizing drug used to treat
65 gnificantly in the rhGH arms (-17.5% in rhGH/rosiglitazone and -22.7% in rhGH) but not in the rosigli
66 r 4 mg twice-daily of rosiglitazone, 4 mg of rosiglitazone and 500 mg of metformin twice-daily, or 4
67        Supplementing with PPARgamma agonists rosiglitazone and GW1929 was sufficient to restore M2 di
68 dipose tissue remodeling similar to those of rosiglitazone and had enhanced antiinflammatory effects.
69 following exposure to the anti-diabetic drug rosiglitazone and increased circulating levels in adipon
70  therapy with rosiglitazone and metformin or rosiglitazone and losartan confers no greater benefit th
71 litazone and metformin in combination versus rosiglitazone and losartan, compared to rosiglitazone al
72 en-label trial was to assess the efficacy of rosiglitazone and metformin in combination versus rosigl
73 orty-eight weeks of combination therapy with rosiglitazone and metformin or rosiglitazone and losarta
74 igate the effects of two antidiabetic drugs, rosiglitazone and metformin, on PepT1 activity/expressio
75  by anti-diabetic PPARgamma ligands, such as rosiglitazone and MRL24.
76                   PPARgamma agonists such as rosiglitazone and pioglitazone are in clinical use for t
77      Microarray analysis revealed that while rosiglitazone and pioglitazone had little effect on gene
78  Compound 6 exhibited comparable efficacy to rosiglitazone and pioglitazone in vivo.
79 some proliferator-activated receptor ligands rosiglitazone and pioglitazone inhibited CYP26A1 with IC
80                                      Whereas rosiglitazone and pioglitazone potentiated cell death, t
81           Thiazolidinediones (TZDs), such as rosiglitazone and pioglitazone, are peroxisome prolifera
82 ects of thiazolidinediones (TZDs), including rosiglitazone and pioglitazone, on cardiac tissue.
83 We tested the effect of two TZD class drugs, rosiglitazone and pioglitazone, on human aortic smooth m
84  (TZD) class of antidiabetes drugs including rosiglitazone and pioglitazone.
85 ceptor phosphorylation, and this response to rosiglitazone and possibly to pioglitazone was PPARgamma
86                                      We used rosiglitazone and primary adipocytes to stringently eval
87         These compounds were far better than rosiglitazone and the other isolated compounds in enhanc
88 ompared with the effects of other PPARgamma (rosiglitazone) and PPARalpha (WY14643) agonists.
89 termine, L-phenylepherine, proglitazone, and rosiglitazone) and seven interferences chosen from off-t
90 duced CH, mice were fed a high-fat diet with rosiglitazone, and cardiac and metabolic consequences we
91  of 234) for metformin alone, metformin plus rosiglitazone, and metformin plus lifestyle intervention
92 ction and insulin sensitivity over time with rosiglitazone appear to be responsible for its superior
93 in resistance, and PPARgamma ligands such as rosiglitazone are insulin sensitizing, yet the mechanism
94 e thiazolidinediones (TZDs) pioglitazone and rosiglitazone are insulin-sensitizing PPARgamma agonists
95 lts suggest that the behavioral responses to rosiglitazone are mediated through PPARgamma-dependent i
96 approved thiazolidinediones pioglitazone and rosiglitazone are peroxisome proliferator-activated rece
97 for human psoriasis, that is, Etanercept and Rosiglitazone, are effective in alleviating the symptoms
98                                        Using rosiglitazone as a model PPARgamma agonist, which decrea
99  used the facility proportion of patients on rosiglitazone as the predictor (instrumental variable ap
100    In this study, we show that, in L6 cells, rosiglitazone- as well as pioglitazone-dependent activat
101                                              Rosiglitazone attenuated bleomycin-induced skin inflamma
102 hereas treatment with the insulin sensitizer rosiglitazone attenuated both metabolic syndrome and ath
103 lled clinical trial compared the efficacy of rosiglitazone (Avandia; GlaxoSmithKline, Philadelphia, P
104  the adiponectin production was prevented by rosiglitazone but not by antioxidants.
105 th AFC improved glucose tolerance similar to rosiglitazone, but AFC did not promote weight gain to th
106                              The addition of rosiglitazone, but not an intensive lifestyle interventi
107            Treatment by the PPARgamma ligand rosiglitazone, but not PI3K modulators, rescued colorect
108                       For colorectal cancer, rosiglitazone, but not pioglitazone, was associated with
109 ype mice with LPS and the PPARgamma agonist, rosiglitazone, but not the PPARalpha agonist (WY-14643),
110 metabolism genes in the heart was altered by rosiglitazone, but these changes were not attenuated by
111 treatment of mice with the PPARgamma agonist rosiglitazone caused a greater improvement in in vivo in
112                The adjusted hazard ratio for rosiglitazone compared with pioglitazone was 1.06 (95% c
113 vents per 100 person-years of treatment with rosiglitazone compared with pioglitazone.
