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1 each other and stimulated by dehydration and hyperosmolarity.
2 elial cell function is adversely affected by hyperosmolarity.
3 esulted from the sustained hyperglycemia and hyperosmolarity.
4 stress and was maintained through 360 min of hyperosmolarity.
5 d that the autophagic flux was unaffected by hyperosmolarity.
6  mass spectrometry, increased in response to hyperosmolarity.
7 exposing confluent endothelial monolayers to hyperosmolarity.
8 xpressing wild-type ASGP-Rs was inhibited by hyperosmolarity.
9 there was normal inhibition by forskolin and hyperosmolarity.
10  pathways mediate the responses to touch and hyperosmolarity.
11 nic and, to an even greater degree, by acute hyperosmolarity.
12  NODM), comprising ketoacidosis (334, 8.1%), hyperosmolarity (131, 3.2%), renal complications (1,286,
13 otrophenol (11-fold), rotenone (7-fold), and hyperosmolarity (8-fold).
14                                              Hyperosmolarity (800 mOsm), achieved by either NaCl/urea
15 l conditions encountered in the lung cavity (hyperosmolarity, acidic pH, and low oxygen tension, amon
16                                              Hyperosmolarity activated both p38 and p42/44 mitogen-ac
17                                              Hyperosmolarity activates different components of severa
18                Exposure of yeast to external hyperosmolarity activates the Hog1 stress-activated prot
19                                              Hyperosmolarity also stimulated the uptake of myo-inosit
20 p38alpha phosphorylation that was induced by hyperosmolarity and anisomycin.
21 erate stresses, including serum deprivation, hyperosmolarity and ionizing radiation.
22                                              Hyperosmolarity and low O2 tension induced the invasive
23  in a greater apoptotic response of cells to hyperosmolarity and microtubule disruption.
24 h conditions found in human tissues, such as hyperosmolarity and presence of aminoglycoside antibioti
25 n kinase (ERK) was diminished in response to hyperosmolarity and serum factors in MEKK1(-/-) cells.
26     These experiments provide a link between hyperosmolarity and tear instability, suggesting that hy
27 ed in cells in response to oxidative stress, hyperosmolarity and treatment with serum.
28                                        Cold, hyperosmolarity, and abscisic acid (ABA) signaling induc
29 es, including exposure to hydrogen peroxide, hyperosmolarity, and carbon starvation.
30 ose biosynthesis, hydrophilins, responses to hyperosmolarity, and hypersalinity, reactive oxygen spec
31 e induced in response to lipopolysaccharide, hyperosmolarity, and interleukin 1.
32 ctivation, which can be induced by oxidants, hyperosmolarity, and proinflammatory cytokines, leading
33 ory neurons mediate responses to nose touch, hyperosmolarity, and volatile repellent chemicals.
34               Tear film instability and tear hyperosmolarity are considered core mechanisms in the de
35                  Sustained hypernatremia and hyperosmolarity are safely tolerated in pediatric patien
36 tivated by UV-C irradiation, heat shock, and hyperosmolarity as well as by tumor necrosis factor alph
37 hough BetT activity increased in response to hyperosmolarity, BetT mediated significant uptake under
38 utations in osm-10 eliminate the response to hyperosmolarity but have no effect on responses to nose
39 fically by methylmethane sulfonate (MMS) and hyperosmolarity but not by ultraviolet radiation, ionizi
40                                              Hyperosmolarity by added sucrose (50 and 100 mM) also in
41                                              Hyperosmolarity by added sucrose inhibited the spontaneo
42 ast, the activation of the stress kinases by hyperosmolarity, by the DNA-cross-linking agent diepoxyb
43 gene, was highly induced under physiological hyperosmolarity conditions.
44 guanylyl cyclase assays indicated that acute hyperosmolarity decreased NPR-B activity in a reversible
45                                         Tear hyperosmolarity, defined by a referent of 316 mOsmol/L,
46 udy was to investigate the role of TonEBP in hyperosmolarity-dependent autophagy in NP.
47 We conclude that in lung venular capillaries hyperosmolarity deteriorates barrier properties, possibl
48                                              Hyperosmolarity did not change the phosphorylation of UL
49        Unlike insulin, activation of NKCC by hyperosmolarity did not involve PI3-kinase but was suppr
50 ophagy in NP cells was not TonEBP-dependent; hyperosmolarity did not upregulate autophagy as previous
51                               Concomitantly, hyperosmolarity diminished total levels of protein synth
52                             We conclude that hyperosmolarity does not play a role in autophagy induct
53                                        Acute hyperosmolarity elevated intracellular calcium in a conc
54                                        Thus, hyperosmolarity enhanced action potential-evoked release
55                               Immunoblots of hyperosmolarity-exposed, cultured rat lung microvascular
56 osmosensor involved in the regulation of the hyperosmolarity glycerol mitogen-activated protein kinas
57 orylated on Ser-38 and Ser-63 in response to hyperosmolarity, heat shock, and arsenite treatment but
58 n of neurotransmitter release was induced by hyperosmolarity, high potassium, or action potential fir
59    alpha-PAK is not activated in response to hyperosmolarity in 3T3-L1 cells.
