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   1 nsor response may be customized to cover the hypo- (0-80 mg/dL), normo- (80-120 mg/dL), and hyperglyc
     2 nce of normal first-pass signal enhancement (HYPO), (2) normal first pass signal followed by hyperenh
     3 week 1, %S was depressed in HYPER, COMB, and HYPO (9+/-8%, 7+/-6%, and 5+/-4%, respectively) and were
     4 nd a normal oncogenic Nras allele (Nras G12D(hypo) and Nras G12D, respectively) to create a gene dose
  
     6 iving Scale), potential prediagnostic motor (hypo- and bradykinesia, tremor, rigidity, postural imbal
     7 re up-regulated in L-NCoRDeltaID mice in the hypo- and euthyroid state, there was little effect seen 
  
     9 n(2+)-binding pocket generated variants both hypo- and hyper-resistant to zinc starvation, and both m
  
  
    12  PTH-iCa curves were constructed by inducing hypo- and hypercalcemia through alterations in dialysate
  
  
  
    16 econciled seemingly disparate themes of both hypo- and hyperconnectivity in the ASD literature; both 
    17 c value in treating disorders resulting from hypo- and hyperdopaminergic activity, without the side e
    18 c value in treating disorders resulting from hypo- and hyperdopaminergic activity, without the side e
    19 yT1+/-), to determine how constitutive NMDAR hypo- and hyperfunction, respectively, affect the glutam
    20 This study was designed to determine whether hypo- and hyperglycaemia modulate the hypoxic ventilator
    21 show for the first time that PHHs exposed to hypo- and hyperglycemia can remain highly functional, bu
    22 olling glucagon and insulin secretion during hypo- and hyperglycemia, respectively, the dose-response
  
  
    25 sants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and c
    26 disorders (periodic ataxia with myokymia and hypo- and hyperkalemic periodic paralysis) are due to mu
    27  mGlu receptor ligands for treatment of both hypo- and hyperkinetic disorders of basal ganglia origin
    28 ing software (SPM5) was used to identify all hypo- and hypermetabolic regions in patients with HD rel
  
    30 les of females; (v) the general dichotomy of hypo- and hypermethylated alleles persisted over the 5 y
    31 nexpectedly, the sequence characteristics of hypo- and hypermethylated domains in cerebellum were dis
  
  
    34 tion levels, thus the dual stability of both hypo- and hypermethylated genomic regions, and (3) spora
    35 e maternally and paternally derived ICRs are hypo- and hypermethylated, respectively, with the former
  
    37 s this an attractive technique to study both hypo- and hypermethylation of regions of the genome like
  
  
    40 , we assess the sensitivity of TRPM7 to both hypo- and hyperosmotic conditions and explored the invol
    41  perturbation of COPI function, because both hypo- and hyperosmotic conditions slowed brefeldin A-ind
  
  
  
  
  
  
    48 ve and regulated pre-mRNA splicing; yet both hypo- and hyperphosphorylation of SR proteins are known 
  
    50 he cilial protein Evc in mice causes various hypo- and hyperplasia defects during molar development. 
    51  changes in aortic cross-sectional area with hypo- and hypertension did not appreciably improve the p
  
    53 vivo, we expressed a biotinylated TRbeta1 in hypo- and hyperthyroid mouse livers, used ChIP-seq to id
  
  
    56 om Necturus basolateral membranes respond to hypo- and hypertonic challenge monotonically around an i
    57 DV volume and pH changes upon ATP depletion, hypo- and hypertonic shock, and rapid withdrawal of perf
    58 inistration of CO(2) as well as by voluntary hypo- and hyperventilation at rest and during steady-sta
  
  
    61 e, anterior hypothalamic (hypo.) n., lateral hypo. area (most extensive and dense message), periventr
  
  
    64 engineered betaTrCP was capable of selecting hypo- but not hyperphosphorylated forms of retinoblastom
  
