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1 tured human epithelial cell lines: HEp-2 and Henle-407.
2 ak cone density, rod-free zone diameter, and Henle fiber layer.
3 vea, consistent with loss in cone nuclei and Henle's fiber layer.
4 es between the outer nuclear layer (ONL) and Henle's fiber layer (HFL) were well defined, showing tha
5 lphaKG) transport in the proximal tubule and Henle's loop from reabsorption (acid load) to secretion
6 ned by the greater length of the cone axons (Henle fibers) in wider foveas.
7                   P2RY5 is expressed in both Henle's and Huxley's layers of the inner root sheath of
8             125I-labeled IpaC binds cultured Henle 407 intestinal cells with an apparent dissociation
9 f serovar Typhimurium to enter into cultured Henle-407 cells or to induce macrophage cell death.
10 r invasion or multiplication within cultured Henle cells; the shuA mutant invaded and produced normal
11 nths, foveal cone cell bodies stack >6 deep, Henle fiber layer (HFL) thickens, and IS/OS length equal
12                             This distinctive Henle fiber layer geometry may reflect an arrested devel
13 orum was noninvasive for cultured epithelial Henle 407, chick kidney, chick ovary, and budgerigar abd
14 molarity conditions and is less invasive for Henle 407 cells.
15 neal birefringence using SLP-VCC can fail if Henle's layer is disrupted by macular disease.
16 nels are essential for NaCl re-absorption in Henle's loop and for potassium secretion by the stria va
17 xtension of the AMN hyperreflective bands in Henle's fiber layer with a Z-shaped morphology on OCT B-
18 different genes with increased expression in Henle cells were identified.
19  which was defective for plaque formation in Henle cell monolayers, had a reduced amount of IcsA dete
20 ponding to SSPiM appeared more frequently in Henle's fiber layer (HFL) than the inner nuclear layer (
21  vitro and during the first 3 h of growth in Henle cells in vivo.
22 ssion when S. flexneri was intracellular (in Henle cells) than when S. flexneri was extracellular (in
23 jury to the Muller glia or photoreceptors in Henle's fiber layer.
24  with the arrangement of macular pigments in Henle fibres; (ii) the morphology of MS is dependent on
25 p and surA mutants failed to form plaques in Henle cell monolayers and were defective in cell surface
26 neri pst mutant to form wild-type plaques in Henle cell monolayers may be due to aberrant expression
27 flexneri pst mutant forms smaller plaques in Henle cell monolayers than does the parental strain.
28  localization or the formation of plaques in Henle cell monolayers.
29 tH promoters was higher when Shigella was in Henle cells than when it was in L broth.
30 ize corneal birefringence based on an intact Henle's layer.
31 C, are translocated into cultured intestinal Henle-407 cells.
32 eria could direct protein translocation into Henle-407 cells as this process occurred in the presence
33 that were cultured with, but did not invade, Henle cells (extracellular).
34               The degP mutant SM1100 invaded Henle cells at wild-type levels and induced apoptosis in
35 ing infection of human epithelial cell lines Henle 407, HEp-2, and HeLa.
36 delineate the axons of photoreceptor nuclei, Henle's fiber layer (HFL).
37 taining of the infundibulum, isthmus, and of Henle's layer of the inner root sheath of the lower anag
38  isolation, cultivation, and confirmation of Henle-Koch's postulate via transmission assays.
39 gulates the cortical thick ascending limb of Henle (cTALH) COX-2 expression via a p38-dependent pathw
40 surrounding cortical thick ascending limb of Henle (cTALH).
41 tion of PTH1R in the thick ascending limb of Henle (TAL) and in distal convoluted tubules (DCTs): Ksp
42  expressed along the thick ascending limb of Henle (TAL), designated NKCC2A, NKCC2B, and NKCC2F.
43 r conductance in the thick ascending limb of Henle (TAL).
44 ed, primarily in the thick ascending limb of Henle (TAL).