60 tant role in cell resistance and adaption to hyperosmolarity in many tissues like kidney and liver.
61             Increased tear evaporation, tear hyperosmolarity, increased ocular surface staining, incr
62                                              Hyperosmolarity induced a significant retrieval of Ntcp
63 eptor potential (TRP) channels, mediates the hyperosmolarity induced Ca(2+) release.
64      In our laboratory, we are interested in hyperosmolarity-induced apoptosis in neuronal cells.
65 uroursodeoxycholate (TUDC) and cAMP reversed hyperosmolarity-induced Fyn activation and triggered re-
66                      Muscle contraction- and hyperosmolarity-induced glucose transport may be regulat
67 ckade of Na(+)/H(+) exchangers prevented the hyperosmolarity-induced IEC inflammatory response.
68 ause p38 and p42/44 inhibition prevented the hyperosmolarity-induced increase in IL-8 production.
69 ficient mutant of focal adhesion kinase, the hyperosmolarity-induced increases in activity of focal a
70 monstrate that PS protects human cornea from hyperosmolarity-induced inflammation and oxidative stres
71 o hyperosmolar filtration (P < 0.01), and by hyperosmolarity-induced Lp increase (P < 0.01).
72 diated ocular surface disease, inhibited the hyperosmolarity-induced MMP production and JNK activatio
73                       TUDC also reversed the hyperosmolarity-induced retrieval of bile salt export pu
74           Kinetic analysis revealed that the hyperosmolarity-induced stimulation was associated with
75                                              Hyperosmolarity is a central mechanism causing ocular su
76 pal slices activates p38 and JNK and whether hyperosmolarity is a potential apoptotic stimulus in thi
77                                    Medullary hyperosmolarity is protected from washout by countercurr
78                  Slow increases in tear film hyperosmolarity may cause the gradual increase in discom
79                    We hypothesized that this hyperosmolarity may contribute to colonic inflammation b
80 of 0 mm/5' in both eyes, accompanied by tear hyperosmolarity, mild meibomian gland dysfunction, reduc
81  drug formulation (polyoxyl 35 castor oil or hyperosmolarity of the SU5416 preparation).
82                 We determined the effects of hyperosmolarity on lung microvascular barrier properties
83         In the present study, the effects of hyperosmolarity on p38 activation and protein synthesis
84 However little is known about the effects of hyperosmolarity on short term regulation of the Na(+)-ta
85  and Caco-2 were used to study the effect of hyperosmolarity on the IEC inflammatory response.
86                             The influence of hyperosmolarity on the uptake of taurine, myo-inositol,
87 nd is activated by cellular stresses such as hyperosmolarity or DNA damage.
88 physiological derivatives (such as oxidants, hyperosmolarity, or glycation products) on tissues direc
89 r dysfunctions by multiple factors including hyperosmolarity, oxidant formation, and protein kinase C
90       gamma-PAK translocation in response to hyperosmolarity parallels Cdc42 translocation to the par
91 n culture study supported that extracellular hyperosmolarity plays no role in promoting autophagy in
92                     This initial response to hyperosmolarity precedes and temporally regulates the ac
93                                              Hyperosmolarity promotes translocation of gamma-PAK from
94  We conclude that a brief period of vascular hyperosmolarity protects against acid-induced ALI when t
95 hese studies provide the first evidence that hyperosmolarity regulates TauT activity and expression i
96 e to our knowledge that in lung capillaries, hyperosmolarity remodels the endothelial barrier and the
97  the combination of low O2 concentration and hyperosmolarity resulted in an approximate 10- to 15-fol
98 was designed to evaluate the effect of donor hyperosmolarity secondary to diabetes insipidus, an almo
99 rophil induced either by stress stimuli (UV, hyperosmolarity, sphingosine) or by anti-Fas antibody or
100  factor, nuclear factor (NF)-kappaB, because hyperosmolarity stimulated both NF-kappaB DNA binding an
101 protein kinases, which effect contributed to hyperosmolarity-stimulated IL-8 production, because p38
102                                  In summary, hyperosmolarity stimulates IEC IL-8 production, which ef
103       No adverse effects of supraphysiologic hyperosmolarity such as renal failure, pulmonary edema,
104 instability produce transient shifts in tear hyperosmolarity that lead to chronic epithelial stress,
105                          Exposure of IECs to hyperosmolarity triggered expression of the proinflammat
106  studies of other cell types have shown that hyperosmolarity triggers autophagy.
107 nts with normal osmolarity (<312 mOsm/L) and hyperosmolarity values (>/=312 mOsm/L) had respective OS
108 vated levels can also activate p38 kinase by hyperosmolarity via a PKC-independent pathway.
109  In addition, the proinflammatory effects of hyperosmolarity were, in a large part, mediated by activ

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