114 nd mortality associated with prescription of rosiglitazone, compared with other oral hypoglycemic age
115                                              Rosiglitazone deactivated the mitogen-activated protein
116 roliferator-activated receptor gamma agonist rosiglitazone decreased activator protein 1 promoter act
117 MC neurons induced by the PPAR-gamma agonist rosiglitazone decreased ROS levels and increased food in
118                                              Rosiglitazone did not affect LV remodeling, increased pe
119                             In control mice, rosiglitazone did not alter plasma aldosterone levels or
120 ny possible effect on myocardial infarction, rosiglitazone does not increase the risk of overall card
121                                              Rosiglitazone-driven adipogenic differentiation of both
122 nal assays in hiPSC-CMs using tacrolimus and rosiglitazone, drugs targeting pathways predicted to pro
123  an EC(50) of 0.045 microM (compare with the rosiglitazone EC(50) of 0.067 microM), while the 13-NO(2
124 g to the ped/pea-15 promoter and blocked the rosiglitazone effect.
125                                              Rosiglitazone effects on cdc42 activation and Caco-2 ShP
126 lormethiazide, but not amiloride, attenuated rosiglitazone effects on volume expansion and CH.
127                                              Rosiglitazone enhanced insulin-induced glucose uptake in
128                The cardiovascular effects of rosiglitazone for patients with coronary artery disease
129 tive pathway and the increased inhibition by rosiglitazone G confirmed the sensitivity of the bacteri
130 vity of AasC was sensitive to triacsin C and rosiglitazone G.
131 spital or death occurred in 61 people in the rosiglitazone group and 29 in the active control group (
132                            321 people in the rosiglitazone group and 323 in the active control group
133                Mean HbA(1c) was lower in the rosiglitazone group than in the control group at 5 years
134 ral hypoglycemic agents, patients prescribed rosiglitazone had significantly higher all-cause (hazard
135 atients who had diabetes and were prescribed rosiglitazone had significantly higher all-cause mortali
136                                              Rosiglitazone has no effect on chloride secretion in the
137                                 In contrast, rosiglitazone has no effect on ENaC activity.
138 ed PPARgamma full agonists, pioglitazone and rosiglitazone, have been reported to produce serious adv
139 , but activates GLUT4 to a similar degree as rosiglitazone, implying gene-specific partial agonism.
140                                              Rosiglitazone improves glycemic control for patients wit
141 activated receptor-gamma (PPARgamma) agonist rosiglitazone improves hippocampus-dependent cognitive d
142 at retains similar anti-diabetic efficacy as rosiglitazone in mice yet does not elicit weight gain or
143 ells induced by a specific PPARgamma agonist rosiglitazone in mice.
144 king pose similarity between telmisartan and rosiglitazone in PPAR gamma active site, two classes of
145                            Administration of rosiglitazone in T1DM-2W mice up-regulated the expressio
146 two insulin-sensitizing drugs (metformin and rosiglitazone) in a genetic model of spontaneously hyper
147 lta12,14-prostaglandin J2, troglitazone, and rosiglitazone) in cat corneal fibroblasts.
148  of the glitazone scaffold, pioglitazone and rosiglitazone, in an effort to identify off-target bindi
149                        The PPARgamma agonist rosiglitazone increases insulin sensitivity and is effec
150                   These results suggest that rosiglitazone increases PHD expression in a PPARgamma-de
151 reviously, we reported that pioglitazone and rosiglitazone induce osteocyte apoptosis and sclerostin
152 phosphorylated at serine 112 but had reduced rosiglitazone-induced activity at lipogenic genes.
153  (PHD) levels significantly increased during rosiglitazone-induced adipocyte differentiation (RIAD).
154 PARgamma-selective antagonist GW9662 blocked rosiglitazone-induced adiponectin expression and antidep
155                            Here we show that rosiglitazone-induced browning of human adipocytes activ
156 tor in human adipocytes that is required for rosiglitazone-induced browning, including the increase i
157 etic furosemide in wild-type mice attenuated rosiglitazone-induced CH, hypertrophic gene reprogrammin
158 esis that volume expansion directly mediates rosiglitazone-induced CH, mice were fed a high-fat diet
159  in the collecting duct, but still exhibited rosiglitazone-induced fluid retention.