45 nel expressed in the thick ascending limb of Henle (TALH) and throughout the distal nephron of the ki
46 o examine whether the thin ascending limb of Henle (tALH) decreases its luminal solute concentration
47  permeability in the thin descending limb of Henle (TDLH) is required for formation of a concentrated
48  reabsorption in the thick ascending limb of Henle and a less well defined role in the inner medullar
49 alizes to the apical thick ascending limb of Henle and BSC2/NKCC1 which was isolated from a mouse IMC
50 lecting duct and the thick ascending limb of Henle and is strongly gated by internal pH in the physio
51 ey in proximal tubule and descending limb of Henle epithelia and in vasa recta endothelia.
52 oid gland and kidney thick ascending limb of Henle to sense and respond to alterations in serum calci
53 changer [NHE3]), the thick ascending limb of Henle's loop (the bumetanide-sensitive Na-K-2Cl cotransp
54 thelial cells of the thick ascending limb of Henle's loop and of the macula densa.
55 alt transport in the thick ascending limb of Henle's loop and/or the distal convoluted tubule, and th
56 ts or in a medullary thick ascending limb of Henle's loop cell line.
57 NF-kappaB pathway in thick ascending limb of Henle's loop cells of UAKD mice was detected by increase
58 yonic kidney 293 and thick ascending limb of Henle's loop cells that were transfected with mutant uro
59 lls and immortalized thick ascending limb of Henle's loop cells with wild-type and mutated uromodulin
60 n ascending limb and thick ascending limb of Henle's loop has increased greatly over the last decade.
61 the proximal tubule, thick ascending limb of Henle's loop, and cortical and medullary collecting duct
62 proximal tubule, the thick ascending limb of Henle's loop, and the collecting duct.
63 luted tubule and the thick ascending limb of Henle's loop, respectively.
64 apical domain of the thick ascending limb of Henle's loop, the connecting tubule, and in some, but no
65  collecting duct and thick ascending limb of Henle's loop.
66  reabsorption in the thick ascending limb of Henle's loop.
67 asma membrane of the thick ascending limb of Henle's loop.
68  reabsorption in the thick ascending limb of Henle's loop.
69 ane of the mammalian thick ascending limb of Henle's loop.
70 ined specifically to thick ascending limb of Henle's loop.
71 the proximal tubule, thin descending limb of Henle, and vasa recta; AQP2, AQP3, and AQP4 in the colle
72 nt in differentiated thick ascending limb of Henle, collecting duct, and stroma; however, it disappea
73 on restricted to the thick ascending limb of Henle, distal convoluted, connecting and cortical collec
74 ptake pathway in the thick ascending limb of Henle, is expressed in three different full-length splic
75 cotransporter of the thick ascending limb of Henle, the Na-Cl cotransporter of the distal convoluted
76 port activity in the thick ascending limb of Henle.
77 proximal tubules and thin descending limb of Henle.
78 a and cortex and in thin descending limbs of Henle's loop in inner medulla.
79 cal membrane of the thick ascending limbs of Henle's loop was strong, whereas outer medullary collect
80 ules, predominantly thick ascending limbs of Henle's loop.
81 highly expressed in thick ascending limbs of Henle's loops and collecting ducts and weakly expressed
82 ollecting ducts and thick ascending limbs of Henle's loops.
83 ecting tubules, and thin descending limbs of Henle's loops.
84  the transport of iron occurs in the loop of Henle (LH) and collecting duct system.
85 n proximal stop flow pressure during loop of Henle (LH) perfusion at 40 nl/min with artificial tubula
86           Sodium handling in the PT, loop of Henle (loop), and distal nephron was assessed at baselin
87 ctivation of ion transporters in the loop of Henle (NKCC2) and distal nephron (NCC, ENaC, and pendrin
88 y in the thick ascending limb of the loop of Henle (TAL).
89 ific contribution of thick ascending loop of Henle (TALH) -derived HO-1, we generated a transgenic mo
90 lume delivery to the thick ascending loop of Henle (TALH) and macula densa, providing the error signa
91 n in the thick ascending limb of the loop of Henle (TALH) in vivo was examined in anaesthetized rats
92 g duct (CCD) and the thick ascending loop of Henle (TALH).
93                We find a decrease in loop of Henle and an increase in collecting duct cells, and diff
94 dney by thick ascending limbs of the loop of Henle and by distal convoluted tubules (DCTs).
95 interstitial fluid resorbed from the loop of Henle and collecting ducts.
96 howed greater Umod expression in the loop of Henle and correspondingly less fibrosis.CONCLUSIONSBioma
97 ged or upregulated, and those in the loop of Henle and distal tubule lineages were downregulated.
