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1 inated in SMKO mice (approximately 5%-10% of control levels).
2 re to hyperoxia but then decreased below the control level.
3 D) activity of only 6 (+/-5) % of the normal control level.
4 -treated cells rescued KGDHC activity to the control level.
5 ssed PRC protein at approximately 15% of the control level.
6 n followed by a recovery significantly below control level.
7 ly through 72 h, enzyme activity returned to control level.
8 es as well as NF-kappaB could be restored to control level.
9 control and brings the depression down to a control level.
10 ing to 80% and 107%, respectively, above the control level.
11 ding to 39% and 38%, respectively, above the control level.
12 ase-specific heparan sulfate, was reduced to control level.
13 beta-amyloid, P-tau] were reduced almost to control level.
14 deficits but fails to enhance growth beyond control level.
15 either prevented or restored mtDNA damage to control levels.
16 use exogenous PKA restored all parameters to control levels.
17 sed mitochondrial aconitase activity back to control levels.
18 ection with a low-dose challenge compared to control levels.
19 and peat, but remained elevated relative to control levels.
20 14 days post-treatment increased again above control levels.
21 monocytes, where DC numbers are about double control levels.
22 icated by decreased relative impedance below control levels.
23 %), and activity ( approximately 108%) above control levels.
24 e (+15%, p<.01), but force did not return to control levels.
25 nockout mice and restored tumor incidence to control levels.
26 ession and cellular location to sinus rhythm control levels.
27 of citrate synthase to levels 36% to 44% of control levels.
28 nal hyperexcitability in epileptic tissue to control levels.
29 rate of apoptosis in active neurons back to control levels.
30 restored PKCepsilon mRNA and protein to the control levels.
31 -LTP by 125% (P<0.001), thus restoring it to control levels.
32 I cell epithelial permeability to protein to control levels.
33 spiking activity and spike amplitude toward control levels.
34 g" myofilament Ca(2+) responsiveness back to control levels.
35 d paired-pulse facilitation deficits back to control levels.
36 rations, and prolonged plasma coagulation to control levels.
37 signaling pathway or proteasome function to control levels.
38 1 and HeyL rescued TrkC(+) neuron numbers to control levels.
39 genesis by surviving interneurons overshoots control levels.
40 rm and rebounded in epileptic animals beyond control levels.
41 ression whereas mGlu3 mRNA was comparable to control levels.
42 ium and cellular ATP content are returned to control levels.
43 maintained in the contralateral hind paw at control levels.
44 ioral and neurochemical measures returned to control levels.
45 unction and intensity of fibrosis to healthy control levels.
46 [(14)C] sucrose permeability, back to saline control levels.
47 ta-stimulated nuclear and cytoplasmic p65 to control levels.
48 ately 2.5-fold [P <0.03], respectively) over control levels.
49 ored mitochondrial and cytoplasmic Ca(2+) to control levels.
50 d biotinylated EAAC1 to approximately 50% of control levels.
51 verapamil to maintain AP duration (APD) near control levels.
52 rate of reepithelialization, which exceeded control levels.
53 egation in embryonic muscles to 3- to 4-fold control levels.
54 levels, which recovers over several hours to control levels.
55 o cartilage-specific matrix proteins fell to control levels.
56 ubB and ubC mRNA levels had all returned to control levels.
57 MKII inhibition could even reduce leak below control levels.
58 JNK phosphorylation was not increased above control levels.
59 hondrial H(2)O(2) emission to non-exercised, control levels.
60 ression of Bcr-Abl is reduced >200-fold from control levels.
61 s was reduced 50 and 91%, respectively, from control levels.
62 cells, the IFNgamma production increased to control levels.
63 terphase duration and checkpoint efficacy to control levels.
64 tivated at 4 h, whereas p-Akt was reduced to control levels.
65 lt offspring, hormone status had returned to control levels.
66 ysin and postsynaptic density-95 back toward control levels.
67 r IS, at a time when CORT was unchanged from control levels.
68 the BCG liver organ load was unaltered from control levels.
69 eturned tumor-infiltrating CD4(+) T cells to control levels.
70 extent, the midbrain-rebounded or surpassed control levels.
71 -Q138 to the cytoplasm restores viability to control levels.
72 rofiles of Trim63 (MuRF1) and Chrna1 back to control levels.