160 iglitazone, Pparg-BKO mice were resistant to rosiglitazone-induced hyperphagia and weight gain and, r
161 al triglyceride accumulation relative to the rosiglitazone-induced maximum.
162 d not modify PepT1 activity but counteracted rosiglitazone-induced PepT1-mediated transport.
163  suppressed PPARgamma expression and blocked rosiglitazone-induced pre-adipocyte differentiation towa
164 2 demonstrated this residue as essential for rosiglitazone-induced receptor activation, but nonessent
165 owed loss of PPARgamma and were resistant to rosiglitazone-induced WAT differentiation.
166  receptor gamma (PPARgamma) agonists such as rosiglitazone induces browning of rodent and human adipo
167                            Pretreatment with rosiglitazone inhibited the Ang II-induced expression of
168     Both pretreatment and posttreatment with rosiglitazone inhibited the occurrence of fatal rupture
169                                      Ten-day rosiglitazone injection not only improved the response t
170              There was no significant rhGH x rosiglitazone interaction for any body composition param
171                                              Rosiglitazone is an insulin sensitiser used in combinati
172                  The use of pioglitazone and rosiglitazone is associated with a decreased liver cance
173                                           As rosiglitazone is clinically used to treat diabetes, our
174 uction of lesions in animals pretreated with rosiglitazone is concomitant with decreased expression o
175 ARgamma phosphorylation in obese patients by rosiglitazone is very tightly associated with the anti-d
176 e activity could be enhanced by lanthanum or rosiglitazone, known stimulators of TRPC5 and TRPC5-cont
177 owever, in subcutaneous inguinal fat (iWAT), rosiglitazone markedly induced molecular signatures of b
178       Studies have suggested that the use of rosiglitazone may be associated with an increased risk o
179 er region of PHDs by ChIP-PCR, implying that rosiglitazone may induce PHD up-regulation directly by P
180                                 Importantly, rosiglitazone-mediated whole-body metabolic improvements
181  were treated for a median of 4.0 years with rosiglitazone, metformin, or glyburide and were examined
182 able adjustment, among patients treated with rosiglitazone, mortality was similar (hazard ratio [HR],
183 spanic black participants and metformin plus rosiglitazone most effective in girls.
184 f 7.9% were randomly assigned to addition of rosiglitazone (n=2220) or to a combination of metformin
185 oliferator-activated receptor-gamma) agonist rosiglitazone, Noc expression was enhanced 30-fold.
186 PP5 are resistant to the negative effects of rosiglitazone on bone, which in wild type animals causes
187 ation of IGF-1R, we determined the effect of rosiglitazone on oxidized LDL (oxLDL)-induced apoptosis.
188 idyl ether or GW9662) blunted the effects of rosiglitazone on PHD regulation.
189 el, separate treatment of hyperglycemia with rosiglitazone or hypertension with lisinopril partially
190 oglitazone use adjusted for sex, age, use of rosiglitazone or metformin, and cardiovascular comorbidi
191                     Moreover, treatment with rosiglitazone or pioglitazone did not significantly alte
192 ge, 74.4 years) who initiated treatment with rosiglitazone or pioglitazone through a Medicare Part D
193 er cancer incidence was found for any use of rosiglitazone (OR: 0.73, 95% CI: 0.65-0.81) or pioglitaz
194    Treating epithelial cells with synthetic (rosiglitazone) or endogenous (10-nitro-oleic acid) PPARg
195          However, when Ucp1 was activated by rosiglitazone, or by iWAT browning in cold-exposed or yo
196                 Treatment with pioglitazone, rosiglitazone, or dexamethasone significantly protected
197 itazone 4 mg twice daily, combination rhGH + rosiglitazone, or double placebo (control) for 12 weeks.
198 inhibitor phloridzin, the insulin-sensitizer rosiglitazone, or insulin.
