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1                                              LAL can be specifically inhibited by a variety of 3,4-di
2                                              LAL defects cause Wolman disease (WD) and CE storage dis
3                                              LAL deficiency causes expansion of CD11b(+)Gr-1(+) immat
4                                              LAL deficiency impaired T cell development in the thymus
5                                              LAL is encoded by LIPA (10q23.31) and the most common mu
6                                              LAL is the standard reagent to test for endotoxin contam
7                                              LAL overexpression increased levels of BAT free choleste
8                         A mouse model with a LAL null mutation was produced by targeting disruption o
9     Humans and mice with defective or absent LAL activity accumulate large amounts of cholesteryl est
10 clusion, our study demonstrates that adipose LAL drives tissue-cholesterol homeostasis and affects BA
11                                           An LAL null (lal-/-) mouse model closely mimics human WD/CE
12  a result, we identified SAOUHSC_02373 as an LAL with high selectivity for L-aspartate and L-methioni
13 me proliferator-activated receptor gamma, an LAL downstream effector, reduces lal(-/-) Treg and Breg
14 xisome proliferator-activated receptor y, an LAL downstream effector, reduces lal(-/-) Treg and Breg
15              Combined inhibition of ATGL and LAL resulted in large LDs, suggesting that lipolysis tar
16 A and LPS were quantified with LTA-ELISA and LAL assay, respectively.
17 nverge on the same genetic subset of FSB and LAL neurons.
18 , and 30 minutes using limulus lysate assay (LAL) and EndoCAb Ig assays.
19 cid (EDTA); limulus amoebocyte lysate assay (LAL); pertussis toxin (PTX); forward scatter (FSC); Inte
20 ed with the initial refractive target before LAL implantation.
21 ffects BAT metabolism, suggesting beneficial LAL activation in anti-obesity approaches aimed at react
22 stiffness in control strips to levels beyond LAL specimens.
23 emical pathways of nanocrystals generated by LAL, providing a rational guideline for the conscious pr
24                     To test how myeloid cell LAL controls myelopoiesis and lymphopoiesis, a myeloid-s
25                                 Myeloid cell LAL expression improved the proliferation and function o
26 n the thymus, reconstitution of myeloid cell LAL restored development of thymocytes at the double-neg
27  using a commercially available colorimetric LAL assay.
28                          Patients completing LAL-CL01 were eligible to enroll in the extension study
29 sue (ATs), from obese patients has decreased LAL expression compared with that from nonobese people.
30            Lysosomal acid lipase deficiency (LAL-D) is caused by mutations in the LIPA gene, which en
31 o disease formation in various organs during LAL deficiency.
32       rscAAVrh74.LP1.LIPA treatment elevated LAL enzyme activity above wild-type levels in all tissue
33                                    Following LAL, myocardial stresses at given strains and circumfere
34  were found in all ethnic groups, except for LAL in the Kinh and Thai groups, and LP1L in the Tay gro
35        These studies provide feasibility for LAL enzyme therapy in human WD and CESD.
36                   We present a mechanism for LAL inhibition by these compounds whereby LAL transientl
37 cal trials of enzyme replacement therapy for LAL deficiency are currently being developed.
38 elop a curative single-treatment therapy for LAL-D using adeno-associated virus (AAV).
39 tential to be a transformative treatment for LAL-D.
40                                     ECs from LAL-deficient (lal(-/-)) mice possess enhanced prolifera
41  that metabolic reprogramming resulting from LAL deficiency enhances the ability of ECs to stimulate
42                                 Furthermore, LAL-deficient mice challenged with RE gavage exhibited l
43                 On a standard chow diet, hep-LAL-ko mice exhibited increased hepatic CE accumulation
44 ral lipid ester phenotype in livers from hep-LAL-ko mice indicates that LAL is limiting for CE turnov
45 specifically lacking LAL in hepatocytes (hep-LAL-ko).
46 sosome-enriched fractions from livers of hep-LAL-ko mice upon VitA/HFD feeding.
