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1 mals, likely because of slower liberation of hepatic lipid.
2 tly accentuated the synthesis and storage of hepatic lipid.
3 MTP(-/-)) mice that have low plasma and high hepatic lipids.
4 dicate that Torc1 activation is required for hepatic lipid accumulation across models of NAFLD, and i
5 alpha and TNF-inducible factors that promote hepatic lipid accumulation and ATP depletion.
6                                          The hepatic lipid accumulation and Cd36 induction were also
7 e in mice results in dilated cardiomyopathy, hepatic lipid accumulation and early neonatal death.
8 -mediated regulation of chronic EtOH-induced hepatic lipid accumulation and hepatotoxicity.
9 w a novel mechanism by which miR-24 promotes hepatic lipid accumulation and hyperlipidemia by repress
10 the underlying mechanisms linking obesity to hepatic lipid accumulation and insulin resistance are in
11 itochondrial respiratory complexes promoting hepatic lipid accumulation and insulin resistance.
12 augmented eIF2alpha signaling, together with hepatic lipid accumulation and insulin resistance.
13 his transcription factor as a contributor to hepatic lipid accumulation and insulin resistance.
14 nder ER stress conditions through repressing hepatic lipid accumulation and maintaining lipoprotein s
15 onectin potently protect against HFD-induced hepatic lipid accumulation and preserve insulin sensitiv
16 down of miR-24 in those mice caused impaired hepatic lipid accumulation and reduced plasma triglyceri
17    Furthermore, GRbeta-Ad mice had increased hepatic lipid accumulation and serum triglyceride levels
18 ficient for GSK3alpha had significantly less hepatic lipid accumulation and smaller atherosclerotic l
19                 Prenatal TBT exposure led to hepatic lipid accumulation and up-regulated hepatic expr
20 nce of glucose metabolism and the control of hepatic lipid accumulation by skeletal muscle.
21              Earlier studies have shown that hepatic lipid accumulation can occur after 4 d of a high
22 c steatohepatitis (NASH) is characterized by hepatic lipid accumulation combined with inflammation, w
23              Acute disruption of Vhl induced hepatic lipid accumulation in an HIF-2alpha-dependent ma
24 of FA represents a far greater potential for hepatic lipid accumulation in burn patients than the end
25 lation between miR-27b expression levels and hepatic lipid accumulation in HCV-infected SCID-beige/Al
26                              The decrease in hepatic lipid accumulation in HF-fed itga1(-/-) mice was
27 related factor 2 (Nrf2) being a modulator of hepatic lipid accumulation in models of NAFLD.
28 d levels, and long-term treatments decreased hepatic lipid accumulation in the NAFLD mice.
29 t, hyperglycemic MPCCs displayed significant hepatic lipid accumulation in the presence of insulin, w
30 navir and lopinavir) significantly increased hepatic lipid accumulation in WT mice.
31 er regeneration is impaired in mice in which hepatic lipid accumulation is suppressed by either pharm
32 ciated with obesity and type 2 diabetes, and hepatic lipid accumulation may contribute to insulin res
33                                     However, hepatic lipid accumulation resulted in negligible change
34  and markedly limited insulin resistance and hepatic lipid accumulation that were induced by prolonge
35                                              Hepatic lipid accumulation was associated with increased
36 ein assembly in the liver, the potential for hepatic lipid accumulation was evaluated.
37                                              Hepatic lipid accumulation was significantly reduced in
38 y diminished CGI-58 expression causes severe hepatic lipid accumulation yet paradoxically improves he
39 yte number, adipocyte size, MSC programming, hepatic lipid accumulation, and hepatic gene expression
40 mproved liver dysfunction markers, decreased hepatic lipid accumulation, and inhibited proinflammator
41                                Liver injury, hepatic lipid accumulation, and proinflammatory cytokine
42 of free and mTORC1-associated Raptor governs hepatic lipid accumulation, and uncover the potentially
43   Fish were stained with oil red O to assess hepatic lipid accumulation, and we also performed quanti
44 ion in Pld1(-/-) liver significantly reduced hepatic lipid accumulation, compared with Pld1(-/-) live
45                 These demonstrated increased hepatic lipid accumulation, higher levels of transcripti
46 for the beneficial effects of polyphenols on hepatic lipid accumulation, hyperlipidemia, and atherosc
47 ent of impaired glucose homeostasis, reduces hepatic lipid accumulation, increases white adipose oxid
48 uctose treatment of larval zebrafish induces hepatic lipid accumulation, inflammation, and oxidative
49              Treatment with fructose induced hepatic lipid accumulation, mitochondrial abnormalities,
50 Tgr5 gene in mice alleviated fasting-induced hepatic lipid accumulation.
51 with tunicamycin or valinomycin also induced hepatic lipid accumulation.