73 n of ISG15 attenuates viral resistance to WT control levels.
74 dietary potassium, which also returned BP to control levels.
75 ued bacterial burden in the ethanol group to control levels.
76 E activities were decreased to 32% to 85% of control levels.
77 ethylated and methylated INS DNA returned to control levels.
78 d total cholesterol (TC) with respect to the control levels.
79 acellular pH and restored enzyme activity to control levels.
80 the cell-cycle distribution and apoptosis to control levels.
81 of respiration with glutamate/malate back to control levels.
82 administered methamphetamine (0.05 mg/kg) at control levels.
83 glycemic ischemia that gradually returned to control levels.
84 C-1alpha target gene expression, compared to control levels.
85 nAg, it was nonetheless significantly above control levels.
86 reducing CP-AMPAR transmission in the NAc to control levels.
87 levels in all tissues examined compared with control levels.
88 fate and beta-hexosaminidase accumulation to control levels.
89 testinal IL-1beta and TNF-alpha cytokines to control levels.
90 not sufficient to restore differentiation to control levels.
91 gned to receive conventional dietary advice [control; level 0 (L0)] or PN advice on the basis of curr
92 the RPP to the left kidney was maintained at control levels (125 +/- 2 mmHg) by continuous servocontr
93 of nitrogen addition, and did not recover to control levels 20 years after nitrogen addition ceased.
98 ws that plant diversity decreased well below control levels after 10 years of chronic high rates (95-
102 tears significantly increased compared with control levels after EDE for 4 and 6 days, respectively,
103 the OVX groups, responding was enhanced from control levels after ExA self-administration in estradio
105 onfirmed by restoration of cell migration to control levels after overexpression of beta1 integrin in
106 lly higher in young Tg1 mice but falls below control levels after postnatal week 12, approximately co
112 H]thymidine incorporation that was twice the control level, along with complete retention of GSIS.
113 creased short-term but recovered only toward control levels, although in epileptic rats excitatory sy
114 creased concentration of RCIIs to 10% of the control level and, interestingly, an increased antenna c
115 l hippocampus restores DA neuron activity to control levels and also blocks the expression of locomot
116 neuroinflammation, return Arc expression to control levels and attenuate cognitive deficits induced
117 y respond to local TGF-beta-induced cues and control levels and distribution of Sox2 to form airways.
118 ce lacking PLN returned I(to,f) and I(K1) to control levels and equalized the APD and QT intervals in
119 hose in striatum and cerebral cortex fell to control levels and hippocampal corticosterone remained e
120 of oleic acid restored hepatic oleyl-CoA to control levels and negated the effects of both central g
121 l myofibres increases transient amplitude to control levels and protects them from loss after OSI.
122 NA returns galactosyltransferase activity to control levels and rescues the defects produced by morph
123 decreased the MKP-1 protein levels to 15% of control levels and was associated with sustained phospho
124 nd UMUC3 in a dose-dependent manner to 6% of control levels and was significant at 1 nmol/L in J82, T
125 on being one of the important processes that controls levels and activities of signaling molecules.
126 reatly elevated ( approximately 50-fold from control levels), and were highly correlated to liver dam
127 cantly increased, NCC expression returned to control levels, and body weight, plasma and urinary elec
128 on, autoantibodies progressively returned to control levels, and both soluble Abeta and axonal degene
129 ributed an anti-inflammatory role at various control levels, and recently we could show that annexin
131 mately 2-fold (P<0.05) over DHF, approaching control levels, and this effect was recapitulated with a
133 ntrol system propose that rules at different control levels are organized along an anterior-to-poster
134 e fundamental frequency partially recover to control levels as concussion symptoms abate, suggesting
136 rotein activation in striatum/GP returned to control level at 3 days after cessation of treatment wit
138 ntly perturbed at 3 or 7 dpi and returned to control levels at 14 or 28 dpi, indicating that the meta
139 heart tissue 10-14 d after MI, returning to control levels at 21 d, whereas NE levels were stable.