47                              Feeding the hep-LAL-ko mice a vitamin A excess/high-fat diet (VitA/HFD)
48                                To assess how LAL in lung epithelial cells plays a role in this inflam
49               Comparisons of mouse and human LAL genes organization revealed identical intron/exon bo
50 nsgenic system was generated to induce human LAL (hLAL) expression in the lal-/- genetic background u
51         Myeloid-specific expression of human LAL (hLAL) in lal(-/-) mice rescues these malignant phen
52 yte, hepatocyte-specific expression of human LAL (hLAL) in lal(-/-) mice was established by cross-bre
53 epithelial cell-specific expression of human LAL (hLAL) in Lipa(-/-) mice was established by crossbre
54  effects and safety of the recombinant human LAL, sebelipase alfa, nine patients received four once-w
55 py was tested using mannose terminated human LAL expressed in Pichia pastoris (phLAL), purified, and
56 oligosaccharide chains was tested with human LAL expressed in Pichia pastoris (phLAL) and CHO cells (
57 rinsic expression of the lysosomal hydrolase LAL (lysosomal acid lipase) to mobilize FA for FAO and m
58                                           In LAL gene-knockout (lal(-/-)) mice, blockage of cholester
59 ekly infusions (0.35, 1, or 3 mg.kg(-1) ) in LAL-CL01, which is the first human study of this investi
60 e hypothesized that ECs are dysfunctional in LAL-deficient (lal(-/-)) mice.
61  MDSCs or mTOR to rejuvenate EC functions in LAL deficiency-related diseases.
62                   One major manifestation in LAL-deficient (Lipa(-/-)) mice is an increase of tumor g
63 ent, LV stresses and stiffness normalized in LAL specimens and microtubule density following colchici
64       Transaminases decreased in patients in LAL-CL01 and increased between studies.
65  density following colchicine was similar in LAL to control.
66 ceiving ongoing sebelipase alfa treatment in LAL-CL04, the mean +/- standard deviation (SD) decreases
67 t week 12 compared to the baseline values in LAL-CL01 were 46 +/- 21 U/L (-52%) and 21 +/- 14 U/L (-3
68                               Interestingly, LAL-deficient mice exhibited increased RE content in the
69 lysosomal acid lipase (hLAL) expression into LAL gene knockout (lal(-/-)) mice.
70 ly used for endotoxin level determination is LAL (Limulus Amebocyte Lysate) assay.
71                        Mice globally lacking LAL accumulate CE most prominently in the liver.
72 actions from livers of mice globally lacking LAL, we detected residual acid hydrolytic activities aga
73 iver, we generated mice specifically lacking LAL in hepatocytes (hep-LAL-ko).
74 h (LM2W); 7.06 mm for lower anterior length (LAL); 26.87 mm for lower posterior length 1 (LP1L); and
75 igh Risk Adult Acute Lymphoblastic Leukemia [LAL-AR/2003]) assigned adolescent and adult patients (ag
76 ton stage 27 following left atrial ligation (LAL) at stage 21 to reduce LV volume load and create lef
77 ding, CTB) or reduced (left atrial ligation, LAL) hemodynamic loading of the embryonic heart.