52 WAT mass and body weight in association with hepatic lipid accumulation.
53 e investigated HIF-1alpha in alcohol-induced hepatic lipid accumulation.
54 nd fatty acid synthase, as well as increased hepatic lipid accumulation.
55 y of weight gain and adiposity and prevented hepatic lipid accumulation.
56 the actions of GCs in the liver, or enhances hepatic lipid accumulation.
57 Rbeta increases inflammation, which leads to hepatic lipid accumulation.
58 (GH) and its mediator, IGF-1, associate with hepatic lipid accumulation.
59 ury correlated positively with the degree of hepatic lipid accumulation.
60 vity and glucose tolerance without affecting hepatic lipid accumulation.
61 curtail glucose production without promoting hepatic lipid accumulation.
62 lation of Insig1, and subsequently decreased hepatic lipid accumulation.
63 ucose is accompanied by different effects on hepatic lipid anabolism and blood TG profiles.
64 itro and in vivo, correlating with decreased hepatic lipid and cholesterol levels and attenuated live
65  Sirt1LKO mice accumulated larger amounts of hepatic lipid and expressed higher levels of inflammator
66   To examine the role of Them2 in regulating hepatic lipid and glucose homeostasis, we generated Them
67        Bile acids are critical regulators of hepatic lipid and glucose metabolism and signal through
68  evidence for the differential regulation of hepatic lipid and glucose metabolism.
69 ism by which CAR down-regulates key genes in hepatic lipid and glucose metabolism.
70 methionine and choline (controls), levels of hepatic lipid and lipoperoxides were elevated at 3 weeks
71  has been shown to have a major influence on hepatic lipid and lipoprotein metabolism.
72 s may be mediated by the fructose effects on hepatic lipids and ATP levels.
73 d more than 80% accompanied by a decrease in hepatic lipids and ER stress response.
74 ake, energy expenditure, and circulating and hepatic lipids) and glucose metabolism (insulin toleranc
75 sulin sensitivity, tracer incorporation into hepatic lipids, and liver triglyceride export.
76 fed G5G8 KO mice had increased liver weight, hepatic lipids, and plasma alanine aminotransferase comp
77                     The overall secretion of hepatic lipid as VLDL may be regulated by (i) changing t
78 ritional pathway an important contributor to hepatic lipid balance.
79 atory fatty acids and concomitant control of hepatic lipid biosynthesis, secretion, and deposition.
80 reased liver neutral lipids and induction of hepatic lipid biosynthetic genes when fasted.
81 tablish that Sar1B promotes the secretion of hepatic lipids but also adds regulation of cholesterol s
82 iver significantly increases accumulation of hepatic lipids, but reduces plasma TG levels in mice.
83  of the liver, which leads to alterations in hepatic lipid, carbohydrate, protein, lactate, and uric
84                                              Hepatic lipid catabolism begins with the transport of li
85                                  In mammals, hepatic lipid catabolism is essential for the newborns t
86 ob/ob mice, suggesting that rFGF1 stimulates hepatic lipid catabolism.
87 f individual molecular species of most mouse hepatic lipid classes were determined from its chlorofor
88 nd PPARalpha mRNA levels as well as impaired hepatic lipid clearance.
89                                              Hepatic lipid composition and histopathology revealed th
90 ablish L-FABP as an important determinant of hepatic lipid composition and turnover, and (iii) sugges
91 G production, VLDL particle composition, and hepatic lipid composition but selectively enhanced clear
92                      Specific alterations in hepatic lipid composition characterize the spectrum of n
93                     beta-Catenin ASO altered hepatic lipid composition in high-fat-fed mice.
94  multiecho and spectroscopic measurements of hepatic lipid concentration (r(2) = 0.99, P < .001).