141 nificantly increased at 14 h and returned to control levels at 38 h after ischemia; the rising slope
142 oportion of cells in S and M phase exceeding control levels at 5-6 and 6 dpi, respectively, suggestin
145 e mitofusins by shRNA to ~45% or ~52% of the control levels attenuated the htau-enhanced mitochondria
148 thylphenidate restored inhibitory ability to control levels but only partially corrected stability de
149 detraining (D7), C/F levels were similar to control levels, but both basal VEGF and TSP-1 were eleva
150 ochondrial complex IV and V proteins were at control levels, but complex IV activity was reduced sign
151 sion of beta1 integrin was reduced to 35% of control levels, but function remained normal at baseline
153 as very high at week 1 and decreased to near control level by 6 weeks without any RMC autophagy.
155 e reduced at 30 minutes and then returned to control levels by 2 hours following induction of LTP.
158 days following vagotomy and were restored to control levels by 30 days and 60 days, respectively.
160 eOL degeneration, preOL density recovered to control levels by 7 days after ischemia and was ~2 fold
165 myocytes from diabetic mice was increased to control levels by insulin treatment or intracellular inf
166 ch to "clamp" CaMKII activity in CAN mice to control levels by interbreeding CAN transgenic mice with
167 ence of retinal waves, but quickly mature to control levels by the end of the second week, suggesting
168 In inflamed tissue, fEPSPs were reduced to control levels by the protein kinase A (PKA) inhibitor,
172 cues, odour matching performance approached control levels, demonstrating an inability to retrieve b
175 ed after 52 h of wakefulness was restored to control levels during a 14-h recovery sleep episode.
176 rate of spinal cord OPCs rose fivefold above control levels during EAE, and numbers of oligodendrogli
178 9 +/- 0.3 mm) responses could be restored to control levels during fetal treatment with NO synthase b
179 eased after hyperoxia at P8, but returned to control levels during recovery between P12 and P15.
180 nic plants, photosynthesis was maintained at control levels during stress and the flag leaf showed in
183 manifests itself in relative impedance above control levels followed by a slower phase of collapse an
184 genotype, but resembled baseline nonpregnant control levels following delivery in mothers with a CC g
185 s was not significantly changed from vehicle control levels following either acute (1, 3, 10, 30 mg/k
187 ays after stroke revealed a normalization to control levels for miR-125b-5p and miR-143-3p starting a
189 pha, HSP70 and Caspase 11 all increased over control levels found in uninjured cells suggesting that
191 nged withdrawal, GABAA receptors returned to control levels in alcohol-dependent nonsmokers, but alco
192 er content, was persistently increased above control levels in AQP4(-/-) mice but not WT mice at 14 a
194 es, but remained below 24 hr vehicle-treated control levels in HCT116 Bax-ko cells (65%, p = 0.004) b
195 y from PI103 treatment, k(PL) remained below control levels in HT29 cells (74%, p = 0.02), and increa
197 ury synuclein immunofluorescence remained at control levels in neurons that were identified as "good
203 are dramatically decreased to 10% to 30% of control levels in the left ventricle of aorta-constricte
204 rleukin-1beta) and restored interleukin-6 to control levels in the renal cortex, indicating the prote
206 also restored PKCepsilon mRNA and protein to control levels in vivo in fetal hearts and in vitro in e
207 d that the density increases to reach almost control levels in volumes further than 50 microm from a
208 n reduced EADs and improved cell survival to control levels in WT beta(2a)-expressing ventricular myo
209 ), whereas CD8 T-cell counts were similar to controls' levels in HIV-positive/CMV-negative subjects.
210 were largely preserved (approximately 80% of control levels) in SMKO mice because of exaggerated acti
211 tistically elevated, when compared with mean control levels, in all treatment and dose groups, while
212 rate-dependent NADPH production above vector control levels, in contrast to the increased production
213 ation and transendothelial migration back to control levels, indicating that stathmin may influence t
214 ned depressed, but lactate levels fell below control levels, likely as a result of rapid renal lactat
216 rker propidium iodide (PI) of 150-500% above control levels, most notably, in the CA1 region pyramida
217 in Ncx1(-/-) (retaining approximately 20% of control level NCX current) and control mice were similar
218 s increased significantly (P < 0.001) from a control level of 0.61+/-0.17% ID/g (percentage of inject
219 e of (64)Cu-NOTA-TRC105-Fab increased from a control level of 3.4 +/- 0.1 to 9.5 +/- 0.4 percentage i
220 ast 10 days of the recovery period, reaching control level of cumulative egg and nauplii production w
221 GABA, leading to "tonic" inhibition that can control levels of excitability and network activity.
222 CAPN3 acts during myogenesis to specifically control levels of membrane-associated but not cytoplasmi
224 cal inputs were designed to spatiotemporally control levels of second messengers, IP3, phosphatidylin
225 his paradigm display resilience, maintaining control levels of social exploration and sucrose prefere
228 are absent on human T cells, were thought to control levels of T-cell activation in chimpanzees and w
230 function associated with impaired ability to control levels of the CTLA-4 ligands, CD80 and CD86.