98 d in the thick ascending limb of the loop of Henle and excreted in the urine.
99 II, to stimulate sodium transport in loop of Henle and the distal nephron, and to induce hypertension
100 y increased reabsorption in both the loop of Henle and the distal nephron, resulting in the observed
101 m-chloride transporter in the kidney loop of Henle and the KCC2 potassium-chloride transporter in neu
102 ting the thick ascending limb of the loop of Henle can cause either acquired Bartter syndrome or hypo
103 ty that matures into thick ascending loop of Henle cells by endogenously activating FGF.
104 ation was significantly elevated and loop of Henle Cl absorption was reduced in microperfused superfi
105      TGF responses to an increase in loop of Henle flow rate from 0 to 30 nl/min, whether determined
106 erulotubular balance response in the loop of Henle is accompanied by increased Na,K-ATPase activity.
107      The thin descending limb of the loop of Henle is crucial for urine concentration, as it facilita
108                 Cl- transport in the loop of Henle is responsible for reclamation of 25-40% of the fi
109 y for Tamm-Horsfall protein (THP), a loop of Henle marker, while Tsc1 deficiency in Osx lineage cells
110 al medicine because they inhibit the loop of Henle Na-K-2Cl cotransporter with much higher affinity.
111 se in THP-, NKCC2- and AQP1-positive loop of Henle nephron segments in mutant DeltaSRM kidneys.
112 hange significantly during prolonged loop of Henle perfusion in e-5'NT/CD73(+/+) mice, a complete dis
113 essure in response to an increase in loop of Henle perfusion rate from 0 to 30 nl/min was comparable
114             In separate experiments, loop of Henle perfusion with 50 microM ouabain decreased TGF res
115 NA and protein were expressed in the loop of Henle region in mouse and human kidneys, and CHAC1 expre
116 o assessment of proximal tubular and loop of Henle sodium handling, to assess sodium exit after loop
117 s, endothelial cells, or proximal or loop of Henle tubular cells, while Osx is known to label tubular
118 ly reabsorbed in proximal tubule and loop of Henle) to the distal nephron in quantities equal to inge
119 al for the coordinated growth of the loop of Henle, a medullary extension of the nephron that elongat
120 , such as podocyte, proximal tubule, loop of Henle, and collecting duct, in addition to macrophages,
121 s of the thin descending limb of the loop of Henle, and principal cells of the collecting system.
122 ule, the thick ascending limb of the loop of Henle, and the distal convoluted tubule.
123 segments to DCT1 and possibly to the loop of Henle, but not to the proximal tubules.
124 tinct distribution pattern along the loop of Henle, but the functional significance of this organizat
125 ific transcripts in proximal tubule, loop of Henle, distal convoluted tubule, and cortical and medull
126 4 expression in the proximal tubule, loop of Henle, distal tubule, and collecting duct and suggest th
127 neages, such as the proximal tubule, loop of Henle, distal tubules, and podocytes, using extracellula
128 ortant in sodium reabsorption in the loop of Henle, is maintained or even increased in Foxa1-deficien
129 proximal tubule (S1/S2 segment), the loop of Henle, the intercalated cells of the distal convoluted t
130 d in the thick ascending limb of the loop of Henle, whereas it is transcellular in the distal convolu
131 tics can curtail their action in the loop of Henle.
132 sodium exit from the proximal tubule/loop of Henle.
133 in the proximal convoluted tubule or loop of Henle.
134 s of the thick ascending limb of the loop of Henle.
135 reased reabsorption in the PT and/or loop of Henle.
136 rogenitor cells and formation of the loop of Henle.
137  and the thick ascending limb of the loop of Henle.
138 ink between proximal tubules and the loop of Henle.
139 ily expressed in the thick ascending loop of Henle.
140 e to the thin descending limb of the loop of Henle.
141 tify the thin descending limb of the loop of Henle.
142 y in the thick ascending limb of the loop of Henle.
143 n in the thick ascending limb of the loop of Henle.
144 ting duct predominantly but also the loop of Henle.
145 ollecting ducts, distal tubules, and loop of Henle.