199 ds repress Retn transcription in adipocytes, rosiglitazone paradoxically stimulates the enhancer acti
200 nt mice with the synthetic PPAR-gamma ligand rosiglitazone partially normalizes the altered gene expr
201                 All three PPARgamma ligands (rosiglitazone, pioglitazone, and 15-deoxy-Delta(12,14)-p
202                             Pioglitazone and rosiglitazone possess a common functional core, glitazon
203                           In the presence of rosiglitazone, PP5 translocates to the nucleus, binds to
204                    When treated with the TZD rosiglitazone, Pparg-BKO mice were resistant to rosiglit
205 lta(12,14)-prostaglandin J(2)) or synthetic (rosiglitazone) PPARgamma ligands enhanced B cell prolife
206                      PPARgamma activation by rosiglitazone prevented the mitochondrial dysfunction an
207 planted fibroblasts and skin organ cultures, rosiglitazone prevented the stimulation of collagen gene
208 -term treatment with metformin, but not with rosiglitazone, prevents the development of severe CHF in
209                             Both nitrite and rosiglitazone produced improvements, relative to saline,
210 ) demonstrated that initial monotherapy with rosiglitazone provided superior durability of glycemic c
211 ses of bexarotene with the PPARgamma agonist rosiglitazone provides effective growth suppression of m
212 lls, we show that activation of PPARgamma by rosiglitazone reduced follistatin mRNA levels in a dose-
213                            20 mumol/liter of rosiglitazone reduced oxidized LDL-induced apoptosis by
214 erentiation induced by the PPARgamma agonist rosiglitazone, reduced obesity development and ameliorat
215 s report, we show that the PPARgamma agonist rosiglitazone reduces autoantibody production, renal dis
216                                  Remarkably, rosiglitazone restored insulin secretion in response to
217 e, PPARgamma activation (i.e. treatment with rosiglitazone) restored euglycemia and reversed high fat
218 ation of human aortic endothelial cells with rosiglitazone resulted in the time- and dose-dependent s
219        Treatment with the PPAR-gamma agonist rosiglitazone reversed the phenotype.
220                                        Here, rosiglitazone (RGZ) activation of GPR40 and p38 MAPK was
221     The insulin sensitizing glitazone drugs, rosiglitazone (ROS) and pioglitazone (PGZ) both have ant
222 tivated Receptor gamma (PPARgamma) activator rosiglitazone (Rosi) or prostaglandin E2 analog (16,16-d
223                                We found that rosiglitazone (Rosi) significantly improved insulin sens
224 or (PPARgamma) ligands pioglitazone (Pio) or rosiglitazone (Rosi) to TGF-beta-treated orbital fibrobl
225 liferation-activated receptor-gamma agonist, rosiglitazone (Rosi), a medication recently reintroduced
226 ted for type II diabetes treatment; however, rosiglitazone (ROSI), a PPARgamma agonist, increases foo
227 utic potential of this pathway, we examined, rosiglitazone (Rosi), a PPARgamma agonist, which has bee
228 to DMSO vehicle, the pharmaceutical obesogen rosiglitazone (ROSI), or TBT (5.42, 54.2, or 542 nM) thr
229 ompared to the multi-billion dollar TZD drug rosiglitazone (Rosi).
230 stimulating cells with the PPARgamma agonist rosiglitazone (Rosi).
231 rator-activated receptor (PPAR)gamma agonist rosiglitazone (RSG) but the consequence of this interact
232 activated receptor gamma (PPARgamma) agonist rosiglitazone (RSG) improved hippocampus-dependent cogni
233                        The PPARgamma agonist rosiglitazone (RSG) promoted quiescence in the activated
234 term labor and that PPARgamma activation via rosiglitazone (RSG) would attenuate the macrophage-media
235 gonists currently in clinical use, including rosiglitazone (RSG), are often associated with severe si
236                            Here we show that rosiglitazone significantly increased dendritic spine de
237 conclude that mesalamine, sulfasalazine, and rosiglitazone significantly reduced the cellular express
238           Stimulation of PPAR-gamma in vivo (rosiglitazone) significantly attenuates biliary damage a
239                                              Rosiglitazone stimulated an increase in the ADP/ATP rati
240 ndothelial cells, and LKB1 was essential for rosiglitazone-stimulated AMPK activity in HeLa cells.
241  the role of AMP-activated protein kinase in rosiglitazone-stimulated NO synthesis.
242 MP-activated protein kinase mutant abrogated rosiglitazone-stimulated Ser-1177 phosphorylation and NO
243 ive capacity are maintained independently of rosiglitazone, suggesting that additional browning facto
244 f this NOC-peptide was partially reversed by rosiglitazone, suggesting that effect of NOC on PPAR-gam
245 accumulation compared with that triggered by rosiglitazone, suggesting that LT175 may have a lower ad
246 R3) counteracted this rescue, suggesting the rosiglitazone survival effect was, at least in part, med
247         Moreover, upon coadministration with rosiglitazone, T2384 was able to antagonize the side eff
248  prevented by suramin, a PTP1B inhibitor, or rosiglitazone that decreased PTP1B levels.