231 ts showed that a key function of Magoh is to control levels of the microcephaly-associated protein Li
232 ined fluorinated nano-building blocks with a controlled level of reactive functionality for the devel
233 ariectomized mice with or without sustained, controlled levels of 17-beta-E2 administered by s.c. imp
234 s, we have generated mice having genetically controlled levels of AM mRNA ranging from approximately
240 negatively regulates cytokinin responses by controlling levels of a key family of transcription fact
241 uences antiviral recognition responses, that controlling levels of adaptor molecules is a recurring s
242 B1 plays an important role in development by controlling levels of cell cycle regulators and thereby
245 ts cargo transport to the Golgi apparatus by controlling levels of phosphatidylinositol 4-phosphate,
246 xide dismutase (SOD) enzymes are critical in controlling levels of reactive oxygen species (ROS) that
248 ntial phase independent of Ler by negatively controlling levels of the regulators GrlA and GrlR throu
249 USP42 forms a direct complex with p53 and controls level of ubiquitination during the early phase
251 midase (GBA2) is one of several enzymes that controls levels of glycolipids and whose activity is lin
252 factor for Skp2, Cdc kinase subunit 1 (Cks1) controls levels of Skp2 in melanoma cells and acts joint
253 nts and 291 matched individuals without IBD (controls); levels of tryptophan were measured using high
254 elial cells from 19 patients with DTS and 16 controls, levels of MMP-9 and its regulating cytokine mR
255 d increased expression of IL28 compared with controls; levels of IL28R were increased in the colonic
256 were able to restore M channel activity to a control level or above, while at saturating voltages the
257 ities in mutant membranes were mostly at the control level or modestly reduced, except mutants of Glu
258 month of hyperglycemia, but most returned to control levels or lower by 3 months, when the same cytok
264 GC-A mRNA in GC-A KO podocytes to 1% of the control level, Podo-GC-A KO mice and control littermates
266 diminished elevated mitochondrial ROS to the control level, prevented structural damage to mitochondr
269 e co-treatment restored most fluxes to their control levels, resulting in steatotic lipid accumulatio
270 GABAergic neurons were reduced to 70% of control levels short-term, where they remained in epilep
271 rylation to approximately 70% of the in vivo control level slows ktr and reduces force generation.
273 ubstances to a maximum of only 50-60% of the control level, suggesting that complex protein-protein i
274 of disinhibited synaptic currents to healthy control levels, suggesting a Src kinase- and actin-depen
275 ated endothelin-converting enzyme to 180% of control levels, suggesting that the Abeta-lowering abili
276 a decrease in neuronal ATP levels (to 48% of control level) that was reversed significantly to 70% of
278 the BLA reduced DAMGO-induced food intake to control levels, this treatment led to exaggerated number
279 maintain glucose concentrations at sedentary control levels, thus not requiring the counter-regulatio
280 it provides a global chromosome-wide nominal control level to clustering, as opposed to previous meth
281 CB1 receptor binding did not recover to control levels until day 7 or 14 after treatment in stri
284 ne in vitro restores hippocampal function to control levels via activation of high-affinity nicotinic
285 ases, 100 controls) and dust (682 cases, 513 controls) levels were treated as natural log-transformed
286 as well as subjects without these disorders (controls); levels were correlated with clinical features
291 maintained miR-133a expression near vehicle control levels, which coincided with (1) a decrease in c
292 resource allocation toward roots returned to control levels, while allocation to the young leaves inc
293 itic spine turnover in adult ngr1-/- mice to control levels, while an acutely enriched environment in
295 vated RyR2 levels in AD mice are restored to control levels with dantrolene treatment, as are synapti
297 ased after METH exposure, but was reduced to control levels with NACA treatment, as measured by dichl
300 ation within the knee, and were decreased to control levels with the use of a specific inhibitor of T
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