95 s likely to have been on the basis increased hepatic lipid content and/or inflammation.
96 to the CNS via osmotic minipumps reduced the hepatic lipid content as assessed by noninvasive (1)H-MR
97                             Metformin lowers hepatic lipid content by activating AMPK, thereby mediat
98                                BPA increased hepatic lipid content concomitant with increased Nrf2 an
99                                    Increased hepatic lipid content is an early correlate of insulin r
100 he individual contributions of ER stress and hepatic lipid content to the pathogenesis of hepatic ins
101                                              Hepatic lipid content was assessed noninvasively in 15 p
102 s used to examine relations between choline, hepatic lipid content, body mass index, glycogen content
103                          BLKO mice had lower hepatic lipid content, increased insulin signaling, and
104 er, both corepressors collaborate to control hepatic lipid content, which likely reflects their coope
105 y and may therefore be predicted to increase hepatic lipid content.
106  mice, which may contribute to the decreased hepatic lipid content.
107 Kalpha negatively regulates ACC activity and hepatic lipid content.
108 H knockout mice display a modest decrease in hepatic lipid contents, but an increase in plasma trigly
109 odel of high-fat feeding was restored by the hepatic lipid control of CNS glycine sensing.
110 get genes and beta-oxidation, which regulate hepatic lipid degradation, were also suppressed in hepat
111 ibition of hepatic mTOR in Am mice increased hepatic lipid deposition and HIRI.
112 py, which additionally led to a reduction in hepatic lipid deposition and improved phosphorylation of
113 ng FADS1 and its polymorphisms in modulating hepatic lipid deposition by altering gene transcription
114 logical liver damage as well as an increased hepatic lipid deposition in double knockout males.
115 in action on glucose metabolism but limiting hepatic lipid deposition.
116 erstanding of the mechanisms by which excess hepatic lipid develops and causes hepatic insulin resist
117 FLD and molecular mechanisms by which excess hepatic lipid develops remain largely unknown.
118 ly Dgat2 ASO treatment significantly reduced hepatic lipids (diacylglycerol and triglyceride but not
119                                         This hepatic lipid droplet accumulation coincides with miR-27
120 pposing effects on the secretion of TRLs and hepatic lipid droplet content.
121 umulation of triglyceride (TG) and PNPLA3 in hepatic lipid droplets (LDs).
122 companied by a 40-fold increase in PNPLA3 on hepatic lipid droplets, with no increase in hepatic PNPL
123 ion of the small GTPase Rac1, which controls hepatic lipid dynamics through ROS-mediated regulation o
124 ring new opportunities to study postprandial hepatic lipid dynamics.
125 r leptin deficiency mediates alcohol-induced hepatic lipid dyshomeostasis, mice were fed alcohol for
126 y acid production and a 2.5-fold increase in hepatic lipid export, both of which explain the reduced
127 the development of fatty liver by modulating hepatic lipid export, uptake, and synthesis, and that th
128 otein (VLDL) formation is the chief route of hepatic lipid export, we hypothesized that the synthesis
129                                              Hepatic lipids extracted from mouse liver, epididymal wh
130                     Despite the reduction in hepatic lipids, fasting glucose and insulin concentratio
131 bsequently to provide a corrected measure of hepatic lipid fraction.
132 ect functional role for both HSL and ATGL in hepatic lipid homeostasis and identifies these enzymes a
133 bolic signals required for the regulation of hepatic lipid homeostasis is complex.
134 se/endoribonuclease, is required to maintain hepatic lipid homeostasis under ER stress conditions thr
135 ggested that CD36 plays an important role in hepatic lipid homeostasis, but the results have been con
136                                      Altered hepatic lipid homeostasis, hepatocellular injury, and in
137 tion and gene expression required for normal hepatic lipid homeostasis.
138 n important role in MAPK-mediated control of hepatic lipid homeostasis.
139 ors known to be involved in VLDL assembly or hepatic lipid homeostasis.
140 derlying these beneficial effects of zinc on hepatic lipid homeostasis.
141 VLDL, respectively, act together to maintain hepatic lipid homeostasis.
142 and Npas2 crosstalk is essential to maintain hepatic lipid homeostasis.
143 CREBH transcriptional activity in regulating hepatic lipid homeostasis.
144 alpha)-regulated genes, and dysregulation of hepatic lipid homeostasis.