    66 lower in the ANTE HYPO group versus the ANTE HYPO + DHEA-S group (2.0 +/- 0.2 vs. 3.3 +/- 0.6 nmol/l;
    67 us the ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (13 +/- 5 vs. 32 +/- 3, 38 +/- 7, a
    68 us the ANTE EUG, ANTE EUG + DHEA-S, and ANTE HYPO + DHEA-S groups (57 +/- 8 vs. 22 +/- 5, 18 +/- 6, a
  
  
    71  mice with 1% of wild-type St14 levels (St14(hypo/-)) display aberrant processing of profilaggrin and
    72  evidence that genome-wide cancer hyper- and hypo- DNA methylation patterns are independent processes
    73 poglycemia (2.8 +/- 0.1 mmol/l; n = 12; ANTE HYPO), euglycemia (6.2 +/- 0.1 mmol/l; n = 12; ANTE EUG)
  
  
  
  
    78  (2VO) or 2VO plus systemic hypotension (2VO+Hypo; mean arterial pressure=30+/-2 mmHg) for 10-20 min.
  
    80 erns of statistically significant hyper- and hypo- methylation in comparisons involving any number of
  
  
  
    84 e pallial commissure, anterior hypothalamic (hypo.) n., lateral hypo. area (most extensive and dense 
    85 po. n., stratum cellulare externum, inferior hypo. n., infundibular hypo. n., median eminence, three 
    86 xtensive and dense message), periventricular hypo. n., lateral to the paraventricular n., ventromedia
    87 re externum, inferior hypo. n., infundibular hypo. n., median eminence, three layers within the strat
    88 eral to the paraventricular n., ventromedial hypo. n., stratum cellulare externum, inferior hypo. n.,
  
  
    91 ase from cerebral microvessels isolated from hypo-, normo- and hyperkalemic rats (2.3+/-0.1, 3.9+/-0.
    92 poglycemia (2.8 +/- 0.1 mmol/l; n = 12; ANTE HYPO), or 4) hyperinsulinemic hypoglycemia (2.8 +/- 0.1 
  
    94 ep output of each locus being either equal-, hypo- or hyper-methylated locus without further post-hoc
  
  
    97 ivo environment, certain cell subsets became hypo- or hyper-responsive, showed profound differences i
    98 iveness and through this mechanism intrinsic hypo- or hyperactive adrenal medullas in some individual
  
   100 , whereas chronic infection can cause either hypo- or hyperchlorhydria, depending on the distribution
   101     Whether these neuroadaptations lead to a hypo- or hyperdopaminergic state during abstinence is a 
   102 entifying an underlying cause and correcting hypo- or hyperfunction of an endocrine gland, however, c
  
   104 ose that the methylation pattern and status (hypo- or hypermethylation) of genomic DNA may determine 
  
  
   107  slices were exposed to different degrees of hypo- or hyperosmolality 15 min prior to and during a 15
  
  
   110 re induced by early drug exposure, producing hypo- or hyperresponsiveness to environmental or pharmac
  
  
   113 )-diabetic (diabetic), and STZ-diabetic kept hypo- or normoglycemic with insulin pellets (diabetic-no
   114 esent investigation, Tregs derived from CD18(hypo) PL/J mice were analyzed for their propensity to di
   115 23/p19 depletion, injection of diseased CD18(hypo) PL/J mice with anti-gammadeltaTCR Abs significantl
  
  
  
  
  
  
   122 in whether recurrent nonsevere hypoglycemia (Hypo) results in long-term cognitive impairment in type 
  
  
  
   126 c regions, and (3) sporadic transitions from hypo- to hypermethylated equilibria as a result of methy
   127 hosphorylation of PERIOD (PER) proteins from hypo- to hyperphosphorylated species, events that are hi
  
   129 ons were small, homogeneously enhancing, and hypo- to isointense on T1-weighted images and iso- to sl
   130  mice (Control and Nrf2(-/-) +/- T1D and +/- Hypo) were subject to recurrent, twice-weekly, insulin o
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