78 dulto (GIMEMA) Leucemia Acuta Linfoblastica (LAL) 2317 protocol investigated the frontline chemothera
79                        Our observations link LAL to metabolic reprogramming in lymphocytes and show t
80 ng dependency on lysosomal acid lipase (LIPA/LAL) and the microphthalmia/transcription factor E (MiT/
81                       Lysosomal acid lipase (LAL) cleaves cholesteryl esters and triglycerides to gen
82 lying mechanisms that lysosomal acid lipase (LAL) deficiency causes infiltration of myeloid-derived s
83                       Lysosomal acid lipase (LAL) deficiency causes systemic expansion and infiltrati
84              Of note, lysosomal acid lipase (LAL) deficiency facilitates melanoma growth and metastas
85                       Lysosomal acid lipase (LAL) has been recently identified as a potential therape
86                       Lysosomal acid lipase (LAL) hydrolyzes cholesteryl ester (CE) and retinyl ester
87                       Lysosomal acid lipase (LAL) hydrolyzes cholesteryl esters and triglycerides to
88                       Lysosomal acid lipase (LAL) is a critical lipid hydrolase that generates free f
89                       Lysosomal acid lipase (LAL) is a key enzyme that cleaves cholesteryl esters and
90                       Lysosomal acid lipase (LAL) is essential for the clearance of endocytosed chole
91                       Lysosomal acid lipase (LAL) is essential for the hydrolysis of cholesteryl este
92                       Lysosomal acid lipase (LAL) is essential for the hydrolysis of the triglyceride
93                       Lysosomal acid lipase (LAL) is required for the hydrolysis of intracellular cho
94                       Lysosomal acid lipase (LAL) is the critical enzyme for the hydrolysis of the tr
95                       Lysosomal acid lipase (LAL) is the critical enzyme for the hydrolysis of trigly
96 bsequent lipolysis by lysosomal acid lipase (LAL) was important for the engagement of elevated oxidat
97                       Lysosomal acid lipase (LAL), a key enzyme in the metabolic pathway of neutral l
98 the metabolic role of lysosomal acid lipase (LAL), highly expressed in adipocytes, is unclear.
99 herited deficiency of lysosomal acid lipase (LAL), is an underappreciated cause of progressive liver
100 anscriptional target, lysosomal acid lipase (LAL).
101 deficient activity of lysosomal acid lipase (LAL).
102  lalistat, a specific lysosomal acid lipase (LAL/Lipa) inhibitor on LD degradation in HSCs during act
103         Deficiency of lysosomal acid lipase (LAL; official name Lipa, encoded by Lipa) in mice (lal(-
104 technologies, with laser ablation in liquid (LAL) being a remarkable technique for their synthesis.
105 ovide input from the lateral accessory lobe (LAL) to the noduli (NO).
106 rons in the premotor lateral accessory lobe (LAL), we gained genetic access to a subset of these neur
107  body (FSB), and the lateral accessory lobe (LAL).
108 s we examined neonatal levator auris longus (LAL) and 4th deep lumbrical (4DL) muscles, as well as ad
109 ersus abdominis (TVA), levator auris longus (LAL) and lumbrical muscles were disrupted in both mouse
110                                 In the lung, LAL is highly expressed in alveolar type II epithelial c
111  as assayed in the Limulus amebocyte lysate (LAL) test.
112 parallelization of Limulus amebocyte lysate (LAL)-based bacterial endotoxin testing using centrifugal
113 ility to coagulate Limulus amebocyte lysate (LAL).
114 netic chromogenic limulus amoebocyte lysate (LAL) assay.
115 arboxymethyl-lysine (CML) and lysinoalanine (LAL) contents.
116 dotoxin using the limulus amebocyte lystate (LAL) gel clot method.
117                          Lentiviral-mediated LAL knockdown in the 3T3L1 mouse cell line to mimic the
118          In this study, we found that murine LAL exhibits RE hydrolase activity.
119 zygote knockout mice (lal -/lal-) produce no LAL mRNA, protein or enzyme activity.
120 ctivity assays revealed the existence of non-LAL acid hydrolytic activities for TG and RE.
121                      Interestingly, this non-LAL acid TG hydrolytic activity was elevated in lysosome
122 +/lal- mice have approximately 50% of normal LAL activity and do not show lipid accumulation.
123  NCTC 8325 and its identification as a novel LAL.
124                           Through week 12 of LAL-CL04, these seven patients also showed mean decrease
125    The unparalleled recognition abilities of LAL biosensors perched with remarkable sensitivity, high
126 acological inhibition or genetic ablation of LAL in murine liver largely reduced in vitro acid RE hyd
127                                  Ablation of LAL suppresses immune rejection and allows growth of hum
128 urring in the tested sample upon addition of LAL.
129                     Western blot analysis of LAL embryos showed an increase in both total and polymer
130 e started from the bibliographic analysis of LAL synthesis of Cu-based nanocrystals to identify the r
131                           The coagulation of LAL is commonly used to signal the presence of endotoxin
132         To understand that the expression of LAL mRNA and protein is tissue and cell specifically reg
133                Pharmacological inhibition of LAL in the human hepatocyte cell line HepG2, incubated w
134 mides, esters, and ketones for inhibition of LAL.