145  ER protein-folding environment and maintain hepatic lipid homeostasis.
146 -oxidant conditions that result in increased hepatic lipid hydroperoxide content.
147 d by VO, and there was a trend for increased hepatic lipid in LO and SO diets.
148 e findings suggest that the sequestration of hepatic lipids in perilipin 2-coated droplets ameliorate
149                                              Hepatic lipids including triglyceride, DAGs, and ceramid
150 leading to its breakdown, and thus promoting hepatic lipid infiltration through reduced fatty acid ox
151                                              Hepatic lipids, insulin sensitivity, and hepatic insulin
152 ressing Acc1, Acc2, or both Acc1 and Acc2 on hepatic lipid levels and insulin sensitivity.
153  in mediating the acute effects of leptin on hepatic lipid levels in lean and DIO animals.
154                            In spite of this, hepatic lipid levels were not affected by the nonsheddin
155 inability to produce bile acids, and whereas hepatic lipid levels were significantly increased, circu
156 ce hepatic malonyl-CoA levels in vivo, lower hepatic lipids (long-chain acyl-CoAs, diacylglycerol, an
157 excessive ER stress in response to increased hepatic lipids may decrease the ability of the liver to
158                    In the 25 human subjects, hepatic lipid measured by using HISTO differed significa
159 out mouse model and characterized changes in hepatic lipid metabolism (this report) and bile metaboli
160  homeostasis contributes to dysregulation of hepatic lipid metabolism and contributes to liver-associ
161 ylated FoxO1 in mice (Foxo1(KR/KR)) improves hepatic lipid metabolism and decreases macrophage inflam
162      We propose that deranged intestinal and hepatic lipid metabolism and defective proglucagon gene
163 npoint the key regulatory role of the UPR in hepatic lipid metabolism and demonstrate the potential c
164 HIF-2 functions as an important regulator of hepatic lipid metabolism and identify HIF-2 as a potenti
165 ion was associated with pathways involved in hepatic lipid metabolism and immunological processes.
166  critical role for both PPARalpha and AOX in hepatic lipid metabolism and in the pathogenesis of spec
167                             Abnormalities in hepatic lipid metabolism and insulin action are believed
168 r macrophages in diet-induced alterations in hepatic lipid metabolism and insulin sensitivity, and su
169 l metabolism.HDAC3 is a critical mediator of hepatic lipid metabolism and its loss leads to fatty liv
170 patocytes and contribute to dysregulation of hepatic lipid metabolism and liver disease.
171 l BVRA-GSKbeta-PPARalpha axis that regulates hepatic lipid metabolism and may provide unique targets
172  Thus, we tested the contribution of ATGL to hepatic lipid metabolism and signaling.
173  growth hormone secretion are known to alter hepatic lipid metabolism and to underlie sexually dimorp
174      These data indicate that TAK1 regulates hepatic lipid metabolism and tumorigenesis via the AMPK/
175 andidate gene/miRNA interactions involved in hepatic lipid metabolism and validated their function in
176 dependent protein deacetylase that regulates hepatic lipid metabolism by modifying histones and trans
177  show that retinol saturase is implicated in hepatic lipid metabolism by regulating the activity of t
178 provides new insights into the regulation of hepatic lipid metabolism by the ubiquitin-proteasome sys
179  of cholestasis, Abcb11 KO mice have altered hepatic lipid metabolism coupled with reduced expression
180 chondrial sirtuin SIRT4 in the regulation of hepatic lipid metabolism during changes in nutrient avai
181          We determined the effect of ATF4 on hepatic lipid metabolism in Atf4(-/-) mice fed regular c
182  We sought to determine the role of ACOT1 in hepatic lipid metabolism in C57Bl/6J male mice 1 week af
183 yses to identify alterations in systemic and hepatic lipid metabolism in mice with disruption of the
184 he importance of cell-specific modulation of hepatic lipid metabolism in promoting fibrogenesis in no
185 hat ATF4 plays a critical role in regulating hepatic lipid metabolism in response to nutritional cues