146 t in the thick ascending limb of the loop of Henle; and claudin-4, -7, and -8 as determinants of coll
147 eabsorbed in the proximal tubule and loop of Henle; and, second, a stimulus to sodium-cation exchange
148  the basement membranes of the thin loops of Henle and spreads from there through the interstitium to
149 luted tubules, collecting ducts and loops of Henle as well as within the cytoplasm of tubule-delineat
150  subset of thin descending limbs of loops of Henle expressed the transgene.
151 ater absorption along microperfused loops of Henle of NKCC2A-/- mice were unchanged at normal flow ra
152 educed in microperfused superficial loops of Henle of NKCC2B-deficient mice.
153  in anaesthetized rats by perfusing loops of Henle of superficial nephrons with solutions containing
154  the kidney within the lumen of the loops of Henle, but no intracellular storage sites were identifie
155 RNA in the epithelial layers of the loops of Henle, distal tubules, and the collecting ducts of the k
156 e aging-related gene alterations in loops of Henle, proximal tubules and collecting ducts in a sex-de
157 duced kidney cysts primarily in the loops of Henle, whereas inactivation in adult mice did not lead t
158  by the thick ascending limb of the loops of Henle.
159 mal tubules and descending limbs of loops of Henle.
160 e phospholipase C, PC-PLC, promotes lysis of Henle 407 cell primary vacuoles in the absence of LLO.
161 -type S. flexneri in confluent monolayers of Henle and Caco-2 cells.
162  not form plaques in confluent monolayers of Henle cells, indicating an inability of this mutant to s
163 rate (EPFR) measurements during perfusion of Henle's loop.
164 channel of the thick ascending limb (TAL) of Henle is critical for Ca(++) reabsorption in the kidney.
165            The thick ascending limb (TAL) of Henle's loop drives paracellular Na(+), Ca(2+), and Mg(2
166         In the thick ascending limb (TAL) of Henle's loop, chloride is reabsorbed transcellularly, wh
167 orption by the thick ascending limb (TAL) of Henle's loop.
168 tro but exhibited normal plaque formation on Henle cell monolayers.
169 the isc mutant was unable to form plaques on Henle cell monolayers because the strain was noninvasive
170 sitA mntH mutant formed wild-type plaques on Henle cell monolayers but had a reduced ability to survi
171 media in vitro but formed smaller plaques on Henle cell monolayers than the parent strain.
172 ron chelator but formed wild-type plaques on Henle cell monolayers, indicating that the sitA mutant w
173 h the suf mutant formed wild-type plaques on Henle cell monolayers, the isc mutant was unable to form
174 eoB iucD) formed slightly smaller plaques on Henle cell monolayers.
175 sitA, feoB, and iucD did not form plaques on Henle cell monolayers.
176 nt SNGFR, SNGFR was manipulated by perfusing Henle's loop to alter TGF activity.
177 also strong labeling of the outer plexiform (Henle fiber) layer with anti-GSTP1.
178 inal thickness, and outer nuclear layer plus Henle fiber layer (ONL+HFL) thickness were measured usin
179 ckness measurements included the ONL and the Henle fiber layer (ONL + HFL), and were obtained using s
180 tion between the outer nuclear layer and the Henle fiber layer.
181  formed by the outer plexiform (OPL) and the Henle fiber layers (HFL): 5.0 x 10(-3) mm(2) vs 15.9 x 1
182 vea in patients with AQP4-IgG+ NMOSD, in the Henle fiber outer nuclear layer (HFONL) and the inner se
183 nteraction of carotenoids and tubulin in the Henle's fiber layer could play an important role in the
184 lly multiple, extending posteriorly into the Henle fiber layer, with reflectivity similar to adjacent
185 face OCT images acquired at the level of the Henle fiber layer highlighted similar concentric rings a
186 e determined from a polarimetry image of the Henle fiber layer.
187  rings occur exclusively at the level of the Henle fiber layer.
188 e determined from a polarimetry image of the Henle fiber layer.
189 bsequent experimental inoculation study, the Henle-Koch-Evans postulates were fulfilled for M. alliga
190 ates that it survived and divided within the Henle cell cytoplasm, but the dksA mutant cells were elo
191 al orientation and size were consistent with Henle fibers.
192 promoters increased when Shigella was within Henle cells, and our data suggest that the intracellular

 
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