135 azole carbamates are effective inhibitors of LAL.
136 oduced system are more than 90% reduction of LAL consumption, from 100 uL/reaction to 9.6 uL/reaction
137            To dissect the functional role of LAL for neutral lipid ester mobilization in the liver, w
138               To test the functional role of LAL in hepatocyte, hepatocyte-specific expression of hum
139 ice provide a model to determine the role of LAL in lipid metabolism and the pathogenesis of its defi
140 also contain retinyl esters (REs), a role of LAL in the clearance of endocytosed REs has not been rep
141     These results indicate a crucial role of LAL-regulated mTOR signaling in the production and funct
142 fied a second population, including a single LAL neuron pair, that bidirectionally regulates ground s
143       Conversely, mice with adipose-specific LAL overexpression (Adpn-rtTA x TetO-hLAL) gained less w
144                         The adipose-specific LAL-overexpressing mouse phenotype depends on the housin
145                         The adipose-specific LAL-overexpressing mouse phenotype depends on the housin
146 only approximately 3%-5% of normally spliced LAL.
147 e eligible to enroll in the extension study (LAL-CL04) in which they again received four once-weekly
148  with a history of laser refractive surgery, LAL implantation and postimplantation adjustment provide
149         These results support a concept that LAL in hepatocytes is a critical metabolic enzyme in con
150         These results support a concept that LAL is a critical metabolic enzyme in lung epithelial ce
151             These observations conclude that LAL-regulated lipid metabolism is essential to maintain
152               These studies demonstrate that LAL in myeloid cells plays a critical role in maintainin
153          These results provide evidence that LAL is an important regulator of myelopoiesis during hem
154                    Our results indicate that LAL has a critical role in regulating MDSCs' ability to
155        In summary, our results indicate that LAL is the major acid RE hydrolase and required for func
156                    Our results indicate that LAL regulates EC functions through interaction with MDSC
157 n livers from hep-LAL-ko mice indicates that LAL is limiting for CE turnover, but not for TG and RE t
158 dial circulating RE content, indicating that LAL is required for efficient nutritional vitamin A avai
159                        Our data suggest that LAL/Lipa is involved in the degradation of a specific pr
160                                          The LAL endotoxin detection limit for samples dispersed in C
161  liposomes, but did not appear to affect the LAL assay sensitivity once the liposomes were completely
162                                 Although the LAL-generated Cu nanocrystals may be present in a range
163 t not DSPG, at 10 mol% further decreased the LAL endotoxin detection limit.
164               Mice double homozygous for the LAL and MMR deficiences (lal-/-;MMR-/-) showed phLAL upt
165                                       In the LAL-deficient (lal(-/-)) mouse model, melanoma metastasi
166 L to consume unpolymerized macromeres in the LAL.
167  ultraviolet light to alter the shape of the LAL and hence its refractive power.
168 solubilization and/or the sensitivity of the LAL assay.
169                 A targeted disruption of the LAL locus produced a null (lal( -/-)) mouse model that m
170 e equation giving the best prediction of the LAL results.
171 tor neurons in the caudal muscle band of the LAL.
172 ents, we applied 2 lock-in treatments to the LAL to consume unpolymerized macromeres in the LAL.
173 ation in HSCs during activation in vitro The LAL inhibitor increased the levels of TAG, cholesteryl e
174 l refractive surgery were implanted with the LAL during cataract surgery performed at a single clinic
175                                   Therefore, LAL, its downstream genes, and lipid mediators all play
176 ral TVA muscle compared with the fast-twitch LAL and lumbrical muscles.
177 ole library of nanomaterials available using LAL, has been until now an empirical endeavor based on c
178 re HPS function relative to controls whereas LAL was associated with delayed conversion to apical ini
179 or LAL inhibition by these compounds whereby LAL transiently carbamoylates the enzyme similarly to pr
180                     LPS were quantified with LAL assay (KQCL test).
181 aching significance (P=0.061) were seen with LAL only.

 
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