186                      This expression affects hepatic lipid metabolism in these animals and thus provi
187                           Optimal control of hepatic lipid metabolism is critical for organismal meta
188 AFLD, but whether this is causally linked to hepatic lipid metabolism is unclear.
189 etabolic reprogramming, suggesting increased hepatic lipid metabolism prior to overt tumor developmen
190        Moreover, COP1-mediated regulation of hepatic lipid metabolism requires optimum ATGL expressio
191 22-treated mice revealed novel regulators of hepatic lipid metabolism that are responsive to miR-122
192 anscriptional regulatory cascade controlling hepatic lipid metabolism that identifies retinoic acid s
193 PPARs) play major roles in the regulation of hepatic lipid metabolism through the control of numerous
194 ow that in the LHA kappaOR directly controls hepatic lipid metabolism through the parasympathetic ner
195                                              Hepatic lipid metabolism was not stimulated during the a
196                                     Study of hepatic lipid metabolism with respect to the contributio
197 nt may have beneficial effects in regulating hepatic lipid metabolism, adipose tissue function, and i
198  the regulation of appetite and body weight, hepatic lipid metabolism, and fibrosis.
199 sential physiological role in the control of hepatic lipid metabolism, and KOR activation is a permis
200  deacetylase HDAC3 is a critical mediator of hepatic lipid metabolism, and liver-specific deletion of
201  HNF6 and Rev-erbalpha coordinately regulate hepatic lipid metabolism, each factor also affects addit
202 istology, and gene expression for markers of hepatic lipid metabolism, ER stress, and inflammation we
203  In this review, we will discuss the role of hepatic lipid metabolism, genetic background, diet, and
204                                     Study of hepatic lipid metabolism, insulin resistance, mitochondr
205 xpression and its functional implications in hepatic lipid metabolism, particularly in the context of
206 tabolism, but since many genes contribute to hepatic lipid metabolism, we hypothesized that other suc
207            To elucidate the role of ACSL1 in hepatic lipid metabolism, we overexpressed an Acsl1 aden
208 y in the lateral hypothalamic area modulated hepatic lipid metabolism, whereas the specific activatio
209 o define the function of Notch1 signaling in hepatic lipid metabolism, wild type mice and Notch1 defi
210 cyte Shp1 in the regulation of PPARgamma and hepatic lipid metabolism.
211 cal role in HIV PI-induced dys-regulation of hepatic lipid metabolism.
212 ry, and this gene plays an important role in hepatic lipid metabolism.
213 ects on the cell-autonomous clock as well as hepatic lipid metabolism.
214 S), particularly the hypothalamus, regulates hepatic lipid metabolism.
215  fatty acid oxidation, linking chemokines to hepatic lipid metabolism.
216  report a novel role for HIF-2 in regulating hepatic lipid metabolism.
217 nges in the expression of genes required for hepatic lipid metabolism.
218 nship using several murine models of altered hepatic lipid metabolism.
219 r (LXR), a nuclear receptor that coordinates hepatic lipid metabolism.
220      Dietary fatty acid composition modifies hepatic lipid metabolism.
221 ck and functions as a circadian regulator of hepatic lipid metabolism.
222 ceptor (LXR) play key roles in regulation of hepatic lipid metabolism.
223 or two distinct pathways for PUFA control of hepatic lipid metabolism.
224 between protein catabolism, ureagenesis, and hepatic lipid metabolism.
225 te transporter involved in nutrient flux and hepatic lipid metabolism.
226 uggests several new miRNAs are regulators of hepatic lipid metabolism.
227 lucidate the role of tribbles-1 in mammalian hepatic lipid metabolism.
228 ifferent enzymatic hydrolyzation methods, on hepatic lipid metabolism.
229 ts functional involvement in fasting-induced hepatic lipid metabolism.
230  action of GH is due to direct regulation of hepatic lipid metabolism.
231 ulin action is required for FGF21 to control hepatic lipid metabolism.
232 as srebp-1 and lxralpha, major regulators of hepatic lipid metabolism.
233 rget gene and demonstrate its involvement in hepatic lipid metabolism.
234 high-fat (AHF) diet, massive accumulation of hepatic lipid metabolites and significant increase in pl
235  a role for OSA in inducing abnormalities in hepatic lipid-metabolizing enzymes, endothelial dysfunct
236 le MR spectroscopic sequence for quantifying hepatic lipid noninvasively.