249 ed cardiovascular outcomes after addition of rosiglitazone to either metformin or sulfonylurea compar
250 y-resistant and -sensitive mice treated with rosiglitazone to generate candidate brite biomarkers fro
251                                  Addition of rosiglitazone to glucose-lowering therapy in people with
252 ce, an effect associated with the failure of rosiglitazone to improve liver insulin receptor signal t
253 FP407 was required for the PPARgamma agonist rosiglitazone to increase Glut4 expression, but was not
254 ith in vitro results, oral administration of rosiglitazone to ob/ob mice for 2 weeks increased adipos
255              We aimed to determine if adding rosiglitazone to rhGH would abrogate the adverse effects
256 hyperphagia and weight gain and, relative to rosiglitazone-treated Pparg(f/f) mice, experienced only
257 le to antagonize the side effects induced by rosiglitazone treatment alone while retaining robust eff
258    Collectively, these results indicate that rosiglitazone treatment attenuates inflammation, dermal
259 se in hepatic insulin sensitivity induced by rosiglitazone treatment during HFD feeding was completel
260 duced insulin-resistant mice and improved by rosiglitazone treatment in the latter.
261                                      A 7-day rosiglitazone treatment increased PepT1 activity and pre
262                                              Rosiglitazone treatment induced volume expansion and CH
263 ternal-fetal interface and systemically, and rosiglitazone treatment partially attenuated these respo
264                        In these experiments, rosiglitazone treatment reduced c-JUN presence at the PE
265                                              Rosiglitazone treatment reduced the induction of the ear
266                                              Rosiglitazone treatment restored insulin sensitivity in
267                                 In addition, rosiglitazone treatment significantly decreased the cort
268 logical concentrations of Adn resulting from rosiglitazone treatment suppressed regeneration by reduc
269 logical concentrations of Adn resulting from rosiglitazone treatment suppressed regeneration by reduc
270                 As with the in vivo studies, rosiglitazone treatment up-regulated PepT1 transport act
271 matched analysis supported an association of rosiglitazone treatment with an increase in major ischem
272 ted receptor (PPAR)gamma activation, through rosiglitazone treatment, reduced the rate of alpha-GalCe
273                                 Furthermore, rosiglitazone treatment, which promotes redistribution o
274 vels, although these effects were reduced by rosiglitazone treatment.
275 ckdown of PP5 results in cells refractory to rosiglitazone treatment.
276 espectively; this suppression was rescued by rosiglitazone treatment.
277      All of these effects were blunted after rosiglitazone treatment.
278 y distinct PPARgamma agonists [pioglitazone, rosiglitazone, troglitazone, and 15-deoxy-Delta12,14-pro
279      Herein, we show that PPARgamma ligands (rosiglitazone, troglitazone, and 15-deoxy-Delta12,14-pro
280  500 mg of metformin twice-daily, or 4 mg of rosiglitazone twice-daily and 50 mg of losartan once-dai
281 eptor (PPAR) gamma agonists pioglitazone and rosiglitazone up-regulated CYP26B1 transcription by as m
282 tic agonists of PPAR-gamma (pioglitazone and rosiglitazone) up-regulates PPAR-gamma-dependent genes,
283           To examine any association between rosiglitazone use and cardiovascular events among patien
284 findings suggest significant associations of rosiglitazone use with higher cardiovascular and all-cau
285 showed more favorable changes over time with rosiglitazone versus metformin or glyburide.
286 ars of follow-up among patients treated with rosiglitazone versus patients not receiving a thiazolidi
287 rescription of pioglitazone, prescription of rosiglitazone was associated with an increased risk of s
288 ve to saline and rosiglitazone, whereas only rosiglitazone was effective at reducing hepatic glucose
289                                              Rosiglitazone was given 1 week before infusion and 1 wee
290      Inhibition of follistatin expression by rosiglitazone was not associated with decreased follista
291                               Metformin plus rosiglitazone was superior to metformin alone (P=0.006);
292                            A novel effect of rosiglitazone was to increase expression of Nrf2 (nuclea
293                                              Rosiglitazone was used as a positive control.
294 rotic process in vivo, the synthetic agonist rosiglitazone was used in a mouse model of scleroderma.
295                             These effects of rosiglitazone were absent in mice lacking adiponectin bu
296 lthough the maximal efficacies of INT131 and rosiglitazone were similar with respect to improvements
297 owered blood pressure relative to saline and rosiglitazone, whereas only rosiglitazone was effective
298 re, the combination of the PPARgamma agonist rosiglitazone with bexarotene synergistically suppressed
299    AFC activated PPARgamma as effectively as rosiglitazone with regard to Adrp, Angptl4, and AdipoQ,
300                          The hypothesis that rosiglitazone would reduce aneurysm expansion or rupture

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