237                     By concurrently lowering hepatic lipid overloading as well as susceptibility of h
238                                              Hepatic lipid overloading mainly in the form of triglyce
239   However, the effect of Notch1 signaling on hepatic lipid oxidation has not yet been directly invest
240                                  To increase hepatic lipid oxidation in the presence of glucose, we p
241 hanol exposure caused a >20-fold increase in hepatic lipids, peaking 12 hours after administration.
242                                Elevations in hepatic lipid peroxidation and CYP2E1 expression that ar
243 urinary dicarboxylic acid excretion; and (5) hepatic lipid peroxidation by immunohistochemical staini
244 vs. 22.0 +/- 3.5%, P = 0.006), and increased hepatic lipid peroxidation compared to the HCR.
245        After liver radiation or cholic acid, hepatic lipid peroxidation levels increased, indicating
246                                              Hepatic lipid peroxidation was also elevated in the nose
247                                The amount of hepatic lipid peroxidation was also significantly decrea
248 acetyl coA oxidase messenger RNA involved in hepatic lipid peroxidation were also markedly increased
249 cohol-induced elevation of plasma endotoxin, hepatic lipid peroxidation, and inhibited TNF-alpha prod
250 tic glutathione concentrations and increased hepatic lipid peroxidation, and the concentrations of li
251  but significantly inhibited alcohol-induced hepatic lipid peroxidation, TNF-alpha production and ste
252 ation with increases in plasma endotoxin and hepatic lipid peroxidation.
253 mature HDL particles by direct lipidation of hepatic lipid-poor apoA-I, slowing its catabolism by the
254 age, or transcription of genes that regulate hepatic lipid processing.
255 gs are that FoxO1 protects against excessive hepatic lipid production during hyperglycemia and that i
256             We sought to further analyze the hepatic lipid profile of these mice by electrospray ioni
257 and show enhanced ethanol clearance, altered hepatic lipid profiles in favor of increased levels of p
258 ed peroxynitrite drove TLR4 recruitment into hepatic lipid rafts and inflammation, whereas the in viv
259  Toll-like receptor (TLR)-4 recruitment into hepatic lipid rafts in nonalcoholic steatohepatitis (NAS
260  liver identifying the role of iPLA2gamma in hepatic lipid second messenger production.
261 on of CAV1 in mice is required for efficient hepatic lipid storage during fasting, liver regeneration
262             MCD feeding triggered steatosis, hepatic lipid storage, and accumulation of free fatty ac
263    Saturated fat ingestion rapidly increases hepatic lipid storage, energy metabolism, and insulin re
264 ing secretion of triglyceride, liver weight, hepatic lipid storage, or transcription of genes that re
265 nd -AII, as well as a sharp depletion of the hepatic lipid stores was also found in PPARbeta-null mic
266 sduction pathways by which insulin regulates hepatic lipid synthesis and degradation remain largely u
267                                              Hepatic lipid synthesis is known to be regulated by food
268 ut its contribution to insulin AKT-regulated hepatic lipid synthesis is unclear.
269 t miR-30c mimic significantly down-regulated hepatic lipid synthesis pathways.
270 ipoprotein levels, in addition to decreasing hepatic lipid synthesis through direct targeting of lyso
271 ce that SCAP and the SREBPs are required for hepatic lipid synthesis under basal and adaptive conditi
272 ulin resistance, because the major source of hepatic lipid synthesis, esterification of preformed fat
273 mbination of increased peripheral lipolysis, hepatic lipid synthesis, loss of hepatoprotective mediat
274 ed capacity to burn fat and suppress de novo hepatic lipid synthesis.
275  fatty liver and dyslipidemia with increased hepatic lipid synthesis/flux associated with elevated he
276 nuclear hormone receptor with known roles in hepatic lipid transport.
277                In addition, the pathways for hepatic lipid uptake and lipogenic program are also down
278 ulation of hepatic TH signaling or decreased hepatic lipid utilization.
279                   Elevated futile cycling of hepatic lipids was also observed.
280  tomography-based method for measurements of hepatic lipids, we resolved the temporal events taking p
281 rstand the role of AMPK in the regulation of hepatic lipids, we studied the effect of metformin on AM
282                                              Hepatic lipids were quantified by capillary gas chromato
283 MET properties and decreased circulating and hepatic lipids when orally administered to dyslipidemic

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